Category Archives: pH Miracle

Cancer is a Preventable and Treatable Disease that Requires Major Lifestyle Changes!

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

Ninety-five-percent (95%) of ALL sickness and diseases are caused by what you eat, what you drink, what you breath and what you think.  Only five-percent (5%) of ALL sickness and diseases are caused by genetics.  The five-percent (5%) of All genetic factors are triggered by the epi-genetics or the alkaline environment of interstitial fluids determined by what you eat, what you drink, what you breath, and what you thing,  Therefore, one-hundred-percent (100%) is caused by what you eat, what you drink, what you breath and what you think.
(Sympathetic Resonance Technology, Scientific Foundations and Summary of Biologic and Clinical Studies, Dec. 2002, Vol. 8, No. 6: 835-842, Alkalizing Nutritional Therapy, medcraveonline.com/IJCAM/IJCAM-02-00046.php Robert O Young and Galina Migalko. Universal Medical Imaging Group, Medical doctor, non-invasive medical diagnostics, USA)

Abstract

This year, more than 1.5 million Americans and more than 18 million people worldwide are expected to be diagnosed with cancer, a disease commonly believed to be preventable. Only 5–10% of all cancer cases can be attributed to genetic defects, whereas the remaining 90–95% have their roots in the environment and lifestyle. The lifestyle factors include cigarette smoking, diet (fried foods, red meat), alcohol, sun exposure, environmental pollutants, infections, stress, obesity, and physical inactivity. The evidence indicates that of all cancer-related deaths, almost 25–30% are due to tobacco, as many as 30–35% are linked to diet, about 15–20% are due to infections, and the remaining percentage are due to other factors like radiation, stress, physical activity, environmental pollutants etc. Therefore, cancer prevention requires smoking cessation, increased ingestion of fruits and vegetables, moderate use of alcohol, caloric restriction, exercise, avoidance of direct exposure to sunlight, minimal meat consumption, use of whole grains, use of vaccinations, and regular check-ups. In this review, we present evidence that inflammation is the link between the agents/factors that cause cancer and the agents that prevent it. In addition, we provide evidence that cancer is a preventable disease that requires major lifestyle changes.

INTRODUCTION

After sequencing his own genome, pioneer genomic researcher Craig Venter remarked at a leadership for the twenty-first century conference, “Human biology is actually far more complicated than we imagine. Everybody talks about the genes that they received from their mother and father, for this trait or the other. But in reality, those genes have very little impact on life outcomes. Our biology is way too complicated for that and deals with hundreds of thousands of independent factors. Genes are absolutely not our fate. They can give us useful information about the increased risk of a disease, but in most cases they will not determine the actual cause of the disease, or the actual incidence of somebody getting it. Most biology will come from the complex interaction of all the proteins and cells working with environmental factors, not driven directly by the genetic code” (http://indiatoday.digitaltoday.in/index.php?

This statement is very important because looking to the human genome for solutions to most chronic illnesses, including the diagnosis, prevention, and treatment of cancer, is overemphasized in today’s world. Observational studies, however, have indicated that as we migrate from one country to another, our chances of being diagnosed with most chronic illnesses are determined not by the country we come from but by the country we migrate to (1–4). In addition, studies with identical twins have suggested that genes are not the source of most chronic illnesses. For instance, the concordance between identical twins for breast cancer was found to be only 20% (5). Instead of our genes, our lifestyle and environment account for 90–95% of our most chronic illnesses.

Cancer continues to be a worldwide killer, despite the enormous amount of research and rapid developments seen during the past decade. According to recent statistics, cancer accounts for about 23% of the total deaths in the USA and is the second most common cause of death after heart disease (6). Death rates for heart disease, however, have been steeply decreasing in both older and younger populations in the USA from 1975 through 2002. In contrast, no appreciable differences in death rates for cancer have been observed in the United States (6).

By 2020, the world population is expected to have increased to 7.5 billion; of this number, approximately 15 million new cancer cases will be diagnosed, and 12 million cancer patients will die (7). These trends of cancer incidence and death rates again remind us of Dr. John Bailer’s May 1985 judgment of the US national cancer program as a “qualified failure,” a judgment made 14 years after President Nixon’s official declaration of the “War on Cancer.” Even after an additional quarter century of extensive research, researchers are still trying to determine whether cancer is preventable and are asking “If it is preventable, why are we losing the war on cancer?” In this review, we attempt to answer this question by analyzing the potential risk factors of cancer and explore our options for modulating these risk factors.

Cancer is caused by both internal factors (such as inherited mutations, hormones, and immune conditions) and environmental/acquired factors (such as tobacco, diet, radiation, and infectious organisms; Fig. 1). The link between diet and cancer is revealed by the large variation in rates of specific cancers in various countries and by the observed changes in the incidence of cancer in migrating. For example, Asians have been shown to have a 25 times lower incidence of prostate cancer and a ten times lower incidence of breast cancer than do residents of Western countries, and the rates for these cancers increase substantially after Asians migrate to the West (http://www.dietandcancerreportorg/?p=ER).

Fig 1

The role of genes and environment in the development of cancer. A The percentage contribution of genetic and environmental factors to cancer. The contribution of genetic factors and environmental factors towards cancer risk is 5–10% and 90–95% respectively. B Family risk ratios for selected cancers. The numbers represent familial risk ratios, defined as the risk to a given type of relative of an affected individual divided by the population prevalence. The data shown here is taken from a study conducted in Utah to determine the frequency of cancer in the first-degree relatives (parents + siblings + offspring). The familial risk ratios were assessed as the ratio of the observed number of cancer cases among the first degree relatives divided by the expected number derived from the control relatives, based on the years of birth (cohort) of the case relatives. In essence, this provides an age-adjusted risk ratio to first-degree relatives of cases compared with the general population.

C Percentage contribution of each environmental factor. The percentages represented here indicate the attributable-fraction of cancer deaths due to the specified environmental risk factor.

The importance of lifestyle factors in the development of cancer was also shown in studies of monozygotic twins (8). Only 5–10% of all cancers are due to an inherited gene defect. Various cancers that have been linked to genetic defects are shown in Fig. 2. Although all cancers are a result of multiple mutations (9, 10), these mutations are due to interaction with the environment (11, 12).

 Fig. 2

Genes associated with risk of different cancers

These observations indicate that most cancers are not of hereditary origin and that lifestyle factors, such as dietary habits, smoking, alcohol consumption, and infections, have a profound influence on their development (13). Although the hereditary factors cannot be modified, the lifestyle and environmental factors are potentially modifiable. The lesser hereditary influence of cancer and the modifiable nature of the environmental factors point to the preventability of cancer. The important lifestyle factors that affect the incidence and mortality of cancer include tobacco, alcohol, diet, obesity, infectious agents, environmental pollutants, and radiation.

RISK FACTORS OF CANCER

Tobacco

Smoking was identified in 1964 as the primary cause of lung cancer in the US Surgeon General’s Advisory Commission Report (http://profiles.nlm.nih.gov/NN/Views/AlphaChron/date/10006/05/01/2008), and ever since, efforts have been ongoing to reduce tobacco use. Tobacco use increases the risk of developing at least 14 types of cancer (Fig. 3). In addition, it accounts for about 25–30% of all deaths from cancer and 87% of deaths from lung cancer. Compared with nonsmokers, male smokers are 23 times and female smokers 17 times more likely to develop lung cancer.

(http://www.cancer.org/docroot/STT/content/STT_1x_Cancer_Facts_and_Figures_2008.asp accessed on 05/01/2008).

The carcinogenic effects of active smoking are well documented; the U. S. Environmental Protection Agency, for example, in 1993 classified environmental tobacco smoke (from passive smoking) as a known (Group A) human lung carcinogen.

(http://cfpub2.epa.gov/ncea/cfm/recordisplay.cfm?deid=2835 accessed on 05/01/2008).

Tobacco contains at least 50 carcinogens. For example, one tobacco metabolite, benzopyrenediol epoxide, has a direct etiologic association with lung cancer (14). Among all developed countries considered in total, the prevalence of smoking has been slowly declining; however, in the developing countries where 85% of the world’s population resides, the prevalence of smoking is increasing. According to studies of recent trends in tobacco usage, developing countries will consume 71% of the world’s tobacco by 2010, with 80% increased usage projected for East Asia.

(http://www.fao.org/DOCREP/006/Y4956E/Y4956E00.HTM accessed on 01/11/08)

The use of accelerated tobacco-control programs, with an emphasis in areas where usage is increasing, will be the only way to reduce the rates of tobacco-related cancer mortality.

 Fig. 3

Cancers that have been linked to alcohol and smoking

Percentages represent the cancer mortality attributable to alcohol and smoking in men and women as reported by Irigaray et al. (see 13).

How smoking contributes to cancer is not fully understood. We do know that smoking can alter a large number of cell-signaling pathways. Results from studies in our group have established a link between cigarette smoke and inflammation. Specifically, we showed that tobacco smoke can induce activation of NF-κB, an inflammatory marker (15,16). Thus, anti-inflammatory agents that can suppress NF-κB activation may have potential applications against cigarette smoke.

We also showed that curcumin, derived from the dietary spice turmeric, can block the NF-κB induced by cigarette smoke (15). In addition to curcumin, we discovered that several natural phytochemicals also inhibit the NF-κB induced by various carcinogens (17). Thus, the carcinogenic effects of tobacco appear to be reduced by these dietary agents. A more detailed discussion of dietary agents that can block inflammation and thereby provide chemopreventive effects is presented in the following section.

Alcohol

The first report of the association between alcohol and an increased risk of esophageal cancer was published in 1910 (18). Since then, a number of studies have revealed that chronic alcohol consumption is a risk factor for cancers of the upper aerodigestive tract, including cancers of the oral cavity, pharynx, hypopharynx, larynx, and esophagus (18–21), as well as for cancers of the liver, pancreas, mouth, and breast (Fig. 3). Williams and Horn (22), for example, reported an increased risk of breast cancer due to alcohol. In addition, a collaborative group who studied hormonal factors in breast cancer published their findings from a reanalysis of more than 80% of individual epidemiological studies that had been conducted worldwide on the association between alcohol and breast cancer risk in women. Their analysis showed a 7.1% increase in relative risk of breast cancer for each additional 10 g/day intake of alcohol (23). In another study, Longnecker et al., (24) showed that 4% of all newly diagnosed cases of breast cancer in the USA are due to alcohol use. In addition to it being a risk factor for breast cancer, heavy intake of alcohol (more than 50–70 g/day) is a well-established risk factor for liver (25) and colorectal (26,27) cancers.

There is also evidence of a synergistic effect between heavy alcohol ingestion and hepatitis C virus (HCV) or hepatitis B virus (HBV), which presumably increases the risk of hepatocellular carcinoma (HCC) by more actively promoting cirrhosis. For example, Donato et al. (28) reported that among alcohol drinkers, HCC risk increased linearly with a daily intake of more than 60 g. However, with the concomitant presence of HCV infection, the risk of HCC was two times greater than that observed with alcohol use alone (i.e., a positive synergistic effect). The relationship between alcohol and inflammation has also been well established, especially in terms of alcohol-induced inflammation of the liver.

