*There are many toxins which modify hormonal responses, activating cells
and altering the immune system (including estrogens and dioxins.) When
these act early in life, extremely small amounts can cause life-long
*When respiratory energy production is blocked in stimulated cells, the
cells are likely to die. (Cortisol, estrogen, polyunsaturated oils have
this effect, especially on thymus cells.)
*Antibodies are involved in removing the debris of cells that have disintegrated.
Intense cellular damage causes many "autoantibodies" to be
produced. People with AIDS have a high incidence of "autoimmunity."
*Endogenous retroviruses are activated by toxins known to be associated
with immunodeficiency. Everyone has endogenous retroviruses. The antibodies
which are used to diagnose "HIV" infection can, in the demonstrated
absence of that virus, be produced in connection with lupus, Sjogren's
syndrome, and arthritis. These autoimmune conditions are promoted by
*Estrogen activates the production of cortisol, and damages the normal
feedback control, causing both cortisol and ACTH to be elevated.
*Estrogen causes chronically elevated free fatty acids, and synergizes
with unsaturated fats.
*Estrogen inhibits thyroid function.
Hypercortisolism is typically associated with hypothyroidism, and both
tend to cause the loss of lean body mass.
*AIDS is often compared to Addison's disease, because of hyponatremia
(loss of sodium) and fatigue. Hypothyroidism causes hyponatremia and
many other features seen in AIDS.
*Increased levels of cortisol, estrogen, and polyunsaturated fatty acids,
and decreased levels of the active thyroid hormone (T3) and (placental)
progesterone have been found to occur in AIDS.
*Progesterone can contribute to the inhibition of HIV replication and
*Common environmental factors can produce hormonal changes leading
One hospital in southern Vietnam admitted 437 septicemia patients
between mid-1993 and 1994; 23% of the adults died.
In 8 months, 17,000 seals died of infections in Europe. In California,
many seals die with an unusual form of metastatic cancer. Seals are
highly contaminated with industrial dioxins.
In Africa, aflatoxin is strongly associated with immunodeficiency. In
animals, both dioxin and aflatoxin activate the expression of viruses.
Endometriosis is stimulated by dioxins. Environmental estrogens affect
the immune system.
It has been over ten years since I wrote about "AIDS" (e.g.,
"Repairing the Immune System," in Cofactors in AIDS and
HIV infection, edited by R.R. Watson, l989) and the official doctrine
that it is caused by the "HIV" virus still hasn't been supported
by anything that resembles real science. Duesberg's arguments have never
been answered (except by bureaucratic thuggery).
In 1989 I pointed out that septicemia, blood stream infection, in young
adults, which used to be a rare thing, and which indicates defective
immunity, has been increasing in a remarkably continuous way since the
late 1940s, and I reviewed the many things in our environment that are
known to suppress immunity, and which
have become increasingly prevalent in our
environment--unsaturated vegetable oils, ferrous iron and carrageenan
in our foods, lead in air, food, and water, exposure to medical, military,
and industrial ionizing radiation, vaccinations, pesticides, chlorinated
hydrocarbons, nitric oxide (smog and medications) and oral contraceptives
and environmental estrogens, in particular. Of these factors, only
radiation and lead exposure have decreased in the last several years,
after several decades of rapid increase. The widespread use of diuretics
in pregnancy, which began in the 1950s and contributed to an epidemic
of premature births, also declined after the late 1960s. Most of these
environmental factors damage the thymus gland, which regulates the immune
system, and by acting on the thymus their effects tend to be additive
with other immunosuppressive factors, including cancer, traumatic injury,
inflammation, toxins in spoiled food (e.g., aflatoxins) and malnutrition.
Cancer, AIDS, and extreme hypothyroidism have several features in common--they
cause tissue loss and organ damage, with immunodeficiency and intense
activation of the stress hormones, including cortisol. In cancer and
AIDS, a good case has been made for the primacy of stress-induced wasting
as the main cause of death. Whatever one might believe to be the cause
of cancer and AIDS, it is always good for the patient to prevent tissue
damage from the stress associated with the sickness. Since the stress
hormones primarily destroy tissues by the activation of specific proteases,
the use of protease inhibitors for treating AIDS could conceivably be
affecting the stress response. However, the body's normal protection
against the cortisol-activated proteases is centered on the protective
hormones, progesterone, thyroid, and the androgens.
