Harold D. Foster,
Professor, Department of Geography
University of Victoria
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.
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
I donít try to describe the future. I try to prevent it.
- Ray Bradbury
Part 2 I
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
then the chief retrovirologist at Harvardís
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
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
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
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
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
While thereís 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
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,
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
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 virusís ability to enter "resting"
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
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
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 HIVís competitive
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
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
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
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-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
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
In sub-Saharan Africa, Senegal stands out like a diamond in the
dirt. Given the widespread polygamy and unprotected promiscuity in
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,
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
Geologically, Senegal is a dried-up Cretaceous and early Eocene sea.
When this desiccation took place, sedimentary rocks were formed from
the dissolved minerals in evaporating sea water. As a result,
calcium phosphates now mined for use in fertilizers are one of
Senegalís chief mineral products. They are derived from
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 worldís 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
environmental selenium has been shown to occur in the United States.
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
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,
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
This is because of the widespread use of more grain grown
outside the selenium deficiency belt, spraying selenium-enriched
fertilizers onto soils and crops, and adding this trace element to
the feed of domestic livestock and to table salt. To illustrate, in
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
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,
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
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 fertilizer 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,
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
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
In Africa, it appears to take some five years
after initial infection until the development of AIDS, which is
characterized 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 Kaposiís 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 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 Kaposiís 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
long before the onset of AIDS.53
If this hypothesis is correct, four corollaries must follow.
AIDS patients should be very deficient in glutathione peroxidase and its components selenium, cysteine, glutamine and
Secondly, any effective treatment for
HIV/AIDS must include normalization 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.
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