How alcohol contributes to carcinogenesis is not fully understood but ethanol may play a role. Study findings suggest that ethanol is not a carcinogen but is a cocarcinogen (29). Specifically, when ethanol is metabolized, acetaldehyde and free radicals are generated; free radicals are believed to be predominantly responsible for alcohol-associated carcinogenesis through their binding to DNA and proteins, which destroys folate and results in secondary hyperproliferation. Other mechanisms by which alcohol stimulates carcinogenesis include the induction of cytochrome P-4502E1, which is associated with enhanced production of free radicals and enhanced activation of various procarcinogens present in alcoholic beverages; a change in metabolism and in the distribution of carcinogens, in association with tobacco smoke and diet; alterations in cell-cycle behavior such as cell-cycle duration leading to hyperproliferation; nutritional deficiencies, for example, of methyl, vitamin E, folate, pyridoxal phosphate, zinc, and selenium; and alterations of the immune system. Tissue injury, such as that occurring with cirrhosis of the liver, is a major prerequisite to HCC. In addition, alcohol can activate the NF-κB proinflammatory pathway (30), which can also contribute to tumorigenesis (31). Furthermore, it has been shown that benzopyrene, a cigarette smoke carcinogen, can penetrate the esophagus when combined with ethanol (32). Thus anti-inflammatory agents may be effective for the treatment of alcohol-induced toxicity.

In the upper aerodigestive tract, 25–68% of cancers are attributable to alcohol, and up to 80% of these tumors can be prevented by abstaining from alcohol and smoking (33). Globally, the attributable fraction of cancer deaths due to alcohol drinking is reported to be 3.5% (34). The number of deaths from cancers known to be related to alcohol consumption in the USA could be as low as 6% (as in Utah) or as high as 28% (as in Puerto Rico). These numbers vary from country to country, and in France have approached 20% in males (18).

Diet

In 1981, Doll and Peto (21) estimated that approximately 30–35% of cancer deaths in the USA were linked to diet (Fig. 4). The extent to which diet contributes to cancer deaths varies a great deal, according to the type of cancer (35). For example, diet is linked to cancer deaths in as many as 70% of colorectal cancer cases. How diet contributes to cancer is not fully understood. Most carcinogens that are ingested, such as nitrates, nitrosamines, pesticides, and dioxins, come from food or food additives or from cooking.

 Fig. 4

Cancer deaths (%) linked to diet as reported by Willett (see 35)

Heavy consumption of red meat is a risk factor for several cancers, especially for those of the gastrointestinal tract, but also for colorectal (36–38), prostate (39), bladder (40), breast (41), gastric (42), pancreatic, and oral (43) cancers. Although a study by Dosil-Diaz et al., (44) showed that meat consumption reduced the risk of lung cancer, such consumption is commonly regarded as a risk for cancer for the following reasons. The heterocyclic amines produced during the cooking of meat are carcinogens. Charcoal cooking and/or smoke curing of meat produces harmful carbon compounds such as pyrolysates and amino acids, which have a strong cancerous effect. For instance, PhIP (2-amino-1-methyl-6-phenyl-imidazo[4,5-b]pyridine) is the most abundant mutagen by mass in cooked beef and is responsible for ~20% of the total mutagenicity found in fried beef. Daily intake of PhIP among Americans is estimated to be 280–460 ng/day per person (45).

Nitrites and nitrates are used in meat because they bind to myoglobin, inhibiting botulinum exotoxin production; however, they are powerful carcinogens (46). Long-term exposure to food additives such as nitrite preservatives and azo dyes has been associated with the induction of carcinogenesis (47). Furthermore, bisphenol from plastic food containers can migrate into food and may increase the risk of breast (48) and prostate (49) cancers. Ingestion of arsenic may increase the risk of bladder, kidney, liver, and lung cancers (50). Saturated fatty acids, trans fatty acids, and refined sugars and flour present in most foods have also been associated with various cancers. Several food carcinogens have been shown to activate inflammatory pathways.

Obesity

According to an American Cancer Society study (51), obesity has been associated with increased mortality from cancers of the colon, breast (in postmenopausal women), endometrium, kidneys (renal cell), esophagus (adenocarcinoma), gastric cardia, pancreas, prostate, gallbladder, and liver (Fig. 5). Findings from this study suggest that of all deaths from cancer in the United States, 14% in men and 20% in women are attributable to excess weight or obesity. Increased modernization and a Westernized diet and lifestyle have been associated with an increased prevalence of overweight people in many developing countries (52).

 Fig. 5

Various cancers that have been linked to obesity. In the USA overweight and obesity could account for 14% of all deaths from cancer in men and 20% of those in women (see 51).

Studies have shown that the common denominators between obesity and cancer include neurochemicals; hormones such as insulinlike growth factor 1 (IGF-1), insulin, leptin; sex steroids; adiposity; insulin resistance; and inflammation (53).

Involvement of signaling pathways such as the IGF/insulin/Akt signaling pathway, the leptin/JAK/STAT pathway, and other inflammatory cascades have also been linked with both obesity and cancer (53). For instance, hyperglycemia, has been shown to activate NF-κB (54), which could link obesity with cancer. Also known to activate NF-κB are several cytokines produced by adipocytes, such as leptin, tumor necrosis factor (TNF), and interleukin-1 (IL-1) (55). Energy balance and carcinogenesis has been closely linked (53). However, whether inhibitors of these signaling cascades can reduce obesity-related cancer risk remains unanswered. Because of the involvement of multiple signaling pathways, a potential multi-targeting agent will likely be needed to reduce obesity-related cancer risk.

Infectious Agents

Worldwide, an estimated 17.8% of neoplasms are associated with infections; this percentage ranges from less than 10% in high-income countries to 25% in African countries (56, 57). Viruses account for most infection-caused cancers (Fig. 6). Human papillomavirus, Epstein Barr virus, Kaposi’s sarcoma-associated herpes virus, human T-lymphotropic virus 1, HIV, HBV, and HCV are associated with risks for cervical cancer, anogenital cancer, skin cancer, nasopharyngeal cancer, Burkitt’s lymphoma, Hodgkin’s lymphoma, Kaposi’s sarcoma, adult T-cell leukemia, B-cell lymphoma, and liver cancer.

Fig. 6

Various cancers that have been linked to infection. The estimated total of infection attributable cancer in the year 2002 is 17.8% of the global cancer burden. The infectious agents associated with each type of cancer is shown in the bracket. HPV Human papilloma virus, HTLV human T-cell leukemia virus, HIV human immunodeficiency virus, EBV Epstein–Barr virus (see 57).

In Western developed countries, human papillomavirus and HBV are the most frequently encountered oncogenic DNA viruses. Human papillomavirus is directly mutagenic by inducing the viral genes E6 and E7 (58), whereas HBV is believed to be indirectly mutagenic by generating reactive oxygen species through chronic inflammation (59–61). Human T-lymphotropic virus is directly mutagenic, whereas HCV (like HBV) is believed to produce oxidative stress in infected cells and thus to act indirectly through chronic inflammation (62, 63). However, other microorganisms, including selected parasites such as Opisthorchis viverrini or Schistosoma haematobium and bacteria such as Helicobacter pylori, may also be involved, acting as cofactors and/or carcinogens (64).

The mechanisms by which infectious agents promote cancer are becoming increasingly evident. Infection-related inflammation is the major risk factor for cancer, and almost all viruses linked to cancer have been shown to activate the inflammatory marker, NF-κB (65). Similarly, components of Helicobacter pylorihave been shown to activate NF-κB (66). Thus, agents that can block chronic inflammation should be effective in treating these conditions.

Environmental Pollution

Environmental pollution has been linked to various cancers (Fig. 7). It includes outdoor air pollution by carbon particles associated with polycyclic aromatic hydrocarbons (PAHs); indoor air pollution by environmental tobacco smoke, formaldehyde, and volatile organic compounds such as benzene and 1,3-butadiene (which may particularly affect children); food pollution by food additives and by carcinogenic contaminants such as nitrates, pesticides, dioxins, and other organochlorines; carcinogenic metals and metalloids; pharmaceutical medicines; and cosmetics (64).

Fig. 7

Various cancers that have been linked to environmental carcinogens. The carcinogens linked to each cancer is shown inside bracket. (see 64).

Numerous outdoor air pollutants such as PAHs increase the risk of cancers, especially lung cancer. PAHs can adhere to fine carbon particles in the atmosphere and thus penetrate our bodies primarily through breathing. Long-term exposure to PAH-containing air in polluted cities was found to increase the risk of lung cancer deaths. Aside from PAHs and other fine carbon particles, another environmental pollutant, nitric oxide, was found to increase the risk of lung cancer in a European population of nonsmokers. Other studies have shown that nitric oxide can induce lung cancer and promote metastasis. The increased risk of childhood leukemia associated with exposure to motor vehicle exhaust was also reported (64).

Indoor air pollutants such as volatile organic compounds and pesticides increase the risk of childhood leukemia and lymphoma, and children as well as adults exposed to pesticides have increased risk of brain tumors, Wilm’s tumors, Ewing’s sarcoma, and germ cell tumors. In utero exposure to environmental organic pollutants was found to increase the risk for testicular cancer. In addition, dioxan, an environmental pollutant from incinerators, was found to increase the risk of sarcoma and lymphoma.

Long-term exposure to chlorinated drinking water has been associated with increased risk of cancer. Nitrates, in drinking water, can transform to mutagenic N-nitroso compounds, which increase the risk of lymphoma, leukemia, colorectal cancer, and bladder cancer (64).

Radiation

Up to 10% of total cancer cases may be induced by radiation (64), both ionizing and non-ionizing, typically from radioactive substances and ultraviolet (UV), pulsed electromagnetic fields. Cancers induced by radiation include some types of leukemia, lymphoma, thyroid cancers, skin cancers, sarcomas, lung and breast carcinomas. One of the best examples of increased risk of cancer after exposure to radiation is the increased incidence of total malignancies observed in Sweden after exposure to radioactive fallout from the Chernobyl nuclear power plant. Radon and radon decay products in the home and/or at workplaces (such as mines) are the most common sources of exposure to ionizing radiation. The presence of radioactive nuclei from radon, radium, and uranium was found to increase the risk of gastric cancer in rats. Another source of radiation exposure is x-rays used in medical settings for diagnostic or therapeutic purposes. In fact, the risk of breast cancer from x-rays is highest among girls exposed to chest irradiation at puberty, a time of intense breast development. Other factors associated with radiation-induced cancers in humans are patient age and physiological state, synergistic interactions between radiation and carcinogens, and genetic susceptibility toward radiation.

Non-ionizing radiation derived primarily from sunlight includes UV rays, which are carcinogenic to humans. Exposure to UV radiation is a major risk for various types of skin cancers including basal cell carcinoma, squamous cell carcinoma, and melanoma. Along with UV exposure from sunlight, UV exposure from sun beds for cosmetic tanning may account for the growing incidence of melanoma. Depletion of the ozone layer in the stratosphere can augment the dose-intensity of UVB and UVC, which can further increase the incidence of skin cancer.

Low-frequency electromagnetic fields can cause clastogenic DNA damage. The sources of electromagnetic field exposure are high-voltage power lines, transformers, electric train engines, and more generally, all types of electrical equipments. An increased risk of cancers such as childhood leukemia, brain tumors and breast cancer has been attributed to electromagnetic field exposure. For instance, children living within 200 m of high-voltage power lines have a relative risk of leukemia of 69%, whereas those living between 200 and 600 m from these power lines have a relative risk of 23%. In addition, a recent meta-analysis of all available epidemiologic data showed that daily prolonged use of mobile phones for 10 years or more showed a consistent pattern of an increased risk of brain tumors (64).