One of the most broadly substantiated principles in biology is that
a great variety of harmful causes all lead to a few forms of biological
harm--the concept of the stress reaction shows the powerful implications
of the principle. Stress, no matter what the specific cause, has a particularly
destructive effect on three organ systems:
The nervous system, the immune system, and the reproductive system.
Inflammation, lipid peroxidation, tissue atrophy, the "calcium
catastrophe" (when almost anything goes wrong, calcium can transmit
and amplify and extend the problem, but isn't itself the source of the
problem), mitochondrial decay, and similar events help to define the
stress reaction in greater detail.
Hans Selye showed that the thymus shrinks very early in the stress reaction.
In his understanding of the process, when adaptation was followed by
the "exhaustion phase," the adrenal glands had simply become
exhausted from overuse. F. Z. Meerson's work showed that cortisol, and
the free fatty acids mobilized by stress, have a toxic influence on
the mitochondrial energy production system. Both cortisol and the free
fatty acids block the efficient use of glucose for producing energy,
creating a diabetes-like condition. The exhaustion problem caused by
excessive stress is generalized, not just a matter of adrenal insufficiency.
Meerson's work created the basis for undersanding several degenerative
processes, especially the phenomenon of "excitotoxicity,"
in which the combination of excessive stimulation and deficient energy
supply damages or kills cells.
Selye believed that some hormones are antagonistic to each other. A
few of the oppositions that he identified have been thoroughly researched,
especially the catabolic/anabolic functions of glucocorticoids and androgens,
and the shock/antishock functions of estrogen and progesterone, respectively.
Puberty, because of hormonal changes, especially increased estrogen,
can be seen as the first stage of a chronic stress, resembling diabetes,
since elevated free fatty acids cause "insulin resistance,"
with slightly impaired oxidation of glucose. The thymus shrinks considerably
at puberty, under the influence of the hormonal changes and the increased
free fatty acids (caused mainly by estrogen). The degenerative diseases
can be seen as the cumulative result of stress, in which tissue damage
results from the diabetes-like impairment of energy production.
The thymus, and the thymus-dependent areas of the spleen, are required
for full and subtle control of immunity. In the absence of thymic control,
the B cells are still able to produce antibodies, but they are more
likely to produce autoantibodies.
Stress produces a variety of cellular changes, including the production
of the "shock proteins." These proteins can make up 20% of
the cell's total protein content. In themselves, the shock proteins
are immunosuppressive. They can be recognized by the immune system as
antigens, and so are a factor in the appearance of "autoimmune"
antibodies. The autoantibodies themselves are often blamed for the diseases
they are sometimes associated with, but since they can be present (for
example, following removal of the spleen) in people who have no symptoms,
their function is probably to facilitate the removal of tissues which
are defective for some other reason. The shock proteins could be one
of the signals that activate the immune system to remove damaged tissue,
and they might be involved in the removal of senescent cells, though
I don't think any experiments have been done to test this idea.
Besides activating the cells to produce massive amounts of the shock
proteins, stress can also activate the so-called hormone receptors,
such as estrogen receptors, even in the absence of the hormones. Stress
also activates the endonucleases, which cut sections out of the DNA
molecules, and activates mobile genetic elements, producing genetic
instability. Like cortisol and estrogen, stress itself activates integrated
retroviruses. The "endogenous retroviruses" make up nearly
10% of the human genome, and many of them locate themselves in regulatory
sites in the chromosomes.
Since stress lowers the discriminatory ability of the immune system,
and stimulates the expression of retroviruses, the antibodies sometimes
seen in association with immunodeficiency may be similar to the various
autoantibodies that are also produced by stress.
