Category Archives: Dr. Robert O. Young

Using Alkalizing Herbs in the Prevention, Treatment and Reversal of Any Cancerous Condition

Dr. Robert O. Young MSc., DSc., Ph.D, ND

“The cure for cancer is found in its prevention NOT in its treatment”  Dr. Robert O. Young

Abstract

An anti-cancer lifestyle and diet is an important strategy you can use to reduce your risk for ANY cancerous condition. The American Cancer Society recommends, for example, that you eat at least five servings of fruit and vegetables daily and eat the right amount of (alkaline) food to stay at a healthy weight. In addition, researchers are finding that certain plant foods or herbs may be particularly useful in protecting and reversing many cancerous condition. The following article covers several of these medicinal herbs and their benefits in the prevention and treatment of brain cancer, lung cancer, breast cancer,  blood cancers,  prostate cancer, oral cancer, liver cancer thyroid cancer, kidney cancer, bowel cancer, stomach cancer, skin cancer and pancreatic cancer.

[Key words; cancer, chemotherapy, herbs, spices, natural cancer treatments, garlic, turmeric, ginger, cayenne, alkalizing, liver disease, oral cancer, prostate cancer, blood cancer, breast cancer, thyroid cancer, stomach cancer, skin cancer, pancreatic cancer, lung cancer, bowel cancer]

Introduction

Make room in your diet for the following foods and drinks to prevent cancer.  Why?  Because an ounce of prevention is worth more than a pound of cure.  The following are eleven herbs or spices that have been shown to be effective in the prevention, treatment and reversal of many cancerous conditions.

Garlic

[Figure 1: Cloves of garlic]

Several large studies have found that those who eat more garlic are less likely to develop various kinds of cancer, especially in digestive organs such as the esophagus, stomach, and colon. Ingredients in the pungent bulbs may keep cancer-causing substances in your body from working, or they may keep cancer cells from multiplying. I recommend a clove a day may be helpful.[1=22 ]

Cayenne Pepper

Most people know cayenne pepper for its spice. But it is actually an extraordinarily strong antioxidant and vaso-dialator. Studies have shown that by consuming cayenne pepper is highly alkaline and a powerful buffer of dietary and metabolic acids that cause cells to become cancerous. If you consume it regularly you can neutralize the acids that cause body cells to become cancerous.[23-29 ]

{Figure 2: Cyenne pepper]

Milk Thistle

Milk thistle is a crucial plant when it comes to liver health and cancer prevention. Milk thistle and the seeds from the plant can be used to eliminate acidic toxins that can bind to the liver, causing damage to the liver setting the stage for a cancerous condition. It protects the alkaline interstitial fluids that surround every body cell protecting them and indirectly preventing the formation of tumors, calcifications and/or cysts which make milk thistle a powerful antioxidant in the chelation of dietary and/or metabolic acids that cause cancer.[30-64 ]

[Figure 3: Milk Thistle]

Turmeric

 [Figure 4: Turmeric root and spice]

This orange-colored spice, a staple in Indian curries, contains an ingredient called curcumin (not the same as cumin) that might be useful in reducing cancer risk. According to the American Cancer Society, curcumin can inhibit some kinds of cancer cells in laboratory studies and slow the spread of cancer or shrink tumors in some animals. Turmeric is easy to find in grocery stores, and you can use it in a variety of recipes.[65-130 ]

Bloodroot

Bloodroot is actually used in a medicine for treating cancer named Black Salve. You can use bloodroot on its own, because it has been shown in tests to be effective in shrinking of tumors.[131-159]

[Figure 5: Bloodroot plant and flower]

Feverfew

Feverfew was used in a study at a university in New York. The study found that it was great at killing off leukemia cells, even better than the actual cancer medication.[160-191]

[Figure 6: Feverfew plant and flower]

Wheatgrass

Consuming one tiny glass of wheatgrass a day either orally or even-better rectally has shown to dramatically increase the health of cancer patients and non-cancer patients alike. It is particularly useful for people who are suffering from the side effects of chemotherapy. It will help purify the blood from dietary and/or metabolic acids, improve blood and lymph circulation, increase the oxygen levels in the microenvironments, and help the body repair and continue to reduce acids loads in the extracellular fluids, interstitial fluids and intracellular fluids to prevent and/or reverse and spoiling of the body cells.[192-204]

[Figure 7: Wheatgrass}

Ruscus Aculeatus

This herb is always known as Butchers Broom and it is great at fighting cancer due to its active ingredient, ruscogenins. The active ingredient has been proven to shrink tumors and increase the cancer fighting cells in the body.[205-221 ]

[Figure 8: Ruscus Aculeatus or Butchers Broom]

Sheep’s Sorrell

Sheep’s Sorrell can be used in people who are suffering the harmful effects of cancer medications. It helps the tissues rebuild and get back to the condition that they were in before the cancer and medication to use it was introduced. Some have suggested that it can be used to ward off cancer cells and keep them from growing.[222-224]

[Figure 9: Sheep’s Sorrel}

Astragalus

This herb is grown in China and has been proven to help with cancer on a couple of different levels. First it boosts your body’s immune system, which in turn helps it identify cancer cells. A study showed that cancer patients who took this herb survived twice as long.[225-250 ]

[Figure 10: Astragalus}

Ginger


[Figure 11: Ginger root]

A new study reveals ginger contains a pungent compound that could be up to 10,000 times more effective than conventional chemotherapy in targeting the cancer stem cells at the root of cancer malignancy. [251]

[Figure 12: Research Shows The Efficacy of Ginger Root as a non-toxic form of chemotherapy]

The authors of the study further affirm these points:

“Cancer stem cells pose serious obstacle to cancer therapy as they can be responsible for poor prognosis and tumour relapse. To add into the misery, very few chemotherapeutic compounds show promise to kill these cells. Several researchers have shown that cancer stem cells are resistant to paclitaxel, doxorubicin, 5-fluorouracil, and platinum drugs [8, 16]. CSCs are thus an almost unreachable population in tumours for chemotherapy. Therefore any compound, that shows promise towards cancer stem cells, is a highly desirable step towards cancer treatment and should be followed up for further development.”

The researchers identified a variety of ways by which 6-shagoal targets breast cancer:

  • It reduces the expression of CD44/CD24 cancer stem cell surface markers in breast cancer spheroids (3-dimensional cultures of cells modeling stem cell like cancer)
  • It significantly affects the cell cycle, resulting in increased cancer cell death
  • It induces programmed cell death primarily through the induction of autophagy, with apoptosis a secondary inducer
  • It inhibits breast cancer spheroid formation by altering Notch signaling pathway through γ-secretase inhibition.
  • It exhibits cytotoxicity (cell killing properties) against monolayer (1-dimensional cancer model) and spheroid cells (3-dimensional cancer model)

It was in evaluating the last mode of 6-shagoal’s chemotherapeutic activity and comparing it to the activity of the conventional chemotherapeutic agent taxol that the researchers discovered an astounding difference. Whereas taxol exhibited clear cytotoxicity in the one-dimensional (flat) monolayer experimental model, it had virtually no effect on the spheroid model, which is a more “real world” model reflecting the 3-dimensionality of tumors and their stem cell subpopulations. Amazingly, this held true even when the concentration of taxol was increased by four orders of magnitude:

 “In contrast [to 6-shagoal], taxol, even though was highly active in monolayer cells, did not show activity against the spheroids even at 10000 fold higher concentration compared to 6-shogoal.”

This is a highly significant finding, as it affirms a common theme in cancer research that acknowledges the primarily role of cancer stem cells: namely, while conventional techniques like surgery, radiation, and chemotherapy are effective at reducing a tumor’s size, sometimes to the point where it is “debulked,” burned,” or “poisoned” out of the body even below the threshold of re-detection, the appearance of “winning the battle” often comes at a steep price, as ultimately the cancer stem cell population regrows the tumors, now with increased vengeance and metastastic invasiveness, resulting in the cancer “winning the war.”

The monolayer model, which does not account for the complex immunity of actual cancer stem-cell based tumors against chemoagents like taxol, represents the old preclinical model of testing cancer treatments. The spheroid model, on the other hand, clearly shows that even 10,000 times higher concentrations of taxol are not capable of beating this ginger component at selectively targeting the root cause of the tumor malignancy.

In their concluding remarks, the authors point out a hugely important distinction between natural anti-cancer agents and conventional ones that have only been introduced in the past half century or so, namely, “Dietary compounds are welcome options for human diseases due to their time-tested acceptability by human bodies.”  

Unlike modern synthetically produced and patented chemicals, ginger, curcumin, garlic, and hundreds of other compounds naturally found in the human diet, have been “time-tested” as acceptable to the human body in the largest and longest running “clinical trials” known: the tens of thousands of years of direct human experience, spanning thousands of different cultures from around the world, that constitute human prehistory. These experientially-based “trials” are validated not by RCTs, or a peer-reviewed publication process, but by the fact that we all made it through this incalculably vast span of time to be alive here today. Consider also that if our ancestors made the wrong dietary choice by simply mistaking an edible berry for a poisonous one, the consequences could be deadly. This places even greater emphasis on how the “time testing” of dietary compounds was not an academic but a life-death affair, and by implication, how the information contained within various cultural traditions as “recipes” passed down from generation to generation are “epigenetic inheritance systems” no less important to our health and optimal gene expression as the DNA in our own bodies.

Ultimately, this new study adds to a growing body of research indicating that cancer stem cell targeting approaches using natural substances present in the human diet for thousands of years are far superior than chemotherapy and radiation, both of which actually increase the relative populations of cancer stem cells versus non-tumorigenic ones.[251]

Cannabis

[Figure 11: Cannabis plant with buds]

Cannabis has been making a lot of noise lately. Multiple states across the United States and countries around the world have successfully legalized medical Marijuana, and the Uruguay parliament recently voted to create the world’s first legal marijuana market.[252-256] This is good news as the health benefits of Cannabis are vast, with multiple medical and scientific studies that confirm them. On the other hand, arguments against the use of marijuana is usually published in Psychiatric journals, which show no scientific evidence that Cannabis is harmful to human health. All psychological evaluations from the intake of cannabis are largely based on assumptions, suggestions and observations (257). When we look at the actual science behind Cannabis, the health benefits can be overwhelming. So what does one who opposes the use of cannabis base their belief on? Nothing, not scientific evidence anyways. The negative stigmatism attached to marijuana is due to it’s supposed psychotropic effects, yet again, there is no scientific evidence to show that marijuana has any psychotropic effects. Nonetheless, cannabis has recently been the focus of medical research and considered as a potential therapeutic treatment and cure for cancer.Cannabis is a great example of how the human mind is programmed and conditioned to believe something. Growing up, we are told drugs are bad, which is true, however not all substances that have been labelled as “drugs” by the government are harmful. Multiple substances are labelled as a “drug” in order to protect corporate interests. One example is the automobile and energy industry, a car made from hemp is stronger than steel, and can be fuelled from hemp alone. Henry Ford demonstrated this many years ago. Hemp actually has over 50,000 uses![258]Let’s take a look at the science behind Cannabis and Cancer. Although Cannabis has been proven to be effective for a large range of ailments, this article will focus mainly on it’s effectiveness in the treatment of cancer. Cannabinoids may very well be one of the best disease and cancer fighting treatments out there. Cannabinoids refer to any of a group of related compounds that include cannabinol and the active constituents of cannabis. They activate cannabinoid receptors in the body. The body itself produces compounds called endocannabinoids and they play a role in many processes within the body that help to create a healthy environment. Cannabinoids also play a role in immune system generation and re-generation. The body regenerates best when it’s saturated with Phyto-Cannabinoids. Cannabinoids can also be found in Cannabis. It is important to note that the cannabinoids are plentiful in both hemp and cannabis. One of the main differentiations between hemp and cannabis is simply that hemp only contains 0.3% THC while cannabis is 0.4% THC or higher. (Technically they are both strains of Cannabis Sativa.)  Cannabinoids have been proven to reduce cancer cells as they have a great impact on the rebuilding of the immune system. While not every strain of cannabis has the same effect, more and more patients are seeing success in cancer reduction in a short period of time by using cannabis.While taking a look at these studies, keep in mind that cannabis can be much more effective for medicinal purposes when we eat it rather than smoking it. Below are 20 medical studies that prove cannabis can be an effective treatment and possible cure for cancer.[ [259-288] Please keep in mind that this is a very short list of studies that support the use of medicinal marijuana. Please feel free to further your research, hopefully this is a good starting point.

Brain Cancer

A study published in the British Journal of Cancerconducted by the Department of Biochemistry and Molecular Biology at Complutense University in Madrid, this study determined that Tetrahydrocannabinol (THC) and other cannabinoids inhibit tumour growth. They were responsible for the first clinical study aimed at assessing cannabinoid antitumoral action. Cannabinoid delivery was safe and was achieved with zero psychoactive effects. THC was found to decrease tumour cells in two out of the nine patients.[289]A study published in The Journal of Neuroscience examined the biochemical events in both acute neuronal damage and in slowly progressive, neurodegenerative diseases. They conducted a magnetic resonance imaging study that looked at THC (the main active compound in marijuana) and found that it reduced neuronal injury in rats. The results of this study provide evidence that the cannabinoid system can serve to protect the brain against neurodegeneration.[290]A study published in The Journal of Pharmacology And Experimental Therapeutics already acknowledged the fact that cannabinoids have been shown to possess antitumor properties. This study examined the effect of cannabidiol (CBD, non psychoactive cannabinoid compound) on human glioma cell lines. The addition of cannabidiol led to a dramatic drop in the viability of glioma cells. Glioma is the word used to describe brain tumour.  The study concluded that cannabidiol was able to produce a significant antitumor activity.[291]A study published in the journal Molecular Cancer Therapeutics outlines how brain tumours are highly resistant to current anticancer treatments, which makes it crucial to find new therapeutic strategies aimed at improving the poor prognosis of patients suffering from this disease. This study also demonstrated the reversal of tumour activity in Glioblastoma multiforme.[292]

Breast Cancer

A study published in the US National Library of Medicine, conducted by the California Pacific Medical Centre determined that cannabidiol (CBD) inhibits human breast cancer cell proliferation and invasion. They also demonstrated that CBD significantly reduces tumour mass.[293]A study published in The Journal of Pharmacology and Experimental Therapeutics determined that THC as well as cannabidiol dramatically reduced breast cancer cell growth. They confirmed the potency and effectiveness of these compounds.[294]A study published in the Journal Molecular Cancer showed that THC reduced tumour growth and tumour numbers. They determined that cannabinoids inhibit cancer cell proliferation, induce cancer cell apoptosis and impair tumour angiogenesis (all good things). This study provides strong evidence for the use of cannabinoid based therapies for the management of breast cancer.[295]A study published in the Proceedings of the National Academy of Sciences of the United States of America (PNAS) determined that cannabinoids inhibit human breast cancer cell proliferation.[296]

Lung Cancer

A study published in the journal Oncogeneby Harvard Medical Schools Experimental Medicine Department determined that THC inhibits epithelial growth factor induced lung cancer cell migration and more. They go on to state that THC should be explored as novel therapeutic molecules in controlling the growth and metastasis of certain lung cancers.[297 ]A study published by the US National Library of Medicine by the Institute of Toxicology and Pharmacology, from the Department of General Surgery in Germany determined that cannabinoids inhibit cancer cell invasion. Effects were confirmed in primary tumour cells from a lung cancer patient.  Overall, data indicated that cannabinoids decrease cancer cell invasiveness.[298 ]A study published by the US National Library of Medicine, conducted by Harvard Medical School investigated the role of cannabinoid receptors in lung cancer cells. They determined its effectiveness and suggested that it should be used for treatment against lung cancer cells.[299 ]

Prostate Cancer

A study published in the US National Library of Medicine illustrates a decrease in prostatic cancer cells by acting through cannabinoid receptors.[300]A study published in the US National Library of Medicine outlined multiple studies proving the effectiveness of cannabis on prostate cancer.[301]Another study published by the US National Library of Medicine determined that clinical testing of CBD against prostate carcinoma is a must. That cannabinoid receptor activation induces prostate carcinoma cell apoptosis. They determined that cannabidiol significantly inhibited cell viability.[302]

Blood Cancer

A study published in the journal Molecular Pharmacology recently showed that cannabinoids induce growth inhibition and apoptosis in matle cell lymphoma. The study was supported by grants from the Swedish Cancer Society, The Swedish Research Council and the Cancer Society in Stockholm.[303]A study published in the International Journal of Cancer also determined and illustrated that cannabinoids exert antiproliferative and proapoptotic effects in various types of cancer and in mantle cell lymphoma.[304]A study published in the US National Library of Medicine conducted by the Department of Pharmacology and Toxicology by Virginia Commonwealth University determined that cannabinoids induce apoptosis in leukemia cells.[305]

Oral Cancer

A study published by the US National Library of Medicine results show cannabinoids are potent inhibitors of cellular respiration and are toxic to highly malignant oral Tumours. [306]

Liver Cancer

A study published by the US National Library of Medicine determined that that THC reduces the viability of human HCC cell lines (Human hepatocellular liver carcinoma cell line) and reduced the growth.[307]

Pancreatic Cancer

A study published in The American Journal of Cancer determined that cannabinoid receptors are expressed in human pancreatic tumor cell lines and tumour biopsies at much higher levels than in normal pancreatic tissue. Results showed that cannabinoid administration induced apoptosis. They also reduced the growth of tumour cells, and inhibited the spreading of pancreatic tumour cells.[308]

Conclusion

According to a 2004 report by Morgan, Ward, and Barton: “The contribution of cytotoxic chemotherapy to 5-year survival in adult malignancies. … survival in adults was estimated to be 2.3% in Australia and 2.1% in the USA.”Jun 16, 2014[309]

Medical oncologists are a long way from using medicinal herbs as an alternative or primary treatment for cancer.  The research is significant and shows that the medicinal herbs discussed in this article are extraordinary plants and have shown excellent results in the prevention, treatment and reversal of many cancerous conditions.

References:

  1. Milner JA. Garlic: Its anticarcinogenic and antitumorigenic properties. Nutrition Reviews1996; 54:S82–S86.
  2. Ross SA, Finley JW, Milner JA. Allyl sulfur compounds from garlic modulate aberrant crypt formation. Journal of Nutrition 2006; 136(3 Suppl):852S–854S.
  3. Amagase H, Petesch BL, Matsuura H, Kasuga S, Itakura Y. Intake of garlic and its bioactive components. Journal of Nutrition 2001; 131(3s):955S–962S.
  4. Amagase H. Clarifying the real bioactive constituents of garlic. Journal of Nutrition 2006; 136(3 Suppl):716S–725S.
  5. Fleischauer AT, Arab L. Garlic and cancer: A critical review of the epidemiologic literature. Journal of Nutrition 2001; 131(3s):1032S–1040S.
  6. Gonzalez CA, Pera G, Agudo A, et al. Fruit and vegetable intake and the risk of stomach and oesophagus adenocarcinoma in the European Prospective Investigation into Cancer and Nutrition (EPIC-EURGAST). International Journal of Cancer 2006; 118(10): 2559–2566.
  7. Steinmetz KA, Kushi LH, Bostick RM, Folsom AR, Potter JD. Vegetables, fruit, and colon cancer in the Iowa Women’s Health Study. American Journal of Epidemiology 1994; 139(1):1–15.
  8. Gao CM, Takezaki T, Ding JH, Li MS, Tajima K. Protective effect of allium vegetables against both esophageal and stomach cancer: A simultaneous case-referent study of a high-epidemic area in Jiangsu Province, China. Japanese Journal of Cancer Research1999; 90(6):614–621.
  9. Setiawan VW, Yu GP, Lu QY, et al. Allium vegetables and stomach cancer risk in China. Asian Pacific Journal of Cancer Prevention 2005; 6(3):387–395.
  10. Hsing AW, Chokkalingam AP, Gao YT, et al. Allium vegetables and risk of prostate cancer: A population-based study. Journal of the National Cancer Institute 2002; 94(21):1648–1651.
  11. Chan JM, Wang F, Holly EA. Vegetable and fruit intake and pancreatic cancer in a population-based case-control study in the San Francisco bay area. Cancer Epidemiology Biomarkers & Prevention 2005; 14(9):2093–2097.
  12. Challier B, Perarnau JM, Viel JF. Garlic, onion and cereal fibre as protective factors for breast cancer: A French case-control study. European Journal of Epidemiology 1998; 14(8):737–747.
  13. Li H, Li HQ, Wang Y, et al. An intervention study to prevent gastric cancer by micro-selenium and large dose of allitridum. Chinese Medical Journal (English) 2004; 117(8):1155–1160.
  14. You WC, Brown LM, Zhang L, et al. Randomized double-blind factorial trial of three treatments to reduce the prevalence of precancerous gastric lesions. Journal of the National Cancer Institute 2006; 98(14):974–983.
  15. Tanaka S, Haruma K, Kunihiro M, et al. Effects of aged garlic extract (AGE) on colorectal adenomas: A double-blinded study. Hiroshima Journal of Medical Sciences 2004; 53(3–4):39–45.
  16. Tilli CM, Stavast-Kooy AJ, Vuerstaek JD, et al. The garlic-derived organosulfur component ajoene decreases basal cell carcinoma tumor size by inducing apoptosis. Archives of Dermatological Research 2003; 295(3):117–123.
  17. Ruddock PS, Liao M, Foster BC, et al. Garlic natural health products exhibit variable constituent levels and antimicrobial activity against Neisseria gonorrhoeae, Staphylococcus aureus and Enterococcus faecalis. Phytotherapy Research 2005; 19(4):327–334.
  18. Shenoy NR, Choughuley AS. Inhibitory effect of diet related sulphydryl compounds on the formation of carcinogenic nitrosamines. Cancer Letters 1992; 65(3):227–232.
  19. Milner JA. Mechanisms by which garlic and allyl sulfur compounds suppress carcinogen bioactivation. Garlic and carcinogenesis. Advances in Experimental Medicine and Biology2001; 492:69–81.
  20. L’vova GN, Zasukhina GD. Modification of repair DNA synthesis in mutagen-treated human fibroblasts during adaptive response and the antimutagenic effect of garlic extract. Genetika 2002; 38(3):306–309.
  21. Boon H, Wong J. Botanical medicine and cancer: A review of the safety and efficacy. Expert Opinion on Pharmacotherapy 2004; 5(12):2485–2501.
  22. Piscitelli SC, Burstein AH, Welden N, Gallicano KD, Falloon J. The effect of garlic supplements on the pharmacokinetics of saquinavir. Clinical Infectious Diseases 2002; 34(2):234–238.Athanasiou A., et al. Vanilloid receptor agonists and antagonists are mitochondrial inhibitors: how vanilloids cause non-vanilloid receptor mediated cell death. Biochem Biophys Res Commun 2007 Mar 2; 354(1): 50-55.
  23. Athanasiou A., et al. Vanilloid receptor agonists and antagonists are mitochondrial inhibitors: how vanilloids cause non-vanilloid receptor mediated cell death.  2007 Mar 2; 354(1): 50-55.
  24. Christensen, Jon. (December 12, 2005). Retrieved from The New York Times. Scientist at work: John Reed; running hot in pursuit of cancer treatment).
  25. Hu, Janny.  (October 12, 2004). Lakers Suite Tomjanovich to a T. San Francisco Chronicle on The Web. Retrieved from http://www.sfgate.com/sports/article/Lakers-suit-coach-Tomjanovich-to-a-T-2641695.php.
  26. Mori, Akio, et al. (March 15, 2006). Capsaicin, A Component of Red Peppers, Inhibits The Growth of Androgen-Independent, p53 Mutant Prostate Cancer Cells. American Association of Cancer Research.
  27. Samid, Dvorit. (1997). Compositions and methods for treating and preventing pathologies including cancer. The USA Dept. of HHS; pg. 56.
  28. Sanchez AM et al. Apoptosis induced by capsaicin in prostate PC-3 cells involves ceramide accumulation, neutral sphingomyelinase, and JNK activation. Apoptosis 2007; 12(11): 2013-24.
  29. Thoennissen NH, O’Kelly J, Lu D, et al. Capsaicin causes cell-cycle arrest and apoptosis in ER-positive and -negative breast cancer cells by modulating the EGFR/HER-2 pathway. Oncogene. 2010, Jan 14;29(2):285-96.  
  30. PDR® for Herbal Medicines™. 2nd ed. Montvale, NJ: Medical Economics, 2000.
  31. Lee DY, Liu Y: Molecular structure and stereochemistry of silybin A, silybin B, isosilybin A, and isosilybin B, Isolated from Silybum marianum (milk thistle). J Nat Prod 66 (9): 1171-4, 2003. [PUBMED Abstract]
  32. Napolitano JG, Lankin DC, Graf TN, et al.: HiFSA fingerprinting applied to isomers with near-identical NMR spectra: the silybin/isosilybin case. J Org Chem 78 (7): 2827-39, 2013. [PUBMED Abstract]
  33. Hruby K, Csomos G, Fuhrmann M, et al.: Chemotherapy of Amanita phalloides poisoning with intravenous silibinin. Hum Toxicol 2 (2): 183-95, 1983. [PUBMED Abstract]
  34. Wagner H, Hörhammer L, Münster R: [On the chemistry of silymarin (silybin), the active principle of the fruits from Silybum marianum (L.) Gaertn. (Carduus marianus L.)] Arzneimittelforschung 18 (6): 688-96, 1968. [PUBMED Abstract]
  35. Campos R, Garrido A, Guerra R, et al.: Silybin dihemisuccinate protects against glutathione depletion and lipid peroxidation induced by acetaminophen on rat liver. Planta Med 55 (5): 417-9, 1989. [PUBMED Abstract]
  36. Farghali H, Kameniková L, Hynie S, et al.: Silymarin effects on intracellular calcuim and cytotoxicity: a study in perfused rat hepatocytes after oxidative stress injury. Pharmacol Res 41 (2): 231-7, 2000. [PUBMED Abstract]
  37. Lettéron P, Labbe G, Degott C, et al.: Mechanism for the protective effects of silymarin against carbon tetrachloride-induced lipid peroxidation and hepatotoxicity in mice. Evidence that silymarin acts both as an inhibitor of metabolic activation and as a chain-breaking antioxidant. Biochem Pharmacol 39 (12): 2027-34, 1990. [PUBMED Abstract]
  38. Zhao J, Agarwal R: Tissue distribution of silibinin, the major active constituent of silymarin, in mice and its association with enhancement of phase II enzymes: implications in cancer chemoprevention. Carcinogenesis 20 (11): 2101-8, 1999. [PUBMED Abstract]
  39. Valenzuela A, Guerra R, Videla LA: Antioxidant properties of the flavonoids silybin and (+)-cyanidanol-3: comparison with butylated hydroxyanisole and butylated hydroxytoluene. Planta Med (6): 438-40, 1986. [PUBMED Abstract]
  40. Valenzuela A, Guerra R, Garrido A: Silybin dihemisuccinate protects rat erythrocytes against phenylhydrazine-induced lipid peroxidation and hemolysis. Planta Med 53 (5): 402-5, 1987. [PUBMED Abstract]
  41. Valenzuela A, Aspillaga M, Vial S, et al.: Selectivity of silymarin on the increase of the glutathione content in different tissues of the rat. Planta Med 55 (5): 420-2, 1989. [PUBMED Abstract]
  42. Mira ML, Azevedo MS, Manso C: The neutralization of hydroxyl radical by silibin, sorbinil and bendazac. Free Radic Res Commun 4 (2): 125-9, 1987. [PUBMED Abstract]
  43. Mira L, Silva M, Manso CF: Scavenging of reactive oxygen species by silibinin dihemisuccinate. Biochem Pharmacol 48 (4): 753-9, 1994. [PUBMED Abstract]
  44. Koch HP, Löffler E: Influence of silymarin and some flavonoids on lipid peroxidation in human platelets. Methods Find Exp Clin Pharmacol 7 (1): 13-8, 1985. [PUBMED Abstract]
  45. Garrido A, Arancibia C, Campos R, et al.: Acetaminophen does not induce oxidative stress in isolated rat hepatocytes: its probable antioxidant effect is potentiated by the flavonoid silybin. Pharmacol Toxicol 69 (1): 9-12, 1991. [PUBMED Abstract]
  46. Bosisio E, Benelli C, Pirola O: Effect of the flavanolignans of Silybum marianum L. on lipid peroxidation in rat liver microsomes and freshly isolated hepatocytes. Pharmacol Res 25 (2): 147-54, 1992 Feb-Mar. [PUBMED Abstract]
  47. Altorjay I, Dalmi L, Sári B, et al.: The effect of silibinin (Legalon) on the the free radical scavenger mechanisms of human erythrocytes in vitro. Acta Physiol Hung 80 (1-4): 375-80, 1992. [PUBMED Abstract]
  48. El-Shitany NA, Hegazy S, El-Desoky K: Evidences for antiosteoporotic and selective estrogen receptor modulator activity of silymarin compared with ethinylestradiol in ovariectomized rats. Phytomedicine 17 (2): 116-25, 2010. [PUBMED Abstract]
  49. Scambia G, De Vincenzo R, Ranelletti FO, et al.: Antiproliferative effect of silybin on gynaecological malignancies: synergism with cisplatin and doxorubicin. Eur J Cancer 32A (5): 877-82, 1996. [PUBMED Abstract]
  50. Bhatia N, Zhao J, Wolf DM, et al.: Inhibition of human carcinoma cell growth and DNA synthesis by silibinin, an active constituent of milk thistle: comparison with silymarin. Cancer Lett 147 (1-2): 77-84, 1999. [PUBMED Abstract]
  51. Zi X, Agarwal R: Silibinin decreases prostate-specific antigen with cell growth inhibition via G1 arrest, leading to differentiation of prostate carcinoma cells: implications for prostate cancer intervention. Proc Natl Acad Sci U S A 96 (13): 7490-5, 1999. [PUBMED Abstract]
  52. Duthie SJ, Johnson W, Dobson VL: The effect of dietary flavonoids on DNA damage (strand breaks and oxidised pyrimdines) and growth in human cells. Mutat Res 390 (1-2): 141-51, 1997. [PUBMED Abstract]
  53. Vailati A, Aristia L, Sozzé E, et al.: Randomized open study of the dose-effect relationship of a short course of IdB 1016 in patients with viral or alcoholic hepatitis. Fitoterapia 64 (3), 219-28, 1993.
  54. Salmi HA, Sarna S: Effect of silymarin on chemical, functional, and morphological alterations of the liver. A double-blind controlled study. Scand J Gastroenterol 17 (4): 517-21, 1982. [PUBMED Abstract]
  55. Parés A, Planas R, Torres M, et al.: Effects of silymarin in alcoholic patients with cirrhosis of the liver: results of a controlled, double-blind, randomized and multicenter trial. J Hepatol 28 (4): 615-21, 1998. [PUBMED Abstract]
  56. Moscarella S, Giusti A, Marra F, et al.: Therapeutic and antilipoperoxidant effects of silybin-phosphatidylcholine complex in chronic liver disease: preliminary results. Current Therapeutic Research 53 (1): 98-102.
  57. Marena C, Lampertico M: Preliminary clinical development of silipide: a new complex of silybin in toxic liver disorders. Planta Med 57 (Suppl 2): A124-5, 1991.
  58. Marcelli R, Bizzoni P, Conte D, et al.: Randomized controlled study of the efficacy and tolerability of a short course of IdB 1016 in the treatment of chronic persistent hepatitis. European Bulletin of Drug Research 1 (3): 131-5, 1992.
  59. Flisiak R, Prokopowicz D: Effect of misoprostol on the course of viral hepatitis B. Hepatogastroenterology 44 (17): 1419-25, 1997 Sep-Oct. [PUBMED Abstract]
  60. Ferenci P: [Therapy of chronic hepatitis C] Wien Med Wochenschr 150 (23-24): 481-5, 2000. [PUBMED Abstract]
  61. Buzzelli G, Moscarella S, Giusti A, et al.: Therapeutic effects of a new silybin complex in chronic active hepatitis (CAH). [Abstract] Hellenic Journal of Gastroenterology 5 (Suppl): A-151, 38, 1992.
  62. Albrecht M, Frerick H, Kuhn U, et al.: Therapy of toxic liver pathologies with Legalon®. Z Klin Med 47: 87-92, 1992.
  63. Rambaldi A, Jacobs BP, Gluud C: Milk thistle for alcoholic and/or hepatitis B or C virus liver diseases. Cochrane Database Syst Rev (4): CD003620, 2007. [PUBMED Abstract]
  64. Yang Z, Zhuang L, Lu Y, et al.: Effects and tolerance of silymarin (milk thistle) in chronic hepatitis C virus infection patients: a meta-analysis of randomized controlled trials. Biomed Res Int 2014: 941085, 2014. [PUBMED Abstract]
  65. Bachmeier BE, Mirisola V, Romeo F, et al. Reference profile correlation reveals estrogen-like trancriptional activity of Curcumin. Cell Physiol Biochem. 2010;26(3):471-482.
  66. Cemil B, Topuz K, Demircan MN, et al. Curcumin improves early functional results after experimental spinal cord injury. Acta Neurochir (Wien). Sep 2010;152(9):1583-1590; discussion 1590.
  67. Seehofer D, Schirmeier A, Bengmark S, et al. Inhibitory effect of curcumin on early liver regeneration following partial hepatectomy in rats. J Surg Res. Aug 2009;155(2):195-200.
  68. Yun JM, Jialal I, Devaraj S. Epigenetic regulation of high glucose-induced proinflammatory cytokine production in monocytes by curcumin. J Nutr Biochem. May 2011;22(5):450-458.
  69. Jantan I, Bukhari SN, Lajis NH, et al. Effects of diarylpentanoid analogues of curcumin on chemiluminescence and chemotactic activities of phagocytes. J Pharm Pharmacol.Mar 2012;64(3):404-412.
  70. Chang KW, Hung PS, Lin IY, et al. Curcumin upregulates insulin-like growth factor binding protein-5 (IGFBP-5) and C/EBPalpha during oral cancer suppression. Int J Cancer. Jul 1 2010;127(1):9-20.
  71. Siwak DR, Shishodia S, Aggarwal BB, et al. Curcumin-induced antiproliferative and proapoptotic effects in melanoma cells are associated with suppression of IkappaB kinase and nuclear factor kappaB activity and are independent of the B-Raf/mitogen-activated/extracellular signal-regulated protein kinase pathway and the Akt pathway.Cancer. Aug 15 2005;104(4):879-890.
  72. Uddin S, Hussain AR, Manogaran PS, et al. Curcumin suppresses growth and induces apoptosis in primary effusion lymphoma. Oncogene. Oct 27 2005;24(47):7022-7030.
  73. Kunnumakkara AB, Guha S, Krishnan S, et al. Curcumin potentiates antitumor activity of gemcitabine in an orthotopic model of pancreatic cancer through suppression of proliferation, angiogenesis, and inhibition of nuclear factor-kappaB-regulated gene products. Cancer Res. Apr 15 2007;67(8):3853-3861.
  74. Selvendiran K, Ahmed S, Dayton A, et al. HO-3867, a curcumin analog, sensitizes cisplatin-resistant ovarian carcinoma, leading to therapeutic synergy through STAT3 inhibition. Cancer Biol Ther. Nov 1 2011;12(9):837-845.
  75. Sreekanth CN, Bava SV, Sreekumar E, et al. Molecular evidences for the chemosensitizing efficacy of liposomal curcumin in paclitaxel chemotherapy in mouse models of cervical cancer. Oncogene. Jul 14 2011;30(28):3139-3152.
  76. Qiao Q, Jiang Y, Li G. Curcumin improves the antitumor effect of X-ray irradiation by blocking the NF-kappaB pathway: an in-vitro study of lymphoma. Anticancer Drugs.Jan 23 2012
  77. Kunnumakkara AB, Diagaradjane P, Guha S, et al. Curcumin sensitizes human colorectal cancer xenografts in nude mice to gamma-radiation by targeting nuclear factor-kappaB-regulated gene products. Clin Cancer Res. Apr 1 2008;14(7):2128-2136.
  78. Ng TP, Chiam PC, Lee T, et al. Curry consumption and cognitive function in the elderly.Am J Epidemiol. Nov 1 2006;164(9):898-906.
  79. Baum L, Lam CW, Cheung SK, et al. Six-month randomized, placebo-controlled, double-blind, pilot clinical trial of curcumin in patients with Alzheimer disease. J Clin Psychopharmacol. Feb 2008;28(1):110-113.
  80. Bundy R, Walker AF, Middleton RW, et al. Turmeric extract may improve irritable bowel syndrome symptomatology in otherwise healthy adults: a pilot study. J Altern Complement Med. Dec 2004;10(6):1015-1018.
  81. Hanai H, Iida T, Takeuchi K, et al. Curcumin maintenance therapy for ulcerative colitis: randomized, multicenter, double-blind, placebo-controlled trial. Clinical Gastroenterol Hepatol. Dec 2006;4(12):1502-1506.
  82. Kuptniratsaikul V, Dajpratham P, Taechaarpornkul W, et al. Efficacy and safety of Curcuma domestica extracts compared with ibuprofen in patients with knee osteoarthritis: a multicenter study. Clin Interv Aging. 2014 Mar 20;9:451-8.
  83. Pungcharoenkul K, Thongnopnua P. Effect of different curcuminoid supplement dosages on total in vivo antioxidant capacity and cholesterol levels of healthy human subjects. Phytother Res. Nov 2011;25(11):1721-1726
  84. Baum L, Cheung SK, Mok VC, et al. Curcumin effects on blood lipid profile in a 6-month human study. Pharmacol Res. Dec 2007;56(6):509-514.
  85. expression in patients with colorectal cancer by administration of curcumin. Cancer Invest. Mar 2011;29(3):208-213.
  86. Dhillon N, Aggarwal BB, Newman RA, et al. Phase II trial of curcumin in patients with advanced pancreatic cancer. Clin Cancer Res. Jul 15 2008;14(14):4491-4499.
  87. Bayet-Robert M, Kwiatkowski F, Leheurteur M, et al. Phase I dose escalation trial of docetaxel plus curcumin in patients with advanced and metastatic breast cancer.Cancer Biol Ther. Jan 2010;9(1):8-14.
  88. Kanai M, Yoshimura K, Asada M, et al. A phase I/II study of gemcitabine-based chemotherapy plus curcumin for patients with gemcitabine-resistant pancreatic cancer. Cancer Chemother Pharmacol. Jul 2011;68(1):157-164.
  89. Epelbaum R, Schaffer M, Vizel B, et al. Curcumin and gemcitabine in patients with advanced pancreatic cancer. Nutr Cancer. 2010;62(8):1137-1141.
  90. Zhang W, Lim LY. Effects of spice constituents on P-glycoprotein-mediated transport and CYP3A4-mediated metabolism in vitro. Drug Metab Dispos. Jul 2008;36(7):1283-1290.
  91. Chen Y, Liu WH, Chen BL, et al. Plant polyphenol curcumin significantly affects CYP1A2 and CYP2A6 activity in healthy, male Chinese volunteers. Ann Pharmacother.Jun 2010;44(6):1038-1045.
  92. Somasundaram S, Edmund NA, Moore DT, et al. Dietary curcumin inhibits chemotherapy-induced apoptosis in models of human breast cancer. Cancer Res. Jul 1 2002;62(13):3868-3875.
  93. Leung AY, Foster S. Encyclopedia of Common Natural Ingredients Used in Food, Drugs and Cosmetics. 2nd ed. New York, NY: John Wiley & Sons; 1996.
  94. Morsy MA, Abdalla AM, Mahmoud AM, et al. Protective effects of curcumin, alpha-lipoic acid, and N-acetylcysteine against carbon tetrachloride-induced liver fibrosis in rats. J Physiol Biochem. Oct 11 2011.
  95. Bulku E, Stohs SJ, Cicero L, et al. Curcumin exposure modulates multiple pro-apoptotic and anti-apoptotic signaling pathways to antagonize acetaminophen-induced toxicity. Curr Neurovasc Res. Feb 1 2012;9(1):58-71.
  96. Alexandrow MG, Song LJ, Altiok S, et al. Curcumin: a novel Stat3 pathway inhibitor for chemoprevention of lung cancer. Eur J Cancer Prev. Dec 7 2011.
  97. Lin SS, Lai KC, Hsu SC, et al. Curcumin inhibits the migration and invasion of human A549 lung cancer cells through the inhibition of matrix metalloproteinase-2 and -9 and Vascular Endothelial Growth Factor (VEGF). Cancer Lett. Nov 28 2009;285(2):127-133.
  98. Chen QY, Lu GH, Wu YQ, et al. Curcumin induces mitochondria pathway mediated cell apoptosis in A549 lung adenocarcinoma cells. Oncol Rep. May 2010;23(5):1285-1292.
  99. Wu SH, Hang LW, Yang JS, et al. Curcumin induces apoptosis in human non-small cell lung cancer NCI-H460 cells through ER stress and caspase cascade- and mitochondria-dependent pathways. Anticancer Res. Jun 2010;30(6):2125-2133.
  100. de H, Tokiwa S, Sakamaki K, et al. Combined inhibitory effects of soy isoflavones and curcumin on the production of prostate-specific antigen. Prostate. Jul 1 2010;70(10):1127-1133.
  101. Wong TF, Takeda T, Li B, et al. Curcumin disrupts uterine leiomyosarcoma cells through AKT-mTOR pathway inhibition. Gynecol Oncol. Jul 2011;122(1):141-148
  102. Bartik L, Whitfield GK, Kaczmarska M, et al. Curcumin: a novel nutritionally derived ligand of the vitamin D receptor with implications for colon cancer chemoprevention.J Nutr Biochem. Dec 2010;21(12):1153-1161.
  103. Watson JL, Hill R, Lee PW, et al. Curcumin induces apoptosis in HCT-116 human colon cancer cells in a p21-independent manner. Exp Mol Pathol. Jun 2008;84(3):230-233.
  104. Yang KY, Lin LC, Tseng TY, et al. Oral bioavailability of curcumin in rat and the herbal analysis from Curcuma longa by LC-MS/MS. J Chromatogr B Analyt Technol Biomed Life Sci. Jun 15 2007;853(1-2):183-189.
  105. Garcea G, Berry DP, Jones DJ, et al. Consumption of the putative chemopreventive agent curcumin by cancer patients: assessment of curcumin levels in the colorectum and their pharmacodynamic consequences. Cancer Epidemiol Biomarkers Prev. Jan 2005;14(1):120-125.
  106. Bishnoi M, Chopra K, Rongzhu L, et al. Protective effect of curcumin and its combination with piperine (bioavailability enhancer) against haloperidol-associated neurotoxicity: cellular and neurochemical evidence. Neurotox Res. Oct 2011;20(3):215-225.
  107. Tsai YM, Chien CF, Lin LC, et al. Curcumin and its nano-formulation: the kinetics of tissue distribution and blood-brain barrier penetration. Int J Pharm. Sep 15 2011;416(1):331-338.
  108. Orr WS, Denbo JW, Saab KR, et al. Liposome-encapsulated curcumin suppresses neuroblastoma growth through nuclear factor-kappa B inhibition. Surgery. Jan 26 2012.
  109. Asai A, Miyazawa T. Occurrence of orally administered curcuminoid as glucuronide and glucuronide/sulfate conjugates in rat plasma. Life Sci. Oct 27 2000;67(23):2785-2793.
  110. Ravindranath V, Chandrasekhara N. Absorption and tissue distribution of curcumin in rats. Toxicology. 1980;16(3):259-265.
  111. Hou XL, Takahashi K, Tanaka K, et al. Curcuma drugs and curcumin regulate the expression and function of P-gp in Caco-2 cells in completely opposite ways. Int J Pharm. Jun 24 2008;358(1-2):224-229.
  112. Zhang W, Tan TM, Lim LY. Impact of curcumin-induced changes in P-glycoprotein and CYP3A expression on the pharmacokinetics of peroral celiprolol and midazolam in rats. Drug Metab Dispos. Jan 2007;35(1):110-115.
  113. Appiah-Opong R, Commandeur JN, van Vugt-Lussenburg B, et al. Inhibition of human recombinant cytochrome P450s by curcumin and curcumin decomposition products.Toxicology. Jun 3 2007;235(1-2):83-91.
  114. Tang M, Larson-Meyer DE, Liebman M. Effect of cinnamon and turmeric on urinary oxalate excretion, plasma lipids, and plasma glucose in healthy subjects. Am J Clin Nutr. May 2008;87(5):1262-1267.
  115. Ulbricht CE, Basch, EM. Natual Standard Herb & Supplement Reference: Evidence-Based Clinical Reviews St. Louis, MO: Elsevier Mosby; 2005.
  116. Lamb SR, Wilkinson SM. Contact allergy to tetrahydrocurcumin. Contact Dermatitis.Apr 2003;48(4):227.
  117. Liddle M, Hull C, Liu C, et al. Contact urticaria from curcumin. Dermatitis. Dec 2006;17(4):196-197.
  118. Prakash P, Misra A, Surin WR, et al. Anti-platelet effects of Curcuma oil in experimental models of myocardial ischemia-reperfusion and thrombosis. Thromb Res. Feb 2011;127(2):111-118.
  119. Jantan I, Raweh SM, Sirat HM, et al. Inhibitory effect of compounds from Zingiberaceae species on human platelet aggregation. Phytomedicine. Apr 2008;15(4):306-309.
  120. Pavithra BH, Prakash N, Jayakumar K. Modification of pharmacokinetics of norfloxacin following oral administration of curcumin in rabbits. J Vet Sci. Dec 2009;10(4):293-297.
  121. Kudva AK, Manoj, MN, Swamy, BM, et al. Complexation of amphotericin B and curcumin with serum albumins: solubility and effect on erythrocyte membrane damage. J Exp Pharmacol. 2011;2011(3):1-6.
  122. Hudson SA, Ecroyd H, Kee TW, et al. The thioflavin T fluorescence assay for amyloid fibril detection can be biased by the presence of exogenous compounds. FEBS J. Oct 2009;276(20):5960-5972.
  123. Egashira K, Sasaki H, Higuchi S, Ieiri I. Food-drug interaction of tacrolimus with pomelo, ginger, and turmeric juice in rats. Drug Metab Pharmacokinet. 2012 Apr 25;27(2):242-7.
  124. Choi HA, Kim MR, Park KA, Hong J. Interaction of over-the-counter drugs with curcumin: influence on stability and bioactivities in intestinal cells. J Agric Food Chem.2012 Oct 24;60(42):10578-84.
  125. Akazawa N, Choi Y, Miyaki A, et al. Curcumin ingestion and exercise training improve vascular endothelial function in postmenopausal women. Nutr Res. 2012 Oct;32(10):795-9.
  126. Sanmukhani J, Satodia V, Trivedi J, et al. Efficacy and safety of curcumin in major depressive disorder: a randomized controlled trial. Phytother Res. 2014 Apr;28(4):579-85.
  127. Niu M, Wu S, Mao L, Yang Y. CRM1 is a cellular target of curcumin: new insights for the myriad of biological effects of an ancient spice. Traffic. 2013 Oct;14(10):1042-52.
  128. Palatty PL, Azmidah A, Rao S, et al. Topical application of a sandal wood oil and turmeric based cream prevents radiodermatitis in head and neck cancer patients undergoing external beam radiotherapy: a pilot study. Br J Radiol. 2014 Jun;87(1038):20130490.
  129. Thomas R, Williams M, Sharma H, Chaudry A, Bellamy P. A double-blind, placebo-controlled randomised trial evaluating the effect of a polyphenol-rich whole food supplement on PSA progression in men with prostate cancer—the U.K. NCRN Pomi-T study. Prostate Cancer Prostatic Dis. 2014 Jun;17(2):180-6.
  130. Daveluy A, Geniaux H, Thibaud L, et al. Probable interaction between an oral vitamin K antagonist and turmeric (Curcuma longa). Therapie. Nov-Dec 2014;69(6):519-520.
  131. Doctor Accused of Aiding Man Who Disfigured Cancer Patients. The Washinton Post.http://www.washingtonpost.com/wp-dyn/content/article/2005/08/13/AR2005081301016.html. Accessed August 17, 2015.
  132. Adhami VM, Aziz MH, Mukhtar H, et al. Activation of prodeath Bcl-2 family proteins and mitochondrial apoptosis pathway by sanguinarine in immortalized human HaCaT keratinocytes. Clin Cancer Res 2003;9(8):3176-82.
  133. Adhami VM, Aziz MH, Reagan-Shaw SR, et al. Sanguinarine causes cell cycle blockade and apoptosis of human prostate carcinoma cells via modulation of cyclin kinase inhibitor-cyclin-cyclin-dependent kinase machinery. Mol Cancer Ther 2004;3(8):933-40.
  134. Basini G, Santini SE, Bussolati S, et al. The plant alkaloid sanguinarine is a potential inhibitor of follicular angiogenesis. J Reprod Dev 2007;53(3):573-9.
  135. Basini G, Santini SE, Bussolati S, et al. Sanguinarine inhibits VEGF-induced Akt phosphorylation. Ann N Y Acad Sci 2007;1095:371-6.
  136. Chaturvedi MM, Kumar A, Darnay BG, et al. Sanguinarine (pseudochelerythrine) is a potent inhibitor of NF-kappaB activation, IkappaBalpha phosphorylation, and degradation. J Biol Chem 1997;272(48):30129-34.
  137. Ding Z, Tang SC, Weerasinghe P, et al. The alkaloid sanguinarine is effective against multidrug resistance in human cervical cells via bimodal cell death. Biochem Pharmacol 2002;63(8):1415-21.
  138. Dzink JL, Socransky SS. Comparative in vitro activity of sanguinarine against oral microbial isolates. Antimicrob Agents Chemother 1985;27(4):663-5.
  139. Eun JP, Koh GY. Suppression of angiogenesis by the plant alkaloid, sanguinarine.Biochem Biophys Res Commun 2004;317(2):618-24.
  140. Eversole LR, Eversole GM, Kopcik J. Sanguinaria-associated oral leukoplakia: comparison with other benign and dysplastic leukoplakic lesions. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;89(4):455-64.
  141. Fetrow C. Professional’s handbook of complementary and alternative medicines 2nd ed. 2001, Springhouse, PA: Springhouse Corp.
  142. Hakim SA, Sanguinarine and hypothalamic glaucoma. J All India Ophthalmol Soc. 1962 Dec;10:83-102.
  143. Jeng JH, Wu HL, Lin BR, et al. Antiplatelet effect of sanguinarine is correlated to calcium mobilization, thromboxane and cAMP production. Atherosclerosis2007;191(2):250-8.
  144. Mascarenhas AK, Allen CM, Loudon J. The association between Viadent use and oral leukoplakia. Epidemiology. 2001;12(6):741-3.
  145. McDaniel S, Goldman GD. Consequences of using escharotic agents as primary treatment for nonmelanoma skin cancer. Arch Dermatol 2002;138(12):1593-6.
  146. Munro IC, Delzell ES, Nestmann ER, et al. Viadent usage and oral leukoplakia: a spurious association. Regul Toxicol Pharmacol 1999;30(3):182-96.
  147. Nandi R, Maiti M. Binding of sanguinarine to deoxyribonucleic acids of differing base composition. Biochem Pharmacol 1985;34(3):321-4.
  148. Scheiner-Bobis G. Sanguinarine induces K+ outflow from yeast cells expressing mammalian sodium pumps. Naunyn Schmiedebergs Arch Pharmacol 2001;363(2):203-8.
  149. Seifen E, Adams RJ, Riemer RK. Sanguinarine: a positive inotropic alkaloid which inhibits cardiac Na+,K+-ATPase. Eur J Pharmacol 1979;60(4):373-7.
  150. Suchomelova J, Bochorakova H, Paulova H, et al. HPLC quantification of seven quaternary benzo[c]phenanthridine alkaloids in six species of the family Papaveraceae. J Pharm Biomed Anal 2007;44(1):283-7.
  151. Wolff J, Knipling L. Antimicrotubule properties of benzophenanthridine alkaloids.Biochemistry 1993;32(48):13334-9.
  152. Mazzio EA, Soliman KF. In vitro screening for the tumoricidal properties of international medicinal herbs. Phytother Res. 2009 Mar;23(3):385-98.
  153. Han MH, Yoo YH, Choi YH. Sanguinarine-induced apoptosis in human leukemia U937 cells via Bcl-2 downregulation and caspase-3 activation. Chemotherapy.2008;54(3):157-65.
  154. Saltzberg F, Barron G, Fenske N. Deforming self-treatment with herbal “black salve”.Dermatol Surg. 2009 Jul;35(7):1152-4.
  155. Sun M, Liu C, Nadiminty N, et al. Inhibition of Stat3 activation by sanguinarine suppresses prostate cancer cell growth and invasion. Prostate. 2011 May 2. doi: 10.1002/pros.21409.
  156. Cienki JJ, Zaret L. An Internet misadventure: bloodroot salve toxicity. J Altern Complement Med. 2010 Oct;16(10):1125-7.
  157. Lee JS, Jung WK, Jeong MH, Yoon TR, Kim HK. Sanguinarine induces apoptosis of HT-29 human colon cancer cells via the regulation of Bax/Bcl-2 ratio and caspase-9-dependent pathway. Int J Toxicol. 2012 Jan-Feb;31(1):70-7.
  158. Eastman KL, McFarland LV, Raugi GJ. Buyer beware: a black salve caution. J Am Acad Dermatol. 2011 Nov;65(5):e154-5.
  159. Schlichte MJ, Downing CP, Ramirez-Fort M, Gordon R, Tyring S. Bloodroot associated eschar. Dermatol Online J. 2014 Jul 15;20(7). pii: 13030/qt05r0r2wr
  160. Martin K, Sur R, Liebel F, et al. Parthenolide-depleted feverfew (Tanacetum parthenium) protects skin from UV irradiation and external aggression. Arch Dermatol Res. Feb 2008;300(2):69-80. doi: 10.1007/s00403-007-0818-x
  161. Izumi E, Morello LG, Ueda-Nakamura T, et al. Trypanosoma cruzi: antiprotozoal activity of parthenolide obtained from Tanacetum parthenium (L.) Schultz Bip. (Asteraceae, Compositae) against epimastigote and amastigote forms. Exp Parasitol. Mar 2008;118(3):324-330. doi: 10.1016/j.exppara.2007.08.015
  162. Mohsenzadeh F, Chehregani A, Amiri H. Chemical composition, antibacterial activity and cytotoxicity of essential oils of Tanacetum parthenium in different developmental stages. Pharm Biol. Sep 2011;49(9):920-926. doi: 10.3109/13880209.2011.556650
  163. Mathema VB, Koh YS, Thakuri BC, et al. Parthenolide, a sesquiterpene lactone, expresses multiple anti-cancer and anti-inflammatory activities. Inflammation. Apr 2012;35(2):560-565. doi: 10.1007/s10753-011-9346-0
  164. Wu C, Chen F, Wang X, et al. Identification of antioxidant phenolic compounds in feverfew (Tanacetum parthenium) by HPLC-ESI-MS/MS and NMR. Phytochem Anal.Sep-Oct 2007;18(5):401-410. doi: 10.1002/pca.995
  165. Diener HC, Pfaffenrath V, Schnitker J, et al. Efficacy and safety of 6.25 mg t.i.d. feverfew CO2-extract (MIG-99) in migraine prevention – A randomized, double-blind, multicentre, placebo-controlled study. Cephalalgia. Nov 2005;25(11):1031-1041. doi: 10.1111/j.1468-2982.2005.00950.x
  166. Cady RK, Goldstein J, Nett R, et al. A double-blind placebo-controlled pilot study of sublingual feverfew and ginger (LipiGesic M) in the treatment of migraine. Headache.Jul-Aug 2011;51(7):1078-1086. doi: 10.1111/j.1526-4610.2011.01910.x
  167. Ferro EC, Biagini AP, da Silva IE, et al. The combined effect of acupuncture and Tanacetum parthenium on quality of life in women with headache: randomised study.Acupunct Med. Dec 2012;30(4):252-257. doi: 10.1136/acupmed-2012-010195
  168. Pattrick M, Heptinstall S, Doherty M. Feverfew in rheumatoid arthritis: a double blind, placebo controlled study. Ann Rheum Dis. Jul 1989;48(7):547-549.
  169. Kim SL, Lee ST, Trang KT, et al. Parthenolide exerts inhibitory effects on angiogenesis through the downregulation of VEGF/VEGFRs in colorectal cancer. Int J Mol Med. May 2014;33(5):1261-1267. doi: 10.3892/ijmm.2014.1669
  170. Al-Fatlawi AA, Al-Fatlawi AA, Irshad M, et al. Effect of parthenolide on growth and apoptosis regulatory genes of human cancer cell lines. Pharm Biol. Jan 2015;53(1):104-109. doi: 10.3109/13880209.2014.911919
  171. Lu C, Wang W, Jia Y, et al. Inhibition of AMPK/autophagy potentiates parthenolide-induced apoptosis in human breast cancer cells. J Cell Biochem. Aug 2014;115(8):1458-1466. doi: 10.1002/jcb.24808
  172. Yip-Schneider MT, Nakshatri H, Sweeney CJ, et al. Parthenolide and sulindac cooperate to mediate growth suppression and inhibit the nuclear factor-kappa B pathway in pancreatic carcinoma cells. Mol Cancer Ther. Apr 2005;4(4):587-594. doi: 10.1158/1535-7163.MCT-04-0215
  173. Zhang S, Ong CN, Shen HM. Involvement of proapoptotic Bcl-2 family members in parthenolide-induced mitochondrial dysfunction and apoptosis. Cancer Lett. Aug 10 2004;211(2):175-188. doi: 10.1016/j.canlet.2004.03.033
  174. Parada-Turska J, Paduch R, Majdan M, et al. Antiproliferative activity of parthenolide against three human cancer cell lines and human umbilical vein endothelial cells.Pharmacol Rep. Mar-Apr 2007;59(2):233-237.
  175. Lesiak K, Koprowska K, Zalesna I, et al. Parthenolide, a sesquiterpene lactone from the medical herb feverfew, shows anticancer activity against human melanoma cells in vitro. Melanoma Res. Feb 2010;20(1):21-34. doi: 10.1097/CMR.0b013e328333bbe4
  176. Carlisi D, D’Anneo A, Angileri L, et al. Parthenolide sensitizes hepatocellular carcinoma cells to TRAIL by inducing the expression of death receptors through inhibition of STAT3 activation. J Cell Physiol. Jun 2011;226(6):1632-1641. doi: 10.1002/jcp.22494
  177. Curry EA, 3rd, Murry DJ, Yoder C, et al. Phase I dose escalation trial of feverfew with standardized doses of parthenolide in patients with cancer. Invest New Drugs. Aug 2004;22(3):299-305. doi: 10.1023/B:DRUG.0000026256.38560.be
  178. Guzman ML, Rossi RM, Neelakantan S, et al. An orally bioavailable parthenolide analog selectively eradicates acute myelogenous leukemia stem and progenitor cells. Blood.Dec 15 2007;110(13):4427-4435. doi: 10.1182/blood-2007-05-090621
  179. Pareek A, Suthar M, Rathore GS, et al. Feverfew (Tanacetum parthenium L.): A systematic review. Pharmacogn Rev. Jan 2011;5(9):103-110. doi: 10.4103/0973-7847.79105
  180. Reuter U, Chiarugi A, Bolay H, et al. Nuclear factor-kappaB as a molecular target for migraine therapy. Ann Neurol. Apr 2002;51(4):507-516.
  181. Sahler J, Bernard JJ, Spinelli SL, et al. The feverfew plant-derived compound, parthenolide enhances platelet production and attenuates platelet activation through NF-kappaB inhibition. Thromb Res. May 2011;127(5):426-434. doi: 10.1016/j.thromres.2010.12.013
  182. Groenewegen WA, Heptinstall S. A comparison of the effects of an extract of feverfew and parthenolide, a component of feverfew, on human platelet activity in-vitro. J Pharm Pharmacol. Aug 1990;42(8):553-557.
  183. Heptinstall S, White A, Williamson L, et al. Extracts of feverfew inhibit granule secretion in blood platelets and polymorphonuclear leucocytes. Lancet. May 11 1985;1(8437):1071-1074.
  184. Johnson ES, Kadam NP, Hylands DM, et al. Efficacy of feverfew as prophylactic treatment of migraine. Br Med J (Clin Res Ed). Aug 31 1985;291(6495):569-573.
  185. Williams CA, Hoult JR, Harborne JB, et al. A biologically active lipophilic flavonol from Tanacetum parthenium. Phytochemistry. Jan 1995;38(1):267-270.
  186. Anderson KN, Bejcek BE. Parthenolide induces apoptosis in glioblastomas without affecting NF-kappaB. J Pharmacol Sci. Feb 2008;106(2):318-320.
  187. Paulsen E, Christensen LP, Andersen KE. Compositae dermatitis from airborne parthenolide. Br J Dermatol. Mar 2007;156(3):510-515. doi: 10.1111/j.1365-2133.2006.07674.x
  188. Killoran CE, Crawford GH, Pedvis-Leftick A. Two cases of compositae dermatitis exacerbated by moisturizer containing feverfew. Dermatitis. Dec 2007;18(4):225-229.
  189. Unger M, Frank A. Simultaneous determination of the inhibitory potency of herbal extracts on the activity of six major cytochrome P450 enzymes using liquid chromatography/mass spectrometry and automated online extraction. Rapid Commun Mass Spectrom. 2004;18(19):2273-2281. doi: 10.1002/rcm.1621
  190. Collins SC, Dufresne RG, Jr. Dietary supplements in the setting of mohs surgery.Dermatol Surg. Jun 2002;28(6):447-452.
  191. Murphy JJ, Heptinstall S, Mitchell JR. Randomised double-blind placebo-controlled trial of feverfew in migraine prevention. Lancet. Jul 23 1988;2(8604):189-192.
  192. Kothari S, Jain AK, Mehta SC, et al. Hypolipidemic effect of fresh Triticum aestivum (wheat) grass juice in hypercholesterolemic rats. Acta Pol Pharm. Mar-Apr 2011;68(2):291-294.
  193. Sethi J, Yadav M, Dahiya K, et al. Antioxidant effect of Triticum aestivium (wheat grass) in high-fat diet-induced oxidative stress in rabbits. Methods Find Exp Clin Pharmacol. May 2010;32(4):233-235.
  194. Shyam R, Singh SN, Vats P, et al. Wheat grass supplementation decreases oxidative stress in healthy subjects: a comparative study with spirulina. J Altern Complement Med. Oct 2007;13(8):789-791.
  195. Ben-Arye E, Goldin E, Wengrower D, et al. Wheat grass juice in the treatment of active distal ulcerative colitis: a randomized double-blind placebo-controlled trial. Scand J Gastroenterol. Apr 2002;37(4):444-449.
  196. Ng SC, Lam YT, Tsoi KK, et al. Systematic review: the efficacy of herbal therapy in inflammatory bowel disease. Aliment Pharmacol Ther. Oct 2013;38(8):854-863.
  197. Marawaha RK, Bansal D, Kaur S, et al. Wheat grass juice reduces transfusion requirement in patients with thalassemia major: a pilot study. Indian Pediatr. Jul 2004;41(7):716-720.
  198. Choudhary DR, Naithani R, Panigrahi I, et al. Effect of wheat grass therapy on transfusion requirement in beta-thalassemia major. Indian J Pediatr. Apr 2009;76(4):375-376.
  199. Singh K, Pannu MS, Singh P, et al. Effect of wheat grass tablets on the frequency of blood transfusions in Thalassemia Major. Indian J Pediatr. Jan 2010;77(1):90-91.
  200. Bar-Sela G, Tsalic M, Fried G, et al. Wheat grass juice may improve hematological toxicity related to chemotherapy in breast cancer patients: a pilot study. Nutr Cancer.2007;58(1):43-48.
  201. Das A, Raychaudhuri U, Chakraborty R. Effect of freeze drying and oven drying on antioxidant properties of fresh wheatgrass. Int J Food Sci Nutr. Sep 2012;63(6):718-721.
  202. Shukla V, Vashistha M, Singh SN. Evaluation of antioxidant profile and activity of amalaki (Emblica officinalis), spirulina and wheat grass. Indian J Clin Biochem. Jan 2009;24(1):70-75.
  203. Gerritsen ME, Carley WW, Ranges GE, et al. Flavonoids inhibit cytokine-induced endothelial cell adhesion protein gene expression. Am J Pathol. Aug 1995;147(2):278-292.
  204. Mukhopadhyay S, et al. The role of iron chelation activity of wheat grass juice in patients with myelodysplastic syndrome. Journal of Clinical Oncology, 2009 ASCO Annual Meeting Proceedings (Post-Meeting Edition). Vol 27, No 15S (May 20 Supplement), 2009: 7012
  205. Blumenthal M, et al. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Austin: American Botanical Council; 1998
  206. Foster S, et al. Tyler’s Honest Herbal: A Sensible Guide to the Use of Herbs and Related Remedies, 3rd ed. New York: Haworth Herbal Press; 1993.
  207. Blumenthal M, et al. Herbal Medicine Expanded Commission E Monographs, 1st ed. Austin: American Botanical Council; 2000.
  208. Vanscheidt W, et al. Efficacy and safety of a Butcher’s broom preparation (Ruscus aculeatus L. extract) compared to placebo in patients suffering from chronic venous insufficiencyArzneimittelforschung 2002;52:243-50.
  209. Cluzan RV, et al. Treatment of secondary lymphedema of the upper limb with CYCLO 3 FORT. Lymphology 1996 Mar;29(1):29-35.
  210. Cappelli R, Nicora M, DiPerri T. Use of extract of Ruscus aculeatus in venous disease in the lower limbs. Drugs Exp Clin Res 1988;14(4):277-83.
  211. Thomas-Anterion C, et al. Unexplained chronic diarrhea, apropos of 4 new cases under Cyclo 3 fort and review of the literature. Rev Med Interne 1993 Apr;14(4):215-7. Review.
  212. Boyle P, Diehm C, Robertson C. Meta-analysis of clinical trials of Cyclo 3 Fort in the treatment of chronic venous insufficiency. Int Angiol. 2003 Sep;22(3):250-62.
  213. Guex JJ, Enriquez Vega DM, Avril L, Boussetta S, Taïeb C. Assessment of quality of life in Mexican patients suffering from chronic venous disorder – impact of oral Ruscus aculeatus-hesperidin-methyl-chalcone-ascorbic acid treatment – ’QUALITY Study’.Phlebology. 2009 Aug;24(4):157-65.
  214. Huang YL, Kou JP, Ma L, et al. Possible mechanism of the anti-inflammatory activity of ruscogenin: role of intercellular adhesion molecule-1 and nuclear factor-kappaB. J Pharmacol Sci. 2008 Oct;108(2):198-205.
  215. Guex JJ, Avril L, Enrici E, et al. Quality of life improvement in Latin American patients suffering from chronic venous disorder using a combination of Ruscus aculeatus and hesperidin methyl-chalcone and ascorbic acid (quality study). Int Angiol. 2010 Dec;29(6):525-32.
  216. De Marino S, Festa C, Zollo F, Iorizzi M. Novel steroidal components from the underground parts of Ruscus aculeatus L. Molecules. 2012 Nov 26;17(12):14002-14.
  217. Longo L, Vasapollo G. Determination of anthocyanins in Ruscus aculeatus L. berries. J Agric Food Chem. 2005 Jan 26;53(2):475-9.
  218. Barbič M, Schmidt TJ, Jürgenliemk G. Novel phenyl-1-benzoxepinols from butcher’s broom (Rusci rhizoma). Chem Biodivers. 2012 Jun;9(6):1077-83.
  219. Facino RM, Carini M, Stefani R, Aldini G, Saibene L. Anti-elastase and anti-hyaluronidase activities of saponins and sapogenins from Hedera helix, Aesculus hippocastanum, and Ruscus aculeatus: factors contributing to their efficacy in the treatment of venous insufficiency. Arch Pharm (Weinheim). 1995 Oct;328(10):720-4.
  220. Barbič M, Willer EA, Rothenhöfer M, Heilmann J, Fürst R, Jürgenliemk G. Spirostanol saponins and esculin from Rusci rhizoma reduce the thrombin-induced hyperpermeability of endothelial cells. Phytochemistry. 2013 Jun;90:106-13.
  221. Sadarmin PP, Timperley J. An unusual case of Butcher’s Broom precipitating diabetic ketoacidosis. J Emerg Med. 2013 Sep;45(3):e63-5.
  222. Tamayo C, et al. The chemistry and biological activity of herbs used in Flor-essence herbal tonic and Essiac. Phytotherapy Res 2000;14:1-14.
  223. Fetrow CW, et al. Professional’s Handbook of Complementary and Alternative Medicines. Philadelphia: Springhouse; 1999.
  224. Newall CA, et al. Herbal medicines: a guide for health-care professionals. Pharmaceutical Press. London. 1996.
  225. Chu DT, Wong WL, Mavligit GM. Immunotherapy with Chinese medicinal herbs. II. Reversal of cyclophosphamide-induced immune suppression by administration of fractionated Astragalus membranaceus in vivoJ Clin Lab Immunol 1988;25:125-9.
  226. Taixiang W, Munro AJ, Guanjian L. Chinese medical herbs for chemotherapy side effects in colorectal cancer patients. Cochrane Database Syst Rev. 2005 Jan 25;(1):CD004540.
  227. McCulloch M, See C, Shu XJ, et al. Astragalus-based Chinese herbs and platinum-based chemotherapy for advanced non-small-cell lung cancer: meta-analysis of randomized trialsJ Clin Oncol. 2006 Jan 20;24(3):419-30.
  228. Cui R, He J, Wang B, et al. Suppressive effect of Astragalus membranaceus Bunge on chemical hepatocarcinogenesis in rats. Cancer Chemother Pharmacol. 2003 Jan;51(1):75-80.
  229. Cho WC, Leung KN. In vitro and in vivo anti-tumor effects of Astragalus membranaceus.Cancer Lett. Jul 8 2007;252(1):43-54.
  230. Yu L, Lu Y, Li J, Wang H. Identification of a gene associated with astragalus and angelica’s renal protective effects by silver staining mRNA differential display. Chin Med J (Engl) 2002;115:923-7.
  231. Ahmed MS, Hou SH, Battaglia MC, et al. Treatment of idiopathic membranous nephropathy with the herb Astragalus membranaceus. Am J Kidney Dis. Dec 2007;50(6):1028-1032.
  232. Ai P, Yong G, Dingkun G, et al. Aqueous extract of Astragali Radix induces human natriuresis through enhancement of renal response to atrial natriuretic peptide. J Ethnopharmacol. Mar 28 2008;116(3):413-421.
  233. Shen HH, Wang K, Li W, et al. Astragalus Membranaceus prevents airway hyperreactivity in mice related to Th2 response inhibition.J Ethnopharmacol. Mar 5 2008;116(2):363-369.
  234. Chen KT, Su CH, Hsin LH, et al. Reducing fatigue of athletes following oral administration of huangqi jianzhong tang. Acta Pharmacol Sin. 2002 Aug;23(8):757-61.
  235. Shi R, He L, Hu Y, et al. The regulatory action of radix astragali on M-cholinergic receptor of the brain of senile ratsJ Tradit Chin Med 2001;21:232-5.
  236. Tang W, et al. Chinese Drugs of Plant Origin. Berlin: Springer-Verlag; 1992.
  237. Qun L, Luo Q, Zhang ZY, et al. Effects of astragalus on IL-2/IL-2R system in patients with maintained hemodialysis. Clin Nephrol. 1999 Nov;52(5):333-4.
  238. Chu DT, Lepe-Zuniga J, Wong WL, et al. Fractionated extract of Astragalus, a Chinese medicinal herb, potentiates LAK cell cytotoxicity generated by a low dose of recombinant interleukin-2J Clin Lab Immunol 1988;26:183-7.
  239. Upton R. Astragalus root: analytical, quality control and therapeutic monograph. American Herbal Pharmacopoeia. 1999;1:1-25.
  240. Wu P, Dugoua JJ, Eyawo O, Mills EJ. Traditional Chinese medicines in the treatment of hepatocellular cancers: a systematic review and meta-analysis. J Exp Clin Cancer Res.2009 Aug 12;28(1):112.
  241. Lu MC, Yao CH, Wang SH, et al. Effect of Astragalus membranaceus in rats on peripheral nerve regeneration: in vitro and in vivo studies. J Trauma. 2010 Feb;68(2):434-40.
  242. Wojcikowski K, Wohlmuth H, Johnson DW, Gobe G. Effect of Astragalus membranaceus and Angelica sinensis combined with Enalapril in rats with obstructive uropathy. Phytother Res. 2010 Jun;24(6):875-84.
  243. Auyeung KK, Woo PK, Law PC, Ko JK. Astragalus saponins modulate cell invasiveness and angiogenesis in human gastric adenocarcinoma cells. J Ethnopharmacol. 2011 Aug 12.
  244. Guo L, Bai SP, Zhao L, Wang XH. Astragalus polysaccharide injection integrated with vinorelbine and cisplatin for patients with advanced non-small cell lung cancer: effects on quality of life and survival. Med Oncol. 2011 Sep 18.
  245. Zhang WJ, Wojta J, Binder BR. Regulation of the fibrinolytic potential of cultured human umbilical vein endothelial cells: astragaloside IV downregulates plasminogen activator inhibitor-1 and upregulates tissue-type plasminogen activator expression. J Vasc Res. 1997 Jul-Aug;34(4):273-80.
  246. Chen HW, Lin IH, Chen YJ,  et al. A novel infusible botanically-derived drug, PG2, for cancer-related fatigue: a phase II double-blind, randomized placebo-controlled study.Clin Invest Med. 2012 Feb 1;35(1):E1-11.
  247. Zhang CZ, Wang SX, Zhang Y, Chen JP, Liang XM. In vitro estrogenic activities of Chinese medicinal plants traditionally used for the management of menopausal symptoms. J Ethnopharmacol. 2005 Apr 26;98(3):295-300.
  248. Fu J, Wang Z, Huang L, et al. Review of the Botanical Characteristics, Phytochemistry, and Pharmacology of Astragalus membranaceus (Huangqi). Phytother Res. 2014 Sep;28(9):1275-83.
  249. Xu X, Li F, Zhang X, et al. In vitro synergistic antioxidant activity and identification of antioxidant components from Astragalus membranaceus and Paeonia lactiflora. PLoS One. 2014 May 9;9(5):e96780. doi: 10.1371/journal.pone.0096780. eCollection 2014.
  250. Ji L, Chen X, Zhong X, et al. Astragalus membranaceus up-regulate Cosmc expression and reverse IgA dys-glycosylation in IgA nephropathy. BMC Complement Altern Med.2014 Jun 18;14:195. doi: 10.1186/1472-6882-14-
  251. Anasuya Ray, Smreti Vasudevan, Suparna Sengupta, 6-Shogaol Inhibits Breast Cancer Cells and Stem Cell-Like Spheroids by Modulation of Notch Signaling Pathway and Induction of Autophagic Cell Death.  Published: September 10, 2015. DOI: 10.1371/journal.pone.0137614
  252. 195.http://www.theguardian.com/world/2013/aug/03/uruguay-cannabis-
  253. lawhttp://www.presstv.ir/detail/2013/08/01/316632/uruguay-passes-bill-on-
  254. marijuana/http://www.ctvnews.ca/business/uruguay-taking-steps-to-become-first-nation-with-legal-marijuana-industry-1.1393211
  255. http://news.yahoo.com/uruguays-house-oks-legal-marijuana-market-plan-024441970.html(1)
  256. http://edrv.endojournals.org/content/27/1/73.fullhttp://rstb.royalsocietypublishing.org/content/367/1607/3326.abstract?sid=20cf2c23-e4fd-49e3-9398-ec8be2e00226.
  257. A.  JOHNS, Psychiatric effects of cannabis. SUBSTANCE MISUSE PAPERS, 
  258. IBID.
  259. Abrams DI, Jay CA, Shade SB, et al. Cannabis in painful HIV-associated sensory neuropathy: a randomized placebo-controlled trial. Neurology. 2007;68(7):515-521.
  260. Ahmedzai S, Carlyle DL, Calder IT, Moran F. Anti-emetic efficacy and toxicity of nabilone, a synthetic cannabinoid, in lung cancer chemotherapy. Br J Cancer. 1983;48(5):657-663.
  261. American College of Physicians. Supporting research into the therapeutic role of marijuana. (Position paper, 2008.) Accessed at http://www.acponline.org/advocacy/where_we_stand/other_issues/medmarijuana.pdf on March 4, 2015.
  262. Bhattacharyya S, Crippa JA, Allen P, et al. Induction of psychosis by {delta}9-tetrahydrocannabinol reflects modulation of prefrontal and striatal function during attentional salience processing. Arch Gen Psychiatry. 2012;69(1):27-36.
  263. Beal JE, Olson R, Laubenstein L, et al. Dronabinol as a treatment for anorexia associated with weight loss in patients with AIDS. J Pain Symptom Manage. 1995;10(2):89-97.
  264. Beal JE, Olson R, Lefkowitz L, et al. Long-term efficacy and safety of dronabinol for acquired immunodeficiency syndrome-associated anorexia. J Pain Symptom Manage. 1997;14(1):7-14.
  265. Cannabis-In-Cachexia-Study-Group, Strasser F, Luftner D, Possinger K, et al. Comparison of orally administered cannabis extract and delta-9-tetrahydrocannabinol in treating patients with cancer-related anorexia-cachexia syndrome: a multicenter, phase III, randomized, double-blind, placebo-controlled clinical trial from the Cannabis-In-Cachexia-Study-Group. J Clin Onc. 2006;24:3394-3400.
  266. Ellis RJ, Toperoff W, Vaida F, et al. Smoked medicinal cannabis for neuropathic pain in HIV: a randomized, crossover clinical trial. Neuropsychopharmacology. 2009;34(3):672-680.
  267. Guzmán M, Duarte MJ, Blázquez C, et al. A pilot clinical study of Delta9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme. Br J Cancer. 2006;95(2):197-203.
  268. Haney M, Rabkin J, Gunderson E, Foltin RW. Dronabinol and marijuana in HIV(+) marijuana smokers: acute effects on caloric intake and mood. Psychopharmacology. (Berl). 2005;181:170-178.
  269. Haney M, Gunderson EW, Rabkin J, et al. Dronabinol and marijuana in HIV-positive marijuana smokers. Caloric intake, mood,and sleep. J Acquir Immune Defic Syndr. 2007;45(5):545-554.
  270. Herman TS, Einhorn LH, Jones SE, et al. Superiority of nabilone over prochlorperazine as an antiemetic in patients receiving cancer chemotherapy. N Engl J Med. 1979;300(23):1295-1297.
  271. Jatoi A, Windschitl HE, Loprinzi CL, et al. Dronabinol versus megestrol acetate versus combination therapy for cancer-associated anorexia: a North Central Cancer Treatment Group study. J Clin Oncol. 2002;20(2):567-573.
  272. Johnson JR, Burnell-Nugent M, Lossignol D, et al. Multicenter, double-blind, randomized, placebo-controlled, parallel-group study of the efficacy, safety, and tolerability of THC:CBD extract and THC extract in patients with intractable cancer-related pain. J Pain Symptom Manage. 2010;39(2):167-179.
  273. Johnson JR, Lossignol D, Burnell-Nugent M, Fallon MT. An open-label extension study to investigate the long-term safety and tolerability of THC/CBD oromucosal spray and oromucosal THC spray in patients with terminal cancer-related pain refractory to strong opioid analgesics. J Pain Symptom Manage. 2013;46(2):207-218.
  274. Karst M, Salim K, Burstein S, et al. Analgesic effect of the synthetic cannabinoid CT-3 on chronic neuropathic pain: a randomized controlled trial. JAMA. 2003;290:1757-1762.
  275. Koppel BS, Brust JC, Fife T, et al. Systematic review: efficacy and safety of medical marijuana in selected neurologic disorders: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2014;82(17):1556-1563.
  276. Kramer JL. Medical marijuana for cancer. CA Cancer J Clin. 2014 Dec 10.
  277. Meiri E, Jhangiani H, Vredenburgh JJ, et al. Efficacy of dronabinol alone and in combination with ondansetron versus ondansetron alone for delayed chemotherapy-induced nausea and vomiting. Curr Med Res Opin. 2007;23(3):533-543.
  278. Musty RE, Rossi R. Effects of Smoked Cannabis and Oral Δ9-Tetrahydrocannabinol on Nausea and Emesis After Cancer Chemotherapy: A Review of State Clinical Trials. Journal of Cannabis Therapeutics. 2001; 1(1): 29-56.
  279. National Cancer Institute. Cannabis and Cannabinoids (PDQ®) Health Professional Version, updated 12/17/14. Accessed at http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional on March 4, 2015.
  280. Portenoy RK, Ganae-Motan ED, Allende S, et al. Nabiximols for opioid-treated cancer patients with poorly-controlled chronic pain: a randomized, placebo-controlled, graded-dose trial. J Pain. 2012;13(5):438-449.
  281. Radwan MM, Elsohly MA, Slade D, et al. Biologically active cannabinoids from high-potency Cannabis sativa. J Nat Prod. 2009;72(5):906-911.
  282. Rog DJ, Nurmikko TJ, Young CA. Oromucosal delta9-tetrahydrocannabinol/cannabidiol for neuropathic pain associated with multiple sclerosis: an uncontrolled, open-label, 2-year extension trial. Clin Ther. 2007;29(9):2068-2079.
  283. Ross SA, ElSohly MA, Sultana GN, et al. Flavonoid glycosides and cannabinoids from the pollen of Cannabis sativa L. Phytochem Anal. 2005;16(1):45-48.
  284. Smith PF. New approaches in the management of spasticity in multiple sclerosis patients: role of cannabinoids. Ther Clin Risk Manag. 2010;6:59-63.
  285. Tramér MR, Carroll D, Campbell FA, et al. Cannabinoids for control of chemotherapy induced nausea and vomiting: quantitative systematic review. BMJ. 2001;323:16-21.
  286. Ware MA, Wang T, Shapiro S, et al. Smoked cannabis for chronic neuropathic pain: a randomized controlled trial. CMAJ. 2010;182(14):E694-701.
  287. Wilsey B, Marcotte T, Deutsch R, et al. Low-dose vaporized cannabis significantly improves neuropathic pain. J Pain. 2013;14(2):136-148.
  288. Woolridge E, Barton S, Samuel J, et al. Cannabis use in HIV for pain and other medical symptoms. J Pain Symptom Manage. 2005;29:358-367.
  289. M Guzmán, M J Duarte, C Blázquez, J Ravina, M C Rosa, I Galve-Roperh, C Sánchez, G Velasco and L González-Feria, A pilot clinical study of Δ9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme, British Journal of Cancer (2006) 95, 197–203. doi:10.1038/sj.bjc.6603236 www.bjcancer.com Published online 27 June 2006.
  290.  M. van der SteltW. B. VeldhuisP. R. BärG. A. VeldinkJ. F. G. Vliegenthart, and K. Nicolay, Neuroprotection by Δ9-Tetrahydrocannabinol, the Main Active Compound in Marijuana, against Ouabain-Induced In Vivo Excitotoxicity.  The Journal of Neuroscience, 1 September 2001, 21(17): 6475-6479.
  291. Paola MassiAngelo VaccaniStefania CerutiArianna ColomboMaria P. Abbracchio and Daniela ParolaroAntitumor Effects of Cannabidiol, a Nonpsychoactive Cannabinoid, on Human Glioma Cell Lines.  JPET March 2004 vol. 308 no. 3 838-845.
  292. Sofía TorresMar Lorente1Fátima Rodríguez-Fornés1Sonia Hernández-Tiedra1María Salazar1,2, A Combined Preclinical Therapy of Cannabinoids and Temozolomide against Glioma.  doi: 10.1158/1535-7163.MCT-10-0688Mol Cancer Therapy, January 2011 10; 90.
  293. McAllister SDMurase RChristian RTLau DZielinski AJAllison JAlmanza CPakdel ALee JLimbad CLiu YDebs RJMoore DHDesprez PY,  Pathways mediating the effects of cannabidiol on the reduction of breast cancer cell proliferation, invasion, and metastasis.  Breast Cancer Res Treat. 2011 Aug;129(1):37-47. doi: 10.1007/s10549-010-1177-4. Epub 2010 Sep 22.
  294. Alessia Ligresti, Aniello Schiano Moriello, Katarzyna Starowicz, Isabel Matias, Simona Pisanti, Luciano De Petrocellis, Chiara Laezza, Giuseppe Portella, Maurizio Bifulco and Vincenzo Di Marzo,  Anti-tumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma.   Endocannabinoid Research Group, Istituto di Chimica Biomolecolare, CNR Pozzuoli, Italy (AL, ASM, KS, IM, VDM); Istituto di Cibernetica, CNR Pozzuoli, Italy (ASM, LDP); Dipartimento di Biologia e Patologia Cellulare e Molecolare “L.Califano”, Università di Napoli “Federico II”(SP, CL, GP, MB) and Dipartimento di Scienze Farmaceutiche, Università degli Studi di Salerno, Fisciano, Italy (SP, MB).
  295. María M CaffarelClara AndradasEmilia MiraEduardo Pérez-GómezCamilla CeruttiGema Moreno-BuenoJuana M FloresIsabel García-RealJosé PalaciosSantos MañesManuel Guzmán and Cristina Sánchez, Cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition, Molecular Cancer20109:196, 22 July 2010.
  296. LUCIANO DE PETROCELLIS, DOMINIQUE MELCK, ANTONELLA PALMISANO§, TIZIANA BISOGNO, CHIARA LAEZZA, MAURIZIO BIFULCO, AND VINCENZO DI MARZO, The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation.  Proc. Natl. Acad. Sci. USA, Vol. 95, pp. 8375–8380, July 1998 Pharmacology.
  297. A Preet, R K Ganju, J E Groopman,  Δ9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo.  Oncogene (2008) 27, 339–346; doi:10.1038/sj.onc.1210641; published online 9 July 2007
  298. Ramer R1, Bublitz KFreimuth NMerkord JRohde HHaustein MBorchert PSchmuhl ELinnebacher MHinz B.,  Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1. FASEB J. 2012 Apr;26(4):1535-48. doi: 10.1096/fj.11-198184. Epub 2011 Dec 23.
  299.  Preet AQamri ZNasser MWPrasad AShilo KZou XGroopman JEGanju RK, Cannabinoid receptors, CB1 and CB2, as novel targets for inhibition of non-small cell lung cancer growth and metastasis. Cancer Prev Res (Phila). 2011 Jan;4(1):65-75. doi: 10.1158/1940-6207.CAPR-10-0181. Epub 2010 Nov 19.
  300. Mimeault MPommery NWattez NBailly CHénichart JP.  Anti-proliferative and apoptotic effects of anandamide in human prostatic cancer cell lines: implication of epidermal growth factor receptor down-regulation and ceramide production.  Prostate. 2003 Jun 15;56(1):1-12.
  301. Juan A. Ramos and  Fernando J. Bianco, The role of cannabinoids in prostate cancer: Basic science perspective and potential clinical applications.  Indian J Urol. 2012 Jan-Mar; 28(1): 9–14.
  302. De Petrocellis LLigresti ASchiano Moriello AIappelli MVerde RStott CGCristino LOrlando PDi Marzo V, Non-THC cannabinoids inhibit prostate carcinoma growth in vitro and in vivo: pro-apoptotic effects and underlying mechanisms. Br J Pharmacol. 2013 Jan;168(1):79-102. doi: 10.1111/j.1476-5381.2012.02027.
  303.  Kristin GustafssonBirger ChristenssonBirgitta Sander and Jenny FlygareCannabinoid Receptor-Mediated Apoptosis Induced by R(+)-Methanandamide and Win55,212-2 Is Associated with Ceramide Accumulation and p38 Activation in Mantle Cell Lymphoma.  Molecular PharmacologyNovember 2006 vol. 70 no. 5 1612-1620.
  304. Kristin Gustafsson, Xiao Wang1, Denise Severa1, Maeve Eriksson1, Eva Kimby2, Mats Merup2, Birger Christensson1, Expression of cannabinoid receptors type 1 and type 2 in non-Hodgkin lymphoma: Growth inhibition by receptor activation. International Journal of Cancer, Volume 123,  Issue 5pages 1025–10331 September 2008.
  305. Jia WHegde VLSingh NPSisco DGrant SNagarkatti MNagarkatti PS, Delta9-tetrahydrocannabinol-induced apoptosis in Jurkat leukemia T cells is regulated by translocation of Bad to mitochondria. Mol Cancer Res. 2006 Aug;4(8):549-62.
  306.  Whyte DAAl-Hammadi SBalhaj GBrown OMPenefsky HSSouid AK.  Cannabinoids inhibit cellular respiration of human oral cancer cells. Pharmacology. 2010;85(6):328-35. doi: 10.1159/000312686. Epub 2010 Jun 2.
  307. Vara DSalazar MOlea-Herrero NGuzmán MVelasco GDíaz-Laviada, Anti-tumoral action of cannabinoids on hepatocellular carcinoma: role of AMPK-dependent activation of autophagy. Cell Death Differ. 2011 Jul;18(7):1099-111. doi: 10.1038/cdd.2011.32. Epub 2011, April 8.
  308. A. Carracedo, M. Gironella, M. Lorente, S. Garcia, M. Guzam, F. Velasco, J. Lovanna, Cannabinoids Induce Apoptosis of Pancreatic Tumor Cells via Endoplasmic Reticulum Stress–Related Genes. Cancer Research, The American Association of Cancer Research, 2006, May 5.
  309. Morgan G1, Ward RBarton M.The contribution of cytotoxic chemotherapy to 5-year survival in adult malignancies.  Clin Oncol (R Coll Radiol). 2004 Dec;16(8):549-60.

– See more at: www.phoreveryoung.com

The Cure for Cancer? That’s an easy question to answer! The Cure for Cancer is Found in its Prevention NOT in its Treatment! – Dr. Robert O. Young

Do you know what rotten apples, grapefruit or bananas look like? If you do then you know what cancer cells look like. Cancer cells are nothing more that healthy cells that are spoiling because of a compromised environment! Look at the picture below and you will see colorized cancerous body cells rotting in their toxic acidic environment.

What compromises the internal environment of a human body that causes body cells to begin spoiling and rotting? The answer is simple! The body’s build-up of acidic metabolic and dietary waste that has not been properly eliminated through the four channels of elimination – urination, defecation, respiration and perspiration!

Cancer is not a noun but an adjective that describes what is happening to body cells in an acidic environment due to an acidic lifestyle and diet. www.phoreveryoung.com
To learn more about Dr. Robert O. Young go to: https://www.linkedin.com/in/drrobertoyoung

Using Sodium and Potassium Bicarbonates in the Prevention and Treatment of ALL Sickness and Disease

Using Sodium and Potassium Bicarbonates in the Prevention and Treatment of ALL Sickness and Disease
Robert Young PhD

Naturopathic Practitioner – The pH Miracle Ti Sana Detox Medical Spa

Using Sodium and Potassium Bicarbonates in the Prevention and Treatment of ALL Sickness and Disease

Abstract

This article suggests that the use sodium and potassium bicarbonates are non-toxic primary alkalizing agents in the prevention and  treatment of all cancers, kidney disease, liver disease, Type I & Type II diabetes, Lupus, heart disease, Pharmacological toxicosis, vascular surgery operation, tonsillar herniation due to cerebral edema, lactic acid toxicosis, and hyponatremia or low salt or loss of salts due to excessive or over-exercise!

