AIDS: The Seleno-Enzyme Solution
Conclusions from an Article by Harold D. Foster: “Death from AIDS is a consequence of four nutritional deficiencies.”
Eating foods grown in selenium-deficient soils, or having a prior infection by a selenium-encoding pathogen are factors which promote susceptibility to HIV infection and ultimately AIDS. 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.
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.
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 people 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. The genetic code of HIV includes a viral requirement for selenium, therefore HIV generally appears to restrict infection to individuals who are deficient in this trace element. This is either because of a diet deficient in selenium, or prior infection by other selenium-encoding pathogens.
To illustrate, glutathione peroxidase is one of the body’s most significant antioxidants. A lack it 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, diarrhea and various neurologic and psychiatric symptoms including dementia. Supplementation with the appropriate nutrients naturally reverses these symptoms.
Author’s Postscript – January 2004
Since I submitted this article for publication, I have learned of a small AIDS trial that is taking place in Botswana. 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 2003:
“I picked two candidates personally who have fully blown AIDS with relevant symptoms like diarrhea, 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, diarrhea 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.
The Seleno-Enzyme Solution
Eating foods grown in selenium-deficient soils or having a prior infection by a selenium-encoding pathogen are factors which promote susceptibility to HIV infection and ultimately AIDS.
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, 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. 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 overoptimistic. By the end of 2000, an estimated 57.9 million people had been infected by HIV, 21.8 million of whom were already dead. Current figures suggest a total of 70 million people have become HIV seropositive since the pandemic began in the early 1980s. 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.
At an overoptimistic 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. 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. 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. 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.,  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. The treatment situation is also made worse by the over-dependence on AZT, a drug which is definitely carcinogenic.
A second characteristic of HIV which makes infection by it so difficult to treat is the virus’s ability to enter “resting” T-cells. 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.
Healing 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. 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. 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. 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.,, 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-workers 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,, , 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. 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.
In sub-Saharan Africa, Senegal stands out like a diamond in the dirt. Given the widespread polygamy and unprotected promiscuity in the country, - 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.
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. 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. Numerous clinical trials, of course, have demonstrated that individuals eating a high-selenium diet are relatively unlikely to develop a wide variety of cancers.
Conversely, a link between elevated AIDS mortality and depressed environmental selenium has been shown to occur in the United States. Cowgill, 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, 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. 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, 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., 
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. 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 Province 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.
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, 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, 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, Berkson 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, 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.,  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., 
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. 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. Many and varied hypotheses have been put forward to explain how HIV-1 causes AIDS. 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, 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.
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.
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, 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-workers 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-workers 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-workers 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 Coxsackie virus infection. As a consequence, myocardial infarctions are quite common even in relatively young people who are HIV seropositive. In addition, autopsies often reveal that AIDS patients,  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. Since this amino acid is one of the body’s major sources of sulphur, they are very deficient in it. 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, 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, 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-workers 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.
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-workers 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. 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 colleagues 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, 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 colleagues have demonstrated that glutamine and antioxidant supplements can reverse the weight loss typically seen in such patients while Kohler and co-workers 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. Similarly plasma tryptophan levels can be increased in HIV-infected patients by nicotinamide supplements. 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-workers 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.
HIV/AIDS patients also often display a hypothyroid or low T3 (tri-iodothyronine) syndrome. 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.
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 Combs 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. 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. 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.
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. 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. 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.
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. 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.
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.
4. National AIDS Trust Fact Sheet 3 Global Statistics posted at http://www.nat.org.uk/press/latest.cfm.
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.
10. Baden D. and others “”HIV-1 drug resistance in newly infected individuals”” JAMA 1999; 282(12):1135-1141.
11. Skelton C. “”New HIV ‘superbug’ emerges in Vancouver: New strain of virus is resistant to every anti-AIDS drug”” The Vancouver Sun August 9 2001 p. A1.
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.
13. Zhang Z.-Q. and others “”Sexual transmission and propagation of SIV and HIV in resting and activated CD4 + T cells”” Science 1999; 286:1353-1357.
14. Cartwright F.F. and Biddiss M.D. Disease and History Dorset Press New York 1991.
15. Hahn B.H. and others “”AIDS as a zoonosis: Scientific and public health implications”” Science 287(5454):607-614.
16. Cartwright and Biddiss op. cit. pp. 144-150.
17. Taylor E.W. and others “”HIV-1 encodes a sequence overlapping env.g p41 with highly significant similarity to selenium dependent glutathione peroxidases”” Journal of AIDS and Human Retrovirology 1997; 15(5):393-394.
18. Taylor E.W. and others “”Genomic structures of viral agents in relation to the biosynthesis of selenoproteins”” Biological Trace Element Research 1997; 56(1):63-91.
19. Taylor E.W. “”Selenium and viral diseases: facts and hypotheses”” J. Orthomolecular Medicine 1997; 12(4):227-239.
20. Zhao L. and others “”Molecular modeling and in vitro activity of an HIV-1- encoded glutathione peroxidase”” Proc Natl Acad SciUSA 2000 June 6; 97(12):6356-6361.
21. 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.
22. Maiorino M. and others “”Probing the presumed catalytic triad of selenium-containing peroxidases by mutational analysis”” Z. Ernahrungswiss 1998; 37 (Suppl 1):118-121.
23. Maiorino M. and others “”Probing the presumed catalytic triad of selenium-containing peroxidases by mutational analysis of phospholipid hydroperoxidase glutathione peroxidase (PH GPX)”” Biol. Chem. Hoppe Seyler 1995; 376(11):650-651.
24. Foster H.D. “”AIDS and the ‘selenium-CDR T cell tailspin’: The geography of a pandemic”” Townsend Letter for Doctors and Patients2000; 209:94-99.
25. Foster H.D. “”Why HIV-1 has diffused so much more rapidly in Sub-Saharan Africa than in North America”” Medical Hypotheses 2003; 60(4):611-614.
26. Meda N. and others “”Low and stable HIV infection rates in Senegal: Natural course of the epidemic or evidence for success of prevention”” AIDS 1999; 13(11):1397-1405.
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).
29. Gulbrandsen R.A. Geochim. Cosmachin. Acta 1966; 30:769 cited by E.A. Keller Environmental Geology Upper Saddle River Prentice Hall New Jersey 1996 p. 352.
30. Howe G.M. “”International Variations in Cancer Incidence and Mortality”” in Global Geocancerology: A World Geography of Human Cancers (ed. G.M. Howe) Churchill Livingston New York 1986 pp. 3-42.
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 Research1997; 56:43-61.
33. Beck M.A. and others “”Rapid genomic evolution of non-virulent Coxsackie virus 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.excDBID=pdq&Type=search&VID=208+01
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.
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.
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 summary visit the website http://www.hdfoster.com.
Extracted from Nexus Magazine Volume 11 Number 1 (December-January 2004)
PO Box 30 Mapleton Qld 4560 Australia. [email protected]
Telephone: +61 (0)7 5442 9280; Fax: +61 (0)7 5442 9381
From our web page at: www.nexusmagazine.com