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- <html>
- <head><title>Immunodeficiency, dioxins, stress, and the hormones</title></head>
- <body>
- <h1>
- Immunodeficiency, dioxins, stress, and the hormones
- </h1>
-
- <strong>
- CRITICAL POINTS</strong>: <p>
- <em>
- *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 changes.
- </em>
- </p>
- <p>
- <em>
- *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.)
- </em>
- </p>
- <p>
- <em>
- *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."
- </em>
- </p>
- <p>
- <em>
- *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.
- </em>
- </p>
- <p>
- <em>
- *Estrogen activates the production of cortisol, and damages the normal feedback control, causing both
- cortisol and ACTH to be elevated.
- </em>
- </p>
- <p>
- <em>
- *Estrogen causes chronically elevated free fatty acids, and synergizes with unsaturated fats.
- </em>
- </p>
- <p>
- <em>
- *Estrogen inhibits thyroid function.
- </em>
- </p>
- <p>
- <em>
- Hypercortisolism is typically associated with hypothyroidism, and both tend to cause the loss of lean
- body mass.
- </em>
- </p>
- <p>
- <em>
- *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.
- </em>
- </p>
- <p>
- <em>
- *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.
- </em>
- </p>
- <p>
- <em>
- *Progesterone can contribute to the inhibition of HIV replication and transmission.
- </em>
- </p>
- <p>
- <em>
- *Common environmental factors can produce hormonal changes leading to immunodeficiency.
- </em>
- </p>
- <p></p>
- <hr />
- 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.
- <hr />
-
- It has been over ten years since I wrote about "AIDS" (e.g., "Repairing the Immune System," in <em>Cofactors in
- AIDS and HIV infection,</em> 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<strong> </strong>
-
- have become increasingly prevalent in our<strong> </strong>
- environment<strong>--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.</strong> 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.
-
- <strong>
- Environmental stress
- </strong>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<strong>: </strong>
-
- 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<strong>:</strong> 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<strong
- >;</strong> Deas, et al., 1998.) Treatments for roundworms and other parasites cause antibodies to retroviruses
- to appear in animals that previously tested negative<strong>;</strong> 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 increases vulnerability. 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 cause. 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.
- <strong><em>
- 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.</em></strong>
- <em>
- Some of these conditions are strongly associated with each other, for example, primary biliary cirrhosis,
- breast cancer, and osteoporosis.
- </em>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 <em>Medical Nemesis,</em>
- 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. <strong>The incidence of low birth-weight babies in the U.S. peaked around 1965, and 28
- years later AIDS mortality in the US peaked.
- </strong>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 probably increasing.
- 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.
-
- <strong>
- A Synthesis
- </strong>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 enviornmental chemicals. 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<strong>; </strong>
- estrogen's effect is to impair the negative feedback, in which cortisol normally shuts down ACTH production.
- This impaired feedback is characteristic of aging. 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 and cortisol. 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
- adaptability. 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 increases excitotoxicity. 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 normally. 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 <strong>increases progesterone synthesis, but decreases estrogen.
- </strong>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, etc. 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.
-
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- </strong>
- Barnham M. Significant streptococcal (non-pneumococcal, non-enterococcal) bacteraemia was detected in 100
- patients in two Health Districts of North Yorkshire in the decade 1978-1988. Transpl Immunol 1998 Jun;6(2):84-93
- <strong>Stress protein-induced immunosuppression: inhibition of cellular immune effector functions following
- overexpression of haem oxygenase (HSP 32).</strong> Woo J, Iyer S, Cornejo MC, Mori N, Gao L, Sipos I,
- Maines M, Buelow R. <strong>The results indicate that overexpression of HO results in the inhibition of several
- immune effector functions and thus provides an explanation for stress-induced immunosuppression.
- </strong>Genome 1998 Oct;41(5):662-8. <strong>A single-primer PCR-based retroviral-related DNA polymorphism
- shared by two distinct human populations.</strong> Deb P, Klempan TA, O'Reilly RL, Singh SM Department of
- Zoology, University of Western Ontario, London, Canada. <strong>"Almost 10% of the human genome consists of DNA
- sequences that share homology with retroviruses.</strong>
- These sequences, which represent a stable component of the human genome <strong>
- (although some may retain the ability to transpose),</strong> remain poorly understood." "Such novel
- polymorphisms should provide useful markers and permit assessment of evolutionary mechanisms associated with
- retroviral-related genomic evolution. " Gen Pharmacol 1998 May;30(5):685-7, <strong>Imprinting of thymic
- glucocorticoid receptor and uterine estrogen receptor by a synthetic steroid hormone at different times
- after birth.</strong> Csaba G, Inczefi-Gonda A. J Clin Endocrinol Metab 1998 Dec;83(12):4373-81.<strong>
- Human immunodeficiency virus induction of corticotropin in lymphoid cells.</strong> Hashemi FB, Hughes TK,
- Smith EM. Eur J Cancer Clin Oncol 1988 Jul;24(7):1179-83. <strong>Abnormal free fatty acids and cortisol
- concentrations in the serum of AIDS patients.</strong>
- Christeff N, Michon C, Goertz G, Hassid J, Matheron S, Girard PM, Coulaud JP, Nunez EA. The serum free fatty
- acid (FFA), cortisol and urinary creatinine, 17-hydzoxycorticosteroid and 17-oxosteroid concentrations of
- acquired immunedeficiency syndrome (AIDS-I: beginning and AIDS-II: end phase) and AIDS-related complex (ARC)
- patients were determined. Both groups were compared to a control group (healthy men). ARC and AIDS-I patients.
- The ratios of stearic (C18:0) to oleic (C18:1) acid were 75%, P less than 0.01 (ARC) and 45%, P less than 0.05
- (AIDS-I) greater than normal, due to a decrease in the relative percentage of monounsaturated fatty acids by
- 25%, P less than 0.001 (ARC) and 20%, P less than 0.01 (AIDS-I). In contrast, <strong>the relative percentage of
- polyunsaturated fatty acids was 85% greater than normal (P less than 0.001) in ARC and 100% greater than
- normal (P less than 0.001) in AIDS-I patients.
- </strong>Total FFA levels did not differ from controls. Serum cortisol levels were 35% (P less than 0.01) above
- normal in ARC and 60% (P less than 0.001) above normal in AIDS-I patients. Urinary 17-hydroxycorticosteroids and
- 17-oxosteroids were very low (2-3-fold lower than normal values, P less than 0.001) in both groups of patients.
- Urinary creatinine did not differ from controls. In AIDS-II patients the total FFA concentration was below
- normal 35% (P less than 0.01) and the stearic/oleic acid ratio was 50% above normal (P less than 0.05). The
- relative percentages of monounsaturated and polyunsaturated fatty acids in this group were similar to those of
- controls. <strong>Serum cortisol concentrations were significantly higher, 50% (P less than 0.001), but the
- urinary 17-hydroxycorticosteroids and 17-oxosteroids were 2-fold lower
- </strong>
- (P less than 0.001) than those of controls. Urinary creatinine did not differ from controls. J Clin Endocrinol
- Metab 1992 May;74(5):1045-52. <strong>Lipids, lipoproteins, triglyceride clearance, and cytokines in human
- immunodeficiency virus infection and the acquired immunodeficiency syndrome.</strong> Grunfeld C, Pang M,
- Doerrler W, Shigenaga JK, Jensen P, Feingold KR. Infection causes disturbances in lipid metabolism that may be
- mediated by cytokines. Therefore we studied plasma lipids, lipoproteins, triglyceride (TG) metabolism, and serum
- cytokines in three groups: patients with the acquired immunodeficiency syndrome <strong>(AIDS) without active
- secondary infection,</strong>
- patients with evidence of human immunodeficiency virus infection but without clinical AIDS (HIV+), and controls.
- <strong>Plasma TGs and FFA were increased in AIDS,</strong> while plasma cholesterol, high density lipoprotein
- (HDL) cholesterol, apolipoprotein-A-1 (Apo-A-1), low density lipoprotein (LDL) cholesterol, and Apo-B-100 levels
- were decreased. J Virol 1991 May;65(5):2231-6.<strong>
- Human immunodeficiency virus type 1 infection of human placenta: potential route for fetal
- infection.</strong>
- Amirhessami-Aghili N, Spector SA. AIDS Res Hum Retroviruses 1997 Sep 20;13(14):1235-42. <strong>Interaction of
- pregnancy steroid hormones and zidovudine in inhibition of HIV type 1 replication in monocytoid and
- placental Hofbauer cells: implications for the prevention of maternal-fetal transmission of HIV.</strong>
- Lee AW, Mitra D, Laurence J. Folia Biol (Krakow) 1996;44(3-4):111-6. <strong>Preovulatory dynamics of ovarian
- steroid hormones in two mouse strains differing in the rate of meiotic maturation.</strong> Krzanowska H,
- Szoltys M. J Clin Invest 1997 Apr 1;99(7):1484-91.<strong>
- Human chorionic gonadotropin hormone prevents wasting syndrome and death in HIV-1 transgenic mice.</strong>
-
- De SK, Wohlenberg CR, Marinos NJ, Doodnauth D, Bryant JL, Notkins AL., Metabolism 1993 Oct;42(10):1270-6.
- Indices of function and weight loss in human immunodeficiency virus infection and the acquired immunodeficiency
- syndrome. Grunfeld C, Pang M, Doerrler W, Jensen P, Shimizu L, Feingold KR, Cavalieri RR. Int J Health Serv
- 1994;24(2):311-35 <strong>Nuclear fallout, low birthweight, and immune deficiency. Gould JM, Sternglass
- EJ</strong> Radiation and Public Health Project, New York, NY 10024. An investigation of the mortality rates
- of young adults born in the postwar period of large-scale atmospheric nuclear testing (1945-1965) in the United
- States and other western industrial nations reveals an increasingly anomalous rise in mortality from its
- previous secular decline. Beginning in the <strong>late 1970s and particularly since 1983, the deterioration in
- the health of the 25-44 age group is related to in utero exposure to fission products in the milk and diet,
- associated with an unprecedented rise in underweight births and neonatal mortality known to be accompanied
- by loss of immune resistance.
- </strong>
- The 1945-1965 rise<strong>
- in the percentage of live births below 2500 grams is highly correlated with the amount of strontium-90 in
- human bone, both peaking in the mid-1960s.</strong> In the 1980s, for the baby boom generation (those
- born<strong>
- between 1945 and 1965), cancer incidence and mortality due to infectious diseases associated with a</strong>
- rising degree of immune deficiency, such as pneumonia, septicemia, and AIDS, increased sharply. This process of
- increasing immune deficiency appears to have been exacerbated by continuing secondary exposures to accidental
- reactor releases and by an acceleration of radiation-induced mutation of pathogenic microorganisms increasingly
- resistant to drugs. Biokhimiia 1987 Sep;52(9):1501-11 <strong>[Activation of lipolysis and ketogenesis in
- tumor-bearing animals as a reflection of chronic stress states].</strong>
- Chekulaev VA, Shelepov VP, Pasha-zade GR, Shapot VS. Arkh Patol 1987;49(6):10-8 <strong>[Combination of
- immunodepression and disorders in nucleic acid metabolism of lymphoid tissue as a manifestation of a
- paraneoplastic syndrome].</strong> [Article in Russian] Potapova GI, Shapot VS Several physiological,
- biochemical, and molecular biological approaches to the study of factors determining immunodepression in
- tumor-bearing animals are considered. Cancer cells release substances of nucleic and peptide nature that
- suppress the functional activity of macrophages and lymphocytes and stimulate cell proliferation in organs and
- tissues of the host. Suppressor T cells capable of inhibiting the function of helper T cells and impairing the
- differentiation of killer T cells are activated. The suppression<strong>
- of T- and B-cell-mediated immunity in the tumor host involves disturbances of nucleic acid metabolism in
- those cells as well as hypersecretion of glucocorticoids.
- </strong>
- The impairments of lymphocyte proliferation and differentiation that result in reduced immune responsiveness are
- attributable to drastic alterations in the metabolism of purine and pyrimidine nucleotides and to the damage
- sustained by the lymphocyte's DNA. Eksp Onkol 1987;9(6):62-7 <strong>[Relation between disorders of glucose
- metabolism, secretion of somatotropic hormone, thyroxine, thyrotropin and hematocrit indices in rats with
- transplanted hepatomas].</strong> Shelepov VP, Pasha-zade GR, Chekulaev VA, Shapot VS. Am J Pathol 1987
- Jan;126(1):103-13 <strong>Dietary fatty acid effects on T-cell-mediated immunity in mice</strong>
- <strong>infected with mycoplasma pulmonis or given carcinogens by injection.</strong> Bennett M, Uauy R, Grundy
- SM. To test whether or not diets enriched in w-6 polyunsaturated fatty acids are significantly immunosuppressive
- . . . mice were fed diets enriched for fatty acids: linoleic (POLY), oleic (MONO), palmitic (SAT), or
- eicosapentanoic (FISH). . . . only mice on the<strong>
- POLY diet were significantly immunosuppressed, and only T-cell-mediated cutaneous sensitivity reactions were
- affected.</strong>
- After instillation, mice on the POLY and MONO diets were suppressed for T-cell cutaneous responses. Deliberate
- infection with Mycoplasma pulmonis resulted in suppressed cutaneous T-cell responses in the POLY group of C3B6F1
- mice, and aspirin partially reversed the immunosuppression. Mice on the FISH diet were resistant to
- immunosuppression. It is tentatively concluded that diets rich in w-6 polyunsaturated diets, while not<strong>
- directly immunosuppressive, do predispose animals to suppression of certain T-cell-mediated immune
- responses. This immunosuppression can be "triggered" by infection and/or by exposure to carcinogens.
- </strong>Tumour Biol 1988;9(5):225-32 <strong>Modulation of cell-mediated immune response by steroids and free
- fatty acids in AIDS patients: a critical survey.</strong> Nunez EA. The overall data presented in this
- review show that cortisol and free fatty acids, in particular long-chain polyunsaturated fatty acids, each have
- immunoinhibitory properties on lymphoblastic transformation of<strong>
- certain T lymphocytes. This effect is enhanced when the two factors are associated. These data could explain
- in part the immunosuppression observed in acquired immunodeficiency syndrome (AIDS) patients where enhanced
- concentrations of cortisol and polyunsaturated fatty acids have been observed.
- </strong>Basic Life Sci 1988;49:615-20 <strong>Vitamin E and immune functions</strong>. Bendich A.
- Supplementation of these diets with higher than nutritionally adequate<strong>
- levels of vitamin E enhances immune responses. High levels of PUFA are immunosuppressive, and vitamin E can
- partially overcome this immunosuppression. High levels of vitamin C can protect tissue levels of</strong>
- vitamin E and may indirectly contribute to the immunoenhancement by vitamin E. Severe selenium deficiency is
- immunosuppressive. Vitamin E can protect some aspects of immune responses from the adverse effects of selenium
- deficiency. These data clearly indicate that nutrients that affect the overall antioxidant status have important
- effects on immune functions. In addition, antioxidant nutrient interactions can synergize to overcome the
- adverse effects of polyunsaturated fatty acids on immune functions. Transplantation 1989 Jul;48(1):98-102
- <strong>Enhancement of immunosuppression by substitution of fish oil for olive oil as a vehicle for
- cyclosporine.</strong>
- Kelley VE, Kirkman RL, Bastos M, Barrett LV, Strom TB. J Am Coll Nutr 1992 Oct;11(5):512-8 <strong>Role of
- nutrition in the management of malnutrition and immune dysfunction of trauma.
- </strong>
- Cerra FB Dept. of Clinical Nutrition, University of Minnesota, Minneapolis. Current nutrition support improves
- patient outcome in trauma patients. It appears to do so by limiting the adverse effects of specific nutrient or
- generalized nutrient deficiencies. Immunosuppression, however, continues as a significant clinical problem. This
- <strong>immunosuppression appears to be part of the inflammatory response that accompanies trauma, and in part,
- to represent the need for conditional</strong> nutrients in this setting. Three nutrients that are being
- evaluated include arginine, uracil as ribonucleic acid and omega-3 polyunsaturated fatty acids. Animal studies
- report improved immune function. Early clinical trials are reporting improved immune function and patient
- outcomes. J Nutr 1996 Mar;126(3):681-92 <strong>Dietary butter protects against ultraviolet radiation-induced
- suppression of contact hypersensitivity in Skh:HR-1 hairless mice.</strong> Cope RB, Bosnic M, Boehm-Wilcox
- C, Mohr D, Reeve VE. Dietary fats modulate a wide variety of T cell functions in mice and humans. This study
- examined the effects of four different dietary fats, predominantly polyunsaturated sunflower oil, margarine, and
- predominantly saturated butter, clarified butter, on the T cell-mediated, systemic suppression of contact
- hypersensitivity by ultraviolet radiation. There was a linear relationship (r > 0.9) between protection
- against<strong>
- photoimmunosuppression and the proportion of clarified butter in mice fed a series of 200 g/kg mixed
- fat</strong> diets that provided varying proportions of clarified butter and sunflower oil. The dietary fats
- did not modulate the contact hypersensitivity reaction in unirradiated animals. The observed phenomena were not
- primary due to the carotene, tocopherol, cholecalciferol, retinol, lipid hydroperoxide or the nonfat solid
- content of the dietary fats used and appeared to be a result of the different fatty acid composition of the
- fats. Cancer Lett 1996 Nov 29;108(2):271-9 <strong>Dependence of photocarcinogenesis and photoimmunosuppression
- in the hairless mouse on dietary polyunsaturated fat.</strong> Reeve VE, Bosnic M, Boehm-Wilcox C. The
- photocarcinogenic response was of increasing severity as the polyunsaturated content of the mixed dietary fat
- was increased, whether measured as tumour incidence, tumour multiplicity, progression of benign tumours to
- squamous cell carcinoma, or reduced survival. When mice were exposed acutely to UV radiation (UVR), a <strong
- >diet of 20% saturated fat provided almost complete protection from the suppression of CHS, whereas feeding 20%
- polyunsaturated fat resulted in 57% suppression</strong>; the CHS of unirradiated mice was unaffected by the
- nature of the dietary fat. These results suggest that the enhancement of photocarcinogenesis by the dietary
- polyunsaturated fat component is mediated by an induced <strong>predisposition to persistent immunosuppression
- </strong>
-
- caused by the chronic UV irradiation, and supports the evidence for an immunological role in dietary fat
- modulation of photocarcinogenesis in mice. Ann Acad Med Singapore 1991 Jan;20(1):84-90.<strong>
- Clinical implications of food contaminated by aflatoxins.</strong> Hendrickse RG. Arch Toxicol
- 1996;70(10):661-71. <strong>Host resistance to rat cytomegalovirus (RCMV) and immune function in adult PVG rats
- fed herring from the contaminated Baltic Sea.</strong> Ross PS, Van Loveren H, de Swart RL, van der Vliet H,
- de Klerk A, Timmerman HH, van Binnendijk R, Brouwer A, Vos JG, Osterhaus AD. In a semi-field study, we
- previously showed that harbour seals (Phoca vitulina) <strong>fed herring from the contaminated Baltic Sea had
- lower natural killer cell activity, T-lymphocyte functionality and delayed-type hypersensitivity
- responses</strong> than seals fed herring from the relatively uncontaminated Atlantic Ocean. A novel model
- was established to assess the specific T-cell response to rat cytomegalovirus (RCMV). When applied to the
- feeding study, no differences between the Atlantic and Baltic groups in the RCMV-induced proliferative
- T-lymphocyte responses could be detected, but virus titres in salivary glands of infected rats of the Baltic Sea
- group were higher. These elevated RCMV <strong>titres and changes in thymus cellularity</strong> suggest that
- the dietary exposure to low levels of contaminants may have been immunotoxic at a level which our immune
- function test could not otherwise detect. While the herring diet per se appeared to have<strong>
- an effect on several immune function parameters, lower plasma thyroid hormone levels in the Baltic Sea group
- of rats confirmed that exposure to the environmental mixture of contaminants led to adverse PHAH-related
- health effects.
- </strong>Environ Health Perspect 1995 Apr;103(4):366-71 <strong>Dioxin activates HIV-1 gene expression by an
- oxidative stress pathway requiring a functional cytochrome P450 CYP1A1 enzyme.</strong> Yao Y, Hoffer A,
- Chang CY, Puga A. <strong>
- Aflatoxin B1, 2,3,7,8-tetrachlorodibenzo-p-dioxin
- </strong>
- (TCDD; dioxin) and benzo[a]pyrene cause a significant increases in CAT expression in mouse hepatoma Hepa-1
- cells. We conclude that induction of a functional CYP1A1 monooxygenase by TCDD stimulates a pathway that
- generates thiol-sensitive reactive oxygen intermediates which, in turn, are responsible for the TCDD-dependent
- activation of genes linked to the LTR. These data might provide an explanation for findings that TCDD increases
- infectious HIV-1 titers in experimental systems and for<strong>
- epidemiologic reports suggesting that exposure to aromatic hydrocarbons, such as found in cigarette smoke,
- is associated with an acceleration in AIDS progression.
- </strong>Ann Trop Med Parasitol 1997 Oct;91(7):787-93 <strong>Of sick turkeys, kwashiorkor, malaria, perinatal
- mortality, heroin addicts and food poisoning: research on the influence of aflatoxins on child health in the
- tropics.
- </strong>
- <hr />
-
- Ann N Y Acad Sci 1986;475:320-8. <strong>Hormonal approaches to immunotherapy of autoimmune disease.</strong>
- Talal N, Ahmed SA, Dauphinee M. Cell Immunol 1998 Nov 1;189(2):125-34.<strong>
- Estrogen increases the number of plasma cells and enhances their autoantibody production in nonautoimmune
- C57BL/6 mice.</strong> Verthelyi DI, Ahmed SA. J Rheumatol 1987 Jun;14 Suppl 13:21-5. <strong>Interleukin 2,
- T cell receptor and sex hormone studies in autoimmune mice.</strong> Talal N, Dang H, Ahmed SA, Kraig E,
- Fischbach M. The <strong>administration of estrogen to pregnant mice late in gestation results in offspring with
- a permanently altered immune system. These mice develop features of autoimmunity similar to those that occur
- spontaneously in genetically susceptible autoimmune mice. T</strong>his phenomenon may have etiopathological
- significance for familial SLE. Endocrinology 1994 Dec;135(6):2615-22. <strong>17 beta-estradiol, but not 5
- alpha-dihydrotestosterone, augments antibodies to double-stranded deoxyribonucleic acid in nonautoimmune
- C57BL/6J mice.</strong> Verthelyi D, Ahmed SA. J Autoimmun 1993 Jun;6(3):265-79 <strong>Antibodies to
- cardiolipin in normal C57BL/6J mice: induction by estrogen but not dihydrotestosterone.</strong>
- Ahmed SA, Verthelyi D. J Autoimmun 1989 Aug;2(4):543-52.<strong>
- Estrogen induces the development of autoantibodies and promotes salivary gland lymphoid infiltrates in
- normal mice.</strong> Ahmed SA, Aufdemorte TB, Chen JR, Montoya AI, Olive D, Talal N. . . . normal mice were
- <strong>prenatally exposed to estrogens.</strong>
- . . . mice prenatally exposed to estrogens had accelerated development of autoimmune salivary gland lesions
- indistinguishable from Sjogren's syndrome (SS) in humans. Further experiments are warranted to confirm these
- findings. The prenatal effects of estrogen may have relevance for familial and neonatal autoimmune syndromes.
- Isr J Med Sci 1988 Dec;24(12):725-8.<strong>
- Sex hormones, CD5+ (Lyl+) B-cells, and autoimmune diseases.</strong> Talal N, Ahmed SA. Ann N Y Acad Sci
- 1986;475:320-8 <strong>Hormonal approaches to immunotherapy of autoimmune disease.</strong> Talal N, Ahmed SA,
- Dauphinee M. Life Sci 1998;63(20):1815-22. <strong>Exacerbated immune stress response during experimental
- magnesium deficiency results from abnormal cell calcium homeostasis.</strong> Malpuech-Brugere C, Rock E,
- Astier C, Nowacki W, Mazur A, Rayssiguier Y. These studies first showed that an <strong>abnormal calcium
- handling induced by extracellular magnesium depression in vivo may be at the origin of exacerbated
- inflammatory response.
- </strong>Magnes Res 1998 Sep;11(3):161-9. <strong>Early morphological and immunological alterations in the
- spleen during magnesium deficiency in the rat.</strong>
-
- Malpuech-Brugere C, Kuryszko J, Nowacki W, Rock E, Rayssiguier Y, Mazur A. Dietary magnesium deficiency in
- rodents, and especially in rats, causes inflammation and leads to alterations in the immune response. Ann Rheum
- Dis 1994 Nov;53(11):749-54 <strong>
- Polymerase chain reaction fails to incriminate exogenous retroviruses HTLV-I and HIV-1 in rheumatological
- diseases although a minority of sera cross react with retroviral antigens.</strong> Nelson PN, Lever AM,
- Bruckner FE, Isenberg DA, Kessaris N, Hay FC. Clin Diagn Lab Immunol 1998, Mar;5(2):181-5. <strong>Reactivity of
- sera from systemic lupus erythematosus and Sjogren's syndrome patients with peptides derived from human
- immunodeficiency virus p24 capsid antigen.</strong> Deas, JE, et al.<strong> </strong>We have previously
- demonstrated that <strong>about one-third of patients with either Sjogren's syndrome (SS) or systemic lupus
- erythematosus (SLE) react to human immunodeficiency virus (HIV)</strong> p24 core protein antigen without
- any evidence of exposure to, or infection with, HIV itself. J Clin Lab Immunol 1988 Feb;25(2):101-3. <strong
- >Effect of diethylcarbamazine on serum antibody to feline oncornavirus-associated cell membrane antigen in
- feline leukemia virus cats.</strong> Kitchen LW, Cotter SM. Department of Cancer Biology, Harvard School of
- Public Health, Boston. Diethylcarbamazine (N,N-diethyl-4-methyl-1- piperazine carboxamide; DEC) is a drug
- frequently used for prevention and treatment of the filariases. An opsonic action of DEC may generate increased
- immune responses to microfilariae. We tested the hypothesis that DEC treatment could result in higher antibody
- levels to other infectious agents. A retroviral animal model was studied, <strong>
- in light of the consideration that use of DEC as an antifilarial agent could conceivably alter
- seroepidemiologic surveys as well as serologic outcomes of vaccine trials in Africa regarding human
- immunodeficiency virus (HIV).
- </strong>The effect of DEC treatment on serum antibody to feline oncornavirus-associated cell membrane antigen
- (FOCMA) in domestic cats exposed to feline leukemia virus (FeLV) was examined. Nine cats that <strong><hr
- /></strong>
- <hr />
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