[Key words: cancer, diabetes, lupus, heart disease, vascular surgery, herniation, cerebral edema, lactic acid toxicosis, liver disease, kidney disease, hyponatremia, Pharmacological toxicosis]

Introduction

Sodium and potassium bicarbonate are excellent agents for a natural alkaline approach in the treatment for all sickness and disease, including cancer. Sodium bicarbonate is the universal mainstream treatment of acidosis. It is used every day by oncologists to neutralize the heavy acidic nature of their chemical and chemotherapeutic agents which are often quite toxic. Sodium bicarbonate is also used routinely in many clinical situations as herein noted including many peer–reviewed journals:

1) Severe diabetic ketoacidosis (1)

2) Cardiopulmonary resuscitation (2)

3) Pregnancy (3)

4) Hemodialysis (4)

5) Peritoneal dialysis (5)6) Pharmacological toxicosis (6)

7) Hepatopathy (7)

8) Vascular surgery operations (8)

Medics and emergency room medical doctors are accustomed to participating in a flurry of activity when trying to save a persons live after a cardiac arrest–inserting IVs and breathing tubes, performing defibrillation to restart the heart, etc. Sodium bicarbonate is a constant performer under such conditions and is more commonly used than magnesium injections, which is traditionally at the top of every doctor’s protocol for cardiac arrest.

Mainstream oncologists recognize the routine involvement of late stage infections which I refer to as outfections in all cancerous conditions. Medical savants also recognize that bacteria, yeast and mold is present in over forty percent of all cancerous conditions. (9) The most recent research in this area demonstrates how even viruses, which I describe as crystallized acid, is present in fifty percent of certain types of cancerous conditions. (10)

Sodium and potassium bicarbonate increases the hydroxyl ions or electron levels through increased alkalinity to the cells buffering the metabolic acids that can cause cancer.(20)  It is also one of the most basic medicines in allopathic and alternative medicine we have for the treatment of kidney disease.  Research by British scientists at the Royal London Hospital shows that sodium bicarbonate can dramatically slow the progress of chronic kidney disease.(11) We don’t need a thousand years of scientific tests to understand something as simple and essential as alkaline water and it is quite the same with sodium and potassium bicarbonate. Sodium and potassium bicarbonate are always present in the best alkaline drinking waters and organic raw green foods and is constantly being produced by the cover cells of the stomach to alkalize the acidic foods and liquids we ingest, including buffering metabolic and respiratory acids in order to maintain the alkaline design of the blood and tissues at a delicate pH of 7.365.(20)

What is Latent Tissue Acidosis?
Medical doctors are not taught in medical school and therefore do not understand or recognize latent tissue acidosis. They understand and recognize compensated acidosis and decompensated acidosis. In compensated acidosis, breathing increases in order to blow off more carbonic acid which decreases PCO2 because of the lowered carbonate or HCO3. When the breathing rate can no longer get any faster and when the kidneys can no longer increase its’ function to keep up with the acid load, then the blood pH starts to change from a pH of 7.365 to 7.3 then to 7.2. At a blood pH of 6.95 the heart relaxes and the client goes into a coma or dies.

Latent “acidosis” is a condition that exists when there are not enough bases in the alkalophile glands because they have been used up in the process of neutralizing the acids adsorbed to the collagen fibers. This leads to compensated “acidosis.” This means the blood pH has not changed but other body systems have changed. This can then lead to decompensated “acidosis” where the alkaline reserves of the blood are used up and the pH of the blood is altered. Decompensated “acidosis” can be determined by testing the blood pH, urine pH and the saliva pH. The decrease in the alkaline reserves in the body  can occur because of hyper-proteinization, (eating meat and cheese!) or too much protein, and hyper-carbonization, or too much sugar or from excessive or over-excercise. This is why young athletes fall over dead or why 80 to 90 year old folks are all shrunk up and look like prunes. They have very little or no alkaline reserves in their alkalophile glands. When all the alkaline minerals are gone, so are you and your battery runs out of charge. The charge of your cellular battery can be measured by testing the ORP or the oxidative reduction potential of the blood, urine or saliva using an ORP meter. As you become more acidic this energy potential or ORP increases.

How Is Sodium Bicarbonate Created In The Body?

The parietal or cover cells of the stomach split the sodium chloride of the blood. The sodium ion is used to bind with water and carbon dioxide to form the alkaline salt, sodium bicarbonate or NaHCO3. The biochemistry is: H20 + CO2 + NaCl = NaHCO3 + HCL. This is why I call the stomach an alkalizing organ NOT an organ of digestion. The stomach DOES NOT digest the food or liquids we ingest but it alkalizes the foods and liquids we ingest.  We have one instrument in the human body to digest food and it is NOT the stomach it is your teeth.  Once we swallow our food or drink the stomach begins to prepare the food by alkalizing it in a bath of sodium bicarbonate.

For each molecule of sodium bicarbonate (NaHCO3) made, a molecule of hydrochloric acid (HCL) is made and secreted into the so-called digestive system – specifically, the stomach (the gastric pits in the stomach) – to be eliminated via the blood. Therefore HCL is an acidic waste product of sodium bicarbonate created by the stomach to alkalize the food and liquids ingested.

Exercise Creates Metabolic Acidic Waste Products Which Are Harmful To The Blood and Tissues

When one exercises or over-exercises the body needs additional alkaline bicarbonate salts to buffer lactic acids.  The additional bicarbonate is created in the stomach lining to buffer the increased amounts of lactic acids produced as a waste product of metabolism.  The production of sodium bicarbonate will always leave an acidic waste product of hydrochloric acid in the gastric pits of the stomach leading to nausea, light headedness, dizziness, muddle thingking, and poor circulation.  If the excessive exercise continues this can then lead to a dificiency of mineral and bicarbonate salts (electrolytes lost through perspiration or urination) which may lead to latent tissue acidosis, pain, edema, hyponatrenia and death.

But how does something like sodium and/or potassium bicarbonate, so seemingly innocuous have such a dramatic effect? During prolonged or intense exercise muscles produce large amounts of acidic waste products, such as lactic acid, that lead to soreness, stiffness, fatigue and possible edema if these acids are not buffered and eliminated through urination or perspiration. Because sodium and potassium bicarbonate naturally reduces metabolic acids, it acts as a buffer against these performance-limiting by-products.

Current research suggests that supplemental sodium bicarbonate, like the pH Miracle pHour Salts (contains sodium and potassium bicarbonate) is particularly helpful in speed-based events, including sprints, football and other fast-moving games, and middle-distance (up to 10km) running, swimming and cycling. “Essentially, sodium bicarbonate is an alkaline substance that increases the pH of the blood,” Dr Folland says. “This seems to reduce and offset the acidity produced in the muscles during intense, anaerobic exercise that produces lactic acid most quickly, such as fast running or swimming.”

In Dr Folland’s study, swimmers who took the sodium bicarbonate knocked 1.5 seconds off their time for 200m, a difference that may seem insignificant to recreational swimmers but which is substantial at elite level.

“At the last Olympics, the top four swimmers in the men’s 200m freestyle were separated by just 1.4 seconds,” Dr Folland says. “So, in theory, it could be the difference between winning a medal and not.”

Anyone can try it, he says, but only those who are serious enough to monitor their times and progress in sports such as running, swimming or cycling may notice the few seconds advantage it might provide. “The increments of improvement are relatively small to the average person, although significant to someone who competes,” Dr Folland says.

Athletes for years have sworn that taking a spoonful of bicarbonate of soda (baking soda) helps them to keep going for longer. For years, experts doubted that there was anything other than a placebo effect to these claims until they subjected the substance to rigorous examination. Most exercise scientists investigating the trend for “soda-doping” among athletes and gym-goers have shown that it offers significant benefits for endurance and speed.”

At Loughborough University, for instance, physiologists reporting in the June issue of the International Journal of Sports Medicine showed that swimmers who took baking soda about one hour before a 200m event were able to shave a significant time off their usual performances. Dr Jonathan Folland, who led the study, says that it is not uncommon for top swimmers to take sodium bicarbonate (another name for the substance) before a competition to give them an edge. Indeed, he showed that of nine swimmers tested, eight recorded their fastest times after ingesting a supplement of the common baking ingredient – sodium bicarbonate.

Where are Bicarbonates Created In The Human Body and Why?

The chloride ion from the sodium chloride (salt) binds to an acid or proton forming HCL as a waste product of sodium bicarbonate production. HCL has a pH of 1 and is highly toxic to the blood and tissues and the cause of indigestion, acid reflux, ulcers, diabetes, cancer, hyponatremia, edema, tonsilar herniation and death.  When large amounts of acids, including HCL, enter the stomach from a rich animal protein or dairy product meal, such as meat and cheese, or from starchy foods from root vegetables like potatoes or during extreme exercise, acid is withdrawn from the acid-base household. The organism would die if the resulting alkalosis – or NaHCO3 (base flood) or base surplus – created by the stomach was not taken up by the alkalophile glands (salivary glands, pancreas, kidney, pylorus glands, Brunner’s glands, Lieberkuhn glands and liver) that need these quick bases in order to build up their strong sodium bicarbonate secretions. These alkalizing glands and organs are the stomach, pancreas, Brunner’s glands (between the pylorus and the junctions of the bile and pancreatic ducts), Lieberkuhn’s glands in the liver and its bile with its strong acid binding capabilities which it has to release on the highly acidic meat, cheese, potato, acid water or metabolic and/or respiratory acids from over-exercise to buffer its strong acids of nitric, sulphuric, phosphoric, uric and lactic acids in daily metabolism, respiration and excessive or over-exercise.

Bicarbonate acts to stimulate the ATPase by acting directly on it.(12)

The simple household product used for baking, cleaning, bee stings, treating asthma, cancer and acid indigestion is so effective in treating disease that it prevents patients from having to be put on kidney dialysis. The findings have been published in the Journal of the American Society of Nephrology. Bicarbonate is a truly strong universal concentrated nutritional medicine that works effectively in many clinical situations that we would not normally think of. Bicarbonates of sodium and potassium are a prime emergency room and intensive care medicine that can save a person’s life in a heartbeat and it is also a supermarket item that you can take right off the shelf and use for more things than one can imagine – including diaper rash.

Dr. SK Hariachar, a nephrologist who oversees the Renal Hypertension Unit in Tampa, Florida stated, upon seeing the research on sodium bicarbonate and kidney disease, “I am glad to see confirmation of what we have known for so long.  I have been treating my patients with bicarbonate for many years in attempts to delay the need for dialysis, and now we finally have a legitimate study to back us up. Not only that, we have the added information that some people already on dialysis can reverse their condition with the use of sodium bicarbonate”.

A dialysis technician at the same center as Dr. Hariachar, who used to be on dialysis himself for 2 years as a result of kidney failure, had his kidneys miraculously start functioning to the point where dialysis was no longer needed. He states that he was prescribed oral doses of sodium bicarbonate throughout his treatment, and still takes it daily to prevent recurrences of kidney failure. Dr. Hariachar maintains though, that not everyone will be helped by taking bicarbonate. He says that those patients who have difficulty excreting acids, even with dialysis using a bicarbonate dialysate bath, that, “oral bicarbonate makes all the difference.”

The Stomach, Pancreas and Kidneys Naturally Produce Sodium Bicarbonate Every Day

The exocrine section of sodium bicarbonate from the stomach and the pancreas have been greatly ignored in the treatment of diabetes and cancer even though its impairment is a well documented condition. The stomach and the pancreas is primarily responsible for the production of sodium bicarbonate necessary for normal alkalization of food and liquids ingested. Sodium bicarbonate is so important for protecting the kidney’s that even the kidneys get into the act of producing sodium bicarbonate.  We now know the common denominator between hyponatremia, inflammation, edema, diabetes, kidney disease, and cancer is the lack of sodium and potassium bicarbonate or the body’s inability to produce sodium and potassium bicarbonate because of a lack of mineral salts in the diet. When the body is hit with reductions in sodium bicarbonate output by these three organs,’ acid conditions build up and then the entire body physiology begins to change from a state of oxygenation to fermentation. Likewise when acid build-up outstrips these organs normal sodium bicarbonate capacity, cellular, tissue, glandular and organ deterioration begins.

The stomach, pancreas and the kidneys alone produce about five hundred
grams (about one pound) of sodium and/or potassium bicarbonate per day in an attempt to neutralize dietary and/or metabolic acid in the blood and interstitial fluids that surround the body cells.

The stomach, pancreas and the kidneys monitor and control the acidity or “acid-base” (pH) balance of the blood and tissues. If the blood and tissues are too acidic, the stomach and/or the kidney’s make sodium bicarbonate to restore the blood and tissue pH back to a delicate pH balance of 7.365. If the blood or tissues are too alkaline, then the kidney excretes sodium bicarbonate into the urine to restore the 7.365 alkaline balance. Acid-base balance is the net result of two processes, first, the removal of sodium bicarbonate subsequent to hydrogen ion production from the metabolism or dietary constituents; second, the synthesis of “new” sodium bicarbonate by the stomach and/or the  kidney’s.(13)  The stomach and kidneys pull salt, water and carbon dioxide from the blood to make sodium bicarbonate to maintain the alkaline design of the body during all functions of the body from the ingestion of food or drink to exercise.  The chemical formula is as follows:  NaCl + H2O + CO2 = NaHCO3 + HCL.  The waste product of sodium bicarbonate is hydrochloric acid which is eliminated by kidneys as an acidic excretion of the urine.
It is considered that normal adults eating ordinary Western diets have chronic, low-grade acidosis which increases with age. This excess acid, or acidosis, is considered to contribute to many diseases and to contribute to the aging or rotting process. Acidosis occurs often when the body cannot produce enough sodium bicarbonate ions (or other alkaline compounds) to neutralize the acids in the body formed from metabolism and eating and drinking highly acid foods and drinks like chicken, pork, beef, dairy products, coffee, tea, alcohol, chocolate, soft drinks, just to name a few.  We are also testing bottled mineral water and finding that these waters are acidic and may contribute to overall tissue acidosis.
Acid-buffering by means of base supplementation (The pH Miracle pHour Salts) of sodium bicarbonate is one of the major roles of dialysis. Sodium bicarbonate concentration in the dialysate (solution containing water and chemicals (electrolytes) that passes through the artificial kidney to remove excess fluids and wastes from the blood, also called “bath.”) should be personalized in order to reach a midweek pre-dialysis serum sodium bicarbonate concentration of 22 mmol/l.(14)  Use of sodium bicarbonate in dialysate has been shown in studies to better control some metabolic aspects and to improve both treatment tolerance and patients’ life quality.  Sodium bicarbonate dialysis, unlike acetate-free biofiltration, triggers mediators of inflammation and apoptosis.(15)

One of the main reasons we become over-acid is from over-consumption of animal protein, dairy products, high sugar fruit, grains, alcohol, coffee, tea, chocolate, soft drinks and over-exercise or under-exercise. Eating meat and dairy products may increase the risk of prostate cancer, research suggests.(16) We would find the same for breast and other cancers as well metastatic cancers.(17) Conversely mineral deficiencies are another reason and when you combine high protein intake with decreasing intake of alkaline minerals you have a dis-ease in the making through lowering of pH into highly acidic conditions. When protein breaks down in our bodies they break into strong acids, such as, nitric, uric, sulphuric and phosphoric acid.

Unless a treatment actually removes acidic toxins  from the body and increases oxygen, water, and nutrients most medical interventions come to naught.

These metabolic and dietary acids must be excreted by the kidney’s because they contain sulfur, phosphorus, and/or nitrogen which cannot break down into water and carbon dioxide to be eliminated as weak acids. In their passage through the kidney’s these strong acids of ntric, sulphuric, phosphoric and uric acid must take a basic mineral with them because in this way they are converted into their neutral salts and don’t burn or destroy the kidney’s on their way out. This would happen if these strong acids were excreted in their free acidic form.

Substituting a sodium bicarbonate solution for saline
infusion prior to administration of radiocontrast
material seems to 
reduce the incidence of nephropathy.(18)
Dr. Thomas P. Kennedy
American Medical Association

Sodium and potassoum bicarbonate ions neutralize the acids that cause chronic inflammatory reactions. Hence, sodium and potassium bicarbonate are of benefit in the treatment of a range of chronic inflammatory and autoimmune diseases. Sodium and potassium bicarbonate are well-studied and used salts with known effects. Sodium and potassium bicarbonate are effective in treating poisonings or overdoses from many chemicals and pharmaceutical drugs by negating their cardiotoxic and neurotoxic effects.(19)  It is the main reason it is used by orthodox oncology – to mitigate the highly toxic effects of chemotherapy.

Sodium and potassium bicarbonates possess the property of absorbing heavy metals, dioxins and furans. Comparison of cancer tissue with
healthy tissue from the same person shows that the cancer tissue
has a much higher concentration of toxic chemicals, pesticides, etc.

Sodium and potassium bicarbonate intravenous infusions are indicated in the treatment of metabolic acidosis, which may occur in severe renal disease, uncontrolled diabetes, and circulatory insufficiency due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest, tonsillar herniation due to cerebral edema, severe primary lactic acidosis and hyponatremia due to excessive or over-exercise.  During heavy exercise, if the the resulting lactic acid is not adsorbed by the collagen fibers, the specific acid catchers of the body, the blood pH will drop and the body will go into a coma and the person will die.

The total collection of these fibers is the largest organ of the body called SCHADE, the colloidal connective tissue organ. NO liquid exchange occurs between the blood and the parenchyma cells, or in reverse, unless it passes through this connective tissue organ. This organ connects and holds everything in our bodies in place. This organ is composed of ligaments, tendons, sinew, and the finer fibers that become the scaffolding that holds every single cell in our bodies in place. When acids are stored in this organ, which includes the muscles, inflammation or edema and pain develop. The production of lactic acid is increased with excessive exercise and the ingestion of milk, cheese, yogurt, butter, ice cream, high sugar fruit and starchy root vegetables like potatoes.

That is why I have stated, “acid is pain and pain is acid or acid is edema and edema is pain”.  You cannot have one without the other. This is the beginning of latent tissue acidosis leading to irritation, inflammation, edema and degeneration of the cells, tissues and organs and eventual or sudden death.  It is why we are seeing so many amateur and professional atheletes pass out and die on the playing fields.  Metabolic, respiratory and gastrointestinal acids can and do kill and death can be overted by simply maintaining the alkaline design of the body fluids with protective hydration of alkaine sodium bicarbonate fluids.

The acid/alkaline balance is one of the most overlooked aspects of diagnostic medicine. In general, the world population is heavily acidic, excepting alkalarian vegans (those who ingest raw, organic green fruit, vegetables, mineral salts, alkaline water and unsaturated seed and nut oils), and even their bodies have to face increasing levels of environmental toxic exposure, which may contribute to an acidic pH condition of the blood and then tissues.

With over 30 years of research and testing over 100,000 individual samples of blood and over 100,000 samples of urine and saliva, I have come to the conclusion that the human body is an acidic producing organism by function – yet, it is an alkaline organism by design. Eating animal protein, especially meat and cheese, sugar, fermented foods, starchy foods like potatoes, acidic water, alcohol, coffee, tea, chocolate,  and excessive exercise or under-exercise, obsessive behaviors, lack of rest, lack of sunshine, and emotional stress are deadly acidic lifestyle choices.

All enervation, under-performance, sensitivity, irritation, inflammation, edema, catarrh, induration, ulcerations, degeneration, aging and cancerous conditions are caused by a four letter word – ACID, which is an acronym which stands for:

A = acidic food and drink, attitudes and activities,
C = compromised internal acidic environment,
I = illness and dis-ease, and,
D = desire for more acidic foods, drinks, attitudes and activities, and the cycle repeats itself.[20]

We ingest acidic medicines to lessen the symptoms of our illness. We stimulate the body with unhealthy forms of energy providing quick, often temporary relief from our symptoms which begins the cycle all over again creating a very powerful pattern of poor health and dis-ease.

Conclusion

The pH Alkalizing Lifestyle and Diet is a low acid producing diet and lifestyle that focuses on the foundational principal that the body is alkaline by design and yet acidic by function. This makes this program the ultimate program for preventing and reversing aging and the onset of sickness and disease. I would say that the pH Alkalizing Lifestyle and Diet is the perfect diet and lifestyle for a longer healthier life.(20)

References

1. Gamba, G., “Bicarbonate therapy in severe diabetic ketoacidosis. A double blind, randomized, placebo controlled trial.” (Rev Invest Clin 1991 Jul-Sep;43(3):234-8). Miyares Gom ez A. in “Diabetic ketoacidosis in childhood: the first day of treatment.” (An Esp Pediatr 1989 Apr;30(4):279-83)

2. Levy, M.M., “An evidence-based evaluation of the use of sodium bicarbonate during cardiopulmonary resuscitation.” (Crit Care Clin 1998 Jul;14(3):457-83). Vukmir, R.B., Sodium bicarbonate in cardiac arrest: a reappraisal (Am J Emerg Med 1996 Mar;14(2):192-206). Bar-Joseph, G., “Clinical use of sodium bicarbonate during cardiopulmonary resuscitation–is it used sensibly?” (Resuscitation 2002 Jul;54(1):47-55).

3. Zhang. L., “Perhydrit and bicarbonate improve maternal gases and acid-base status during the second stage of labor.” Department of Obstetrics and Gynecology, Xiangya Hospital, Hunan Medical University, Changsha 410008. Maeda, Y., “Perioperative administration of bicarbonated solution to a patient with mitochondrial encephalomyopathy.” (Masui 2001 Mar;50(3):299-303).

4. Avdic. E., “Bicarbonate versus acetate hemodialysis: effects on the acid-base status.” (Med Arh 2001;55(4):231-3).

5. Feriani, M., “Randomized long-term evaluation of bicarbonate-buffered CAPD solution.” (Kidney Int 1998 Nov;54(5):1731-8).

6. Vrijlandt, P.J., odium bicarbonate infusion for intoxication with tricyclic antidepressives: recommended inspite of lack of scientific evidence. Ned Tijdschr Geneeskd 2001 Sep 1;145(35):1686-9). Knudsen, K., “Epinephrine and sodium bicarbonate independently and additively increase survival in experimental amitriptyline poisoning.” (Crit Car e Med 1997 Apr;25(4):669-74).

7. Silomon, M., “Effect of sodium bicarbonate infusion on hepatocyte Ca2+ overload during resuscitation from hemorrhagic shock.” (Resuscitation 1998 Apr;37(1):27-32). Mariano, F., “Insufficient correction of blood bicarbonate levels in biguanide lactic acidosis treated with CVVH and bicarbonate replacement fluids.” (Minerva Urol Nefrol 1997 Sep;49(3):133-6).

8. Dement’eva, I.I., “Calculation of the dose of sodium bicarbonate in the treatment of metabolic acidosis in surgery with and deep hypothermic circulatory arresta.” (Anesteziol Reanimatol 1997 Sep-Oct;(5):42-4).

9. “I believe that, conservatively, 15 to 20 percent of all cancer is caused by infections; however, the number could be larger — maybe double,” (Dr. Andrew Dannenberg, Director of the Cancer Center at New York-Presbyterian Hospital/Weill Cornell Medical Center.”) Dr. Dannennberg made the remarks in a speech in December 2007 at the annual international conference of the American Association for Cancer Research.

10. A sexually transmitted virus that causes cervical cancer is also to blame for half of all cases of cancer of the penis.

11.  www.nelm.nhs.uk/en/NeLM-Area/News/2009—July/20/
Bicarbonate-supplementation-may-slow-renal-decline-in-chronic-kidney-disease/

12. Origin of the Bicarbonate Stimulation of Torpedo Electric Organ Synaptic Vesicle ATPase. Joan E. Rothlein  1 Stanley M. Parsons. Department of Chemistry and the Marine Science Institute, University of California, Santa Barbara, Santa Barbara, California, U.S.A.

13. Levine DZ, Jacobson HR: The regulation of renal acid secretion: New observations from studies of distal nephron segments. Kidney Int 29:1099–1109, 1986

14.  www.uptodate.com/patients/content/abstract.do?topicKey=~G/p55S8w8sQDwqG&refNum=28

15.  www.ncbi.nlm.nih.gov/pubmed/16523427

16.  news.bbc.co.uk/2/hi/health/7655405.stm

17.  Cancer Res. 2009 Mar 15;69(6):2260-8. Epub 2009 Mar 10.
Bicarbonate increases tumor pH and inhibits spontaneous metastases.
Robey IFBaggett BKKirkpatrick NDRoe DJDosescu JSloane BFHashim AIMorse DLRaghunand NGatenby RAGillies RJ. Source: Arizona Cancer Center, University of Arizona, Tucson, Arizona, USA

18.  JAMA 2004;291:2328-2334,2376-2377.www.urotoday.com/56/browse_categories/renal_transplantation_vascular_disease/
sodium_bicarbonate_may_prevent_radiocontrastinduced_renal_injury.html

19. These include, Benzotropines (valium) cyclic antidepressants (amytriptayine), organophosphates, methanol (Methyl alcohol is a cheap and potent adulterant of illicit liquors) Diphenhydramine (Benedryl), Beta blockers (propanalol) Barbiturates, and Salicylates (Aspirin).   Poisoning by drugs that block voltage-gated sodium channels produces intraventricular conduction defects, myocardial depression, bradycardia, and ventricular arrhythmias. Human and animal reports suggest that hypertonic sodium bicarbonate may be effective therapy for numerous agents possessing sodium channel blocking properties, including cocaine, quinidine, procainamide, flecainide, mexiletine, bupivacaine, and others.

20. www.phmiracle.com. Young.R.O., Young, S.R., The pH Miracle Revised and Updated, Hachett, 2010.

Harvard Trained Immunologist Demolishes California Legislation That Terminates Vaccine Exemptions

78764-babyandvaccines

The following open letter by a PhD Immunologist completely demolishes the current California legislative initiative to remove all vaccine exemptions. That such a draconian and cynical state statute is under consideration in the ‘Golden State’ is as shocking as it is predictable.  After all, it was mysteriously written and submitted shortly after the manufactured-in-Disneyland measles ‘outbreak’.

The indisputable science that is employed by Tetyana Obukhanych, PhD ought to be read by every CA legislator who is entertaining an affirmative vote for SB277.  Dr. Obukhanych skillfully deconstructs the many false and fabricated arguments that are advanced by Big Pharma and the U.S Federal Government as they attempt to implement a nationwide Super-Vaccination agenda.

When the California Senate refuses to consider authoritative scientific evidence which categorically proves the dangerous vaccine side effects on the schoolchildren, something is very wrong. Such conduct by the Senate constitutes criminal action that endangers the lives and welfare of children. Their official behavior must be acknowledged for what it is — CRIMINAL — and prosecuted to the fullest extent of the law.

An Open Letter to Legislators Currently Considering Vaccine Legislation from Tetyana Obukhanych, PhD in Immunology

Re:  VACCINE LEGISLATION

Dear Legislator:

My name is Tetyana Obukhanych. I hold a PhD in Immunology.  I am writing this letter in the hope that it will correct several common misperceptions about vaccines in order to help you formulate a fair and balanced understanding that is supported by accepted vaccine theory and new scientific findings.

Do unvaccinated children pose a higher threat to the public than the vaccinated?

It is often stated that those who choose not to vaccinate their children for reasons of conscience endanger the rest of the public, and this is the rationale behind most of the legislation to end vaccine exemptions currently being considered by federal and state legislators country-wide. You should be aware that the nature of protection afforded by many modern vaccines – and that includes most of the vaccines recommended by the CDC for children – is not consistent with such a statement. I have outlined below the recommended vaccines that cannot prevent transmission of disease either because they are not designed to prevent the transmission of infection (rather, they are intended to prevent disease symptoms), or because they are for non-communicable diseases. People who have not received the vaccines mentioned below pose no higher threat to the general public than those who have, implying that discrimination against non-immunized children in a public school setting may not be warranted.

  1. IPV (inactivated poliovirus vaccine) cannot prevent transmission of poliovirus (see appendix for the scientific study, Item #1). Wild poliovirus has been non-existent in the USA for at least two decades. Even if wild poliovirus were to be re-imported by travel, vaccinating for polio with IPV cannot affect the safety of public spaces.  Please note that wild poliovirus eradication is attributed to the use of a different vaccine, OPV or oral poliovirus vaccine. Despite being capable of preventing wild poliovirus transmission, use of OPV was phased out long ago in the USA and replaced with IPV due to safety concerns.
  1. Tetanus is not a contagious disease, but rather acquired from deep-puncture wounds contaminated with C. tetani spores. Vaccinating for tetanus (via the DTaP combination vaccine) cannot alter the safety of public spaces; it is intended to render personal protection only.
  1. While intended to prevent the disease-causing effects of the diphtheria toxin, the diphtheria toxoid vaccine (also contained in the DTaP vaccine) is not designed to prevent colonization and transmission of C. diphtheriae. Vaccinating for diphtheria cannot alter the safety of public spaces; it is likewise intended for personal protection only.
  1. The acellular pertussis (aP) vaccine (the final element of the DTaP combined vaccine), now in use in the USA, replaced the whole cell pertussis vaccine in the late 1990s, which was followed by an unprecedented resurgence of whooping cough. An experiment with deliberate pertussis infection in primates revealed that the aP vaccine is not capable of preventing colonization and transmission of B. pertussis (see appendix for the scientific study, Item #2). The FDA has issued a warning regarding this crucial finding.[1]
  • Furthermore, the 2013 meeting of the Board of Scientific Counselors at the CDC revealed additional alarming data that pertussis variants (PRN-negative strains) currently circulating in the USA acquired a selective advantage to infect those who are up-to-date for their DTaP boosters (see appendix for the CDC document, Item #3), meaning that people who are up-to-date are more likely to be infected, and thus contagious, than people who are not vaccinated.
  1. Among numerous types of H. influenzae, the Hib vaccine covers only type b. Despite its sole intention to reduce symptomatic and asymptomatic (disease-less) Hib carriage, the introduction of the Hib vaccine has inadvertently shifted strain dominance towards other types of H. influenzae (types a through f).These types have been causing invasive disease of high severity and increasing incidence in adults in the era of Hib vaccination of children (see appendix for the scientific study, Item #4).  The general population is more vulnerable to the invasive disease now than it was prior to the start of the Hib vaccination campaign.  Discriminating against children who are not vaccinated for Hib does not make any scientific sense in the era of non-type b H. influenzae disease.
  1. Hepatitis B is a blood-borne virus. It does not spread in a community setting, especially among children who are unlikely to engage in high-risk behaviors, such as needle sharing or sex. Vaccinating children for hepatitis B cannot significantly alter the safety of public spaces. Further, school admission is not prohibited for children who are chronic hepatitis B carriers. To prohibit school admission for those who are simply unvaccinated – and do not even carry hepatitis B – would constitute unreasonable and illogical discrimination.

In summary, a person who is not vaccinated with IPV, DTaP, HepB, and Hib vaccines due to reasons of conscience poses no extra danger to the public than a person who is.  No discrimination is warranted.

How often do serious vaccine adverse events happen?

It is often stated that vaccination rarely leads to serious adverse events. Unfortunately, this statement is not supported by science. A recent study done in Ontario, Canada, established that vaccination actually leads to an emergency room visit for 1 in 168 children following their 12-month vaccination appointment and for 1 in 730 children following their 18-month vaccination appointment (see appendix for a scientific study, Item #5).

When the risk of an adverse event requiring an ER visit after well-baby vaccinations is demonstrably so high, vaccination must remain a choice for parents, who may understandably be unwilling to assume this immediate risk in order to protect their children from diseases that are generally considered mild or that their children may never be exposed to.

Can discrimination against families who oppose vaccines for reasons of conscience prevent future disease outbreaks of communicable viral diseases, such as measles?

Measles research scientists have for a long time been aware of the “measles paradox.” I quote from the article by Poland & Jacobson (1994) “Failure to Reach the Goal of Measles Elimination: Apparent Paradox of Measles Infections in Immunized Persons.” Arch Intern Med 154:1815-1820:

“The apparent paradox is that as measles immunization rates rise to high levels in a population, measles becomes a disease of immunized persons.”[2]

Further research determined that behind the “measles paradox” is a fraction of the population called LOW VACCINE RESPONDERS. Low-responders are those who respond poorly to the first dose of the measles vaccine. These individuals then mount a weak immune response to subsequent RE-vaccination and quickly return to the pool of “susceptibles’’ within 2-5 years, despite being fully vaccinated.[3]

Re-vaccination cannot correct low-responsiveness: it appears to be an immuno-genetic trait.[4]  The proportion of low-responders among children was estimated to be 4.7% in the USA.[5]

Studies of measles outbreaks in Quebec, Canada, and China attest that outbreaks of measles still happen, even when vaccination compliance is in the highest bracket (95-97% or even 99%, see appendix for scientific studies, Items #6&7). This is because even in high vaccine responders, vaccine-induced antibodies wane over time.  Vaccine immunity does not equal life-long immunity acquired after natural exposure.

It has been documented that vaccinated persons who develop breakthrough measles are contagious. In fact, two major measles outbreaks in 2011 (in Quebec, Canada, and in New York, NY) were re-imported by previously vaccinated individuals.[6] – [7]

Taken together, these data make it apparent that elimination of vaccine exemptions, currently only utilized by a small percentage of families anyway, will neither solve the problem of disease resurgence nor prevent re-importation and outbreaks of previously eliminated diseases. 

Is discrimination against conscientious vaccine objectors the only practical solution?

The majority of measles cases in recent US outbreaks (including the recent Disneyland outbreak) are adults and very young babies, whereas in the pre-vaccination era, measles occurred mainly between the ages 1 and 15. Natural exposure to measles was followed by lifelong immunity from re-infection, whereas vaccine immunity wanes over time, leaving adults unprotected by their childhood shots. Measles is more dangerous for infants and for adults than for school-aged children.

Despite high chances of exposure in the pre-vaccination era, measles practically never happened in babies much younger than one year of age due to the robust maternal immunity transfer mechanism. The vulnerability of very young babies to measles today is the direct outcome of the prolonged mass vaccination campaign of the past, during which their mothers, themselves vaccinated in their childhood, were not able to experience measles naturally at a safe school age and establish the lifelong immunity that would also be transferred to their babies and protect them from measles for the first year of life.

Luckily, a therapeutic backup exists to mimic now-eroded maternal immunity. Infants as well as other vulnerable or immunocompromised individuals, are eligible to receive immunoglobulin, a potentially life-saving measure that supplies antibodies directed against the virus to prevent or ameliorate disease upon exposure (see appendix, Item #8).

In summary: 1) due to the properties of modern vaccines, non-vaccinated individuals pose no greater risk of transmission of polio, diphtheria, pertussis, and numerous non-type b H. influenzae strains than vaccinated individuals do, non-vaccinated individuals pose virtually no danger of transmission of hepatitis B in a school setting, and tetanus is not transmissible at all; 2) there is a significantly elevated risk of emergency room visits after childhood vaccination appointments attesting that vaccination is  not risk-free; 3) outbreaks of measles cannot be entirely prevented even if we had nearly perfect vaccination compliance; and 4) an effective method of preventing measles and other viral diseases in vaccine-ineligible infants and the immunocompromised, immunoglobulin, is available for those who may be exposed to these diseases. 

Taken together, these four facts make it clear that discrimination in a public school setting against children who are not vaccinated for reasons of conscience is completely unwarranted as the vaccine status of conscientious objectors poses no undue public health risk. 

Sincerely Yours,

Tetyana Obukhanych, PhD

Tetyana Obukhanych, PhD, is the author of the book Vaccine Illusion.  She has studied immunology in some of the world’s most prestigious medical institutions. She earned her PhD in Immunology at the Rockefeller University in New York and did postdoctoral training at Harvard Medical School, Boston, MA and Stanford University in California.

Dr. Obukhanych offers online classes for those who want to gain deeper understanding of how the immune system works and whether the immunologic benefits of vaccines are worth the risks:  Natural Immunity Fundamentals.

Appendix

Item #1. The Cuba IPV Study collaborative group. (2007) Randomized controlled trial of inactivated poliovirus vaccine in CubaN Engl J Med 356:1536-44

http://www.ncbi.nlm.nih.gov/pubmed/17429085

The table below from the Cuban IPV study documents that 91% of children receiving no IPV (control group B) were colonized with live attenuated poliovirus upon deliberate experimental inoculation.  Children who were vaccinated with IPV (groups A and C) were similarly colonized at the rate of 94-97%.  High counts of live virus were recovered from the stool of children in all groups.  These results make it clear that IPV cannot be relied upon for the control of polioviruses.

polio chart

Item #2. Warfel et al. (2014) Acellular pertussis vaccines protect against disease but fail to prevent infection and transmission in a nonhuman primate model.Proc Natl Acad Sci USA 111:787-92

http://www.ncbi.nlm.nih.gov/pubmed/24277828

“Baboons vaccinated with aP were protected from severe pertussis-associated symptoms but not from colonization, did not clear the infection faster than naïve [unvaccinated] animals, and readily transmitted B. pertussis to unvaccinated contacts. By comparison, previously infected [naturally-immune] animals were not colonized upon secondary infection.”

Item #3. Meeting of the Board of Scientific Counselors, Office of Infectious Diseases, Centers for Disease Control and Prevention, Tom Harkins Global Communication Center, Atlanta, Georgia, December 11-12, 2013

http://www.cdc.gov/maso/facm/pdfs/BSCOID/2013121112_BSCOID_Minutes.pdf

Resurgence of Pertussis (p.6)

“Findings indicated that 85% of the isolates [from six Enhanced Pertussis Surveillance Sites and from epidemics in Washington and Vermont in 2012] were PRN-deficient and vaccinated patients had significantly higher odds than unvaccinated patients of being infected with PRN-deficient strains.  Moreover, when patients with up-to-date DTaP vaccinations were compared to unvaccinated patients, the odds of being infected with PRN-deficient strains increased, suggesting that PRN-bacteria may have a selective advantage in infecting DTaP-vaccinated persons.”

Item #4. Rubach et al. (2011) Increasing incidence of invasive Haemophilus influenzaedisease in adults, Utah, USA. Emerg Infect Dis 17:1645-50

http://www.ncbi.nlm.nih.gov/pubmed/21888789

The chart below from Rubach et al. shows the number of invasive cases of H. influenzae(all types) in Utah in the decade of childhood vaccination for Hib.

Hib chart

Item #5. Wilson et al. (2011) Adverse events following 12 and 18 month vaccinations: a population-based, self-controlled case series analysis. PLoS One 6:e27897

http://www.ncbi.nlm.nih.gov/pubmed/22174753

“Four to 12 days post 12 month vaccination, children had a 1.33 (1.29-1.38) increased relative incidence of the combined endpoint compared to the control period, or at least one event during the risk interval for every 168 children vaccinated.  Ten to 12 days post 18 month vaccination, the relative incidence was 1.25 (95%, 1.17-1.33) which represented at least one excess event for every 730 children vaccinated.  The primary reason for increased events was statistically significant elevations in emergency room visits following all vaccinations.”

Item #6. De Serres et al. (2013) Largest measles epidemic in North America in a decade–Quebec, Canada, 2011: contribution of susceptibility, serendipity, and superspreading events. J Infect Dis 207:990-98

http://www.ncbi.nlm.nih.gov/pubmed/23264672

“The largest measles epidemic in North America in the last decade occurred in 2011 in Quebec, Canada.”

“A super-spreading event triggered by 1 importation resulted in sustained transmission and 678 cases.”

“The index case patient was a 30-39-year old adult, after returning to Canada from the Caribbean.  The index case patient received measles vaccine in childhood.”

“Provincial [Quebec] vaccine coverage surveys conducted in 2006, 2008, and 2010 consistently showed that by 24 months of age, approximately 96% of children had received 1 dose and approximately 85% had received 2 doses of measles vaccine, increasing to 97% and 90%, respectively, by 28 months of age.  With additional first and second doses administered between 28 and 59 months of age, population measles vaccine coverage is even higher by school entry.”

“Among adolescents, 22% [of measles cases] had received 2 vaccine doses.  Outbreak investigation showed this proportion to have been an underestimate; active case finding identified 130% more cases among 2-dose recipients.”

Item #7. Wang et al. (2014) Difficulties in eliminating measles and controlling rubella and mumps: a cross-sectional study of a first measles and rubella vaccination and a second measles, mumps, and rubella vaccination. PLoS One9:e89361

http://www.ncbi.nlm.nih.gov/pubmed/24586717

“The reported coverage of the measles-mumps-rubella (MMR) vaccine is greater than 99.0% in Zhejiang province.  However, the incidence of measles, mumps, and rubella remains high.”

Item #8. Immunoglobulin Handbook, Health Protection Agency

http://webarchive.nationalarchives.gov.uk/20140714084352/http://www.hpa.org.uk/webc/HPAwebFile/HPAweb_C/1242198450982

HUMAN NORMAL IMMUNOGLOBULIN (HNIG):

Indications

  1. To prevent or attenuate an attack in immuno-compromised contacts
  2. To prevent or attenuate an attack in pregnant women
  3. To prevent or attenuate an attack in infants under the age of 9 months

[1] http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm376937.htm

[2] http://archinte.jamanetwork.com/article.aspx?articleid=619215

[3] Poland (1998) Am J Hum Genet 62:215-220

http://www.ncbi.nlm.nih.gov/pubmed/9463343

“ ‘poor responders,’ who were re-immunized and developed poor or low-level antibody responses only to lose detectable antibody and develop measles on exposure 2–5 years later.”

[4] ibid

“Our ongoing studies suggest that seronegativity after vaccination [for measles] clusters among related family members, that genetic polymorphisms within the HLA [genes] significantly influence antibody levels.”

[5] LeBaron et al. (2007) Arch Pediatr Adolesc Med 161:294-301

http://www.ncbi.nlm.nih.gov/pubmed/17339511

“Titers fell significantly over time [after second MMR] for the study population overall and, by the final collection, 4.7% of children were potentially susceptible.”

[6] De Serres et al. (2013) J Infect Dis 207:990-998

http://www.ncbi.nlm.nih.gov/pubmed/23264672

“The index case patient received measles vaccine in childhood.”

[7] Rosen et al. (2014) Clin Infect Dis 58:1205-1210

http://www.ncbi.nlm.nih.gov/pubmed/24585562

“The index patient had 2 doses of measles-containing vaccine.”

Second Thoughts About Viruses, Vaccines, and the HIV/AIDS Hypothesis

HIV-budding-Color

In the sciences, people quickly come to regard as their own personal property that which they have learned and had passed on to them at the universities and academies. If however, someone else now comes along with new ideas that contradict the Credo (that has been recited for years and passed on in turn to others) and in fact even threaten to overturn it, then all passions are raised against this threat and no method is left untried to suppress it. People resist it in every way possible: pretending not to have heard about it; speaking disparagingly of it, as if it were not even worth the effort of looking into the matter. And so a new truth can have a long wait before finally being accepted.

-Goethe

Viruses

Introduction

The first isolation of a virus was achieved in 1892 by Russian bacteria hunter Dimitri Iwanowski, who gathered fluid from diseased tobacco plants. He passed this liquid through a filter fine enough to retain bacteria; yet to Iwanowski’s surprise, the bacteria-free filtrate easily made healthy plants sick. In 1898 a Dutch botanist, Martinus Willem Beijerinck, repeating the experiment, also recognized that there was an invisible cause and named the infectious agent “tobacco mosaic virus.” In the same year as Beijerinck’s report, two German scientists purified a liquid containing filterable viruses that caused foot-and-mouth disease in cattle (viruses were at one time called “filterable viruses,” but eventually the term “filterable” came to apply only to viruses, and was dropped). Walter Reed followed in 1901 with a filtrate responsible for yellow fever, and soon dozens of other disease-causing viruses were found.

In 1935 another American, Wendell M. Stanley, went back to the beginning and created pure crystals of tobacco mosaic virus from a filtered liquid solution. He affirmed that these crystals could easily infect plants, and concluded that a virus was not a living organism, since it could be crystallized like salt and yet remain infectious. Subsequently, bacteriologists all over the world began filtering for viruses, and a new area of biology was born-virology.

Historically, medical science has vacillated on the question of whether a virus is alive. Originally it was described as nonliving, but is currently said to be an extremely complex molecule or an extremely simple microorganism, and is usually referred to as a parasite having a cycle of life. (The term “killed” is applied to certain viral vaccines, thus implying an official conviction that viruses live.) Commonly composed of either DNA or RNA cores with protein coverings, and having no inherent reproductive ability, viruses depend upon the host for replication. They must utilize the nucleic acids of living cells they infect to reproduce their proteins (i.e., trick the host into producing them), which are then assembled into new viruses like cars on an assembly line. Theoretically, this is their only means of surviving and infecting new cells or hosts.

{Key words: Vaccines, Vaccination, Virus, HIV, AIDS, Ebola, Hunta virus, Hepatitis C, Pleomorphism, Yeast, Candida albicans, Koch’s postulate, Farr’s law, Virology, Louis Pasteur, Antione BeChamp, Microzyma]

Birth of Virology-a Miscarriage?