People who have autoimmune diseases such as lupus and Sjogrens syndrome
(which are promoted by estrogen: Ahmed and Talal) have antibodies
which sometimes react positively in the AIDS test, and searches for
the HIV virus in such people have found no evidence of it. (Nelson,
et al., 1994; Deas, et al., 1998.) Treatments for roundworms
and other parasites cause antibodies to retroviruses to appear in animals
that previously tested negative; this might account for the high
rates of positive tests for HIV in areas such as Africa in which treatment
for filiariasis is common (Kitchen and Cotter, 1988).
Organisms are most sensitive to environmental damage early in life,
especially prenatally. This is the period in which normal hormone exposure
masculinizes the brain, for example. The term "imprinting"
refers to the extreme responsiveness of the organism at this time, and
it has been extended to include long lasting influences which may result
from abnormally high or low levels of natural substances, or from the
presence of other, abnormal substances during the sensitive period.
The effects of early "imprinting" can cause permanently altered
sensitivities. In animal studies, L. C. Strong showed that prenatal
influences determine the age at which puberty and reproductive senescence
occur. In humans, premature birth, a powerful stressor, is associated
with premature puberty. The thymus is damaged both by premature birth
and by puberty. The effects of damage early in life will increase vulnerability
in subsequent decades.
When babies are imprinted by the mother's disturbed hormones, or by
diuretics, by milk substitutes, or by industrial effluents, the worst
effects are likely to be seen decades later, or even generations later.
A similar long-range effect can be produced by nutritional deficiencies.
Although more mature organisms are less sensitive to stress, both early
imprinting, and the cumulative effects of exposure, will cause some
individuals to be much more sensitive than others, and aging itself
If the present epidemic of immunodeficiency is produced by environmental
stress, then we should expect to see a variety of other stress-related
diseases increasing at roughly the same time. When a stressor is acting
through imprinting, then the harmful effects may not be seen until 20
or 30 years later, but when the stressor has acute and immediate effects,
the effects should rise and fall at roughly the same time as the environmental
The rise of the Acquired Immunodeficiency Syndrome during the last 50
years hasn't been the only health problem that has grown rapidly during
that time. The "flesh eating bacteria," causing necrotizing
fasciitis and related conditions, should probably be classed along with
septicemia/bacteremia as the consequence of a weakened immune system,
but there are many other diseases that have followed a similar pattern,
which might be caused by the same factors which are causing immunodeficiency.
Thyroid diseases (mostly in women), some autoimmune diseases including
primary biliary cirrhosis (mostly in women) and inflammatory bowel disease,
liver cancer, diabetes (doubling in children since 1949), prostate cancer,
decreased sperm counts, premature births and birth defects, minimal
brain dysfunction-attention deficit-hyperactivity, cerebral palsy, premature
puberty (which is associated with premature birth), congestive heart
failure, osteoporosis (independently of the changing age-structure of
the population), depression (most common in women, more than doubling
among children in recent decades), and multiple sclerosis have increased
in prevalence during this period. Some of these conditions
are strongly associated with each other, for example, primary biliary
cirrhosis, breast cancer, and osteoporosis.
It is common knowledge, among people who study immunity, that radiation,
polyunsaturated fatty acids, estrogens, and dioxins are toxic to the
thymus gland, and can produce immuno-deficiency. They mimic or accelerate
the thymic atrophy of aging, causing a deficient thymus-dependent immune
response, usually without harming the ability of B cells to produce
antibodies. There are probably many examples of damage to immune systems,
besides immunodeficiency, caused by these agents. Slight damage to the
immune system, such as can be produced by hypoglycemia or other energy
deficit--creates an exaggerated inflammatory response, and the release
of the mediators of inflammation, including histamine, serotonin, and
prostaglandins, activates the stress hormone system, leading to further
biological damage. Liver disease and several other "autoimmune"
diseases involve abnormal immune responses, probably including thymic
deficiency and an intensified inflammatory response. The fact that livers
transplanted from female donors to male recipients are less successful
than are livers from male donor transplanted into female recipients,
is consistent with the idea that autoantibodies (which are far more
common in women than in men) are a relatively harmless response to changes
in the organs themselves.
