Category Archives: Health

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.

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

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.

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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/

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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

The 4 Best Natural Organic Oils For Beautiful Wrinkle-Free Skin!

The 4 Best Natural Oils For Beautiful Wrinkle-Free Skin!

Dr. Robert Young

 MSc., DSc., PhD., N.D.

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

The 4 Best Natural Oils For Beautiful Wrinkle-Free Skin!

Putting oils on your face sounds very unusual and people usually turn to oil-free products thinking that oil will make the skin greasy and blemished. However, it has NOW been proven that using natural oil based skincare products is basically the best thing you can do when it comes to beautiful skin. The natural cole-pressed oil has the ability to soothe and nourish the skin, allowing the active ingredients in the skincare to penetrate deeper into the skin, boosting their beneficial properties.

There are various amazing cold-pressed organic oils out there, but the following are the best ones due to their proven skin-loving benefits:

Extra Virgin Cold-Pressed Avocado Oil

This oil is best for dry and dehydrated skin. It serves as a great moisturizer thanks to its vitamin A, vitamin E, and fatty acids content. It resembles the oils naturally produced by our skin, allowing it to be easily absorbing. This characteristic contributes to boosting the skin`s elasticity. The antioxidant in this oil, lutein may even prevent skin cancer. It can be applied prior taking a shower or be added to luscious bath. The warm water contributes to better absorption of moisture from the oil, and the towel dries off the excess. You will be surprised with the amazing unit-aging and anti-wrinkle benefits after 4 weeks of use!  To purchase USA grown organic raw cold-pressed avocado oil from Dr. Young’s Rancho del Sol go to: www.phoreveryoung.com or www.phmiracle.com

Rosehip Oil

The rosehip oil is best oil for acne-prone skin, fine lines, anti-aging, and uneven scars. It is capable of deep penetration into the skin, which in turn helps in the regeneration of the cells and increase of collagen production. It is high in omega-3 fatty acids, omega-6 fatty acids, and vitamin C, known to reduce inflammation and heal scar tissue. It also contains retinoic acid, the main ingredient in retinol products, which helps in the reduction of fine lines and wrinkles. It offers a whole range of anti-aging properties.

Besides its ability to prevent signs of premature aging, it can help repair acne-probe skin with mild scares and blemishes and it can also prevent more breakouts. This is due to the linoleic acid it contains, which when combined with avocado oil it becomes an amazing remedy. Hello clear, radiant skin!

Sesame Oil

This oil is ideal for wound-prone skin as well as for sun lovers. Apart from being one of the most commonly used cooking oils; the sesame oil has a significant part in the skincare world. As a matter of fact, this golden toned oil is a skin`s secret weapon. It resembles the sunscreens we normally use, as it protects the skin from sun damage, resisting up to 30 percent of UV rays. Moreover, it can help you a lot in case you`ve cut yourself. Just apply some sesame oil on cuts or wounds, and thanks to its anti-acid properties, it can help them heal faster. It is beneficial for skin conditions, such as eczema and psoriasis as well, because it provides anti-inflammatory or anti-acid properties, it nourishes the skin, and it gives the necessary moisture. It is rich in potent antioxidants, sesamol, and vitamin E. This content allows the oil to buffer excess metabolic and dietary acids as well as to repair and nourish acid-damaged skin cells, thanks to its high viscosity.

Extra Virgin Cold-Pressed Coconut Oil

It is best for eczema, normal, sensitive and/or dry skin. However, it is perfect for extra sensitive skin. It provides anti-acid, anti-inflammatory, and anti-mycotoxin properties. It also contains a small molecular structure, allowing easier absorption and giving the skin a smooth and soft texture. What contributes to its ability to treat skin conditions like eczema is the medium chain fatty acids which helps to retain the moisture content of the skin. This oil can be used all year round because it replenishes moisture after a direct sun exposure and it soothes the skin in the cold, windy months. Finally, it contains lauric acid which protects the skin`s surface and it serves as an amazing remedy for rough and dry skin.

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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.

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A Day To Never Forget – A Testimony of Joy and Peace!

A Day To Never Forget - A Testimony of Joy and Peace!
Dr. Robert Young

 MSc., DSc., Ph.D, ND

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

Monday September 21, 2015 A day to never forget. For this day was a day that brought the same feelings of elation and joy as did the days my daughters we born and put into my arms for the first time! Speechless as I looked in wonder and awe at their stunning beauty and unimaginable perfection.

Today, as I again looked in amazement at the scans that were repeated from August 17, just 5 weeks ago. Tears of joy ran down my cheeks as comparisons were made to the then and now. I was speechless to find the tumors had shrunk and were dying off. To that I now refer to all of you who have contributed in faith.

For all the prayers that were offered on my behalf. For all the heads that humbly bowed, For all the arms that were reverently folded and knees bent upon the floors of your dwelling spaces. For all of the kind and sincere acts of faith, expressed even in fasting. I now express my deepest gratitude to all of you. We can all celebrate our Father in Heaven, collectively. Our faith combined as increased and I feel honored to be the recipient of your “faith” and “His Will.”

My dear friends and family, not only were the areas of cancer concerns definitively reduced. But, many others areas of concern, within my body in were in trouble.

There is no doubt, that had I taken the conventional approach as the treatment at this time, these other areas of concern, that were not even on the radar would have not withstood the effects of chemotherapy and radiation, not to mention, it is at the cellar leve very dipilatingl. Because of the promptings (inspiration) that I felt guided to pursue, my body has shown tremendous healing and as a result of diet & lifestyle change. Miracles have taken place.

I express my deep and sincere gratitude to all of you for caring and being so kind and selfless in your contributing to help save my life. I feel as though, I have been holding my breath in anticipation of this monumental day. I felt ashamed that I had any level of doubt or fear. My Dad quickly reassured me that we are all human and those emotions are at times unavoidable.

The first call I made was to my Mom & Dad, then my Doll & Mcke. We all through cracking voices & flowing tears of joy, began expressing to God. While dad struggled through tears to offer a prayer of our emmense gratitude we once again had been a witness to Gods tender Mercies, as they have now begun to take place.

One might ask, “just how many miracles can one woman experience?” The answer, perhaps is there is no limit. Gods “Will” always comes first. Then When Mercy collides with Grace, I don’t think there is a score board keeping track
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For me, this journey has become a fascinating opportunity to really take a serious look at the bigger picture. This isn’t just about cancer at all. It’s about opportunity and the gift of friends and family coming together no matter the distance and uniting in love and faith, to help lift and cheer one another.

Thankfully, it’s me. Most of you know, that I have an amazing capacity to overcome and succeed. Sometimes, I forget that God knows me better than I know myself, the “what next?” really doesn’t matter because, He’s got my back… He always has and always will and it’s the same for all of us.

Remember, the times that are the most difficult, when we may feel that we are alone and fears, sneaks up on us? There are always only one set of footprints. He not only carries us to but through them.

It really all comes down to one thing and one thing and one thing only, that we have as strong as possible a trust in our Savior.

One response today came in a txt, as this scripture in Luke 8:48, And he said unto her, Daughter, be of good comfort; thy faith hath made thee whole; go in peace.

Today, when I did just that as I left doctor’s office. I walked outside I was acutely aware that what I was feeling was a sense of Peace. For a huge burden of the unknown had been lifted. Yay!

Riding home, I sent a few groups, txt announcing the wonderful news. “ALL PRAYERS ANSWERED” Fantastic news!!! My body is healing and I am so healthy and strong thanks to the pH Miracle for Cancer protocol!!! All areas are improving. My next apt. 12/21/15. Can you imagine the gift of “life” this years holiday season will bring? I am already in the “Joy Zone” as the messages went out, I would like to share the responses received back:

1. That’s great news Diana. I’s so happy to hear that your body is healing and recovering. We will keep the prayers coming.
2. Tears of joy for you beautiful
3. Great news! congratulations.
4. Hallelujah, that is wonderful news!!!!
5. Awesome news!!!
6. Yay! Praise God!! and you for working so hard to get healthier.
7. Oh Diana, this is such awesome news!!! I am thrilled for you. Prayers certainly have been answered.
8. Making me tear!!! Wonderful… I knew it! You are amazing and truly a light. I’m thinking and praying for you throughout the day! Everyday!
9. Oh, that is wonderful, Thank you heavenly Father for answered prayers!!!!
10. I knew you would overcome!! Just s speed bump like I said. Hooray Xxox
11. Praise God!
12. Amen! we will definitely continue to keep praying!
13. Great news! keep getting better
14. I am so happy for you!
15. This is great!! I am hopeful for you.
16. I was just thinking about you. So positive!!! That is such good news Di.
17. Hi Diana, I am so happy… I have been praying for you. I will call you soon.
18. Wonderful news
19. Yay!!! So exciting!!
20. That is amazing news!!! Just heard from cke too!!! So happy to read this. Stay strong!!! Xoxo
21. Omg! Tha’ts the best news ever!!! I can’t wait to hear all about it.
22. There is no limit to the number of miracles is there? That is awesome news. Thank you for sharing with me. Excellent to hear!!!
23.Omg!!! That’s wonderful Di!!!
24. What Awesome News. Lu very much and thanks so much. Can’t wait to see . Xxoo
25. Awesome

So many of you mentioned the word ” Good news,” to that I say “He Lives” Thank you for all your wonderful words of inspiration, where friends and faith have come together, as well as many prayers still being said. The outpouring of love. Wow, with 56 exclamation marks, that sets a record for so many, in the shortest time ever. Your enthusiasm is overwhelming.

Thank you all so very much!

Blessings, Di

To learn more read The pH Miracle, The pH Miracle revised and updated, Reverse Cancer Now and The pH Miracle for Cancer – http://www.phoreveryoung.com

The Future for Cancer Prevention and Treatment Here Today – The pH Miracle for Cancer!

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Cancer Metastasis Rev. 2014 Dec;33(4):1095-108. doi: 10.1007/s10555-014-9531-3.

Microenvironmental acidosis in carcinogenesis and metastases: new strategies in prevention and therapy.

Fais S 1, Venturi GGatenby B.