Underlying the birth of virology was the doctrine of monomorphism-that all microorganisms (herein called microforms) are fixed species, unchangeable; that each pathological type produces (usually) only one specific disease; that microforms never arise endogenously, i.e., have absolute origin within the host; and that blood and tissues are sterile under healthy conditions. This last point warrants immediate comment. Theoretically, under ideal health conditions the blood might be sterile, though it has the inherent potential to develop morbid microforms, as discussed in the main text of this book. Long and repeated observation of live blood in the phase-contrast, dark-field microscope, however, shows that the blood can contain various microforms in an otherwise asymptomatic host, or in a condition defined as normal or healthy in orthodox terms. The forms are easily visible before other physical symptoms arise. (Since long and repeated observation has correlated their presence with other disease symptoms and their disappearance with the return of health, they serve as indicators of impending outward signs of disease.)

Monomorphism was the cornerstone of developments in 20th-century medical research and treatments. Refusal by the mainstream to examine fairly, much less accept, the demonstrated facts of pleomorphism-that viruses and bacteria (and also yeast and fungi) are evolutions from the microzyma (see Section 1 of this Appendix); that microforms can rapidly change their form (evolve and “devolve”) in vivo, one becoming another dependent upon conditions in the inner terrain (environment); that blood and tissues are not necessarily sterile; and that there are no specific diseases, but only specific disease conditions-was the foundation of a latter day “Galileo debate.” It is so called because those who wore the “robes” of scientific authority, reprising the religious fanatics who punished the noted astronomer for his truths, would not be swayed from folly when presented with its contrary proofs. These proofs began in earnest with Antoine Bechamp in the last century (who also endured the indignation of a fanatical clergy).

In the early third of the 20th century, the heated debate took place over filterable bacteria versus non-filterable. This was a major battle concerning micromorphology (discussed briefly below). The orthodox view prevailed: bacterial forms were not small enough to pass, or did not have a smaller, earlier stage. What passed through “bacteria-proof filters was something else, i.e., viruses. Standard medical textbooks long made this fdtering distinction between bacteria and viruses. Subsequently, however, the cellular nature of many filterable forms originally thought to be viruses, such as some mycoplasmas, rickettsias, and various other groups, has been established. In this writer’s opinion, with the victory of the monomorphic view, deeper understanding of infectious “disease” was lost, setting the stage for cancer, degenerative symptoms and AIDS.

What You See?

A typical bacterium is about 1 micron in size. Most filterable forms now called viruses range in size from .3 microns (300 millimicrons) to .01 micron (10 millimicrons)-partially in the colloidal range (.1 to .001 micron). Most of the larger viruses are a third to a quarter the size of the average bacterium. Size is critical because .3 microns is the resolution limit of modern-day light microscopes (except for the claimed resolution of Canadian microscopist Gaston Naessens’ Somatoscope, at .015 microns). Thus, as viruses were discovered (except for the very large ones, such as mumps), they required an electron microscope to be seen, especially given the fact that Royal Rife’s microscope technology and career were destroyed by vested interests (see Section 1). Unfortunately, electron microscopes and the process of chemical staining disorganize all specimens, whereas Rife’s technology allowed life to proceed and thus evolve under its lens. As viruses became visible to advancing technology, the ramification was that the technology revealed, to minds infected with monomorphism, protein structures deemed foreign to the body.

A New Theory

Formulated by Bechamp in the 19th century, microzymian principle is the basis of a new theory about “viruses.” Briefly, this principle holds that in all living organisms are biologically indestructible anatomical elements, which he called microzymas. They are independently living organized ferments, capable of producing enzymes and capable of evolution into more complex microforms, such as bacteria. Bechamp’s thesis is that disease is a condition of one’s internal environment (terrain); that disease (and its symptoms) are “born of us and in us”; and that disease is not produced by an attack of microentities but calls forth their endogenous evolution. (The common biological basis for this is discussed below.)

My studies and research suggest that the complexes science calls viruses and retroviruses originate in the cell as microzymian principle suggests. However, they are created in response to an alarming situation (condition of disease) for the purpose of genetic repair. They are repair proteins evolved from anatomical elements (microzymas), not pathogenic organisms.

It is known that normal cell activity includes genetic repair. Both enzymes and proteins must be involved. What is the mechanism? Viruses are organized around DNA or RNA, not both. Thus, they are quite probably intended to repair genetic molecules or other structures, and show up with disease symptoms because the body needs them. Since viruses require a living cell/host for reproduction, how do we know that the scenario is not set in motion for a purpose by the cell (i.e., its microzymas), rather than being the result of invasion? Because disease (disturbance of balance in the organism) is so prevalent, especially that which has not yet become indicated by common symptoms, repair proteins may be frequently or constantly present. A toxified cell may easily suffer localized damage to the genome. Since most observers are not even aware of microzymian principle, much less understand or even consider it, and since monomorphism stresses invasion, these protein complexes are regarded as foreign and disease is attributed to them.

Another note of interest is the size of viruses compared to the microzyma. Viruses are considered to be some of the smallest biological particles and are frequently of colloidal size: e.g., hepatitis A, 27 nanometers (.027 microns); hepatitis B (.042 microns); poliovirus (.03 microns); EBV (.042 microns); fflV (.080 to .12 microns), influenza (.08 to .12 microns); mumps (.15 to .30 microns); smallpox (.30 x .24 microns); and, according to Bechamp, the microzyma (.0005 microns). This coincides with what Gaston Naessens says about the size of his somatid, which ranges from “a few Angstroms to a tenth of a micron.”[1]

In his book, The Blood and Its Third Anatomical ElementBechamp states: “The microzyma is at the beginning and at the end of all organization. It is the fundamental anatomical element whereby the cellules, the tissues, the organs, the whole of an organism are constituted living. … In a state of health the microzymas act harmoniously and our life is, in every meaning of the word, a regular fermentation. In the condition of disease, the microzymas do not act harmoniously, the fermentation is disturbed, the microzymas have either changed their function or are placed in an abnormal situation by some modification of the medium.”[2]  The virus is either a self-ordered microzymian polymerization, or (less likely) a structure made by microzymas. It is enveloped in protein which is also composed of microzymas, and could well be thought of as an autonomous molecular tool box.

Along with Drs. Glen Dettman and Archie Kalokerinos, I wonder, “whether Bechamp’s writing anticipated, in some respects, the discovery of RNA and DNA?” Could the genetic structure be the construct, thus a tool, of the microzyma? They quote a personal communication (1974) from a Professor Bayev of the USSR Academy of Sciences, who discusses his work showing that molecular self-restoration from its parts of pure transfer RNA from brewer’s yeast is possible (see Section 1 of this Appendix for full quotation).[3]

In my own research I have found molecular restorations similar to that described by Bayev. In my experiment I used five-year-old coagulated capillary blood from a woman with cancer. With one drop of 0.9% of sodium chloride, the blood was restored to an appearance and level of activity characteristic of a freshly drawn sample. In other words, the anatomical microzymas of the dried blood were restored to activity. Even the white globules became active. One might eagerly ask for an explanation of the reversal of polymers made during clotting. It is unclear at this point how this reversal takes place, except to say that what can evolve apparently has the potential to devolve. It is observable, however. For example, I have seen, and recorded on video, rod microforms retrograding without any visible decomposition from 10 microns in length to the vicinity of .1 micron.

This research supports the very important postulate that the cell is not the smallest living biological unit, as promulgated by conventional medical science. In fact, a smaller biological unit is the imperishable microzyma, which is an organized, living being “of a special category without analogue,” said Bechamp, who found them ready to become active in chalk deposits at least 11 million years old.[4]

The Pleomorphic Cycle

I suggest a developmental cycle in vivo consisting of three macrostages: (1) a primitive stage comprising the repair protein complexes; (2) an intermediate, or bacterial, stage including filterable forms such as the cell-wall deficient forms described by Lida Mattman, Ph.D. (in Cell Wall Deficient Forms, Stealth Pathogens); and (3) a culmination stage consisting of yeast and fungal phases, and then mold, the end phase. The usual course of development would be from microzyma to repair protein and then to bacterium, etc. However, under certain conditions, such as trauma for example, it is highly likely that the microzymas can skip the primitive stage and become bacteria directly. Although these transformations are as astounding as that of a larva to a butterfly, what is equally impressive under observation is the rapidity with which they can take place-in minutes, even seconds, sometimes. By the same token, when provoked by conditions and the cycle proceeds to yeast, fungus and then mold, it may occur so rapidly that the bacterial stage, if it happens, has no time to be of any significance.

Thus, symptogenic microforms can originate within higher organisms without invasion, via a permutation of the endogenous microzymas when the situation calls for such change. The situation is an imbalance referred to by Bechamp as a “modification of the medium.” Endogenous evolution is evident under the microscope when bacterial, yeast, and fungal forms are seen coming out of red blood cells which initially appear normal.

Biological Basis for the Pleomorphic Cycle

There is a common biological basis for the pleomorphic cycle and its increasing complexity of organization: More complex forms evolve inherently upon the death of an organism for the purpose of recycling its anatomical and chemical structures in the carbon cycle. The process of rapid evolution (which is reversible) is an essential life process which, beyond the repair stage, is necessary to return a dead organism to the earth. The second and third-stage microforms degenerate the body’s vital substances and tissues via putrefaction (bacteria) and fermentation (yeast and fungus). Fermentation results in acid waste products, which further break down tissue. Disease symptoms, then, especially the degenerative type, are not produced by viruses, but manifest as chemical decomposition, or attempted recycling via fermentation and acid toxins, but with “host” survival processes still operable (see Section 3 and discussion of pH in the main text). Obviously, certain other factors may play important roles in producing symptoms, such as heavy metal toxicity, or state of mind, for example. Some of the body’s survival methods also produce symptoms commonly called diseases. An example is eczema, an emergency expulsion of acid toxins via the skin.

The aforementioned causal (alarming) situation, or modification of the medium, is chronic acidification (pH imbalance) and oxygen deprivation in the blood and tissues due to acid-forming foods, adverse lifestyle, emotional stress, and environmental stress. This is not oversimplification. Acidification/hypoxia biochemically signals a dead host to the microzymas, while creating collapsed areas (dead zones) of the colloidal system in the intercellular fluid (see Section 2), and it is the primary physiological disease condition out of which the symptoms commonly called specific diseases arise.

Thus, we distinguish between this disease condition and its consequent symptoms, which include both the morbidly evolved microzymas and the physiological signs commonly thought of as specific diseases. As they develop, microforms (bacteria, yeast, fungus and mold) are actually scavenging forms of the microzyma, developed when disease in the cell life requires tissue to be broken up. These upper development forms are the ones easily visible in the blood before physical symptoms arise. They disappear (devolve) when the recycling task is complete, once again becoming microzymas of the earth and/or air.

Virus or Toxin?

Regarding the early period of virus isolation, a question is whether the unseen entities isolated in filtered fluids were accompanied by the waste products (mycotoxins) of fermentation by yeast and fungus of cellular elements, such as DNA. If virus filtrates are injected into a host to prove virulence, it is almost certain that easily filterable molecular toxins will be introduced as well. Could Dr. Stanley’s “pure crystals of tobacco mosaic virus” have been crystallized toxins? If so, they would certainly be highly symptogenic, as are exotoxins at the intermediate stage of the cycle, for example. However, it is not proof of anything that you can create illness by poison injection, except proof of that tautological fact.

In my research utilizing dark-field and phase-contrast microscopy, it is common to see crystallizations in the blood. It is normal for the body to use calcium or other mineral salts, and fats as well, to chelate the waste products from the morbid fermentation of body proteins, fats and sugars. Such crystal deposits are found in cancer tissue as well. A malignant tumor removed from the breast of one of my research clients was found to have numerous calcium deposits attached to it. It is an attempt to render inactive the substances that make our inner streams filthy, poison our cells, and coagulate colloidal systems in blood and intercellular fluid.

The term “virus” is the Latin word for poison, and gives us insight into the immediate cause of disease symptoms-poisons: mycotoxins, endotoxins, exotoxins, and toxins from environmental sources (many of which are primary or secondary mycotoxins). Orthodox medicine is well aware that it is bacterial toxins more than the bacteria themselves (they feed in us), that cause the symptoms referred to as infectious disease. Little if any emphasis is placed on this fine but important distinction. Always, the germ is emphasized. There is little to no awareness (or acknowledgment), either, of the same role played by toxins of the culminate microforms of the pleomorphic cycle. Their action and the body’s response to them are frequently ascribed to viruses, which do not produce toxins but are said to wreak havoc by a number of other means. However, if they participate in symptogenesis in a host it is because they are stimulated to evolve into more complex, toxigenic forms. Somewhat less likely is the possibility that they cause damage as a result of erroneous construction or function, for one reason or another-missing mineral nutrients leading to enzyme deficiencies, for example.

Misconception Breeds Contempt

In addition to chemical toxicity, however, what is the impact of the fear (emotional toxicity) that the word “virus” brings to mind and heart? It has been said that fear is the most deadly of disease conditions. If a “disease” kills one person, the fear of it may kill twenty. General prejudice concerning the danger of viruses is fundamental biological error based on Louis Pasteur’s germ theory, and is itself a perpetrator of auto-suggested illness. For example, in Africa doctors attribute some AIDS sickness to “voodoo death” syndrome, the term for illnesses induced psychologically. According to one nurse, “We had people who were symptomatically AIDS patients. They were dying of AIDS, but when they were tested and found out they were negative they suddenly rebounded and are now perfectly healthy.”[5]  Ironically, if the germ theory were founded on facts it would be correct to fear viruses, except there would be few, if any, humans living to discuss the issues. These socalled pathogenic entities are to researchers, medical practitioners and the press what criminals are to detectives-the focus and justification of their existence.

The Encyclopaedia Britannica has this to say about bacteria, which relates also to viruses:

The common idea of bacteria in the minds of most people is that of a hidden and sinister scourge lying in wait for mankind. This popular conception is born of the fact that attention was first focused upon bacteria through the discovery, some 70 years ago, of the relationship of bacteria to disease in man, and that in its infancy the study of bacteriology was a branch of medical science. Relatively few people assign to bacteria the important position in the world of living things that they rightly occupy, for it is only a few of the bacteria known today that have developed in such a way that they can live in the human body, and for every one of this kind, there are scores of others which are perfectly harmless and far from being regarded as the enemies of mankind, must be numbered among his best friends.

It is in fact no exaggeration to say that upon the activities of bacteria the very existence of man depends; indeed, without bacteria there could be no other living thing in the world; for every animal and plant owes its existence to the fertility of the soil, and this in turn depends upon the activity of the micro-organisms which inhabit the soil in almost inconceivable numbers. It is one of the main objects of this article to show how true is this statement; there will be found in it only passing reference to the organisms which produce disease in man and animals- for information on these see Pathology and Immunity. {Encyclopaedia Britannica, 14th ed., Vol. 2, p. 899)

The general message of the foregoing article applies even more aptly to viruses in the sense that much fear has been bred and cultivated around them, although they never produce disease symptoms, whereas some bacteria do. The writer of the above understands bacteria, with the exceptions that symptogenic bacteria found in man and animals do not produce disease (only secondary symptoms), that their precursors are endogenous to higher organisms, and they have not “developed in such a way that they can live in the human body.” If anything, the reverse is true. According to one theory of microbiology, microforms have colonized over eons to become higher organisms. In one sense, then, the human body has developed as a specialized environment for them.

An important dimension of the bacterial dependence of higher life forms is the floral population in the human digestive tract. Literally, these “foreign species” keep us alive.

Most bacteria have the same underlying function, whether found in soil, sewage, in the human digestive tract, or elsewhere in nature: they are an essential part of the life processes of higher organisms. They will not or cannot attack healthy cells or tissues, but certain ones will recycle sick or dead tissue in much the same way insect pests are drawn to weaker plants. As Bechamp said, “Nothing is the prey of death; all things are the prey of life.”

Following in the wake of misconceptions arising from the fundamental biological error known as the germ theory of disease, defining the filtrates of diseased tissue as a newly discovered infectious microform was the birth of a major corollary error in bioscience.

Viral Behavior Reconsidered

Listed below are ways viruses are said to disrupt or destroy host cells according to orthodox medical science and the germ theory. Following each in italics is a different interpretation following from microzymian principle:

1. Viral proteins insert into the host cell’s plasma membrane and directly damage its integrity to promote cell fusion (HIV, measles, and herpes viruses).

Proteins are attempting to repair membrane damage, or enter cells to make other repairs. There is the question as to whether viruses on cell walls are coming or going. In both cases it would be a matter of whether or not a cell has been disturbed by excess fermentation and acidity. But in the former case the cell would be dysfunctional before attachment occurs, thus requiring the repair complex. Another possibility, perhaps remote, is that dysfunctional receptors on cells are in need of repair, or they are covered by these complexes to inactivate malfunctioning cells. Positive electrical charges in a compromised terrain, primarily on acid molecules from fermentations, discharge cell membranes and act as mortar to stick cells together.

2. Viruses inhibit host cell DNA, RNA, or protein synthesis. For example, poliovirus inactivates cap-binding protein, which is essential for protein synthesis directed by capped host cell mRNAs, while allowing protein synthesis from uncapped poliovirus
mRNAs.

Protein inactivation is probably being done by fermentation or by acidic toxins from fermentation, while “poliovirus” is produced in the cell to reverse the damage.

3. Viruses replicate efficiently and lyse host cells, e.g., liver cells by yellow fever, and neurons by poliovirus.

Highly unlikely. The lysing is more likely caused by acid mycotoxicosis, or by free radicals (ROTS) released in response to mycotoxic stress, or from other sources (ionizing radiation, for example). Repair particles are residual after cell wall disruption.

4. Slow-virus infections (e.g., subacute sclerosing panencephalitis, caused by the measles virus) culminate in severe progressive diseases after a long latency period.

How is this demonstrated? Perhaps “latency” is a period of successful or attempted repair that eventually falters. Symptomology naturally appears in the weakest parts of the body. Excess acidity is always a systemic problem that localizes, just as cancer is a systemic condition that localizes, even though its symptogenic influence may later spread.

5. Viral antigen proteins on the surface of the host cells are recognized by the immune system, and the host lymphocytes attack the virus-infected cells (e.g., liver cells infected with hepatitis B).

Liver cells are damaged beyond repair by mycotoxicosis, and the immune system, our elaborate janitorial service, is cleaning up the garbage. Perhaps the repair protein antigen is expressed to signal immune response (because the cell is beyond repair), which is one explanation for why there are antibodies to these proteins.

6. Viruses damage cells involved in host antimicrobial defense, leading to secondary infections.

The function of immune cells is damaged by fungal infestation and/or overwork by toxic overload, preventing proper cleanup and elimination of disharmonious, symptogenic elements.

7. Viral killing of one cell type causes the death of other cells that depend on them, e.g., degeneration of muscle cells enervated by the attack of poliovirus on motor neurons.

Once again, a misinterpretation and lack of understanding that it is not viral microforms that damage neurons. Toxins from bacteria, yeast, fungus and mold-as well as the fermentation of glucose, proteins, hormones and fats-produce, or influence the body to produce, disease symptoms. Not recognizing the “virus,” for what it is, observers attribute disease to it.

8. Host cell responses to viruses include metabolic derangements and transformations resulting in neoplastic changes.

Metabolic derangement has occurred prior to the appearance of repair proteins, due to toxic overload in the cell. It is more likely that the proteins attempt to prevent cell transformation, and that cancerous development is cell conversion from primarily oxidative to wholly fermentative metabolism, mediated by fungus and mold.

Listed below are further orthodox views regarding virus replication, etc., with alternative interpretations in italics.

9. According to orthodox theory, viruses enter a host cell and replicate at the host’s expense. Replication is accomplished using enzymes which are distinct for each virus family. For example, RNA polymerase is used by negative-stranded RNA viruses to generate positive-stranded mRNA, whereas reverse transcriptase is used byretroviruses to generate DNA from their RNA template and to integrate that DNA into the host genome.

It is normal for repair proteins to generate enzymes to do their work.

10. One reason suggested for viral tropism (the tendency to infect some cells but not others) is the presence or absence of host cell receptors that allow the virus to attach. It is said, for example, that HIV binds to the protein (CD4) involved with antigen presentation on helper T-lymphocytes, that Epstein-Barr virus binds to the complement receptor (CD2) on macrophages, that rabies virus binds to the acetylcholine receptor on neurons, and that rhinoviruses bind to the adhesion protein (ICAM-1) on mucosal cells.

See number 1 above.

Theoretically, once attached, the entire virion, or a portion containing the genome and essential polymerases, penetrates into the cell cytoplasm in one of three ways: (1) Translocation of the entire virus across the plasma membrane; (2) receptor-mediated endocytosis of the virus and fusion with endosomal membranes; or( 3) fusion of the viral envelope with the cell membrane. Theory suggests that within the cell the virus uncoats, separating its genome from its structural components and losing its infectivity before replication. In either the nucleus or cytoplasm, newly synthesized viral genomes and capsid proteins are assembled into progeny virions, which may then bud through the plasma membrane. Unencapsulated viruses may be released also, directly through the membrane.

It is interesting, however, that viruses can somehow choose the “infection” to be abortive, latent or persistent, meaning respectively: (1) viral infections with incomplete replication cycles; (2) persisting in a cryptic state, like herpes zoster within a dorsal root ganglion, which suddenly becomes active to produce shingles;( 3) continuously synthesized virions, with or without altered cell function (e.g., hepatitis B). These three ideas, especially latency, have arisen as feeble excuses for the untenable virus theory.

11. In order for viruses to reproduce, they must complete the following four steps:

a). Adsorption and penetration of a cell. The viral particle binds to the host cell membrane. This is usually a specific interaction in which a viral encoded protein on the capsid or a glycoprotein embedded in the virion envelope binds to a host cell membrane receptor and is then internalized. This internalization occurs by endocytosis or by fusion of the virion envelope with the host cell membrane.

This is the mechanism whereby the viral particle enters the cell for the purposes of carrying out repairs to the damaged DNA orRNA.

b). Uncoating of the virus, so that the nucleic acid can be released from the capsid into the nucleus or cytoplasm.

Repair work may require uncoating. An uncoated “virus” in the cytoplasm may have come from the nucleus and not yet have a coat, as in the case of hepatitis B according to medscience. A coat is then created to protect the nucleic acid, to make a communicative or responsive protein complex, or to allow exiting the cell for remote function or for neutralization and recycling by the immune system.

c) Synthesis and assembly of viral products as well as inhibition of the host cell’s own DNA, RNA and protein synthesis.

Protein complexes produced in response to an alarming situation-fermentative and mycotoxic stress-are capable of self-ordered replication. As suggested by Bechamp, the microzyma is specific for each organ, therefore specific repair proteins will be needed for specific cells that make up specific organs that are being disturbed. There is the question of why the great numbers in some cases. One possibility is simply overreaction; for example, fever can be extreme.

d) And finally, release of virions from the host cell either by budding or lysis.

(1) Complexes leave the cell for remote function or to be neutralized; (2) Repairs have failed, and complexes are released prior to or during the breakdown of the cell by acid toxins or the immune system.

Further Considerations

Virologists refer to certain microforms as passenger viruses, which are present in asymptomatic situations, riding on their host’s genetic molecule like a passenger. To the conventional mind searching for new diseases or for a viral cause of unexplained ones, they are most interesting, because the status of virologists in the scientific community depends upon the pathogenic potential of the viruses they study. Due to their location, passenger viruses are thought to have much disease potential, thus their true function goes unnoticed. These colloidal passengers are the silent majority of animal and human intranuclear proteins essential for genetic repair.

Kalokerinos and Dettman quote Dr. Fred Klenner regarding the changeability of viruses: “I am of the opinion that virus units have the potential of going from one type to another by altering their protein coat. We see chicken pox at Thanksgiving, mumps at Christmas, red measles in the spring, and polio and Coxsackie in the summer.”[6]  Seasonal appearance of different forms may be mediated by variations of imbalance in the biological terrain or nutritive medium due to the fermentation of dietary excesses such as sugar and animal proteins that accompany holidays and seasons, calling for different repair proteins.

For example, outbreaks of polio have been associated with sugar consumption in summer. Various psycho-emotional stresses correspond to these seasons as well.

Supporting the general idea of dietary culpability is a statement published by the great English physician, Sir Robert McCarrison in 1936: “Obsessed with the invisible microbe, virus, protozoa as all important excitants of disease, subservient to laboratory methods of diagnosis, hidebound by our system of nomenclature, we often forget the most fundamental of all rules for the physician, that the right kind of food (nutrition) is the most important single factor in the promotion of health and the wrong kind of food the most important single factor in the promotion of disease.”7

Six years before Bechamp identified the microzyma as a ferment and, with his devoted associate, Professor Estor, began a 13-year odyssey of research into its nature, Florence Nightingale published a statement about the germ theory. In Notes on Nursing, 1st ed., 1860, she said of infection:

Diseases are not individuals arranged in classes, like cats and dogs, but conditions growing out of one another.

Is it not living in a continual mistake to look upon diseases, as we do now, as separate entities, which must exist, like cats and dogs, instead of looking upon them as conditions, like a dirty and a clean condition, and just as much under our own control; or rather, as the reactions of kindly Nature against the conditions in which we have placed ourselves?

I was brought up … distinctly to believe that smallpox, for instance, was a thing of which there was once a first specimen in the world, which went on propagating itself in a perpetual chain of descent, just as much as that there was a first dog, (or a first pair of dogs), and that smallpox would not begin itself any more than a new dog would begin without there having been a parent dog.

Since then I have seen with my eyes and smelt with my nose smallpox growing up in first specimens, either in close rooms or in overcrowded wards, where it could not by any possibility have been “caught,” but must have begun. Nay, more, I have seen diseases begin, grow up, and pass into one another. … I have seen, for instance, with a little overcrowding, continued fever grow up; and with a little more, typhoid fever; and with a little more, typhus, and all in the same ward or hut.

Would it not be far better, truer, and more practical, if we looked upon disease in this light? For diseases, as all experience shows, are adjectives, not noun-substantives.

That is, symptoms (called diseases) are describers of a situation.

I find legitimate Bechamp’s conclusion that what are called germs of the air are fundamentally microzymas of beings which are being consumed by the recycling process, i.e., some kind of vegetative digestion-putrefaction or fermentation. In short, there are no pre-existing disease-germ species. The principles of microbian medicine constitute a fundamental biological error. As Bechamp said, “The microbian doctrine is the greatest scientific silliness of this age.” This is not to say that there is no transmission, only that invasion is not necessary for symptogenesis, nor is it the primary mechanism for illness. It is to say that for transmission to take place, susceptibility in the form of a compromised terrain must pre-exist in the receiver, who is then likely to be ill anyway. With the exception of the immune component in the mucosal barrier, primary host “resistance” is a function of terrain condition rather than immunity per se.

Phantom Viruses Hepatitis

Hepatitis can be a painful symptom that has yielded profitable virus-hunting opportunities in recent years. Although there are several categories of this disorder, three main varieties of what is called “acute viral hepatitis” exist: Type A (formerly “infectious hepatitis”), Type B (formerly “serum hepatitis”), and hepatitis C (formerly “non-A, non-B”). The corresponding viruses are HAV, HBV, and the non-A, non-B “group,” now called C. Type A is said to be caused by an RNA virus, spread primarily by fecal contamination of water and food, with blood and secretions also possibly being infectious (but it is due to the toxins associated with unsanitary conditions). Hepatitis B, discovered in the ’60s, is said to be caused by a DNA virus which replicates in the hepatocyte nucleus and receives its surface coat in the cytoplasm. It is said to be transmitted by transfused blood or blood products, or via common use of needles by intravenous drug users (but it is due primarily to over-acidification from the drugs, especially heroin. The exchange of body fluids into the blood, whether by unsterilized needles, abusive sexual activity, etc., can also play a role over time because of repeated immune stress caused by foreign proteins. See Section 1 for Bechamp’s view of the invasion of blood by injection of proteins). Third World babies with poor nutrition and unsanitary conditions around the time of birth are also susceptible.

The third type of hepatitis, discovered in the ’70s, is found among drug users and alcoholics, and accounts for 80 to 90% of hepatitis caused by blood transfusion. It is thus akin to B type and was at first thought by scientists to be hepatitis B until thorough testing of subjects revealed no virus B-nor A, for that matter. It was thus called “non-A, non-B” hepatitis and thought to be at least two viruses and perhaps more.

In 1987 scientists believed they found a single virus causing the third type, what is known today as the hepatitis C virus. However, what they identified was an antibody they associated with a virus. Now, just as with HIV, they could test patients for antibodies against an elusive or invisible virus. With this new observation, however, new paradoxes confronted the viral hypothesis. Huge numbers of people testing positive for the phantom C virus never developed any symptoms. Hepatitis is truly the result of over-acidification or toxification of the largest filter in the human body by such substances as lactic acid, acetic aldehyde and ethanol-not the disease of a pathological virus. It is interesting to note also that all these hepatitis viruses have incubation periods of 2 to 25 weeks, violating Farr’s Law (see below), yet are not classified as slow viruses. Also, the point at which a “natural invasion” takes place, as opposed to a highly artificial injective one, and thus, how true incubation periods are determined, is another interesting question.

Hantavirus

A recent example of unwarranted panic in American biomedicine was the eminent hantavirus of 1994. Presumably it had jumped species, from mouse to man (the American Navaho Indians). However, after supposedly killing a number of people, this phantom virus apparently made peace with the Indians and retired to its mouse reservoir. The virus failed to materialize.[8] A front-page article in the San Francisco Chronicle reported that CDC “epidemiologists across the nation are carefully monitoring the deer mouse population and the level of virus within it.” But all that was left to discover of the former “Navaho flu” by the CDC epidemiologists (shown in their space suits) were healthy mice in the mountains.[9]  The Navaho flu is nothing new to the native Americans and is most likely tied to sanitation, nutrition and lifestyle.

Ebola

In May 1995 the CDC announced the new, threatening Ebola virus. The deadly killer virus was expected to leave its hidden reservoir in the rain forests of Africa to claim Europe and the United States. An article in Time magazine was peppered with men in space suits and colored electron micrographs of the virus (even though electron microscopes cannot take color pictures). A CDC virologist suggested the virus could leave the rain forest if “we get a virus that is both deadly to man and transmitted in the air.” We are thus asked to fear the image of viruses somehow being launched into the air, perhaps by ejection from a host, and then floating on killer breezes to other lands. A more imaginable scenario was suggested by a European epidemiologist who heads the United Nations AIDS program. Echoing the CDC’s alarm, he stated, “It’s theoretically feasible that an infected person from Kuwait could go to Kinshasa, get on a plane to New York, fall ill, and present transmission risk there.” But within a month the virus had disappeared in Africa, and not a single Ebola case was reported in the United States or Europe. [10]

The World Health Organization announced on December 19, 1995 that the Ebola virus epidemic that killed 245 people in West Africa was over. All tests on any remaining suspected cases were negative. A somewhat unsettling revelation was that every Ebola outbreak in Africa “is associated to have spread through public hospitals.”[11]  As it turned out, it was associated with re-used hypodermic needles in these hospitals. Just like hantavirus, Ebola vanished, never to be heard from again. Most interesting is that this epidemic, as epidemics will, stopped without vaccines or other drugs. But consider the impact such stories have made upon our minds and on the way we view and understand germs. What’s next in virodrama, the Andromeda Strain?

There is one insidious possibility that must be mentioned in passing. Some mysterious outbreaks of the past have been shown years later to have been man-made. In some cases, government agency has used the public to test releases of organisms and weak biochemical toxins in order to verify, through medical reports, expectations of biowarfare activity. These incidents and the whole story of such behavior is well documented in the book, A Higher Form ofKillingby Robert Harris and Jeremy Paxman (Hill & Wang, 1982). In this scenario, the cause of such an incident would be constructed officially, or left as a mystery, in order to draw attention away from the truth.

Vaccines

Haphazard Beginnings

The greatest danger of the germ theory half-truth is its promulgation and acceptance as the whole truth, thus diverting attention from endogenous factors, primarily host ecology-resistance and susceptibility. Such factors are highly significant if Bechamp and his many followers, including me, are correct. Distraction from host factors has been quite thorough, with the exception of the false notion that the immune system is the “first line of defense” against infectious symptoms.

Louis Pasteur is credited with improving and successfully using the technique of vaccination, a practice blindly begun in 1796 by British physician Edward Jenner. Jenner happened to notice that dairy maids who had contracted the relatively mild disease cowpox did not later contract smallpox. On a hunch, he took pus from the running sores of sick cows and injected it into the blood of an eight-year-old boy. As the story goes, the boy developed cowpox. Several weeks later Jenner inoculated the boy with smallpox, but the disease failed to develop. Upon this single anecdotal event was based the supposition that this practice was safe and effective. The process has changed little to this day except perhaps to have been worsened with additives. Its understanding is still clouded by Pasteur’s theory, and it is as recklessly pursued as it was begun.

Theoretically, vaccination works by introducing a diluted and weakened (attenuated) or “killed” version of the pathogen into the body, causing the immune system’s memory function to prepare for any subsequent contact, which is met with much greater response. It is commonly thought that infectiosity, or germ-virulence, tests are performed on laboratory animals and then vaccines are made which boost the immune system against germs. However, like Jenner’s, the tests are primarily toxicity tests, and vaccines, especially viral ones, activate the immune system primarily in response to injected toxins. Whether the response is to toxins, microforms, or both, it is a misguided approach at best. Bypassing the mucosal barrier and thus the segment of the immune system which is the organism’s interface with the environment, makes such experimentation, and vaccination itself, flawed, unscientific practice ipso facto.

A Toxin Pathway

Bacteria secrete a variety of enzymes (leukocidins, hemolysins, coagulases, hyaluronidases, fibrinolysins), any of which are disruptive in the body. For example, diphtheria toxin is composed of the enzymatic fragment A, which is at the amino end of the molecule, and fragment B at the carboxyl end, which allows entry into host cells. The two fragments are linked by a disulfide bond. Once bound diphtheria accesses the cell cytoplasm, the disulfide bond is broken, releasing fragment A. This enzyme catalyzes the covalent transfer of adenosine diphosphate ribose (ADPR) from nicotinamide adenine dinucleotide (NAD) to EF-2. The latter, a ribosomal elongation factor involved in protein synthesis, is thus inactivated. One molecule of diphtheria toxin can kill a cell by ADP-ribosylating more than a million EF-2 molecules. In diluted form this toxin, along with other toxic chemicals and fragments of bacteria, is what is introduced directly into the blood of infants under the guise of a health measure.

Diphtheria toxin creates a layer of dead cells in the throat, on which Corynebacterium diphtheriae outgrows competing bacteria (the diphtheria microform is an intermediate stage of a morbidly evolved microzyma, and competing bacteria also evolve out of sick cells). Subsequent wide dissemination of diphtheria toxin causes the characteristic neural and myocardial dysfunctions. Diphtheria toxin also causes disseminated intravascular coagulation, which activates the various alarm responses of the body. Thus, we know that toxins produce symptoms, but what is it that produces the condition which creates or supports the toxin producer?

Bordetella pertussis is a fascinating organism to study. A certain amount of empiricism, as opposed to logic, is required for success with pertussis. Diagnostic cultures are difficult and sometimes unreliable. Different lots of vaccine, made in the same way from the same strains, sometimes show different properties. Experimental work is not always reproducible from one laboratory to another, but this is common in biological research. The diagnostic culture problems and the unexpected variability in vaccines and in pertussis strains themselves are not easy to explain.

-Charlotte Parker Department of Microbiology, U. of Texas at Austin

Vaccine Recipes

To make a vaccine you need to acquire the disease germ-a toxic bacterium or a live virus. The mumps virus is a sterile, lyophilized preparation of the Jeryl Lynn (B level) strain of mumps virus. It is adapted to, and propagated in, cell cultures of chick embryo, free and stabilized with sorbitol and hydrolyzed gelatin. The rubella virus (Wistar RA 27/3 strain) is grown in human diploid cell cultures. Measles (from Eners’ attenuated Edmonston strain) is grown in cell cultures of chick embryo.[12]  The various so-called virus strains are stored by pharmaceutical companies for later culture. Where these stockpiles come from and the specific methods used seem to be guarded secrets, but as Bechamp emphasized, they must originally be obtained from diseased higher organisms, for they are found nowhere else in nature. If protein complexes exist in the viral stores, their replication in culture is simply the behavior pattern of the repair proteins they are. It is highly likely that toxins accompany these strains as a means of stressing the culture cells.

To make a live vaccine, the microform must be attenuated, or weakened. This is accomplished by serial passage-passing the microform/toxin many times through animal tissues, e.g., monkey kidneys, human diploid cells (the dissected organs of an aborted fetus), chick embryos and calfs.[13]  Killed vaccines are prepared with heat or radiation, or else chemically, usually by using the mycotoxin formaldehyde.[14]

The weakened microform must be mixed with antibody-boosting and immune-activating adjuncts such as the antibiotics neomycin and streptomycin, as well as stabilizers such as sodium chloride, sodium hydroxide, aluminum hydroxide, aluminum hydrochloride, sorbitol, hydrolyzed gelatin, formaldehyde, and thimerosal (a mercury-based antiseptic).

For example, diphtheria, pertussis and tetanus (DPT) vaccine consists of a combination of tetanus and diphtheria exotoxins with pertussis microforms. Diphtheria toxin is produced by growing Corynebacterium diphtheriae in a medium composed of pig pancreatic hydrolysate of casein. Tetanus toxin is produced by growing Clostridium tetani in a medium composed of pig tryptic digest of casein. Both toxins are combined with formaldehyde, ammonium sulfate (a mycotoxin), and diluted with saline containing thimerosal. They are then adsorbed on aluminum phosphate and combined with a suspension of Bordetella pertussis organisms.[15]

The first pertussis (whooping cough) vaccine was created in 1912 by two French bacteriologists, Jules Bordet and Octave Gengou, who wanted to use it on the children of Tunisia. After growing the pertussis bacteria in large pots, they killed them with heat, preserved the mixture with formaldehyde, and injected it into the children.

One change made in the original Bordet/Gengou recipe was to add an “adjuvant.” This material, usually a metal salt, somehow heightens the capacity of the pertussis vaccine to produce antibodies in the host. In 1943 a pioneer American pertussis vaccine researcher, Pearl Kendrick, reported that alum had this adjuvant effect. The vaccine was said to be more protective, and fewer pertussis bacteria had to be included. After her report, alum or alum-based substances were added to the vaccine. Kendrick was also instrumental in having pertussis combined with diphtheria and tetanus vaccines already in use in the 1940s.

The vaccine is made in essentially the same way today as in the time of Bordet and Gengou, although each manufacturer prepares it differently, and the exact processes and formulas are considered trade secrets. Pertussis bacteria are usually grown on a casein hydrolysate medium with yeast dialysate, supplemented with agar and charcoal. The mixture is prepared in vats, then washed, and the bacteria killed with heat and formaldehyde The resulting toxoid is preserved with thimerosal. Other possible ingredients are hydrochloric acid, the adjuvant (usually an aluminum compound), sodium hydroxide, and salt.

In the past, human blood was often added. This is now prohibited by federal law, but manufacturers are still permitted to add blood from “lower animals other than the horse.” The microzymas of horse blood destroy human blood.

The vaccine is stored for a while at near-freezing temperatures, then combined with the diphtheria and tetanus exotoxins and poured into vials for distribution. Ultimately it is shipped to pharmacies, private physicians, and public health clinics, whence it is injected into the blood of infants.

Calf Serum

The precedent of cruelty to animals, promoted, if not set, by Louis Pasteur, is apparently a hallmark of germ theory. It is not better demonstrated than by the following description of the preparation of so-called calf serum dreamt up in the early days of vaccine manufacture, and continuing, as far as I can tell, into the late 1980s, if not to this day:

A calf is strapped down to an operating table. A space on the abdomen of about 12-15 inches is shaved with a razor, then about 100 slashes are cut into the flesh. The seed virus, consisting of a culture of smallpox passed through a solution of glycerine, is rubbed into the wounds.

Made to stand in a headstock so it cannot lick its belly, the calf grows very sick and the wounds become swollen and inflamed. In a few days, as the body reacts to the poison, small blisters appear, scabs form over the wounds and fill with pus. In five to seven days, the wounds are ulcerated, issuing pus and morbid cells. The calf is again strapped to the operating table, and the infested area is washed with warm water. Each scab is scraped off and its contents are pressed out of the sores into a container. An equal amount of glycerine is added to the pus, and the whole is stirred. Once thoroughly mixed, the concoction is passed through a sieve to remove solids such as pieces of flesh, scabs and hair. After being stirred once again, the mixture is put into vials, sealed, and distributed as “pure calf lymph,” commonly known as smallpox vaccine.[16]

These aforementioned concoctions are obviously poisonous products of disease. By injecting these products into the blood of school children, physicians, via legal manipulation of health boards and school boards, potentiate illness and ensure that medical products and services will continue to be in high demand.

It is interesting to note that the vaccine given to those considered to be at high risk for hepatitis A (such as highly overactive homosexual males, users of illicit injectable drugs, residents of a community experiencing hepatitis A, hemophiliacs and other recipients of therapeutic blood products), or those testing positive for hepatitis A, is made of immune serum globulin obtained by ethanol fractionation of plasma pooled from hundreds of donors. Considering that microzymas and morbidly evolved microzymas are being transferred from one individual to another, one might conclude that this could have disastrous consequences. (The fact that animal blood and fluids are transferred to humans by vaccination bears no further comment, except to say that Frankenstein would be proud.)

It is also very interesting that the vaccine given to those testing positive for hepatitis B is created by cloning the antigen HBsAg in a bed of yeast {Saccharomyces cerevi’s Jae, the culminate stage of the morbidly evolved microzyma) and formulated as a suspension of the antigen adsorbed on aluminum hydroxide. [17] Such morbid, poisonous vaccines are given to infants at 2, 4, and 15 months of age. The vaccine is enough to disturb the central balance of the biological terrain and cause an array of symptomologies in anyone, especially an infant. That more people are not quickly poisoned to death by this practice is testimony to the astounding resilience of human physiology.

Vaccination Results

Does the vaccinal approach produce wellness or any health benefit? Kalokerinos and Dettman point out that statistics in England and Wales, presented at the Presidential Address of the British Association for the Advancement of Sciences (Porter, 1971), show that deaths of children under 15 years of age attributed to scarlet fever, diphtheria, whooping cough and measles saw a 90% decline from 1850 to 1940. Yet, antibiotics and compulsory (i.e., widespread) vaccination against diphtheria were not introduced until 1940. The death rate due to these illnesses dropped from over 6,000 per million children in 1850 to under 1,000 per million children in 1940, a period marked by vastly improved public health, sanitation and nutrition.[18]

Along the same lines, an English doctor, D. Powles, observed: “The major contributing factor toward improved health over the past 200 years has been improved nutrition. Nearly 90% of the total decline in the death rate in children between 1860 and 1965 due to whooping cough, scarlet fever, diphtheria and measles occurred before the introduction of antibiotics and widespread immunization against diphtheria.”[19]  Also, it has not been well publicized by authorities that infectious epidemics are naturally cyclic in populations. The procedure has generally been to introduce vaccines as the downcurve begins, giving the impression of effectiveness. In addition, there are numerous instances in history of violent outbreaks of illness following near-total immunizations of population groups.

Once I looked into this subject and its history, microzymian principle brought it into focus for me. Since germs evolve out of, or take advantage of, the susceptible state, and are symptoms themselves, drugging or vaccinating susceptible individuals cannot render them immune, and may have the reverse effect. When and if a vaccine works as intended, the result is only to suppress the appearance of a specific set of symptoms, not to prevent disease. Therefore, it is not conferring wellness, nor reducing susceptibility, but simply creating an effect in a highly artificial and dangerous manner, while allowing the disease condition to worsen. Is there a price to pay for this invasive and unscientific approach? In this writer’s view, it is what we’ve got-pandemic degenerative disease, cancer and AIDS, because we are not dealing with the foundational disease, which may then get worse and re-expresses itself in more intense ways.

Contaminants

The November/December 1995 issue of The Vaccine Reaction, Volume 1, No. 5, issued by the National Vaccine Information Center, reveals that Swiss scientists have reported finding the enzyme reverse transcriptase (RT) in the live measles/mumps/rubella (MMR) vaccine. This has been traced to the chicken embryos whose cells are used to create the vaccines. It has reportedly been detected in yellow fever and some influenza vaccines, also prepared in chicken embryo cells. No disease has been attributed to RT in the MMR vaccine, but it is a factor in retroviral disease theory and its presence in this case is a mystery. RT, which is officially said to be produced by many “tumor-producing” viruses, supposedly the retroviruses, catalyzes the transformation of RNA into DNA. However, there is no proof of viral production of tumors-only theory.

I suggest the following process to explain how it gets into the vaccine, based on microzymian principle: Disruption of the embryo cells, by toxins or other means, probably damages their DNA. The response is endogenous microzymian production of repair protein complexes (“retroviruses”), which in turn produce RT in order to effect repairs. As the toxification process continues, central balance in the embryo cells is disturbed sufficiently and the ensuing endogenous pleomorphic development of upper development forms results in excess fermentations, with corresponding increase in the level of toxins. In order not to “spoil the broth,” however, preservatives are added at a certain point to arrest development.

Experiments with fertile eggs, which I later discovered were described by Bechamp, provide evidence of endogenous microzymian development. I have observed that the hypodermically extracted serum of a fresh egg looks normal under a high powered light microscope. However, when the central balance is disturbed by shaking the egg, which is then allowed to sit for a period of time, extracted serum shows the presence of bacteria, yeasts, and their associated toxins, i.e., acetic, sulfuric and butyric acids. An equally elegant, but even simpler, demonstration is bruising an apple without breaking the skin. Soon the area begins to turn brown and rot from the inside. This is a life process mediated by endogenously developed microforms.