Are antiviral therapies working? Ivan Ilich, in Medical Nemesis,
showed that historically, many diseases have had characteristic incidence
curves, rising to a maximum, and then falling away to relative insignificance,
independently of what people were doing as treatment or prevention.
As susceptible people are exposed to conditions that cause a disease,
they will get sick, and then either die or develop resistance. The conditions
which at first caused increasing disease incidence, will eventually
tend to affect only children who haven't developed resistance.
If AIDS mortality rose rapidly to a peak a few years ago, and then began
falling, we should ask whether this pattern fits that of other diseases
discussed by Ilich. Looking for causes other than the virus, we might
find a parallel in the rise and fall of some other factor.
In the 1950s, new diuretics came on the market, and millions of pregnant
women took them. It was predicted that there would be an epidemic of
brain damage as a result, and in fact the incidence of hyperactivity,
attention-deficit, and other "minimal" brain damage disorders
did rise during those years. After about 15-20 years, experiences such
as the Thalidomide episode caused physicians to temper their enthusiasm
for the use of drugs during pregnancy. The incidence of low birth-weight
babies in the U.S. peaked around 1965, and 28 years later AIDS mortality
in the US peaked. The rising curve had followed both the increase
in radioactive fallout from atmospheric testing of large numbers of
atomic bombs up to 1963, and the intense promotion of the new diuretics
beginning in the early 1950s. The peak in AIDS mortality in 1993 came
ten or twelve years after the long decline in SAT scores had stopped.
(The most extreme declines in SAT scores had occurred among the brightest
students, disproving the contention that the average score fell simply
because more students were taking the tests.) The same prenatal damage
which caused the extreme decline in SAT scores 18 years later (when
the damaged babies reached that age) would have left many of the same
individuals with weakened immune systems, which would fail prematurely,
but at varying intervals, depending on the exposure to other factors.
The use of unleaded gasoline increased into the 1990s, and there was
a corresponding decrease in tissue lead content, reflecting the smaller
amount of lead being put into the environment. According to some reports,
medical and dental x-ray exposures were declining during this period.
Yet other factors, including dioxins and unsaturated dietary fats, were
Although the new protease inhibitors wouldn't be used until years after
the AIDS mortality had begun falling, the government and drug companies
are claiming that it is the drugs which are decreasing the mortality.
Many things in our environment are increasing the incidence of certain
kinds of liver disease. The liver processes things that are ingested
or that enter the blood stream after being inhaled or absorbed through
the skin, so in a toxic environment it is susceptible to injury. If
deprived of good nutrition or adequate thyroid hormone it is especially
sensitive to toxins. The body's own estrogen is a burden on the liver,
causing women's livers to be on average slower than men's in processing
Almost any kind of toxin causes the liver to be less efficient at excreting
other substances, including hormones. In malnutrition, sickness, and
in aging, there is a tendency for higher levels of estrogen to remain
circulating in the blood.
Natural estrogen, and environmental substances that act like estrogen,
act as excitants in many types of cell, and at the same time, reduce
the efficiency of energy production. Both of these properties relate
to its known ability to activate the adrenal glands. A. L. Soderwall,
who was my thesis adviser at the University of Oregon, found that estrogen
caused hamsters' adrenal glands to enlarge, and that larger doses overstimulated
the glands sufficiently to cause tissue damage. It is now known that
estrogen acts directly on the adrenal cells to stimulate cortisol production,
and that it also stimulates the pituitary to produce more adrenocorticotropin
(ACTH), which also stimulates the adrenals;
estrogen's effect is to impair the negative feedback, in which cortisol
normally shuts down ACTH production. This impaired feedback is characteristic
Estrogen directly causes the thymus gland to atrophy, and several of
its effects, such as increased adrenal activity and elevated free fatty
acids, also contribute to the shrinkage of the thymus and the inhibition
of its functions. While this is happening, the B cells, which normally
are under the control of the thymus cells, are not killed by estrogen,
and actually seem to be stimulated by estrogen to produce certain types
of antibodies. This combination of effects, weakening the thymus and
stimulating antibody production, is thought to contribute to the development
of autoimmune diseases. Estrogen also stimulates mast cells and similar
cells to release histamine and other promoters of inflammation, and
these effects are probably closer to the actual problem in the autoimmune
diseases. Several of the substances formed under the influence of estrogen
interfere with energy production and contribute to cellular excitation,
causing tissue injury.
Cortisol also stimulates antibody production while suppressing thymic
immunity (Norbiato, et al., 1997).
Estrogen and stress cause increased levels of free fatty acids to circulate.
The polyunsaturated fatty acids are immunosuppressive, antithyroid,
diabetogenic, inhibit respiration, and promote the actions of estrogen
People suffering from AIDS have been found to have increased estrogen,
with high cortisol and ACTH, and very low T3. (Unfortunately, some researchers
and the editors who publish their ideas, conclude that the hormones
don't cause the stress and wasting symtpoms, because they call thyroid
a "catabolic hormone," and because they describe the fatigue
and sodium deficiency as evidence of "deficiency of cortisol."
Such is the state of the research establishment.)
In animal experiments, and a few human tests, the HIV and similar viruses
have produced effects that could plausibly explain some of the conditions
seen in AIDS, such as damage to brain cells (C. Pert, R. Sapolsky),
and altered steroid secretion. But this is real science, that promises
to link up with information about stress, aging, allergy, and biological
For example, Sapolsky's group (Brooke, et al., 1998) found that the
nerve toxicity caused by a viral protein (called gp120) synergizes with
glucocorticoid toxicity, lowering the ATP level and inhibiting mitochondrial
function, and that simply supplying the nerve with additional energy
protects it from destruction. In other words, the viral peptide just
Another group (Amirhessami-Aghili and Spector, 1991) found that the
presence of the virus can decrease the production of progesterone. Since
progesterone blocks (Lee, et al., 1997) the expression (and transmission)
of the virus, this suggests how the overgrowth of the virus might be
triggered by stress--once progesterone synthesis falls, a vicious circle
could get started.
Lee, et al., found that progesterone can help to prevent transmission
of the virus from an infected mother to the fetus. But the most interesting
study of the virus in pregnancy involved mice that were engineered to
contain extremely large quantities of the HIV provirus (De, et al.,
1997). At birth, they seemed normal, but within a few days their skin
became diseased, and they quickly wasted away and died. The experimenters
realized that something present in the mother's body had permitted normal
development up to the point of birth, and then the wasting disease set
in. The placental hormone, chorionic gonadotropin, is produced in large
amounts during pregnancy. The experimenters gave newborn infected mice
regular doses of human chorionic gonadotropin (hCG), and they developed
Rodents don't respond to gonadotropins or other ovarian stimulation
exactly the way pigs and primates and people do. For example, prolactin
and melatonin usually inhibit progesterone synthesis in people, but
in rodents, they increase it. So it's necessary to see exactly what
happens to the ovarian hormones when a mouse is given hCG. In 1996,
another group (H. Krzanowska and M. Szoltys) had done that, and found
that hCG greatly increases progesterone synthesis, but decreases
Considering the progesterone-HIV experiments together, I am reminded
of a science fiction movie, in which a disease from another planet killed
everyone in the lab that was studying it, except for one woman, who
turned out to be pregnant.
The medical version of AIDS research, though, pushes aside all of the
real science, in favor of a simplistic idea that the virus kills the
cells of the immune system, and uses false diagnostic methods and deadly
drugs to treat something which too often doesn't exist, while denying
that there are other real causes of immune deficiency and wasting-sickness,
Aging is characterized by loss of lean body mass, immunodeficiency,
and a variety of autoimmune reactions. My perennial argument has been
that decreased thyroid and progesterone, associated with increased estrogen
and stress hormones, are largely responsible for those changes. The
huge investment in AIDS research has found that these occur in AIDS,
but, because of the medical pharmaceutical culture which has created
myths about these hormones, no one is yet interpreting the hormone imbalances
in ways that would reveal their responsibility for the symptoms. While
the institutionalized theory claims that the HIV virus is responsible
for the syndrome, the hormones are reduced to epiphenomena.