Fruits, vegetables, spices, condiments and cereals with potential to prevent cancer. Fruits include 1 apple, 2apricot, 3 banana, 4 blackberry, 5 cherry, 6 citrus fruits, 7 dessert date, 8 durian, 9 grapes, 10 guava, 11 Indian gooseberry, 12 mango, 13 malay apple, 14 mangosteen, 15 pineapple, 16 pomegranate. Vegetables include 1artichok, 2 avocado, 3 brussels sprout, 4 broccoli, 5 cabbage, 6 cauliflower, 7 carrot, 8 daikon 9 kohlrabi, 10onion, 11 tomato, 12 turnip, 13 ulluco, 14 water cress, 15 okra, 16 potato, 17 fiddle head, 18 radicchio, 19komatsuna, 20 salt bush, 21 winter squash, 22 zucchini, 23 lettuce, 24 spinach. Spices and condiments include 1 turmeric, 2 cardamom, 3 coriander, 4 black pepper, 5 clove, 6 fennel, 7 rosemary, 8 sesame seed, 9 mustard, 10 licorice, 11 garlic, 12 ginger, 13 parsley, 14 cinnamon, 15 curry leaves, 16 kalonji, 17 fenugreek, 18camphor, 19 pecan, 20 star anise, 21 flax seed, 22 black mustard, 23 pistachio, 24 walnut, 25 peanut, 26 cashew nut. Cereals include 1 rice, 2 wheat, 3 oats, 4 rye, 5 barley, 6 maize, 7 jowar, 8 pearl millet, 9 proso millet, 10 foxtail millet, 11 little millet, 12 barnyard millet, 13 kidney bean, 14 soybean, 15 mung bean, 16 black bean, 17 pigeon pea, 18 green pea, 19 scarlet runner bean, 20 black beluga, 21 brown spanish pardina, 22green, 23 green (eston), 24 ivory white, 25 multicolored blend, 26 petite crimson, 27 petite golden, 28 red chief.

Click here to read the entire article:
To learn more about a healthy lifestyle and diet for the prevention of all sickness and disease read The pH Miracle revised and updated and The pH Miracle for Cancer – http://www.phoreveryoung.com

Lecture in Dubai – The Annual Conference on Bacterial, Viral and Infectious Diseases

Join Robert O Young PhD and Galina Migalko MD in Dubai on December 5th and 6th, 2018 for the Annual Conference on Bacterial, Viral and Infectious Diseases. They will be Key Note Speakers and doing a workshop on the New Biology.

For more information and to register go to: https://bacterialdiseases.infectiousconferences.com/organizing-committee.php

The following is the abstract for Dr. Young’s lecture:

The Dismantling of the Viral Theory

Robert O Young CPT, MSc, DSc, PhD, Naturopathic Practitioner

Abstract

There is now over 100 years of documented history and research on the Polio virus and whether or not its treatment by inoculation has been successful in eradicating Polio. I am suggesting in this article and in my lecture that there are significant findings based on historical and past and current research, including my own that the viral theory of Polio and possibly other modern-day diseases, such as Post-Polio Syndrome, Polio Vaccine-Induced Paralysis, Legionnaires, CNS disease, Cancer, HIV/AIDS and now Zika may be caused by acidic chemical poisoning from DDT (dichloro-diphenyl-trichloroethane) and other related DDT pesticides, acidic vaccinations, and other factors including lifestyle and dietary factors rather than from a lone infectious virus. I will present ten historical graphs outlining the history of Polio, the production of DDT, BHC, Lead, Arsenic, Polio vaccinations and the author’s theory that chemical poisoning, vaccination, and lifestyle and dietary choices are a more likely causes for the symptoms of Polio, neurological diseases, Cancer, HIV/AIDS and now Zika.

THE POSSIBLE CAUSE OF POLIO, POST-POLIO, CNS, PVIPD, LEGIONNAIRES, AIDS and the CANCER EPIDEMIC – MASS ACIDIC CHEMICAL POISONING?

References

1. L. N. Kolonel, D. Altshuler, and B. E. Henderson. The multiethnic cohort study: exploring genes, lifestyle and cancer risk. Nat. Rev. Cancer. 4:519–27 (2004) doi:10.1038/nrc1389. [PubMed]

2. J. K. Wiencke. Impact of race/ethnicity on molecular pathways in human cancer. Nat. Rev. Cancer. 4:79–84 (2004) doi:10.1038/nrc1257. [PubMed]

3. R. G. Ziegler, R. N. Hoover, M. C. Pike, A. Hildesheim, A. M. Nomura, D. W. West, A. H. Wu-Williams, L. N. Kolonel, P. L. Horn-Ross, J. F. Rosenthal, and M. B. Hyer. Migration patterns and breast cancer risk in Asian-American women. J. Natl. Cancer Inst.85:1819–27 (1993) doi:10.1093/jnci/85.22.1819. [PubMed]

4. W. Haenszel and M. Kurihara. Studies of Japanese migrants. I. Mortality from cancer and other diseases among Japanese in the United States. J. Natl. Cancer Inst.40:43–68 (1968). [PubMed]

5. A. S. Hamilton and T. M. Mack. Puberty and genetic susceptibility to breast cancer in a case-control study in twins. N. Engl. J. Med.348:2313–22 (2003) doi:10.1056/NEJMoa021293. [PubMed]

6. A. Jemal, R. Siegel, E. Ward, T. Murray, J. Xu, and M. J. Thun. Cancer statistics, 2007. CA Cancer J. Clin.57:43–66 (2007). [PubMed]

7. F. Brayand, and B. Moller. Predicting the future burden of cancer. Nat. Rev. Cancer. 6:63–74 (2006) doi:10.1038/nrc1781. [PubMed]

8. P. Lichtenstein, N. V. Holm, P. K. Verkasalo, A. Iliadou, J. Kaprio, M. Koskenvuo, E. Pukkala, A. Skytthe, and K. Hemminki. Environmental and heritable factors in the causation of cancer—analyses of cohorts of twins from Sweden, Denmark, and Finland. N. Engl. J. Med.343:78–85 (2000) doi:10.1056/NEJM200007133430201. [PubMed]

9. K. R. Loeb, and L. A. Loeb. Significance of multiple mutations in cancer. Carcinogenesis. 21:379–85 (2000) doi:10.1093/carcin/21.3.379. [PubMed]

10. W. C. Hahn, and R. A. Weinberg. Modelling the molecular circuitry of cancer. Nat. Rev. Cancer. 2:331–41 (2002) doi: 10.1038/nrc795. [PubMed]

11. L. A. Mucci, S. Wedren, R. M. Tamimi, D. Trichopoulos, and H. O. Adami. The role of gene-environment interaction in the aetiology of human cancer: examples from cancers of the large bowel, lung and breast. J. Intern. Med.249:477–93 (2001) doi:10.1046/j.1365-2796.2001.00839.x. [PubMed]

12. K. Czene, and K. Hemminki. Kidney cancer in the Swedish Family Cancer Database: familial risks and second primary malignancies. Kidney Int.61:1806–13 (2002) doi:10.1046/j.1523-1755.2002.00304.x.[PubMed]

13. P. Irigaray, J. A. Newby, R. Clapp, L. Hardell, V. Howard, L. Montagnier, S. Epstein, and D. Belpomme. Lifestyle-related factors and environmental agents causing cancer: an overview. Biomed. Pharmacother.61:640–58 (2007) doi:10.1016/j.biopha.2007.10.006. [PubMed]

14. M. F. Denissenko, A. Pao, M. Tang, and G. P. Pfeifer. Preferential formation of benzo[a]pyrene adducts at lung cancer mutational hotspots in P53. Science. 274:430–2 (1996) doi:10.1126/science.274.5286.430.[PubMed]

15. R. J. Anto, A. Mukhopadhyay, S. Shishodia, C. G. Gairola, and B. B. Aggarwal. Cigarette smoke condensate activates nuclear transcription factor-kappaB through phosphorylation and degradation of IkappaB(alpha): correlation with induction of cyclooxygenase-2. Carcinogenesis. 23:1511–8 (2002) doi: 10.1093/carcin/23.9.1511. [PubMed]

16. S. Shishodiaand, and B. B. Aggarwal. Cyclooxygenase (COX)-2 inhibitor celecoxib abrogates activation of cigarette smoke-induced nuclear factor (NF)-kappaB by suppressing activation of IkappaBalpha kinase in human non-small cell lung carcinoma: correlation with suppression of cyclin D1, COX-2, and matrix metalloproteinase-9. Cancer Res. 64:5004–12 (2004) doi:10.1158/0008-5472.CAN-04-0206. [PubMed]

17. H. Ichikawa, Y. Nakamura, Y. Kashiwada, and B. B. Aggarwal. Anticancer drugs designed by mother nature: ancient drugs but modern targets. Curr Pharm Des. 13:3400–16 (2007) doi:10.2174/138161207782360500. [PubMed]

18. A. J. Tuyns. Epidemiology of alcohol and cancer. Cancer Res. 39:2840–3 (1979). [PubMed]

19. H. Maier, E. Sennewald, G. F. Heller, and H. Weidauer. Chronic alcohol consumption—the key risk factor for pharyngeal cancer. Otolaryngol. Head Neck Surg.110:168–73 (1994). [PubMed]

20. H. K. Seitz, F. Stickel, and N. Homann. Pathogenetic mechanisms of upper aerodigestive tract cancer in alcoholics. Int. J. Cancer. 108:483–7 (2004) doi:10.1002/ijc.11600. [PubMed]

21. R. Doll, and R. Peto. The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. J. Natl. Cancer Inst. 66:1191–308 (1981). [PubMed]

22. R. R. Williams, and J. W. Horm. Association of cancer sites with tobacco and alcohol consumption and socioeconomic status of patients: interview study from the Third National Cancer Survey. J. Natl. Cancer Inst.58:525–47 (1977). [PubMed]

23. N. Hamajima et al. Alcohol, tobacco and breast cancer—collaborative reanalysis of individual data from 53 epidemiological studies, including 58,515 women with breast cancer and 95,067 women without the disease. Br. J. Cancer. 87:1234–45 (2002) doi:10.1038/sj.bjc.6600596. [PMC free article] [PubMed]

24. M. P. Longnecker, P. A. Newcomb, R. Mittendorf, E. R. Greenberg, R. W. Clapp, G. F. Bogdan, J. Baron, B. MacMahon, and W. C. Willett. Risk of breast cancer in relation to lifetime alcohol consumption. J. Natl. Cancer Inst.87:923–9 (1995) doi:10.1093/jnci/87.12.923. [PubMed]

25. F. Stickel, D. Schuppan, E. G. Hahn, and H. K. Seitz. Cocarcinogenic effects of alcohol in hepatocarcinogenesis. Gut. 51:132–9 (2002) doi:10.1136/gut.51.1.132. [PMC free article] [PubMed]

26. H. K. Seitz, G. Poschl, and U. A. Simanowski. Alcohol and cancer. Recent Dev Alcohol. 14:67–95 (1998) doi:10.1007/0-306-47148-5_4. [PubMed]

27. H. K. Seitz, S. Matsuzaki, A. Yokoyama, N. Homann, S. Vakevainen, and X. D. Wang. Alcohol and cancer. Alcohol Clin. Exp. Res.25:137S–143S (2001). [PubMed]

28. F. Donato, U. Gelatti, R. M. Limina, and G. Fattovich. Southern Europe as an example of interaction between various environmental factors: a systematic review of the epidemiologic evidence. Oncogene. 25:3756–70 (2006) doi:10.1038/sj.onc.1209557. [PubMed]