The enzyme that orthodox researchers associate with retroviruses is being found in live vaccines such as MMR and polio. But RT does not cause disease. It is toxins which taint the vaccine, whether produced in culture or introduced as ingredients, that have the potential to interact with each individual’s immune system and DNA and disrupt the body such that various symptoms are produced. This practice of introducing foreign (genetic/viral) proteins directly into the blood may result in morbid pleomorphosis with further potential for toxification. Of course, that is precisely what has been occurring for many years, with the blessing of the allopathic medical system, whose financial health depends on disease.

Another example of unwanted or unpredictable vaccine contaminants: polio vaccines grown on monkey kidney have been identified as a source of simian viral (SV40) and spherical retroviral structures.[20]  Such stray protein structures and fragments in vaccines can be regarded as a large, uncontrolled, cross-species genetic experiment in which a gene from one species might be spliced as a repair protein into another.

Reactions

Though secondary to the failure to address disease, vaccine reaction has become the more common issue because of its immediacy. It results from the aggressive willingness of medical authorities to play Russian roulette with people’s lives. When asked about potential, dangerous reactions, officials reply, “The benefits outweigh the risks.” The simple fact is, there are no benefits, even before we get to the fact that this assertion is based upon statistical information that seems far from complete. According to the U.S. National Vaccine Information Center, more than 54,000 adverse events following vaccination, including convulsions, encephalitis and deaths, were reported to the FDA during a three-year period ending October 1993. However, since the FDA estimates that only 10 percent of doctors report adverse events, the real number could have been extremely high, more than half a million, including 50 or 60,000 serious injuries and 10-11,000 deaths. Connaught Laboratories, a vaccine manufacturer, estimates a 50-fold under-reporting of adverse events.

I can find no accurate statistical estimate for how many deaths and serious injuries are caused by vaccinations each year in the United States. It appears as though the government would rather not release such information, although a federal fund has been set up to cover the millions of dollars in lawsuits that are always pending. Thus, the law has been constructed so that perpetrators of this damaging practice cannot be sued, but continue to profit, while the government shields them with the people’s money.

Perhaps the government feels that with no way to enforce accurate reporting from doctors, it is futile to indulge in a guessing game. From the doctors’ perspective, there is little to gain from reporting, except an inexorable and embarrassing statistical slide toward collision with the truth. Consider these words from Kalokerinos and Dettman 20 years ago: “Moreover, it is disappointing to observe the futility and ineffectiveness of many ‘flu’ vaccines that have been accepted by an unwary public.”[21] In this writer’s opinion, the statement applies to all vaccines.

Taken in the Rear

Montague R. Leverson, M.D., Ph.D., M.A., an American physician, happening to come across some of Professor Bechamp’s writings in New York, became fascinated with his views. Realizing that the dated works anticipated Pasteurian “revelations” in certain important points, he decided to go to France to meet Professor Bechamp, where he heard the story of Pasteur’s plagiarism of the professor’s work directly. In a lecture entitled “Pasteur, the Plagiarist,” delivered at Claridge’s Hotel, London, on May 25, 1911, he outlined briefly Bechamp’s claim to be the first to produce a ferment in a medium containing no albuminoid matter, something thought impossible up to that time. (Ethel Douglas Hume’s book about Bechamp was based on work begun by Leverson, who is also the translator of Bechamp’s masterwork, The Blood.)

Understanding microzymian principle, he had this to say about inoculation:

When a drug is administered by the mouth, as was beautifully pointed out by Dr. J. Garth Wilkinson, in proceeding along the alimentary canal it encounters along its whole line a series of chemical laboratories, wherein it is analyzed, synthesized, and deleterious matter is prepared for excretion, and finally excreted, or it may be ejected from the stomach, or overcome by an antidote.

But when nature’s coat of mail, the skin, is violated, and the drug inserted beneath the skin, nature’s line of defense is taken in the rear, and rarely can anything be done to hinder or prevent the action of the drug, no matter how injurious, even fatal it may be. All the physicians of the world are incompetent either to foresee its action or to hinder it. Even pure water has been known to act as a violent. . . poison when injected into the bloodstream. How much more dangerous is it, then, to inject poisons known to be such, whether modified in the fanciful manner at present fashionable among vivisectionists or in any other manner. . . . Inoculation should be regarded as malpractice to be tolerated only in case of extreme danger where the educated physician sees no other chance of saving life.

Now the forcing of these inoculations upon individuals by law is one of the worst of tyrannies imaginable, and should be resisted, even to the death of the official who is enforcing it….

. . . The entire fabric of the germ theory of disease rests upon assumptions which not only have not been proved, but which are incapable of proof, and many of them can be proved to be the reverse of truth. The basic one of these unproven assumptions, the credit for which in its present form is wholly due to Pasteur, is the hypothesis that all the so-called infectious and contagious disorders are caused by germs, each disease having its own specific germ, which germs have existed in the air from the beginning of things, and that though the body is closed to these pathogenic germs when in good health, when the vitality is lowered the body becomes susceptible to their inroads.

Dr. Leverson goes on to describe disease as nature’s attempt to eliminate waste, and diseased tissues as being due to improper living. He suggests plenty of fresh air, the best sanitation, scanty clothes, and a scientific study of diet. He saw overeating as the precursor to “an enormous number of diseased conditions.”[22]

Vaccine Causes Polio Symptoms

Although Leverson is correct in his criticism of inoculation, even the body’s amazing “coat of mail” sometimes fails to be enough, as oral vaccine also poses danger. In a report on the Internet by Nando.net/Associated Press, we have a statement by Dr. Rebecca Prevots of the Center for Disease Control in Atlanta (Jan. 30, 1977) that almost every case of polio in the United States between 1980 and 1994 was caused by, or related to, the oral vaccine itself, “which consists of a live but weakened virus,” the CDC said. But, they hasten to add, there is a new, safer plan. “This emphasizes the timeliness of the change in policy,” said Prevots. Time is said to pass in a different manner for different personalities, but it still seems a bit of a stretch to apply “timeliness” to a period of 14 years with 133 impacted lives involved.

The new policy is “expected” not to eliminate risk but to cut it in half. In the official oddsmanship game of risk versus benefit, this is tendered as comfort to those yet to be afflicted. It consists of two preliminary killed-virus injections given to infants in the first four months “… to build up their immunity to polio. Then they are given two oral doses of ‘weakened-virus’ vaccine between ages 1 and 6.” One can only hope that these microbists desist from this folly because, in addition to their misplaced belief in germ theory, they do not yet understand that the extent of vaccine risk goes beyond reaction.

Compulsory Vaccination

As Leverson emphasized, people are forced to this abomination by law in many cases, especially schoolchildren. Overcoming this assault on human rights usually requires extreme persistence, courage and a knowledgeable approach. (I don’t recommend his approach, but it is self-defense!) The argument is literally that those at risk for damage must be sacrificed to save millions of others (i.e., “the benefits outweigh the risks”). But there is no science or even logic to this. If one is vaccinated, theoretically one is safe. If one chooses not to be vaccinated, then s/he does not threaten vaccinated people, but only those who have chosen that risk. Yet, the responsibility for the decision has been stolen from families under the guise of government responsibility to protect children from parents.

The unvaccinated, threatened by medical authority with the risk of developing a serious “disease,” are not told that said risk is greatly increased by germ theory mentality itself. It’s the medical equivalent of a mob protection racket, and the law has been manipulated to maintain the profitability of ill health produced by this practice. Holistic means of preventing or dealing with these symptoms are not even in the equation.

To summarize, if we consider Bechamp’s thesis that bacteria are evolved forms of anatomical elements called microzymas, that there are specific disease conditions rather than specific diseases, and that the microform is not the antecedent of disease, but arises in it; and if we add to this my thesis that the primitive stage of evolution, viruses, are apathological and created as response to structural breakdown, and that yeast, fungus, mold and their symptogenic poisons produce the symptoms attributed to viruses, is it possible that medical science is misdirected, if not malfeasant, in its intense pursuit of vaccinal answers? Was Bechamp on the right track? Are his many followers, including myself, correct as well? Is this why we cannot make a successful vaccine, and have, in fact, made dangerous and deadly ones?

On a final note of sanity, Edgar Cayce, the renowned psychic who could diagnose illnesses and treatments while in trance, was asked and answered the following question during a diagnostic session:

Q. Can immunization against contagious diseases be set up in any other manner than by inoculations?

A. If an alkalinity is maintained in the system-especially with lettuce, carrots and celery, these in the blood supply will maintain such a condition as to immunize a person. In an alkaline system there is less effect of cold and congestion.[23]

HIV/AIDS and the Monomorphic Disease Model

In 1960 a veteran retrovirologist urged his peers to “raise questions whether the known facts about viruses suffice to account for it.” The subject was cancer, the veteran was Peyton Rous, and the quote is from a paper in Cancer Research. Mindful of that example, in 1987 I asked a similar question in a paper likewise published in Cancer Research: whether the known facts about two human retroviruses suffice to account for leukemia and AIDS.

Clearly, following Rous’s example did not make me very popular with the multinational club of retrovirologists. My article was officially ignored and not “dignified” with a response because the AIDS virus establishment was “too busy . . . saving lives” and testing for antibodies to HIV. I was often shunned like an AIDS patient by my former fellow retrovirologists. My views were unwelcome for several reasons: after a frustrating, twenty-year-long search for a human cancer virus, the retrovirologists were craving for clinical relevance and hence happily adopted HIV-“the AIDS virus”-as the cause of AIDS. The discovery of HIV was announced in the U.S. at a press conference and the virus-AIDS hypothesis became instant national dogma. On this basis, the retrovirologists convinced their governments to spend billions of dollars to stop the predicted viral epidemic, already being labelled “the epidemic of the 20th century.” The virus was also the immediate darling of the biotechnology companies. Due to its very low complexity, it can be readily cloned for diagnostic test kits and vaccines. In turn, the virus was a hit with the press because it mobilized in readers the instinctive fears of a contagious disease, and appealed to the public prejudice that all evil comes from without.

-Peter H. Duesberg, Ph.D.

What Proof?

Perhaps the foremost thing that should be said about HIV is that it has never been proven to be the cause of AIDS, or any human illness for that matter. Not one scientific paper exists that demonstrates it. Based on activity in contrived situations in test tubes, among other illogical things, its culpability was a pronouncement handed down by an authority figure at the National Institute of Health. It is the same authority (Dr. Robert Gallo, head of NTH cancer labs) behind the expenditure of around a trillion dollars in cancer research which has produced nothing but an epidemic that is virtually out of control. (One wonders what it will take before people finally get the idea and stop creating walks, rides, telethons and cake sales to contribute money to the bottomless pit of biased, misdirected, wasteful and cruel orthodox medical research in cancer and degenerative disease.) And it is the same authority who has taken out two patents whose value depends upon HIV being accepted as the cause or a co-factor. One patent is for the technique of testing for HIV, and the other for a method of laboratory cultivation. No one in a position to do anything about it questions this obvious conflict of interest.

Kary Mullis, microbiologist inventor of the Polymerase Chain Reaction, says, “I can’t find a single virologist who will give me references which show that HIV is the probable cause of AIDS …. If you ask a virologist for that information, you don’t get an answer, you get fury.”[24]  Mullis has continued his outspoken criticisms of the AIDS establishment: “Where is the research that says HIV is the cause of AIDS? We know everything in the world about HIV now. There are 10,000 people in the world now who specialize in HIV.

None have any interest in the possibility HIV doesn’t cause AIDS, because if it doesn’t, their expertise is useless.”[25] Their embarrassment would also be considerable.

AIDS exists on paper. It is just a new label applied to a defined combination of immune-deficiency symptoms, which are not new, and a group of existing “diseases.” Intense public attention has been focused on the combination using statistical manipulation and fear that is bred in a general lack of understanding about health and disease. The question is whether all the destruction of AIDS can be laid at the feet of a nearly undetectable virus that defies every rule of medical microbiology. For example, HIV is said to cause AIDS after the appearance of antiviral immunity. Furthermore, the establishment has shown irresponsibility in referring to this syndrome as a disease. And the fact that it has been given the handy four-letter word encourages others to do likewise. This reinforces programmed notions, especially the idea of a single evil entity causing the whole thing. To emphasize these important points, AIDS will be here designated as “AIDSyndrome” in many instances.

A Medical Establishment on the Elastic Band Wagon

The HIV/AIDS theory is so elastic it stretches to embrace all reasonable criticism. Typical of this elasticity is the so-called latent period of the virus, which has gone from about one year to twelve, and shows potential of going to twenty. The elasticity is equaled only by the degree of credulousness required to accept HIV dogma. For example, it is said that in spite of the extremely low incidence of HIV in the body, it (mysteriously) tricks the immune system into attacking itself! I use the term HIV/Elastic Theory, or HIV/ET.

Another major factor is oppressive socio-economic and political conditions. Such conditions exist in the Third World particularly, but in their own way in sections of the United States. This aspect will not be detailed here, but includes such phenomena as corporate dumping of banned drugs on unregulated Third World markets, pesticide manufacture and use with frightening disregard for safety, squalid living conditions, and rainforest destruction. These, not HIV, are among the primary causes of what is labeled AIDSyndrome in the Third World. Pharmaceutical companies are heavily involved in the pesticide market. The corporate-interest connection with these abominations goes: pharmaceuticals, pesticides, agriculture, petroleum, international banking. Therefore, since the HIV/ET hoax has to cover a lot of financial territory, it must have considerable stretchability.

AIDSyndrome Scenarios

1. The first recorded AIDSyndrome case in history, one of five reported by the CDC in June 1981, was a 33-year-old Los Angeles male. He was engaged in a lifestyle which we now consider high risk; but there are reasons for risk other than those defined by AIDSyndrome “viromania” (a word coined by microbiologist Peter Duesberg). For one thing, he admitted using “poppers,” the aphrodisiac amyl nitrite (a poisonous secondary mycotoxin), then popular in homosexual bathhouses and discos. We are familiar with nitrites, used in tiny amounts as a preservative in meat. Sodium nitrite, a relatively weak member of the family, has been regulated for years as a potential carcinogen. It is well known that once in the body it is converted into carcinogenic nitrosamines (via its reaction with mycotoxins-not so well known).

Few mycotoxins, however, are more toxic than the organic nitrites (poppers), which react violently with almost anything. In water, they form the unstable nitrous acid, which destroys any biological molecule within reach. Nitrites and their breakdown products have long been known to scientists for their ability to mutate DNA, a point recently verified by direct experiment.[26]

During the 1960s and ’70s, poppers and other drugs were heavily abused, especially by sections of the male gay community. As a result, in 1969 prescription laws were tightened, and as usual, contaminated illegal products appeared on the streets adding insult to injury. In addition, impure products were marketed as “room odorizers.” According to a former nitrite researcher with the CDC, doses from inhalation are likely to exceed those from eating preserved meats by a million times.[27]  Yet this massive insult to the body, and the drug abuse factor in general, including filthy street injectables, OTC drugs, and especially prescription drugs such as antibiotics, antifungals and other immunosuppressive chemicals, are not considered causative, in favor of a scarce, barely detectable, inactive, difficult-to-transmit retrovirus. However, HIV/ET would respond by saying that, if anything, the drug factor increased susceptibility to a virus that invaded him and destroyed his immune system.

Popper use has been associated with one “AIDS indicator”- Pneumocystis carinii pneumonia (PCP)[28] – officially said to be caused by a protozoa. But the corresponding organism is not a protozoa; studies show the DNA sequencing of PCP to be identical to that of the Saccharomyces cerevisiae yeast.[29]  PCP is responsible for 62% of all AIDSyndrome mortality in America and Europe, candidiasis is responsible for 23%, and Cryptococcus neoformans is responsible for 12%. This means that yeast and fungus-the culminate microform symptoms of disease-contribute 97% of all AIDS-related mortality in those continents.

Thus, in the first recorded AIDSyndrome patient, a yeast infestation of the lung instigated pneumonia (symptom of over-acidification from fermentation processes), and oral thrush, a thick overgrowth of Candida albicans, choked him to death. He died, not from the ravages of a scapegoat retrovirus, but from an overdose of mycotoxins-nitrites-and the mycotoxins of yeast and fungal infestation-acetyl aldehyde, alcohol, and uric acid.

In Kenya, Africa, a 39-year-old woman from Zaire entered the hospital for treatment of her lung condition, which had begun with a relatively innocent cough and an unexpected drop in weight. Soon her coughs began to bring up blood, and tuberculosis was the diagnosis. But the patient had a strong allergic reaction to prescribed drugs, and her condition progressed from bad to worse, producing diarrhea, uncontrollable fever, swollen lymph nodes, and anemic blood disorders (all symptoms of a compromised biological terrain, as described in the main text). The woman was then diagnosed with AIDSyndrome (but not I-AIDS-Iatrogenic-AIDS).

The woman’s husband, whom doctors assumed must have transmitted AIDSyndrome to his wife, was suffering entirely different symptoms. He had pneumonia, a Candida infestation in his mouth, and lesions of Kaposi’s sarcoma on his now irregularly pigmented skin. He lost weight to a relentless diarrhea and was constantly fighting off episodes of gonorrhea. Their children had no symptoms.[30]

We are asked by national public health officials to believe that the Los Angeles case and the two Zaireans all suffered the same affliction from the same cause. The irony is that in terms of germ theory this is highly questionable, but when considered in the light of microzymian principle, it is highly plausible. With one instance of overlap, each person was affected with radically different symptoms-a Pneumocystis pneumonia (as noted, yeast in the lungs); a tuberculosis (symptom of exotoxin from an intermediate pleomorphic stage); and a Kaposi’s sarcoma, or papular tumors of the skin and mucous membranes (caused by mycotoxins). Before AIDSyndrome, these conditions never would have been connected by clinical doctors. Now they are struggling to believe that the common factor is the presence of nearly undetectable antibodies against HIV, and they could not be at a much worse disadvantage.

African AIDS

The World Health Organization’s definition for African AIDSyndrome includes some opportunistic infections, like tuberculosis; also, the African version of wasting called “slim disease,” a composite of weight loss, diarrhea, and fever; plus such conditions as persistent cough, skin problems and swollen lymph nodes. These signs comprise old, indigenous African health problems. But here is another example of HIV/ET. Compromised immunity makes “diseases” worse, so whatever “diseases” are already common become the indicators. All we have to do is plug HIV into the equation and we have AIDS. This makes sense to most people.

On the other side of the coin, malaria, for example, the leading killer in the Third World, produces fever and other symptoms frequently misdiagnosed as AIDS.[31]  Tuberculosis, also a common killer and part of the defined African syndrome, presents a challenging situation there, as described by a Nigerian medical professor: “The serologic demonstration of HIV infection in patients with tuberculosis in Africa is very important because it aids the separation of seropositive from the seronegative patients, since such a separation may be impossible in all cases on clinical grounds.”[32]

According to a Ugandan doctor treating AIDS cases, “A patient who has TB and is HIV-positive would appear exactly the same as a patient who has TB and is HIV-negative. Clinically, both patients would present with prolonged fever; both patients would present with loss of weight-massive loss of weight, actually; both patients would present with prolonged cough, and in both cases the cough would equally be productive. Now, therefore, clinically I cannot differentiate the two.”[33]  What can be the difference? Of course, a major one is that the AIDS case may be given expensive poison drugs which are nearly certain to end the patient rather than the illness, while filling pharmaceutical coffers.

Doctor Konotey-Ahulu has illustrated the confusion created by the HIV/ET: “Immunosuppressive diseases, of course, there always have been in Africa and elsewhere before antiquity was born. … I have clinical photographs from 1965 of a Ghanaian man who looked like some of the AIDS patients I saw in Africa recently. The man, who was like a skeleton, had severe nonbloody diarrhea (more than twenty bowel actions a day); he had what looked like fungus in the mouth [candidiasis], skin changes, periodic fever and cough-all the classical features of African AIDS. . . . The patient (according to relatives) had literally consumed on average one and a half bottles of whisky [a mycotoxin] every single day for the previous eighteen months before admission. We found it difficult to believe the story, but there are photographs today showing a complete reversal in 1966 of physical signs and symptoms, including the diabetes, when hospitalization cut short his alcohol supply and active treatment was administered, with gradual protein calorie buildup and pancreatin supplements.”[34]

Ongoing HIV testing since 1985 has revealed that eight times more Africans than Americans are infected (6 to 8 million)[35], yet the continent has produced fewer AIDS cases: 129,000 by 1992 and 345,639 as of December 1994.[36]  By contrast, several large studies recently published findings that among thousands of randomly selected Africans with standard AIDS diseases, fewer than half were HIV-positive.[37]  What does this say about a supposedly raging epidemic?

A completely separate epidemic seems to affect rural Africans, this one having no identified risk group. Some reports suggest a correlation between AIDS there and the symptoms of malnutrition. Doctors observe that AIDS patients who eat least often, or whose diets are skewed by food availability, suffer the most rapid decline in health. This should surprise no one. In rural Africa, the most important aspects to be considered, as in the entire history of epidemics, are: sanitation, which rarely exists; clean water supplies, also rare or nonexistent; and decent nutrition. It would seem that HIV/AIDS has created no new epidemic in Africa. But since HIV/ET is such a well-received hoax, it jumps in and “takes credit,” while obfuscating relevant issues.[38]

In 1985, 250 patients from a local hospital in a remote area of Zaire, none of whom had clinical AIDS, were tested for HIV. Twelve percent clearly showed positive, while another 12 percent were borderline; but there was no correlation with any health complaints. The researcher concluded, “Thus, if antibodies indicate prior exposure to [the AIDS virus], this population must have had and survived [AIDS-virus] infection without lasting health problems.”[39] In a similar situation in Venezuela, Indians who live cut off from the rest of the country’s people were found with from 3.3 to 13.3 percent infection, with no symptoms.40 Being so isolated, they are highly unlikely to have been infected within the latent period. In both these cases, investigators concluded that people could have been living with the virus for a generation or more.

One might be challenged, as the Ugandan doctor was, to distinguish between an AIDS/tubercuIosis and a traditional one. Since the clinical symptoms are identical, the CDC has stipulated in its current definition that tuberculosis must be renamed AIDS if HIV antibodies are also found. In the absence of HIV antibodies, the disease is classified under its old name, tuberculosis, and treated accordingly. Therefore, simply by definition/elasticity, HIV antibodies can never be found apart from AIDS, and vice versa; and any symptomology has the potential to become an AIDS indicator with HIV around. In general, if doctors can tell the difference between AIDS on the one hand, and non-AIDS presence of its indicator diseases on the other, only by testing for antibodies to HIV, which sometimes don’t even have to be present (discussed below), it would seem we have a syndrome of contrived or arbitrary origin, circularly defined.

HIV/AIDS and Koch’s Postulates

Koch’s postulates is a set of conditions long accepted as the requirements for establishing a fixed microorganism as the cause of a specific disease. The case for HIV as the AIDS virus, as with the identification of any causative infectious agent, should depend upon meeting these parameters, of which there are four. (Keep in mind that researchers disagree about what constitutes proof that any germ causes a disease.)

1.  The germ must be found in all cases of the disease. Tissues said to be affected by HIV include primarily the white blood cells of the immune system, particularly the T-cells, the brain neurons in dementia, skin cells in lesions of Kaposi’s sarcoma, as well as, theoretically, any cell in the body expressing the CD4 surface receptor said to be the key to HIV cell entry. But no trace of the virus can be found in either the Kaposi’s sarcoma or the neurons of the central nervous system. HIV/ET has now moved from involving only immune cells to other types of cells in order to explain certain AIDS-defining symptoms which are not immune deficiencies anyway, including the cancers, dementia and wasting diseases, and which have not been, or cannot be, explained in terms of a germ-theory virus model that involves destruction of the immune system.

And if HIV were actively infecting T-cells or other members of the body’s immune system, extracellular virions should easily be found circulating in the blood. But in most individuals suffering from AIDSyndrome, no particles can be found anywhere in the body.

Another aspect of HIV/ET is that now several HIV “reservoirs” have been suggested. One encyclopedia, which will go unnamed, says: “Researchers have also been able to show direct infection of bone-marrow cells-the precursors of circulating blood cells-and the proliferation of the virus within these cells. Thus bone marrow may represent an important reservoir of HIV in an infected person and provide a potential mechanism for dissemination of the virus through the body.” This is misinformation, pure speculation, a conclusion based on laboratory pyrotechnics, or scientific fraud. It is also said that macrophages can support HIV replication while harboring the virus from immune surveillance. Circulating macrophages are said to play an important role in the distribution of HIV throughout the body, including the brain. The question is, wouldn’t there be significant amounts of virus in a reservoir? The fact remains: it is nearly impossible to recover HIV from its “victims.” (See below under “Autoimmune Theory.”) One paper published in March 1993 reported two individuals with about 100,000 particles per milliliter of blood, among dozens of patients with little or no detectable extracellular particles.[41]

The abundance of uninfected T-cells (about one in 500) in all AIDSyndrome patients is the definitive argument against the false claims for high cell-wall particle “loads,” or “burdens,” in AIDS patients. The absence of active, infectious virus automatically disqualifies HIV as a player in the AIDSyndrome.

2.  The germ must be isolated from the host and grown in pure culture. Even for the most experienced virus hunters, a virus that is so extremely scarce is difficult to find. Only with rare luck and extreme persistence has HIV been extracted from an antibody-positive person. This amounts to finding the proverbial needle of HIV in a haystack of human DNA. This difficulty speaks to HIV’s lack of potential in disease.

3.  The purified germ must cause the disease again in another host. There is no animal or human model for HIV and AIDS, and where there is no animal or human model, you cannot establish Koch’s postulates. (It is more than disconcerting to think of the number of primates that have been injected to this day in an attempt to produce AIDS.) HIV/ET jumps in and says that HIV should receive special dispensation from Koch’s postulates. A major stumbling block is the latency which is claimed, but whose modus is not explained by authorities. In 1989 the official latent period between HIV infection and the onset of AIDS was one year. This period of “incubation” has since been stretched to 1012 years. For each year that passes without the predicted explosion in AIDS cases, approximately one year is added to this period. Even this is insufficient; with only 5 percent of infected Americans developing AIDS each year, the average latent period would have to be revised to more than 20 years for 100 percent to become sick.

HIV should cause AIDS within two weeks of infection at most, but it does not, and with the complete lack of a demonstrated process by which HIV diminishes immune function, belief in a decade or more of unexplained latency requires a level of “faith” beyond this writer’s capacity. Another major stumbling block is that even once the latent period is apparently over, there is still precious little development of the virus.

4. The germ must then be isolable from the newly infected host. We are now back to the problem of meeting requirement number 2.

The Antibody That Isn’t

According to germ theory, an antibody is a certain antidote to a pathogen. According to HIV/ET, however, the more antibodies you have to HIV, the sicker you are said to be. AIDSyndrome is the only “disease” in the allopathic file cabinet in which antibodies to the causative agent mean you’re in trouble; and it defies just about every known law, rule, guideline, fact, and behavior in the germ theory book. This includes, as we have seen, Koch’s postulates, and, as we will see below, Farr’s Law. Furthermore, vaccine research proceeds on the basis of producing antibodies to HIV in the patient. Apparently, these “synthetic” antibodies will signal recovery, while one’s own signal death.

The Autoimmune Theory

One explanation put forth for the deadliness of such a scarce pathogen is that it somehow induces a self-destructive immune response (the system attacks itself). Evidence for this is said to be low white cell counts in people with AIDSyndrome; however, there is nothing to support the hypothesis, i.e., no plausible process by which this occurs has been suggested (see “What’s Overlooked” below).

For the sake of discussion, let us allow germ-theory interpretation of immune function and autoimmunity. With only one in 500 immune cells said to be infected in HIV positives, it would seem to require a virus of extraordinary cunning to get uninfected cells to attack each other and not infected ones, which would be self-defeating for the virus. Or in the latter event, such cunning could be matched only by the adroitness required to move quickly from one host cell to another just before destruction. Or, if macrophages are involved, the process should lead either to increasing titers of virions in the blood, lymph, etc., as infected cells are lysed, or to increasing concentrations in macrophages if they are ingesting T-cells. This supports the reservoir notion (if there were any viruses to be found in them). It is thus easy to expand HIV/ET.

HIV/AIDS and Farr’s Law

Established in the early 1900s, Farr’s Law, which is fundamental to virology, states that viral disease develops exponentially, and dictates that illness will strike soon after infection. The rate-determining factor of the exponential growth of viruses is viral generation time, which is between 8 and 48 hours. Since laws are made to be broken or excepted, viruses with incubation periods longer than allowed by Farr’s Law are called “slow viruses.” And since HIV joins an exonerated class of viruses by not multiplying according to this law of virology, virologists stretch HIV/ET to accommodate it. The question arises, though, of how anyone can determine or demonstrate when a “natural” HIV infection takes place, and thus determine latency, since no one is being tested daily or weekly, etc., and there is no animal model. Within the slow-virus concept, adopted as an exception to Farr’s Law, retrovirologists can find refuge, hold on to their theory, hibernate in their labs, and hope the long winter of HIV latency is over before they expire.

According to expert retrovirologist Dr. Peter Duesberg, “The slow virus concept has never been reconciled with the short generation time of viruses and the immune system. Once the virus lies totally dormant, an intact immune system will never allow any virus to be reactivated to multiply into numbers that would threaten the host. For a virus to be reactivated, the immune system first must be destroyed by something else-the real cause of a disease. A reactivated virus would just contribute an opportunistic infection. Thus, there are no slow viruses, only slow virologists.”42 Also, says Duesberg, “Retroviruses are all very similar. I mean, there are differences, but as far as pathology is concerned, you don’t see a marker in one which is going to explain why it supposedly wakes up from sleep and becomes active.”[43]

The Chemotherapy Drug Azidothymidine (AZT)

HIV-antibody-positive individuals suffer major health risks from AIDS medications routinely administered by physicians uncritical of drug-company propaganda. AZT, an isolate from herring sperm, was first synthesized in 1964 by Jerome Horwitz, heading a lab at Detroit Cancer Foundation and financed by an NIH grant. Designed to kill cancer cells, Horwitz’s creation is a chemically modified form of a DNA building block. When a cell divides, it must copy its complete genetic code, which is stored in long chromosome chains. The DNA components (nucleotides) are linked to one another in a sequence. But Horwitz’s altered DNA building block enters the growing DNA chain while a cell is preparing to divide and acts as a premature terminator, blocking addition of DNA components. Being unable to copy its DNA sequence, the cell dies.

AZT was the perfect killer of dividing cancer cells. When the compound was tested on cancer-ridden mice, however, it failed to perform as expected and instead revealed its extraordinarily deadly nature. The experimental drug was withdrawn from testing and never approved for human use-until AIDSyndrome. Side effects of AZT include ulcerations and hemorrhaging; damage to hair follicles and skin; destruction of mitochondria, the energy dynamos of cells; wasting of muscles; and the destruction of the immune system and other blood cells. Children are affected more severely, because many more of their cells are dividing than in adults.

Amid scandal-(l) the single, human trial that was ruined, yet was claimed to have proven effectiveness; (2) free corporate (Burroughs Wellcome) acquisition of large amounts of National Cancer Institute (taxpayer) raw material and technology; and (3) government stonewalling of other, potentially less expensive antivirals-AZT was first approved for treatment of AIDS in 1987.44 The cost was $250 a shot, or about $18,000 per year, per case. In 1990 it was approved for AIDS prevention, and has currently reached an average cost of $6,000 per year.

I have worked with many HIV-antibody-positive individuals who have for years remained completely free of any AIDS-indicator symptoms or any other significant ones. When treated with medications like AZT, however, people are observed to sicken and die from “wasting disease” in a short period of time. I, as well as other molecular cell biologists, know of no one who has been treated with AZT and lived for more than around one year. Fortunately, it has begun to fall out of favor as the drug of choice.

Use of AZT is a good example of two other medical phenomena: (1) the odds game called the therapeutic index, or the relationship between a drug’s effectiveness and its toxicity; and (2) the dependence upon destruction that informs “scientific medicine.” The acceptable toxicity of a drug is directly proportional to, and established by, the deemed deadliness of the disease. However, to this date the Physicians’ Desk Reference quotes the low toxicity of AZT reported by Broder, Barry, Bolognesi, and colleagues in 1986. According to at least four independent studies published since, however, the toxicity of the drug is a thousand times higher.[45]

Broder, Barry, Bolognesi, and colleagues overlooked or disregarded two basic factors in their lab experiments: (1) In the test tube in which they tested AZT, there was a high concentration of “infected” cells. But, as noted earlier, in a person with HIV, titers are very low, and the ratio of infected to healthy cells is very low (only 1 in about 500 T-cells in HIV antibody-positive persons is ever “infected”); (2) Like all other chemotherapy drugs, AZT is unable to distinguish between target cells and healthy cells. The disastrous consequence is that AZT must poison 499 good T-cells in order to poison one inhabited by the AIDS “virus.”

Real Fallout

Various individuals diagnosed with AIDS who were paraded in the media, trapped into following the AIDS “company line,” later died of AIDS-related symptoms. Many were treated with AZT from the very beginning, even though they showed no signs, or few signs, of ill-health at the start of the program. Two examples are Kimberly Bergalis (featured in the October 22, 1990 issue of People magazine) who supposedly “caught” HIV from her Florida dentist, and Arthur Ashe, the heterosexual tennis professional. (Kimberly had only a minor yeast infection at the start of her AZT program.) In typical fashion, the news media focused upon, and widely broadcast, the details of their gradual degeneration and painful deaths, which exhibited all the classic symptoms of AZT poisoning. “AIDS” death and AZT death are outwardly indistinguishable. Here is a perfect combination: an illness incorrectly billed as universally fatal, treated by a useless, frequently fatal drug.

What’s Overlooked

Shades of doubt concerning HIV/ET validity in terms of germ theory have arisen since three-quarters of the 20,000 hemophiliacs in the United States were infected by HIV through the blood supply a little more than a decade ago. During that period, clotting factor VIII doubled life expectancies, while relatively few developed AIDSyndrome. HIV has made no measurable impact on the well-being of hemophiliacs, except for devastation of those who are treated with AZT.[46] No evidence has shown that death rates from blood transfusions ever increased from HIV transmission, nor has anyone demonstrated that death rates declined once the virus was screened out of the blood supply.

Even if AIDSyndrome does exist as a new phenomenon, perhaps insufficient scrutiny has been paid to the idea that it is not virus-based, but related to an inverted way of living and eating. For these reasons, and the sociopolitical ones mentioned earlier, illness is simply on the rise in general, and individual cases are often more intense and intractable. Cancer is now epidemic, for example. “Flesh-eating” bacteria have made an appearance. Disease intensity and statistics must also be considered in terms of the ineffectiveness and iatrogenic influence of the orthodox approach to illness-the equivalent of trying to remove a screw with a hammer. HIV/ET attempts to divert responsibility for health disaster from an inept, sometimes malfeasant, pharmaceutically controlled medical tradition. A century of medical practice and health concepts based on the scientifically erroneous germ theory is as much the cause of AIDS as any single factor-probably more. AIDS could easily have been predicted epidemiologically as an aspect of the burgeoning crisis in health. It had to be blamed on a virus on order to distract attention from the real problems.

Speaking of prediction: Several doctors and writers have made a strong connection between AIDSyndrome and syphilis. The consequences of misdiagnosed or improperly treated (including penicillin) syphilis may be misinterpreted as AIDS indicators. According to one researcher, almost every AIDSyndrome indicator has been seen in syphilis.[47]  An interesting corollary here is the Tuskegee Alabama Syphilis Study, in which 400 Alabama sharecroppers were allowed to suffer and die with untreated syphilis (which they were not told they had) for 40 years until the study was exposed in 1972. Did a medical establishment (CDC, Public Health Service, NIH) capable of such behavior learn anything about syphilis which might have helped predict, and formulate a description of, the “new” AIDSyndrome epidemic?

With the primary U.S. AIDS groups, or with any group for that matter, if you understand microzymian principle and consider the blood as a flowing tissue, it will be seen in general that body fluids which find their way from one individual directly into the blood of another are a stress factor on the body. This is by virtue of the introduction of foreign tissue and possibly morbidly evolved microzymas. Total impact depends on the degree to which the terrain is already compromised. In fact, a major danger is blood transfusion itself, essentially a “tissue transplant,” which is a threat or irritant to immune function. There is no reason to believe that such repeated stress will not, by itself, overwork and weaken immune function and drain overall energy reserves.

Current medical science gives credence to the so-called autoimmune response, where white cells said to be deranged indiscriminately destroy and/or clear out healthy and unhealthy cells. This misconception arises as a consequence of germ theory mentality, which misunderstands the central function of the immune system. It is essentially a sophisticated janitorial service. It operates to keep the place clean and to recycle usable material. Should “self cells or tissue become useless or even dangerous to the body, the immune system will clean them out. Thus, it is not deranged, but is doing its job correctly. The host is somehow not doing its job, however, to maintain a balanced internal environment, which is the first line of defense, not immunity, against tissue destruction and infection. This is because infection can come from within. And it bears repeating that the fundamental misconception of the germ theory is that infection must be invasion, rather than an endogenous morbid change in chemistry or micromorphology.

Compromised or weakened by fungal infestation (evidence for which is obvious and strong) or by drugs and chemicals such as mycotoxins, the immune system may weaken and fail to be efficient, but it will not attack healthy cells. There is a situation where this may appear to be so-when free radicals produced by the immune system in response to mycotoxins and morbidly evolved microforms damage local cells and tissue by the “shotgun” effect – but it is not a direct attack on “self,” and is frequently an overreaction to the alarming situation.

What Constitutes AIDS in 1998?

HIV/ET responds to the question of why the syndrome hasn’t spread into the general population with the reply that it just needs a little more time. To accomplish this, however, the situation requires a little massage as well. On occasion, the definition of AIDS has been expanded (along with the latency period), with more indicator diseases being added to the list. In 1987, purportedly for surveillance purposes, a major change was made to the definition, which not only added diseases to the list, but removed, in the presence of a positive HIV test, exclusions for other known causes of immune suppression. The rationale was to provide consistent statistical data for public health purposes. Thus, a person could now be diagnosed with a surveillance case of AIDS.

In the CDC guideline, the caveat was given that clinicians would not rely on this definition alone to diagnose serious disease caused by HIV. Good medical practice, which was apparently expected to be employed later, could be expected to catch cases that somehow slip through the vast surveillance net because they have either a negative H1V-antibody test or, in the presence of HIV antibody, an opportunistic disease not listed in the definition. With the new rules, in the case of diagnosis of any one of several indicator diseases by a “definitive method,” AIDS had to be diagnosed even if the patient were HIV negative.

One question would seem to be: Why not employ good medical practice at the outset? Also, with the vast range of conditions listed, one is hard pressed to imagine what might not be included, except perhaps the common cold. But the overall effect of this change was to boost statistics and bring more people into the web of fear surrounding the syndrome. In 1992 another statistic-bumping revision was handed down.

Today the AIDS-indicator list includes, but is not limited to, Pneumocystis pneumonia, Kaposi’s sarcoma, non-Hodgkin’s lymphoma, candidiasis, cryptococcosis, tuberculosis, herpes simplex, cryptosporidiosis, coccidioidomycosis, toxoplasmosis, wasting disease and dementia. And symptomologies such as syphilis, chronic fatigue, anemia, arthritis, nephritis, pneumonitis, diarrhea, cervical cancer, and a T-cell count of less than 200 cells per microliter, or less than 14% of the expected level, have been added to the diagnostic list. It appears that when a higher rate of new AIDS cases is needed “for public health data,” the CDC expands the definition. With the stroke of a pen an illusion of the spread of AIDS is created. To include the major symptoms of malnutrition (wasting) as an AIDSyndrome indicator, especially in Africa and the Third World, is to ensure a burgeoning statistical picture.

Nor is this the first time such statistical manipulation has occurred in medical history, polio being an excellent example. According to Dr. Herbert Ratner, former public health officer for Oak Park, Illinois, prior to vaccine introduction, doctors were being paid $25 apiece by the National Foundation for Infantile Paralysis for polio case reports. Also, Ratner indicated, it was known that paralytic polio went away in 50 percent of cases within 60 days. After the arrival of the Salk vaccine, the case definition for polio was changed to require symptoms for 60 days before a diagnosis could be reported. Thus, if someone had it and it went away within that time, it was never counted, making the vaccine look better.48 After vaccine introduction, cases previously reported as poliomyelitis were differentiated as aseptic meningitis. Despite this subterfuge, case incidence increased dramatically after vaccine introduction (80 percent from 1958 to 1959) but the Public Health Service manipulated statistics and made statements to give the opposite impression.[49]

Should anyone question the idea that the CDC at any time “needed” a higher case rate, consider the following: In the early years of AIDSyndrome, while this supposed epidemic was developing, the CDC stood back and did nothing to identify and help the sexual contacts of AIDSyndrome patients. It was a departmental “do-nothing” policy. This has been documented and published by a former Public Health Adviser and AIDS researcher who worked at the CDC at the time.[50]

A Final Thought

To prove that HIV is the cause of AIDS and make HIV/ET more than a speculative hypothesis, it would be necessary to show the presence of HIV among patients with AIDS diseases whose personal history did not include: (1) chronic, abusive, male homosexual activity with associated chronic drug abuse and antibiotic dependency; (2) massive ingestion or injections of recreational drugs; and (3) use of toxic prescription medications, including AZT and antifungals. Likewise, one would have to show HIV absent among groups of healthy, asymptomatic individuals. In spite of the millions which have been spent on AIDS research, such a study has never been undertaken, although we have seen instances of long-term HIV presence with no correlated illness.

In my research, I can see only minor differences among dried blood samples of people with cancer, dementia, MS, and diabetes on the one hand, and the person with AIDS on the other. They all show excess fermentation processes and disseminated intravascular coagulation. They are all rotting from the inside out. There seems to be one model that makes sense and consistently validates clinical observation and research: There is only one physiological disease-terrain imbalance seen as acidification, due primarily to an inverted way of eating and living. Acidification leads to the one sickness, or primary symptom of disease-morbid microzymian response, or the overgrowth of microforms whose poisons result in secondary symptoms (commonly called “diseases”), these being produced in or by the body in keeping with the uniqueness of each individual. Forms of toxicity such as environmental chemicals and heavy metals also play a role, but in most cases will also disturb the central balance of the microzymas, thus complicating the situation with morbid microzymian evolution.

There are no “diseases” created by “microbes” invading from without. Viruses are not even symptogens. HIV has no causative connection with disease, and no new epidemic exists.

References 

[1]  L’Orthobiologie Somatidienne. Video by Gaston Naessens, 1991.

[2]  Bechamp, Pierre Jacques Antoine. The Blood and Its Third Anatomical Element, (Montague R. Leverson, translator). London: John Ouseley Ltd., 1912, pp. 205 and 229.

[3]  Kalokerinos, A. and Dettman, G. Second Thoughts About Disease: A Controversy and Bechamp Revisited. Warburton, Victoria, Australia: Biological Research Institute, p. 9 [booklet published from an article in Journal of the International Academy olPreventive Medicine, July 1977; 4(1)].

[4]  Hume, E. Douglas. Bechamp or Pasteur? Ashingdon, Rochford, Essex, England: The C.W. Daniel Co. Ltd., 1923, p. 109.

[5]  Farber, C. Out of Africa, Part I. Spin Magazine, March 1993: 61-63, 86-87.

[6]  Kalokerinos and Dettman, op. cit., p. 12.

[7]  Ibid.

[8]  Denetclaw, T.H. and Denetclaw, W.F.J. Is “Southwest U.S. mystery disease” caused by hantavirus? Lancet, 1994; 343: 53-54.

[9]  Russel, S. On the Trail of Hantavirus. San Francisco Chronicle, July 4,1995: AI, AI2.

[10]  Russel, S. Signs that Ebola Virus Is Fading Away. San Francisco Chronicle, May 24,1995: A6.

[11]  Kaiser, R. Africa State Hospitals Make Viruses, Not Patients, Feel at Home. Washington Post, June 4,1995: A6.

[12]  Physicians’ Desk Reference (PDR), 1997, p. 1730.

[13]  Beale, A.J. Vaccines and Antiviral Drugs. In: Topley and Wilson, Principles of Bacteriology, Virology and Immunity, (Publisher, Year?), p. 149.

[14]  Jegede, V.A. et al. Vaccine Technology. In: Encyclopedia of Chemical Technology, (Publisher, Year?), p. 629.

[15]  PDR, op. cit., p. 2650.

[16]  Rappaport, John. Touching All Bases-Exploring Alternative Theories of AIDS. The Reader (Los Angeles Free Weekly), August 7, 1987; Vol. 9, No. 42: 10. [Note: Reference pertains to evidence that calves were recently, or are still, cruelly used for this purpose. Minor details of the process differ from those described in the article.]

[17]  PDR, op. cit., p. 2656.

[18]  Kalokerinos and Dettman, op. cit. (Ref. 3), p. 13.

[19]  Ibid., p. 12.

[20]  Goldberg, B. Origin of AIDS. Lancet, 1992; 339: 1548.

[21]  Kalokerinos and Dettman, op. cit.

[22]  Pearson, R.B. The Dream and Lie of Louis Pasteur. Collingwood, Australia: Sumeria Press, 1994, pp. 32-35.

[23]  Cayce Reading #480-19. The Cayce readings are on fde at the Association for Research and Enlightenment, Virginia Beach, VA.

[24]  Hodgkinson, N. Experts Mount Startling Challenge to AIDS Orthodoxy. Sunday Times (London), April 26,1992; I: 12-13.

[25]  Carroll, John. The Weird Way to Win a Nobel Prize. San Francisco Chronicle, October 21,1993: E9.

[26]  Mirvish, S.S., Williamson, J., Badcook, D., Sheng-Chong, C. Mutagenicity of Iso-butyl nitrite vapor in the Ames test and some relevant chemical properties, including the reaction of iso-butyl nitrite with phosphate. Environmental. Molecular Mutagen, 1993; 21: 247-252.