Author information:

  • 1Department of Therapeutic Research and Medicines Evaluation, Unit of Antitumor Drugs, Istituto Superiore di Sanità, Viale Regina Elena 299, Rome, Italy, stefano.fais@iss.it.

Abstract

Much effort is currently devoted to developing patient-specific cancer therapy based on molecular characterization of tumors. In particular, this approach seeks to identify driver mutations that can be blocked through small molecular inhibitors. However, this approach is limited by extensive intratumoral genetic heterogeneity, and, not surprisingly, even dramatic initial responses are typically of limited duration as resistant tumor clones rapidly emerge and proliferate. We propose an alternative approach based on observations that while tumor evolution produces genetic divergence, it is also associated with striking phenotypic convergence that loosely correspond to the well-known cancer “hallmarks”. These convergent properties can be described as driver phenotypes and may be more consistently and robustly expressed than genetic targets. To this purpose, it is necessary to identify strategies that are critical for cancer progression and metastases, and it is likely that these driver phenotypes will be closely related to cancer “hallmarks”. It appears that an antiacidic approach, by targetting a driver phenotype in tumors, may be thought as a future strategy against tumors in either preventing the occurrence of cancer or treating tumor patients with multiple aims, including the improvement of efficacy of existing therapies, possibly reducing their systemic side effects, and controlling tumor growth, progression, and metastasis. This may be achieved with existing molecules such as proton pump inhibitors (PPIs) and buffers such as sodium bicarbonate, citrate, or TRIS.

To learn more about the prevention and non-invasive treatment for Cancer  read the following introduction to the pH Miracle for Cancer  by Dr. Robert O. Young:

 The pH Miracle for Cancer is coming out next week. I thought you might enjoy a preview by reading the introduction – I am very, very grateful to be able to share with you my cancer research I call the New Biology(R). I also refer to my research as the pH Miracle – a new way of living, a new way of eating, a new way of thinking. Some of the questions I will be covering in the pH Miracle for Cancer include:

What is Cancer?
What is the cause of all cancers? (Is cancer a mutant cell, a virus, a mold? Or is cancer an acidic liquid?) Is cancer a noun or is it actually an adjective that explains what’s happening to the body cells? Are tumors bad or good? What role does the lymphatic system play in preventing and reversing a cancerous condition? The focus for preventing and reversing cancer must be on the alkaline pH of the body fluids as a systemic acidic condition. The key to preventing and/or reversing cancer is to obtain the necessary sustainable energy for optimal body function and the elimination of toxic acidic waste products from diet, metabolism, respiration and the environment that all contribute to the cause of a cancerous condition.

Most of the last 30 years of my cancer research has been focused on what is happening to the cells as it pertains specifically to the environment around those cells. I love this quote by Ralph Waldo Emerson: “What lies behind us and what lies before us are tiny matters compared to what lies within us.” The focus of my cancer research has been specifically on what lies within us and, more specifically, how the internal fluids of the body affect the health, energy, and vitality of the human cell, tissues, organs and glands. Dr Benjamin Rush, eminent physician and signer of the Declaration of Independence, said: “Unless we put medical freedom into the Constitution, the time will come when medicine will organize into an underground dictatorship. To restrict the art of healing to one class of men and deny equal privileges to others will constitute the Bastille of medical science. All such laws are un-American and despotic.”

As I think about my vision, the relative purpose of medicine I believe medicine must include not just the treatment but also the prevention of illness and the promotion of health and fitness, rather than just focusing all of our attention on a specific diagnosis or even the treatment of the disease. Because disease is an illusion! In reality, disease is the body trying to prevent over-acidification or fermentation or breakdown of the body cells, tissues, organs or glands.

Disease is the body in preservation mode trying to maintain the homeostasis of the internal fluids of the body, which are all alkaline.

I believe that the ultimate purpose of medicine is to help people discover something fundamental within themselves. And that is an awareness of the true source of wellbeing, the true source of joy, the true source of contentment that we all seek which lies in one’s mind and in one’s heart – which are the emotions and the spirit. And this is important so that you and I can all begin to be free from the process of grasping for happiness in a physical world.
To support this approach, this theory, I believe we must begin to embrace a more spiritual vision of ourselves and of humanity as a whole, while at the right time providing great love, care, and attention to the physical body. Then, and only then, will medicine (or the treatments that medicine is current performing) help people discover this non-physical, spiritual dimension of themselves. And when this happens I believe that we can live and work with less fear.

Rather than working in fear you can work in its opposite – you can work in faith. You are going to have less stress grasping to preserve the physical body at all costs, then I believe you can truly be happy, energetic, and free from ALL sickness and disease, especially cancer.

Several years ago Shelley and I had the opportunity to have a wonderful experience with Dr. Lawrence Carter who is the caretaker of the estate of Martin Luther King, at Morehouse College and also the protégé of M. L. King, and there he honored. The most important thing that I learned about Dr. Carter was his openness to not just thinking outside the box, because we talk a lot about thinking outside the box, but making our box of knowledge bigger. I would like to suggest rather than thinking outside the box as you contemplate my theories on the prevention and treatment of cancer but making your box bigger to include all truth. I would also suggest as you read this book that you do not have to think outside the box, you just need to make your box of knowledge bigger to allow for new technology, new biology, and new protocols that are effectively making the difference, specifically in the prevention and treatment of cancer.

I truly believe in the words of Gandhi when he said, “you must be the change you want to see.”

If you are looking for the cure for cancer, I believe you must be change you want to see. You’ll have to look at cancer differently, not outside the box but inside the box making it bigger. Expanding your views and your perspective as it relates to prevention and the true cause of cancer.

Now, before you start exploring the pH Miracle for Cancer, I must start by defining a ‘pH miracle’. I would suggest that a ‘pH miracle’ is a natural phenomenon, that is not currently understood by medical researchers, specifically in the cause and effect relationship. What is the cause? Is cancer a cause for disease? I say NO! Cancer is the body perfectly attempting to maintain alkaline homeostasis. Cancer is the body in perfect preservation mode trying to maintain its natural healthy alkaline design. So first, you must understand that cancer is unequivocally not a disease, but a symptom or better yet an effect of gastrointestinal, respiratory, environmental and metabolic acids that build up in the blood and then thrown off into the tissues poisoning and suppressing our immune system making it increasingly difficult to maintain the alkaline pH of the internal fluids of the body. Metabolic, respiratory, environmental and dietary acids also destroy the white cells’ ability to remove toxins and the cells which they spoil or degenerate.

What I’m simply suggesting is that cancer is not a cell, but an acidic toxic liquid that spoils and degenerated the body cells that make up our tissues, organs and glands. This happens when toxic acidic waste products are not properly eliminated through the four channels of elimination, which are urination, perspiration, respiration and defecation.

Let’s now look at the current medical definition of cancer. What is it? Cancer is a group of diseases characterized by uncontrolled growth and spread of abnormal body cells. If the spread is not controlled it can result in death. Cancer is caused by both external factors, some of which are known and are common in our society such as tobacco, chemicals, radiation (from our cellular phones) and internal factors: hormone imbalances, immune deficiency and gene mutations – which is what they’re suggesting. These factors may act together in a sequence to promote what is called carcinogenesis. This is the classical definition of cancer, taken directly from the American Cancer Society.

What is being suggested by current medical science is that the cancer is some mutating cell – a transmutation of the genes – triggered by internal or external factors. This is true but what is not understood is these internal or external factors are the acidic waste products of diet, metabolism, respiration and the environment. When you are dealing with any symptom or an effect, you need to look at the cause. Whether externally or internally, the focus traditionally has been to look at the matter or cells that make up your tissues, organs and glands rather than looking at the internal environment around the matter. And, to understand the cause of cancer is very simple just like the treatment. The New Biology® explains the cause and effect of all sickness and disease and specifically cancer as well as how to improve the quality and quantity of life without chemical therapy, radiation or surgery. The pH Miracle for Cancer is a drug-free protocol to a cure for cancer!

Let me give you an example. Enervation (ie, lack of energy), muscle weakness, you’ve probably seen the commercials on television, it’s a new disease they call restless legs syndrome (RLS) for which there are drugs that supposedly treat the syndrome. Current medical researchers want to put everything in a disease modality – a nice little box – that has a specific treatment. Yet restless legs syndrome is weakness or loss of electrical power to the muscles. It’s not a disease. But, by causing a flagging of the toxic elimination from the tissue, the blood becomes charged with these metabolic toxic acids and when it’s charged with these metabolic toxic acids the blood has to purify itself by throwing these metabolic toxic acids into the tissues to maintain its delicate pH balance of 7.365. This is what I call the body in preservation mode, which leads to what I refer to as latent tissue acidosis or acid build-up in the connective and fatty tissues. Acid is poison in the blood, and if that poison is not eliminated through urination, defecation, respiration or perspiration the body has to purify itself so it eliminates this acidic poison into the connective and fatty tissues. This is the disease, or is it? Not even skin challenges when the acids accumulate beyond the toleration point, a crisis takes place, which means that the acidic poison is being eliminated through the pores of the skin.

Looking at the 2012 statistics for cancer, this coming year in America we’re looking at 1,400,000 new cases of cancer. By the way, this statistic doesn’t even include skin cancer, which is actually bigger than lung cancer, breast cancer or prostate cancer combined. And, prostate cancer is known to be the leading cause of death in men while lung cancer being the leading cause of death in women. And yet when we look at cancer, the new incidents of cancer and the new diagnoses are skin cancers because the skin is the third kidney – the largest acid elimination organ for removing acidic toxic waste products. And if acids are not properly eliminated through normal elimination channels, then those acids are thrown out into the tissues and this is what’s not currently recognized or understood by medical science.

This is the way the blood maintains its delicate alkaline pH and purity by either eliminating acid through urination or defecation or throwing it into the connective or fatty tissues which leads to this crisis, this poisoning, this elimination through the pores of the skin, again the third kidney! And this is not a disease! The only disease is systemic, because acids flow out through your whole body. They are the waste products of metabolism, diet, respiration and the external toxic environment.

Your body is like a car. You are constantly on 24/7 and you require energy and when energy is being used, a waste product like carbon dioxide or carbon monoxide or lactic acid or uric acid is being created. So acid is constantly being created by the body cells, which has to be eliminated or it will cause cancer!
When energy is being used to think, to move, to breathe, at the same time an acidic waste product is being created and this acidic waste product needs to be eliminated. If the acid is not eliminated, it is pushed out into the connective tissue. It is your connective tissue that becomes the ‘acid catcher’ in order to maintain the purity and alkalinity of the blood. The blood has to maintain its purity and alkalinity and this is why the blood has a constant pH of 7.365. If it varies even just one-tenth of one point you can have ill effects. The proper healthy pH balance of the blood is 7.365. If the blood pH starts dropping or if it starts going up, the body will do whatever it can to maintain its delicate pH. This is very significant in order to understand the cause and treatment of cancer and why it’s not a cell but the spoiling of the cells by dietary and/or metabolic acids, which have not been properly eliminated through normal elimination. When you are enervated or fatigued you do not have the energy to move the acidic waste products out of the body to maintain the purity of the blood. When this happens the blood pushes these acidic waste products out into the connective and fatty tissues.

For example, when acidic waste elimination takes place through the mucus membrane of the nose, it is called a cold – catarrh of the nose. And when this crisis is repeated for years the mucus membrane thickens and ulcerates, and the bones enlarge, closing the passages. At this stage hay fever, then asthma develops. When the tonsils or any other respiratory passages become the seat of the crisis of acidity (because the acids were not properly eliminated through urination or defecation or respiration or perspiration) then we have tonsillitis, laryngitis, bronchitis, asthma, pneumonia, and finally cancer. You see, it’s progressive. It’s the same disease at different levels of acidity. All of these symptoms are happening in different progressions from the same thing – just different levels of states of acidosis.

When acid is located in the cranial cavity we have dementia, Alzheimer’s, Parkinson’s, muddle thinking, and/or forgetfulness. If the acids accumulate in the digestive area, we end up with irritable bowel syndrome, gastro intestinal problems, stenosis, and colitis. And, when the acids locate in the pelvic tissue, or in the breasts, we end up with micro-calcifications and finally cancerous breast and reproductive organs. When the body is in the preservation mode, it is using alkaline buffers such as calcium, potassium, magnesium and sodium to neutralize or solidify the acidic liquid waste.

This is why I first see, using Ultrasound imaging, micro-calcifications in the pelvic area and in the breast tissue prior to the cancerous breast condition. The buffering of toxic acidic waste, forming micro-calcifications always precedes the cancerous condition of the tissue, organ or gland. Even in prostate cancer.

Hence all cancerous conditions are the expulsion of acids from the blood and then the tissues, organs and glands at different points and are essentially the same character evolving from the same cause, namely systemic acidosis – a crisis of toxemia. The description can be extended to every organ of the body: the lung, the liver, the pancreas, the bowels, the brain, including the largest organs which have the highest incidents, the skin. Any organ that is enervated or fatigued below the average standard (from stress of habit, from overstressed at work, from worry, anxiety, fear, injury, etc.) may become the location of the crisis of systemic latent tissue acidosis. The symptoms are presented differently depending upon which organ is being affected. Which is what makes it appear as if every symptom complex is a separate and distinct disease. You need to begin thinking inside the box and make your box bigger.

I give thanks to this new light and knowledge shed upon nomen culture naming disease by the philosophy of The New Biology(R), every symptom complex goes back to the one and only cause of all so-called cancers, namely systemic latent tissue acidosis. To find the cause of all symptomologies – lung cancer, breast cancer, brain cancer, bowel cancer, pancreatic cancer, thyroid cancer, and prostate cancer – you start with colds and catarrh, and watch the pathology as is it travels from irritation to catarrh to inflammation to induration to ulceration and finally to degeneration or cancer – Nothing more than rotting degenerating tissues, organs or glands. And what is causing this transformation or the degeneration of the cell(s), including the gene transmutation? It is simply the spoiling of the cell(s) due to the build-up of dietary, respiratory, environmental and/or metabolic acids, which have not been properly eliminated through urination, defecation, respiration or perspiration!

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Have you ever opened a refrigerator and smelt the spoiling of food at the back? What you are smelling is the acidic wastes from spoiling food! It’s not some germ, it’s not some virus, it’s not some mold that’s breaking the food down, it’s the acidic waste products that are breaking the tissue down and giving rise to the symptomatology. Mold is like a smoking gun, the bullet being the acid. And yet it’s not the bullet or the acid that kills, and surely not the smoke or some gene mutation, or some bacteria or virus, but it is the person himself or herself that is pulling the acidic lifestyle and dietary trigger which then releases the acids that then tenderizes or spoils or rots the cells that make up your tissues, organs and glands. And, a cancerous condition always expresses itself first in the weakest parts of the body.

Nature’s order is interfered with by innovating acidic lifestyle and dietary habits until acidosis is established.

A vaccination as evidenced by the Spanish flu epidemic or an infection, in truth is literally an out-fection from the same source causing the most vulnerable organ, specifically the bowels, to take on organic or anatomical changes. The organ however has nothing to do with the cause, and directing treatment to the organ is actually compounding the problem. You cannot treat disease when in reality disease is the body in preservation mode trying to re-establish alkaline homeostasis when in a state of systemic acidosis that is affecting the weakest parts of the body, first!

When you realize that breast cancer is the second leading cause of death in women and these fatty tissues (breast areas) are being used by the body to bind or collect acidic waste products in order to protect the organs that sustain life. And, by the way, when one does a mammogram and sees these micro-calcification in the breast tissue, this is an indication of a state of tissue acidosis – the body’s defensive mechanism to relieve or remove or neutralize and solidify acidity that has not been properly eliminated though urination, defecation, respiration or perspiration.

If you are dealing with a cancerous prostate, you are dealing with localized acidity. If you are dealing with lung cancer, you are dealing with localized acidity that has been caused by external or internal forces even though a cancerous condition begins from within. As you take in tobacco smoke, there are acids or toxins or poisons – one being sugar which breaks down to acetaldehyde, which tenderizes and rots the lung tissues. Tobacco smoking is not an addiction of nicotine alone. It is an addiction of sugar, which causes excess acidity in the lung causing lung cancer. The cause is always constant, ever-present, always the same, only the effects change. To illustrate, a catarrh of the stomach presents first irritation, then inflammation, then ulceration, induration and finally degeneration or a cancerous stomach. Cancer is not at the first, it’s the culmination of deteriorating or broken tissue spoiled by an over-acidic stomach from an over-acidic lifestyle and diet.

Most people in the world are challenged with the symptomatology of indigestion, which can include acid reflux, bloating, heartburn, burping, diarrhea, or even constipation. The proper way to study a disease is to study health in every aspect. Disease is perverted health. Cancer is perverted health – any influence that lowers energy becomes disease-producing.

There’s an important question now to answer. Why do I crave sugar? It’s interesting when doing an MRI or a CAT scan. What is used but radioactive sugar that is taken up by the acidic cancerous cells – not cancer cells because we don’t have cancer cells, we have acidic cells or cancerous cells – cells that have been spoiled by the environment in which they live. So sugar cravings are the body’s need for sustainable energy. And energy can only be transported through a matrix of salt. Therefore sugar cravings are the body’s needs for salt, not sugar. I would suggest that sugar is an acid of cellular transformation – a waste product – not a product of energy, but a by-product of what the body truly uses which is electrical potential in the form of electrons.

The body doesn’t use carbohydrates, the body uses electrons to run. The body is electrical. And sugar is nothing more than an acidic waste product of cellular breakdown and transformation. Isn’t that what happens to the banana? As the banana moves from irritation to inflammation to induration and then to cancer, going from green to yellow to brown, getting its “liver spots” the same way you get liver spots, through excess fermentation and rotting. You do not say the banana has cancer, you say the banana is spoiling. In the same way you shouldn’t say that the lung has cancer but rather that the lung is spoiling – it is cancerous. Cancer is not a noun but an adjective expressing the process of cellular transformation. Again, sugar is the waste product. In fact, that’s why a banana gets sweeter and sweeter as it ferments. Consistently in my cancer research I see that we have a release of sugar from the breakdown of tissues, organs or glands. And to overcome sugar cravings you don’t have to eat sugar, you need to eat more salt. The secondary metabolites of this primary acid or sugar are acetaldehyde and ethanol alcohol. So sugar cravings are the body’s signal that the body needs more sustainable energy. You need energy to remove the acids of diet and metabolism – the body utilizing electrons for energy purposes. Food, water, sun, minerals, vitamins, drugs… are common choices made by us to achieve sustainable energy, but yet what you are looking for are the electrons from these sources. And your choices will determine whether or not your cravings will lead to true sustainable energy which maintains the alkaline integrity of the fluids of body and therefore the integrity of the tissues, organs and glands, or gives you false energy which creates this over-acidic state that leads to latent tissue acidosis which begins the process of spoiling of the tissues, organs and glands and finally a degenerative or cancerous condition.

Sugar stimulates and gives the body a deceptive quick-fix – it’s illusionary – whereas salt provides the matrix of life and gives your body the rise in sustainable energy, over a longer period of time, without the high and extreme lows that come from eating an acid – whether it be sugar or any other acidic foods or drinks.

It is the skin that suffers most, because if the body can’t eliminate the acids that are created through energy use, it throws the acidic wastes out into the connective and fatty tissues and into the lymphatic system. This is why the lymphatic system is so critical in the prevention of cancer and in the treatment of cancer, because it is the lymphatic system that is the vacuum cleaner of the acids that are in the interstitial fluids of the body, pulling these poisonous acids out in order to maintain the integrity of the tissue through diaphramic breathing and perspiration (that is if you are perspiring, which is one of the most important things you need to do on a daily basis to remove cancer causing acids). If you cannot eliminate your acidic wastes completely through urination, respiration or defecation then your body urinates through the skin – which is why there is over a million cases of skin cancer a year in the United States alone. It’s not talked about. Why? Because the etiology of skin cancer is not understood. It is unknown. Scientists don’t know what causes basal cell carcinoma, melanoma, they do not understand it because they don’t understand latent tissue acidosis and the importance of the lymphatic system as the vacuum cleaner to remove poisonous acidic wastes out via the kidneys and through perspiration. But people are not exercising, and this is why obesity and a lack of exercise have been associated with cancer. Yet when you are moving your body you are moving the acidic wastes out of the connective and fatty tissues, organs and glands. The lymphatic system, unlike the circulatory system, does not have a pump (the heart), it actually flows through movement. It is the diaphragm muscle that acts as a pump for the lymphatic system that moves acidic wastes through the system – out through perspiration or back into general circulation to be eliminated through urination.

And if you have a cancerous condition you have to pee your way to health. Because cancer is not a cell, but a poisonous acidic liquid. A cancer cell is a cell that has been spoiled or poisoned by the metabolic, respiratory, environmental and/or gastrointestinal acids that are produced internally, or may be taken in via the lungs or skin. That’s when the body will go into the preservation mode by forming fibrous materials, which cross-link to encapsulate the spoiled cancerous cells and thus forming the protective tumor. Hence, the tumor is the body’s protective mechanism to encapsulate spoiled or poisoned acidic cells from excess acidic wastes which have not been properly eliminated through urination, defecation, respiration and/or perspiration. The tumor is the body’s solution to protect healthy cells that make up tissues, organs and glands of the body. So, the tumor is not the problem. Let the tumor go. Let it do its job. The focus must be placed not on the tumor but on the internal environment around the tumor, which is full of acidic cells. One of the common acids which is in higher concentration around all tumors is lactic acid. Lactic acid is a by-product of metabolism when you are in a state of oxygen deprivation. Think of any cancerous condition as a systemic acidic condition that affects first the weakest parts of the body, not a local problem that metastasizes. You see metastasis is localized acids that spoil other cells much like a rotten apple placed in the center of a bushel of healthy apples will spoil the whole bushel. I call this the ‘domino effect’ where one acidic cell spoils another healthy cell causing a chain reaction. The body stops the ‘domino effect’ by forming the tumor around the cancerous or acidic body cells.

Therefore, there is no such thing as a cancer cell. A cancer cell in reality is a cancerous cell. Cancer is an adjective expressing the spoiling body cells that are rotting in an over-acidic environment. A cancerous cell was once a healthy cell that has been spoiled from an over-acidic lifestyle and diet and the body’s inability to remove these acids through the proper channels of elimination.
The only solution to the acidic toxic liquids that poison our body cells causing the effect that medical doctors call cancer, is to change the environment. It has to be a contextual approach. You must restore and maintain the alkaline design of the human body if you want to prevent or reverse a cancerous condition. This has been my great discovery of the 21st century – that the human organism is alkaline by design and acidic by function. Every part of the body that makes up every anatomical element, that makes up your genetic material, that makes up your body cells, every single part has to be bathed in an alkaline fluid which needs to be purified every 24 hours to remain healthy.

Early in the 19th century, beginning on January 17, 1912, a famous French physiologist of the Rockefeller Institute and Nobel Prize winner, Dr. Alexis Carrel, removed a very small piece of heart muscle from an un-hatched chicken embryo—still warm and living—and placed it in fresh nutrient solution in a glass flask of his own design. He transferred the tissue every forty-eight hours, during which time it doubled in size and had to be trimmed before being moved to its new flask. Every time he moved the heart he would put it into an alkaline saline solution with the appropriate alkalizing minerals. Twenty years later the heart tissue was still growing. Keep in mind that the average chicken lives for 5 – 7 years. So, after getting bored of singing “Happy Birthday” to the chicken heart for over twenty years he decided to pull the plug and not change the fluids every 48 hours and the heart finally died.

This is a very important discovery, which very few people know about. Why? Because it answers the question about why cells live and why cells die. You see, the life expectancy of the human cell is infinite. The body cells become compromised by their environment. Once you understand that matter cannot be created nor can it be destroyed it can only change its form or function, then you will realize that the environment is everything, the terrain is everything, and the cell is subservient to that.

The secret to Dr. Carrel’s chicken heart surviving for twenty years lies in this knowledge, this New Biology, this new way of living and thinking as we expand the box rather than thinking outside the box, that the cell is only as healthy as the alkaline fluids it is bathed in. The heart is only as healthy as the cells and the fluids they are bathed in. If you have any cancerous condition, this cancerous condition is the expression of your internal environment. The human cell will only breakdown in an acidic environment and become cancerous.

Carrel’s experiment brought me to the modern New Biology, the new understanding, the new expansion, the new medicine and the new definition of cancer – that the composition of our body fluids that bath the outside of our cells must be controlled very carefully from moment to moment and day-to-day with no single important constituent varying more than a one percent. This condition of health can be controlled and you can do it yourself!

In 1932 Otto Warburg received his Nobel Prize in medicine for discovering the cause of cancer. He described it as a cell changing its mode of respiration, its mode of metabolism – from respiration to fermentation. He suggested that cancer was the result of acidic environment, a state of oxygen deprivation. Warburg also wrote a paper entitled, “The Prime Cause and Prevention of Cancer.” He states: “There is no disease whose prime cause is better known – over acidity.”

When you understand this you realize that all conditions of cancer potentially can be reversed if the treatments are focused on the fluids and not the cells of the body. Therefore it doesn’t matter what the cancerous condition is, because cancer is not the cause but the effect of an over-acidic lifestyle and diet which is the cause of cancer. It’s you pulling the acidic lifestyle and dietary trigger that causes cancer. You do NOT get CANCER – You DO CANCER with your daily lifestyle and dietary choices!

After 30 years of doing blood research, after looking at thousands and thousands of cancerous patients, I’ve never seen healthy blood or an alkaline internal environment – whether testing the pH of the saliva, or the urine, or the blood, or the sweat, or the tears – they are all acidic in an over-acidic internal environment. I have come to understand that the human organism is alkaline by design and acidic by function, and if you maintain this alkaline design of your body through an alkaline lifestyle and diet you WiLL prevent all cancerous conditions. For the cure of cancer is not found in its treatment, because a cancerous condition is the body in preservation mode trying to restore its alkalinity. The cure for a cancerous condition will not be found in its treatment of the tissues but in maintaining the alkaline design of the body fluids.

As Thomas Edison said: “The doctor of the future will give no medicine, but will involve the patient in the proper use of food, fresh air and exercise.

The future is here and NOW and is found in the following chapters of pH Miracle for Cancer.

My hope is The pH Miracle for Cancer will expand your box of truth and knowledge to protect you from the acidic condition medical science calls Cancer.

To pre-order The pH Miracle for Cancer go to: http://www.phoreveryoung.com

The digital version of The pH Miracle for Cancer is NOW Available just order on line at: http://www.phoreveryoung.com

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References

1. Hanna G, Fontanella A, Palmer G, Shan S, Radiloff DR, Zhao Y, Irwin D, Hamilton K, Boico A, Piantadosi CA, Blueschke G, Dewhirst M, McMahon T, Schroeder T. Automated measurement of blood flow velocity and direction and hemoglobin oxygen saturation in the rat lung using intravital microscopy. American Journal of Physiology. Lung Cellular and Molecular Physiology. 2013;304(2):L86–L91.[PubMed]

2. Yang, K.R., Mooney, S., Zarif, J.C., Coffey, D.S., Taichman, R.S. & Pienta, K.J. (2014). Niche inheritance: a cooperative pathway to enhance cancer cell fitness through ecosystem engineering. Journal of Cellular Biochemistry. [PMC free article]  [PubMed]

3. Gatenby RA, Gillies RJ. Why do cancers have high aerobic glycolysis? Nature reviews. Cancer. 2004;4(11):891–899.  [PubMed]

4. Lee WY, Huang SC, Hsu KF, Tzeng CC, Shen WL. Roles for hypoxia-regulated genes during cervical carcinogenesis: somatic evolution during the hypoxia-glycolysis-acidosis sequence. Gynecologic Oncology. 2008;108(2):377–384.  [PubMed]

5. Ibrahim-Hashim A, Cornnell HH, Abrahams D, Lloyd M, Bui M, Gillies RJ, Gatenby RA. Systemic buffers inhibit carcinogenesis in TRAMP mice. The Journal of Urology. 2012;188(2):624–631.[PMC free article]  [PubMed]

6. Estrella V, Chen T, Lloyd M, Wojtkowiak J, Cornnell HH, Ibrahim-Hashim A, Bailey K, Balagurunathan Y, Rothberg JM, Sloane BF, Johnson J, Gatenby RA, Gillies RJ. Acidity generated by the tumor microenvironment drives local invasion. Cancer Research. 2013;73(5):1524–1535.[PMC free article]  [PubMed]

7. Robey IF, Baggett BK, Kirkpatrick ND, Roe DJ, Dosescu J, Sloane BF, Hashim AI, Morse DL, Raghunand N, Gatenby RA, Gillies RJ. Bicarbonate increases tumor pH and inhibits spontaneous metastases. Cancer Research. 2009;69(6):2260–2268. [PMC free article]  [PubMed]

8. Warburg O. On the origin of cancer cells. Science (New York, N.Y.) 1956;123(3191):309–314.[PubMed]

9. Zu XL, Guppy M. Cancer metabolism: facts, fantasy, and fiction. Biochemical and Biophysical Research Communications. 2004;313(3):459–465.  [PubMed]

10. Kroemer G. Mitochondria in cancer. Oncogene. 2006;25(34):4630–4632.  [PubMed]

11. Hume DA, Weidemann MJ. Role and regulation of glucose metabolism in proliferating cells. Journal of the National Cancer Institute. 1979;62(1):3–8.  [PubMed]

12. Vander Heiden MG, Cantley LC, Thompson CB. Understanding the Warburg effect: the metabolic requirements of cell proliferation. Science (New York, N.Y.) 2009;324(5930):1029–1033.[PMC free article]  [PubMed]

13. DeBerardinis RJ, Mancuso A, Daikhin E, Nissim I, Yudkoff M, Wehrli S, Thompson CB. Beyond aerobic glycolysis: transformed cells can engage in glutamine metabolism that exceeds the requirement for protein and nucleotide synthesis. Proceedings of the National Academy of Sciences of the United States of America. 2007;104(49):19345–19350. [PMC free article]  [PubMed]

14. Lemons JM, Feng XJ, Bennett BD, Legesse-Miller A, Johnson EL, Raitman I, Pollina EA, Rabitz HA, Rabinowitz JD, Coller HA. Quiescent fibroblasts exhibit high metabolic activity. PLoS Biology. 2010;8(10):e1000514. [PMC free article]  [PubMed]

15. Gillies RJ, Robey I, Gatenby RA. Causes and consequences of increased glucose metabolism of cancers. Journal of Nuclear Medicine: Official Publication, Society of Nuclear Medicine. 2008;49(Suppl 2):24S–42S.  [PubMed]

16. Gatenby RA. The potential role of transformation-induced metabolic changes in tumor-host interaction. Cancer Research. 1995;55(18):4151–4156.  [PubMed]

17. Gillies RJ, Martinez-Zaguilan R, Martinez GM, Serrano R, Perona R. Tumorigenic 3T3 cells maintain an alkaline intracellular pH under physiological conditions. Proceedings of the National Academy of Sciences of the United States of America. 1990;87(19):7414–74

18. [PMC free article]  [PubMed]18. Gatenby RA, Gillies RJ. A microenvironmental model of carcinogenesis. Nature Reviews. Cancer. 2008;8(1):56–61.  [PubMed]

19. Garcia SB, Novelli M, Wright NA. The clonal origin and clonal evolution of epithelial tumours. International Journal of Experimental Pathology. 2000;81(2):89–116. [PMC free article]  [PubMed]

20. Nowell PC. The clonal evolution of tumor cell populations. Science (New York, N.Y.) 1976;194(4260):23–28.  [PubMed]

21. Ilyas M, Straub J, Tomlinson IP, Bodmer WF. Genetic pathways in colorectal and other cancers. European Journal of Cancer (Oxford, England: 1990) 1999;35(3):335–351.  [PubMed]

22. Fearon ER, Vogelstein B. A genetic model for colorectal tumorigenesis. Cell. 1990;61(5):759–767.[PubMed]

23. Silva AS, Gatenby RA, Gillies RJ, Yunes JA. A quantitative theoretical model for the development of malignancy in ductal carcinoma in situJournal of Theoretical Biology. 2010;262(4):601–613.  [PubMed]

24. Gatenby RA, Smallbone K, Maini PK, Rose F, Averill J, Nagle RB, Worrall L, Gillies RJ. Cellular adaptations to hypoxia and acidosis during somatic evolution of breast cancer. British Journal of Cancer. 2007;97(5):646–653. [PMC free article]  [PubMed]

25. Smallbone K, Gatenby RA, Gillies RJ, Maini PK, Gavaghan DJ. Metabolic changes during carcinogenesis: potential impact on invasiveness. Journal of Theoretical Biology. 2007;244(4):703–713.[PubMed]

26. Wykoff CC, Beasley N, Watson PH, Campo L, Chia SK, English R, Pastorek J, Sly WS, Ratcliffe P, Harris AL. Expression of the hypoxia-inducible and tumor-associated carbonic anhydrases in ductal carcinoma in situ of the breast. The American Journal of Pathology. 2001;158(3):1011–1019.[PMC free article]  [PubMed]

27. Huber V, De Milito A, Harguindey S, Reshkin SJ, Wahl ML, Rauch C, Chiesi A, Pouyssegur J, Gatenby RA, Rivoltini L, Fais S. Proton dynamics in cancer. Journal of Translational Medicine. 2010;8:57.[PMC free article]  [PubMed]

28. Webb BA, Chimenti M, Jacobson MP, Barber DL. Dysregulated pH: a perfect storm for cancer progression. Nature Reviews. Cancer. 2011;11(9):671–677.  [PubMed]

29. Rich IN, Worthington-White D, Garden OA, Musk P. Apoptosis of leukemic cells accompanies reduction in intracellular pH after targeted inhibition of the Na(+)/H(+) exchanger. Blood. 2000;95(4):1427–1434.  [PubMed]

30. Che XF, Zheng CL, Akiyama S, Tomoda A. 2-Aminophenoxazine-3-one and 2-amino-4,4alpha-dihydro-4alpha,7-dimethyl-3H-phenoxazine-3-one cause cellular apoptosis by reducing higher intracellular pH in cancer cells. Proceedings of the Japan Academy. Series B, Physical and Biological Sciences. 2011;87(4):199–213. [PMC free article]  [PubMed]

31. Nagata H, Che XF, Miyazawa K, Tomoda A, Konishi M, Ubukata H, Tabuchi T. Rapid decrease of intracellular pH associated with inhibition of Na+/H+ exchanger precedes apoptotic events in the MNK45 and MNK74 gastric cancer cell lines treated with 2-aminophenoxazine-3-one. Oncology Reports. 2011;25(2):341–346.  [PubMed]

32. Di Sario A, Bendia E, Omenetti A, De Minicis S, Marzioni M, Kleemann HW, Candelaresi C, Saccomanno S, Alpini G, Benedetti A. Selective inhibition of ion transport mechanisms regulating intracellular pH reduces proliferation and induces apoptosis in cholangiocarcinoma cells. Digestive and Liver Disease: Official Journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver. 2007;39(1):60–69.  [PubMed]

33. Roepe PD. Analysis of the steady-state and initial rate of doxorubicin efflux from a series of multidrug-resistant cells expressing different levels of P-glycoprotein. Biochemistry. 1992;31(50):12555–12564.  [PubMed]

34. Murakami T, Shibuya I, Ise T, Chen ZS, Akiyama S, Nakagawa M, Izumi H, Nakamura T, Matsuo K, Yamada Y, Kohno K. Elevated expression of vacuolar proton pump genes and cellular PH in cisplatin resistance. International Journal of Cancer. Journal International Du Cancer. 2001;93(6):869–874.[PubMed]

35. Martinez-Zaguilan R, Raghunand N, Lynch RM, Bellamy W, Martinez GM, Rojas B, Smith D, Dalton WS, Gillies RJ. pH and drug resistance. I. Functional expression of plasmalemmal V-type H+-ATPase in drug-resistant human breast carcinoma cell lines. Biochemical Pharmacology. 1999;57(9):1037–1046.[PubMed]

36. Keizer HG, Joenje H. Increased cytosolic pH in multidrug-resistant human lung tumor cells: effect of verapamil. Journal of the National Cancer Institute. 1989;81(9):706–709.  [PubMed]

37. Altan N, Chen Y, Schindler M, Simon SM. Defective acidification in human breast tumor cells and implications for chemotherapy. The Journal of Experimental Medicine. 1998;187(10):1583–1598.[PMC free article]  [PubMed]

38. Belhoussine R, Morjani H, Sharonov S, Ploton D, Manfait M. Characterization of intracellular pH gradients in human multidrug-resistant tumor cells by means of scanning microspectrofluorometry and dual-emission-ratio probes. International Journal of Cancer. Journal International Du Cancer. 1999;81(1):81–89.  [PubMed]

39. Becelli R, Renzi G, Morello R, Altieri F. Intracellular and extracellular tumor pH measurement in a series of patients with oral cancer. The Journal of Craniofacial Surgery. 2007;18(5):1051–1054.  [PubMed]

40. Raghunand N, Mahoney B, van Sluis R, Baggett B, Gillies RJ. Acute metabolic alkalosis enhances response of C3H mouse mammary tumors to the weak base mitoxantrone. Neoplasia (New York, N.Y.) 2001;3(3):227–235. [PMC free article]  [PubMed]

41. Simon S, Roy D, Schindler M. Intracellular pH and the control of multidrug resistance. Proceedings of the National Academy of Sciences of the United States of America. 1994;91(3):1128–1132.[PMC free article]  [PubMed]

42. Ouar Z, Bens M, Vignes C, Paulais M, Pringel C, Fleury J, Cluzeaud F, Lacave R, Vandewalle A. Inhibitors of vacuolar H+-ATPase impair the preferential accumulation of daunomycin in lysosomes and reverse the resistance to anthracyclines in drug-resistant renal epithelial cells. The Biochemical Journal. 2003;370(Pt 1):185–193. [PMC free article]  [PubMed]

43. Federici C, Petrucci F, Caimi S, Cesolini A, Logozzi M, Borghi M, D’Ilio S, Lugini L, Violante N, Azzarito T, Majorani C, Brambilla D, Fais S. Exosome release and low pH belong to a framework of resistance of human melanoma cells to cisplatin. PloS One. 2014;9(2):e88193. [PMC free article][PubMed]

44. Parolini I, Federici C, Raggi C, Lugini L, Palleschi S, De Milito A, Coscia C, Iessi E, Logozzi M, Molinari A, Colone M, Tatti M, Sargiacomo M, Fais S. Microenvironmental pH is a key factor for exosome traffic in tumor cells. The Journal of Biological Chemistry. 2009;284(49):34211–34222.[PMC free article]  [PubMed]

45. Fais S. Proton pump inhibitor-induced tumour cell death by inhibition of a detoxification mechanism. Journal of Internal Medicine. 2010;267(5):515–525.  [PubMed]

46. Nishi T, Forgac M. The vacuolar (H+)-ATPases—nature’s most versatile proton pumps. Nature Reviews. Molecular Cell Biology. 2002;3(2):94–103.  [PubMed]

47. Sennoune SR, Martinez-Zaguilan R. Plasmalemmal vacuolar H+-ATPases in angiogenesis, diabetes and cancer. Journal of Bioenergetics and Biomembranes. 2007;39(5–6):427–433.  [PubMed]

48. Chung C, Mader CC, Schmitz JC, Atladottir J, Fitchev P, Cornwell ML, Koleske AJ, Crawford SE, Gorelick F. The vacuolar-ATPase modulates matrix metalloproteinase isoforms in human pancreatic cancer. Laboratory Investigation; A Journal of technical Methods and Pathology. 2011;91(5):732–743.[PMC free article]  [PubMed]

49. Sennoune SR, Bakunts K, Martinez GM, Chua-Tuan JL, Kebir Y, Attaya MN, Martinez-Zaguilan R. Vacuolar H+-ATPase in human breast cancer cells with distinct metastatic potential: distribution and functional activity. American Journal of Physiology. Cell Physiology. 2004;286(6):C1443–C1452.[PubMed]

50. Martinez-Zaguilan R, Lynch RM, Martinez GM, Gillies RJ. Vacuolar-type H(+)-ATPases are functionally expressed in plasma membranes of human tumor cells. The American Journal of Physiology. 1993;265(4 Pt 1):C1015–C1029.  [PubMed]

51. Xu J, Xie R, Liu X, Wen G, Jin H, Yu Z, Jiang Y, Zhao Z, Yang Y, Ji B, Dong H, Tuo B. Expression and functional role of vacuolar H(+)-ATPase in human hepatocellular carcinoma. Carcinogenesis. 2012;33(12):2432–2440.  [PubMed]

52. Avnet S, Di Pompo G, Lemma S, Salerno M, Perut F, Bonuccelli G, Granchi D, Zini N, Baldini N. V-ATPase is a candidate therapeutic target for Ewing sarcoma. Biochimica et Biophysica Acta. 2013;1832(8):1105–1116.  [PubMed]

53. Philippe JM, Dubois JM, Rouzaire-Dubois B, Cartron PF, Vallette F, Morel N. Functional expression of V-ATPases in the plasma membrane of glial cells. Glia. 2002;37(4):365–373.  [PubMed]

54. Hinton A, Sennoune SR, Bond S, Fang M, Reuveni M, Sahagian GG, Jay D, Martinez-Zaguilan R, Forgac M. Function of a subunit isoforms of the V-ATPase in pH homeostasis and in vitro invasion of MDA-MB231 human breast cancer cells. The Journal of Biological Chemistry. 2009;284(24):16400–16408. [PMC free article]  [PubMed]

55. Lu Q, Lu S, Huang L, Wang T, Wan Y, Zhou CX, Zhang C, Zhang Z, Li X. The expression of V-ATPase is associated with drug resistance and pathology of non-small cell lung cancer. Diagnostic Pathology. 2013;8:145. [PMC free article]  [PubMed]

56. Michel V, Licon-Munoz Y, Trujillo K, Bisoffi M, Parra KJ. Inhibitors of vacuolar ATPase proton pumps inhibit human prostate cancer cell invasion and prostate-specific antigen expression and secretion. International Journal of Cancer. Journal International Du Cancer. 2013;132(2):E1–E10. [PMC free article][PubMed]

57. Nishisho T, Hata K, Nakanishi M, Morita Y, Sun-Wada GH, Wada Y, Yasui N, Yoneda T. The a3 isoform vacuolar type H(+)-ATPase promotes distant metastasis in the mouse B16 melanoma cells. Molecular Cancer Research: MCR. 2011;9(7):845–855.  [PubMed]

58. Luciani F, Spada M, De Milito A, Molinari A, Rivoltini L, Montinaro A, Marra M, Lugini L, Logozzi M, Lozupone F, Federici C, Iessi E, Parmiani G, Arancia G, Belardelli F, Fais S. Effect of proton pump inhibitor pretreatment on resistance of solid tumors to cytotoxic drugs. Journal of the National Cancer Institute. 2004;96(22):1702–1713.  [PubMed]

59. De Milito A, Marino ML, Fais S. A rationale for the use of proton pump inhibitors as antineoplastic agents. Current Pharmaceutical Design. 2012;18(10):1395–1406.  [PubMed]

60. Xu K, Mao X, Mehta M, Cui J, Zhang C, Mao F, Xu Y. Elucidation of how cancer cells avoid acidosis through comparative transcriptomic data analysis. PloS One. 2013;8(8):e71177. [PMC free article][PubMed]

61. Katara, G.K., Jaiswal, M.K., Kulshrestha, A., Kolli, B., Gilman-Sachs, A. & Beaman, K.D. (2013). Tumor-associated vacuolar ATPase subunit promotes tumorigenic characteristics in macrophages. Oncogene.  [PubMed]

62. Huang L, Lu Q, Han Y, Li Z, Zhang Z, Li X. ABCG2/V-ATPase was associated with the drug resistance and tumor metastasis of esophageal squamous cancer cells. Diagnostic Pathology. 2012;7:180.[PMC free article]  [PubMed]

63. Garcia-Garcia A, Perez-Sayans Garcia M, Rodriguez MJ, Antunez-Lopez J, Barros-Angueira F, Somoza-Martin M, Gandara-Rey JM, Aguirre-Urizar JM. Immunohistochemical localization of C1 subunit of V-ATPase (ATPase C1) in oral squamous cell cancer and normal oral mucosa. Biotechnic & Histochemistry: Official Publication of the Biological Stain Commission. 2012;87(2):133–139.  [PubMed]

64. Ohta T, Numata M, Yagishita H, Futagami F, Tsukioka Y, Kitagawa H, Kayahara M, Nagakawa T, Miyazaki I, Yamamoto M, Iseki S, Ohkuma S. Expression of 16 kDa proteolipid of vacuolar-type H(+)-ATPase in human pancreatic cancer. British Journal of Cancer. 1996;73(12):1511–1517. [PMC free article][PubMed]

65. De Milito A, Canese R, Marino ML, Borghi M, Iero M, Villa A, Venturi G, Lozupone F, Iessi E, Logozzi M, Della Mina P, Santinami M, Rodolfo M, Podo F, Rivoltini L, Fais S. pH-dependent antitumor activity of proton pump inhibitors against human melanoma is mediated by inhibition of tumor acidity. International Journal of Cancer. Journal International Du Cancer. 2010;127(1):207–219.  [PubMed]

66. Malo ME, Fliegel L. Physiological role and regulation of the Na+/H+ exchanger. Canadian Journal of Physiology and Pharmacology. 2006;84(11):1081–1095.  [PubMed]

67. Daniel C, Bell C, Burton C, Harguindey S, Reshkin SJ, Rauch C. The role of proton dynamics in the development and maintenance of multidrug resistance in cancer. Biochimica et Biophysica Acta. 2013;1832(5):606–617.  [PubMed]

68. Harguindey S, Arranz JL, Polo Orozco JD, Rauch C, Fais S, Cardone RA, Reshkin SJ. Cariporide and other new and powerful NHE1 inhibitors as potentially selective anticancer drugs–an integral molecular/biochemical/metabolic/clinical approach after one hundred years of cancer research. Journal of Translational Medicine. 2013;11:282. [PMC free article]  [PubMed]

69. Amith SR, Fliegel L. Regulation of the Na+/H+ exchanger (NHE1) in breast cancer metastasis. Cancer Research. 2013;73(4):1259–1264.  [PubMed]

70. Magalhaes MA, Larson DR, Mader CC, Bravo-Cordero JJ, Gil-Henn H, Oser M, Chen X, Koleske AJ, Condeelis J. Cortactin phosphorylation regulates cell invasion through a pH-dependent pathway. The Journal of Cell Biology. 2011;195(5):903–920. [PMC free article]  [PubMed]

71. Bourguignon LY, Singleton PA, Diedrich F, Stern R, Gilad E. CD44 interaction with Na+-H+ exchanger (NHE1) creates acidic microenvironments leading to hyaluronidase-2 and cathepsin B activation and breast tumor cell invasion. The Journal of Biological Chemistry. 2004;279(26):26991–27007.  [PubMed]

72. Halestrap AP. The monocarboxylate transporter family—structure and functional characterization. IUBMB Life. 2012;64(1):1–9.  [PubMed]

73. Ganapathy V, Thangaraju M, Prasad PD. Nutrient transporters in cancer: relevance to Warburg hypothesis and beyond. Pharmacology & Therapeutics. 2009;121(1):29–40.  [PubMed]

74. Pinheiro C, Reis RM, Ricardo S, Longatto-Filho A, Schmitt F, Baltazar F. Expression of monocarboxylate transporters 1, 2, and 4 in human tumours and their association with CD147 and CD44. Journal of Biomedicine & Biotechnology. 2010;2010:427694. [PMC free article]  [PubMed]

75. Miranda-Goncalves V, Honavar M, Pinheiro C, Martinho O, Pires MM, Pinheiro C, Cordeiro M, Bebiano G, Costa P, Palmeirim I, Reis RM, Baltazar F. Monocarboxylate transporters (MCTs) in gliomas: expression and exploitation as therapeutic targets. Neuro-Oncology. 2013;15(2):172–188.[PMC free article]  [PubMed]

76. Wahl ML, Owen JA, Burd R, Herlands RA, Nogami SS, Rodeck U, Berd D, Leeper DB, Owen CS. Regulation of intracellular pH in human melanoma: potential therapeutic implications. Molecular Cancer Therapeutics. 2002;1(8):617–628.  [PubMed]

77. Fang J, Quinones QJ, Holman TL, Morowitz MJ, Wang Q, Zhao H, Sivo F, Maris JM, Wahl ML. The H+-linked monocarboxylate transporter (MCT1/SLC16A1): a potential therapeutic target for high-risk neuroblastoma. Molecular Pharmacology. 2006;70(6):2108–2115.  [PubMed]

78. Sonveaux P, Vegran F, Schroeder T, Wergin MC, Verrax J, Rabbani ZN, De Saedeleer CJ, Kennedy KM, Diepart C, Jordan BF, Kelley MJ, Gallez B, Wahl ML, Feron O, Dewhirst MW. Targeting lactate-fueled respiration selectively kills hypoxic tumor cells in mice. The Journal of Clinical Investigation. 2008;118(12):3930–3942. [PMC free article]  [PubMed]

79. Swietach P, Hulikova A, Vaughan-Jones RD, Harris AL. New insights into the physiological role of carbonic anhydrase IX in tumour pH regulation. Oncogene. 2010;29(50):6509–6521.  [PubMed]

80. Swietach P, Vaughan-Jones RD, Harris AL. Regulation of tumor pH and the role of carbonic anhydrase 9. Cancer Metastasis Reviews. 2007;26(2):299–310.  [PubMed]

81. Wykoff CC, Beasley NJ, Watson PH, Turner KJ, Pastorek J, Sibtain A, Wilson GD, Turley H, Talks KL, Maxwell PH, Pugh CW, Ratcliffe PJ, Harris AL. Hypoxia-inducible expression of tumor-associated carbonic anhydrases. Cancer Research. 2000;60(24):7075–7083.  [PubMed]

82. Pastorek J, Pastorekova S, Callebaut I, Mornon JP, Zelnik V, Opavsky R, Zat’ovicova M, Liao S, Portetelle D, Stanbridge EJ. Cloning and characterization of MN, a human tumor-associated protein with a domain homologous to carbonic anhydrase and a putative helix-loop-helix DNA binding segment. Oncogene. 1994;9(10):2877–2888.  [PubMed]

83. De Simone G, Supuran CT. Carbonic anhydrase IX: biochemical and crystallographic characterization of a novel antitumor target. Biochimica et Biophysica Acta. 2010;1804(2):404–409.  [PubMed]

84. Pastorekova S, Parkkila S, Parkkila AK, Opavsky R, Zelnik V, Saarnio J, Pastorek J. Carbonic anhydrase IX, MN/CA IX: analysis of stomach complementary DNA sequence and expression in human and rat alimentary tracts. Gastroenterology. 1997;112(2):398–408.  [PubMed]

85. Chia SK, Wykoff CC, Watson PH, Han C, Leek RD, Pastorek J, Gatter KC, Ratcliffe P, Harris AL. Prognostic significance of a novel hypoxia-regulated marker, carbonic anhydrase IX, in invasive breast carcinoma. Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology. 2001;19(16):3660–3668.  [PubMed]

86. Giatromanolaki A, Koukourakis MI, Sivridis E, Pastorek J, Wykoff CC, Gatter KC, Harris AL. Expression of hypoxia-inducible carbonic anhydrase-9 relates to angiogenic pathways and independently to poor outcome in non-small cell lung cancer. Cancer Research. 2001;61(21):7992–7998.  [PubMed]

87. Generali D, Fox SB, Berruti A, Brizzi MP, Campo L, Bonardi S, Wigfield SM, Bruzzi P, Bersiga A, Allevi G, Milani M, Aguggini S, Dogliotti L, Bottini A, Harris AL. Role of carbonic anhydrase IX expression in prediction of the efficacy and outcome of primary epirubicin/tamoxifen therapy for breast cancer. Endocrine-Related Cancer. 2006;13(3):921–930.  [PubMed]

88. Roos A, Boron WF. Intracellular pH. Physiological Reviews. 1981;61(2):296–434.  [PubMed]

89. Cardone RA, Casavola V, Reshkin SJ. The role of disturbed pH dynamics and the Na+/H+ exchanger in metastasis. Nature Reviews. Cancer. 2005;5(10):786–795.  [PubMed]

90. Harguindey S, Orive G, Luis Pedraz J, Paradiso A, Reshkin SJ. The role of pH dynamics and the Na+/H+ antiporter in the etiopathogenesis and treatment of cancer. Two faces of the same coin–one single nature. Biochimica et Biophysica Acta. 2005;1756(1):1–24.  [PubMed]

91. Reshkin SJ, Cardone RA, Harguindey S. Na+-H+ exchanger, pH regulation and cancer. Recent Patents on Anti-Cancer Drug Discovery. 2013;8(1):85–99.  [PubMed]

92. Harguindey S, Arranz JL, Wahl ML, Orive G, Reshkin SJ. Proton transport inhibitors as potentially selective anticancer drugs. Anticancer Research. 2009;29(6):2127–2136.  [PubMed]

93. Perez-Sayans M, Somoza-Martin JM, Barros-Angueira F, Rey JM, Garcia-Garcia A. V-ATPase inhibitors and implication in cancer treatment. Cancer Treatment Reviews. 2009;35(8):707–713.  [PubMed]

94. Perez-Sayans M, Somoza-Martin JM, Barros-Angueira F, Diz PG, Rey JM, Garcia-Garcia A. Multidrug resistance in oral squamous cell carcinoma: the role of vacuolar ATPases. Cancer Letters. 2010;295(2):135–143.  [PubMed]

95. Bowman EJ, Siebers A, Altendorf K. Bafilomycins: a class of inhibitors of membrane ATPases from microorganisms, animal cells, and plant cells. Proceedings of the National Academy of Sciences of the United States of America. 1988;85(21):7972–7976. [PMC free article]  [PubMed]

96. Boyd MR, Farina C, Belfiore P, Gagliardi S, Kim JW, Hayakawa Y, Beutler JA, McKee TC, Bowman BJ, Bowman EJ. Discovery of a novel antitumor benzolactone enamide class that selectively inhibits mammalian vacuolar-type (H+)-atpases. The Journal of Pharmacology and Experimental Therapeutics. 2001;297(1):114–120.  [PubMed]

97. Beutler JA, McKee TC. Novel marine and microbial natural product inhibitors of vacuolar ATPase. Current Medicinal Chemistry. 2003;10(9):787–796.  [PubMed]

98. Lu X, Qin W, Li J, Tan N, Pan D, Zhang H, Xie L, Yao G, Shu H, Yao M, Wan D, Gu J, Yang S. The growth and metastasis of human hepatocellular carcinoma xenografts are inhibited by small interfering RNA targeting to the subunit ATP6L of proton pump. Cancer Research. 2005;65(15):6843–6849.  [PubMed]

99. You H, Jin J, Shu H, Yu B, De Milito A, Lozupone F, Deng Y, Tang N, Yao G, Fais S, Gu J, Qin W. Small interfering RNA targeting the subunit ATP6L of proton pump V-ATPase overcomes chemoresistance of breast cancer cells. Cancer Letters. 2009;280(1):110–119.  [PubMed]

100. Capecci J, Forgac M. The function of vacuolar ATPase (V-ATPase) a subunit isoforms in invasiveness of MCF10a and MCF10CA1a human breast cancer cells. The Journal of Biological Chemistry. 2013;288(45):32731–32741. [PMC free article]  [PubMed]

101. Mullin JM, Gabello M, Murray LJ, Farrell CP, Bellows J, Wolov KR, Kearney KR, Rudolph D, Thornton JJ. Proton pump inhibitors: actions and reactions. Drug Discovery Today. 2009;14(13–14):647–660.  [PubMed]

102. Olbe L, Carlsson E, Lindberg P. A proton-pump inhibitor expedition: the case histories of omeprazole and esomeprazole. Nature Reviews. Drug Discovery. 2003;2(2):132–139.  [PubMed]

103. Ferrari S, Perut F, Fagioli F, Brach Del Prever A, Meazza C, Parafioriti A, Picci P, Gambarotti M, Avnet S, Baldini N, Fais S. Proton pump inhibitor chemosensitization in human osteosarcoma: from the bench to the patients’ bed. Journal of Translational Medicine. 2013;11:268. [PMC free article]  [PubMed]

104. Chen M, Zou X, Luo H, Cao J, Zhang X, Zhang B, Liu W. Effects and mechanisms of proton pump inhibitors as a novel chemosensitizer on human gastric adenocarcinoma (SGC7901) cells. Cell Biology International. 2009;33(9):1008–1019.  [PubMed]

105. Chen M, Huang SL, Zhang XQ, Zhang B, Zhu H, Yang VW, Zou XP. Reversal effects of pantoprazole on multidrug resistance in human gastric adenocarcinoma cells by down-regulating the V-ATPases/mTOR/HIF-1alpha/P-gp and MRP1 signaling pathway in vitro and in vivoJournal of Cellular Biochemistry. 2012;113(7):2474–2487. [PMC free article]  [PubMed]

106. Udelnow A, Kreyes A, Ellinger S, Landfester K, Walther P, Klapperstueck T, Wohlrab J, Henne-Bruns D, Knippschild U, Wurl P. Omeprazole inhibits proliferation and modulates autophagy in pancreatic cancer cells. PloS One. 2011;6(5):e20143. [PMC free article]  [PubMed]

107. Spugnini EP, Baldi A, Buglioni S, Carocci F, de Bazzichini GM, Betti G, Pantaleo I, Menicagli F, Citro G, Fais S. Lansoprazole as a rescue agent in chemoresistant tumors: a phase I/II study in companion animals with spontaneously occurring tumors. Journal of Translational Medicine. 2011;9:221.[PMC free article]  [PubMed]

108. De Milito A, Iessi E, Logozzi M, Lozupone F, Spada M, Marino ML, Federici C, Perdicchio M, Matarrese P, Lugini L, Nilsson A, Fais S. Proton pump inhibitors induce apoptosis of human B-cell tumors through a caspase-independent mechanism involving reactive oxygen species. Cancer Research. 2007;67(11):5408–5417.  [PubMed]

109. Marino ML, Fais S, Djavaheri-Mergny M, Villa A, Meschini S, Lozupone F, Venturi G, Della Mina P, Pattingre S, Rivoltini L, Codogno P, De Milito A. Proton pump inhibition induces autophagy as a survival mechanism following oxidative stress in human melanoma cells. Cell Death & Disease. 2010;1:e87.[PMC free article]  [PubMed]

110. Yeo M, Kim DK, Kim YB, Oh TY, Lee JE, Cho SW, Kim HC, Hahm KB. Selective induction of apoptosis with proton pump inhibitor in gastric cancer cells. Clinical Cancer Research: An Official Journal of the American Association for Cancer Research. 2004;10(24):8687–8696.  [PubMed]

111. Shen W, Zou X, Chen M, Shen Y, Huang S, Guo H, Zhang L, Liu P. Effect of pantoprazole on human gastric adenocarcinoma SGC7901 cells through regulation of phosphoLRP6 expression in Wnt/beta-catenin signaling. Oncology Reports. 2013;30(2):851–855.  [PubMed]

112. Perut F, Avnet S, Fotia C, Baglio SR, Salerno M, Hosogi S, Kusuzaki K, Baldini N. V-ATPase as an effective therapeutic target for sarcomas. Experimental Cell Research. 2014;320(1):21–32.  [PubMed]

113. Bellone M, Calcinotto A, Filipazzi P, De Milito A, Fais S, Rivoltini L. The acidity of the tumor microenvironment is a mechanism of immune escape that can be overcome by proton pump inhibitors. Oncoimmunology. 2013;2(1):e22058. [PMC free article]  [PubMed]

114. Calcinotto A, Filipazzi P, Grioni M, Iero M, De Milito A, Ricupito A, Cova A, Canese R, Jachetti E, Rossetti M, Huber V, Parmiani G, Generoso L, Santinami M, Borghi M, Fais S, Bellone M, Rivoltini L. Modulation of microenvironment acidity reverses anergy in human and murine tumor-infiltrating T lymphocytes. Cancer Research. 2012;72(11):2746–2756.  [PubMed]

115. Vishvakarma NK, Singh SM. Immunopotentiating effect of proton pump inhibitor pantoprazole in a lymphoma-bearing murine host: Implication in antitumor activation of tumor-associated macrophages. Immunology Letters. 2010;134(1):83–92.  [PubMed]

116. Singh, S., Garg, S.K., Singh, P.P., Iyer, P.G. & El-Serag, H.B. (2013). Acid-suppressive medications and risk of oesophageal adenocarcinoma in patients with Barrett’s oesophagus: a systematic review and meta-analysis. Gut. [PMC free article]  [PubMed]

117. Kastelein F, Spaander MC, Steyerberg EW, Biermann K, Valkhoff VE, Kuipers EJ, Bruno MJ, ProBar Study Group Proton pump inhibitors reduce the risk of neoplastic progression in patients with Barrett’s esophagus. Clinical Gastroenterology and Hepatology: The Official Clinical Practice Journal of the American Gastroenterological Association. 2013;11(4):382–388.  [PubMed]

118. Harley W, Floyd C, Dunn T, Zhang XD, Chen TY, Hegde M, Palandoken H, Nantz MH, Leon L, Carraway KL, 3rd, Lyeth B, Gorin FA. Dual inhibition of sodium-mediated proton and calcium efflux triggers non-apoptotic cell death in malignant gliomas. Brain Research. 2010;1363:159–169.[PMC free article]  [PubMed]

119. Yang X, Wang D, Dong W, Song Z, Dou K. Inhibition of Na(+)/H(+) exchanger 1 by 5-(N-ethyl-N-isopropyl) amiloride reduces hypoxia-induced hepatocellular carcinoma invasion and motility. Cancer Letters. 2010;295(2):198–204.  [PubMed]

120. Wong P, Kleemann HW, Tannock IF. Cytostatic potential of novel agents that inhibit the regulation of intracellular pH. British Journal of Cancer. 2002;87(2):238–245. [PMC free article]  [PubMed]

121. Chang WH, Liu TC, Yang WK, Lee CC, Lin YH, Chen TY, Chang JG. Amiloride modulates alternative splicing in leukemic cells and resensitizes Bcr-AblT315I mutant cells to imatinib. Cancer Research. 2011;71(2):383–392.  [PubMed]

122. Miraglia E, Viarisio D, Riganti C, Costamagna C, Ghigo D, Bosia A. Na+/H+ exchanger activity is increased in doxorubicin-resistant human colon cancer cells and its modulation modifies the sensitivity of the cells to doxorubicin. International Journal of Cancer. Journal International Du Cancer. 2005;115(6):924–929.  [PubMed]

123. Lauritzen G, Jensen MB, Boedtkjer E, Dybboe R, Aalkjaer C, Nylandsted J, Pedersen SF. NBCn1 and NHE1 expression and activity in DeltaNErbB2 receptor-expressing MCF-7 breast cancer cells: contributions to pHi regulation and chemotherapy resistance. Experimental Cell Research. 2010;316(15):2538–2553.  [PubMed]

124. Kellen JA, Mirakian A, Kolin A. Antimetastatic effect of amiloride in an animal tumour model. Anticancer Research. 1988;8(6):1373–1376.  [PubMed]

125. Matthews H, Ranson M, Kelso MJ. Anti-tumour/metastasis effects of the potassium-sparing diuretic amiloride: an orally active anti-cancer drug waiting for its call-of-duty? International Journal of Cancer. Journal International Du Cancer. 2011;129(9):2051–2061.  [PubMed]

126. Reshkin SJ, Bellizzi A, Cardone RA, Tommasino M, Casavola V, Paradiso A. Paclitaxel induces apoptosis via protein kinase A- and p38 mitogen-activated protein-dependent inhibition of the Na+/H+ exchanger (NHE) NHE isoform 1 in human breast cancer cells. Clinical Cancer Research: An Official Journal of the American Association for Cancer Research. 2003;9(6):2366–2373.  [PubMed]

127. Pacchiano F, Carta F, McDonald PC, Lou Y, Vullo D, Scozzafava A, Dedhar S, Supuran CT. Ureido-substituted benzenesulfonamides potently inhibit carbonic anhydrase IX and show antimetastatic activity in a model of breast cancer metastasis. Journal of Medicinal Chemistry. 2011;54(6):1896–1902.  [PubMed]

128. Touisni N, Maresca A, McDonald PC, Lou Y, Scozzafava A, Dedhar S, Winum JY, Supuran CT. Glycosyl coumarin carbonic anhydrase IX and XII inhibitors strongly attenuate the growth of primary breast tumors. Journal of Medicinal Chemistry. 2011;54(24):8271–8277.  [PubMed]

129. Lou Y, McDonald PC, Oloumi A, Chia S, Ostlund C, Ahmadi A, Kyle A, Auf dem Keller U, Leung S, Huntsman D, Clarke B, Sutherland BW, Waterhouse D, Bally M, Roskelley C, Overall CM, Minchinton A, Pacchiano F, Carta F, Scozzafava A, Touisni N, Winum JY, Supuran CT, Dedhar S. Targeting tumor hypoxia: suppression of breast tumor growth and metastasis by novel carbonic anhydrase IX inhibitors. Cancer Research. 2011;71(9):3364–3376.  [PubMed]

130. Dubois L, Peeters S, Lieuwes NG, Geusens N, Thiry A, Wigfield S, Carta F, McIntyre A, Scozzafava A, Dogne JM, Supuran CT, Harris AL, Masereel B, Lambin P. Specific inhibition of carbonic anhydrase IX activity enhances the in vivo therapeutic effect of tumor irradiation. Radiotherapy and Oncology: Journal of the European Society for Therapeutic Radiology and Oncology. 2011;99(3):424–431.  [PubMed]

131. Halestrap AP, Price NT. The proton-linked monocarboxylate transporter (MCT) family: structure, function and regulation. The Biochemical Journal. 1999;343(Pt 2):281–299. [PMC free article]  [PubMed]

132. Colen CB, Shen Y, Ghoddoussi F, Yu P, Francis TB, Koch BJ, Monterey MD, Galloway MP, Sloan AE, Mathupala SP. Metabolic targeting of lactate efflux by malignant glioma inhibits invasiveness and induces necrosis: an in vivo study. Neoplasia (New York, N.Y.) 2011;13(7):620–632. [PMC free article][PubMed]

133. Matsubara T, Kusuzaki K, Matsumine A, Shintani K, Satonaka H, Uchida A. Acridine orange used for photodynamic therapy accumulates in malignant musculoskeletal tumors depending on pH gradient. Anticancer Research. 2006;26(1A):187–193.  [PubMed]

134. Hashiguchi S, Kusuzaki K, Murata H, Takeshita H, Hashiba M, Nishimura T, Ashihara T, Hirasawa Y. Acridine orange excited by low-dose radiation has a strong cytocidal effect on mouse osteosarcoma. Oncology. 2002;62(1):85–93.  [PubMed]

135. Kusuzaki K, Aomori K, Suginoshita T, Minami G, Takeshita H, Murata H, Hashiguchi S, Ashihara T, Hirasawa Y. Total tumor cell elimination with minimum damage to normal tissues in musculoskeletal sarcomas following photodynamic therapy with acridine orange. Oncology. 2000;59(2):174–180.[PubMed]

136. Kusuzaki K, Hosogi S, Ashihara E, Matsubara T, Satonaka H, Nakamura T, Matsumine A, Sudo A, Uchida A, Murata H, Baldini N, Fais S, Marunaka Y. Translational research of photodynamic therapy with acridine orange which targets cancer acidity. Current Pharmaceutical Design. 2012;18(10):1414–1420.[PubMed]

137. Kusuzaki K, Murata H, Matsubara T, Miyazaki S, Shintani K, Seto M, Matsumine A, Hosoi H, Sugimoto T, Uchida A. Clinical outcome of a novel photodynamic therapy technique using acridine orange for synovial sarcomas. Photochemistry and Photobiology. 2005;81(3):705–709.  [PubMed]

138. Kusuzaki K, Murata H, Matsubara T, Miyazaki S, Okamura A, Seto M, Matsumine A, Hosoi H, Sugimoto T, Uchida A. Clinical trial of photodynamic therapy using acridine orange with/without low dose radiation as new limb salvage modality in musculoskeletal sarcomas. Anticancer Research. 2005;25(2B):1225–1235.  [PubMed]

139. Matsubara T, Kusuzaki K, Matsumine A, Murata H, Nakamura T, Uchida A, Sudo A. Clinical outcomes of minimally invasive surgery using acridine orange for musculoskeletal sarcomas around the forearm, compared with conventional limb salvage surgery after wide resection. Journal of Surgical Oncology. 2010;102(3):271–275.  [PubMed]

140. Liu, J., Huang, Y., Kumar, A., Tan, A., Jin, S., Mozhi, A. & Liang, X.J. (2013). pH-Sensitive nano-systems for drug delivery in cancer therapy. Biotechnology Advances.  [PubMed]

141. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646–674.[PubMed]

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