29. G. Poschl, and H. K. Seitz. Alcohol and cancer. Alcohol Alcohol. 39:155–65 (2004) doi:10.1093/alcalc/agh057. [PubMed]

30. G. Szabo, P. Mandrekar, S. Oak, and J. Mayerle. Effect of ethanol on inflammatory responses. Implications for pancreatitis. Pancreatology. 7:115–23 (2007) doi:10.1159/000104236. [PMC free article][PubMed]

31. B. B. Aggarwal. Nuclear factor-kappaB: the enemy within. Cancer Cell. 6:203–208 (2004) doi:10.1016/j.ccr.2004.09.003. [PubMed]

32. M. Kuratsune, S. Kohchi, and A. Horie. Carcinogenesis in the esophagus. I. Penetration of benzo(a) pyrene and other hydrocarbons into the esophageal mucosa. Gann. 56:177–87 (1965). [PubMed]

33. C. La Vecchia, A. Tavani, S. Franceschi, F. Levi, G. Corrao, and E. Negri. Epidemiology and prevention of oral cancer. Oral Oncol.33:302–312 (1997). [PubMed]

34. P. Boffetta, M. Hashibe, C. La Vecchia, W. Zatonski, and J. Rehm. The burden of cancer attributable to alcohol drinking. Int. J. Cancer. 119:884–887 (2006) doi:10.1002/ijc.21903. [PubMed]

35. W. C. Willett. Diet and cancer. Oncologist. 5:393–404 (2000) doi:10.1634/theoncologist.5-5-393.[PubMed]

36. S. A. Bingham, R. Hughes, and A. J. Cross. Effect of white versus red meat on endogenous N-nitrosation in the human colon and further evidence of a dose response. J. Nutr.132:3522S–3525S (2002).[PubMed]

37. A. Chao, M. J. Thun, C. J. Connell, M. L. McCullough, E. J. Jacobs, W. D. Flanders, C. Rodriguez, R. Sinha, and E. E. Calle. Meat consumption and risk of colorectal cancer. JAMA. 293:172–182 (2005) doi:10.1001/jama.293.2.172. [PubMed]

38. N. Hogg. Red meat and colon cancer: heme proteins and nitrite in the gut. A commentary on diet-induced endogenous formation of nitroso compounds in the GI tract. Free Radic. Biol. Med.43:1037–1039 (2007) doi:10.1016/j.freeradbiomed.2007.07.006. [PubMed]

39. C. Rodriguez, M. L. McCullough, A. M. Mondul, E. J. Jacobs, A. Chao, A. V. Patel, M. J. Thun, and E. E. Calle. Meat consumption among Black and White men and risk of prostate cancer in the Cancer Prevention Study II Nutrition Cohort. Cancer Epidemiol. Biomarkers Prev. 15:211–216 (2006) doi:10.1158/1055-9965.EPI-05-0614. [PubMed]

40. R. Garcia-Closas, M. Garcia-Closas, M. Kogevinas, N. Malats, D. Silverman, C. Serra, A. Tardon, A. Carrato, G. Castano-Vinyals, M. Dosemeci, L. Moore, N. Rothman, and R. Sinha. Food, nutrient and heterocyclic amine intake and the risk of bladder cancer. Eur. J. Cancer. 43:1731–1740 (2007) doi:10.1016/j.ejca.2007.05.007. [PubMed]

41. A. Tappel. Heme of consumed red meat can act as a catalyst of oxidative damage and could initiate colon, breast and prostate cancers, heart disease and other diseases. Med. Hypotheses. 68:562–4 (2007) doi:10.1016/j.mehy.2006.08.025. [PubMed]

42. L. H. O’Hanlon. High meat consumption linked to gastric-cancer risk. Lancet Oncol. 7:287 (2006) doi:10.1016/S1470-2045(06)70638-6. [PubMed]

43. T. N. Toporcov, J. L. Antunes, and M. R. Tavares. Fat food habitual intake and risk of oral cancer. Oral Oncol. 40:925–931 (2004) doi:10.1016/j.oraloncology.2004.04.007. [PubMed]

44. O. Dosil-Diaz, A. Ruano-Ravina, J. J. Gestal-Otero, and J. M. Barros-Dios. Meat and fish consumption and risk of lung cancer: A case-control study in Galicia, Spain. Cancer Lett.252:115–122 (2007) doi:10.1016/j.canlet.2006.12.008. [PubMed]

45. S. N. Lauber, and N. J. Gooderham. The cooked meat derived genotoxic carcinogen 2-amino-3-methylimidazo[4,5-b]pyridine has potent hormone-like activity: mechanistic support for a role in breast cancer. Cancer Res.67:9597–0602 (2007) doi:10.1158/0008–5472.CAN-07-1661. [PubMed]

46. D. Divisi, S. Di Tommaso, S. Salvemini, M. Garramone, and R. Crisci. Diet and cancer. Acta Biomed. 77:118–123 (2006). [PubMed]

47. Y. F. Sasaki, S. Kawaguchi, A. Kamaya, M. Ohshita, K. Kabasawa, K. Iwama, K. Taniguchi, and S. Tsuda. The comet assay with 8 mouse organs: results with 39 currently used food additives. Mutat. Res.519:103–119 (2002). [PubMed]

48. M. Durando, L. Kass, J. Piva, C. Sonnenschein, A. M. Soto, E. H. Luque, and M. Munoz-de-Toro. Prenatal bisphenol A exposure induces preneoplastic lesions in the mammary gland in Wistar rats. Environ. Health Perspect.115:80–6 (2007). [PMC free article] [PubMed]

49. S. M. Ho, W. Y. Tang, J. Belmonte de Frausto, and G. S. Prins. Developmental exposure to estradiol and bisphenol A increases susceptibility to prostate carcinogenesis and epigenetically regulates phosphodiesterase type 4 variant 4. Cancer Res.66:5624–32 (2006) doi:10.1158/0008-5472.CAN-06-0516.[PMC free article] [PubMed]

50. A. Szymanska-Chabowska, J. Antonowicz-Juchniewicz, and R. Andrzejak. Some aspects of arsenic toxicity and carcinogenicity in living organism with special regard to its influence on cardiovascular system, blood and bone marrow. Int. J. Occup. Med. Environ. Health. 15:101–116 (2002). [PubMed]

51. E. E. Calle, C. Rodriguez, K. Walker-Thurmond, and M. J. Thun. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med. 348:1625–1638 (2003) doi:10.1056/NEJMoa021423. [PubMed]

52. A. Drewnowski, and B. M. Popkin. The nutrition transition: new trends in the global diet. Nutr. Rev.55:31–43 (1997). [PubMed]

53. S. D. Hursting, L. M. Lashinger, L. H. Colbert, C. J. Rogers, K. W. Wheatley, N. P. Nunez, S. Mahabir, J. C. Barrett, M. R. Forman, and S. N. Perkins. Energy balance and carcinogenesis: underlying pathways and targets for intervention. Curr. Cancer Drug Targets. 7:484–491 (2007) doi:10.2174/156800907781386623. [PubMed]

54. A. Nareika, Y. B. Im, B. A. Game, E. H. Slate, J. J. Sanders, S. D. London, M. F. Lopes-Virella, and Y. Huang. High glucose enhances lipopolysaccharide-stimulated CD14 expression in U937 mononuclear cells by increasing nuclear factor kappaB and AP-1 activities. J. Endocrinol.196:45–55 (2008) doi:10.1677/JOE-07-0145. [PubMed]

55. C. H. Tang, Y. C. Chiu, T. W. Tan, R. S. Yang, and W. M. Fu. Adiponectin enhances IL-6 production in human synovial fibroblast via an AdipoR1 receptor, AMPK, p38, and NF-kappa B pathway. J. Immunol.179:5483–5492 (2007). [PubMed]

56. P. Pisani, D. M. Parkin, N. Munoz, and J. Ferlay. Cancer and infection: estimates of the attributable fraction in 1990. Cancer Epidemiol. Biomarkers Prev.6:387–400 (1997). [PubMed]

57. D. M. Parkin. The global health burden of infection-associated cancers in the year 2002. Int. J. Cancer. 118:3030–3044 (2006) doi:10.1002/ijc.21731. [PubMed]

58. S. Song, H. C. Pitot, and P. F. Lambert. The human papillomavirus type 16 E6 gene alone is sufficient to induce carcinomas in transgenic animals. J. Virol.73:5887–5893 (1999). [PMC free article] [PubMed]

59. B. S. Blumberg, B. Larouze, W. T. London, B. Werner, J. E. Hesser, I. Millman, G. Saimot, and M. Payet. The relation of infection with the hepatitis B agent to primary hepatic carcinoma. Am. J. Pathol.81:669–682 (1975). [PMC free article] [PubMed]

60. T. M. Hagen, S. Huang, J. Curnutte, P. Fowler, V. Martinez, C. M. Wehr, B. N. Ames, and F. V. Chisari. Extensive oxidative DNA damage in hepatocytes of transgenic mice with chronic active hepatitis destined to develop hepatocellular carcinoma. Proc. Natl. Acad. Sci. U S A. 91:12808–12812 (1994) doi:10.1073/pnas.91.26.12808. [PMC free article] [PubMed]

61. A. L. Jackson, and L. A. Loeb. The contribution of endogenous sources of DNA damage to the multiple mutations in cancer. Mutat. Res.477:7–21 (2001) doi:10.1016/S0027-5107(01)00091-4. [PubMed]

62. N. De Maria, A. Colantoni, S. Fagiuoli, G. J. Liu, B. K. Rogers, F. Farinati, D. H. Van Thiel, and R. A. Floyd. Association between reactive oxygen species and disease activity in chronic hepatitis C. Free Radic. Biol. Med.21:291–5 (1996) doi:10.1016/0891–5849(96)00044-5. [PubMed]

63. K. Koike, T. Tsutsumi, H. Fujie, Y. Shintani, and M. Kyoji. Molecular mechanism of viral hepatocarcinogenesis. Oncology. 62(Suppl 1):29–37 (2002) doi:10.1159/000048273. [PubMed]

64. D. Belpomme, P. Irigaray, L. Hardell, R. Clapp, L. Montagnier, S. Epstein, and A. J. Sasco. The multitude and diversity of environmental carcinogens. Environ. Res.105:414–429 (2007) doi:10.1016/j.envres.2007.07.002. [PubMed]

65. Y. S. Guan, Q. He, M. Q. Wang, and P. Li. Nuclear factor kappa B and hepatitis viruses. Expert Opin. Ther. Targets. 12:265–280 (2008) doi:10.1517/14728222.12.3.265. [PubMed]

66. S. Takayama, H. Takahashi, Y. Matsuo, Y. Okada, and T. Manabe. Effects of Helicobacter pylori infection on human pancreatic cancer cell line. Hepatogastroenterology. 54:2387–2391 (2007). [PubMed]

67. K. A. Steinmetz, and J. D. Potter. Vegetables, fruit, and cancer prevention: a review. J. Am. Diet Assoc.96:1027–1039 (1996) doi:10.1016/S0002–8223(96)00273-8. [PubMed]

68. P. Greenwald. Lifestyle and medical approaches to cancer prevention. Recent Results Cancer Res.166:1–15 (2005). [PubMed]

69. H. Vainio, and E. Weiderpass. Fruit and vegetables in cancer prevention. Nutr. Cancer. 54:111–42 (2006) doi:10.1207/s15327914nc5401_13. [PubMed]

70. L. W. Wattenberg. Chemoprophylaxis of carcinogenesis: a review. Cancer Res. 26:1520–1526 (1966).[PubMed]

71. B. B. Aggarwal, and S. Shishodia. Molecular targets of dietary agents for prevention and therapy of cancer. Biochem. Pharmacol.71:1397–1421 (2006) doi:10.1016/j.bcp.2006.02.009. [PubMed]

72. H. Nishino, M. Murakosh, T. Ii, M. Takemura, M. Kuchide, M. Kanazawa, X. Y. Mou, S. Wada, M. Masuda, Y. Ohsaka, S. Yogosawa, Y. Satomi, and K. Jinno. Carotenoids in cancer chemoprevention. Cancer Metastasis Rev.21:257–264 (2002) doi:10.1023/A:1021206826750. [PubMed]

73. K. B. Harikumar, and B. B. Aggarwal. Resveratrol: A multitargeted agent for age-associated chronic diseases. Cell Cycle. 7:1020–1037 (2008). [PubMed]

74. G. L. Russo. Ins and outs of dietary phytochemicals in cancer chemoprevention. Biochem. Pharmacol. 74:533–544 (2007) doi:10.1016/j.bcp.2007.02.014. [PubMed]

75. R. Agarwal, C. Agarwal, H. Ichikawa, R. P. Singh, and B. B. Aggarwal. Anticancer potential of silymarin: from bench to bed side. Anticancer Res. 26:4457–98 (2006). [PubMed]

76. E. G. Rogan. The natural chemopreventive compound indole-3-carbinol: state of the science. In Vivo. 20:221–228 (2006). [PubMed]

77. N. Juge, R. F. Mithen, and M. Traka. Molecular basis for chemoprevention by sulforaphane: a comprehensive review. Cell Mol Life Sci. 64:1105–27 (2007) doi:10.1007/s00018-007-6484-5. [PubMed]

78. L. Chen, and H. Y. Zhang. Cancer preventive mechanisms of the green tea polyphenol (−)-epigallocatechin-3-gallate. Molecules. 12:946–957 (2007). [PMC free article] [PubMed]

79. P. Anand, C. Sundaram, S. Jhurani, A. B. Kunnumakkara, and B. B. Aggarwal. Curcumin and cancer: An “old-age” disease with an “age-old” solution. Cancer Lett. in press (2008). [PubMed]

80. F. Khanum, K. R. Anilakumar, and K. R. Viswanathan. Anticarcinogenic properties of garlic: a review. Crit. Rev. Food Sci. Nutr.44:479–488 (2004) doi:10.1080/10408690490886700. [PubMed]

81. G. Sethi, K. S. Ahn and B. B. Aggarwal. Targeting NF-kB activation pathway by thymoquinone: Role in suppression of antiapoptotic gene products and enhancement of apoptosis. Mole Cancer Res. in press (2008). [PubMed]

82. Y. J. Surh. Anti-tumor promoting potential of selected spice ingredients with antioxidative and anti-inflammatory activities: a short review. Food Chem. Toxicol.40:1091–1097 (2002) doi:10.1016/S0278-6915(02)00037-6. [PubMed]

83. Y. Shukla, and M. Singh. Cancer preventive properties of ginger: a brief review. Food Chem. Toxicol.45:683–690 (2007) doi:10.1016/j.fct.2006.11.002. [PubMed]

84. M. M. al-Harbi, S. Qureshi, M. Raza, M. M. Ahmed, A. B. Giangreco, and A. H. Shah. Influence of anethole treatment on the tumour induced by Ehrlich ascites carcinoma cells in paw of Swiss albino mice. Eur. J. Cancer Prev.4:307–318 (1995) doi:10.1097/00008469-199508000-00006. [PubMed]

85. C. K. Sen, K. E. Traber, and L. Packer. Inhibition of NF-kappa B activation in human T-cell lines by anetholdithiolthione. Biochem. Biophys. Res. Commun.218:148–53 (1996) doi:10.1006/bbrc.1996.0026.[PubMed]

86. R. A. Lubet, V. E. Steele, I. Eto, M. M. Juliana, G. J. Kelloff, and C. J. Grubbs. Chemopreventive efficacy of anethole trithione, N-acetyl-L-cysteine, miconazole and phenethylisothiocyanate in the DMBA-induced rat mammary cancer model. Int. J. Cancer. 72:95–101 (1997) doi:10.1002/(SICI)1097-0215(19970703)72:1<95::AID-IJC14>3.0.CO;2-9. [PubMed]

87. Y. Nakagawa, and T. Suzuki. Cytotoxic and xenoestrogenic effects via biotransformation of trans-anethole on isolated rat hepatocytes and cultured MCF-7 human breast cancer cells. Biochem. Pharmacol.66:63–73 (2003) doi:10.1016/S0006-2952(03)00208-9. [PubMed]

88. S. Lam, C. MacAulay, J. C. Le Riche, Y. Dyachkova, A. Coldman, M. Guillaud, E. Hawk, M. O. Christen, and A. F. Gazdar. A randomized phase IIb trial of anethole dithiolethione in smokers with bronchial dysplasia. J. Natl. Cancer Inst.94:1001–1009 (2002). [PubMed]

89. S. Shishodia, and B. B. Aggarwal. Diosgenin inhibits osteoclastogenesis, invasion, and proliferation through the downregulation of Akt, I kappa B kinase activation and NF-kappa B-regulated gene expression. Oncogene. 25:1463–1473 (2006) doi:10.1038/sj.onc.1209194. [PubMed]

90. R. Ghosh, N. Nadiminty, J. E. Fitzpatrick, W. L. Alworth, T. J. Slaga, and A. P. Kumar. Eugenol causes melanoma growth suppression through inhibition of E2F1 transcriptional activity. J. Biol. Chem.280:5812–5819 (2005) doi:10.1074/jbc.M411429200. [PubMed]

91. K. Sukumaran, M. C. Unnikrishnan, and R. Kuttan. Inhibition of tumour promotion in mice by eugenol. Indian J. Physiol. Pharmacol.38:306–308 (1994). [PubMed]

92. K. Imaida, M. Hirose, S. Yamaguchi, S. Takahashi, and N. Ito. Effects of naturally occurring antioxidants on combined 1,2-dimethylhydrazine- and 1-methyl-1-nitrosourea-initiated carcinogenesis in F344 male rats. Cancer Lett.55:53–59 (1990) doi:10.1016/0304-3835(90)90065-6. [PubMed]

93. M. Pisano, G. Pagnan, M. Loi, M. E. Mura, M. G. Tilocca, G. Palmieri, D. Fabbri, M. A. Dettori, G. Delogu, M. Ponzoni, and C. Rozzo. Antiproliferative and pro-apoptotic activity of eugenol-related biphenyls on malignant melanoma cells. Mol Cancer. 6:8 (2007) doi:10.1186/1476-4598-6-8.[PMC free article] [PubMed]

94. S. S. Kim, O. J. Oh, H. Y. Min, E. J. Park, Y. Kim, H. J. Park, Y. Nam Han, and S. K. Lee. Eugenol suppresses cyclooxygenase-2 expression in lipopolysaccharide-stimulated mouse macrophage RAW264.7 cells. Life Sci. 73:337–348 (2003) doi:10.1016/S0024–3205(03)00288-1. [PubMed]

95. H. P. Deigner, G. Wolf, U. Ohlenmacher, and J. Reichling. 1¢-Hydroxyeugenol- and coniferyl alcohol derivatives as effective inhibitors of 5-lipoxygenase and Cu(2+)-mediated low density lipoprotein oxidation. Evidence for a dual mechanism. Arzneimittelforschung. 44:956–961 (1994). [PubMed]

96. C. J. Rompelberg, M. J. Steenwinkel, J. G. van Asten, J. H. van Delft, R. A. Baan, and H. Verhagen. Effect of eugenol on the mutagenicity of benzo[a]pyrene and the formation of benzo[a]pyrene-DNA adducts in the lambda-lacZ-transgenic mouse. Mutat. Res.369:87–96 (1996) doi:10.1016/S0165-1218(96)90052-X. [PubMed]

97. D. P. Richardson. The grain, the wholegrain and nothing but the grain: the science behind wholegrain and the reduced risk of heart disease and cancer. Nutr. Bull.25:353–360 (2000) doi:10.1046/j.1467-3010.2000.00083.x.

98. H. E. Miller, F. Rigelhof, L. Marquart, A. Prakash, and M. Kanter. Antioxidant content of whole grain breakfast cereals, fruits and vegetables. J. Am. Coll. Nutr.19:312S–319S (2000). [PubMed]

99. J. L. Slavin, D. Jacobs, and L. Marquart. Grain processing and nutrition. Crit. Rev. Food Sci. Nutr.40:309–326 (2000) doi:10.1080/10408690091189176. [PubMed]

100. L. Chatenoud, A. Tavani, C. La Vecchia, D. R. Jacobs, Jr, E. Negri, F. Levi, and S. Franceschi. Whole grain food intake and cancer risk. Int. J. Cancer. 77:24–8 (1998) doi:10.1002/(SICI)1097-0215(19980703)77:1<24::AID-IJC5>3.0.CO;2-1. [PubMed]

101. D. R. Jacobs, Jr, L. Marquart, J. Slavin, and L. H. Kushi. Whole-grain intake and cancer: an expanded review and meta-analysis. Nutr. Cancer. 30:85–96 (1998). [PubMed]

102. L. Marquart, K. L. Wiemer, J. M. Jones, and B. Jacob. Whole grains health claims in the USA and other efforts to increase whole-grain consumption. Proc. Nutr. Soc.62:151–160 (2003) doi:10.1079/PNS2003242. [PubMed]

103. M. Eastwood, and D. Kritchevsky. Dietary fiber: how did we get where we are? Annu. Rev. Nutr.25:1–8 (2005) doi:10.1146/annurev.nutr.25.121304.131658. [PubMed]

104. A. McIntyre, P. R. Gibson, and G. P. Young. Butyrate production from dietary fibre and protection against large bowel cancer in a rat model. Gut. 34:386–391 (1993) doi:10.1136/gut.34.3.386.[PMC free article] [PubMed]

105. J. L. Slavin, D. Jacobs, L. Marquart, and K. Wiemer. The role of whole grains in disease prevention. J. Am. Diet Assoc.101:780–5 (2001) doi:10.1016/S0002-8223(01)00194-8. [PubMed]

106. K. S. Ahn, G. Sethi, K. Krishnan, and B. B. Aggarwal. Gamma-tocotrienol inhibits nuclear factor-kappaB signaling pathway through inhibition of receptor-interacting protein and TAK1 leading to suppression of antiapoptotic gene products and potentiation of apoptosis. J. Biol. Chem.282:809–820 (2007) doi:10.1074/jbc.M610028200. [PubMed]

107. F. H. Sarkar, S. Adsule, S. Padhye, S. Kulkarni, and Y. Li. The role of genistein and synthetic derivatives of isoflavone in cancer prevention and therapy. Mini Rev. Med. Chem.6:401–407 (2006) doi:10.2174/138955706776361439. [PubMed]

108. K. W. Lee, H. J. Lee, Y. J. Surh, and C. Y. Lee. Vitamin C and cancer chemoprevention: reappraisal. Am. J. Clin. Nutr.78:1074–1078 (2003). [PubMed]

109. B. A. Ingraham, B. Bragdon, and A. Nohe. Molecular basis of the potential of vitamin D to prevent cancer. Curr. Med. Res. Opin.24:139–149 (2008) doi:10.1185/030079907X253519. [PubMed]

110. F. W. Booth, M. V. Chakravarthy, S. E. Gordon, and E. E. Spangenburg. Waging war on physical inactivity: using modern molecular ammunition against an ancient enemy. J. Appl. Physiol.93:3–30 (2002).[PubMed]

111. G. A. Colditz, C. C. Cannuscio, and A. L. Frazier. Physical activity and reduced risk of colon cancer: implications for prevention. Cancer Causes Control. 8:649–67 (1997) doi:10.1023/A:1018458700185.[PubMed]

112. A. R. Shors, C. Solomon, A. McTiernan, and E. White. Melanoma risk in relation to height, weight, and exercise (United States). Cancer Causes Control. 12:599–606 (2001) doi:10.1023/A:1011211615524.[PubMed]

113. A. Tannenbaum, and H. Silverstone. The initiation and growth of tumors. Introduction. I. Effects of underfeeding. Am. J. Cancer. 38:335–350 (1940).

114. S. D. Hursting, J. A. Lavigne, D. Berrigan, S. N. Perkins, and J. C. Barrett. Calorie restriction, aging, and cancer prevention: mechanisms of action and applicability to humans. Annu. Rev. Med.54:131–152 (2003) doi:10.1146/annurev.med.54.101601.152156. [PubMed]

115. M. H. Ross, and G. Bras. Lasting influence of early caloric restriction on prevalence of neoplasms in the rat. J. Natl. Cancer Inst.47:1095–1113 (1971). [PubMed]

116. D. Albanes. Total calories, body weight, and tumor incidence in mice. Cancer Res.47:1987–92 (1987).[PubMed]

117. L. Gross, and Y. Dreyfuss. Reduction in the incidence of radiation-induced tumors in rats after restriction of food intake. Proc. Natl. Acad. Sci. U S A. 81:7596–7598 (1984) doi:10.1073/pnas.81.23.7596. [PMC free article] [PubMed]

118. L. Gross, and Y. Dreyfuss. Prevention of spontaneous and radiation-induced tumors in rats by reduction of food intake. Proc. Natl. Acad. Sci. U S A. 87:6795–6797 (1990) doi:10.1073/pnas.87.17.6795.[PMC free article] [PubMed]

119. K. Yoshida, T. Inoue, K. Nojima, Y. Hirabayashi, and T. Sado. Calorie restriction reduces the incidence of myeloid leukemia induced by a single whole-body radiation in C3H/He mice. Proc. Natl. Acad. Sci. U S A. 94:2615–2619 (1997) doi:10.1073/pnas.94.6.2615. [PMC free article] [PubMed]

120. V. D. Longo, and C. E. Finch. Evolutionary medicine: From dwarf model systems to healthy centenarians? Science. 299:1342–1346 (2003) doi:10.1126/science.1077991. [PubMed]

The Earth & Humanity Are Dying

How Long Can We Fool Ourselves or be Fooled by Others?

Animals Must Be Off the Menu if this World and Humanity are Going to Survive! Eating meat is killing OUR planet and killing us and our children.

Please watch the video below and listen carefully. This great man speaks the truth to those who have a heart and especially a soul!

To learn more about the foods that kill and the foods that heal!

Please read the following article for yourself and your family by Professor Robert O Young and then share this information with everyone you love and care about and even those who you should love and care about! Just click on the link below:

https://www.wix.com/…/app/61f33d50-3002-4882-ae86-d319c1a24…

Give yourself and your loved ones a blessing and STOP eating the flesh, blood, organs and eggs of animals!

www.drrobertyoung.com

Tom Brady’s pH Alkaline Lifestyle and Diet

New England Patriots quarterback Tom Brady — a five-time Super Bowl Champion and three-time NFL MVP — is widely considered to be one of the greatest athletes of all time. Lately, however, Brady has been following an alkaline lifestyle and diet.

In September 2017, Brady released his book, The TB12 Method: How to Achieve a Lifetime of Sustained Peak Performance. In this book, Brady detailed exactly what he eats every day. One main feature of his diet is liberal amounts of alkaline foods and liquids.

 

In the mornings, Brady doesn’t eat a full meal. When he wakes up at 6:00 am, he drinks 20 ounces of alkaline water infused with electrolytes, including sodium, potassium, magnesium and calcium. He then drinks a smoothie and/or juices containing alkalizing grasses, vegetables, fruit, nuts and seeds. Two hours later, he has another glass of alkaline electrolyte-infused water, and a post-workout protein shake. Brady claims to drink somewhere between 12 and 25 glasses of alkaline water per day.

 

He also heavily encourages snacking. He usually snacks at around 11:00 am, just before lunch. For lunch, Brady will usually have a piece of fatty fish like salmon and a lot of green vegetables. In the afternoon, he may have another protein shake or protein bar, and around 6:00 pm, Brady eats dinner, which, again, consists of mostly green vegetables.

His book provides recipes for green juices, green soups, green salads, and a few carbohydrate recipes such as his pasta dish — which is odd, considering that he supposedly rarely eats carbs. But even Brady treats himself sometimes. He doesn’t often eat dessert, but he does give a recipe for his famous alkaline avocado ice cream.

 

His book also contains several alkalizing rules for eating. Brady won’t eat carbohydrates and protein together. He recommends eating carbs or protein with green vegetables instead, as he knows that this is better for assimilation and elimination.

Brady’s chef Allen Campbell says that 80 per cent of his diet is green vegetables and the rest of his diet is grass-fed organic steak and wild salmon.

Brady follows what he refers to as an alkaline lifestyle and diet created by Robert O. Young PhD, in order to minimize muscle inflammation caused by the buildup of lactic acid in the interstitial fluids of the Interstitium (see illustration below). This entails limiting ‘acidifying foods,’ which mostly includes starchy foods like potato, pasta, bread and ALL dairy products.

What is even more interesting is the list of acidic foods that Brady doesn’t eat. For Brady, caffeine, white sugar, white flour, dairy, and some nightshade vegetables —  eggplant and mushrooms — are completely off the table. He also won’t consume olive oil if it’s used in cooking — but he’ll have it raw. And he won’t eat high sugar fruit, unless it’s in a smoothie.

Since there are profound benefits with Brady’s pH alkaline diet, and it is clearly sustaining his play on the field, there a 100’s of specific health and fitness benefits of the pH alkaline lifestyle and diet which are backed by published scientific evidence.

 

He claims that limiting acidic foods helps control the body’s pH balance. What one eats, drinks, breaths and thinks has a huge effect on the body fluids, including the blood plasma, interstitial and intracellular fluid pH which is ideal at 7.365.

Brady also knows that the alkaline lifestyle and diet can decrease the lactic acids that causes inflammation in the body, leading to ALL sickness and disease, including connective tissue disorders that can end an athlete’s career.

 

At 41 years young, which is considered ancient in football years, Brady says he wants to play at least another five years. While he is certainly capable, his pH Miracle lifestyle and diet will be a major reason he WILL achieve HIS goal.

To learn more about the pH alkaline lifestyle and diet read The pH Miracle revised and updated – http://www.phoreveryoung.com

To learn more about the lifestyle and attend a pH Miracle Retreat in Marbella, Spain or Sardenia, Italy, go to: http://www.phmiracleretreat.com

SuperGreens – The World’s First Organic Vegetable, Fruit and Grass Powder!

InnerLight SuperGreens – by Dr Robert O. Young – The Original Super Greens Powder – 49 Grasses, Leaves, Vegetables, Sprouts & Herbs – Organic & Wild Crafted Ingredients – Great Tasting – No Cameron Fillers

Screen Shot 2018-07-13 at 4.40.04 AM

About the product

ORIGINALLY CREATED IN 1988 by Dr. Robert Young (author of the best-selling pH Miracle books), this product was one of the 1st greens powders on the market and has stood the test of time, helping thousands of people maintain their health.
ALL THE GREENS YOUR BODY NEEDS – InnerLight SuperGreens is a super-concentrated organic combination of 49 different grasses, leaves, vegetables, sprouts, and herbs
Screen Shot 2018-07-13 at 4.41.07 AM
DOES NOT CONTAIN any fillers, artificial sweeteners, colorings, flavorings, additives, preservatives, spirulina, algae, mushrooms or probiotics.
MICRO FINE POWDER that makes it easy to mix with water and consume.
CHILDREN LOVE THE TASTE of the InnerLight SuperGreens powder which gets them started on the road to Optimal Health.

Product description

Screen Shot 2018-07-13 at 4.40.47 AM

 InnerLight SuperGreens is a super-concentrated organic combination of 49 different grasses, leaves, vegetables, sprouts & herbs; all the “greens” your body needs. Originally created in 1988 by Dr. Robert Young (author of the best-selling pH Miracle books), this product was one of the 1st greens powders on the market and has stood the test of time, helping thousands of people maintain their health.
Tony Robbins, internationally known motivational speaker, talked about InnerLight SuperGreens in a 1 1/2 hour “Power Talk” interview he did with Dr Robert Young in the early 2000’s. This helped get the word out about our excellent product.
Tony-robbins
InnerLight SuperGreens powder is a micro fine powder which makes it easy to mix with water and digest. The greens powder smells great and has a mild taste.
InnerLight SuperGreens DOES NOT CONTAIN any fillers, artificial sweeteners, colorings, flavorings, additives, preservatives, spirulina, algae, mushrooms or probiotics. Our product is also formulated with Non GMO ingredients.
SuperGreens powder has four times the power of ordinary green powders. Drinking InnerLight SuperGreens is the quickest way to get a high concentration of chlorophyll which can assist with building healthy cells.
As Dr Young says, “When the Fish is Sick, Change the Water”. SuperGreens is an organic, colloidal, concentrated, charged high frequency food. There is nothing else like it. We invite you to commit to a 120-day program and take your health to the next level.
0-8
If you’re worried that you’re not getting enough greens in, InnerLight SuperGreens is the answer for you.
Try some InnerLight SuperGreens today!
p.s.- We have a “no-quibble guarantee” so you have nothing to lose!
Screen Shot 2018-07-13 at 4.39.47 AM

Is There a Cure for Brain Cancer?

Is There Any Cure for a Brain Tumor?

Robert Young

Robert Young

Research Scientist at the pH Miracle Center

This was a question asked by Sahar Sahar (a face book friend) and here is my answer:

My own young and beautiful daughter Ashley, at the age of 21 followed the pH Miracle Alkaline Lifestyle and Diet with great success. She has now been in remission from brain cancer for over 15 years. She elected not to have brain surgery, radiation or chemotherapy.

 

Ashley was married and pregnant with her first child and in her 3rd trimester when she had a shocking seizure while at the movie theater. She was rushed to the hospital and after brain scans was found to have a large complex mass in her brain.

She was told that she needed emergency surgery and that since she was pregnant the Doctors recommended the termination of her pregnancy by C-section so they could begin treating her cancer.

With the help of her husband Matthew and Ashley’s strong faith and courage she decided no surgery and no taking the baby prematurely. She rested at home for several weeks until it was time to give birth.

She gave birth to a healthy boy (who is now 16 pictured below loving his sisters) and was told by the Doctors that she would not be able to have any more children because of her brain condition.

 

Ashley did not believe what she was hearing and had faith in God and the truth she had learned from her parents. She now has 4 beautiful healthy children – 1 boy and 3 girls. The newest addition came to their family just one year ago.

 

Her decision to follow the pH Miracle alkaline lifestyle and diet was her own decision and was supported by her loving husband and her parents.

 

As her Father who loves his daughter is so happy she is alive, healthy and able to attend to all her family needs. She is a wonderful example of Motherhood, a wonderful wife and has a strong abiding faith in God. I am so proud of Ashley and her bravery, courage and especially her faith to make such a bold decision at the young age of 21.

With love I share this very personal story that has a happy ending with many tears and trails knowing Ashley is healthy and alive today because she followed her heart with the knowledge that healing comes from within and is our personal responsibility.

Each person must decide for themselves (not the government) the path they will choose to go. It is all about free-agency to choose YOUR own healing path. Ashley listened to her parents, to her husband and especially to that still-small voice that speaks to our minds and through prayer and the support of family members made a wise choice. That choice is why she is alive today!

You might remember in the story of Alice in Wonderland when Alice came to a crossroads on her path and encountered the Cheshire Cat. As the story goes Alice asked the Cheshire Cat which road she should choose to go. The Cheshire Cat answered wisely, “If you do not know where you want to go any road will do.”

 

May God bless all of you who are at the crossroads of life with the depth of perception and the faith to choose YOUR own road wisely. Listen to that still-small voice that will speak to your mind and tell YOU the path YOU should choose. This voice will never deceive YOU or lead you astray!

Believe in Miracle even pH Miracles!

With sincere gratitude, love and healing light,

Robert O Young (Ashley’s Father)

To learn more about Ashley’s choice and the pH Miracle alkaline lifestyle and diet go to: www.drrobertyoung.com and www.phmiracleretreat.com

PS I believe that the road Ashley chose was the road that gave her a cancer cure and a healthy life, including the protection and love of her family, friends and a living and loving Father in Heaven!

PSS Ashley’s husband Mathew operates the pHmlife.com that sells the pH Miracle alkaline nutritional products.

Why Tony Robbins Promotes The Alkaline Lifestyle & Diet

Tony Robbins Shares the Reasons Why the pH Miracle Alkaline Lifestyle and Diet is the Best Way to Live a Healthy and Disease Free Life!

Did you know that Tony Robbin’s health day is based upon the work, research and findings of Robert O Young, PhD

0-5

Watch the following video as Tony shares the pH Miracle Alkaline way of living, eating, breathing and thinking at the following link:

 

Tony Robbins on alkalinity – the power of alkaline water – alkalinity – health – alkaline diet In this video Tony Robbins explains all the benefits of alkalinity. The power of alkaline water and diet.

To learn more about the pH Miracle alkaline lifestyle and diet go to: http://www.drrobertyoung.com and http://www.phmiracleretreat.com

Join the millions around the World that are enjoying good health and fitness free of ALL sickness and disease. Read The pH Miracle revised and updated book and other books written by Robert O Young PhD – https://www.amazon.com/pH-Miracle-Balance-Reclaim-https://www.amazon.com/Robert-O.-Young/e/B001ILKCSU/ref=sr_tc_2_0?qid=1529539204&sr=8-2-ent

Would YOU like to come to a pH Miracle Health and Fitness Retreat?  To learn more go to: http://www.phmiracleretreat.com
Screen Shot 2018-05-19 at 3.05.26 PM

SHOCKING STUDY IN 2016: Chemo Kills up to 51% of Patients within 30 days

cause of death

For decades now, many scientists have been raising red flags that chemotherapy can oftentimes do more harm than good, and in a surprisingly large number of cases, it simply does not work.

Dr. Hardin B. Jones, a former Professor of Medical Physics and Physiology at Berkeley, California, studied the impact of chemotherapy, radiation, and surgery on the survival rates of cancer patients, and found that instead of prolonging lives, these treatments actually make the patients die almost four times sooner. This was found more than 40 years ago, and yet not much has changed in the way the hospitals treat cancer.

For terminal patients as well, a 2016 study in the peer-reviewed journal of the American Cancer Society CANCER found that living at home instead of being treated at the hospital prolonged their lives by about 45%.

And now, a new study was just published earlier this month that analyzed 30-day mortality rates caused by the treatment itself: chemotherapy and chemotherapy plus radiation.

Cancer Study: Early Mortality Rate Caused by Chemotherapy

The study, published in The Lancet’s Oncology, looked at 23,228 breast and 9,634 lung cancer patients in England.

download-58

The results showed high death rates linked to the treatment, increased use of SACTs (systematic anticancer therapies – cytotoxic chemotherapy). The researchers stated it was due “poor clinical decision making.”

“Patients dying within 30 days after beginning treatment with SACT are unlikely to have gained the survival or palliative benefits of the treatment, and in view of the side-effects sometimes caused by SACT, are more likely to have suffered harm,” states the study.

The researchers write that while there a few patients who may have benefited from SACTs, there were too many who were harmed by it, or even killed by the treatment.

chemotherapy-448578_960_720

In 2014 , the year the study was researched, almost 1,400 patients in England died within 30 days of their first chemotherapy treatment. In some hospitals, the mortality rate was significantly higher than in the others: up to 51% of breast cancer patients died in Milton Keynes (although the number of total patients was small), and up to 29% of lung cancer patients died in Lancashire Teaching Hospitals.

“Simply reducing doses of or avoiding SACT altogether would reduce or eliminate instances of treatment-related early mortality.”

The study was done after noticing a clear lack of data analyzing the risk versus gain of using chemotherapy and mortality rates caused by it in the first 30 days of treatment. As the researchers state, this is the first time this topic has been brought up and investigated at a national level.

The “million dollar questions” (or perhaps “billion dollar” since this is the cancer treatment industry we’re talking about) raised by the researchers included: is chemotherapy use still advocated based on small clinical studies — most sponsored by the pharmaceutical industry?

And it has never been fully studied how well it works in a real hospital setting?

Do Most Hospitals Know What They Are Even Doing?

The study points out two problems. One is that mortality rate is high due to poor clinical decisions. Perhaps because in most hospitals chemotherapy is given in a one-size-fits all manner or a fixed-dose with no consideration to a patient’s health history, and characteristics such as weight and age.

In England’s database, it was found that for many patients, the doctors did not include why the chemotherapy was given, and the overall health of the patient and the severity of their cancers was never recorded.

Both of these factors, as the study points out, could significantly change the outcome for these patients.

In America, another study found that doctors gave palliative chemotherapy to terminal cancer patients, and in at least two-third of cases, the patient did not know that the treatment could not cure them, but it only alleviated some symptoms, such as pain.

Knowing that the treatment could not help them in the end, would they have searched for alternative options that may have worked better?

Death Rates from Chemotherapy Are Rarely Properly Documented

The second issue the study found is that mortality rates are hard to analyze because they are not well or properly recorded.

In England’s case, many dates of deaths were simply missing from the national database. Some were documented twice, and the two dates did not match.

 

800px-Death_certificate_of_John_Otto_Siegel,_front_view

In America, the national statistic of cancer mortality comes from the death certificates. This is what the National Center for Health Statistics (NCHS) along with the doctors use to see how many people are die from cancer, and how many people die from the treatment. Unfortunately, the National Cancer Institute reports “cancer” as the cause of death for almost all cancer patients, regardless of what actually caused it, as pointed out in a 2002 article.

This article raised concern that “cancer death rates are systematically underestimated, in that many patients who die as a result of cancer treatment do not have cancer recorded as the underlying cause of death.”

For example, they studied patients who died within one month after a cancer-surgery between 1994 and 1998, and 41% of these deaths were not properly recorded. The authors write that cancer treatment was the likely cause of death.

“…Many deaths subsequent to 1 month after cancer-directed surgery may be similarly miscoded.”

Unfortunately, even though the study points out that many death certificates quote some condition other than cancer as the cause of death (such as liver failure), they want the cause of death to be just “cancer.” That would lead to further incorrect data as many patients do die from cancer treatments, and liver failure that would not happen from cancer, is often caused by the toxic chemo drugs. But what this study does show us, is that because of a 1999 revision in the International Statistical Classification of Diseases and Related Health Problems (ICD), instead of a cancer or cancer-related death, death certificates now have to show the “underlying” cause of each death, such as: thromboembolism (blood vessel obstruction), infections, organ failures, and hemorrhage (excessive bleeding).This leads to improper classification and underestimated cancer death rates and statistics.

How many patients die from the treatment instead of cancer?

That is hard to say until every doctor and hospital begins classifying the causes of deaths correctly. Until then, it is important to keep studies like this in mind when considering pros and cons of starting a chemotherapy treatment.

There are more and more alternative options out there – and for many, they do work. (Just look up testimonials from the Nutritional Oncology Research Institute, or even studies on carotenoids antioxidants derived from natural sources, and even IV curcumin and sodium bicarbonate).

“I think it’s important to make patients aware that there are potentially life threatening downsides to chemotherapy. And doctors should be more careful about who they treat with chemotherapy,” writes one of the study’s co-authors, Professor David Dodwell, Institute of Oncology, St James Hospital, Leeds, UK.

This article is for informational purposes only. Consult a doctor before beginning any treatment. See our full disclaimer here. 

Want to learn more about the most effective ways to prevent and reverse cancer?  Read The pH Miracle revised and updated and The pH Miracle for Cancer –

https://www.amazon.com/Robert%20O.%20Young/e/B001ILKCSU/ref=la_B001ILKCSU_pg_1?rh=n%3A283155%2Cp_82%3AB001ILKCSU&sort=author-pages-popularity-rank&ie=UTF8&qid=1528305583

Screen Shot 2018-06-07 at 8.31.48 AM.png

References

1) https://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(16)30383-7/abstract?code=lancet-site

2) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2360753/

3) https://althealthworks.com/8088/berkeley-scientist-cancer-patients-live-4x-longer-by-refusing-chemotherapyyelena/

4) https://academic.oup.com/jnci/article/94/14/1044/2519814

5) Alkalizing Nutritional Therapy in the Prevention and Treatment of Any Cancerous Condition – https://www.amazon.com/Alkalizing-Nutritional-Prevention-Treatment-Cancerous-ebook/dp/B01JKCXJRY/ref=la_B001ILKCSU_1_14?s=books&ie=UTF8&qid=1528429047&sr=1-14&refinements=p_82%3AB001ILKCSU

6) The pH Miracle for Cancer: Discover the Truth about the Cause, Prevention, Treatments, and Reversal of ALL Types of Cancers – https://www.amazon.com/PH-Miracle-Cancer-Prevention-Treatments-ebook/dp/B01JJX1Q8S/ref=la_B001ILKCSU_1_6?s=books&ie=UTF8&qid=1528428158&sr=1-6&refinements=p_82%3AB001ILKCSU

7) Using Sodium and Potassium Bicarbonates in the Prevention and Treatment of All Sickness and Disease – https://www.amazon.com/Potassium-Bicarbonates-Prevention-Treatment-Sickness-ebook/dp/B01JLHJ1Y8/ref=la_B001ILKCSU_1_30?s=books&ie=UTF8&qid=1528429161&sr=1-30&refinements=p_82%3AB001ILKCSU

The pH Miracle Performance Center

 

Robert Young

Robert Young

Research Scientist at The pH Miracle Center

Total personalization, maximum results

The pH Miracle Performance Center powered by Acquaforte is a centre of excellence for professional and amateur sports players, who want a personalized training strategy to achieve the best results in terms of muscle balance, personalized improvement in their individual sport, weight loss and general health, fitness and well-being.

Under the guidance of an extraordinary and close-knit team of athletics trainers, sports doctors, massage therapists, osteopaths, chiropractors and nutritionists, the Performance Center provides the most accurate analysis of every pathological condition and then an effective course of treatment, even when time is short, such as on holiday.

The training method of the Performance Center, aimed at improving skills, is based on the search for a new kind of balance, the result of resolving any postural issues and at the same time introducing new training methods that are personalized on the basis of the analyses provided by the Forte Lab medical team.

 

Each type of training is designed to the needs of the guests and takes place in the state-of-the-art Fitness Room at Acquaforte Thalasso & Spa. Depending on the different cases in question, activity in the gym is combined with the thalassotherapy course, which, in a weightless environment, allows you to effortlessly perform a series of exercises that are totally effective for getting your body back in shape.

To learn more or to register for your personalized pH Miracle Retreat email us at: phmiraclelife@gmail.com or give us at call at: 760 484 1075 or 760 751 8321.

#ph, #phmiracle, #alkalinelifestyleandiet, #alkaline, #alkalinebydesign, #acidicbyfunction, #drrobertoyoung, #dryoung, #phmiracleretreat, #alkalineretreat, #drgalina,

Thalassotherapy at Acquaforte Thalasso The pH Miracle Spa Detox, Regeneration, Wellness and Enhancement Protocol

Screen Shot 2018-05-19 at 2.09.33 AM
Acquaforte Thalasso Spa thalassotherapy is based on the revolutionary principle of sea water at different temperatures and different saline densities. Set in a wonderful garden, the thalassotherapy course consists of six pure Sardinian sea water pools, with water drawn from just over a hundred metres from the shoreline at a depth of ten metres.
The first three pools – at a high temperature and with a high saline concentration – have an extraordinary detox effect. The final three – with a lower saline concentration and at lower temperatures – round off the regenerating program, stabilizing the exchanges between the body and the mineral salts.
Screen Shot 2018-05-19 at 2.09.11 AM
1st sea oil or brine pool Temperature: 37°-38°
Draining, muscle-relaxing and energizing action The very high concentration of magnesium salt allows the body to float, performing a draining and anti-inflammatory action and delightfully relaxing the muscles. The high temperature of the water has a vasodilatory effect, and when combined with the high saline density, it increases metabolic exchanges by osmosis, thereby aiding the draining and detox effect.
2nd sea oil, or brine, pool with aloe and mint Temperature: 37°- 38°
Action that stimulates the production of endorphins In this pool, thalassotherapy and phytotherapy join forces: sea oil is mixed with refreshing mint and aloe vera, appreciated for centuries for its therapeutic properties for the skin. The combination of phytotherapeutic elements and magnesium salt provides extraordinary results in terms of skin pathologies (psoriasis). The first and second pools also have a stimulating and gratifying effect, thanks to the production of endorphins.
Screen Shot 2018-05-19 at 2.08.57 AM
3rd high saline density pool Temperature: 37°-38°
Action complementing the exchanges between the sea and body Thanks to osmosis, a dip in this sodium-rich pool continues and increases the exchanges between the sea water and the body, stimulating the elimination of toxins, introducing sea salt that is full of minerals, and continuing the relaxation of the muscles. Furthermore, the high temperature of the water generates extraordinary mental and physical relaxation and transforms the pool into a place of silent enchantment, where you can discover all the wellbeing of one of the most original and exclusive Acquaforte Thalasso & Spa massages.
4th pure sea water pool Temperature: 37-38°
Toning and sensory action This high temperature, pure sea water pool features whirlpools that stimulate microcirculation from the soles of the feet to the abdominal muscles and the back. The movement and the water pressure and vigorously and sensorially stimulate various body areas, complementing the muscle-relaxing effect of the previous pools.
5th sea oil Temperature: 30-32°
Draining, muscle-relaxing and energiZing action The very high concentration of magnesium salt allows the body to float, performing a draining and anti-inflammatory action and delightfully relaxing the muscles. The high temperature of the water has a vasodilatory effect, and when combined with the high saline density, it increases metabolic exchanges by osmosis, thereby aiding the draining and detox effect.
6th pure sea water pool Temperature: 25°-27°
High-impact reaction completing vasoconstriction This spectacularly sized pool with pure sea water at a lower temperature is the perfect end to vascular exercise and the toning action all over the body, thanks to its remarkable vasoconstrictor action. The upstream lane and the variety of whirlpools set in the pool’s bays instil a wonderful feeling of lightness and energy.
Signature Treatments Light, lightness, seduction
Screen Shot 2018-05-19 at 1.55.10 AM
The medical team of Acquaforte Thalasso & Spa have spent years of research to design and develop a wonderful collection of extraordinarily effective and appealing exclusive treatments.
Screen Shot 2018-05-19 at 2.08.46 AM
Heavenly legs
A walk through sea water, divided into a series of stages with different saline densities and decreasing temperatures, from 34° to 10°. It is ideal for toning the legs and working on vascular diseases, with its extraordinary anti-edema action. The result: lighter, more toned, more seductive legs.
Natural sea salt exfoliation In the fragrant steam of the Turkish bath, a salt-based scrub removes toxins and dead cells from the skin, draining excess liquid, and preparing the body to receive the benefits of thalassotherapy and the sun.
Honey and salt massage
One of life’s rules is that opposites attract, as this extraordinary massage proves, where the softness of honey and the energy of salt, combined with essential oils, purify and smooth the skin, preparing it to welcome the smiling sun and every caress.
Sea oil cryotherapy
 
Drawing on the property of sea oil, which freezes at -40 °, the treatment combines the benefits  Forte Village Sardegna of low temperature with the draining and toning properties of this extraordinary natural magnesium-based liquid.
Thanks to the skilled massage of the therapists, the microcirculation is reactivated and the body becomes wonderfully light again, with a remarkable skin anti-aging effect.
Sea mud
Thanks to its wealth of minerals and trace elements, boosted by the waters of the Mediterranean, when applied over the whole body or on specific areas, sea mud complements the benefits of thalassotherapy, toning and working therapeutically on skin pathologies and the bone/muscle system with a very remarkable anti-inflammatory effect.
To register for the pH Miracle Retreat at the Forte Village, Sardegna, Italy, email: phmiraclelife@gmail.com or call at: 760 484 1075.
case-study_c200
Check out the following youtube video on all the benefits you will experience at the pH Miracle at the Forte Village, Sardegna, Italy!
 https://youtu.be/zbBlwsUMMHI
Screen Shot 2018-05-19 at 1.54.54 AM.png
#phmiracleretreat, #phmiracle, #ph, #alkalinelifestyleanddiet, #alkalarian

What is the Interstitial Fluid or Interstitum?

 Scientists Have Discovered a New Organ in the Human Body validating the Work, Research, Findings and Discoveries of Robert O Young MSc, DSc, PhD, Naturopathic Practitioner Over 30 Years Ago! What is the Interstitial Fluid or the Interstitium?

The interstitial fluids are the fluid areas that surround every cell of the body and hold alkalinity or electrons for cellular energy and acidic wastes that are waiting to be removed by the lymphatic system through the 4 channels of elimination (perspiration, urination, defecation and respiration).

These fluid-filled spaces or compartments are what I call the acid-catchers of the blood and body cells and are at an ideal pH of 7.2 – just slightly more acidic than the blood at a base of 7.365. This organ makes up over 50% of the entire body fluids and contains all the evidence that validates my 30 year old theory that the human body is alkaline by design when healthy although acidic by function and the key to health and vitality. The key to health, energy and vitality is achieved by maintaining the alkaline design of the body fluids, especially the interstitial fluids and eliminating metabolic, dietary, environmental and respiratory acidic waste. This is why I continue to declare the same ideology of sickness, disease and health – “There is only one sickness and one disease and the cause is the over-acidification of the blood and then the tissues (interstitial fluids) due to an inverted way of living, eating, breathing and thinking. The cure for all disease and sickness is found in its prevention NOT in its treatment. Education not medication is the answer to empower people with their personal responsibility to manage their own health and well-being.

In my published paper, “Alkalizing Nutritional Therapy in the Prevention and Reversal of any Cancerous Condition” you learn of the importance of testing the chemistry (pH, minerals, proteins, etc) of the interstitial or interstitium to understand the true picture of health and wellness rather than just the chemistry of the blood. WHY IS TESTING THE CHEMISTRY AND PH of the INTERSTITIAL FLUIDS SO IMPORTANT? Because everything from the blood that is toxic or in excess is pushed out into the acid catchers or interstitial fluids in order to purify the blood and to maintain its delicate pH balance and chemistry at a pH of 7.365. If it were not so you would surely die from metabolic, dietary, environmental and respiratory acidosis.

It is extremely important to understand this organ system needs to be tested regularly (At least twice a year more frequently if you are dealing with a serious health challenge) for chemistry and pH to determine true homeostasis, metabolic alkalosis, metabolic acidosis and mineral levels for accurate picture of health, fitness and vitality. This cannot be done with current blood tests (CBC’s and Chemistry’s of the blood) because deficiencies in the blood do not show up until the interstitial fluids have been seriously compromised by an acidic lifestyle and diet.

In a study published in Scientific Reports, a New York University-led team of researchers finally described my discovery of the interstitium, which is a series of connected, fluid-filled spaces found under skin as well as throughout the gut, lungs, blood vessels and muscles.

The bubble wrap-like network only became visible when the pathologists used a new laser endoscope, called a confocal laser endomicroscope, that allowed them to see microscopic tissues in living people. Most studies of tissues missed the interstitium because they rely on biopsies of tissues that are then dried and fixed onto microscope slides; the desiccated samples never showed the fluid-filled spaces.

But when the endoscopic laser was used to remove the pancreas and bile duct in a dozen patients with cancer, the odd spaces became obvious.

In the study, the authors speculate that the spaces could be important for a number of functions, including generating the collage that supports cells in certain tissues, as well as housing the stem cells that rush in to repair damaged tissues. They may also play a role in conducting electrical signals as cells move and stretch. Because the spaces form a fluid-highway linking tissues and organs, it may also explain why some cancers, if they invade the spaces, spread more quickly than others.

The bottom-line is the compartments of the interstitial fluids are where everything is taking place when determining true homeostasis and pH balance.

The idea that you cannot control the chemistry or the pH of the blood or body fluids as suggested by current medical savants is a false theory/hypothesis. The break-through research of Prof Robert O Young will continue to prove that managing and maintaining the pH or chemistry’s of the interstitial fluids is an accurate and efficient way to prevent any and ALL sickness and disease.

To learn more about the chemistry’s of blood compared to the chemistry’s of the interstitial fluids read, “Alkalizing Nutritional Therapy in the Prevention and Reversal of any Cancerous Condition”.

Read “The pH Miracle for Cancer”. To order go to: https://www.amazon.com/…/dp/B01JKCX…/ref=la_B001ILKCSU_1_19…

Read the “Metabolic and Dietary Acids Are the Fuel That Lights the Fuse That Ignites Inflammation That Leads to Cancer!” https://www.amazon.com/…/dp/B01JKGP…/ref=la_B001ILKCSU_1_52…

Read “The pH Miracle revised and updated” – https://store.phoreveryoung.com/…/the-ph-miracle-original-2…

Read “The pH Miracle for Cancer” https://store.phoreveryoung.com/…/the-ph-miracle-for-cancer…

For inquires for non-invasive, non-radioactive interstitial chemistry and pH email: phmiraclelife@gmail.com

For health and wellness coaching email: phmiraclelife@gmail.com

%d bloggers like this: