More on the origin of AIDS.
Archive for the 'AIDS' Category
HIV-AIDS was created with the use of Gay men as targets for Eugenic experiments suggests U.S. doctor
Published by April 4th, 2008 in AIDS. 0 CommentsWell worth reading.
Is HIV a virus-like form of acid-fast Tuberculosis-type bacteria?
Published by April 4th, 2008 in AIDS. 0 CommentsMore background to the creation of AIDS.
Join the dots to see the big picture.
Another gift to the pharmaceutical lobby that paves the way into US meddling in other parts of Africa.
Uganda: Uganda Launches HIV Vaccine Trials for Babies
Published by January 13th, 2007 in AIDS, Eugenics, Corporate Crime and Medical Mafia. 0 CommentsThe East African (Nairobi), Esther Nakkazi, Nairobi
December 26, 2006
http://allafrica.com/stories/200612270406.html
Uganda has screened and vaccinated at least a quarter of the 50 babies needed for vaccine trial focused on prevention of HIV transmission from mother to child during breastfeeding.
The first baby in the vaccine trials was enrolled in October and by last week 14 of them had received either the vaccine or placebo saline solution (for control) while 16 have been screened to participate.
The study is in its phase I, randomised double blind - where the researchers will not know which babies receive the vaccine or the placebo solution, while 40 babies will randomly receive the vaccine and 10 the placebo.
In this first phase of the trial, the researchers are testing whether the vaccine, formally known as Alvac-HIV, is safe for use in children, following which they will study whether it can stop mother-to-child transmission of the Aids-causing virus during breastfeeding.
Last week, Prof Francis Mmiro, the lead investigator, said the baby vaccine trial has been successful so far, adding that he hoped the vaccine will be added to the many given to babies at birth and thereafter like polio, tetanus, hepatitis B and measles.
Preliminary results are expected by mid 2007 in the-two -and a half-year study.
The Alvac-HIV vaccine is being given to children less than or equal to three days of age, who weigh at least 2kg, have normal blood levels and are born to HIV positive mothers.
The babies enrolled are also not participating in other trials, have not received blood transfusions, do not have serious illnesses, and can be monitored for 24 months. Their families should, therefore, be living around Mulago referral hospital in Kampala.
The study primarily aims at evaluating the safety and immunogenicity of the vaccine in infants born to HIV-infected women.
If successful, the vaccine could prevent at least 25,000 infections in newborns in East Africa alone. The trial is being carried out by the Uganda in collaboration with US Aids researchers.
Many children, especially in the developing world, are infected by their HIV positive mothers who cannot afford to buy milk based formulas and are forced to breastfeed them.
In Uganda, at least 8,000 babies were infected last year. At least 22,000 infections are registered in children each year.
So far, 535 women have been referred to Makerere University John Hopkins Collaboration at Mulago Hospital.
Copyright © 2006 The East African. All rights reserved. Distributed by AllAfrica Global Media (allAfrica.com). Click here to contact the copyright holder directly for corrections — or for permission to republish or make other authorized use of this material.
AIDS: THE SELENO-ENZYME SOLUTION
AIDS is a consequence of HIV infection which causes deficiencies of the enzyme glutathione peroxidase and its four components, yet this syndrome and viral activity can be reversed with dietary supplementation.
Part 2 of 2
Extracted from Nexus Magazine, Volume 11, Number 2 (February-March 2004)
PO Box 30, Mapleton Qld 4560 Australia. editor@nexusmagazine.com
Telephone: +61 (0)7 5442 9280; Fax: +61 (0)7 5442 9381
From our web page at: www.nexusmagazine.com
by Harold D. Foster, PhD © 2003
Professor, Department of Geography
University of Victoria
PO Box 3050
Victoria, BC, V8W 3P5, Canada
Email: hfoster@mail.geog.uvic.ca
Website: http://www.hdfoster.com or http://www.hetn.org/
COROLLARY ONE: Deficiencies of Glutathione Peroxidase and its Components in HIV/AIDS
There is strong evidence to show that HIV-seropositive individuals are deficient in glutathione peroxidase. Gil and colleagues,54 for example, compared levels of it in the blood of 85 HIV/AIDS patients with those in 40 healthy controls, confirming the presence of a significant (p<0.05) reduction of the selenoenzyme in the infected group. Beyond this, Batterham and co-workers55 showed that such depressed glutathione peroxidase levels in men with HIV/AIDS could be raised by supplementation with selenium and other antioxidants.
If Aumann and co-workers56 are correct, then HIV/AIDS patients should also be very deficient in the four nutritional components that these researchers believe are required by the body to produce glutathione peroxidase—namely, selenium, cysteine, glutamine and tryptophan. There is certainly good evidence to prove that such individuals are selenium deficient.
Several studies have documented declining plasma selenium levels in patients with HIV/AIDS. Probably the most convincing of these was conducted by Baum and co-workers57 in Florida. These researchers monitored 125 HIV-1–seropositive male and female drug users in Miami over a period of 3.5 years. This study collected data on CD4 T-cell count, antiretroviral treatment and plasma levels of vitamins A, E, B6 and B12 as well as selenium and zinc. A total of 21 of these patients died during the study. Only plasma selenium levels and CD4 T-cell counts could have been used to predict which of the 125 patients would die, with selenium levels being more accurate predictors than CD4 T-cell counts. The same research group also monitored 24 HIV-infected children over a five-year period, during which time half of them died of AIDS. As with adults, the lower their serum selenium levels, the faster that death occurred.
It also appears as if the selenium deficiency seen in HIV/AIDS patients, as expected, makes them more susceptible to Coxsackievirus infection. As a consequence, myocardial infarctions are quite common even in relatively young people who are HIV seropositive.59 In addition, autopsies often reveal that AIDS patients60, 61 have been suffering from, and perhaps have died of, Keshan disease—an endemic heart disease normally limited to the populations of regions of extreme selenium deficiency.
HIV/AIDS patients also display low plasma levels of cysteine at every stage of infection.62 Since this amino acid is one of the body's major sources of sulphur, they are very deficient in it.63 Interestingly, depressed cysteine is also characteristic of SIV-infected rhesus macaques.
Several researchers have documented glutamine deficiencies in HIV/AIDS patients.65–67 Shabert and colleagues, for example, discovered that much of the weight loss seen in individuals could be reversed by glutamine–antioxidant supplementation.
If HIV is producing glutathione peroxidase for its own purposes and if this selenoenzyme contains tryptophan, then HIV/AIDS patients should be deficient in this amino acid. This appears to be the case. Werner and co-workers,68 for example, have shown that, in male patients with advanced HIV infection, tryptophan serum levels are less than half of those found in matched healthy controls. Since tryptophan is required for the biosynthesis of both serotonin and niacin, it is not surprising that their levels are also depressed in patients with HIV/AIDS.69, 70
It is clear from the literature just cited that HIV/AIDS patients are indeed very deficient in glutathione peroxidase and in the four components of this selenoenzyme—namely, selenium, cysteine, glutamine and tryptophan. In short, the clinical and scientific evidence supports the truth of corollary one.
COROLLARY TWO: Effective Treatment for HIV/AIDS Should Involve Correcting Deficiencies of Glutathione Peroxidase and its Nutritional Precursors
There is a wealth of evidence that correcting one or more of the deficiencies of selenium, cysteine, glutamine and tryptophan, which are characteristic of HIV/AIDS, has significant health benefits. Selenium, for example, is a key immunological enhancement agent that has a strong impact on lymphocyte proliferation.
This relationship was confirmed by Peretz and co-workers,71 who monitored enhanced lymphocyte response in elderly subjects given a daily 100-microgram selenium supplement over a six-month clinical trial. This seems to be because selenium is essential for lymphocytes—as shown by Porter and colleagues,72 who demonstrated that plasma proteins carry selenium to lymphocytes which absorb it. Further, Wang and co-workers73 have demonstrated that selenium enhances lectin-stimulated T-lymphocyte proliferation and is an important modulator for immune response. It is not surprising, therefore, that HIV/AIDS patients with depressed plasma selenium also show T-lymphocyte abnormalities.74
There have been numerous clinical trials to explore the impact of cysteine supplementation (usually given as N–acetylcysteine) on HIV/AIDS symptoms. De Rosa and co-workers76 at Stanford University, for example, have shown that the oral administration of N–acetylcysteine significantly replenished glutathione in HIV-infected individuals. This is very significant, since subsequent research has established that glutathione levels in HIV-positive patients is a predictor of survival rates.77
As previously mentioned, cysteine is a significant source of sulphur and HIV/AIDS patients are very deficient in this element. A trial carried out in Germany by Breitkreutz and colleagues77 showed that N–acetylcysteine supplementation helped to correct this sulphur deficiency while simultaneously improving immunological functions in HIV/AIDS patients.
Glutamine is a major requirement of cells which are rapidly proliferating. As a result there is a significant requirement for it in the digestive tract, where it is essential for intestinal cell proliferation, intestinal fluid/electrolyte absorption and mitogenic response to growth factors. Since glutamine deficiency is so characteristic of HIV/AIDS, it is not surprising that patients typically suffer badly from digestive malfunction and diarrhoea. It has been demonstrated by Noyer and co-workers,78 at the Albert Einstein College of Medicine, that glutamine therapy improves intestinal permeability in AIDS patients, although the amount required to enhance intestinal absorption may be as much as 20 grams per day.
Glutamine is also essential for muscle building; in HIV/AIDS patients, deficiencies of it seem linked to loss of body cell mass. Shabert and his colleagues79 have demonstrated that glutamine and antioxidant supplements can reverse the weight loss typically seen in such patients, while Kohler and co-workers80 also have shown that glycyl-glutamine improves lymphocyte proliferation in AIDS patients.
I am not aware of any clinical trials conducted to test the impact of tryptophan supplementation on HIV/AIDS. However, it is interesting to note that antiretroviral drug therapy, designed to prevent HIV-1 replication, slows the rate of tryptophan loss seen in seropositive individuals.81 Similarly, plasma tryptophan levels can be increased in HIV-infected patients by nicotinamide supplements.82 This is perhaps not surprising, given the close chemical association between this nutrient and the tryptophan derivative, niacin.
Simply put, there is a great deal of evidence that HIV/AIDS patients are typically deficient in glutathione peroxidase and its precursors—selenium, cysteine, glutamine and tryptophan. Beyond this, it is clear from clinical trials that survival rates and patients’ symptoms are improved by supplementation with such nutrients.
Indeed, one might go so far as to say it would be medical malpractice not to give these nutrients to those who are HIV seropositive.
COROLLARY THREE: Reversing Deficiencies of the Precursors of Glutathione Peroxidase Should Reverse the Symptoms of HIV/AIDS
The hypothesis presented here suggests that HIV/AIDS is a disease that is caused by the combined deficiencies of glutathione peroxidase and its precursors. If this is correct, then the symptoms normally associated with a deficiency of each one of these substances ought to occur in AIDS patients. There is a wealth of evidence that suggests this is the case.
Baum and co-workers83 have shown that adults and children dying of AIDS display both depressed CD4 T-lymphocyte counts and very depleted plasma selenium stores. This seems to be part of a positive feedback system, since one of the most significant symptoms of selenium deficiency is a reduction of CD4 T-lymphocytes, which occurs because this trace element is needed for their production. A lowering of CD4 T-lymphocyte levels causes a drop in the efficiency of the immune system, encouraging infection by other pathogens and resulting in a further decline in selenium. I have termed this positive feedback system the selenium CD4 T-cell tailspin.84
HIV/AIDS patients also often display a hypothyroid or low T3 (tri-iodothyronine) syndrome.85 This seems to occur because selenium deficiency causes a reduction in deiodinase, the enzyme required to convert T4 (thyroxine) to T3. It has been further suggested that such a selenium deficiency abnormality of the thyroid may be a significant factor in the AIDS wasting process.86
Selenium deficiency has been linked to depression in the general population.87, 88 It is not surprising, therefore, that this is also a characteristic of people with HIV/AIDS.
It would appear, therefore, that at least three of the major symptoms of HIV/AIDS—namely, depressed CD4 T-lymphocyte count, lowered tri-iodothyronine production and depression—can be explained, at least in part, by the inadequate selenium levels seen in such patients.
In 1981, Bunk and Combs89 described an experiment demonstrating that, in chickens, selenium deficiency impaired the conversion of the S–amino acid methionine into cysteine. It is highly likely that this is true for humans. If it is, then, by encoding for the selenoenzyme glutathione peroxidase, HIV-1 causes a deficiency of cysteine in infected individuals in two distinct ways. Firstly, the virus removes cysteine directly from the body as it replicates. Secondly, it creates a selenium deficiency which impairs the conversion of methionine to cysteine, so reducing the availability of the latter. Simply put, HIV-1 both increases the demand for and reduces the supply of cysteine in patients who are HIV-1 positive. Cysteine deficiency, in and of itself, has been shown to be associated with depressed glutathione, poor wound and skin healing, psoriasis, abnormal immune function and greater susceptibility to secondary infections and cancers.90 All these characteristics of cysteine deficiency are seen in HIV/AIDS patients.
Glutamine is a major nutrient required by rapidly proliferating cells and is of particular significance in the digestive tract. Deficiencies cause abnormal intestine permeability and digestive malfunction, often associated with diarrhoea.91 Glutamine is also a favourite with body-builders, who use it in large quantities to promote muscle growth. It is not surprising that muscle protein wasting, therefore, is a symptom of glutamine inadequacy. Both diarrhoea and muscle wasting are characteristics of HIV/AIDS.92
Tryptophan deficiencies, in and of themselves, have led to major health problems in the past. Probably the worst of these was pellagra, which developed in children eating diets high in corn. Maize is very deficient in tryptophan and so such children quickly developed pellagra, which is thought to be due to a co-deficiency of both tryptophan and its metabolite, niacin.93 As a consequence of these two deficiencies, such individuals could not produce adequate nicotinamide adenine dinucleotide and so developed pellagra. The symptoms of this disease were known as “the four Ds”—namely, dermatitis, diarrhoea, dementia and, ultimately, if not treated effectively, death.94 AIDS patients commonly experience all such symptoms and also display inadequate levels of nicotinamide adenine dinucleotide. This can be reversed, at least in vitro, by the administration of nicotinamide.95
It would appear, therefore, that corollary three is correct and that the great majority of the symptoms of HIV/AIDS (with the exception of those caused by opportunistic pathogens) are a combination of symptoms seen in individuals who are extremely deficient in glutathione peroxidase or in one or more of its precursors.
COROLLARY FOUR: HIV-1 Seropositive Individuals Who Eat a Diet Elevated in Selenium, Cysteine, Glutamine and Tryptophan Should Never Develop AIDS
Obviously, the easiest way to test the truth or otherwise of this fourth corollary would be to arrange for a double-blind, placebo-controlled pilot study in which half the HIV/AIDS patients are given injections of glutathione peroxidase and supplements of selenium, cysteine, glutamine and tryptophan.
Unfortunately, geographers are not expected to develop new disease-related hypotheses that have the potential for undermining genetic, biochemical and clinical authority. As a result, I have been attempting to gain support for testing this concept for more than two years. Given the enormous power of the pharmaceutical industry and its lack of interest in the discovery of a cheap and simple treatment for HIV/AIDS, it has not been an easy row to hoe. To date, all I can point to are two AIDS patients who quickly reversed their major symptoms when attempting to follow my suggested regime.96 Beyond this, there are research teams in South Africa, Tanzania, Botswana and Morocco who have contacted me to express a willingness to conduct such trials, should funding ever become available.
CONCLUSIONS
Death from AIDS is a consequence of four nutritional deficiencies. Fortunately, HIV infection does not need to be a death sentence because such deficiencies are cheap and easy to reverse. And while the four nutrients won’t eradicate HIV, they activate the virus’s own “warning system”, preventing its replication.
The genetic code of HIV includes a homologue for the essential human selenoenzyme glutathione peroxidase. Paradoxically, this viral requirement for selenium generally appears to restrict infection to individuals who, because of a diet deficient in selenium or because of prior infection by other selenium-encoding pathogens, are deficient in this trace element.
Unfortunately, the human population is becoming ever more susceptible to infection by HIV-1 (and HIV-2 to a lesser extent) as well as other selenoenzyme-encoding viruses because of acid rain, which reduces the bioavailability of selenium.
To be replicated, HIV must compete with its host for glutathione peroxidase and its four constituent nutrients—selenium, cysteine, glutamine and tryptophan. As a consequence, replication of the virus gradually depletes seropositive individuals of these substances. AIDS is the end product of these nutritional declines, and most of its symptoms are caused by them. As a consequence, it is likely that AIDS can be easily reversed by correcting such deficiencies.
To illustrate, glutathione peroxidase is one of the body’s most significant antioxidants. A lack of this selenoenzyme therefore accelerates free radical damage and oxidative stress. Beyond this, having inadequate selenium and cysteine undermines the immune system in a process that is accelerated by other infectious pathogens. A deficiency of glutamine encourages muscle wasting and digestive malfunction, while a lack of tryptophan and the compounds it biosynthesises (such as niacin and serotonin) results in dermatitis, diarrhoea and various neurologic and psychiatric symptoms including dementia. Supplementation with the appropriate nutrients naturally reverses these symptoms.
It is ironic, but not really surprising, that our continuous destruction of the global ecosystem is promoting the spread of viral infections (and various chronic degenerative diseases) that threaten humanity’s domination of the planet.
POSTSCRIPT (as at early January 2004)
Since I submitted this article for publication, I have learned of a small AIDS trial that is taking place in Botswana.97 The trial is funded by a Canadian vitamin company and is using the nutrient regimen suggested in my book. Here is a quotation from the initial email report that I received in late September:
“I picked two candidates personally who have fully blown AIDS with relevant symptoms like diarrhoea, skin rash, loss of weight and a lack of appetite. One of these candidates has a severe complication of syphilis which has slowed his recovery somewhat, but still, within two weeks of trials, his skin rash, diarrhoea and fatigue have all but disappeared. The lady candidate gained 3 kg in two weeks and now eats ‘like a horse’. She resumed work last Tuesday after several weeks of absence. I am gaining confidence in this treatment by the day and I hope the same would apply to the remainder of the trial candidates…
“A lady who started the regimen three weeks back has just tested negative for HIV, and her CD4 count has shot up from 500 to 700!” (It’s unknown if this is the same lady who ate “like a horse”!)
In the meantime, I have set up a small company, HD Foster Research Inc., which is having the nutrients made up into a product called HELP. We are giving this away to doctors who treat AIDS patients. The first taker is a physician in South Africa, and I have mailed him enough treatment for 10 patients. The idea is to find medical supporters who can vouch that the treatment works. Beyond this, the small Canadian company that is using my treatment in Botswana (anecdotal evidence suggests a 99% success rate in reversing AIDS) has spread its activities into Zambia.
We have decided to produce a video in which I describe my theory of HIV/AIDS, and which also shows patients recovering. We are looking for financial and other assistance to do this. The idea is to give this away to TV stations in Africa and elsewhere.
Recently I checked the progress of the two Victoria, BC, patients mentioned in my book, who were dying of AIDS in 2001. They are now both in good health and are back at work.
I have also had two more HIV/AIDS papers published in Chinese in the proceedings of two different medical conferences held in Shanghai in November 2003. Two additional papers have been accepted for publication in Chinese medical journals. On 17 March I am scheduled to give a lecture on AIDS at the Centennial AGM of the Association of American Geographers in Philadelphia.
Things are moving along. Hopefully, the world will soon know that the treatment does indeed work. ∞
Author’s Note:
Readers wanting more detailed information about the HIV/AIDS environmental link are directed to the website http://www.hdfoster.com, where they can download a free copy of the book, What Really Causes AIDS.
About the Author:
Harold D. Foster, PhD, was born and educated in England. He specialised in geology and geography, earning a BSc in 1964 from University College London and a PhD in 1968 from London University. He is a Canadian by choice, and has been a faculty member in the Department of Geography, University of Victoria, British Columbia, Canada, since 1967.
A tenured professor, Dr Foster has authored or edited some 235 publications, the majority of which focus on reducing disaster losses or identifying the causes of chronic disease or longevity. He has published hypotheses on the origins of numerous diseases including myocardial infarction, SIDS, cancer, diabetes, schizophrenia, multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), Alzheimer’s and Parkinson’s diseases, and stroke.
His numerous books include: Disaster Planning: The Preservation of Life and Property (Springer Verlag, New York, 1980); Reducing Cancer Mortality: A Geographical Perspective (Western Geographical Press, Victoria, 1986); The Ozymandias Principles: Thirty-one Strategies for Surviving Change (Southdowne Press, Victoria, 1997); and What Really Causes AIDS (Trafford Publishing, Victoria, 2002; see review in NEXUS 10/05). His new book, What Really Causes Schizophrenia, is to be published by Trafford in late 2003.
Harold Foster is a member of the Explorers Club as well as several academic organisations including The New York Academy of Sciences, The Royal Geographical Society and The Royal Society of Literature. He is also the editor of both the International and Canadian Western Geographical Series and is a member of the boards of the Journal of Orthomolecular Medicine and the International Schizophrenia Foundation.
He has been a consultant to numerous organisations, including the United Nations and NATO, and to the governments of Canada, Ontario and British Columbia. He is also a member of the Science Advisory Panel for the Healthy Water Association.
Every day, Dr Foster makes a point of taking at least the recommended daily allowance of the known essential nutrients. He is also currently pursuing offers for his suggested nutrient mixture to be produced for use in clinical trials with AIDS patients. For a more detailed résumé, visit the website http://www.hdfoster.com.
Endnotes
54. Gil, L. and others, “Contribution to characterization of oxidative stress in HIV/AIDS patients”, Pharmacol Res 2003; 47(3):217-224.
55. Batterham, M. and others, “A preliminary open label dose comparison using an antioxidant regimen to determine the effect on viral load and oxidative stress in men with HIV/AIDS”, Eur J Clin Nutr 2001; 55(2):107-114.
56. Aumann, K.D. and others, “Glutathione peroxidase revisited – simulation of the catalytic cycle by computer-assisted molecular modelling”, Biomed Environ Sci 1997; 10(2-3):136-155.
57. Baum, M.K. and others, “High risk of HIV-related mortality is associated with selenium deficiency, J Acquir Immune Defic Syndr Hum Retrovirol 1997; 15(5):370-374.
58. Campa, A. and others, “Mortality risk in selenium deficient HIV-positive children”, J Acquir Immune Defic Syndr Hum Retrovirol 1999; 20(5):508-513.
59. Law, M. and others, “Modelling the 3-year risk of myocardial infarction among participants in the Data Collection on Adverse Events of Anti-HIV Drug (DAD) study”, HIV Med 2003; 4(1):1-10.
60. Dworkin, B.M., “Selenium deficiency in HIV infection and the acquired immunodeficiency syndrome (AIDS)”, Chem Biol Interact 1994; 91(2-3):181-186.
61. Dworkin, B.M. and others, “Reduced cardiac selenium content in the acquired immunodeficiency syndrome”, J Parenter Enteral Nutr (JPEN) 1989; 13(6):644-647.
62. Droge, W. and others, “Functions of glutathione and glutathione disulfide in immunology and immunopathology”, FASEB J 1994; 8:1131-1138.
63. Breitkreutz, R. and others, “Improvement of immune functions in HIV infection by sulfur supplementation: two randomized trials”, J Mol Med 2000; 78(1):55-62.
64. Droge, W. and others, “HIV-induced cysteine deficiency and T-cell dysfunction – a rationale for treatment with N–acetylcysteine”, Immunol Today 1992; 13(6):211-214.
65. Shabert, J.K. and others, “Glutamine-antioxidant supplementation increases body cell mass in AIDS patients with weight loss: a randomized double-blind controlled trial”, Nutrition 1999; 15(11/12):860-864.
66. Noyer, C.M. and others, “A double-blind placebo-controlled pilot study of glutamine therapy for abnormal intestinal permeability in patients with AIDS”, Am J Gastroenterol 1998; 93(6):972-975.
67. Kohler, H. and others, “Glycyl-glutamine improves in vitro lymphocyte proliferation in AIDS patients”, Eur J Med Res 2000; 5(6):263-267.
68. Werner, E.R. and others, “Tryptophan degradation in patients infected by human immunodeficiency virus”, Biol Chem Hoppe Seyler 1988; 369(5):337-340.
69. Murray, M.F, “Niacin as a potential AIDS preventative factor”, Med Hypotheses 1999; 53(5):375-379.
70. Sidibe, S. and others, “Effects of serotonin and melanin on in vitro HIV-1 infection”, J Biol Regul Homeost Agents 1996; 10(1):19-24.
71. Peretz, A. and others, “Lymphocyte response is enhanced by supplementation of elderly subjects with selenium-enriched yeast”, Am J Clin Nutr 1991; 53(5):1323-1328.
72. Porter, E.K. and others, “Uptake of selenium-75 by human lymphocytes in vitro”, J Nutr 1979; 109(11):1901-1908.
73. Wang, R.D. and others, “Investigation of the effect of selenium on T-lymphocyte proliferation and its mechanisms”, J Tongji Med Univ 1992; 12(1):33-38.
74. Baum, M.K. and others, “High risk of HIV-related mortality is associated with selenium deficiency”, J Acquir Immune Defic Syndr Hum Retrovirol 1997; 15(5):370-374.
75. De Rosa, S.C. and others, “N–acetylcysteine replenishes glutathione in HIV infection”, Eur J Clin Invest 2000; 30(10):915-929.
76. James, J.S., “NAC: First Controlled Trial, Positive Results”, AIDS Treatment News 1996; 250:1-3, posted at http://www.aids.org/immunet/atn.nsf/ page/ZQX25002.html.
77. Breitkreutz, R., “Improvement of immune functions in HIV infection by sulfur supplementation: two randomized trials”, J Mol Med 2000; 78(1):55-62.
78. Noyer, C.M. and others, “A double-blind placebo-controlled pilot study of glutamine therapy for abnormal intestinal permeability in patients with AIDS”, Am J Gastroenterol 1998; 93(6):972-975.
79. Shabert, J.K. and others, “Glutamine-antioxidant supplementation increases body cell mass in AIDS patients with weight loss: a randomized double-blind controlled trial”, Nutrition 1999; 15(11/12):860-864.
80. Kohler, H. and others, op. cit.
81. Zangerle, R. and others, “Effective antiretroviral therapy reduces degradation of tryptophan in patients with HIV-1 infection”, Clin Immunol 2002; 104(3):242-247.
82. Murray, M.F. and others, “Increased plasma tryptophan in HIV-infected patients treated with pharmacologic doses of nicotinamide”, Nutrition 2001; 17(7-8):654-656.
83. Baum, M.K., op. cit.
84. Foster, H.D., “AIDS and the ’selenium-CDR T cell tailspin’: The geography of a pandemic”, Townsend Letter for Doctors and Patients 2000; 209:94-99.
85. Bourdoux, P.P. and others, “Biochemical thyroid profile in patients infected with the human immunodeficiency virus”, Thyroid 1991; 1:149.
86. Geelhoed-Duijvestijn, P.H. and others, “Effect of administration of growth hormone on plasma and intracellular levels of thyroxine and tri-iodothyronine in thyroidectomized thyroxine-treated rats”, J Endrocrin 1992; 133:45-49.
87. Hawkes, W.C. and others, “Effect of dietary selenium on mood in healthy men living in a metabolic research unit”, Biol Psychiatry 1996; 39:121-128.
88. Finley, J.W. and others, “Adequacy or deprivation of dietary selenium in healthy men: clinical and psychological findings”, J Trace Elem Exp Med 1998; 11:11-27.
89. Bunk, M.J. and others, “Evidence for an impairment in conversion of methionine to cysteine in the Se-deficient chicken”, Proc Soc Ex Biol Med 1981; 167:87-93.
90. Braverman, E.R. (with C.C. Pfeiffer), The Healing Nutrients Within: Facts, Findings and New Research on Amino Acids, Keats Publishing, New Canaan, 1987.
91. Rhoads, M., “Glutamine signalling in intestinal cells”, J Parenter Enteral Nutr 1999; 23(5 Suppl):S38-40.
92. Ward, D.E., The AmFAR AIDS Handbook: the Complete Guide to Understanding HIV and AIDS, W.W. Norton, New York, 1999.
93. Braverman, E.R., op. cit.
94. ibid.
95. Murray, M.F. and others, “HIV infection decreases intracellular nicotinamide adenine dinucleotide (NAD)”, Biochem Biophys Res Commun 1995; 212(1):126-131.
96. Foster, H.D., 2000, op. cit.
97. Email to author, September 25, 2003.
Cancer & AIDS Successfully Treated with Induced Remission Therapy - Part 2
Published by December 30th, 2006 in AIDS, Cancer and Corporate Crime. 0 CommentsINDUCED REMISSION THERAPY
Our Best Hope Against Cancer?
Part 2
Dr Sam Chachoua has identified ‘nemesis organisms’ that can control and even cure diseases such as cancer and AIDS, but his therapies have been largely ignored by the medical establishment.
Extracted from Nexus Magazine, Volume 5, #4(June-July 1998).
PO Box 30, Mapleton Qld 4560 Australia. editor@nexusmagazine.com
Telephone: +61 (0)7 5442 9280; Fax: +61 (0)7 5442 9381
From our web page at: www.nexusmagazine.com
From a lecture presented by
Sam Chachoua, MB, BS
on “Revolutionary New Therapies in the Treatment of Incurable Diseases”
at the 2nd World Congress on Cancer Sydney, Australia
15-19 September 1995
[We published the first part of Dr Sam Chachoua’s story in NEXUS 5/01 and promised to follow up with further detail on his Induced Remission Therapy. Here we present an edited transcript of the lecture he gave at the 2nd World Congress on Cancer, held in September 1995, followed by a recent update from Dr Chachoua.–Editor]
My name is Sam Chachoua and I’m an MD from Melbourne, Australia. What I’m going to talk to you about now is something quite new and revolutionary. It’s called Induced Remission Therapy and it’s a treatment that is based on three natural phenomena: organ resistance, organism resistance, and spontaneous remission.
I first got into cancer research at an early age when my father was diagnosed with multiple myeloma, and I basically tried to see whether I could find something that could help him where conventional therapies were failing. One thing that I noted in all the studies I had was that there are parts of the human body-for example, the small intestine-which are consistently resistant to cancer. Regardless of how far and wide cancer usually spreads, it usually leaves the small intestine alone.
There’s also something known as “organism resistance”, which means that most other animals that we try to give human cancer to are able to reject it. So I set about designing an experimental protocol where I was going to find out what it was about the small intestine that made it resistant to cancer, and I was going to find out what it was about horses, cats and dogs and other animals that made them resistant to human cancer.
To cut a long story short, I managed to isolate the immunological factors which I used in experimental protocols at the Peter McCallum Cancer Institute. At age 18 I’d written my first paper, and the following year I presented it before the Clinical Oncology Society of Australia. Let me tell you, I was pretty proud of myself. I thought: “Kid, you’ve got it made; you’ve helped your dad now, and this therapy is going to be adopted soon.” And I could just see it. I was going to walk into the Clinical Oncology Society of Australia. Everybody’s going to cheer and get on the phone and say: “Hey, we’ve got a young kid here; give me the Nobel Committee.” Naïve! I was actually greeted with all the warmth one usually reserves for a venereal disease or an acute attack of hemorrhoids!
Let me just jump to how this form of therapy can apply to AIDS. We’ve known for a very long time that it’s impossible to give animals AIDS by injecting them with HIV. Now there are two possibilities: either animals are inherently resistant, i.e., they don’t have receptor sites for HIV; or maybe, just maybe, they have an immune system which is capable of fighting and destroying the virus. Well, hey, let’s check it out!
So the initial data all showed promise that you could raise an immune response out of a horse, for example, that would selectively destroy HIV. What intrigued and amazed me was seeing the thought processes or, rather, not being able to see the thought processes in the AIDS researchers who for years now have tried to find some way of developing an immune system resistant to AIDS. They sit there and say: “Well, we need to make an animal model. Once we have an animal model, once we’ve made an animal sick with AIDS we can find a way to cure it.” So they get their little test animals; they get their rats, their dogs, their horses and cats; they inject them with HIV-and they can’t give them AIDS! They get really upset about that: “How am I supposed to find a cure for AIDS if I can’t give this animal AIDS? I’m injecting it with HIV to try to find an immune response that will kill HIV, and it won’t take it. How am I supposed to do my job?” Are you following the thought pattern here? It’s looking right at them.
It would seem a bit of an anticlimax if I were to tell you that one of the easiest ways to deal with the greatest plague today is to use an animal system that’s resistant to the plague, and treat and cure the people suffering from the disease. A hundred years ago, before we had antibiotics, the only therapy we had for pneumonia, smallpox and polio was horse serum. They’d get a horse, shoot it with a disease, draw the horse serum out, shoot that into the person and cure them. If that therapy was good enough to deal with the plagues a hundred years ago, why isn’t it being applied now?
But what happens if you do apply it now? Here’s the case of a young man with AIDS. He’s 32 years old. He’s got a pneumocystis pneumonia, he’s short of breath, he’s got a T-cell count of 80 and a T4/T8 imbalance. So, essentially, his blood, his virus, is extracted out; an animal, such as a horse, is vaccinated with his blood; the antiserum from the animal is then purified against this patient’s blood so it doesn’t cause allergic reactions; and the patient is treated with the horse’s serum. And we see that within 24 hours, the pneumocystis pneumonia clears up. That’s pretty remarkable considering that the best that antibiotics can do, if they can clear it, is take days to weeks. This patient’s symptoms resolved; his T-cell count went up to 780 within 10 days from a low of 80, and his T4/T8 ratio became normal.
Now what I’ve just told you is pretty dramatic, but doesn’t it make some sense to you? Isn’t it common sense? We have a disease that can ravage our immune systems but can’t ravage a horse’s, can’t ravage another animal’s. Why not use those animals’ immune systems to destroy the disease?
So, off I went to the big hospitals in the US, and I said, “Hey, guys, look at this!” I showed them the case study and the patient I brought with me. I showed them ‘befores’ and ‘afters’ which were done on US soil, and they said: “Inject a person with horse serum? Are you insane? We’d never do that.”
A few months later, some of the people whom I was speaking to from a related centre-friends of theirs, actually-came out with the announcement that they’re going to give a baboon’s bone marrow to an AIDS patient because baboons are resistant to HIV!
At that stage, feeling dejected and rather silly, I set about trying to investigate as much in the way of alternative therapy and conventional therapy as I could-and believe me, I investigated just about everything, down to laughter therapy!
Now one thing that really struck me very quickly on in the piece when I was reviewing all the alternative, natural and conventional therapies is that there are two misnomers that exist in this world. One of them is “natural therapy”.
Please, don’t take me the wrong way. There’s a lot of good in alternative therapy, there’s a lot of good in vitamins and diet, but what on Earth is natural about shoving 50,000 units of vitamin C intravenously? What’s natural about injecting ozone into somebody’s backside? What’s natural about cappuccino enemas?
The other great misnomer in the medical field of conventional therapy are the terms “radiotherapy” and “chemotherapy”. How the world “chemo” ever got side by side with the word “therapy” is beyond me. Never before has a therapy repeatedly failed for 80 years, caused the most hideous side effects known to man, and continued to prosper and flourish. It amazes me that chemotherapy has spread its wings without people knowing.
For example, how many people know that the commonest therapy for aggressive psoriasis these days is chemotherapy? Teenagers and people of child-bearing age will go to the doctor, and their doctor will say: “I’ll give you a folic acid antagonist called Methotrexate.” You see, “folic acid antagonist” sounds better than “chemotherapy”, doesn’t it, but it’s chemo. These kids are swallowing poison, and they and their kids will suffer the consequences.
Did you hear about the latest breakthrough, a new form of contraception that’s now on the market? It’s a one-shot abortion injection. Well, the abortion injection is a folic acid antagonist. It’s chemotherapy.
Let’s be blunt about something. Alternative therapy is great, and we can probably extend and improve the quality of life of people who are ill, and, heaven knows, we can prevent a lot of diseases from happening; but when you cut down to the chase, conventional therapy and alternative therapy are joined by one thing.
Over the past hundred years in the war against cancer, we’ve failed abysmally. Let’s be frank here: if a hundred people were to do the most arduous alternative therapy available, we would not cure a hundred cancer patients; we would not cure a hundred AIDS patients.
There are only three reasons why we’re failing in our war. One possibility is that the weaponry isn’t powerful enough. Now, in chemotherapy and radiotherapy we have weaponry that can cremate a person! So, it can’t be that one; rule that one out. The second possibility is that the target is invisible. Now we know that to be true; we know that cancer cells are immunologically invisible. The third possibility is that there’s another target.
The one thing I found depressing about alternative and conventional therapy is that they both totally ignored the phenomenon of “spontaneous remission” which is perhaps the most natural phenomenon which repeatedly tells us how to cure terminal disease. “Spontaneous remission” is a term given to miraculous healings, where people on their death bed ‘rise from the dead’ within two to three days without a trace of their disease. It’s a phenomenon that’s been reported in the literature but hardly ever investigated.
The data on spontaneous remission strongly suggest that just before a person with cancer, heart disease, arthritis or any of the other terminal diseases has a spontaneous remission or a cure of their disease, they suffer what seems to be a viral or bacterial or some form of severe infection.
This was noticed by a Dr Didot, in France, who noted that the existence of syphilis precluded the appearance of cancer. If prostitutes had syphilis, they were very unlikely to develop cancer. This doctor actually treated 20 cancer patients with syphilis and, of those 20, 14 went into total remission. As the syphilis grew, it munched up the cancer; the cancer went away. Another three patients did pretty well, and a couple of them died of the syphilis. But this was a few hundred years ago, and given the choice between “the Big C” and “the Big S”-well, today we can cure syphilis with a couple of shots of penicillin, or so I’ve been told!
Late last century, Dr William Coley had a patient who had bone cancer and developed a severe syphilis or skin infection. As the skin infection grew, it munched on the bone cancer and the bone cancer disappeared. Dr Coley went on to develop what he called “Coley’s toxins” and used them for many years as a therapy that got quite good results.
The trouble here is that Dr Coley succumbed to what I call “macho medicine”. The infection he isolated from the patient, and which cured the patient, had remarkable successes in subsequent patients treated with the same infection, but he wasn’t happy with that. Coley wanted something that would do better, so he found a more toxic infection. Instead of using the specific Streptococcus strain which he’d isolated from the patient, he found a Streptococcus that kills people, reasoning that it’s more toxic, therefore it will kill more cancer, and therefore the chances of cure are better.
It’s been long known that in areas where malaria exists, there’s no cancer; and when you get rid of malaria, drain the swamps, kill the mosquitoes, the cancer rate rises. People who have cancer and who catch malaria have a chance of going into remission. Just recently, Dr Henry Heimlich [who developed the Heimlich manoeuvre for preventing choking] injected a few AIDS patients with malaria and managed to get them into some form of remission where they improved and stayed stable at the improved level.
All these observations led me to come up with something I call “nemesis theory”, which states that for every disease there’s an antidisease organism which will specifically attack and destroy it.
This then led to the development of “nemesis therapy”, where I make extracts of these “nemesis organisms” with which to treat specific diseases.
And how do you find nemesis organisms? Well, you look around. Where there’s a disease and there’s less of another disease, the chances are that they’re antagonistic to each other. Or, you work on basic levels, as I like to do, and do test after test after test to check.
What I did in the laboratory was get thousands of bottles and place leukemia lymph node tumour biopsies in them. Each bottle had a particular organism growing inside it. The one with affinity for the cancer actually grabbed hold of the cancer and ate it. This protein ‘web’-actually, a fungus-shot up and encapsulated the tumour. Within a few days, there was a little bit of the cancer left. A couple of weeks later, no cancer-just the fungus!
So what this does is it gives us this new therapeutic modality. This nemesis organism can now give us highly specific chemicals that it used to kill the cancer, but which can be made so they do not attack any other sort of tissue. Two, it can give us tagging complexes which stick to the outside of the cancer and make the cancer highly visible to the immune system. And three, it can give us a complete range of digestive enzymes which are specific for digesting the cancer and the cancer alone. So this little baby not just kills the disease, it also cleans up after itself!
With use of the tagging system, if the immune system looks at this fibrillary network of protein stuck onto the outside of the cancer, it doesn’t see cancer; it sees a bug and it wants to go after the bug. Now, you don’t inject the bug; you purify the protein extract that sticks to the cancer and you inject that. That then sticks to the cancer in the body. The body can then see it and recognise it because it’s tagged with bacterial, fungal or viral protein.
You and I have no trouble getting rid of a cough or a cold in a week or two. We can get rid of cancer: make the cancer look like a cough or a cold by sticking cough or cold particles on it, and the body will attack it, destroy it and remove it.
However, there were instances where patients had a regression several months or years after treatment of their tumours with a tagging complex. This suggested that tagging the cancer was not the be-all and end-all, that tagging the cancer cell still didn’t cure cancer the disease. There was another factor at work.
An interesting observation was made about 20 years ago when leukaemia patients were treated by wiping out their bone marrow and then giving them somebody else’s bone marrow. It was found that the leukaemia would invariably recur. And you know how they say how cancer comes back? Well, the doctor says: “Sorry, Mr Jones; it seems that when I was operating on you and I was giving you the chemo and the radio, one cell spilt, and this one cell hid and then went all over the place and grew again-just this one cell, the spilt cell.” One cell or a few cells get loose and the disease comes back. This may account for some of the cancer recurrences, but to try to explain all cancer recurrences that way, the medical term for that is “crap”!
What we know from those leukaemia trials is that they wiped out the patient’s bone marrow. There was nothing left! They gave him someone else’s bone marrow. Six months later, the leukaemia came back. Now, if it was a leftover cell, then when you check that leukaemia cell you should find that it’s the same as the leukaemia you treated before the patient went into remission, true? It should be the same cell come back. However, when they ran DNA checks, they found that not only wasn’t it the same cell, but it belonged to the donor. It was the donor’s bone marrow that had turned into leukaemia cells!
This finding has been published in the conventional medical literature, and it means that cancer the disease is not cancer the cell. There is something in the body of a patient which regenerates and augments cancer, the cancer cell. And if you don’t address that, then you won’t get rid of the disease.
So there I was, with all these little bottles, cooking up these nemesis organisms and tagging them, but something kept showing up over and over and over again which was driving me nuts. I would incubate the cancer with another organism-say, an E. coli-and I’d find other organisms growing when the cancer cells died, that I hadn’t put in there. They would usually be staphylococcal or streptococcal in appearance. Acid-fast bacilli sometimes would show up, depending on what culture medium was used and for how long I cultured them.
Now this is really interesting. What you notice is what some people would call “pleomorphism” in progress. A couple of elements would develop these elongated rodlike structures, and you could actually see a coccal form changing into a rodlike form. Pleomorphism in action.
I went to my colleagues and said: “Look, why do I keep getting these bugs? It’s a sterile cancer I’m putting into the bottle, for goodness sake. I’m incubating with something completely different, and these bugs keep showing up.” And they said: “Well, Sam, you know what you’re like. You probably sneezed and contaminated the whole lot!” Then I said: “It’s happened over and over and over again. So it’s contamination?” “Yes, yes, absolutely.”
A hundred years ago, everybody blamed this contamination as the cause of cancer. I have the literature. There were thousands of articles written on bacteria-bacterial and fungal organisms-being the cause of cancer. But, as technology gets more and more advanced, we have to reject what’s obvious; and when we reject what’s obvious, the truth becomes very hard to find.
So how could I prove to these people that these organisms are actually intricately involved in the cancer process or in the AIDS process?
The first thing to do is to grow a bunch of them out of some cancer cells, inject them into a few animals and see how many animals get cancer-and a lot of them do. Because the bug does not kill the animal, the animal develops cancer. In a strange way, it actually appears that developing the cancer makes the animal live longer.
Now, let me warp your minds a little bit here. Believe me, what I’m about to say to you is just a theory, and it has no bearing at all on the efficacy of the therapy, but what if these bugs can’t entice an immune response? They are contained in the middle of the cancer; the body is not doing anything to fight them, and yet they’re not spreading. What’s containing them? What if cancer isn’t really the enemy? What if it’s the body’s last-chance attempt at getting these bugs and localising them in an area so they don’t spread and kill us in a hurry? What if cancer is actually doing us a favour? Is that why every time we fry a cancer lesion with radiotherapy and chemotherapy, the whole thing then comes back and explodes all over the place because we’re actually releasing the cause from its entrapment? Just a theory!
This therapy at the very least can control the disease, and at best can cause dramatic, rapid improvement. There are many cases of cancer tumour reducing to half its size within a week or two.
For example, fig. 1a shows the mammogram of a breast cancer in a 65-year-old woman. After 10 days of treatment, the breast is normal (fig. 1b). Fig. 2a shows a case of non-Hodgkin’s lymphoma in a 32-year-old woman. After two weeks of treatment, her lymphoma was considerably reduced in size (fig. 2b).
It’s unheard of to be able to do that and not have significant die-off or toxic effects-and yet they don’t exist with this treatment. When you follow nature and follow the guidelines of what happens in spontaneous remission, Induced Remission Therapy can achieve cures with minimal side effects.
I didn’t choose the public forum to come here and speak to you today. Please understand me: I would much rather be addressing medical practitioners, peers, and getting this out not as an alternative therapy but as a conventional therapy. I’ve spent 12 years trying to get my research published in the conventional literature, and 12 years going from hospital to hospital and being treated like something they’d stepped in.
In light of what I read in the paper today-somebody wrote an article condemning this conference-it appears that the message being sent by that person is that if the conventional medical establishment in all its holiness doesn’t agree with a concept or a therapy, then the public is just too stupid to be able to understand it fully and evaluate it for themselves. The attitude is that the public is just so dumb that they shouldn’t be given the opportunity. Well, my apologies to the author, but the greatest fool I know is a blind fool who’ll say opinions about things he hasn’t even bothered experiencing or investigating himself.
In this “Kevorkian age”, as I call it, where people champion the concept of death with dignity when faced with suffering, pain and disease, I’m offering a technology that can end suffering, pain and disease; and I pray that the emphasis will shift now from trying to support death with dignity to championing life with dignity.
INDUCED REMISSION THERAPY: 1998 UPDATE
After years of lectures, presentations to peers and public appearances as well as numerous radio, television, newspaper and magazine appearances, I find that conventional medicine still has little awareness of the efficacy of my therapies-as evidenced, for example, in the advances achieved using IRT in AIDS remission (see table 1).
Any doctor can make amazing claims, but independent, unbiased testing is a credible way to determine the efficacy of a treatment. It would not only document the effectiveness of my vaccines but would also stir interest in any promising new therapy.
So I brought case studies of AIDS patients I’d treated to Cedar Sinai Medical Center for evaluation. Dr Shlomo Melmed was impressed with the results, and at his suggestion I sent samples of my vaccine to the AIDS and Immune Disorders Center’s Division of Infectious Diseases for in vitro analysis. The clinical analysis performed by Dr Eric Daar indicated that out of the 22 samples tested, 20 of them showed 99% efficacy in neutralising HIV-1.
This analysis was followed up with an independent evaluation by University of Southern California clinical laboratories. This involved the electron microscopy of blood samples taken by a control group infected with HIV. This group yielded over 100 photos that demonstrate the attack, death, disintegration and purge of the HIV virus. The PhD who conducted this test remarked that “the number of intact viral particles has declined for each patient following vaccine administration at a level approximating 50%”.
Examples of this progression from attack to purge are shown in figures 3a to 3d. The first electron microscope photograph (fig. 3a) shows the fragmenting cell full of HIV particles. The next photo (fig. 3b) shows the cell three days later, with improved stability and decreased viral particle count. The third photo (fig. 3c) was taken six days after vaccine treatment and shows fewer viral particles per cell. The final photo (fig. 3d), taken nine days after therapy, shows no intracellular viral particles and the now-visible cell nucleus.
This evidence from the cellular level demonstrates that AIDS and cancer can be attacked genetically without causing significant damage to the healthy, fast-multiplying cells needed to maintain a healthy life.
You’d think that the media, the medical community and others would be alerted to the fantastic results of this treatment.
It’s hard to imagine that institutes entrusted with the public faith and public funds to discover and research new therapies would delay the application of life-saving technology and treatments. It was my hope that knowledge of IRT would be disseminated and the FDA would allow the practice of this therapy upon the countless AIDS and cancer victims who had little hope otherwise. But these doctors and medical institutes denied having any affiliation with me. They denied the impressive test data and even denied knowing me-until forced to declare otherwise before a judge in a civil legal action in San Diego, CA (case no. 700406). It was their incomprehensible behaviour that led me to bring a lawsuit, if for no other reason than to make these test results a record of the court, but I had to pursue these medical organisations so as to have access to further laboratory evidence.
We tend to worship our doctors as gods who will save us from diseases. If these false gods let us down, is it not time to take back responsibility for our lives and well-being? As the public begins to learn of this promising healing technology, IRT, they demand to know why it is being withheld.
I’ve always resented my work being associated under the catch-all phrase “alternative medicine”. My treatment involves an extremely focused hybrid of what is considered “conventional medicine”. However, in my pursuit of any form of therapy that could augment or even supersede my own findings, I’ve always been interested in alternatives as opposed to conventional, toxic and often barbaric treatments.
Although there is hope of finding other practitioners who have medical information to offer, I have yet to find any breakthroughs that would complement my own.
I’ve been appalled to find alternative health organisations that sell juice drinks, vitamin C shots and laetrile powders to desperate patients-products costing hundreds and often thousands of dollars yet only costing a few cents to make.
It was in this spirit that I made this offer: US$100,000 to any “alternative” therapy that can prove 10 cases of full cancer remission.
Additionally, I made this offer to the sceptical world of conventional medicine: US$100,000 to any reputable medical organisation that will test and publish the results of my AIDS and cancer vaccines.
No one has yet come forward to make a claim on these offers.
With the realisation that Induced Remission Therapy can offer favourable results now, and with the assistance of additional resources, medical industry professionals who are truly dedicated to curing disease, and have the ability to catalogue, store and culture autogenous vaccines on a large scale, could and would alter medical treatment as recognised today. Historically, institutions are resistant to change. Change comes slowly. So for any promising therapy to be accepted into the mainstream of medical practice, this would require a paradigm shift in medical science as we know it today.
IRT deals with maladies at the genetic level. Indeed, it is the only therapy now in application that concentrates on disease at this level. The matrix of many diseases is at the genetic level, so many types of illness can be treated with IRT.
Genetic correction is the only hope for achieving a cure in such disease conditions as AIDS and cancer, and starkly contrasts the available toxic and inferior modalities that attack disease mechanisms and symptoms while leaving a damaged blueprint.
The best demonstration of this remarkable ability can be seen in the cases where HIV virus is genetically removed from the cell nucleus. Not only is the body purged of the disease, but it is able to repair damage suffered during the course of the illness. This opens up a new field of cellular regeneration never before possible.
The capacity to reverse age-and disease-related DNA damage opens a new world of therapeutic opportunity and almost limitless applications.
Editor’s Notes:
You can contact Dr Sam Chachoua via Gilbert Burciaga on +1 310 229 5275
Cancer & AIDS Successfully Treated with Induced Remission Therapy - Part 1
Published by December 30th, 2006 in AIDS, Cancer, Corporate Crime and Medical Mafia. 0 CommentsInduced Remission Therapy
Our Best Hope Against Cancer?
Part 1
Dr Sam Chachoua has developed a safe, effective vaccine for healing cancer, AIDS and other terminal illnesses, but medical authorities continue to ignore his work and try to prevent his treatments from becoming widely known.
Extracted from Nexus Magazine, Volume 5, #1 (December 1997 - January 1998).
PO Box 30, Mapleton Qld 4560 Australia. editor@nexusmagazine.com
Telephone: +61 (0)7 5442 9280; Fax: +61 (0)7 5442 9381
From our web page at: www.nexusmagazine.com
©1997 All Rights Reserved
by Sam Chachoua, MB, BS
You can contact Dr Sam Chachoua via Gilbert Burciaga on +1 310 229 5275
TRUTH, LIES AND CONSPIRACIES
Cancer, AIDS, heart disease: three faces of death that devastate so many lives. Many believe that modern medicine will someday develop effective therapies. Those afflicted, their friends, family, lovers, pray that the breakthroughs will come one day soon.
Imagine that the world was offered new treatments and even cures. Newspapers, television, radio and magazines would carry images of medical triumph supported not only by hard data but by living, walking, healthy miracles. Imagine the impact this gift would have on millions of lives: the fulfillment of dreams, the awakening of hope. Try to imagine that the announcement was made, but the world slept through it. Try to picture a public reception with indifference and a medical society charged not to embrace but to destroy all embers of this success.
If the scenario is hard to picture, then don’t try to imagine it but try to remember. It happened. I know. I developed the technology. I made the announcement.
I had always known that the medical system would take some time to change, to develop, but I could not have believed that the public announcement would fall on the deaf ears of victims, nor that my peers would challenge me not on the science of my achievements but with baseless rumours, lies and personal attacks. I could never have anticipated that in answering the dreams of so many, my life would turn into a nightmare.
A THREAT TO THE STATUS QUO
The summer of 1995 was the proudest in my life. Fifteen years of research and medical trials had been building up to this one moment: the triumphant return to my adopted homeland Australia, and the fulfillment of a promise I had made to myself as I watched my father die of cancer so many years before.
Investigating three previously overlooked phenomena-organ resistance, organism resistance and spontaneous remission-I had developed effective vaccines for the prevention and treatment of many killer diseases. The genesis of what I call “Induced Remission Therapy” had begun in Australia more than a decade earlier, but I had spent five years touring the world, lecturing and training doctors in hospitals and institutes. I was returning with independent proof: dramatic and overwhelming evidence that a new age of health was being ushered in. I was returning home to present my discoveries and to fund all research and development in this field.
Armed with X-rays, blood tests, preliminary data from the Colorado University Medical School, UCLA, Cedars Sinai Medical Center and undoubtedly the strongest proof: patients in remission from cancer, AIDS and heart disease-rescued after all other options had been exhausted. This should have been the realisation of my life’s goals. Via the media, millions would meet the success stories and hear of my offer of A$100,000 to initiate investigations in Australia of this new therapy. Then, suddenly, silence. All research institutes were eligible for the $100,000 grant but none came.
I found myself suddenly in the vacuum of a media blackout. Interviews were cancelled, news stories were not run. The public returned to its comfortable staple of cancer “breakthroughs” that may come to be in the next 10 years, the almost weekly announcements from the familiar research institutes. Soon, to the public, I became a forgotten memory. To other interests, however, I was a threat that needed to be destroyed.
A direct frontal assault on Australian soil was not the way, though. I am a medical doctor in Australia; that gives me certain powers and rights. I had offered money to have my therapies proved or disproved, and I had reached out to the public. Attacking me overtly would have raised too many questions. Backed by data from some of the world’s most prestigious research institutes, I was offering my technology with no strings attached.
Australian Medical Board representatives attempted to chastise me for what they believed were obvious lies and deception. They demanded to know who had evaluated my data and where. They accused me of falsely raising hope in poor, dying individuals. It seemed okay to announce that you can cure an occasional rat and raise millions in public donations if you are an institute; however, to say that you can help people and not ask for, but offer money to prove your point was not quite the done thing. Interestingly, the Medical Board enquiry into my “unprofessional” behaviour was the first time I had divulged details of the contacts and institutes investigating my technology. Incredibly, within days, these centres would not only cancel their collaboration with me but also, paradoxically, begin to deny that one had ever existed.
In the USA and Mexico clinics opened up, offering my therapy but delivering heaven-knows-what to unsuspecting patients. I initiated legal action to shut them down, but then became a victim of intense personal and professional attacks as well as physical attempts on my life. I was disgusted to learn that members of UCLA and Cedars Sinai took part in my denigration, but I was in for an even greater shock. When the names of individuals from the Australian Medical Board were used against me, I asked them to intervene; they would not. It seemed that my own Medical Board was supporting the attacks, even if only by inaction.
What is even more incredible is that amongst all the lies were claims that my MB, BS (the Australian medical degree) was not that of a doctor but rather of a nurse or undergraduate. In court, American expert witnesses testified to that and the Australian Medical Board seemed to go along for the ride. Despite incredible resistance and bias, I won the court battle-but the war to save lives still rages.
Unlike stories of conspiracies and cover-ups from long ago, this is happening now. I am still alive; the dream need not be lost, then mourned. The proof is there if you would only look.
I would never have imagined that the hardest part of healing cancer and AIDS would be to get people to listen.
This is my story and our dream. Please read; read and remember.
ACCELERATED DREAMS
Every child has dreams and aspirations, major contributions to make, marks to be left, fame to be found-and what feels like an eternity in which to accomplish these objectives. Curing cancer, growing up to be a hero, saving mankind-these must be some of the commonest fantasies of the young. Impossible tasks seem achievable because there is so much time-time to study, time to grow, time to prepare. Time allows for attainable fantasies, for pleasant dreams. When time is shortened by age or situation, when there is a need for rapid realisation of the dream, reality destroys fantasies and dreams are either abandoned or are often transformed into tangible despair that mourns its loss by cutting harsher than reality ever could.
My father was first diagnosed with cancer in 1975. He was aware of the multiple myeloma (a cancer of the bone marrow) several months prior to submitting to investigations and therapy. Multiple myeloma at the time was treated only when symptomatic, as therapy was felt to decrease lifespan, so he felt no rush to confirm his diagnosis.
He also felt no rush in informing me of his condition. My brother and sister had already entered medical school; I had entered puberty. My father worried that the news would devastate me and affect my studies. Even when faced with death, his concerns were for my life and future. So much changed in the next few years. My father, the workaholic, became much more the family man; always my hero, now my best friend.
STEPPING STONES, ALTERED PERCEPTIONS
Cancer is a disease that has repeatedly thwarted a cure. To defeat it, surely one did not simply need to understand current teachings, one needed to excel. Curing cancer was not within current knowledge, therefore one needed not only to master existing technology but to surpass it.
When seen as stepping stones to achieving my dream, teachings were devoured. I top-marked in several exams and received the T. F. Ryan Roentgen Prize in physics. I tried to apply every new nugget of information to my father’s situation. Biochemistry taught of new agents that could increase the efficacy of chemotherapy and radiotherapy, and of cellular toxic agents that were presented in other contexts. Review of old and new medical research often showed that these agents had been used, and failed to demonstrate efficacy. Chemical therapy of cancer was receiving such intense worldwide scrutiny that it was virtually impossible to generate an original thought or concept from within the field.
Perhaps the answer then lay in the application of unrelated technology to the cancer problem. In physics we were taught that ultrasonic waves would have different heating coefficients depending on the density of the target; that is, the harder something was, the hotter it would become when exposed to ultrasonic frequencies. Cancer was usually denser than normal tissue, and my father’s cancer, being surrounded by bone, could be heated up much more so than surrounding soft tissue. Perhaps such preferential heat damage could kill the cancer.
I approached several cancer researchers. They seemed as excited as I was but cautioned me to check past publications on the subject. Thirty years previously, someone had applied that effect to cancer with marginal and occasionally harmful responses.
If preferential attacks on cancer were not the answer, perhaps protection of normal structures against toxic agents would allow for more savage attacks against cancer. I discovered entire fields of science on the topic of radioprotective and chemoprotective agents. It was almost impossible to generate an original thought within the confines of chemotherapy and radiotherapy, yet despite continued failure these modalities seemed so powerful, so alluring. Cancer was killing my father; I wanted to hit back, hard!
Searching for metabolic weaknesses; poisoning some pathway essential to cancer but not to normal cells; combining modalities of chemotherapy with each other, with radiation, with hormones-everything had previously been done and had failed.
Cancer was seen as a disease of excess (too much smoking, radiation, pollution etc.); the generation of an evil, foreign life-form which battles and invariably destroys its host. Excess must be cut down, taken away, burned or poisoned. This logic, combined with the frustration and hatred generated by this invulnerable nemesis, had locked us into the mindset that dominates current therapies-therapies that have failed us for so long, yet which we refuse to abandon.
STANDARD CONCEPTS OF CANCER
I would like to outline the concepts that have dominated cancer research and therapies over the past few decades. Understanding failure is a useful tool in attaining success.
By definition, cancer is a rogue cell which multiplies without respect for normal systems of cellular control and develops into a mass that invades and destroys normal tissue and structures. It is a powerful, mindless beast that spreads, grows more rapidly than normal tissue and ultimately leads to the death of the host.
Cancer growth rate may be slowed or accelerated by a variety of infections. Even in its natural history, cancer growth is not constant, for during the life of the patient the disease often grows in spurts. It is not uncommon for some cancer metastases to shrink, while most increase in size.
Cancer, the “mindless beast”, starts in a localised area, invades circulatory and lymphatic systems, then spreads throughout the body. Certain cancers exhibit specific patterns of spread, long held by conventional teachings to be dictated by the pattern of circulatory distribution of micro-tumour emboli. This belief furthers the concept that cancer is a rampaging monster, cast by chance to spread its deadly seeds. Passively carried by blood and lymph to their new targets, cancer cells are undifferentiated, non-specific parcels of destruction that care not where they lodge and are not part of the decision-making process in their travels to new organs.
SEARCHING FOR MISSING DEFENCES
A few observations regarding cancer in its population and age distribution are cited repeatedly in immunotherapy literature. Essentially, increased cancer incidence occurs with immunodeficiency; and age, particularly past puberty, also appears to be a promoting factor.
If one considers only these observations, one can conclude that after puberty there is a loss of some vital immune-protective agent. If only we could identify it and replenish it, perhaps we could then triumph over this living nightmare.
The most likely candidate for our source of white blood cells in shining armour seemed to be the thymus gland, a master immune- cell generator which atrophies by early teenage years. Its degeneration seemed to correlate with increased appearance of cancer.
Therapies have proliferated over the years where part or all of the thymus, its products and hormones were used to treat cancer patients. Results were marginal to non-existent, yet, of all the borderline alternative therapies, thymus supplementation persists most stubbornly. Propelled by a romantic notion, hope does not fade-even when it is a false hope.
This restricted logic may have been sound. Perhaps we had fixated on the wrong atrophied organ.
ORGAN RESISTANCE
A common observation, even in the most advanced of malignancies, is that some organs and tissues appear resistant to cancer spread and invasion. The small intestine not only resists spread but also very rarely develops primary cancer. Perhaps there is specific immunologic capacity in the small intestine that prevents cancer from developing and protects it from tumour spread.
A quick search of anatomy and immunology books revealed that the small intestine is blessed with its own immune protection in the form of lymphoid aggregates called “Peyer’s patches”. Much of the function of this line of defence is restricted to the small intestine and does not circulate. This could account for the cancer resistance being local.
Studies of lower animals, particularly birds, indicated that their main immune-processing organ was not the thymus but was located in their embryonic and foetal intestine. Could this part of human immunology have been delegated an unfairly low status? In the animals, their capacity to transfer immune resistance to the entire body is optimal early in life. What if human correlation exists whereby there is transfer of resistant factors between Peyer’s patches (and immune responses localised to the small intestine in later life) and the rest of the body early in life?
In view of the logic supporting thymic supplementation and the hope that restoration of an atrophied organ would destroy disease, there was another interesting observation with relation to Peyer’s patches. Intestinal lymphoid aggregates atrophied with age. We had been so obsessed with the thymus that perhaps we had overlooked the real saviour.
THOUGHT TO ACTION
I had yet to start medical school but spent a good deal of time at the Peter McCallum Cancer Institute in Melbourne where my father was receiving treatment. He had introduced me to several oncologists and I approached them with my ideas. The general response was condescending but usually polite. Dr Ian Cooper, chief haematologist, was not only supportive but also advised me to formulate my ideas as an experimental protocol and present it to Dr Jose of the Immunology Department.
The reply to my preliminary correspondence was surprisingly encouraging: I was invited to address the weekly group meeting of the immunology research team. I prepared theory, protocol and an experimental design.
The presentation was informal and pleasant. Researchers from around the world had submitted protocols for review by this unit. Immunostimulants, interferon, interleukin, lymphocyte harvest pre-chemotherapy: the suggestions were complicated but the themes familiar. I had heard or read about all these concepts before; worse yet, the experiments had been done and repeated years previously. I felt encouraged; my protocol was the only original idea being presented on that day. Surely a new concept would be more appealing to a research unit on the cutting edge of technology than simple repetition of prior failures?
To demonstrate that Peyer’s patches could be stimulated to produce anti-cancer activity, I proposed that lymphocytes isolated from these aggregates be tested against those taken from the spleen and other sources for efficacy against cancer. For obvious reasons I chose multiple myeloma as the cancer system to attack. An important design feature was the testing of ordinary extracts to check for inherent activity and the evaluation of lymphocytes exposed to the cancer during the animal’s life to search for induced activity.
I was aware that the members of the unit had not been previously exposed to this approach; it was new to them. I was also aware that they were not in the least interested.
The first question I was asked was by Dr Jose, requesting the sources and literature supporting this concept as well as data on previous trials and their conclusions on this issue.
“This experiment hasn’t been done before!” I claimed proudly.
“But we need to see prior work in this field,” he countered. “That is a key factor in our accepting experimental protocols!”
In that instant, I understood an intrinsic flaw in the cancer research industry. In order to realise easy acceptance of ideas and receive grants, it was important to show that you were travelling down the same well-worn path of prior investigations.
“I don’t understand,” I replied. “Are you telling me that you won’t do this because it hasn’t been done before?”
“It is hard for me to allocate funds to work lacking prior experimental and data references.” (In essence, he meant “yes”.)
“We have no cure for cancer; we aren’t even close. How will we find it if we don’t explore new avenues?” I did not mean to sound cocky, but all of my hope and courage were suddenly dissipating. I was being rejected.
“We are on a strict budget and have defined guidelines.”
I would not be dismissed; my chance to save my father demanded their acceptance.
“Okay, I’ll pay for it!” (The first of many times that this phrase would pass my lips, and about the only time that I would not regret it.)
Dr Jose smiled and relented. “We’ll see,” he said. “Go do an intensive literature search; we’ll start arranging things next week. Your ideas are interesting and worth exploring.”
My father, Isaac, was by now confined to a wheelchair and my mother, Catherine, catered to his every need and whim. He had been a whirlwind, an active workaholic who delighted in helping the ill. Now confined to a chair and to bed, he exhibited a spirit and attitude that I have since come to realise is far from common. Isaac wasted no time cursing his debility but would focus on how long he was able to stay in his garden, tending to his plants, or on how active and pain-free he could be on a particular day.
That day, my father and mother awaited my return from the conference with anticipation. That night, my home was filled with intense happiness, hope and prayer.
SIMPLE MIRACLES
The experiment I had proposed was amateurish in its simplicity. The small intestine dealt with foreign challenges from ingested food on a continuous basis. Mechanisms for immunologically dealing with harmful agents had to be dramatic, rapid and effective. Every time an organism entered our intestine, we did not have the luxury of mounting a slow response with temperature, lethargy and all the normal physiologic and metabolic features of an immune response. It had to be eliminated with prejudice and finality.
Neighbourhood lymphocytes in the blood and other organs would never meet such overwhelming numbers of challenges, as several barriers needed to be passed first; their response therefore could afford to be more delayed. Immune cells from respiratory passages would also be expected to act rapidly, but they did not appear resistant to the spread and appearance of cancer. Peyer’s patches would protect the small intestine against direct invasion from the large bowel cancers as well as blood-borne metastases. I reasoned that their cancer-killing ability should be visible within minutes.
Others in the laboratory were sceptical, and with reason. Data repeated from decades of studies indicated that it would take the incubation of 50,000 to 100,000 white blood cells for three days with cancer cells and immunostimulants for some of these cells to kill one cancer cell. The effect was often so subtle that radio-uptake and leakage studies had to be undertaken to detect differences. This involved incubating cancer cells with radioactive isotopes of an agent such as caesium, to allow the cancer cells to absorb it. When damaged, cancer cells would then leak the radioactive caesium and that leakage can be measured to indicate cell damage. I reasoned that the effect would be easily seen on light microscopy with oesin uptake. This technique is one where a red dye is added to the cells. Living cells have an active pump system and patent membranes that stop dye entry, whereas damaged and dying cells would be coloured by the oesin.
Control studies using cells from Peyer’s patches that had not been exposed to cancer, showed cancer viability close to 95 per cent. Spleen cells from unexposed animals did the same. Spleen cells from animals that had been carrying the cancer gave me a surprising finding of 100 per cent viability of cancer and an actual increase in cancer count after short-term incubation. It appeared that spleen extract from a diseased animal was actually promoting tumour growth. I did not pay much attention to that finding at the time; I was searching for a cure, not riddles.
Cells from Peyer’s patches of mice that had been carrying the cancer surpassed my expectations. As opposed to the 50,000 to 100,000 cells destroying one cancer cell as previously mentioned over a three-day period, it took one lymphocyte from sensitised aggregates to kill 400 cancer cells in a one-hour-or-less time period. The cancer cells would uptake the red oesin dye and soon collapse.
The experiment would be repeated over and over before I would let myself believe it, before I would show others. Exposed to a very small amount of Peyer’s patch extracts, the cancer cells would turn red with embarrassment, then shrivel and die. Mass slaughter of an invulnerable enemy-it was intoxicating and delicious.
I beckoned for Dr Jose to review the carnage. With just a hint of excitement he exclaimed, “They’re all dead!” He then added in standard clinical “Vulcan” coldness: “Interesting.”
The following weeks were filled with more magic. Tests confirmed no toxicity to healthy cells from my lymphocyte extracts. They were able to protect animals against cancer inoculations, and single low-dose treatment was able to keep the animals living longer once they had the disease. Other cancer systems were tested, including the hepatoma rat model, with identical successes.
FADING DREAMS
I asked when this discovery could be put to use in terminally-ill humans. “Not for a long, long time,” I was told condescendingly.
None of my colleagues or superiors in the laboratory seemed to share my excitement; worse yet, they seemed to resent my success-and me, too, for that matter. Perhaps their egos were bruised. I was often reminded that I had no formal training or education in the field, whereas they had years of it. My work at the Clinical Sciences Building (Royal Melbourne Hospital) and the Ludwig Institute became more and more isolated.
Other affiliates and collaborators who had donated animals and lab space to me included the Department of Biochemistry at Melbourne University. Dr Schreiber, the department head, called me in to advise me personally that in the few days I had been there I had created friction as I was not qualified, paid or a member of their ‘group’ and that structurally they could not support another worker. I had not fought with anybody, or argued or insulted anyone. I was unpaid and, above all, my work was yielding incredible results. How could they terminate investigation on such a promising avenue? These extracts were killing cancer more effectively and more safely than anything else in history!
“It doesn’t matter,” Dr Schreiber replied.
Dr Jose reminded me that publication was the only way for a scientist to achieve recognition, and offered me a poster presentation at the Clinical Oncology Society of Australia (COSA) annual meeting in 1981. Hopes rekindled; I prepared for the big time. Perhaps amongst doctors, the idea of an effective therapy would be better received than in the sterile field of research.
A few months later I was standing proudly by my poster; the youngest-ever presenter of an original project at the prestigious COSA meeting. Few people stopped by my exhibit and most did so only to advise me to leave research and concentrate on my medical studies. I was simply too young and naïve, they said. “What about the work?” I asked. “Interesting,” they replied, and moved on.
Most people spent their time around a diagnostic antibody exhibit. The attractive researcher’s mini-skirt and plunging neckline were also on exhibit. Hell, even I found myself distracted by her monoclonals!
I had come with aspirations of recognition, of encountering someone who would carry the investigation where I could not: in the human field. If I had harboured any illusions of discovery, fame or acceptance, they were quickly shattered. Scientists and doctors alike had greeted me and my discoveries with the same warmth one reserves for an acute attack of haemorrhoids or outbreak of herpes.
While I found the displays worthwhile, the conferences themselves were electrifying. I learned of new techniques being used and the latest trials of hormonal agents, immunostimulants and chemotherapy. Immunotherapy remained an exciting field, whereas the latest chemotherapy evaluations were delivered in gritty, realistic and defeatist manner. Hormones were finding increasing application in general disease management. Bone damage and pain in cancer such as multiple myeloma were shown to be preventable and treatable with anabolic hormones. Just that tidbit of information was worthwhile. It represented a concrete, usable way to help my father.
During the presentations I was to strike a friendship with an oncologist who would later do his best to destroy me. It would be a recurring theme of my life. My greatest enemies would always start as respected friends.
When I suggested to my father’s oncologist that anabolic hormones be added to strengthen his bones and diminish his pain, he became annoyed. I had stepped on his toes by daring to suggest a therapy. Had I hurt his ego? Was there a better way to ask him? Who cares? I just wanted the best for my father. He refused to recommend it and my father refused to try anything his specialist did not recommend.
In one presentation I managed to offend my father’s doctor and be ignored by virtually all others. I had presented a technology for curing cancer, and no one cared.
EGOS AND LIES IN THE HEALING ARTS
One of modern medicine’s greatest achievements is the claim that no one needs to suffer, for there is supposedly no pain that cannot be eliminated by modern pharmaceuticals. That is perhaps true even in severe terminal pain, if one does not mind existing instead of living; existing with clouded perceptions, blunted emotions, a drug-induced stupor; a waking coma where you struggle to comprehend the world racing around you, where you try to communicate but mouth gibberish, where you dig deep, searching for the spark, the joy, the will to continue but find not even a memory of it.
This desperation, this depression, this torment, this torture is often the price paid for physical comfort. “We can prevent suffering in terminal disease” is a statement often made by a medical fool more concerned with perpetuating and reaffirming his illusions of godhood without any regard for reality.
Cancer is nothing if not relentless. Chemotherapy and radiotherapy had failed to arrest the progress of my father’s disease. As the multiple myeloma spread its physical domination, shattered my father’s skeleton and destroyed his immune function, fractures, recurrent infections and pain, constant pain, became features of his life. As he lay bedridden with bone compression, multiple rib breaks and a disintegrating pelvis, my father refused painkillers except at night so that he could sleep. He would not permit any loss of mental clarity during his waking hours: time was short and he wanted to live it, experience it fully. With his body deteriorating, his mind remained the only undesecrated sanctuary, haven, drive to continue. He would not allow this most cherished possession to be tainted; he would not allow his loved ones to see him as anything less than the best he could be.
I was beginning to have major problems at medical school. I could not see the relevance of many topics, nor fathom the time-wasting techniques in teaching other subjects. We learned, for example, how to launch a projectile into orbit around Jupiter (useful knowledge if your practice caters for outer-space aliens and you wish to post them a prescription; of course that would necessitate a pharmacy on Uranus, which could prove uncomfortable). Plutonium purification in the manufacture of nuclear warheads was another priceless inclusion in our study of the healing arts. Important topics were noted by their absence. Preventive medicine was never discussed. In the late 1970s and early 1980s, when I undertook my formal medical studies, diet and nutrition were considered alternative heresy.
The study of anatomy was done in a particularly inefficient manner. We were given cadavers to dissect for two years. A group of eight students would spend hours, scalpels in hand, digging at a corpse, hoping to find and trace nerves and arteries to their origins and distributions. Dead bodies do not handle the same as living tissue, and rarely look the same as in book illustrations. I studied my anatomy from a book. Much more could have been learned had each group been assigned one person who was well-trained and who could have guided and educated us. My memories of these sessions are ones of the stench of formalin, of a student eating someone’s biceps on a dare, and of others skipping rope using a corpse’s small intestine or playing football with a hardened lung. This abhorrent lack of respect for men and women who had donated their bodies to science and medicine sickened me.
MEDICAL RESEARCH: STAGNANT, DIRECTIONLESS
In this era of genetic engineering and daily promises of medical marvels, it is hard to imagine a period where innovative thought seemed to be at a standstill; yet back then, as now, in the playing fields of clinical trials, one finds variations of intricate protocols and slight modifications of rules and tools to search for slightly improved responses from the same tired players: surgery, radiation and chemotherapy. This points to the stagnant nature of real options available to the public.
As a medical student, I was now becoming exposed to rigid, inhumane insanity often associated with clinical trials and questionable measures of success. Only in cancer, for example, would a chemotherapeutic agent being evaluated be considered a success if it shrank a cancer mass, even if it shortened patient survival.
Decades ago, hospitals had carried out unethical and repulsive procedures in the name of science. Pregnant women were injected with high doses of radioactive isotopes to gauge the effect on embryos; prisoners’ testicles were irradiated to study changes; relatives were inoculated with patients’ cancers to study their response (at least one case of cancer transfer and death of a patient’s mother occurred).
Modern-day inhumanity was present, but not quite as overt. It lay in protocol objectives and structures.
I remember the case of a patient, a 22-year-old mother, who entered a monitored trial situation where she was slotted into the hormone-blocker evaluation group. This breast cancer study was designed to evaluate survival with various treatment options: surgery alone (localised), surgery alone (extensive), with radiation, with chemotherapy, with hormonal blocker therapy, with combinations of the preceding.
This data had already been gathered to reasonable precision from studies too numerous to mention worldwide, and certain guidelines for combinations had been enforced for many years. This particular design protocol did not allow for such flexibility. How could we achieve accurate readings if we contaminated one group with the therapy of another group?
The cruelty of the last statement could be seen in the plight of the patient referred to above. Having been assigned to the hormone group, other therapy was withheld-even when it became obvious that it was not working, and spreading cancer had broken several bones in her spine. (This was not an unusual occurrence in breast cancer. The standard therapy of the time, which remains to this day, is the use of radiation to allow for fracture-healing and to resolve the associated pain. This was denied her; actually, never offered, for the ’sake’ of the trial.) The insanity of this situation must be restated: this trial was confirming many others which had already outlined the relative merits of therapy. Why this theme of repetitive rediscovery of the known, regardless of human consequence? Because it gives the illusion of work, progress and motion in a stagnant cesspit of medical impotence.
In Australia, the natural health revolution had only just begun and was struggling for acceptance. The adamant claims of this new field of medicine were both inspiring and confusing. The response from conventional medicine was cutting. Alternative medicine was deemed fraudulent and rejected outright, its practitioners shunned and persecuted. Disgrace and deregistration awaited doctors who preached or practised its beliefs.
Supporters of this emerging field dealt in an inexact science, yet the detractors refused to carry out investigations to disprove the claims of alternative medicine. What resulted was a slinging match with a confused public as the victim. Patients were often punished if they saw a naturopath or asked a doctor advice on supplements; they would be treated curtly, and it was not unusual for the doctor to refuse their ongoing care. New options had been thrust onto patients, yet proof of efficacy was as lacking as proof of inefficacy.
My mother and I had been searching constantly for anything in research, folklore or overseas programs. The sudden influx of claims from natural medicine brought a range of new modalities to try: mind power, herbs, vitamins, vegetarianism, macrobiotics. My father tried them all, to no avail.
Fasting, juices, meditation, simple do-it-yourself techniques with a universal appeal could restore a person’s capacity to help themselves against a condition so foreign, so overwhelming that grown adults would revert to child-like dependency on their doctors. Even if only of marginal efficacy in the physical long-run, the psychological advantage of regaining some measure of control of one’s life was a feature conventional medicine could not compete with. There was also a link that had only been hinted at previously. Alternative medicine heavily promoted the concept that proper activation of immune function could eliminate cancer-again, an empowering concept.
Perhaps in an effort to compete with the new challenger, or perhaps finally disgusted with the toxic failures called “standard therapy”, the powers-that-be launched a major thrust into immunotherapy. I was part of the “IF” generation. Conventional medicine brought out a new warrior, an immunostimulant called “interferon”-the “IF” drug. I cannot claim to know or understand what changes the emphasis of investigative pathways in modern medicine, only to say that the industry is particularly well tuned to public views and needs. In the 1970s it was immune function, so interferon and interleukin occupied the forefront of research for a decade or so. In the 1980s the public cried out for natural medicine, so Taxol, a natural extract, was released.
If the above passage alluded to a sinister, manipulative arm to the industry, it is because I believe it to be inherent in this field. Interferon, hailed as the new champion in the 1970s, had actually been discovered at least 50 years previously and then shelved. Why turn to it now unless the above were true? Public manipulation and public gullibility are extreme in many areas; cancer, however, leads the field.
STOLEN HOPE
The interferon onslaught was savage. Newspapers, magazines, television and radio programs were at saturation levels with details of miraculous cures. Like a well-oiled machine, the Cancer Institute announced it would commence interferon trials; then, soon after, hospital fundraising events were commenced. This ‘dance’ of announcing breakthroughs, then a program for implementation followed by appeals for public donation, was monotonous and obvious, year after year.
Many controversial figures have been accused of preying on desperate victims and profiting from false hope. With decades of failure behind them but excellent marketing and publicity, with daily announcements of breakthroughs and assurances of imminent success, with billions raised within this format, could the cancer industry not also be accused of the same? Yesterday’s heroes fade into oblivion and new hopeful contenders are found to blaze in glory for a time, then fail. They may fail in living up to therapeutic expectation but always succeed in maintaining the illusion of dynamic progress and in raising phenomenal income.
Interferon was showing initial remarkable activity in several cancer types; most importantly, and repeatedly, cases of advanced multiple myeloma were shown recovering with this new therapy. My father’s hospital had announced that it would investigate its efficacy in the treatment of multiple myeloma. A dream come true, a hope reignited!
My father was a doctor. He had worked at the Peter McCallum Cancer Institute and was on first-name basis with most of the specialists there. He was also one of few long-term survivors of multiple myeloma at that hospital, so surely he would be one of those enrolled in the trial now that all other therapies were failing him.
Reality hardly ever fulfils all your dreams and prayers. It is also not usually as needlessly cruel as it was to my father. Following months of anticipation and planning into what had seemed a bleak future, we awaited notification of the interferon trial. My father was not accepted.
In medical trials, patient selection is often optimised for demonstrating good results. The healthier the patient, the more likely they are to survive the trial (no point investing in someone who may die prior to accumulation of data), and the more likely they are to make the product look good. My father was a risk. Death loomed closer; cancer laughed and marched on, its progress accelerated by a weary body and a spirit shattered not by disease but by hope that was taken away.
Extracted from Nexus Magazine, Volume 11, Number 1 (December-January 2004)
PO Box 30, Mapleton Qld 4560 Australia. editor@nexusmagazine.com
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From our web page at: http://www.nexusmagazine.com
by Harold D. Foster, PhD © 2003
Professor, Department of Geography
University of Victoria
PO Box 3050
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Email: lia. hfoster@mail.geog.uvic.ca
Website: http://www.hdfoster.com
I don’t try to describe the future. I try to prevent it.
- Ray Bradbury
THE MOST PROBABLE FUTURE
In 1992, in a lecture to the French Academy of Sciences, William A. Haseltine pointed out that “the future of AIDS is the future of humanity”. Haseltine,1 then the chief retrovirologist at Harvard’s Dana-Farber Cancer Institute, went on to add that “Unless the epidemic of AIDS is controlled, there is no predictable future for our species”. Later, testifying at a US Senate hearing, he predicted that by the year 2000 we could expect 50 million people to have been infected by HIV.2 In his opinion, by 2015 the total number of dead or dying could reach one billion - that is, some sixth of the current global population.
Time has proven Haseltine to have been over-optimistic. By the end of 2000, an estimated 57.9 million people had been infected by HIV, 21.8 million of whom were already dead.3 Current figures suggest a total of 70 million people have become HIV seropositive since the pandemic began in the early 1980s.4
As a consequence of our inability to halt the spread of HIV/AIDS, several of the worst-affected countries in sub-Saharan Africa are now on the verge of total social collapse as life expectancies, productivity, tax revenues and GDP dramatically fall and the need for expanded healthcare rises. There are many signs that suggest this situation will continue to worsen rapidly in the foreseeable future.5
PAST FAILURES
At an over-optimistic press conference held in 1984, Margaret Heckler, at that time the US Health and Human Services Secretary, announced the discovery of HIV, the virus believed responsible for the AIDS pandemic. She then went on to predict that a vaccine against this virus should be available within five years.6 Heckler was clearly no Nostradamus, since almost 20 years later - after the expenditure of untold billions of research dollars - there is still no effective vaccine against either HIV-1 or HIV-2. Of course, there is no shortage of those willing to continue the expensive search to find one.
In June 2003, for example, 24 co-authors, including Nobel Prize winners, college presidents, heads of major US public health departments and AIDS researchers from around the world combined to argue for a Manhattan Project against AIDS. This, of course, would focus its efforts on the discovery of the long-awaited vaccine against HIV.7 While there’s no doubting the need for such a vaccine, there seems to me to be a very distinct possibility that it will not be available before 2015 and the infection of one sixth of the global population.
The news is not much better from the treatment front. HIV-1 exhibits at least two characteristics that make it extremely difficult to eradicate. Firstly, it lacks the ability to “proofread” its genetic sequences during replication.8 The large number of resulting genetic errors results in the creation of endless variants, some of which inevitably will be immune to the antiretroviral drugs being used in treatment. As a consequence, inhibitors of reverse transcriptase and protease have promoted the evolution of drug-resistant strains of HIV that are now spreading rapidly in the developed world.9, 10 At least one of these new strains is resistant to all three classes of drugs that are currently used to treat HIV/AIDS. Patients infected by this new strain have gone from being totally asymptomatic to having fully developed AIDS within a few months.11 The treatment situation is also made worse by the overdependence on AZT, a drug which is definitely carcinogenic.12
A second characteristic of HIV which makes infection by it so difficult to treat is the virus’s ability to enter “resting” T-cells.13 Such cells are particularly good places for a virus to hide because they are inactive and, therefore, ignored by the immune system. Similarly, “resting” T cells are not targeted by drugs, which in order to work also require some form of activity by either the infected cell or the virus. Since such “resting” T cells can remain dormant for years, even decades, HIV can exist undetected in infected individuals for a similar length of time.
HALTING THE AIDS PANDEMIC
Throughout recorded human history, pandemics have ravaged the known world. Typically, millions died from infection by a particular pathogen which then retreated, only to return later as community immunity declined. Cholera, influenza, typhoid, smallpox and bubonic plague, for example, have taken repeated heavy tolls of the human population.14 There is, however, no convincing evidence of repetitive AIDS pandemics. The current scourge, already threatening to overtake the devastation associated with the Black Death, appears to be the first.
Simian immunodeficiency viruses (SIV) have been collected from 26 different species of African non-human primates. Two of these appear to have given rise to HIV-1 and HIV-2 in humans.15 That is, these human viruses evolved from simian viruses as a result of zoonotic, cross-species transmission. A close examination of the genomes of these viruses seems to indicate that HIV-1 originated as the chimpanzee (Pan troglodytes) virus SIVcpz, while SIVsm, a sooty mangabey (Cercocebus atys) monkey virus, gave rise to HIV-2.
However, mankind has been in close contact with chimpanzees, sooty mangabeys and other non-human primates for hundreds of thousands of years. Obviously there must have been endless opportunities through hunting and the bushmeat trade for human exposure to simian body fluids and for the cross-species transmission of viruses. Why, then, did HIV only begin to infect the human population on a global scale, for the first time, in the last two decades of the 20th century? After all, the 16th to 19th centuries saw the inhumanity of the slave trade, with the movement of millions of West Africans to Europe, North America and elsewhere. Had HIV-1 or HIV-2 been endemic in West Africa at the time, these viruses would certainly have been diffused around the globe by both slaves and slavers. Indeed, exotic diseases were spread by the slave trade from Africa to Europe and elsewhere; these included yellow fever, but they did not include AIDS.16
Viruses are like all other life-forms: they thrive in specific physical and social environments, and not in others. The most likely reason why HIV/AIDS is pandemic now is that certain changes in the environment, occurring in the latter part of the 20th and early part of the 21st century, have greatly improved HIV’s competitive position.
What these changes were can be deduced from the work of E. W. Taylor and his colleagues at the University of Georgia. In the mid-1990s, these researchers discovered there was a series of viruses that encoded for a selenium-dependent glutathione peroxidase. These included HIV-1 and HIV-2, Coxsackievirus B, and the hepatitis B and C viruses.17,18,19 What this means is that the genomes of such viruses include a gene that is virtually identical to that seen in humans, which allows them to manufacture the essential enzyme glutathione peroxidase. Subsequently, to prove that this apparent section of the HIV-1 genetic code really permitted it to produce the mammalian selenoenzyme glutathione peroxidase, Taylor and his co-workers20 cloned the hypothetical HIV-1 gene and transfected canine kidney cells and MCF7 cells with it. In both cases, the cells given the HIV-1 gene greatly increased their production of the selenoprotein glutathione peroxidase. This proves beyond any reasonable doubt that HIV-1 (and probably HIV-2, Coxsackievirus B and the hepatitis B and C viruses) is capable of producing glutathione peroxidase for its own purposes.
More or less simultaneously, K. D. Aumann and co-workers,21,22,23 of the Department of Biological Chemistry, University of Padova, Italy, were studying the biochemistry of the glutathione peroxidases. In three articles, they argued that glutathione peroxidase is characterised by catalytically active selenium which forms the centre of a strictly conserved triad composed of selenocysteine, glutamine and tryptophan. That is, they believed that it consisted of the trace element selenium and three amino acids, namely cysteine, glutamine and tryptophan. Their suggestion, it should be noted, ran contrary to the conventional belief that glutathione peroxidase consists of selenium, cysteine, glutamine and not tryptophan but glycine.
Regardless of the true composition of glutathione peroxidase, there is no doubt that this enzyme contains selenium. Since, as researchers at the University of Georgia have established, HIV-1 and HIV-2, Coxsackievirus B and the hepatitis B and C viruses all encode for this enzyme, it would seem logical to expect that infections from them would peak in high-selenium regions. Interestingly, there is abundant evidence that the reverse is true and that a high dietary selenium intake gives a great deal of immunity against all of these viruses.24
Indeed, it is believed by the author that this inability to diffuse, in areas where the population has a relatively high selenium intake, represents the Achilles heel of HIV/AIDS and currently offers the best available strategy for halting, or at least slowing, the pandemic.25
In sub-Saharan Africa, Senegal stands out like a diamond in the dirt. Given the widespread polygamy and unprotected promiscuity in the country,26-27 one would expect that its mortality from AIDS would have been enormous. After all, Senegal is located in sub-Saharan Africa, close to the region where the simian immunodeficiency virus (SIVcpz) is believed to have been transmitted from chimpanzees to humans on several occasions and where it subsequently evolved into HIV-1. However, in Dakar, Senegal’s major urban centre, HIV-1 prevalence among women attending antenatal clinics has remained at one per cent or less since the time that surveillance began in the mid-1980s until the present. Similar very-low-prevalence rates are also recorded in the Senegalese hinterland.28
Geologically, Senegal is a dried-up Cretaceous and early Eocene sea. When this dessication took place, sedimentary rocks were formed from the dissolved minerals in evaporating sea water. As a result, calcium phosphates now mined for use in fertilisers are one of Senegal’s chief mineral products. They are derived from phosphorite, a rock type that is always selenium-enriched.29
It appears to be no coincidence that HIV-1 has had great difficulty diffusing in Senegal, a country which also has the world’s lowest incidence of cancer.30 Numerous clinical trials, of course, have demonstrated that individuals eating a high-selenium diet are relatively unlikely to develop a wide variety of cancers.31
Conversely, a link between elevated AIDS mortality and depressed environmental selenium has been shown to occur in the United States. Cowgill,32 for example, used analysis of variance to compare selenium in local alfalfa with AIDS mortality for 1990. Where selenium levels were depressed, AIDS mortality was elevated. This relationship was particularly evident amongst Afro-Americans, who Cowgill believed were less mobile and therefore more likely to eat locally grown foods. This inverse relationship between dietary selenium intake and risk of infection does not seem limited to HIV-1, but also appears to be true of other viruses that encode for glutathione peroxidase.
Beyond that, Beck and her co-workers,33 for example, have shown that a normally benign Coxsackievirus can mutate to cause significant heart damage in selenium-deficient mice. Such new viral strains differed significantly from the original virus and were also then able to cause heart problems in selenium-adequate animals.
This relationship between the virulence of the Coxsackievirus and heart disease in mice is of more than just academic concern. A frequently fatal cardiomyopathy called Keshan disease is widespread and endemic in the selenium-deficient areas of China.34 It occurs in those who are both selenium deficient and infected by the Coxsackievirus. It is therefore a disease caused by a virus that encodes for glutathione peroxidase, but only infects those who are eating a diet containing inadequate selenium.
This problem may not be limited only to regions of extreme selenium-deficiency. Nicholls and Thomas,35 for example, showed that 10 out of 38 patients suffering acute myocardial infarction (heart attack), admitted to the King Edward VII Hospital in Midhurst, Sussex, England, during a two-month period, had serological evidence of very recent Coxsackievirus B infection. That is, approximately 25 per cent of these British heart attack patients had suffered from an influenza-like illness caused by the Coxsackievirus B within seven days prior to admission. Even more interesting is the fact that heart attack patients who subsequently took selenium supplements suffered far fewer secondary episodes of myocardial infarction.36, 37
Further evidence that selenium supplementation can greatly reduce infection by the Coxsackievirus has been provided from China, where the incidence and mortality rates for Keshan disease are in decline.38 This is because of the widespread use of more grain grown outside the selenium deficiency belt, spraying selenium-enriched fertilisers onto soils and crops, and adding this trace element to the feed of domestic livestock and to table salt. To illustrate, in Sichuan Province39 the use of selenium-fortified table salt was able to reduce the incidence of Keshan disease in children from 7.1 to 0.12 per thousand during the period 1974 to 1983. Everywhere in the great Chinese selenium deficiency belt, as the level of this trace element has risen in local diets Coxsackievirus infection has fallen and, with it, Keshan disease incidence and mortality.40
The Chinese also have provided evidence that increased dietary selenium can reduce the rates of infection by two more pathogens that encode for glutathione peroxidase: the hepatitis B and C viruses. In Qidong County, Jiangsu Province,41 20,847 residents of one town were given table salt fortified with 15 ppm of anhydrous sodium selenite. Those in the six surrounding townships continued to use normal table salt. Prior to and during the first year of the study, there was no statistically significant difference in hepatitis infection between the selenium supplementation and control populations. However, by the third year, a drop in the incidence of hepatitis had occurred in the selenium-supplied township (4.52 per 1,000) compared with those communities using normal salt (10.48 per 1,000; 56.8% reduction, p<0.002). A similar study in the same county, also conducted by Yu and colleagues,42 further established that daily selenium-yeast (200 micrograms of selenium) supplementation could significantly reduce the primary liver cancer often associated with hepatitis B and C infection. Interestingly, Berkson43 has demonstrated that the liver damage caused by hepatitis C can be reversed by a combination of alpha- lipoic acid, silymarin and selenium, often negating the need for expensive liver transplantation.
In summary, infection from HIV-1, Coxsackievirus B and the hepatitis B and C viruses occurs far more frequently in regions and populations that are selenium deficient. It has been established further that rates of infection by and death from Coxsackievirus B and hepatitis B and C viruses can be greatly reduced by increasing dietary selenium intake. It seems extremely likely, therefore, that the same strategy would be just as effective in slowing the diffusion of HIV-1 and so lowering the AIDS death rate.
Unfortunately, the reverse seems to be occurring. During the latter half of the 20th century, precipitation became increasingly acidic, soil pH fell, and heavy metal and fertiliser contamination increased. As a consequence, selenium bioavailability declined and levels of this element in the food chain fell,44 making it much easier for viruses that encode for glutathione peroxidase to diffuse. This is why we are now experiencing pandemics caused by HIV-1, the Coxsackievirus and the hepatitis B and C viruses.45, 46 Together they have infected more than one third of the global human population and show no sign of halting their rapid spread. Their devastation, of course, is most obvious in those regions of the planet where, for geological reasons, the soil levels of selenium are naturally very low. These include most of sub-Saharan Africa and the "disease belt" that crosses China from northeast to southwest.
If we are going to have any hope of halting the AIDS pandemic and of slowing the diffusion of hepatitis B and C, the dietary intake of selenium must be increased in such areas. It is clear also that, even in the developed world, additional selenium could greatly reduce cancer incidence and lower mortality from myocardial infarction.47, 48
THE REVERSAL OF AIDS
After infection with HIV-1 there is an initial brief illness, with lymph node enlargement and fatigue. These symptoms are like those of mononucleosis, but far more transient. However, usually several years later, diverse new symptoms occur that typically include night sweats, diarrhoea, psoriasis, muscle wasting, immune incompetence and depression.49 In Africa, it appears to take some five years after initial infection until the development of AIDS, which is characterised by these symptoms. In the developed world, this period is somewhat longer, probably nearer 10 years.50
Many and varied hypotheses have been put forward to explain how HIV-1 causes AIDS.51 Unfortunately, they appear unconvincing since they tend to focus on immune incompetence and do not adequately explain the wide range of other symptoms seen in AIDS patients, including the abnormal incidence of Kaposi’s sarcoma.
Recently in my book, What Really Causes AIDS,52 I put forward an alternative hypothesis that not only explains why HIV-1 takes so long to cause AIDS but why this disease has the specific symptoms it does. It was suggested that since HIV-1 encodes for the human selenoenzyme glutathione peroxidase, as it is replicated its genetic needs cause it to deprive seropositive individuals not only of glutathione peroxidase but also of its four basic components: selenium, cysteine, glutamine and tryptophan. Eventually, after a period of time (the length of which depends on the diet being eaten), this depletion process causes severe deficiencies of all these nutrients.
These in turn are responsible for the major symptoms of AIDS, which include immune system collapse, increased cancer and myocardial infarction susceptibility, muscle wasting, depression, psychosis, dementia and diarrhoea. Naturally, since these nutritional deficiencies cause immune system failure, other pathogens can infect the patient and become responsible for their own unique symptoms.
One of these symptoms is Kaposi’s sarcoma, which is linked to the human herpes virus 8 (HHV-8), a virus that was endemic for years in Uganda and other selenium-deficient regions of sub-Saharan Africa long before the onset of AIDS.53
If this hypothesis is correct, four corollaries must follow.
Firstly, AIDS patients should be very deficient in glutathione peroxidase and its components selenium, cysteine, glutamine and tryptophan.
Secondly, any effective treatment for HIV/AIDS must include normalisation of body levels of glutathione, glutathione peroxidase, selenium, cysteine, glutamine and tryptophan.
Thirdly, since deficiencies of these nutrients cause the main symptoms of AIDS, correcting them should reverse the disorder. The only symptoms remaining might be expected to be those caused by other opportunistic pathogens.
Fourthly, since the symptoms of AIDS are those of extreme deficiencies of one trace element and three amino acids, it follows that individuals who are HIV-1 seropositive but who eat diets elevated in these four nutrients should never develop AIDS.
Evidence exploring these four corollaries is presented in part two of this series.
Continued in Part 2.
Author’s Note:
Readers wanting more detailed information about the HIV/AIDS environmental link are directed to the website http://www.hdfoster.com, where they can download a free copy of the book, What Really Causes AIDS.
About the Author:
Harold D. Foster, PhD, was born and educated in England. He specialised in geology and geography, earning a BSc in 1964 from University College London and a PhD in 1968 from London University. He is a Canadian by choice, and has been a faculty member in the Department of Geography, University of Victoria, British Columbia, Canada, since 1967.
A tenured professor, Dr Foster has authored or edited some 235 publications, the majority of which focus on reducing disaster losses or identifying the causes of chronic disease or longevity. He has published hypotheses on the origins of numerous diseases including myocardial infarction, SIDS, cancer, diabetes, schizophrenia, multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), Alzheimer’s and Parkinson’s diseases, and stroke.
His numerous books include: Disaster Planning: The Preservation of Life and Property (Springer Verlag, New York, 1980); Reducing Cancer Mortality: A Geographical Perspective (Western Geographical Press, Victoria, 1986); The Ozymandias Principles: Thirty-one Strategies for Surviving Change (Southdowne Press, Victoria, 1997); and What Really Causes AIDS (Trafford Publishing, Victoria, 2002; see review in NEXUS 10/05). His new book, What Really Causes Schizophrenia, is to be published by Trafford in late 2003.
Harold Foster is a member of the Explorers Club as well as several academic organisations including The New York Academy of Sciences, The Royal Geographical Society and The Royal Society of Literature. He is also the editor of both the International and Canadian Western Geographical Series and is a member of the boards of the Journal of Orthomolecular Medicine and the International Schizophrenia Foundation.
He has been a consultant to numerous organisations, including the United Nations and NATO, and to the governments of Canada, Ontario and British Columbia. He is also a member of the Science Advisory Panel for the Healthy Water Association.
Every day, Dr Foster makes a point of taking at least the recommended daily allowance of the known essential nutrients. He is also currently pursuing offers for his suggested nutrient mixture to be produced for use in clinical trials with AIDS patients. For a more detailed résumé, visit the website http://www.hdfoster.com.
Endnotes:
1. “More cases, same old question”, The Philadelphia Inquirer, June 6, 1993, Review and Opinion, p. D1.
2. “Large AIDS increases predicted by early 2005″, The Vancouver Sun, December 15, 1992, p. A12.
3. Worldwatch Institute, Vital Signs 2001: The trends that are shaping our future, W.W. Norton, New York.
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5. Foster, H.D., What Really Causes AIDS, Trafford, Victoria BC, 2002.
6. Elliott, V.S., “AIDS research: Still one step forward and one step back”, American Medical News, April 22/29, 2002, posted at http://www.ama-assn.org/sci-pubs/amnews/pick_02/hlsb0422.htm.
7. Klausner, R.D. and others, “Enhanced: The need for a global HIV vaccine enterprise”, Science Magazine, posted at http://.aidscience.org/Science/Science–Klausner_et_al_300(5628)2036.htm.
8. Brown, P., “How does HIV cause AIDS?”, New Scientist, July 18, 1992, pp. 31-35.
9. Garrett, L., “HIV/Multidrug-resistant strains worry 3 research teams”, Newsday, September 22, 1999, posted at http://www.aegis.com/news/newsday/1999/ND990901.html.
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12. National Toxicology Program, “Summary Data and Level of Evidence for Technical Reports Reviewed at the Meeting of the Board of Scientific Counselor’s Technical Reports Review Subcommittee”, December 11-12, 1996, posted at http://ntpserver.niehs.nih/gov/Main_Pages/PR_Actions.html.
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16. Cartwright and Biddiss, op. cit., pp. 144-150.
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27. Hecht, D., “AIDS rate among Senegalese sex workers inexplicably low”, Drum, April 1, 1997.
28. UNAIDS/WHO, “Epidemiological fact sheet on HIV/AIDS and sexually transmitted infections: Senegal”, 2000 Update (revised).
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31. Foster, H.D., “Selenium and Cancer: a geographical perspective”, Journal of Orthomolecular Medicine 1998; 13(1): 8-10.
32. Cowgill, G.M., “The distribution of selenium and mortality owing to Acquired Immune Deficiency Syndrome in the continental United States”, Biological Trace Element Research 1997; 56:43-61.
33. Beck, M.A. and others, “Rapid genomic evolution of non-virulent Coxsackievirus B3 in selenium-deficient mice results in selection of identical virulent isolates”, Nature Medicine 1995; 1(5):433-436.
34. Oldfield, J.E., Selenium World Atlas, Selenium-Tellurium Development Association, Grimbergen, Belgium, 1999.
35. Nicholls, A.C. and Thomas, M., “Coxsackie virus infection in acute myocardial infarction”, The Lancet, April 23, 1977, pp. 883-884.
36. Foster, H.D., “Coxsackie B virus and myocardial infarction”, The Lancet, March 2, 2002, p. 804.
37. Kuklinsk, B. and others, “Coenzyme Q10 and antioxidants in acute myocardial infarction”, Mol. Aspects Med. 1994; 15(suppl):143-147.
38. Tan, J. and others, “Medical Geography”, in Geographical Society of China (ed.), Recent Developments of Geographical Science in China, Science Press, Beijing, 1990, pp. 259-279.
39. Cheng, Y.-Y., “Selenium and Keshan disease in Sichuan Province, China”, in G.F. Combs, Jr, and others (eds), Selenium in Biology and Medicine, Van Nostrand Reinhold, New York, 1987, pp. 877-891.
40. Editorial Board, The Atlas of Endemic Diseases and the Environment in the People’s Republic of China, Science Press, Beijing, 1985, pp. 42-83.
41. Yu, S.Y. and others, “Chemoprevention trials of human hepatitis with selenium supplementation in China”, Biological Trace Element Research 1989; 20(1-2):15-22.
42. Yu, S.Y. and others, “A preliminary report on the intervention trials of primary liver cancer in high-risk populations with nutritional supplementation of selenium in China”, Biological Trace Element Research 1991; 29:289-294.
43. Berkson, B.M., “A conservative triple antioxidant approach to the treatment of hepatitis C. Combination of alpha lipoic acid (thioctic acid), silymarin, and selenium: three case histories”, Med. Klin. 1999; 94(Suppl3):84-89.
44. Frost, D.V., “Why the level of selenium in the food chain appears to be decreasing”, in G.F. Combs, Jr, and others (eds), Selenium in Biology and Medicine, Van Nostrand Reinhold, New York, 1987, pp. 534-547.
45. WHO Information Fact Sheet/204 Hepatitis B, posted at http://www.who.int/inf-fs/en/fact204.html.
46. WHO Information Fact Sheet/164 Hepatitis C, posted at http://www.who.int/inf-fs/en/fact164.html.
47. Combs, G.F., Jr, “Selenium as a cancer-protective agent”, The Bulletin of the Selenium-Tellurium Development Association, February 1997, pp. 1-4.
48. Rayman, M.P., “The importance of selenium to human health”, The Lancet 2000; 356:233-241.
49. Ward, D.E., The AmFAR AIDS Handbook: the Complete Guide to Understanding HIV and AIDS, W.W. Norton, New York, 1999.
50. “The Durban Declaration”, Nature 2000; 406:15-16.
51. Brown, P., op. cit.
52. Foster, H.D., 2000, op. cit.
53. CancerNet, National Cancer Institute, “Kaposi’s Sarcoma Treatment - Health Professionals”, posted at http://cancernet.nci.nih.gov/cgibin/srchcgi.exc?DBID=pdq&Type=search&VID=208+01