[27]  Rappaport, John. AIDS Inc. Scandal of the Century., San Mateo, Cal.: Human Energy Press, 1988, p. 38.

[28]  Ibid., p. 40.

[28]  Fungalbionics Convention: The Fungal/Mycotoxin Etiology of Chronic and Degenerative Disease. Metro Toronto Convention Centre, September 30,1994.

[29]  Konotey-Ahulu, F.I.D. What is AIDS? Watford England: Tetteh-A’Domeno Co., 1989, p. 109.

[30]  Rappaport, op. cit. (Ref. 27), p. 73.

[31]  Williams, A.O. AIDS: An African Perspective. Boca Raton, Fla.: CRC Press, 1992, p. 238.

[32]  Duesberg, Peter H. Inventing the AIDS t7ras,(**Publisher, YEAR?), p. 293.

[33]  Konotey-Ahulu, op. cit., pp. 56-57.

[34]  World Health Organization, The Current Global Situation of the HIV/AIDS Pandemic, 1995.

[35]  Duesberg, Peter H. AIDS acquired by drug consumption and other noncontagious risk factors. Pharmacology and Therapeutics, 1992; 55: 258.

[36]  Ibid., p. 240.

[37]  Rappaport, op. cit. (Ref. 27), pp. 71-82.

[38]  Biggar, R.J. et al. Seroepidemiology of HTLV-III antibodies in a remote population of Eastern Zaire. British Medical Journal, 1985; 290: 808-10 (cited in Coulter, Harris L. AIDS and Syphilis, The Hidden Link. Berkeley, Cal.: North Atlantic Books; and Washington: Wehawken Books, 1987; p. 61).

[39]  Duesberg, Peter H. Retroviruses as carcinogens and pathogens: Expectations and reality. Cancer Research, 1987; 47: 1199-1220 (cited in Coulter, Harris L., op. cit. [Ref. 38], p. 61).

[40]  Lemonick, M.D. Return to the Hot Zone. Time International, May 22,1995; 145: 56-57.

[41]  Duesberg, Peter H. AIDS acquired by drug consumption . . . (Ref. 36), pp. 237-38, 241, 247.

[42]  Rappaport, op. cit., p. 130.

[43]  Committee on Government Operations. AIDS Drugs: Where Are They? 73rd Report. U.S. Government Printing Office; October 3, 1988. (Cited in Culbert, Michael L., D.Sc. AIDS: Hope Hoax and Hoopla. Chula Vista, Cal.: The Bradford Foundation, 1898, pp. 10-11).

[44]  Chiu, D. and Duesberg, P.H. The toxicity of Azidothymidine (AZT) on human and animal cells in culture at concentrations used for antiviral therapy. Genetica 95, 1995: 103-109. Duesberg, Peter H. AIDS acquired by drug consumption . . . (Ref. 36), pp. 201-77.

[45]  Yarchoan, R, Pluda, J.M., Perno, C.-F., Mitsuya, H., Broder, S. Anti-retroviral therapy of human immunodeficiency virus infection: Current strategies and challenges for the future. Blood, 1991; 78: 859-84. McLeod, G.X., Hammer, S.M. Zidovudine: Five years later. Annals of Internal Medicine, 1992; 117: 487-501.

[46]  Duesberg, Peter H. Is HIV the cause of AIDS? Lancet, 1995; 346: 1371-72.

[47]  Coulter, Harris L. AIDS and Syphilis, The Hidden Link. Berkeley, Cal.: North Atlantic Books; and Washington: Wehawken Books, 1987, p. 37.

[48]  Rappaport, op. cit. (Ref. 27), pp. 152-53.

[49]  Hearings before the House Committee on Interstate and Foreign Commerce. House of Representatives, 87th Congress, 2nd Session, H.R. 10541, May 1962, pp. 94, 96, 112 (cited in: James, Walene. Immunization: The Reality Behind the Myth, 2nd edition. Westport, CT: Bergin & Garvey (Greenwood Publishing Group, Inc.), 1995, pp. 35-36).

[50]  Sermos, Gus G. Doctors of Deceit and the AIDS Epidemic-A View From the Inside. McComb, Miss.: GGS Publishing, 1988, p. 3.

Pathological Blood Coagulation and the Mycotoxic Oxidative Stress Test

 Robert Young PhD

Naturopathic Practitioner – The pH Miracle Ti Sana Detox Medical Spa and Universal Medical Imaging Group

Abstract

Historical analysis suggests that conventional understandings of Disseminated Intravascular Coagulation (DIC) may be misguided; further examination may be necessary.  Here, a theoretical analysis provides an alternative explanation for DIC pathology; it is suggested that the cause and mechanics of DIC are largely due to the proliferation of several intravascular microforms and their associated metabolic toxic acidic waste products — Mycrozymian Acidic Toxins (MAT) and Exotoxic-Mycotoxic-Producing Microorganisms (EMPO).  The Mycotoxic Oxidative Stress Test (MOST) is presented here as an easy, inexpensive and non-invasive alternative to conventional measurements for the detection of intravascular  acidic toxins, DIC  and oxidative stress.

Introduction and Historical Perspective

More than 150 years ago, British physician T. W. Jones asked the question, “Why does the blood circulating in the vessels not coagulate?”[1]  though a general answer to this question is now obvious, the biochemical mechanisms involved in how the blood coagulates (clots) are complex and varied, and all the intricacies have not yet been explained. A. Trousseau, recognized that the blood of cancer patients is in a hyper-coagulable state in the process of coagulation, even while confined in the blood vessels.[2]  The name given to this discovery is still in use today, as “Trousseau’s Syndrome.”[2]  Early in his career, Rudolph Virchow, the Father of Pathology, was interested in thrombosis and embolism.  He speculated that intravascular blood could be altered so it would clot as a result of a stimulus too weak to clot normal blood.[3]  In 1856 Virchow delivered a lecture setting forth this concept.

Although the concept of partial clotting within vessels reaches back to the beginnings of modern medicine, much of the discovery of its biochemical mechanisms – the activation of clotting factors – has been left to chance.  The admission of a patient to the hospital with an unceplained bleeding disorder challenged researchers to discover the cause of hemorrhaging.  Analysis of blood from normal persons helped in the study of the patient with the blood disorder. A new clotting factor was hereby discovered which was missing from the  patient’s blood.  For this reason, several clotting factors have been named after the individuals in which they were missing: e.g., Christmas factor (factor IX)[4], Hageman factor (factor XII)[4].

In this article, the causes of pathological (intravascular) clotting will be described, as will various methods of detecting this condition, especially a blood test I call the Mycotoxin Oxidative Stress Test (MOST).

The Mechanics of Blood Coagulation

Blood clotting is a highly detailed chemical-mechanism involving many distinct components.  The problem for the hematologist hs been to understand it at the biochemical level.  Undoubtedly, efforts to fully understand blood clotting will continue for many more years.

Recalling Antione Bechamp’s[8] and Gunther Enderlein’s[9] research into the sub cellular living elements and combining this with what is known of colloidal flocculation[6], it is suggested that the clotting of blood begins with the end-linking (polymerizing) of the fundamental protein unit called by Bechamp the microzyma[8].  A chain of these living units constitutes fibrinogen, which is still dispersed 9micro-hetergenous0 in the blood, and it may or may not be further processed.  If processing continues, it will be either by continued end-linking or by cross-linking.  End-linked fibrinogen is referred to here as fibrin monomer, which I have suggested is a repair protein also dispersed in the blood. Due to a number of blood clotting factors, the process may continue until the excess fibrin monomer and/or until fibrin becomes excessively end-linked.

Cross-linking the polymerized strands to form a three-dimensional network results in what is called the hard clot (fibrin – the major protein of clotting blood).  Factor XIII, which instigates the forming of these blood networks. is always present but latent in the blood, and must be activated before the formation can occur.  Persons who are producing fibrin monomer or excessively linked fibrinogen are said to be in a hyper-coagulable state, while those having diminished  ability to form clots are in a hypo-coagulated state.  It is the activation of the colloidal clotting factors which is so complex.  Blood clotting may occur through many pathways and be initiated by many different stimuli.  Regardless of initiation factors, the process is a sequence of events in which the activation of one factor triggers another, until, after a series of discrete steps, fibrin is formed.

When blood is clotted prematurely, and the factors involved are consumed (incorporated into) the body recognizes a deficiency of clotting agents and generates more.  Thus, people with a tendency to clot excessively will alternate between a hyper coagulable state and a hypo-coagulatable state.  When in the hypo coagulated state, such people hemorrhage until the deficient clotting factors are replaced.[4]  When only fibrin monomer or excessively linked fibrinogen is formed (no cross-linking), it is quite subtle and may go undetected.  It may be detected by a change in blood viscosity (sedimentation rate), by the Mycotoxic Oxidative Stress Test (described later), or by other more subtle means.  If strands of fibrinogen are cross-linked, however, a suggicient amount of insoluble precipitate of fires may result, and these can be detected microscopically using a phase contrast and dark-field microscopy in prepared slides of fresh tissue or blood.  An excessive formation of fibrin leads to  an impairment in circulation, and eventual organ failure usually results.[5]

With this background, we are in a position to consider a standard medical term: disseminated intravascular coagultion (DIC).[6]  This term encompasses the hyper coagulable state, i refer to as pathological blood coagulation which consists of both insoluble and excess dispersed polymers of colloidal proteins.

Key Ingredients of Pathological Blood Coagulation

Before discussing DIC in more detail, it si necessary to introduce its fur important ingredients according to this view – mycotoxins, endotoxins, exotoxins, and tissue factor.  Any of these elements, or any combination of them, can play a major role in initiating unwanted DIC.[6]  However, mycotoxins or the acids from yeast have been found to be the underlying element which instigates and intensifies the participation of the other three.[6]  Each will now be described in turn and brought into the clotting picture.

(Micrograph 1: left, shows normal hyper-coagulated blood in a healthy blood clot sample and right, hypo coagulated blood in an unhealthy blood clot sample)

Mycotoxins and Metabolism by Fermentation

As discussed in the main text of my published book, Sick and Tired book[7 ]. acidification of blood and body tissues and organs and the accompanying lack of oxygen lead to pathological metabolic fermentation, which is carried out primarily by yeast and mold.  Such pathological microorganisms, or their precursors, ar inherent to the human body and to all higher organisms.  Their precursors according to Bechamp, the microzymas, carry on a nominal and homeostatic fermentation themselves. under healthy conditions.[8]  The primary function of yeast and mold is to decompose the body upon the death of the animal or human organism.  Their premature overgrowth indicates a biochemical environment akin to death.  During pathological metabolic fermentation, high concentrations of several acidic substances called mycotoxins are created.  They are highly damaging, always acidic, metabolic products.  If not immediately buffered by specific antioxidants, such as hydrogen peroxide and the hydroxyl free-radical, mycotoxins can seriously disrupt the physiology by disrupting normal metabolism and by penetrating blood and body cells and poisoning them.  As will be seen, they interact with many of the mechanisms for DIC in various pathological symptomologies.

In my published article called The Finger on the Magic of Life: Antoine Bechamp, 19th Century Genius (1816-1908),  I discuss pleomorphism in some detail.[7] Understanding this phenomenon – the rapid evolution of microorganisms across traditional taxonomic  lines is helpful in getting a complete picture of DIC.  Briefly stated, collodial living microzymas evolve intracellularly into more complex forms (microorganisms), beginning with a healthy primitive stage comprising of repair proteins.  As the disease condition worsens, morbid intermediate forms (filterable bacteria or viruses, cell-wall deficient forms and full bacteria) develop from repair proteins, or directly from microzymas.  A third macrostage comprises the commonly recognized culminate microorganisms which are yeast, fungus to mold.  In terms of pleomorphism, all of these microorganisms represent a single family of variously functioning forms.[8]  The culminate forms produce the lions share of acids, which are mycotoxins and the primary focus of my research.[7][8][9]  For convenience, bacteria, yeast, fungus and mold that produce acidic metabolic wastes and protein cellular fragments called exotoins, endotoxins and mycotoxins will here be referred to collectively ash EMPO, or exotoxic, mycotoxic-producing microorganisms.

What follows is a shortened description or the description and origin of several exotoxins and mycotoxins, referred to collectively microzymian acidic toxins of MAT, which are involved in the processes leading to DIC.  The bio-effects, or the pathology of cellular fermentation, of these toxic metabolites are know as mycotic illness, mycotoxicosis, or mycotoxic stress as seen in the MOST and described and published by Dr. Bolin in the 1940’s.[10]

One such metabolic product is acetyl aldehyde, which is formed by  cellular breakdown of food, especially carbohydrate and the birth of  EMPO.  Acetyl aldehyde can also break down into a secondary substance know as ethyl alcohol.  Although acetyl aldehyde presents an immediate hazard to health and well-being, nature has provided a means of buffering of neutralizing this acidic by-product of cellular digestion and fermentation almost as soon as it is created.[11] The controls of acetyl aldehyde (and ethyl alcohol) are the sulfur amino acids, cysteine, taurine, methionine and the peptide glutathione which is found in red blood cells and almost all cells utilizing oxygen.[12]  In an attempt to buffer or neutralize MAT, the body will also bind or chelate both fats and minerals to them.[12]

Another member of the MAT family is uric acid, which is formed by the digestion of protein and the creation of EMPO.[13]  Uric acid can also break down into secondary substance, on of which is alloxan.[14] This has been shown to damage the insulin-producing pancreatic beta cells leading to diabetes [Refer to Tables 1 and 2]

A shortage of alkalizing nutrients or an excess of MAT initi­ates an immune response in which a special class of free radicals which I call microzymian oxidative buffering species (MOBS) are released.[15] These oxygen metabolites carry unpaired electrons and are intended to disrupt bacteria, yeast, fungus and mold, and buffer exotoxins, endotoxins, and mycotoxins. Current medical savants believe that they can disrupt just about any­thing they contact, including healthy cells and tissue: this is not accurate. The fact is that MOBS carriers a nega­tive surface-charge and repel healthy cells, which also have a negative surface-charge. [16] It is the positively surface-charged bacteria, yeast/fungus, mold, exotoxins, endotoxins, and myco­toxins that MOBS bind too.[17]  This aspect gives some insight into autoimmune phenomena, which are not, as is often maintained, the result of an overburdened immune system. They result either as a side-effect of the immune system’s attempt to remove foreign or toxic ele­ments, or as a direct attempt by the immune system to remove cells or tissue rendered useless or disturb­ing to the body by MAT.

In every degenerative symptomatology I have studied, I have found excessive MAT and MOBS (see Tables 1-3). Some of these degenerative symptoms and their underlying disease conditions, including cancer are described in my recently published paper on a deficiency on alkaline nutrition and cancer. [15] But the fact that myco­toxins cause harm to humans and other animals is purely a secondary effect, since, as noted, the prima­ry function of the microorganism is not to cause illness. We know from the fossil record that pleomorphic microforms existed long before animals.[19] In fact, humans and animals developed in terms of micro­organisms.[20] The reverse, however, is not true. Since micro­organisms appeared first in the developmental sequence, they are not physiologically aware of humans and animals. There is much evidence that human and animal physiologies are highly aware of, and respond to MAT – these acidic compounds signaling the presence of bacteria, yeast, fungi and/or mold or  EMPO.[21].

Endotoxins

Also involved in the process leading to DIC are endotoxins, substances endogenous to symptogenic (i.e., “pathogenic” in orthodox terms) bacteria. Endotoxins are a family of related substances having certain common characteristics, but differing from one bacterial form (or strain) to another. Endotoxins are lipopolysaccharides (LPS). LPS form a widely diversified group because of (1) the number of long- chain fatty acids composing lipids; (2) the number of individual sugars as well as their modes of linkage to one another; (3) the branching of sugar chains; and (4) the number of possible arrangements of these units. Endotoxins also contain proteins, further com­pounding the structural diversity.[22]

One theory on endotoxin states that its purpose is to act as a semi-permeable membrane for the bac­terium, limiting and regulating substances entering the organism.[22] Endotoxin resides solely on or near the interior surface of the cell membrane and is shed into the surrounding medium only upon the death of the bacterium. Thus, as these microforms die off, or are lysed by bodily activity, endotoxin is released. (This fact may well be an explanation for the Herxheimer reaction, in which a patient becomes worse following the administration of toxic drugs or other forms of treatment that drastically alter the associated organ­ism.[23]) Another endotoxin theory states that LPS are a constituent of the membrane, and as the organism grows, endotoxin fragments are repeatedly sloughed off into the medium. This phenomenon has been observed in the digestive tract.[24] Since bacterial translocation into the blood is not only possible but common where epithelial hyperpermeability exists, one can assume that the process will continue there. Both theories may be correct if we think of the first one as true of “adult” forms, and the second as true of newly developed and expanding ones.

Basic to the structure of an endotoxin is the lipid common to all forms, designated lipid A, to which is attached a “core” polysaccharide, identical for large groups of bacteria. To the core polysaccharide is attached the O-antigen, consisting of various lengths of polysaccharide chains which are chemically unique for each type of organism and LPS. These chains pro­vide endotoxin specificity.[25] Experiments conducted over many years indicate that most, if not all, of the toxic effects of an endotoxin may be attributed to the lipid portion, and it is sometimes used per se in experiments rather than the entire molecule.[26] An important additional feature of lipid A is its phos­phate content. Each phosphate group carries a nega­tive charge, and since lipid A is a rather large mole­cule, it provides, essentially, a negatively charged sur­face. The importance of this will be seen shortly.

Exotoxins

These are the metabolic excretions of bacteria. While endotoxin’s ongoing effect is, in a manner of speaking, in the background, exotoxins, like myco­toxins, present a double-edged sword. Not only do they initiate DIC, but they produce, or influence the body to produce, the various and numerous infec­tious symptomatologies, such as typhoid fever, diph­theria, etc. (See “Vaccination Reconsidered” in Section 4 of the Appendix of Sick and Tired for details on the action of diphtheria toxin.)[7] By comparison, mycotoxins not only initiate DIC, but there is much evidence to sug­gest that they produce, or influence the body to pro­duce, degenerative symptomatologies, such as arthri­tis, diabetes, etc., and cancer and AIDS as well.

Tissue Factor

Crucial to the understanding of DIC is recogni­tion of the role of tissue factor (TF), formerly known as thromboplastin. This transmembrane lipoprotein exists on the surface of platelets, vas­cular endothelial cells, leukocytes, monocytes, and most cells producing EMPO.[27] It plays a major role in several biochemical mechanisms leading to DIC.

TF is the primary cell-bound initiator of the blood coagulation cascade. Its gene is activated in wound healing and other conditions. By itself it is capable of initiating clotting, but also becomes active when complexed with factor VII or activated factor VII (Vila).[28] TF has been described as the receptor for factor VII because of the close association between the two proteins and because it causes a shape change (conformational) in factor VII, allowing it to attain activity. Both factor Vila and the TF/VII com­plex activate factors IX and X, which initiate the clotting cascade and the formation of thrombin.[29]

Development of Disseminated
Intravascular Coagulation
(DIC)

DIC Induced by MAT and Tissue Factor

An infusion of toxins into the blood has a direct effect on TF gene expression in leukocytes. Contact of MAT, endotoxins (lipid A), or exotoxins with leukocytes, activates proteins that bind to DNA nucleotide sequences, thereby activating the TF gene.[30] (See Tables 4-6.)

Endothelial cells damaged in culture by exotoxins, endotoxins, or mycotoxins attract polymorphonuclear leukocytes (PMNs), which adhere to the damaged cells. Once the leukocytes are bound, they can still have their TF gene activated if it hasn’t yet occurred, and they may release MOBS in response to toxins and to organisms of disease, possibly creating further dis­turbances. (Cellular disorganization then releases acti­vating proteins into the blood, which is discussed in more detail later.) Research shows that exotoxic and mycotoxic stress resulting in bound PMNs can be blocked by “antioxidants.”[31] These might better be called anti-exotoxins or antimycotoxins. Both observa­tion and study have led the author to conclude that cellular disorganization is initiated and primarily caused by fermentation pathology, not, as is the cur­rent belief, by the MOBS, or free radicals, generated to destroy toxins and microorganisms. MOBS or free radicals, because of their negative charge, are released to chelate or bind EMPO and MAT. It is suggested by current savants that free radical tissue damage is the secondary, “shotgun” effect of intense immune response to EMPO toxification and MAT-damaged cells. This could not be the case since healthy cells or their membranes carry a negative charge and would resist any electromagnetic attraction because of simi­lar charge. The concentration and instability of MAT generated in a compromised terrain, as opposed to the fleeting existence of free radicals, especially exoge­nous ones, also lead to this conclusion.

Endothelial cells grown in culture can be induced to express tissue factor. In one experiment, no procoagulant activity could be detected in the absence of toxins. However, the addition of mycotoxins from Aspergillus niger or Micrococcus neoformas (Mucor racemosus Fresen) resulted in procoagulant activity which reached a maximum in four to six hours and was dose-dependent. The same experiment was applied using E. coli and Salmonella enteritidis endo­toxin with a similar result.[32] A single intravenous injection of a mycotoxin from Aspergillus niger into experimental animals resulted in circulating endothelial cells within five minutes. In other exper­iments with the mycotoxin, detachment of endothe­lial cells from the basement membrane was noted.[33] (See Table 8.)

Removal of endothelial cells has dire conse­quences from two standpoints: First, the surface of these cells is covered with a specific prostaglandin (PGI2) known as prostacyclin. If blood contacts a surface not covered with PGI2, it will clot. For example, surfaces devoid of this prostaglandin are formed whenever a vessel is cut or punctured. An abrasion or other injury may also expose a surface on which PGI2 is lacking. The removal of endothelial cells by exotoxins or mycotoxins creates a surface devoid of PGI2, leading to blood clotting (see Table 7). Secondly, disorganization of endothelial cells cre­ates increased levels of EMPO and MAT which are attracted to an exposed surface (basement mem­brane) which expresses a negative charge. This also leads to clotting.

DIC Induced by Electrostatic Attraction

It was discovered in 1964 that blood will clot sim­ply from contacting a negatively charged surface.[34] Previously it was believed that the clotting process comprised a cascade of enzyme activity in which one activated the next, etc. The discovery that blood could be clotted simply by contacting a negatively charged surface ruled out the purely enzyme hypoth­esis. Only some of the known clotting factors have been shown to be enzymes.[35] As a result of this sur­prising discovery, detailed research was conducted in an attempt to describe the process. In some experi­ments, the negatively charged surfaces of selected, finely divided, inorganic crystals, including alu­minum oxide, barium sulfate, jeweler’s rouge, quartz, and titanium oxide, were considered.[36]

The clotting factor eventually shown to be activat­ed when whole blood contacted negatively charged surfaces was factor XII, also known as the Hageman factor. This is a positively charged protein migrating in an electric field (electrophoresis) toward the anode.[37] It is believed that factor XII is normally in the shape of a hairpin which binds to the negatively charged sur­face at the bend. Electrostatic attraction forces the two arms to lie flat on the surface, thereby exposing the inner faces and activating the molecule.

It was discovered that if the negatively charged particles were smaller than the clotting factor itself, activation was minimal. Or, if the concentration of clotting factor was too great, there was little or no activation.[38] Both of these observations indicated that the process was one of electrostatic attraction between the negatively charged surface and the clot­ting factor, which is a “basic” protein, that is, posi­tively charged.[39]

Activation of factor XII allows the activation of factor XI, which then activates factor IX. Thus, the blood clotting cascade continues to the formation of fibrin in the normal manner.[40] However, due to a series of activations begun by contact of factor XII with a negatively charged surface, trace amounts of factor Xa also show up in the blood. Factor VII is activated to Vila by factor Xa. Factor Vila then acti­vates factors IX and X, leading to the formation of thrombin. Factor Xa, with co-factor Va, continues the clotting cascade until fibrinogen is activated, leading to fibrin formation.[41] (See Table 5.)

As discussed earlier in terms of prostacyclin, beneath endothelial cells is another surface—the basement membrane. Called the extracellular matrix, it is a thin, continuous net of specialized tis­sue between endothelial cells and the underlying connective tissue. It has four or more main con­stituents, including proteoglycans (protein/polysac- charide).[42] The removal of endothelial cells by’MAT exposes this membrane, which is negatively charged by virtue of its sulfonated polysaccharides in the pro­teoglycans. This brings a reduced negatively charged surface into direct contact with the blood, which activates factor XII and the clotting cascade.[43]The positively charged toxic components of MAT also activate factor XII, as do disturbed disorganized cells, yeast/fungus cells, moldy cells, and the phos­phate groups in the lipid A component of endotoxin. (See Tables 2-5.)

To summarize this section, exotoxic, mycotoxic, and oxidative stress resulting from the overgrowth of bacteria, yeast/fungus, and then mold, has multiple actions, all leading to disseminated intravascular coagulation:

MAT activation of tissue factor gene in leukocytes; subsequent activation of factors VII, IX, and X, resulting in the blood clotting cascade.

MAT activation of tissue factor gene in endothelial cells, again leading to the clotting cascade.

MAT damage to endothelial cells, resulting in neu­trophil attraction, with TF gene activation and generation of MOBS, which, in turn, neutralize MAT, protecting healthy endothelial cells or the basement membrane and supporting the janitorial services of the leukocytes.

Removal of negatively charged endothelial cells by positively charged exotoxins, endotoxins, and mycotoxins, creating a surface devoid of PGI2, also exposes the negatively charged basement membrane, leading to the activation of factor XII and initiation of the clotting cascade. Positively charged components of EMPO, exotoxins and mycotoxins, and several other elements, including the lipid A component of bacterial endotoxin, also activate factor XII and the clotting cascade.

Endothelial Cells as Antithrombotics or Procoagulants

Normal, resting (unstimulated) endothelial cells show antithrombotic activity in several ways: (1) by the inhibition of prostacyclin (platelet adhesion and aggregation); (2) the inhibition of thrombin genera­tion; and (3) the activation of the fibrinolytic system, leading to clot lysis.[45] We will take a brief look at the thrombin aspect.

On the surface of endothelial cells is a protein called thrombomodulin, which acts as a receptor for thrombin. When bound to thrombomodulin, throm­bin can activate protein C. Activated protein C then catalyzes the proteolytic cleavage of factors Va and Vila, thereby destroying their participation in blood clotting. Thus thrombin, which normally activates fib­rinogen, plays an opposite role in this case and inhibits the clotting process.[46,47] (See Table 7.)

On the other side of the coin, the endothelial cell becomes a procoagulant agent when acted on by cer­tain lymphokines, such as interleukin-1. Not only can interleukin-1 induce TF gene expression, but it also suppresses transcription of the thrombomodulin gene in endothelial cells. As in other situations, the lymphokine-activated endothelial cell expresses TF on its surface as a result of TF gene activation. This leads to the production of thrombin and the trigger­ing of the blood clotting cascade.[48] (See Table 5.) Many lymphokines also stimulate adhesion of leuko­cytes to endothelial cells damaged by MAT, resulting in recycling of the cells by MOBS, as described later.

DIC Induced by Intracellular Exotoxic, Mycotoxic, Oxidative Stress by Bacteria, Yeast/Fungus and/or Mold

Any cell which has gone from an oxidative to a fer­mentative state can biochemically cause macrophage production of the lymphokine tumor necrosis factor (TNF). This protein has been shown to activate the gene for TF in fermenting cells, which are so behaved due to morbid evolution of bacteria, yeast/fungus, and then mold.[49,50] In the author’s view, a cell having been switched entirely to fermentation metabolism as a result of a physical or emotional disturbance of that cell, is what constitutes cancer (see Tables 5 and 13). (One might argue that this definition does not fit all “forms” of cancer, such as leukemia, for example. This is because leukemia is not cancer, but an immune response to the rise in EMPO and MAT in the body, and a relatively easy compensation to correct.)

The surface of many disorganizing or fermented cells (cancer cells) is characterized by small projec­tions in the plasma membrane which pinch off, becoming free vesicles containing toxins as well as TF complexed with factor VII. These vesicles can aggre­gate and/or lodge anywhere, ultimately releasing their contents. Also, the presence of excessive amounts of TF/factor VII complexes on the surface of fermented cells allows the formation of a fibrin net around the cell and around the entire mass of cells (tumor). This seems to be an attempt by the body to encapsulate and contain the mass. However, fermented cells do escape from the primary fibrin net, perhaps due to some electromagnetic effect, and become free-float­ing in the circulation. They may thus lodge elsewhere and instigate the fermentation of other cells by fungal penetration or by poisoning them and provoking a morbid evolution of their inherent microzymas.

Because of the surrounding fibrin net, these mobi­lized fermenting cells are protected from collection by the immune system while in transit.[51,52] (See Table 4.) The blockage or dissolution of fibrin net forma­tion by an anticoagulant such as heparin allows freed, fermenting (metastasizing) cells to be dismantled by natural killer cells and other immune cells (see Tables 5, 12 and 13).

DIC Induced by MAT/EMPO and Immune System Response (Release of MOBS)

Unsaturated fatty acids are highly susceptible to EMPO as well as MAT. Linoleic acid, a long-chain fatty acid present in white cells, has 18 carbons and 2 unsaturations. Subjected to MAT, linoleic acid binds the exotoxin, endotoxin, or mycotoxin, there­by forming an epoxide at the first unsaturation.[53] Research has revealed that this compound, named leukotoxin, is highly disturbing to other cells. It caus­es platelet lysis, thereby releasing TF and initiating DIC.[54] (See Table 10.) The fact that MAT result in fermented fats lends further credence to the sugges­tion that the initial and primary degenerative damage to structures and substances in the body is caused by exotoxins and/or mycotoxins, and that damage by MOBS, or by other free radicals, is not possible.

Another mechanism leading to DIC is the release of a special glycoprotein, sialic acid, from the terminal ends of cell-membrane polysaccharides, where it is always found. Polysaccharides play a highly significant role in biochemical processes, with both enzymes and membrane receptors recognizing various groupings of specific sugars linked in highly specific ways.

Immediately preceding the release of sialic acid in the polysaccharide chain is the sugar galactose. The sialic acid/galactose arrangement is utilized as a biolog­ical indicator of cellular and molecular aging. As cells age, sialic acid is naturally expressed from the terminal ends of polysaccharides, thereby exposing galactose. A membrane-bound enzyme from the liver, galactose oxi­dase, recognizes galactose and eventually disorganizes it, disrupting cell function integrity and hastening demise. Aged red blood cells, which have expressed a significant amount of sialic acid, are removed from the blood by this process. (I theorize that the biological ter­rain may be at work in normal cell aging. That is, the rate at which sialic acid is expressed is determined by the levels of corrosive acids in the system and the body’s ability to remove them, although there are no doubt intracellular factors at work as well.)

I suggest from my years of  clinical research  that cellular breakdown is compounded by the fermentation of the galactose by the microzyma. This is a process that begins from within and not necessarily from without. Not only does this action create more sialic acid, it creates other toxic waste products such as acetic aldehyde, alcohol, uric acid, oxalic acid, etc. The increase in cellular disturbances and fermenta­tion of the galactose creates biochemical signals for more galactose oxidase. This leads to greater cellular disorganization and developmental morbidity, espe­cially in the red blood cells, and a rise in the level of detrital serum proteins, which encourages clotting. From this perspective, diabetes, arthritis, atheroscle­rosis and other symptomatologies become more clearly “degenerative” (see Tables 2-5, 12 and 13).

Fibrinogen is a rather elaborate protein having the structure of three beads on a string. Expressed on the end beads is sialic acid, which indicates the beginning of disorganization of the fibrinogen and a declining negative charge to the positive. Prior to the declining charge and the expression of sialic acid on the end beads, fibrinogen, which is negatively charged, will not polymerize the healthy blood due to mutual repulsion. However, fibrinogen will poly­merize to damaged cells, EMPO, MAT and other positively charged areas of the body for repair pur­poses. Thus, as more and more sialic acid is expressed, there will be a significant reduction in the charge of the fibrinogen, acting as the primary requirement for the polymerization of fibrinogen (hypercoagulable state). The resulting polymer, fib­rin monomer, is the protein chain used in the repair of cells and clotting of blood.[55] End-linking will take place after the release of sialic acid (positive charge) by whatever means.

With this background, it is interesting to note that blood taken from persons suffering from anxiety is expressing sialic acid from fibrinogen, and is halfway toward clotting. Hormones released during anxiety states are easily fermented, giving more momentum to MAT and thereby resulting in this important change in fibrinogen. It leads to a clotting pattern characteristic of anxiety stress, and is readily identi­fied in the MOST. As can be seen in this picture, the pattern is a “snowstorm” of protein polymeriza­tions measuring from 2 to 10 microns.

allergiesbefore

 

 

 

 

 

 

 

[Micrograph 2: An Anxiety Profile showing a ‘snowstorm’ of 2 to 10 micron protein polymerizations starting from the center of the clot and moving out towards the edge]

As mentioned earlier, despite the attempt by the body to neutralize EMPO and MAT, an excess will initiate the release of MOBS by immune cells. A major MOBS is superoxide, designated chemically as O 2. It may exist alone or be attached to another ele­ment, such as potassium (KO’2) or sulfur (SO). Again, however, nature has provided a means of pro­tecting healthy cells—their negative charge[1]. Another protection against superoxide is the enzyme superox­ide dismutase (SOD), also found in all healthy cells.

A second member of the MOBS family is hydro­gen peroxide (H202). This molecule is very unstable and tends to react rapidly with other biological mol­ecules, damaging them. The release of hydrogen per­oxide in the body is a response to the overgrowth of decompositional organisms in a declining pH (com­promised biological terrain). The control for healthy cells against hydrogen peroxide is their negative charge and the protective enzyme catalase, one of the most efficient enzymes known.

When leukocytes and other white blood cells are stimulated by the presence of bacteria, yeast/fungus and mold, they treat these organisms as foreign par­ticles to be eliminated. During and prior to phagocy­tosis, the foregoing oxidative cytotoxins, along with the hydroxyl radical (OH’), are generated and released specifically for neutralizing microforms or harmful substances. This release is referred to as an “oxidative burst.” As a result of fermentation and the production of exotoxins and mycotoxins that fer­ment galactose from cells, the immune system is activated. An oxidative burst is released to neutralize the morbid microforms and mycotoxicity.[56] Like other biological processes faced with constantly alarming situations, the continued release of MOBS can get out of control. This may damage endothelial cells, the basement membrane, or other body ele­ments, and this activates fibrinogen to fibrin monomer (repair protein), leading to DIC [see Table 9]. Interestingly, the white blood cells capable of neutralizing MAT through MOBS production are the same ones capable of phagocytosis, the process by which foreign matter, waste products and microor­ganisms are collected and dumped in the liver.[57]

To summarize this section, pathological microforms and their acids create DIC by a number of pathways:

Leukotoxin (linoleic acid bound to mycotoxin) is highly toxic to cells. It causes platelet lysis, there­by releasing TF and initiating DIC.

The expression or release of sialic acid residues from healthy cells that have been disturbed allows for the fermentation of galactose, creating exotox­ins and mycotoxins, biochemically activating galactose oxidase, which further disturbs and dis­organizes healthy cells. This cycle loads the blood with debris.

EMPO and MAT disturb fibrinogen, which releas­es sialic acid and reduces the charge, allowing it to polymerize into fibrin monomer and fibrin nets.

The presence of exotoxins, endotoxins, and myco­toxins and their poisoning of cells activates the immune system. White blood cells generate MOBS (e.g., superoxide [0′2] or hydrogen perox­ide [H202]). These substances bind to and neu­tralize EMPO and MAT. MOBS are repelled by healthy endothelial cells and the basement mem­brane because of their negative charge. Cellular disturbances and disorganization stimulate the generation of fibrin monomer for repair purposes, leading to DIC.

Detection of Disseminated Intravascular Coagulation

The Sonodot Analyzer

The Sonoclot Coagulation Analyzer provides a reaction-rate record of fibrin and clot formation with platelet interaction. An axially vibrating probe is immersed to a controlled depth in a 0.4 ml sample of blood. The viscous drag imposed upon the probe by the fluid is sensed by the transducer. The electronic circuitry quantifies the drag as a change in electrical output. The signal is transmitted to a chart recorder which provides a representation of the entire clot for­mation, clot contraction and clot lysis processes. The analyzer is extremely sensitive to minute changes in visco-elasticity and records fibrin formation at a very early stage. The Sonoclot has been evaluated scientif­ically and shown to provide an accurate measurement of the clotting process.[58,59]

One application of the Analyzer has been the development of a test to distinguish non-advanced breast cancer from tumors that are benign. The ratio­nale for the test is the hypercoagulable state seen in cancer patients (Trousseau’s Syndrome), resulting from the generation of TF by leukocytes (mono­cytes).[60] (See Table 4.)

Fibrin Degradation
Products and Fibrin Monomer

DIC can be seen as a two-step process. First, fib­rinogen, which is always present in the blood, is acti­vated by any of several mechanisms. This activation leads to an automatic polymerization (chain forma­tion) resulting in fibrin monomer. This is not apparent in a microscope unless the blood is allowed to clot, as in the MOST.[61,62] The second step is the precipitation or deposition of fibrin (hard clot) by several other mechanisms. One of these is the formation of cross­links through the action of factor XIII. Another such mechanism may be poor circulation in an organ already blocked by deposited fibrin. The deposition of precipitated fibrin may be detected microscopically in tissue sections and diagnosed as DIC.[62]

Because fibrin monomer is not readily detected, a chemical test for it is of immense value in diagnosing DIC. Research has indicated that its detection may be very useful in the early diagnosis of DIC and MAT.[63] There are three fundamental physiologic areas related to blood clotting: (1) the prevention of blood clotting, (2) the clotting of blood, and (3) the removal of clotted blood once it has formed.

Enzymes are present that are capable of removing (lysing) clotted blood, one of which is plasmin. Another enzyme, plasminogen, is always present in the blood, but is inactive as a proteolytic agent. Plasminogen acti­vator converts plasminogen to plasmin, which can degrade deposited fibrin. This process is not specific for fibrin, however, and other proteins may be affected. When fibrin is degraded (fibrinolysis), fibrin monomer, as well as several other products, are formed. Commercial kits are available for the analysis of fibrin degradation. This test is an indirect measure of the pres­ence of DIC and MAT.[64]

Other tests include:

Protamine Sulfate: Protamine sulfate is a heparin binder sometimes used in surgery for excessive bleed­ing. The test, which indicates fibrin strands and fibrin degradation products, is conducted in a test tube, with fibrin monomer and fibrin forming early and polymer­ization of fibrin degradation products occurring later.[65] Ethanol Gelation: A white precipitate is formed by the addition of ethanol to a solution in a test tube containing fibrin monomer as a degradation product of fibrin, indicating DIC and MAT.[66]

The Mycotoxic Oxidative Stress Test (MOST)

Up to now, blood chemistries have been the prima­ry mode of diagnosis or analysis for the presence of pathology. In the view presented here, the bright-field microscope, is used to easily and inexpensively reveal a disease state as reflected by changes in certain aspects of blood composition and clotting ability. DIC is char­acterized by the abnormal presence in the blood of fib­rin monomer. When allowed to clot, blood containing such an abnormal artifact will exhibit distortions of normal patterns. The presence in the blood of soluble fragments of the extracellular matrix and soluble fibronectin, as well as other factors, will also create abnormal blood clotting patterns as described below.

A small amount of blood from a fingertip is con­tacted with a microscope slide. A series of drops is allowed to dry and clot in a normal manner. Under the compound microscope, the pattern seen in healthy subjects is essentially the same—a dense mat of red areas interconnected by dark, irregular lines, completely filling the area of the drop. The blood of people under mycotoxic/oxidative stress exhibits a variety of characteristic patterns which deviate from nor­mal, but with one striking, common abnormality: “clear” or white areas, in which the fibrin net/red blood cell conglomerate is missing.

BowelCancerLive Blood Dried Blood_0166

 

 

 

 

 

 

 

 

[Micrograph 3; An abnormal clot with striking ‘clear’ or white areas or protein polymerization as seen in the hyper coagulated blood of a patient with lower bowel imbalances]

Why the fibrin net is missing may be understood from the following: Two peptides—A and B—in the central protein bead of the fibrinogen structure become bound in the cross-linking process. There are two ways this can be configured: (1) Thrombin is capable of activating peptides A and B, resulting in the formation of a polymer loosely held together only by hydrogen bonds; (2) With peptides A and B acti­vated normally, the resulting hard clot is insoluble, indicating that the peptides are linked by covalent bonds. The difference in bonds results from factor XIII, an enzyme which links the two fibrin strands with a glutamine-lysine peptide bond.

Additional research has shown that the release of sialic acid from fibrinogen inhibits the action of factor XIII, resulting in a soft, white clot. In addition, acetic aldehyde has been shown to inactivate factor XIII directly. The soft clotting, compounded by other polymeric aggregations (described below), results in clear areas in the dry specimens. In the opposite extreme, high serum levels of calcium, for the pur­pose of neutralizing MAT, activates factor XIII, lead­ing to excessive cross-linking of fibrin to form a clot harder than normal. This is reflected in the MOST pattern characteristic of definite hypercalcemia— that of a series of cracks in the clot radiating outward from the center, resembling the spokes of a wheel. High serum calcium is the body’s attempt to com­pensate for the acidity of mycotoxic stress by pulling this alkalizing mineral from bone into the blood. This demand creates endocrine stress in turn, because reabsorption of bone is mediated by parathormone (PTH). Therefore, this clotting pattern indicates cal­cium deficiency and thyroid/parathyroid imbalance.

calciumpattern

 

 

 

 

 

 

 

[Micrograph 4: A mineral deficiency or more specifically a calcium deficiency pattern associated with an imbalance of they thyroid and/or parathyroid}

Advanced research has shown that there are seven carbohydrate chains in fibrinogen (each terminated by sialic acid). A second action of factor XIII is to ferment a large amount of carbohydrate during clot­ting. Because carbohydrate is most often water solu­ble, the loss of this material undoubtedly adds to the insolubility of a clot, while pathological retention contributes to the softness of the abnormal clot.

Clinical experience demonstrates that the MOST is a reliable indicator of exotoxic and mycotoxic stress and, concurrently, of various disorganizing symptoma­tologies associated with fermentative and oxidative processes. As various cellular degradation occurs, the blood-borne phenomena which accompany such symptoms as diabetes, arthritis, heart attack, stroke, atherosclerosis and cancer show up in the MOST, often with sialic acid beads in the clear areas of poly­merized proteins. (Determination of the liberation of sialic acid from carbohydrate has been approved by the U.S. Food and Drug Administration as an accept­ed indicator for cancer, and is clinically available.)

sialicacid

[Micrograph 5: Sialic acid beads are seen inside the protein
polymerization of the hypocoagulated blood as black dots]

The extent and shape of the clear areas are reflec­tive of particular symptomatologies which have arisen from the way in which the disease condition manifests in a given individual. This observation is borne out by having the patient undergo appropriate alkalizing therapy. With success of treatment based on the patient’s freedom from symptoms, sense of well-being, and live blood exams discussed in the main text of Sick and Tired, Reclaim Your Inner Terrain, Appendix C,[7] repeated analysis with the MOST reveals a progressively improving clotting pattern.

[Micrographs 6 and 7: Medically diagnosed cancer patient with large polymerized protein pools (PPP) in the hypo-coagulated blood above. In the picture below PPP’s have significantly reduced in size and the blood is moving to a more hyper-coagulated state as a result of reducing acid loads with an alkaline lifestyle and diet (7, 70)]

Because of its very nature, the MOST is emi­nently suited to reveal and measure the presence in the blood of abnormal substances, clotting factors, and disorganization of cells due to an inverted way of living, eating, and thinking, which gives rise to MAT. The MOST indicates both the direct and indirect activity of MAT on blood clotting, endothelium, and the extracellular matrix (described next), as well as on biochemical pathways, including hormonal ones. The generation of excessive MOBS in response to EMPO and MAT, the inability that accompanies all degenerative symptoms to neutralize or eradicate EMPO and MAT, and the recognized hyper- and hypocoagulable states seen in various symptomatolo­gies, will beyond doubt be revealed in the MOST.

Aspergillusnigercrystal

 

 

 

 

 

[Micrograph 8 and 9: Medically Diagnosed HIV/AIDS micrograph showing above an Aspergullus niger mold crystal using dark field microscopy and below a hypocoagulated blood clot with systemic protein polymerizations measuring in excess of 40 microns using bright field microscopy}

HIV

 

 

 

 

 

 

As mentioned, hormones are easily fermented, and this will show up as a hypocoagulated blood pattern in the MOST. It is my opinion, this hypocoagulated blood appears in the MOST as misty clouds of protein polymerizations throughout the clot, as seen in the accompanying picture.

poorfibrin

[Micrograph 10: Poor fibrin interconnection in the clot associated with endocrine or hormonal imbalance]

The MOST from Solubilized Extracellular Matrix

There is now a clearer picture of the biochemical rationale for correlating abnormal blood clotting patterns with the presence of degenerative symptoms.  A link between symptoms and the distorted clotted blood patterns has been delineated in the MOST.
Another reason for the abnormal clotting patterns accompanying pathological states, in addition to insufficient bonding of fibrinogen peptides as seen in the MOST, is presence in the blood of water-soluble fragments of the extracellular matrix.

Extracellular Matrix Degradation by MAT

The extracellular matrix (EM) is a three-dimen­sional gel, binding cells together and composed of five or more major constituents: collagen (protein), hyaluronic acid (polysaccharide), proteoglycans (pro- tein/polysaccharide), fibronectin and laminin. Also included are glycosaminoglycans and elastin.[67] In every degenerative disease studied by this author, evidence has been found for MAT activity destruc­tive of EM.

One of the proteolytic enzymes activated in response to EMPO and MAT is alpha-1 antitrypsin (capable of neutralizing MAT), normally not active in the presence of the enzyme trypsin. The active por­tion of this anti-exotoxin and antimycotoxin contains the amino acid methionine, which includes a C-S-C linkage. When chelated by the hydroxyl radical (one of the MOBS oxidants), methionine’s central sulfur atom acquires one or two oxygen atoms (forming the sulfone or sulfoxide respectively). The fermentation of methionine is a secondary effect of immune response to an alarming situation, intended to neutral­ize MAT and prevent degradation of the EM. Once alpha-1 antitrypsin is exhausted, MAT will have more access to the EM. If the EM is damaged beyond repair, then the enzyme trypsin is released to disorganize and recycle the cells involved.[68]

A similar scenario holds for the enzymes collage- nase and elastase. Thus, the absence of alpha-1 antitrypsin in the presence of EMPO and MAT activates three enzymes which degrade the extracellular matrix. Degradation of the EM by enzymes and MAT puts into the blood the water-soluble fragments (proteins and glycoproteins) of normally insoluble EM components (see Table 11). The presence of these fragments modifies the normal clotting pattern (described below), as seen in the M/OST, and is therefore an indication of EM degradation, which is always found with degenerative symptoms. (Also present is fibrin monomer, which has been found in the blood of patients suffering from collagen dis­ease.[69] See Table 11.)

Fibronectin is a molecule in EM having several binding sites for various long-chain molecules— heparin (a sulfonated polysaccharide) and collagen, for example. As such, it functions as a cellular glue, bind­ing cells together as well as various components of the EM. A soluble form of fibronectin is normally found free in the blood, and enters into the formation of a blood clot through the action of factor XIII. This form of fibronectin binds to fibrin. Elevated, bound-serum fibronectin results from EM fragmentation by MAT, and accompanies degenerative symptoms such as arthritis and emphysema (collagen diseases).

Water-soluble fragments of the EM bound by fibronectin form a three-dimensional network or gel in the pathologically clotted blood (fibrin and com­ponents of the blood clotting cascade). Since fibronectin binds to both fibrin and collagen, the two polymeric networks are superimposed and intermin­gled, resulting in a modification of the normal clot­ting pattern. Exactly how the pattern is modified depends upon the nature of the collagen abnormally present, the nature and extent of hyaluronate pre­sent, and the degree to which EM fibronectin has been released by MAT.

Conclusion

Thus, it is easily seen that there are many forms which the pattern of clotted blood may take, depending on the individual and the internal terrain that produced the modifying substances. The MOST reveals not only the presence of exotoxic and mycotoxic stress, but indicates as well the nature of the symptom(s) resulting from the stress (see Table 12). Since MAT underlie the entire complex of events which degrade the extracellular matrix, I must conclude that the absence of these exotoxins, endotoxins and mycotoxins would provide substantial improvements in tissue integrity and the overall physiology and functionality of the organism or animal and human.

­

­

References

[1]  Jones, T.W., “Observations on some points in the anatomy, physiology and pathology of the blood.”  British Foreign Medical Review, 1842. 14 : 585.

[2] Trousseau, A., Phlegmasis alba delens. “Clinque Medicale de L’Hotel Dieu de Paris.”, 1865, 3:94

[3]  Virchow, R., “Hypercoagulability: A review of its development, clinical application, and recent progress.”  Gesammelte Abhandlungen our Wussenschaftlichen Medizin, 1856, 26:477.

[4]  Rapaport, S.I., “Blood Coagulation and its Alterations in Hemorrhagic, and Thrombotic Disorders.”  The Western Journal of Medicine, 1993; 158: 153.

[5]  Hamilton, P.J. et al., “Disseminatied Intravascular Coagulation: A Review.”  Journal of Clinical Pathology, 1978, 31: 609

[6] The Harper Collins Illustrated Medical Dictionary, 1994, p.13.

[7] Young, RO, “Sick and Tired, Reclaim Your Inner Terraine,” Woodland Publishing, 1999.

[8] BeChamp, A., “The Blood and Its Third Anatomical Element,”  Hikari Omni Publishing, 1999.

[9]  Schwerdtle, C, Arnoul, F, Enerlein, G, “Introduction to Darkfield Diagnostics”, Semmelweis-Verlag (2006).

[10]  Hawk, BO, Thoma, GE, Inkley, JJ, The Evaluation of the Bolen Test as a Screening Test for Malignancy*, cancerres.aacrjournals.org on December 5, 2015. © 1951 American Association for Cancer Research.

[11]  Uchida, K., “Role of Reactive Aldehyde in Cardiovascular Diseases”,  Labortory of Food and Biodynamics, Nagoya University Graduate School of Bioagricultural Sciences, Nagoya, Japan , Free Radical Biology and MedicineVolume 28, Issue 12, 15 June 2000, Pages 1685–1696

 [12] Chang JCvan der Hoeven LHHaddox CH, “Glutathione reductase in the red blood cells”,  Ann Clin Lab Sci. 1978 Jan-Feb;8(1):23-9.

[13] Kutzing, MK, Firestein, BL, “Altered Uric Acid Levels and Disease States”, Department of Cell Biology and Neuroscience (M.K.K., B.L.F.), Graduate Program in Biomedical Engineering (M.K.K.), Rutgers University, Piscataway, New Jersey. Address correspondence to: Dr. Bonnie L. Firestein, Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 08854-8082. E-mail: firestein@biology.rutgers.edu

[14] Claudino, M,. Ceolin,,DS, Alberti, S.,  Cestari, TM,  Spadella, CT, Fischer Rubira-Bullen, IR, Gustavo Pompermaier Garlet, Gerson Francisco de Assis, ” Alloxan-Induced Diabetes Triggers the Development of Periodontal Disease in Rats”,  Published: December 19, 2007. DOI: 10.1371/journal.pone.0001320

[15] Young RO (2015), “Alkalizing Nutritional Therapy in the Prevention and Reversal of any Cancerous Condition. Int J Complement Alt Med 2(1): 00046. DOI: 10.15406/ijcam.2015.02.00046

[16] Heloise Pöckel FernandesCarlos Lenz Cesar, and  Maria de Lourdes Barjas-Castro, “Electrical properties of the red blood cell membrane and immunohematological investigation”, Rev Bras Hematol Hemoter. 2011; 33(4): 297–301. doi:  10.5581/1516-8484.20110080 PMCID: PMC3415751

[17] Harris, JO, “The Relationship Between the Surface Charge and the Absorption of Acid Dyes by Bacterial Cells”, Department of Bacteriology, Kansas Agricultural Experiment Station, Manhattan,Kansas, Received for publication March 3, 195.

[18] Young, RO, “Metabolic and Dietary Acids are the Fuel That Lights the Fuse that Ignites Inflammation that Leads to Cancer”. https://www.linkedin.com/pulse/metabolic-dietary-acids-fuse-ignites-inflammation-causes-young. 2015.

[19] Snaders, R, “Did Bacteria Spark Evolution of Multicellular Life?” Berkeley News, Research, Science and Environment,  October 24, 2012.

[20] Wenner, M, “Humans Carry More Bacterial Cells than Human Ones”. Scientific American, November 30th, 2007.

[21} Animals and humans respond to MAT as a poison.

[22]  Morrison, D.C. et al. The effects of bacterial endotox­ins on host mediation systems. American Journal of Pathology, 1978; 93: 526.

[23]  Ibid.

[24]  Ibid.

[25]  Van Deventer, S.J.H. et al. Intestinal Endotoxemia. Gastroenterology, 1988; 94(3): 825-831.

[26]  Morrison, D.C. et al., op. cit.

[27]  Ibid.

[28]  Hu, T. et al. Synthesis of tissue factor messenger RNA and procoagulant activity in breast cancer cells in response to serum stimulation. Thrombosis Research, 1993; 72: 155.

[29]  Rapaport, op. cit. (Ref. 4).

[30]  Ibid.

[31]  Mackman et al. Lipopolysaccharides—mediated tran­scriptional activation of the human tissue factor gene in THP-1 monocytic cells requires both activator protein 1 and nuclear factor kappa B binding sites. Journal of Experimental Medicine, 1991; 174: 1517.

[32]  Yamada, O. et al. Deleterious effects of endotoxins on cultured endothelial cells: An in vitro model of vascular injury. Inflammation, 1981; 5: 115.

[33]  Colucci, M. et al. Cultured human endothelial cells: An in vitro model of vascular injury. Journal of Clinical Investigation, 1983; 71: 1893.

[34]  Cho, T.H. et al. Effects of Escherichia coli toxin on structure and permeability of myocardial capillaries.

[35]  Acta Pathologica Japonica, 1991; 41: 12.

[36]  Rapaport, op. cit. (Ref. 4).

[37]  Ibid.

[38]  Margolis, J. The interrelationship of coagulation of plasma and release of peptides. Annals of the New York Academy of Sciences, 1963; 104: 133.

[39]  23-25. Ibid.

[40]  Morrison, D.C. et al., op. cit.

[41]  Rapaport, op. cit. (Ref. 4).

[42]  Alberts, B. et al, eds. Molecular Biology of the Cell. New York: Garland Publishing, Inc., 1989 (2nd ed.), p. 818.

[43]  Rapaport, op. cit. (Ref. 4).

[44] Bertz, A., et al. Modulation by cytokines of leukocyte endothelial cell interactions. Implications for thrombo­sis. Biorheology, 1990; 27: 455.

[45]  Rapaport, op. cit. (Ref. 4).

[46]  Nachman, R.L. et al. Hypercoagulable states. Annab of Internal Medicine, 1993; 119: 819.

[47]  Ibid.

[48]  Tallman, M.S., et al. New insights into the pathogene­sis of coagulation dysfunction in acute promyelocytic leukemia. Leukemia and Lymphoma, 1993; IT. 27.

[49]  Silberberg, J.M., et al. Identification of tissue factor in two human pancreatic cancer cell lines. Cancer Research, 1989; 49: 5443.

[50]  Grimstad, I.A. et al. Thromboplastin release, but not content, correlates with spontaneous metastasis of can­cer cells. International Journal of Cancer, 1988; 41: 427.

[51]  Gunji, Y. et al. Role of fibrin coagulation in protection of murine tumor cells from destruction by cytotoxic cells. Cancer Research, 1988; 48: 5216.

[52]  Sugiyama, S. et al. The role of leukotoxin (9, 10- epoxy-12-octadecenoate) in the genesis of coagulation abnormalities. Life Sciences, 1988; 43: 221.

[53]  Ibid.

[54]  White, A. et al, eds. Principles of Biochemistry. McGraw-Hill Book Co., New York, 1964, p. 648.

[55]  Mueller, H.E. et al. Increase of microbial neu­raminidase activity by the hydrogen peroxide concen­tration. Experientia, 1972; 23: 397.

[56]  Young, Robert O. Fermentology and oxidology. The study of fungus-produced mycotoxic species and the activation of the immune system and release of microzymian oxidative buffering species (MOBS). Self- published: InnerLight Biological Research Foundation, Alpine, Utah, 1994.

[57]Chandler, WL. et al. Evaluation of a new dynamic vis­cometer for measuring the viscosity of whole blood and plasma. Clinical Chemistry, 1986; 32: 505.

[58]  Saleem, A. et al. Viscoelastic measurement of clot for­mation: A new test of platelet function. Annals of Clinical and Laboratory Science, 1983; 13: 115.

[59]  Spillert, C.R. et al. Altered coagulability: An aid toselective breast biopsy. Journal of the National Medical Association, 1993; 85: 273.

[60]  Bowie, E.J. et al. The clinical pathology of intravascular coagulation. Bibliotheca Haematologica, 1983; 49: 217.

[61]  Muller-Berghaus, G. et al. The role of granulocytes in the activation of intravascular coagulation and the pre­cipitation of soluble fibrin by endotoxin. Blood, 1975; 45: 631.

[62]  Bick, R.L. Disseminated intravascular coagulation. Hematology/Oncology Clinics of North America, 1993; 6: 1259.

[63]  Bredbacka, S. et al. Laboratory methods for detecting disseminated intravascular coagulation (DIC): New aspects. Acta Anaesthesiologica Scandinavica, 1993; 37: 125.

[64]  Sigma Diagnostics, St. Louis, MO 63178; tel: 314- 771-5765.

[65]  Nachman, R.L. et al. Detection of intravascular coag­ulation by a serial-dilution protamine sulfate test. Annals of Internal Medicine, 1971; 75: 895.

[66]  Breen, F.A. et al. Ethanol gelation: A rapid screening test for intravascular coagulation. Annals of Internal Medicine, 1970; 69: 1197.

[67] Hay, E.D., ed. Cell Biology of Extracellular Matrix. New York: Plenum Press, 1981, p. 653.

[68]  Carp, H. et al. In vitro suppression of serum elastase- inhibitory capacity by ROTS generated by phagocytos- ing polymorphonuclear leukocytes. Journal of Clinical Investigation, 1979; 63: 793.

[69]  Wilson, C.L. The alternatively spliced V region con­tributes to the differential incorporation of plasma and cellular fibronectins into fibrin clots. Journal of Cell Biology, 1992; 119: 923.

[70] Young, RO, Young, SR, “The pH Miracle Revised and Updated”, Hachette Publishing, 2010.

Tables

Table 1

Expression of Sialic Acid/Galactose [MAT] from Cell and Protein Degeneration (From All Serum Proteins, RBC/WBC and Other Cell Surfaces)

  1.  Carbohydrate, Proteins, and Fats From Diet, Body Cells or Reserves
  2. As cells breakdown or ferment they give birth to bacteria, yeast, fungus and mold [EMPO] and their associated metabolic acidic waste [MAT]
  3. Exotoxins, Endotoxins, and Mycotoxins [MAT]
  4. Acetyl Aldehyde, Ethyl Alcohol, Uric Acid, Alloxan, Lactic Acid are examples of MAT
  5. MAT  Ferments Other Body Cells and their Extracellular Membranes and Proteins
  6. MAT Modifies Glycoprotein
  7. Binds to liver Galactosidase
  8. Creating an Increase in Cell and Protein Fermentation and Degeneration and Increased Amounts of Exotoxins, Endotoxins and Mycotoxins [MAT]

Table1a

Table 2

Expression of Sialic Acid [MAT] From the Fermentation of Degeneration of Insulin Producing Pancreatic Beta-Cells in Type I, Type II and Type III Diabetes

  1. Pancreatic Insulin producing Beta-Cells with no or minimal Surface Sialic Acid [MAT]A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Diet
  2. Normal regulation of Insulin Production
  3. A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Dietary choicesdd
  4. Leads to cellular fermentation and degeneration and the birth of EMPO
  5. This lead to increased abnormal amounts of MAT that the immune system, the alkaline buffering system and the elimination organs has to deal with
  6. Fermenting and degenerating Insulin Producing Beta Cells
  7. Giving Rise to Surface Cell Sialic Acid [MAT}
  8. Increased Amounts of Sialic Acid Activates the Immune Response [MOBS] and Sialidase [AB]
  9. Leads to Lowered or No Insulin Production
  10. Symptoms of Type I, Type II or Type III Expressed
  11. The insulin producing beta cells of the Islets of Langerhans express silica acid on their surface as a break down metabolite.  I have suggested that when insulin producing beta cells are physically disturbed by MAT they begin to disorganize and express sialic acid on the surface of the cell.  This indicates the death of the cell and insulin production will stop.

Table2a

Table 3

HIGH BLOOD PRESSURE, ATHEROSCLEROSIS, HEART ATTACKS, STROKES, and CONGESTIVE HEART FAILURE

  1. A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Dietary choices
  2. Leads to cellular fermentation and degeneration and the birth of EMPO
  3. This lead to increased abnormal amounts of MAT that activates the immune system to chelate the MAT.
  4. Increased amounts of MAT will cause endothelial breakdown and the expression of Sialic acid.
  5. Increased Amounts of Sialic Acid and damage to the endothelial will cause a reduction in the negative surface-charge leading to the release of Glycoproteins.
  6. The release of Glycoproteins will cause the activation of Factor XII and the blood clotting cascade.
  7. This cause the creation and formation of fibrin monomers and the increase of Platelet Deposition out of the red blood cells for clotting purposes
  8. The immune system will activate and MOBS will be released as well as sodium bicarbonate, calcium, lipids and other alkaline buffers to reduce metabolic acidity.
  9. The build-up of fibrin monomers in the clotting cascade will lead to fibrin nets and clots causing an increase in blood pressure and the risk of blockages potentially causing a Stroke or Heart Attack.

Table3a

Table 4

DISSEMINATED INTRAVASCULAR COAGULATION RESULTING
FROM INTRACELLULAR DISORGANIZATION OR FERMENTATION WHICH GIVES RISE TO MAT
 AND EMPO

  1. A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Dietary choices
  2. Leads to cellular fermentation and degeneration and the birth of EMPO
  3. This lead to increased abnormal amounts of MAT that activates the Tumor Necrosis Factor (TNF).
  4. Increased amounts of TNF activates the Tissue Factor Gene (TF)
  5. Increased Amounts of TF causes the release of Thromboplastin.
  6. The release of Thromboplastin activates the release of clotting Factors VII (VIIa) and trace amounts of Factor Xa into the blood.
  7. This activates the release of Factors IX and X to IXa and the increase of Factor Xa.
  8. The activation of the blood clotting cascade leads to Disseminated Intravascular coagulation and the clotting or thickening of the blood inside the blood vessels.
  9. The DIC or hyper-coagulation will mask the fermentation of healthy cells to unhealthy cells or cancerous cells.
  10. As the unhealthy cells or cancerous cells increase the body will go into preservation mode and begin forming fibrin nets to encapsulated these unhealthy cells to protect healthy body cells.
  11. As body and blood cells breakdown from MAT this causes an increase of MAT and EMPO leading to systemic latent tissue acidosis and a potential metastatic cancerous condition.

Table4a

 Table 5

DISSEMINATED INTRAVASCULAR COAGULATION RESULTING
IN CELLULAR DISORGANIZATION OR FERMENTATION/OXIDATON AND THE INCREASE OF MAT AND EMPO

  1. A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Dietary choices.
  2. Leads to cellular fermentation and degeneration and the birth of EMPO
  3. This lead to increased abnormal amounts of MAT that activates the Tumor Necrosis Factor (TNF).
  4. Increased amounts of TNF activates the Tissue Factor Gene (TF)
  5. Increased Amounts of TF causes the release of Thromboplastin.
  6. The release of Thromboplastin activates the release of clotting Factors VII and Factor Xa in the blood.
  7. This activates the release of Factors IX and X to IXa and the increase of Factor Xa.
  8. The activated blood clotting cascade leads to Disseminated Intravascular coagulation and the clotting or thickening of the blood inside the blood vessels.
  9. The DIC or hyper-coagulation will mask the fermentation of healthy cells to unhealthy cells or cancerous cells.
  10. As the unhealthy cells or cancerous cells increase the body will go into preservation mode and begin forming fibrin nets to encapsulated the unhealthy cells.
  11. This leads to tumor formation of the unhealthy or cancerous cells.
  12. As the body and blood cells breakdown this causes an increase of MAT and EMPO leading to an increased risk of  systemic metastatic cancer.

Table5aTable 6

ENDOTHEIAl CELL CONVERSION FROM AN
ANTITHROMBOTIC STATE TO A PROCOAGULANT STATE
CELLULAR DISORGANIZING PATHWAY

  1. A Physical and/or Emotional Disturbance Occurs from Lifestyle and/or Dietary choices
  2. Leads to cellular fermentation and degeneration and the birth of EMPO
  3. This leads to increased abnormal amounts of MAT that damages the protective endothelial cover cells leading to a reduction of PGI2
  4. The absence of PGI2 causes the release of Interleukin-1 and/or Tumor Necrosis Factor (TNF).
  5. In addition the loss of protective endothelial cover cells leads to Tissue Factor Gene Activation and the release of Thrombin causing a pro-coagulate state leading to DIC
  6. Another pathway to DIC would be the loss of protective endothelial cover cells and the absence of PGI2 causes the suppression of Thromomodulin, Protein C leading to procogradulation and DIC.

Talble6

 Table 7

ENDOTHELIAL CELL CONVERSION
FROM AN ANTITHROMBOTIC STATE
(NORMAL PATHWAY)

Table7

Table 8

MECHANISM OF DISSEMINATED INTRAVASCULAR COAGULATION GENERATED BY MAT

Table8Table 9

ACTIVATION OF SIALIDASE AND MICROZYMIAN OXIDATIVE BUFFERING SPECIES (MOBS) BY EMPO AND MAT

Table9

Table 10

DISSEMINATED INTRAVASCULAR COAGULATION RESULTING FROM PHAGOCYTIC OXIDATIVE BURST

Table10

Table 11

MOST BLOOD TEST and DISSEMINATED INTRAVASCULAR COAGULATION WITH SOLUBILIZED EXTRACELLULAR MATRIX

Table11

Table 12

TYPICAL SOURCES OF FERMENTATION INSULT (MAT) IN BIOLOGICAL SYSTEMS INITIATING DIC

Table12

Table 13

POSITIVE CHARGE OF CANCEROUS CELLS AND TUMORS AND THE FORMATION OF FIBRIN NETS AND TREES IN RESPONSE TO MAT

Table13

Cystic Fibrosis and Pulmonary Adenocarcinoma Lung Cancer – Stage Seven Metabolic and Dietary Acidosis

 
Robert Young PhD

Robert Young M.Sc., D.Sc.,PhD

Naturopathic Practitioner – The pH Miracle Ti Sana Detox Medical Spa

Abstract

Cystic fibrosis (CF)[1][2] and Pulmonary Adenocarcinoma (PAC)[3] have similar symptomologies and are chronic, progressive, and frequently fatal acidic conditions of the respiratory system (lungs), lymphatic system (lymph nodes), intestines, pancreas, urinary tract system, reproductive organs and the skin as the alkaloid glands (the salivary glands, stomach, and small and large intestines) produce and secrete alkaline compounds, such as sodium bicarbonate to buffer and preserve the alkaline design of the body and the specific organs and glands affected.  These metabolic and dietary acidic conditions resulting in the buildup of mucous[3] can affect any organ or organ system but primarily affects the respiratory, lymphatic system, digestive, and reproductive tracts in children and young adults with CF and the lungs and surrounding lymph nodes in PAC.  I have suggested from own clinical research that both of these conditions are the result of latent tissue acidosis (LTA) from metabolism, diet and environmnent and may be successfully treated and reversed with an alkaline lifestyle and diet (ALD).[4]

Key Words: Cancer, Terminal Cancer, Lung Cancer, Cystic Fibrosis, Pulmonary Adneocarcinoma, Bronchitis, Asthma, Shortness of breath, Thick mucous, Wheezing, Chronic sinisitits, Nasal Polyps, Weight loss, Water retention, Abdominal pain, Excessive sweating, cirrhosis of the liver, Inflammation of the pancreas, Pancreas, Liver, Liver disease, Latent tissue acidosis, fatigue, smoking, air pollution, chemical exposure, alkaline lifestyle and diet, alkalizing, nutritional IV’s, massage, infrared sauna, colon hydrotherapy, nebulizing, alkaline nebulizing, L-arginine, glutathione, N-actyl-cysteine, detoxification, live and red blood tests, acupuncture.

Introduction

According to the Cystic Fibrosis Foundation, about 30,000 Americans have CF. This condition occurs mostly in whites whose ancestors came from northern Europe, although it cuts across all races and ethnic groups. About 3,500 babies are born with this acidic condition each year in the United States. Moreover, about one in every 30 Americans suffer from CF.[1][3]

Nearly 40% of lung cancers in the US are adenocarcinoma, which usually originates in peripheral lung tissue.[5] Most cases of adenocarcinoma are associated with smoking; however, among people who have smoked fewer than 100 cigarettes in their lifetimes (“never-smokers”),[6] adenocarcinoma is the most common form of lung cancer.[7] Its incidence has been increasing in many developed Western nations in the past few decades, where it has become the most common major type of lung cancer in smokers (replacing squamous cell lung carcinoma) and in lifelong nonsmokers.[3] According to the Nurses’ Health Study, the risk of adenocarcinoma of the lung increases substantially after a long duration of previous tobacco smoking, with a previous smoking duration of 30 to 40 years giving a relative risk of approximately 2.4 compared to never-smokers, and a duration of more than 40 years giving a relative risk of approximately 5.[8]

Signs and Symptoms of CF and PAC:

CF and PAC have similar symptomologies and are often accompanied by the following signs and symptoms:

  • Thick, viscous mucus in the lungs caused by the glandular secretion of sodium bicarbonate in the chelation of excess dietary and/or metabolic acids.[3][9][[10]
  • Changes in color and amount of sputum (material coughed up from the lungs) is in direct relationship to the build-up of acidic waste products that are not being properly eliminated through the four channels of elimination – the lungs, bowels, kidneys and skin.[3][9][[10]
  • Chronic cough, possibly with blood streaking is a result of increased acidic and the lung and other elimination organs ridding itself of excess dietary and/or metabolic acids.[3][9][[10]
  • Wheezing is caused by an increase in sticky acidic mucous.[3][9][[10]
  • Bronchitis is stage four acidosis.[3][9][[10]
  • Chronic sinusitis is an acidic condition or stage two acidosis which is experienced by congestion and irritation.[3][9][[10]
  • Asthma is a higher valance of congestive acidosis leading to congestive acidic mucous.[3][9][[10]
  • Nasal polyps (fleshy growths inside the nose) are groups of cells bound together with dietary and/or metabolic acids.[3][9][[10]
  • Weight loss, failure to thrive in infants, abdominal swelling all caused by the retention of acids.  Weight loss due to dietary acids destroying the delicate villi in the small intestines.[3][9][[10]
  • Excessive salt in sweat, dehydration due to the build-up of acids that are not being properly eliminated through the four channels of elimination – lungs, bowels, kidneys and/or skin.[3][9][[10]
  • Failure of newborn in CF to pass stool is the result of ingesting acidic foods and/or drinks.[9][10]
  • Abdominal pain, flatulence are both caused by trapped acids that have not been properly eliminated through the bowels or urinary tract system.[3][9][[10]
  • Fatigue is the first sign congestion of the elimination organs and dietary and/or metabolic acids are building up.[3][9][[10]
  • Other acidic conditions that are caused by an acidic lifestyle and diet such as late onset of puberty, intestinal obstruction, inflammation of the pancreas, cirrhosis (a liver condition), and infertility may also be signs of CF.[3][9][[10]

What Causes Cystic Fibrosis According to Conventional Medicine?

CF is caused by a mutation in the gene cystic fibrosis transmembrane conductance regulator (CFTR). The most common mutation, ΔF508, is a deletion (Δ signifying deletion) of three nucleotides[11] that results in a loss of the amino acid phenylalanine (F) at the 508th position on the protein. This mutation accounts for two-thirds (66–70%[12]) of CF cases worldwide and 90% of cases in the United States; however, there are over 1500 other mutations that can produce CF.[13] Although most people have two working copies (alleles) of the CFTR gene, only one is needed to prevent cystic fibrosis. CF develops when neither allele can produce a functional CFTR protein. Thus, CF is considered an autosomal recessive disease.

What Causes Pulmonary Adenocarcinoma Lung Cancer According to Conventional Medicine?

Pulmonary Adenocarcinoma cancer is usually seen peripherally in the lungs, as opposed to small cell lung cancer and squamous cell lung cancer, which both tend to be more centrally located,[3][10] although it may also occur as a central lesions.[10] For unknown reasons according to current medical science, it often arises in relation to peripheral lung scars. The current theory is that the scar probably occurred secondary to the tumor, rather than causing the tumor.[10] The adenocarcinoma has an increased incidence in smokers, and is the most common type of lung cancer seen in non-smokers and women.[10] The peripheral location of adenocarcinoma in the lungs is due to the use of filters in cigarettes which prevent the larger particles from entering the lung.[14][15]Deeper inhalation of cigarette smoke results in peripheral lesions that are often the case in adenocarcinomas of the lung. Generally, adenocarcinomas grow more slowly and form smaller masses than the other subtypes.[12] However, they tend to form metastases widely at an early stage.[12] Adenocarcinoma is a non-small cell lung carcinoma, and as such, it is not as responsive to radiation therapy as is small cell lung carcinoma, but is rather treated surgically, for example by pneumonectomy or lobectomy.[12]

What Causes Cystic Fibrosis According to the Research of Dr. Robert O. Young?

When I talk about disease or “dis-ease”, such as CF or PAC, I am really focusing on the state of imbalance in the body, especially the lungs, that is brought on by an inverted way of living, eating and thinking.[15][16]  I have suggested that all disease or dis-ease, including CF and PAC  are caused by individual lifestyle and dietary choice, or for children, how parents are feeding and caring for their children.  I have also suggested that you do not get sick you have to do sick by making personal acidic lifestyle and dietary choices.  In other words disease is a personal choice just like health and fitness are personal choices.

When one chooses or parents choose for their children to eat acidic foods or drinks, such as animal flesh, eggs, dairy products, like cheese, yogurt and ice cream, soda pop, sport drinks, coffee or tea you set yourself up for excess latent tissue acidosis (LTA).  This is when a serious health challenge can begin to develop, such as cystic fibrosis of the lungs for a child or young adult or pulmonary adenocarcinoma lung cancer for people that smoke, breast cancer in women, prostate cancer for men.[15][16]

Over 30 years ago I postulated a theory that ALL sickness and disease is the result of an inverted way of living, eating and thinking.  And, that genetic defects were caused by acidic dietary and lifestyle choices that caused the genetics to express themselves in abnormal ways.  In the case of CF and PAC, the alkaphile glands (salivary glands, stomach, pancreas, gallbladder, Lieberkuhn glands in the intestines) are secreting sodium bicarbonate into the acidic tissues or organs, such as the lungs to maintain the alkaline design of the body fluids and protect the lung cells and tissues from breaking down.  The result is when sodium bicarbonate binds to dietary and/or metabolic acid it creates mucous.  The mucous secretion is the effect of the body protecting itself from excess dietary, environmental and/or metabolic acid. [15][16]

The intelligence of the cell or its genetics is only as healthy as its environment.  I like to compare the intelligent expression of the cellular genetics to a dangerous game called Russian Roulette.  To play the game you put one bullet in the chamber, spin the chamber and then put the gun up to your head and pull the trigger.  The object of the game is to avoid blowing your head off.  The bullet is a metaphor for the genetics and the trigger represents your daily personal lifestyle and dietary choices.  The result in cellular genetics will always be, if you continue to pull the acidic lifestyle and dietary trigger, the genetic bullet will be fired and the symptom(s) will be expressed.  The expression of cellular genetics in producing excess mucous in the condition of CF and PAW can be stopped when you stop pulling the acidic lifestyle and dietary trigger.  The human cell is only as healthy as the fluids it is bathed in just as a fish is only as healthy as the water it swims in.  Change the water and you will change the genetic expression.[15][16]

This new science is called epigenetics and it is showing that the genetic expression of a cell can be turned on or turned off depending on changes in the cellular environment affected by lifestyle and dietary choice.[17]

It is critical to understand this foundational principal in achieving and maintaining a healthy body and a healthy respiratory function.  The foundational hypothesis of my research is the understanding that the human body is alkaline by design and acidic by function.[16]  The mucous in the body is the evidence that the body is protecting itself from its acidic functions (breathing, thinking, moving, eating) when dietary and/or metabolic acids are not properly eliminated through the four channels of elimination.[16]

When you understand that the body needs to be maintained in an alkaline state in order to have sustainable energy, health, fitness and vitality, then everything you drink, everything you eat, every activity you engage in, even your thoughts, produce acidic waste products that affect the health, fitness and vitality of the blood, tissues, organs and glands.[16]

Your health, fitness, energy and vitality is an expression of what you are eating, what you are drinking and what you are thinking.  If you are ingesting an abundance of acidic foods and liquids, or smoking cigarettes or exposed to environmental pollutants, that’s creating an internal acid environment leading to a breakdown or fermentation of the lung cells, this will lead to a host of dis-ease conditions, including CF or PAC.[16]

There are seven stages of ALL sickness and dis-ease or acidity even though there is only one sickness and one disease.

The one sickness and one disease or dis-ease theory is the over-acidification of the blood and then tissues due to an inverted way of living, eating and thinking.  This one sickness and one disease or dis-ease theory has seven stages or or seven expressions, which have been categorized by medical science as separate or different types of disease without any association or connection.  But, there is NOT many diseases only one disease and one health![18]

For example, cancer is part of that one acidic disease.  Lung cancer is an acidic condition that spoils healthy cells making them cancerous.  Multiple sclerosis is part of that one disease as acid destroys the myelin sheath.  Heart disease is the result of acid damage as is diabetes.  Cystic fibrosis is also part of this one disease as healthy body cells are being protected from dietary and/or metabolic acids creating sticky mucous.  Allergies, arthritis, osteopenia, osteoarthritis, osteoporosis, bowel restrictions and constipations, from diverticulitis to diverticulosis, IBS, ulcerated colitis, Crohn’s, all of these so-called diseases are the result of a compromised alkaline environment from individual acidic lifestyle and dietary choice.[18]

The seven stages of disease or dis-ease or excess acidity begins in the bowels, then in the blood, pushed out into the tissues, organs and glands and expressed as follows:

1) The first stage of acidosis is enervation or the loss of energy.  In this stage the body does not have the sufficient energy to completely remove dietary and/or metabolic acidic waste products which build up first in the blood and then in the connective and fatty tissues.

2) The second stage of acidosis are sensitivities and irritation.  An example of stage two acidosis are sensitivities to food and/or air-born allergies.

3)  The third stage of acidosis is catarrh or mucous buildup.  An example of stage three acidosis would be the acidic condition of the lungs called cystic fibrosis.  It is important to understand that mucous is created when the glands of the body release the alkaline compound sodium bicarbonate for the purpose of binding up dietary and/or metabolic acids.  The combining of sodium bicarbonate to acid creates a sticky mucous.  Since dietary, environmental and metabolic acids can breakdown and destroy healthy tissues and organs the glands of the body, such as the salivary glands, the pylorus glands, the pancreas and even the stomach release the alkalizing compound, sodium bicarbonate to protect and preserve healthy body cells that make up our tissues and organs.

4) The fourth stage of acidosis is inflammation.  There is only one cause of inflammation and that is acid.  Acid equal pain and pain equals acid.  There is no other cause.  Any pain or inflammation in the body is the result of localized acid that has not been properly removed by the lymphatic system.  That is why exercise is so important because the lymphatic circulation is activated by the contraction of muscle and especially the calf muscles.  Therefore, inflammation is always caused by dietary, environmental and/or metabolic acid.

5) The fifth stage of acidosis is induration or fibrotic tissue or the hardening of the tissues or organs.  This is the classic symptomology of cystic fibrosis.  The tissues and organs are turning into leather.  Another classic symptomology of induration is atherosclerosis or the hardening of the vascular system.

6)  The sixth stage of acidosis is the ulceration of tissues and/or organs such as in ulcerated colitis, or cirrhosis of the liver, or any lesion where ever it may appear.

7)  And, the seventh and final stage of acidosis prior to death is the degeneration of tissues, organs and glands.  All degenerative conditions are caused by dietary, environmental and/or metabolic acids, such as in the symptomologies of osteoporosis, multiple sclerosis, ALL cancerous conditions, heart disease and all respiratory dis-eases, including cystic fibrosis.[18]

It is important to keep in mind that whatever the disease or dis-ease condition there is only one cause.  And, that one cause is the retention of excess acids first in the blood and then the tissues and organs.  This excess acid is not eliminated through the four channels of elimination they are then deposited into the connective and fatty tissues.  This is why I call the connective tissues the “acid catchers” of the blood.[16][18]

You do not need a doctor to tell you your stage of acid imbalance. You can know this based upon your the symptom(s) you are experiencing or feeling.  If you are overweight this is an acidic condition and the body protecting the organs that sustain life from excess dietary, environmental and/or metabolic acids.  In other words, obesity is NOT a fat problem any more then cystic fibrosis is a genetic problem.  They are both an acid problem.[19]

Cystic fibrosis (CF) or Pulmonary Adenocarcinoma (PAC) are both progressive latent tissue acidosis (LTA)  conditions that begin with fatigue, then congestion, then retention, irritation, mucous build up, inflammation, induration, ulceration, degeneration and finally death.[18]

The Self-Care to a Self-Cure Can Be Simple

1) Open the channels of elimination.

2)  Heal the root system or the intestinal villi of the small intestines.

3) Build healthy stem cells and red blood cells.

4) Hyper-perfuse the blood and tissues with alkalinity.[18]

Who’s Most At Risk?

CF and PAC are caused by the genetic expression of body cells to excess dietary, metabolic and environmental acidity.[18] To change the genetic expression of the body cells one must restore the alkaline design of the body fluids with an alkaline lifestyle and diet (ALD).[18]  To have CF, a child must inherit the acidic lifestyle and diet of the parents that then causes two abnormal genes — one from each parent.  The new science of epigenetics suggests that genes can change their expression as a result of diet and lifestyle changes.[17]  In other words, when a child with CF changes his/her diet from a standard acidic American diet to the AFD diet or one stops smoking the genes will change and begin slowing down and even stopping their secretion of acid-binding sodium bicarbonate.  This in turn will reduce congestion from sticky mucous that can builds up in the lungs another organs and tissues.[20]

What to Expect at Conventional Medical Doctor’s Office for Diagnostic Testing

A baby born with the CF gene usually has symptoms during its first year, although signs of the disease may not appear until adolescence or even later.

Your child’s health care provider can help make a diagnosis and guide you in determining which treatment or combination of therapies will best alleviate symptoms of the disease. Your health care provider will perform a physical exam and run laboratory tests, including a sweat test, which checks for higher than normal amounts of sodium and chloride in the sweat. Other tests include a sputum test, genetic screening, and a stool analysis. Imaging techniques may help reveal lung conditions and abdominal obstruction.[21][22]

Tests that examine the lungs are used to detect (find), diagnose, and stage CF and PAC.

Tests and procedures to detect, diagnose, and stage CF and PAC are often done at the same time. Some of the following tests and procedures may be used:

  • Physical exam and history : An exam of the body to check general signs of health, including checking for signs of disease, such as lumps or anything else that seems unusual. A history of the patient’s health habits, including smoking, and past jobs, illnesses, and treatments will also be taken.
  • Laboratory tests : Medical procedures that test samples of tissuebloodurine, or other substances in the body. These tests help to diagnose disease, plan and check treatment, or monitor the disease over time.
  • Chest x-ray: An x-ray of the organs and bones inside the chest. An x-ray is a type of energy beam that can go through the body and onto film, making a picture of areas inside the body.
  • CT scan (CAT scan): A procedure that makes a series of detailed pictures of areas inside the body, such as the chest, taken from different angles. The pictures are made by a computer linked to an x-ray machine. A dye may be injected into a vein or swallowed to help the organs or tissues show up more clearly. This procedure is also called computed tomography, computerized tomography, or computerized axial tomography.
  • Sputum cytology : A procedure in which a pathologist views a sample of sputum (mucus coughed up from the lungs) under a microscope, to check for cancer cells.
  • Fine-needle aspiration (FNA) biopsy of the lung: The removal of tissue or fluid from the lung using a thin needle. A CT scan, ultrasound, or other imaging procedure is used to locate the abnormal tissue or fluid in the lung. A small incision may be made in the skin where the biopsy needle is inserted into the abnormal tissue or fluid. A sample is removed with the needle and sent to the laboratory. A pathologist then views the sample under a microscope to look for cancer cells. A chest x-ray is done after the procedure to make sure no air is leaking from the lung into the chest.
  • Bronchoscopy : A procedure to look inside the trachea and large airways in the lung for abnormal areas. A bronchoscope is inserted through the nose or mouth into the trachea and lungs. A bronchoscope is a thin, tube-like instrument with a light and a lens for viewing. It may also have a tool to remove tissue samples, which are checked under a microscope for signs of cancer.
  • Thoracoscopy : A surgical procedure to look at the organs inside the chest to check for abnormal areas. An incision (cut) is made between two ribs, and a thoracoscope is inserted into the chest. A thoracoscope is a thin, tube-like instrument with a light and a lens for viewing. It may also have a tool to remove tissue or lymph node samples, which are checked under a microscope for signs of cancer. In some cases, this procedure is used to remove part of the esophagus or lung. If certain tissues, organs, or lymph nodes can’t be reached, a thoracotomy may be done. In this procedure, a larger incision is made between the ribs and the chest is opened.
  • Thoracentesis : The removal of fluid from the space between the lining of the chest and the lung, using a needle. A pathologist views the fluid under a microscope to look for cancer cells.
  • Light and electron microscopy : A laboratory test in which cells in a sample of tissue are viewed under regular and high-powered microscopes to look for certain changes in the cells.
  • Immunohistochemistry : A test that uses antibodies to check for certain antigens in a sample of tissue. The antibody is usually linked to a radioactive substance or a dye that causes the tissue to light up under a microscope. This type of test may be used to tell the difference between different types of cancer.[23]

Alkalizing Treatment Protocol for Cystic Fibrosis (CF) and Pulmonary Adenocarcinoma Lung Cancer (PAC)

Prevention and Alkalizing is the Self-Care to a Self-Cure for Cystic Fibrosis (CF) and Pulmonary Adenocarcinoma Lung Cancer (PAC)

The best self-care to a self-cure for Cystic Fibrosis (CF) and Pulmonary Adenocarcinoma Lung Cancer (PAC) will be found in its prevention NOT in its treatment. Preventing CF and PAC must begin with the parents switching to an alkaline lifestyle and diet before conception.  At birth the parents can help avoid the symptoms of CF or any other dis-ease with the Alkalizing Lifestyle and Diet Protocol.

Natural Non-Invasive Treatment Plan for Cystic Fibrosis (CF) and Pulmonary Adenocarcinoma (PAC) Lung Cancer[15][16][18]

The hope for the future is that the Alkalizing Lifestyle and Diet (ALD) therapy can repair or replace the defective CF or PAC gene and cause the gene to express itself differently by changing the environment and restoring the alkaline design of the body fluids.  This will cause the gene to express itself in an alkaline way rather than in a defensive way to protect itself from an acidic lifestyle and diet.  This environmental approach for treating CV and PAC may prove to be the cure for this acidic lifestyle and dietary symptom.

CF and PAC patients suffer from frequent lung infections that may lead to obstructed breathing caused by an acidic lifestyle and diet. So, the mainstays of a treatment plan are:

1) Open up the channels of elimination of dietary and metabolic acids.

2) Hyper-perfuse the tissues with alkalinity to buffer the retained dietary and/or metabolic acids.

3) Heal the root system or bowels of the body or the intestinal villi of the small intestines to improve the quality and quantity of stem cell and red blood cell production.

4)  Alkalizing physical therapy to remove acids out of the tissues, especially the lungs.

5) Alkalizing  exercise to remove dietary and/or metabolic acids in the connective tissues out through the pores of the skin, and

6) Alkalizing natural organic and colloidal natural medications for reducing the acids that cause mucus that is congesting and blocking the lung’s airways.

Natural Alkalizing Lifestyle and Dietary (ALD) Therapies[15][16][18]

Natural organic colloidal nutrients can by pass the alimentary canal and go directly into the blood and tissues through a process of nebulization or misted alkaline nutrients that are inhaled through the mouth and nose.[16] These include the following:

  • Nebulizing 5ml of Glutathione and 5ml of N-acetyl-cysteine to reduce acidic mucous in the sinuses and lungs 2 to 3 times a day.
  • Nebulizing 10ml of a mucolytic such as colloidal silver at 5 to 10 ppm once a day
  • Nebulizing 10 ml of colloidal silica which acts as a decongestant (which reduce swelling of the membranes of the breathing tubes).
  • Antibiotics are highly acidic and should NEVER be used with CF or PAC.  To reduce infection in the blood and tissues you reduce tissue acidity which is the cause of infections.[18]

The alimentary canal problems of congestion caused by an acidic diet leading to the symptoms of CF and PAC are managed with the following natural organic remedies.

  • Whole leaf cold pressed aloe vera juice will reduce inflammation caused by increased amounts of hydrochloric acid when the stomach is producing sodium bicarbonate to buffer the retention of tissue acids.[24]
  • Alkalizing hydrocolon therapy or colonics and enemas with mucolytic agents such as magnesium oxide, magnesium chloride, sodium bicarbonate, potassium bicarbonate, calcium glutamate and Vitamin C to treat intestinal obstructions and to infuse alkalizing compounds into the blood stream via the messenteric blood vessels.[25]

Food and Nutritional Supplements in the Prevention and Reversal of Cystic Fibrosis (CF) and Pulmonary Adenocarcinoma Lung Cancer (PAC)[26]

Natural organic colloidal nutrients can by-pass the alimentary canal and go directly into the blood and tissues through a process of nebulization or misted alkaline nutrients that are inhaled through the mouth and nose. These include the following:

Following these dietary nutritional tips will help reduce ALL acidic symptomologies associated with CF and PAC:[15][16][18]

1)  Eliminate all inflammatory acidic liquids and foods that increase sodium bicarbonate and the formation of mucous, including dairy products (milk, cheese, sour cream, and ice cream), wheat (gluten), processed soy except for non-GMO organically sprouted soy, corn, potatoes, all high-sugar fruit including bananas, oranges, pineapple, berries, apples, all forms of sugar including honey, maple syrup, fructose, maltose, dextrose, glucose, preservatives, food additives and excessive salt and all animal meats including fish, poultry, beef and pork.[15][16][18]

2)  Eat more foods that decrease acids and the formation of mucous, including garlic, onions, watercress, horseradish, mustard, parsley, celery, cucumber, broccoli, spinach, rose hips tea, lemon, lime, tomato, avocado and anti-inflammatory/anti-acid oils from nuts and seeds.[15][16][18]

3)  Eat more foods that are high in potassium, such as avocado sprouts and kale.[15][16][18]

4)  Avoid all processed and refined foods, such as white breads, pastas, and sugar.[15][16][18]

5)  Eliminate all red meats and lean meats, pork, poultry, fish, processed soy and all legumes.  Increase plant based proteins from avocado, hemp and sprouted organic soy.[15][16][18]

6)  Use healthy oils in foods, such as cold pressed olive oil and avocado oil.[15][16][18]

7)  Eliminate trans fatty acids, found in commercially baked goods such as cookies, crackers, cakes, French fries, onion rings, donuts, processed foods, and margarine.[15][16][18]

8)  Eliminate all grains from the diet.[15][16][18]

9)  Eliminate all corn products.[15][16][18]

10)  Eliminate peanuts.[15][16][18]

11)  Eliminate all forms of vinegar.[15][16][18]

12)  Eliminate all forms of mushrooms.[15][16][18]

13)  Eliminate coffee, black teas and other stimulants, alcohol, and tobacco.[15][16][18]

14)  Eliminate sport drinks, energy drinks and soft drinks.[15][16][18]

15)  Drink 4 to 6 liters of 9.5 alkaline water daily based upon 1 liter per 30 kg of weight.  Add 10 grams of pH Miracle green powder with 5 drops of pH Miracle puriphy in each liter of water.  This will help build healthy stem cells and blood in the crypts of the small intestines and reduce latent tissue acidosis which may be the cause of CF and PAC.[15][16][18]

16)  Alkalizing exercise moderately, for 60 minutes daily, 6 days a week.  Choose from walking, jogging, elliptical machines, rebounding, swimming, biking, Younga Yoga, isotonic weight lifting, just to name a few.[15][16][18]

Address nutritional deficiencies and excess latent tissue acidosis (LTA) with the following supplementation to the daily diet:[15][16][18][36]

1)  Omega-3 fatty acids, such as Hemp, Flax and Borage oils, 4 – 6 capsules or 1 tablespoonful of a 2 to 1 to 1 (Omega 3 to 6 to 9) combination of these three oils at least three to four daily, to help decrease inflammation caused by dietary and/or metabolic acids and improve the health and strength of the lipid membranes of stem, blood and body cells.[15][16][18][27][28][29][31]{34]

2)  A multivitamin daily, containing the acid chelating antioxidant vitamins A, D, E, K, the B-vitamins and trace minerals, such as sodium, magnesium, potassium, calcium, zinc, and selenium.[15][16][18][31]

3)  Digestive acid buffers of sodium bicarbonate, potassium bicarbonate, magnesium chloride and calcium chloride to reduce hydrochloric acid in the stomach, bowels, blood and tissues, 1 – 2 capsules 4 times daily with 9.5 pH alkaline water.[15][16][18][31]

4)  Magnesium oxide with Vitamin C to breakdown undigested acid foods of animal protein, dairy products and mucous in the 9 yards of the small intestines.[15][16][18][31]

5)  Coenzyme Q10, 100-200 mg at bedtime, for antioxidant and supporting the white blood cells in removing bacteria, yeast and solidified acids from the the blood and tissues.[15][16][18][31]

6)  N-acetyl-cysteine (NAC), 2000 mg daily 3 times a day, for antioxidant effects for buffering metabolic acids of acetylaldehyde and ethanol alcohol that effect the respiratory and neurological systems. NAC can also be given by IV at 5ml where each ml equals 200mgs.[15][16][18][31]

7)  Grapefruit seed extract (Citrus paradisi), 100 mg capsule or 5 – 10 drops (in alkaline water) 3 times daily, for buffering the acids of diet, metabolism, bacteria and yeast for increasing the alkaline pH of the gastrointestinal system to 8.4.[15][16][18][31][32][33][34]

8)  Methylsulfonylmethane (MSM), 3,000 mg twice a day, to help decrease the acids that cause inflammation.[15][16][18][31]

9)  Organic hemp protein, 10 – 20 grams daily mixed in fresh organic hazel or almond milk, for supporting the white blood cells and blood building.[15][16][18][31]

10)  L-Arginine, 10 grams 3 times a day to break up solidified acid crystals causing circulation problems of the vascular and lymphatic system.[15][16][18]

11)  Magnesium chloride, 2 grams 3 times a day to oxidize dietary and metabolic acids.[15][16][18]

12)  Pure organic chlorophyll from sprouted Moringa,  5 to 10 drops in 4 ounces of 9.5 pH alkaline water 3 times a day.  This mixture at 10ml can also be put into a nebulizer to reduce acid congestion in the sinuses and lungs.[15][16][18]

13)  Glutathione, 2000mg 3 to 4 times daily, neutralizes harmful acids or oxidants introduced into the lungs from the air or blood or those released by cells. Exotoxins from bacteria can overload the endobronchial terrain and feed the fires of acidic inflammation. This staggering burden increases the oxidative sensitivity of the CF lung, resulting in further injury of lung parenchyma. Data supports evidence of a decrease in the antioxidant tri-peptide glutathione. [15][16][18]

Glutathione is always in great demand and is rapidly consumed when we experience any sort of emotional or physical stress, fatigue and even moderate exercise. Some well-known causes of glutathione depletion are as follows:[15][16][18][30]

1) Acidic lifestyle and diet

2) Air and Water pollution

3) Prescription and recreational drugs

4) Ultraviolet and Radiation from cells phones, computers, electrical cars, power lines, hair dryers, etc.

5) Emotional and physical stress

6) Injury, trauma or burning

7) Heavy metals

8) Cigarette smoke

9) Household chemicals

10) Acetaminophen poisoning

11) Exhaust from motor vehicles

12) Septic shock caused by the retention of metabolic and/or dietary acid.

All of these above factors lead to a build up of acidic toxins that cause the loss of glutathione as a non-nutritive buffer leading to cellular aging, dis-ease and finally death.[30]

Alkalizing Medicinal Herbs and Organically Sprouted Grasses

1)  Medicinal herbs, grasses, fruit and vegetables is a safe way to strengthen and tone the body’s alkalizing buffering system, detox the alimentary canal and build blood in the crypts of the small intestines. You should use the whole unprocessed or non-fermented herbs, grasses, fruit and vegetables titrated to a fine powder so they that can be mixed in 9.5 pH alkaline water or put into veggie caps to be taken orally.[15][16][18][31][34]

2)  Ginkgo (Ginkgo biloba), 40 – 80 mg 3 times daily, for inflammation and as an antioxidant to buffer acids in the blood, tissues and organs.[15][16][18][31][34]

3)  Wheat, Barley and Kamut rrganically sprouted grasses, 250 – 500 mg daily, for building blood, detoxing the alimentary canal,  buffering dietary and metabolic acids and supporting the white blood cells in the removal of solidified acids. You may also prepare teas from these grasses.[15][16][18][31][34]

3)  Cat’s claw (Uncaria tomentosa) , 20 mg 3 times a day, for inflammation caused by dietary and/or metabolic acids,  supporting the white blood cells and reducing acids from bacteria, yeast and mold in the blood and tissue fluids.[15][16][18][31][34]

4)  Milk thistle (Silybum marianum), 80 – 160 mg 2 – 3 times daily, for detoxification of acids in the blood, liver and kidneys.[15][16][18][31][34]

5)  Bromelain (Ananus comosus), 40 mg 3 times daily, for pain and inflammation caused by dietary acids.[15][16][18][31][34]

6)  Ground Ivy (Hedera helix) , 50 mg 3 times daily, to decrease acids and the build-up of mucous and to loosen phlegm.[15][16][18][31][34]

Intravenous (IV) Alkalizing Therapy

The main purpose of IV therapy is to hyper-perfuse the tissues with alkaline compounds of sodium bicarbonate, magnesium chloride, potassium bicarbonate and calcium glutamate and thus buffer the retention of excess dietary and/or metabolic acids in the body tissues, especially the lungs reducing inflammation, mucous, solidfication of tissues, and cysts.

Acupuncture 

Acupuncture may alleviate symptoms of cystic fibrosis. Acupuncture may help enhance blood and lymph circulation to the lungs which in turn will help the immune function to remove cellular debris and acid crystals.  Because acupuncture improves circulation it also helps remove acids throughout the alimentary canal, and strengthen.

Massage

Therapeutic lymphatic massage can help drain acidic mucus from the lungs and remove latent tissue acidosis.

Infrared Sauna

Therapeutic infared sauna can help increase blood and lymphatic circulation and open up the pores of the skin to eliminate excess dietary, environmental and metabolic acids from the tissues.  This passive form of exercise will cause you to sweat at every pore removing latent tissue acids.  I recommend at least 30 minutes a day or until you start sweating.  Once you start sweating remain in the sauna for at least 15 minutes.  Make sure you are adequately hydrated with alkaline mineral rich water at a pH of 9.5.  To adequately hydrate drink at least 1 liter of akaline fluids for every 30 kg of weight.  You can also drink before, during and after your infared sauna. Prognosis/Possible Complications Respiratory problems due to acid build-up and the solidification of dietary, environmental and/or metabolic acids forming acid crystals and cysts in the lungs are the most common complication from CF and PAC.

Following Up

CF and PAC patients receive pulmonary function tests every 3 – 6 months. They also receive chest x-rays every 2 – 4 years, or more often if needed.

Case Study of the Alkalizing Lifestyle and Diet (ALD) for Terminal Metastatic Pulmonary Adenocarcinoma Lung Cancer

A 58 year old Danish woman was diagnosed by X-ray, Cat Scan and biopsy of the lung with Pulmonary Adenocarcinoma Lung Cancer with metastasis to the axillary lymph nodes at the Roskilde Hospital on June, 2011.  She was not offered conventional invasive surgery because the cancer had spread throughout her left lung to the lymphatic system and the axillary lump nodes.  Chemotherapy and radiation were suggested but would only extend life for a few weeks beyond her 6 month life expectancy.  She started the ALD protocol a week after diagnosis.  She was retested in October, 2015 with Ultrasound and Bronchoscopy  and found to have no pulmonary adenocarcinoma cancer in the lungs or in the axillary lymph nodes.  The medical doctors found her to be in good health and attribute her cancer remission to the Alkalizing Lifestyle and Diet (ALD) that she followed and is still following as of to date.

Conclusion

Cystic Fibrosis (CF) and Pulmonary Adenocarcinoma (PAC) of the lungs are terminal chronic acidic conditions, theoretically caused by LTA with no current conventional treatments to slow-down the aggressive nature of these conditions.  The Alkalizing Lifestyle and Diet (ALD) have shown great promise in improving symptoms of both CF and PAC and in one case reversing PAC, a terminal cancer condition with a 5 year life expectancy of 1 percent.[37]

Further Research

Further research needs to be done with larger groups with CF or PAC to show that the ALD cancer treatment protocol is a viable therapy for the prevention and/or reversal of Cystic Fibrosis (CF) and Pulmonary Adenocarcinoma (PAC).  The author of this article is hopeful that more research scientist will be open to investigating the efficacy of the ALD protocol as a potential non-invasive treatment for the cure of CF and PAC.

References

  1.  O’Sullivan, BP; Freedman, SD (30 May 2009). “Cystic fibrosis.”. Lancet 373 (9678): 1891–904. doi:10.1016/s0140-6736(09)60327-5PMID 19403164.
  2. Hodson, Margaret; Geddes, Duncan; Bush, Andrew, eds. (2012). Cystic fibrosis (3rd ed.). London: Hodder Arnold. p. 3. ISBN 978-1-4441-1369-3.
  3. Travis, William D; Brambilla, Elisabeth; Müller-Hermelink, H Konrad; Harris, Curtis C, eds. (2004). Pathology and Genetics of Tumours of the Lung, Pleura, Thymus and Heart (PDF). World Health Organization Classification of Tumours. Lyon: IARC Press. ISBN 92-832-2418-3. Retrieved 27 March 2010.
  4. Young, R.O. (25 February 2015). “The Blood Jerk Reaction – A Rise In The Alkaline pH of the Blood! What Does It Really Mean?” http://blog.phoreveryoung.com/tag/latent-tissue-acidosis/
  5. Smokers defined as current or former smoker of more than 1 year of duration. See image page in Commons for percentages in numbers. Reference:
    1.  Horn, L; Pao W; Johnson DH (2012). “Chapter 89”. In Longo, DL; Kasper, DL; Jameson, JL; Fauci, AS; Hauser, SL; Loscalzo, J. Harrison’s Principles of Internal Medicine(18th ed.). McGraw-Hill. ISBN 0-07-174889-X.
  6. Subramanian, J; Govindan R (February 2007). “Lung cancer in never smokers: a review”. Journal of Clinical Oncology (American Society of Clinical Oncology) 25 (5): 561–570. doi:10.1200/JCO.2006.06.8015PMID 17290066.
  7. Kenfield, S. A.; Wei, E. K.; Stampfer, M. J.; Rosner, B. A.; Colditz, G. A. (2008). “Comparison of aspects of smoking among the four histological types of lung cancer”Tobacco Control 17 (3): 198–204. doi:10.1136/tc.2007.022582PMC 3044470PMID 18390646.
  8. Flume PA, Mogayzel Jr PJ, Robinson KA, et al. (March 2010). “Cystic Fibrosis Pulmonary Guidelines: Pulmonary Complications: Hemoptysis and Pneumothorax”. Am J Respir Crit Care Med 182 (3): 298–306. doi:10.1164/rccm.201002-0157OCPMID 20299528.
  9. Mitchell, Richard Sheppard; Kumar, Vinay; Robbins, Stanley L.; Abbas, Abul K.; Fausto, Nelson (2007). Robbins basic pathology. Saunders/Elsevier. ISBN 1-4160-2973-7.
  10. “Profile : Lap-Chee Tsui”. Science.ca. 1989-05-09. Retrieved 2013-01-23.
  11. Mitchell, Richard Sheppard; Kumar, Vinay; Robbins, Stanley L.; Abbas, Abul K.; Fausto, Nelson (2007). Robbins basic pathology. Saunders/Elsevier. ISBN 1-4160-2973-7.
  12. Bobadilla JL, Macek M, Fine JP, Farrell PM (June 2002). “Cystic fibrosis: a worldwide analysis of CFTR mutations—correlation with incidence data and application to screening”. Hum. Mutat. 19 (6): 575–606. doi:10.1002/humu.10041PMID 12007216.
  13. Goljan USMLE Audio Tapes, 2001
  14. Young, RO, “Sick and Tired”, Woodland Publishing, Orem, Utah, 2001.
  15. Young, RO, Young, SR, “The pH Miracle Revised and Updated”, Grand Central Publishing, New York, NY, 2010.
  16. McGowan P.O., Meaney M.J., Szyf M. (2008).  Diet and the epigenetic (re)programming of phenotypic differences in behavior. Brain Research, 1237: 12-24 (subscription required).
  17. Young,R.O., Young, SR, “The pH Miracle for Cancer”, Hikari Omni Media Publishing, Alpine, Utah, 2015.
  18. Young,R.O., Young, S.R., “The pH Miracle for Weight Loss”, Grand Central Publishing, New York, NY, 2005.
  19. Rubin BK. The pharmacologic approach to airway clearance: Mucoactive agents. Paediatr Respir Rev. 2006;7 Suppl 1:S215-9.
  20. The Cystic Fibrosis Foundation, “Testing for CF”, https://www.cff.org/What-is-CF/Testing/
  21. Farrell P, Rosenstein B, White T, et al. Guidelines for Diagnosis of Cystic Fibrosis in Newborns through Older Adults: Cystic Fibrosis Foundation Consensus Report. Journal of Pediatrics. 2008;153(2).
  22. The National Cancer Institute, “Testing for Non-Small Cell Lung Cancer”‘ http://www.cancer.gov/types/lung/patient/non-small-cell-lung-treatment-pdq
  23. Young, R.O., “The Real Scientific Truth Concerning The pHysiology of the Stomach”,  http://blog.phoreveryoung.com/2015/02/02/the-real-scien…of-the-stomach/
  24. Young, R.O., “Alkalizing Colon Hydrotherapy – The Secret of the Ancient Healers”,  http://blog.phoreveryoung.com/2015/08/01/the-secret-of-…ient-healers-
  25. Adde FV, Rodrizues JC, Cardoso AL. Nutritional follow-up of cystic fibrosis patients: the role of nutrition education. J Pediatr (Rio J). 2004;80(6):475-82.
  26. Mizejewski GJ, Pass KA. Fatty acids, alpha-fetoprotein, and cystic fibrosis. Pediatrics. 2001;108(6):1370-3.
  27. Caramia G, Cocchi M, Garliardini R, et al. Fatty acids composition of plasma phospholipids and triglycerides in children with cystic fibrosis. The effect of dietary supplementation with an olive and soybean oils mixture. Pediatr Med Chir. 2003;25(1):42-9.
  28. Beckles Willson N, Elliot TM, Everard ML. Omega-3 fatty acids (from fish oils) for cystic fibrosis. Cochrane Database Syst Rev. 2002;(3):CD002201.
  29. Roum JH, Buhl R, McElvaney NG, et al. Systemic Deficiency of Glutathione in Systic Fibrosis. J Appl Physiol 1993; 75:19-24
  30. Young, R.O. “Herbal Nutritional Medications”, Hikari Omni Publishing, Alpine, Utah, 1992.
  31. Cvetnic Z, Vladimir-Knezevic S. Antimicrobial activity of grapefruit seed and pulp ethanolic extract. Acta Pharm. 2004;54(3):243-50.
  32. Heggers JP, Cottingham J, Gussman J, et al. The effectiveness of processed grapefruit-seed extract as an antibacterial agent: II.
    Mechanism of action and in vitro toxicity. J Altern Complement Med. 2002;8(3):333-40.
  33. Guo R, Pittler MH, Ernst E. Herbal medicines for the treatment of COPD: a systematic review. Eur Respir J. 2006;28(2):330-8.
  34. Simopoulos AP. Omega-3 fatty acids in inflammation and autoimmune diseases. J Am Coll Nutr. 2002;21(6):495-505.
  35. Murray KL, Lee CK, Mogayzel PJ Jr, Zeitlin PL, Rosenstein BJ. Dietary supplement use in pediatric patients with cystic fibrosis. Am J Health Syst Pharm. 2008;65(6):562-5.
  36. The American Cancer Society, “Non-Small Cell Lung Cancer Survival Rates by Stage”, http://www.cancer.org/cancer/lungcancer-non-smallcell/detailedguide/non-small-cell-lung-cancer-survival-rates

What Happens to ALL the Disappearing Can

12311128_1639530499647197_8412997691509003664_nWhat Happens to ALL the Disappearing Cancer Patients?

It’s been almost 20 years since I met my first disappearing patient — a nurse in her early 40s, let’s call her Kate. Kate was diagnosed with breast cancer. As a nurse, she had seen the results of breast cancer treatments. She was terrified, and determined. She was not heading for surgery, nor chemotherapy, nor radiation.

But Kate worked in a hospital. She worked with the doctors who diagnosed her cancer, and she worked with the surgeon, who wanted to schedule her into surgery “as soon as possible.”

The first thing Kate did was slow down. She did some research. It didn’t take her long to remind herself that in Canada, and in the USA, the treatments for cancer are akin to law. No hospital would dare deviate from the deadly three (cut, poison, burn).

Kate’s cancer was not large. She had been tested for cancer last year and no cancer was found. She knew it took many years for cancers to develop. At first, she was furious, “If it is here today, it must have been here last year. Why didn’t you find it last year?” It had not metastasized. It was not growing rapidly and was not affecting her health in any way. In theory, she had lots of time. So, she took some time.

But Kate didn’t look for magic cures. She didn’t search for the latest “cancer medicine.” She wasn’t interested in curing herself. She knew she was a nurse, not a doctor. She searched instead for the “cured” – patients who were diagnosed with cancer, and no longer had cancer. She knew from her work in the hospital, from conversations with patients, and with some staff, that these people existed — but from the perspective of the medical establishment, they seemed to disappear.

It didn’t take her long to find some patients who claimed they were cured. They hadn’t disappeared from life. They were eating, drinking, loving, and living full healthy and prosperous lives. But according to the medical records, they didn’t exist. They were “never cured.”

The medical system treated their cures as “anecdotal.” It ignored them. There was no attempt by any doctors to understand what happened to these cancer patients. They were no longer sick. The medical system looks after sick patients, treats sick patients. These patients were not sick.

Kate looked and listened. Her interest was not clinical science vs. anecdotal evidence. Her interest was personal. She talked, listened, compared stories. From several, she learned about a clinic that did not claim to cure cancer. It did not use medicines to treat cancers. But patients were cured, somehow. This clinic was not in Canada. It was not in the USA. She would have to go to Mexico to learn more.

There are lots of alternative treatment clinics in Mexico. Are some of them valid, using important techniques to cure cancers? Are some of them scams, wanting to take money from desperate clients? Do some of them have a cure that works sometimes, but might not work for her? Kate didn’t know. She did more research. She called the clinic.

The staff did not claim to cure cancer. Claiming to cure cancer is dangerous, even for a clinic outside of North America. They suggested Kate visit the clinic and see what happens there, no charge for a visit, but she would need to pay for her travel to Mexico. Kate had done her research. She had met and talked to patients whose cancers had disappeared.

Kate made her decision. She was familiar with cancer diagnosis techniques in Canada. She had undergone a physical examination, a mammogram, that detected a lump in her breast. Then she had a biopsy, where tissue was taken from the lump and was sent to a lab for analysis. The lab technician tested and examined the sample and issued a diagnosis “cancer” or “not cancer.” Once the diagnosis is issued, everybody swings into action. Kate knew that the mammogram had a high false positive rate and a false negative rate. Many people who are diagnosed with a “possible cancer” by a mammogram do not actually have cancer. She was also aware that cancer biopsies have a false positive rate and a false negative rate, as well. Her work in the hospital, with real patients, had made this very clear.

She didn’t really know for certain if she had cancer. Her surgeon, on the other hand, was still pressing her to schedule treatment.

Kate knew one thing. She had time. She cashed out some savings and booked a “holiday” in Mexico.

At the clinic, Kate was surprised that there was no “cancer diagnosis.” They did check the presence and size of the lump on her breast. But they didn’t repeat the biopsy. The clinic read her diagnostic reports, but did not investigate them further. There was instead a very thorough analysis completed by a suite of doctors. It took two full days of tests and interviews, if I remember correctly.

Kate was asked about her family’s medical histories. She gave blood samples. She was questioned extensively about her diet, about what she eats on a regular basis. What foods does she like and eat often. What foods does she not like and never eat. Doctors examined her lungs, her heart, liver, and other bodily organs with various tests. Her immune system was tested. Extensive interviews about her life, her work, her relationships, and more.

At the time I talked to Kate, I didn’t realize that she was not getting a “medical analysis,” she was actually getting a “healthicine analysis.” Her tests and questions fit perfectly to the hierarchy of healthicine: genetics, nutrition, cells, tissues, organs, bodily systems, body, mind, spirit, and community.

Kate’s genetics were analyzed through family history. There may have been further genetic analysis, I don’t remember all of the details. Her nutritional status was analyzed, not just by analyzing what she ate, and what she preferred to eat, but also by studying what she didn’t like to eat, what she deliberately never ate, what foods she believed she was allergic to. Her cells and tissues were analyzed directly, through blood samples and physical examination, and indirectly through medical history and other tests. Many of her organs were tested for healthiness. Her bodily systems, immune system, circulatory system, respiratory system, hormonal systems and more were analyzed and assessed. Her physical body was measured, weighed, and examined. Her mental health was assessed, as well as her spiritual healthiness. She was in good spirits, even in light of a potentially life threatening illness. Her community health was analyzed as well. Her family, her relationships with her children, her spouse, her parents, her work community, and more.

After a few days, Kate met with a group of doctors to discuss her health, not her illness, her healthiness. Diagnosing illness is difficult. Analyzing healthiness is more complex. It took several doctors and several hours for Kate to learn and understand what they had learned about her healthinesses and her unhealthinesses.

They then “prescribed” two weeks, if I remember correctly, of healthiness training, tailored to Kate’s specific situation. She spent the next two weeks at the clinic, learning to be healthier, not learning how to be “healthier in principle,” rather – learning what Kate needed to do to make her diet, her body, her mind, her spirits, and even her relationships with her communities healthier. She could not change her work community. But she could change how she reacted to and interacted with it – to improve her own health. After two weeks of learning at the clinic, her breast lump had started to shrink.

Kate went back to Canada, to put her learning into action. The lump disappeared. Her diagnosis was still there on paper. But her “cancer” had disappeared. She was retested at her hospital and no cancer was found.

Then Kate began to disappear.

When the surgeon asked again, she explained that she was not going to surgery. The surgeon looked away. He refused to look her in the eye after that.

But Kate didn’t disappear from her family. She went back to her family. She didn’t disappear from her job. She went back to her job. She disappeared from the cancer system. Her cancer disappeared, so, as a cancer patient, she disappeared.

Was she cured? We don’t know. There is no useful definition of a cancer cure. No medical or scientific test that can prove a patient has been cured of cancer. Our cancer treatment statistics have no count for people who are cured of cancer. Patients that are cured, whether they are cured with medicines or not, are not counted. No breast cancer patients are officially cured by medicine. If their cancer goes away without treatment, they disappear from statistics. If their cancer is killed by radiation, chemotherapy or surgery, they are not cured, they are a “survivor.” Everyone knows that cancer survivors are always waiting for the cancer to reappear. Their symptoms are in remission, but their cancer is not cured. They are not cured. With no proof of a cure, it might just be hidden.

Kate no longer has cancer. She paid, from her own pocket, for her trip to a clinic in Mexico. After the trip, her cancer disappeared. She had medical insurance. But her insurance wouldn’t pay for her trip. Insurance pays for treatments, not for cures. It pays for treatments, even if they fail. But it does not pay for success. Success disappears.

There are two ways for a cancer patient to disappear. You might be cured by health. Or you might be cured by a medicine that is not approved. In both cases, the medical system will ignore the cure, and ignore the patient.

In healthicine, there are no incurable diseases. If it is not curable – it is not a disease, it is a handicap, a disability, a deficiency, or simply an attribute of the person. All diseases can be cured by definition.

I have since met several cancer patients who have disappeared, and not just cancer patients. Maybe you have too? I’ve met more by internet, email, etc. There is no way for me to determine if a disappeared patient actually had cancer, if their treatment cured their cancer, if their body cured their cancer or if they still have cancer. We can only tell if there is another cancer diagnosis. Nothing can be told from the absence of a diagnosis.

There is no way for any doctor to tell either. There are no tests for a cancer cure. There is no way to recognize, much less document a cancer cure. There are no statistics for cancers cured.

Many cured patients don’t disappear quietly. They speak out. They write books and newspaper articles. They blog. But it doesn’t matter. They still don’t count. Once cured, they disappear. The medical system does not study their cases, does not study their diagnosis, does not study their cures. For chronic diseases, like cancer, arthritis, diabetes, heart disease, even obesity, and many more, there are no techniques to document “cured patients.” As a result, there are no statistics for “cured patients” of any chronic illness.

Once they are cured, they disappear. Health doesn’t cure illness, it disappears illness. And medicine doesn’t count people who have disappeared.

To your health

Scientific Breakthrough! The Most Powerful Selective Anti-Oxidant, Alkalizer, Energizer and Cell Hydrator

The Incredible Power of Molecular Reduced Magnesium ... Bringing Cutting Edge Nutritional Science To You Now!
Dr. Robert Young

Naturopathic Practitioner – The pH Miracle Ti Sana Detox Medical Spa

The Incredible Power of Molecular Reduced Magnesium … Bringing Cutting Edge Nutritional Science To You Now!

Nov 11, 2015

Scientific Breakthrough!

The Most Powerful Selective Anti-Oxidant, Alkalizer, Energizer and Cell Hydrator in the World!

With An Instant Impact on Alkalinity, Blood Quality and Energy!

My mission is to make optimal health as easy and as cost effective as possible. I am  constantly researching to find the most effective and natural ways to achieve and maintain optimal health, fitness and vitality for myself, my family, my friends and my clients. So I am extremely excited to share with you mu latest and greatest breakthrough research in nutritional science!

My 30 years of research has shown that nearly every health condition and chronic dis-ease have three factors often associated with them:

  • Excess metabolic and dietary acidity in the interstitial body fluids
  • That excess interstitial acidity triggers tissue inflammation
  • This tissue inflammation activates cell signaling  to release anti-oxidants or acid buffers to protect the tissues, glands and organs.

Medical Science has been looking at a way of tackling these three issues for quite some time now. 

I have recently discovered that molecular activated and reduced magnesium (MgOH-) that is potentiated with lithium ions tackles all of these problems! It acts as a super anti-oxidant or a super anti-acid, a super anti-inflammatory, a super neutralizer of excess metabolic, dietary, respiratory and environmental acids, acting alone as its own cell signaling molecule!

In our body’s, activated and reduced magnesium that carries an extra electron (MgOH-) acts as a very powerful and selective anti-oxidant helping to prevent cellular damage from acid caused inflammationprotecting DNA and combating out of control metabolic and dietary acids that are the primary cause of cellular degeneration.

According to my recent research published in the medical journal, “The International Journal of Complimentary and Alternation Medicine”, entitled, “Alkalizing Nutritional Therapy in the Prevention and Reversal of Any Cancerous Condition!”, I suggest:

As deficiencies are corrected in the intracellular and interstitial fluids with key alkalizing nutritional treatments, patients see the difference  in the improved interstitial pH and chemistry counts through follow-up tests using quantitative non-invasive 3-D FBBES.  They also feel the difference physiologically and functionally with increased energy and vitality.

This is how I know proper alkalizing nutritional support in any cancerous condition is important in the prevention and treatment of cancer, the metastasis of cancer, and the shrinking of a cancerous cyst or mass without chemotherapy and-or radiation. The best part about these alkalizing nutritional treatments is they are helpful in most, if not in all cancerous conditions.”  (To read the full article go to: https://www.linkedin.com/pulse/alkalizing-nutritional-therapy-prevention-reversal-any-young-6057087895716507648?trk=mp-reader-card)

There are now well over 1000 studies from peer reviewed medical journals discussing the countless health benefits from elemental magnesium.

Activated and reduced magnesium (MgOH-) has been shown to reduce inflammation and joint discomfortincrease stamina and energy.

Activated and reduced magnesium (MgOH-) has shown promise to be cardio protectiveneuro protective, offer intestinal protectionskin rejuvenation and many more conditions caused by metabolic and dietary acids that are not properly eliminated via the four channels of elimination – skin, lungs, bowels and kidneys.

Activated and reduced magnesium (MgOH-) also acts as a powerful cell signalling molecule to maintain our cellular communications system. The interference in this through excess metabolic and dietary acidity is the cause of many health and fitness problems in the body.

The Benefits of Activated and Reduced Magnesium

The health benefits of activated and reduced magnesium are new to the world.

This was because, until NOW, the delivery was only attainable through:

  • Electron-enriched ionized water (inefficiently delivered from water current electrical ionization)
  • Electrons release through hydroxyl Gas from a metallic cylinder under high pressure

The problem with these delivery systems is that electrons disappear very quickly and therefore are not very accessible to our cells to buffer or neutralize metabolic and/or dietary acids.

Basic chemistry has demonstrated that in the stomach, the generation of electrons carried by sodium bicarbonate is more complete and faster than any other means.

I took it upon myself to find some way of getting a highly accessible form of elections stabilized by magnesium that was  easy to use and highly bioavailable to the body.

I discovered the first reduced form of magnesium potentiated by lithium that would deliver a concentration of free-electron for buffering the dietary, respiratory, environmental and metabolic acids that cause ALL sickness and disease.

I have found that this is the most efficient and easiest way of getting the benefits of activated and reduced magnesium loaded with electron energy.

Benefits Include:

  • FAST RED BLOOD CELL TRANSFORMATION: Immediate improved difference which is viewable using phase contrast microscopy in just five minutes.
  • ALKALIZING EFFECTs: Pure Energy(TM) is a potent alkalizer serving to effectively neutralise all types of metabolic and dietary acids in our body including lactic acid.
  • NEGATIVE-CHARGED ORP EFFECT: Pure Energy(TM) has a high Negative-Charged Oxidative Reduction Potential.  My electron tests show an ORP of up to -1000mV!  In this case the negative-charge is good, not bad and represents a concentration of free electron energy! As we age, we oxidize or ferment, like an old car that rusts. Things that oxidize have a positive ORP or positive-charge. Therefore if we want to slow down the aging (rusting or fermenting) process, then it’s a good to ingest foods, liquids or supplements that carry a negative-charged ORP. This was only available before with an expensive water ionizers – but is now available in supplement form to all through my latest invention called Pure Energy(TM)
  • BIO-AVAILABLE:  Pure Energy(TM) is activated and reduced magnesium potentiated with lithium and is 100% bio-available, so it will act on ALL of the body’s fluids, tissues, glands and organs.
  • ANTI-INFLAMMATORY: Pure Energy(TM) acts as a powerful anti-inflammatory in the body because it neutralizes the metabolic, respiratory, dietary and environmental acids that cause inflammation.
  • ENHANCED CELLULAR HYDRATION: Pure Energy(TM) has been shown to increase cellular hydration by enhancing the ability to move alkalizing extracellular water into the cell.
  • ENERGY PRODUCTION: Pure Energy(TM) when added to distilled or purified water will activate and reduce and potentiated with lithium as it releases electron-energy which becomes available to the mitochondria in our cells.  Activated and reduced magnesium potentiated with lithium also increases electron stores in the liver and may improve functioning of all organs in the body by increasing stores of available electron energy.
  • ANTI-AGING: Aging is created by the body being broken down by metabolic and dietary acids. By having a continual supply of electrons released from activated and reduced magnesium potentiated with lithium, the body can use the increased electrons to neutralize the acids that cause aging and slow down the aging process.
  • SPORTS RECOVERY & LEGAL PERFORMANCE ENHANCER: By increasing alkalizing cellular hydration, reducing the acids that cause inflammation and most importantly reducing the lactic acid by up to 18% that causes inflammation that leads to pain, Pure Energy(TM) is a powerful (and fully permittedsports performance and recovery enhancer.
  • POWERFUL ANTIOXIDANT: Due to its extremely small size (0.24 Trillionth of a Meter), it can spread throughout the body in seconds and penetrate all tissue, cells, and cell components providing rapid protection from metabolic and dietary acids.
  • SELECTIVE ANTIOXIDANT: Activated and reduced magnesium has special SELECTIVE properties that allow the abundant release of electrons to deal with the “bad” acid but leave the “good” alkalizing buffers, such as sodium bicarbonate and hydrogen peroxide to do their tissue protective jobs.
  • HOLISTIC ANTIOXIDANT: Due to its molecular size, Pure Energy(TM) can provide protection to the inside and outside of body cellsexternal surface of the cell membrane (lipid-bi-layer), the extra-cellular matrixplasmainterstitial fluids and all external surfaces of cells, organs, and all tissue.
  • PURE ENERGY(TM) ENABLES THE PRODUCTION OF YOUR BODY’S OWN ANTIOXIDANTS: Acts as a natural Nrf2 transcription factor activator that allows the body to make its own antioxidant compounds (e.g., superoxide dismutase (SOD), catalase, and glutathione peroxidase).
  • CELL SIGNALLING: Cell signalling is a way the body can send a message to different parts of the body to supply it with required red blood cells. The released hydroxyl ions or OH- that releases an extra electron has recently been found to act as a cell signalling molecule.  The release of this electron from reduced and activated magnesium acts as a powerful antioxidant and anti-inflammatory.
  • NATURAL & SAFEPure Energy(TM) contains natural mineral ingredients and tested to be 100% safe, even at high doses. There are no known negative direct or side-effects.
  • Pure Energy(TM) can ONLY be obtained by calling this special phone number: 760-484-3797 or you can order on line at: http://store.phoreveryoung.com/products/pure-energy?variant=10089006916, or email us at: phmiraclelife@gmail.com
  • www.phoreveryoung.com and www.phoreveryoung.wordpress.com

How To Prepare the Pure Energy(TM) Magnesium for Activation and Reduction:

1) Take a 12 ounce surgical stainless steel bottle and fill the bottle to the top with distilled or purified water.  Make sure there is no air at the top of the bottle where electrons might escape.

2) Drop one Pure Energy(TM) magnesium tablet in the water and immediately seal the bottle with the screw on top in order to trap all the electrons inside.

3) Let the distilled or purified water sit for 2 hours while the magnesium activates and reduces.

4) When you are ready to drink the Pure Energy(TM) activated and reduced magnesium water you can take off the lid or you can flip up the straw to drink.  Drink the whole 12 ounces once opened.

Please note that the Pure Energy(R) activated reduced magnesium water is stable and drinkable for up to 1 year as long as the cap or the lid has not been opened.

Recommendations:

Drink one 12 ounce Pure Energy(TM) activated reduced magnesium water in the morning and one 12 ounce Pure Energy(TM) activated reduced magnesium water in the afternoon.

To order your Pure Energy(TM) go to: http://store.phoreveryoung.com/products/pure-energy?variant=10089006916

You will receive with your Pure Energy(TM) order, free shipping, Dr. Robert O. Young’s “Alkalizing Nutritional Therapy” book, a special container for your Pure Energy(TM) tablets and two stainless steel 12 ounce bottles, with each order of one month supply or a minimum of 60 tablets of Pure Energy(TM).

Alkalizing Fruit, Vegetables, Nuts, Seeds and Sprouts May Prevent or Reverse Depression!

Alkalizing Fruit, Vegetables, Nuts, Seeds and Sprouts May Prevent or Reverse Depression!
Dr. Robert Young

 M.Sc., D.Sc., Ph.D., N.D.

Naturopathic Physician at the pH Miracle Ti Sana Medical Spa, Arlate, Italy

Alkalizing Fruit, Vegetables, Nuts, Seeds and Sprouts May Prevent or Reverse Depression!

Eating a plant-based alkaline diet comprising of fruit, vegetables, sprouts, legumes, and healthy polyunsaturated oils is associated with preventing the onset of depression, according to research published in the open access journal BMC Medicine. A large study of 15,093 people suggests depression could be linked with nutrient deficits.

Following extensive research into diet and its effect on our physical health, researchers are now exploring the link between nutrition and mental health. This is the first time that several healthy dietary patterns and their association with the risk of depression have been analyzed together.

The researchers compared three diets; the Mediterranean diet, the Pro-vegetarian Dietary Pattern and Alternative Healthy Eating Index-2010. Participants used a scoring system to measure their adherence to the selected diet, i.e. the higher the dietary score indicated that the participant was eating a healthier diet.

Food items such as meat and sweets (sources of animal fats: saturated and trans fatty acids) were negatively scored, while nuts, fruit and vegetables (sources of omega-3 fatty acids, vitamins and minerals respectively) were positively scored.
Lead researcher, Almudena Sanchez-Villegas, University of Las Palmas de Gran Canaria, says “We wanted to understand what role nutrition plays in mental health, as we believe certain dietary patterns could protect our minds. These diets are all associated with physical health benefits and now we find that they could have a positive effect on our mental health.”

“The protective role is ascribed to their nutritional properties, where nuts, legumes, fruit and vegetables (sources of omega-3 fatty acids, vitamins and minerals) could reduce the risk of depression.”

The study included 15,093 participants free of depression at the beginning of the study. They are former students of the University of Navarra, Spain, registered professionals from some Spanish provinces and other university graduates. All are part of the SUN (Seguimiento Universidad de Navarra) Project, a cohort study started on 21st December 1999. The cohort has been used to identify dietary and lifestyle determinants of various conditions, including diabetes, obesity and depression.

Questionnaires to assess dietary intake were completed at the start of the project and again after 10 years. A total of 1,550 participants reported a clinical diagnosis of depression or had used antidepressant drugs after a median follow-up of 8.5 years.

The Alternative Healthy Eating Index-2010 was associated with the greatest reduction of risk of depression but most of the effect could be explained by its similarity with the Mediterranean Diet. Thus, common nutrients and food items such as omega-3 fatty acids, vegetables, fruits, legumes, nuts and moderate alcohol intake present in both patterns (Alternative Healthy Eating Index-2010 and Mediterranean diet) could be responsible for the observed reduced risk in depression associated with a good adherence to the Alternative Healthy Eating Index-2010.
Almudena Sanchez-Villegas says, “A threshold effect may exist. The noticeable difference occurs when participants start to follow a healthier diet. Even a moderate adherence to these healthy dietary patterns was associated with an important reduction in the risk of developing depression. However, we saw no extra benefit when participants showed high or very high adherence to the diets.
So, once the threshold is achieved, the reduced risk plateaus even if participants were stricter with their diets and eating more healthily. This dose-response pattern is compatible with the hypothesis that suboptimal intake of some nutrients (mainly located in low adherence levels) may represent a risk factor for future depression.”

A limitation of this study was that the results are based on self-reported dietary intake and a self-reported clinical diagnosis of depression. More research is needed to predict the role of nutrient intake for neurophysiological requirements and identify whether it is minerals and vitamins or proteins and carbohydrates that cause depression.

Read more: https://phoreveryoung.wordpress.com
Follow us: @drrobertyoung on twitter and The pH Miracle Fan Club on Facebook

The Cure for Cancer? That’s an easy question to answer! The Cure for Cancer is Found in its Prevention NOT in its Treatment! – Dr. Robert O. Young
Do you know what rotten apples, grapefruit or bananas look like? If you do then you know what cancer cells look like. Cancer cells are nothing more that healthy cells that are spoiling because of a compromised environment! Look at the picture below and you will see colorized cancerous body cells rotting in their toxic acidic environment.

What compromises the internal environment of a human body that causes body cells to begin spoiling and rotting? The answer is simple! The body’s build-up of acidic metabolic and dietary waste that has not been properly eliminated through the four channels of elimination – urination, defecation, respiration and perspiration!

Cancer is not a noun but an adjective that describes what is happening to body cells in an acidic environment due to an acidic lifestyle and diet. http://www.phoreveryoung.com

To learn more about Dr. Robert O. Young go to: https://www.linkedin.com/in/drrobertoyoung
To read more of Dr. Young’s articles go to: http://www.phoreveryoung.wordpress.com
To join Dr. Young on Twitter go to: @drrobertyoung
To watch more videos on YouTube go to: https://www.youtube.com/user/pHMiracleCenter
Join Dr. Young on Facebook at: The PH Miracle Medical Association or The pH Miracle
To purchase Dr. Young’s books or nutritional productts go to: http://www.phoreveryoung.com or http://www.phmiracle.com

From Beer to Greens

12111976_895303250518987_8060493019611639627_n

Aquí las consecuencias de una Dieta Alcalina, de seguir a la naturaleza, de actuar de acuerdo a tu biología, de dedicarse tiempo, de levantarse más temprano, de limpiar el extractor, de aguantar el “bullying”, de manejar el stress, de soltar, de enfocarse, de amarse……

Cambio de insumos = cambio de resultados, la ciencia (naturaleza) es tan simple que solo con seguir sus pasos podemos sanar y vivir mejor!!

Aplausos y admiración para Noel, su esfuerzo y disciplina, por tomar el toro por los cuernos, por poner su salud en sus propias manos, y claro para sus super coaches VIP, Sofia ReyesOfelia Reyes y Sofía De la Rosa

Sus resultados son un motivo más para seguir trabajando de “salmones” nadando contracorriente, pero seguimos avanzando.

Read morehttp://phoreveryoung.wordpress.com
Follow us: @drrobertyoung on twitter and The pH Miracle Fan Club on Facebook

The Cure for Cancer? That’s an easy question to answer! The Cure for Cancer is Found in its Prevention NOT in its Treatment! – Dr. Robert O. Young

Do you know what rotten apples, grapefruit or bananas look like? If you do then you know what cancer cells look like. Cancer cells are nothing more that healthy cells that are spoiling because of a compromised environment! Look at the picture below and you will see colorized cancerous body cells rotting in their toxic acidic environment.

What compromises the internal environment of a human body that causes body cells to begin spoiling and rotting? The answer is simple! The body’s build-up of acidic metabolic and dietary waste that has not been properly eliminated through the four channels of elimination – urination, defecation, respiration and perspiration!

Cancer is not a noun but an adjective that describes what is happening to body cells in an acidic environment due to an acidic lifestyle and diet. www.phoreveryoung.com or http://www.phmiracle.com

To learn more about Dr. Robert O. Young go to: https://www.linkedin.com/in/drrobertoyoung

To read more of Dr. Young’s articles go to: www.phoreveryoung.wordpress.com and http://www.articlesofhealth.blogspot.com

To join Dr. Young on Twitter go to: @drrobertyoung

To watch more videos on YouTube go to: https://www.youtube.com/user/pHMiracleCenter

To Join Dr. Robert O. Young on Facebook go to:

1) The pH Miracle Fan Club: https://www.facebook.com/groups/50864627953/

2) Dr. Robert O. Young Fan Club: https://business.facebook.com/Dr.Robert.O.Young?business_id=10152751050143317

3) The pH Miracle Center: https://business.facebook.com/ThepHMiracle?business_id=10152751050143317

4) The pH Miracle Medical Association: https://www.facebook.com/pHMiracleMedicalAssociation?fref=ts
To purchase Dr. Young’s books or nutritional productts go to: www.phoreveryoung.com for wholesale or www.phmiracle.com for retailTo become a pH Miracle Coach or Microscopist go to: http://www.phoreveryoung.com or http://www.phmiracle.com or call: 760-751-8321 or 760-484-1075

To become a distributor for Dr. Robert O. Young’s nutritional and water products call: 760-751-8321 or 760-484-1075

To purchase a water purification system and ionizer go to: http://www.phoreveryoung.com or call: 760-751-8321 or 760-484-1075

%d bloggers like this: