HIV Does Not Cause AIDS: Contribution of Corticosteroids, Illicit Drugs, and Malnutrition to the Pathogenesis of AIDS

By Mohammed Ali Al-Bayati

Original Publication
Feb. 2001

Abstract

Review of the medical literature concerning the causes and the pathogenesis of AIDS worldwide revealed the following facts: 1) AIDS in drug users and homosexuals in the USA and Europe is probably caused by the heavy ancillary use of glucocorticoids and other immunosuppressive agents to medically treat the wide range of the chronic serious illnesses. 2) AIDS in hemophiliacs is clearly related to the use of corticosteroids and other immunosuppressive agents to prevent the development of antibodies for factors VIII and IX and to treat chronic illnesses. 3) AIDS in people receiving blood and/or tissue is related to the use of glucocorticoids to prevent reactions of transfusion and tissue rejection. 4) AIDS in infants and children is probably caused by their exposure to drugs and corticosteroids in utero and their exposure to corticosteroids after birth used to treat their chronic illnesses. 5) AIDS in Africa is caused by malnutrition, release of endogenous cortisol, and by opportunistic diseases. A trophy in the lymphoid tissue has been observed in HIV-negative people suffering from malnutrition. 6) Damage to the immune system is rapidly reversible after removal of the true insulting agent or treatment of the true causes in both HIV-positive and HIV-negative AIDS patients. 7) Kaposi’s sarcoma (KS) and lymphoma are probably induced by the use of steroids and drugs, and the release of endogenous cortisol. 8) HIV appears to be a harmless virus both in the in vivo and the in vitro settings. 9) The uses of glucocorticoids, AZT, and protease inhibitors to treat AIDS are contraindicated.

Introduction

The following case history was the spark that ignited this in-depth investigation of the causes and pathogenesis of acquired immune deficiency syndrome (AIDS). A 60 year-old-white male, HIV-negative, developed Acquired Immune Deficiency Syndrome (AIDS) following treatment with a two month course of prednisone (60 mg per day) and a two week course of azathioprine (50-100 mg per day) for lung fibrosis. His blood CD4+ T cells count was 255/µL, the CD4+ T cells /CD8+ T cells ratio was 0.6, and he had severe lymphocytopenia. He also suffered from pneumonia and severe fungal infection in his mouth and skin. Cessation of the treatment with prednisone and azathioprine lead to the reversal of the damage in his immune system. He fully recovered from pneumonia and the fungal infection after a short course of antibiotics and the use of antifungal lotion. Twenty-two days after the last dose of prednisone, his CD4+ T cells count was back to normal at 657 cells/µL (Al-Bayati, 1999).

Review of the literature of the causes and the pathogenesis of AIDS worldwide revealed that approximately 90% of AIDS cases in the USA and Europe are observed in homosexual men and drug users. The regular uses of alcohol, heroin, cocaine, amphetamines, and alkyl nitrite cause chronic health problems of the nervous system, respiratory system, cardiovascular system, kidneys and other tissues in these individuals. The majority of these health problems are usually diagnosed as idiopathic currently, and treated with high doses of glucocorticoids and/or cytotoxic drugs. In addition, homosexual men are usually heavy user of illicit drugs, alcohol, and rectal glucocorticoids (Fauci et al., 1998; Al-Bayati, 1999).

The HIV-hypothesis states that HIV causes AIDS by killing the CD4+ T cells directly or indirectly after long incubation times (about 10 years), and the number of these cells will reach very low levels (<300/ml) which lead to severe immune deficiency. Patients with severe immune deficiency (CD4+ T cells < 200/µL) usually suffer from opportunistic infections (viral, bacterial, fungal, yeast, and/or parasitic) and certain form of cancer such Kaposi’s sarcoma and lymphoma. It follows that treatment of patients with antiviral drugs such as inhibitors of reverse transcriptase (AZT) or protease is believed to delay the progression of AIDS by preventing HIV replication in the cells (Gallo, 1987; Fauci et al., 1998).

However, the treatment of a patient with prednisone at 60 mg per day for about three months can actually cause AIDS as described above. This treatment and doses often given to patients suffering from lung fibrosis, thrombocytopenia, or other chemically induced chronic illnesses. For example, Fauci et al., 1998 (p. 1463) described the treatment for patient with lung fibrosis as follows: "A trial of oral prednisone is begun at a dose of 1 mg/kg daily and continued for about 8 weeks. Should the disease not respond or be progressive, additional immunosuppression with cyclophosphomide should be considered. The objective is to reduce the white blood cell count to approximately half the normal baseline value, causing a distinct drop in the total lymphocyte count. However, a minimum count of 1000 PMNs/ul should be maintained". At this dose levels, the CD4+T cells count in the peripheral blood of the treated individual is expected to be <300/ul which meets the definition for AIDS set by the US Center For Diseases Control and Prevention (CDC).

Further investigation also revealed an astonishing result: the majority of AIDS patients who participated in the four major Zidovudine (AZT) clinical trials in the US between 1987-1992 were HIV-negative prior to their treatment with AZT. Briefly, a total of 2,349 patients participated in these studies, and at least 77% of them were HIV-negative prior to their treatment with AZT. HIV status of participants upon entrance to these studies are: a) Fischl et al., 1987: 282 patients participated; HIV was isolated at entry from 160 patients (57 percent of the AZT group and 58 percent of the placebo group); b) Fischl et al., 1990: 406 AIDS patients were treated with AZT but only 50 percent of these subjects had detectable serum levels of HIV antigen before treatment; c) Volberding et al., 1990: 1338 subjects participated; only 117 patients (9%) had detectable levels of HIV p24 antigen at baseline; and d) Hamilton et al., 1992: 321 AIDS patients received AZT but only 63 patients (20%) had detectable level of p24 antigen at base-line.

The reversal of CD4+ T cells depletion in the peripheral blood was reported in HIV+ homosexual men after the termination of their treatment with glucocorticoids. Sharpstone et al., 1996 reported that eight HIV+ males with inflammatory bowel disease who used rectal steroid preparation had a decline in their CD4+ T cells at a rate of 85 cells/µL per year. Four of them underwent coloectomy that eliminated the need for the steroid and their CD4+ T cells increased 4 cells/µL per year. Eight case-matched controls who did not have surgery continued to have a decline of 47 cells/µL per year as the result of the use of rectal steroid.

Furthermore, the reversal of the reduction in CD4+T cell count in HIV+ pregnant women following proper feeding was also reported by Fawzi et al., 1998. Briefly, the influence of diet on T cells counts in peripheral blood in 1,075 HIV-infected pregnant women who had poor nutritional status were studied. The CD4+ T cell counts of the women who received multivitamin increased from 424/µL to 596/µL during six months of proper feeding.

The reversal of damage in the immune system in HIV-positive patients following the cessation of the insulting agents and the existence of large number of HIV-negative AIDS patients as described above, combined with the wide use of immunosuppressive agents in modern medicinal practice to treat a variety of drug induced chronic illnesses gave me the incentive to review the medical literature to evaluate the validity of the HIV-hypothesis and the contribution of the illicit drugs, alcohol, and therapeutic agents, and malnutrition to the pathogenesis of AIDS worldwide.

Methods

The correct approach for solving AIDS causes or pathogenesis questions or any other complicated chronic medical problems is by evaluating all medical evidence concerning each risk group. Namely, a differential diagnosis that considers both infectious and noninfectious causes of diseased should be performed. To test the validity of the HIV-hypothesis, I reviewed the medical literature to evaluate the role of drugs, malnutrition, and infectious agents in the pathogenesis of AIDS worldwide. Detailed descriptions of the studies that I reviewed to evaluate the validity of the HIV-hypothesis were reported. The results indicate that the medical evidence show AIDS is probably caused by the use of illicit drugs, therapeutic use of corticosteroids, and malnutrition. Differential diagnosis indicated that HIV is not involved.

Findings

I. Causes and pathogenesis of AIDS in drug user and homosexuals:

In the USA, the total cases of AIDS in adults was 573,800 as of January 1, 1997 and about 90% of these cases were male homosexuals and heterosexuals and homosexual drug users (Fauci, et al., 1998). The appearance of AIDS in the USA and Europe in drug users and homosexuals in the late 1970’s and early 1980’s coincided with the synergistic actions of several events. Briefly, these include the spread of illicit drug use, especially smoking crack cocaine and heroin in 1970’s, the approval of glucocorticoids aerosol by the US FDA in 1976, the wide use of the glucocorticoid inhalers to treat chronic respiratory illnesses resulting from inhaling cocaine and heroin, the wide use of alkyl nitrites by homosexuals to facilitate anal sex in 1970’s, and the wide use of corticosteroids to treat chronic gastrointestinal tract illness in homosexuals. Furthermore, the approval of antiviral drugs (AZT and protease inhibitors) and the steroids by the U.S. FDA to treat patients with AIDS and asymptomatic patients infected with HIV has exacerbated the problem (Al-Bayati, 1999).

The HIV-hypothesis states that HIV cause AIDS by killing the CD4+ T cells directly or indirectly (Fauci, et al., 1998). It appears that there is no scientific evidence to show that HIV can kill infected T4 cells (CD4+ T cells) in vitro or in vivo. In addition, the abnormalities in the immune system of patients with AIDS are not restricted to the reduction of T4 cells as predicted by the HIV-hypothesis. Hoxie et al. (1985) observed no evidence of death in T cells infected with HIV in tissue culture. These cells continued to produce virus particles for more than four months after inoculation with the virus. Many reports describe the changes in the lymph nodes of patients infected with HIV and these changes range from extensive cellular hyperplasia of T and B lymphocytes and the supporting stroma to severe atrophy of the glands. Changes in the lymph nodes of 505 HIV infected patients who were asymptomatic or had AIDS demonstrate three distinct stages. These are hyperplasia (245 patients), atrophy (117 patients), and mixed stage (172 patients) (Al-Bayati, 1999). The presence of hyperplasia in the infected lymph nodes contradicts the HIV-hypothesis which states HIV destroys infected T cells (Gallo, 1987; Fauci et al., 1998).

Further elucidation is provided by the proponents of the HIV-hypothesis. Muro-Cacho, Pantaleo, and, Fauci (1995) examined 29 HIV+ lymph nodes and found twelve of these lymph nodes with follicular hyperplasia and extensive germinal centers, five with follicular hyperplasia mixed with follicular involution, twelve lymph nodes with a mixture of follicular involution and lymphocyte depletion, and five lymph nodes with lymphocyte depletion. They stated that "apoptosis was not restricted only to CD4+ T cells; both B cells and CD8+ T cells were found to undergo apoptosis. Taken together, these results indicate that the increased intensity of the apoptotic phenomenon in HIV infection is caused by the general state of immune activation, and is independent of the progression of HIV activities and the levels of viral load". HIV provirus was also found in CD4+ T cells, CD8+ T cells, and B cells lymphocytes in the lymph nodes of HIV infected patients and its ability to infect cells is not restricted to cells that have CD4 receptor as predicted by the HIV-hypothesis (Al-Bayati, 1999).

The changes in the lymph nodes described above are not unique to HIV infected individuals but also were described in HIV-negative patients in risk groups. The lymph nodes from 215 HIV-negative homosexual and drug users men showed hyperplasia and atrophy and 15 lymph nodes showed Kaposi’s sarcoma and lymphoma. These changes are AIDS-indicator diseases based on the CDC’s criteria, yet the subjects were HIV-negative (Al-Bayati, 1999).

In addition to the information presented above that demonstrate the invalidity of the HIV-hypothesis, the rate of T cells infection by HIV, and the rate of the thymus and the lymphoid tissue regeneration also conflict with the HIV-hypothesis.

Duesberg, (1992a) stated that HIV infects on the average only 0.1% (1 out of 500 to 3000) of T-cells in AIDS patients, and at least 3% of all T-cells are regenerated during the two days it takes a retrovirus to infect a cell. HIV could never kill enough T cells to cause immunodeficiency. Thus, even if HIV killed every infected T cell, it could deplete T cells only at 1/30 of their normal rate of regeneration, not considering activated regeneration.Gallo agreed with Duesberg that 1 in 10000 T cells are infected with HIV (Booth, 1988). Baltimore and Feinberg, 1989 also stated that in the late stage of AIDS disease, HIV infects 1 in 100 CD4+ T cells or 1 in 400 mononuclear cells. Furthermore,the study of Al-Bayati et al. (1990) also showed that the rate of regeneration in the damaged thymus and lymphoid tissue of mice treated with a lymphotoxic agent (vanadate) is very rapid. In this study, a total of 120 mice were treated with metavanadate solution (15.5 mg/kg). Severe necrosis in the thymus of treated mice were observed at 2 days following treatment and the thymus healed completely in about 10 days.

In addition to illicit drug and alcohol abuse, homosexuals are also heavy users of alkyl nitrites that relax the anal muscle and facilitate anal sex. It has been stated that the use of alkyl nitrites permeated the gay life by 1977 (Al-Bayati, 1999). Some of the studies cited by Duesberg, (1992a and 1992b) clearly showed the heavy use of alkyl nitrites and illicit drugs by homosexuals. These are: 1) 86.4% of 420 homosexual men attending clinics for sexually transmitted diseases in New York, Atlanta and San Francisco reported that they frequently used amyl-and butyl nitrites as sexual stimulants and the frequency of nitrite use was proportional to the number of sexual partners; 2) a total of 170 male homosexuals from sexual disease clinics, including 50 with KS and pneumonia, and 120 without AIDS were surveyed showing 50-60% had used cocaine, 50-70% amphetamines, 40% marijuana, 10% heroin, over 50% had also used prescription drugs, about 80% had past or current gonorrhea, 40-70% had syphilis, 15% mononucleosis, 50% hepatitis, and 30% parasitic diarrhea; 3) A study of a group of 359 homosexual men in San Francisco reported in 1987 that 84% had used cocaine, 82% alkyl nitrites, 64% amphetamines, 51% methaqualone and 41% barbiturates; 4) a total of 3916 self-identified American homosexual men were surveyed, among which 83% had used one, and about 60% of them used two or more drugs with sexual activities during the previous six months (similar drug use has been reported from European homosexuals at risk); and 6) survey of homosexual men from Boston, conducted between 1985 and 1988, documented that among 206 HIV-positives, 92% had used nitrite inhalants, 73% cocaine, 39% amphetamines, 29% lysergic acid in addition to six other psychoactive drugs as sexual stimulants.

Homosexuals usually suffer from acute and chronic rectal and gastrointestinal diseases that dictate the heavy therapeutic use of rectal steroids. Among 7 selected studies that included 736 patients (97% of them were homosexual or bisexual men) who were infected with HIV and/or had AIDS. They show clearly that homosexual men suffer from extensive rectal and gastrointestinal problems that result in chronic use of therapeutic rectal steroids (Al-Bayati, 1999).

Review of the medical literature revealed that the short and the long term use of glucocorticoids at therapeutic doses, resulted in a variety of effects on the immune system that range from a transient reduction in T cells count in peripheral blood to the development of full blown AIDS. Fauci, (1975) and Fauci et al., (1976) described in detail the effects of corticosteroids on the immune system. These effects resemble the immune abnormalities that are found in patients suffering from AIDS or Idiopathic CD4 T cells lymphocytopnea (ICL) which are also described by Fauci et al.,1998. For example, Fauci et al., 1976 stated that "we have reviewed many aspects of the host defenses that are altered by corticosteroids, and the combined effects of these changes must be considered in trying to understand the relation between corticosteroids and infections. Since the defect with corticosteroids is broad, it is not surprising that many types of infections seem to occur more often in patients treated with corticosteroids. Of the bacterial infections, staphylococcal and Gram-negative infections, as well as tuberculosis and Listeria infections, probably occur most often. Certain types of viral, fungal, and parasitic infections also occur often. Patients with lupus erythematous, rheumatoid arthritis, and renal transplant have more infection with steroid administration. Studies of bronchial aerosols showed that with higher doses of steroid in the aerosol, Candida infections of the larynx and pharynx occurred more often".

In addition, Kaposi’s sarcoma (KS) can develop in patients chronically treated with glucocorticoids independently of HIV. For example, KS developed eight months after initiation of prednisone treatment (40 mg per day for three months) in a 58-year-old man with systemic rheumatoid disease. He also had lymphocytopenia (896/µL), reduction of T4 cells (215/µL ), and T4/ T8 ratio of 0.7. This man was HIV-negative as tested by western blot (Schottstaedt et al., 1987). In addition, there are many cases who developed KS following treatment with glucocorticoids. They had reversal of their lesions after the termination of the treatment (Al-Bayati, 1999).

Furthermore, review of the medical literature revealed that the majority of AIDS patients suffer from metabolic and endocrine abnormalities. Changes were observed in the adrenal gland function of 182 AIDS patients (Al-Bayati, 1999). The high prevalence of adrenal insufficiency among AIDS patients provides very strong evidence that AIDS in these patients is caused by the use of corticosteroids. Fauci et al., (1998) stated that endocrine and metabolic abnormalities are frequently seen in HIV-infected individuals and most HIV-infected individuals studied at autopsy had involvement of adrenal glands. The most common abnormality seen in HIV infected individuals is hyponatremia, seen in up to 30 percents of patients. They also stated that the presence of a low sodium level combined with a high serum potassium level in a patient should alert one to the possibility of adrenal insufficiency and adrenocortical insufficiency as seen following prolonged administration of excess glucocorticoids. However; the use of corticosteroids by AIDS patients was not considered by Fauci and his colleagues.

Furthermore, as stated above, that the CD4+ T cells depletion in the peripheral blood of HIV -positive homosexual men was reversed after the termination of their treatment with glucocorticoids and at least 77% of 2,349 patients participated in the four major AZT clinical trials (1987-1992) were HIV-negative prior to their treatment with AZT. These studies demonstrate clearly that HIV is not the cause of AIDS (Al-Bayati, 1999).

Some studies show increases in CD4+ T cells in HIV-positive individual after treatment with the antiviral drugs (Al-Bayati, 1999). This information was interpreted as a good response to the medications. On the contrary, the elevation of T cells is not a good response in these conditions, but rather, it indicates severe tissue damage and infection. This explains the death of the patients following treatment with these drugs For example, the CD4+ T cells were also increased following the treatment of HIV negative nurses with AZT who took AZT as a prophylactic. They developed severe symptoms following 3 weeks of treatment with AZT (Al-Bayati, 1999). In addition to the failure of the antiviral drugs, AIDS patients suffering from immune deficiency are treated with glucocorticoids (Fauci et al., 1998). This practice is not supported by any known biomedical mechanism of action.

II. Causes and pathogenesis of AIDS in infants and children in USA and Europe:

As of January 1, 1997, the number of infants and children in USA diagnosed with AIDS was 6,891 and ninety percent of these cases had mothers who were drug users (Fauci et al., 1998; Al-Bayati, 1999). The prevalence of drug and alcohol abuse during pregnancy is very high both in the USA and Europe. The results of nine large studies surveying the prevalence of drug use in relation to the outcome of pregnancy in the USA showed that up to 15% of pregnant women used cocaine during pregnancy based on a positive urine test. The impact of illicit drug and alcohol abuse during pregnancy on infant health is very serious as shown in nine studies that included 1,295 drug using mothers and 4,293 nonusers. The use of cocaine during pregnancy was usually associated with a high prevalence of premature births and low birth weights. Drug exposed infants usually had immature lung profiles and other serious health problems that were treated with glucocorticoids (Al-Bayati, 1999).

Fauci et al., (1998) also explained the serious impact of illicit drugs on the pregnant mothers and her infants. They stated that "women who abuse cocaine have reported major derangement in menstrual cycle function, including galactorrhea, amenorrhea, and infertility. Chronic cocaine abuse may cause persistent hyperprolactinemia as a consequence of cocaine-induced disorders of dopaminergic regulation of prolactin secretion by the pituitary. Cocaine abuse, particularly the smoking of crack by pregnant women, has been implicated as causing an increased risk of congenital malformations and of prenatal cardiovascular diseases in the infants. Cocaine abuse per se is probably not the sole reason for these prenatal disorders since many problems associated with maternal cocaine abuse, including poor nutrition and health care status as well as polydrug abuse, also contribute to the risk of prenatal diseases". Furthermore, Fauci et al., (1998) also reported that a special case of opiate withdrawal is seen in the newborn passively addicted by the mother’s drug misuse during pregnancy. Some level of addiction develops in 50 to 90 percent of children of heroin-dependent mothers. The syndrome consists of irritability, crying, and tremor in 80%; increased reflexes, increased respiratory rate, diarrhea, and hyperactivity in 60%; vomiting in 40%; and sneezing, yawning, and hiccuping in 30%. The affected child usually has a low birth weight and may be otherwise unremarkable until the second day, when symptoms are likely to begin.

The treatment of the mother expected to have a premature birth with glucocorticoids has been used as a standard procedure since 1970s. Glucocorticoids are used to facilitate the development of the lung and to reduce the incidence of necrotizing enterocolitis in premature infant. In addition, the natural cortisol levels in plasma and urine of the cocaine-exposed preterm neonates is significantly higher than in normal infants (Al-Bayati, 1999).

Infants and children with AIDS are dying from opportunistic infections as a result of malnutrition and the excessive use of therapeutic steroids to treat the wide range of illnesses in these children. For example, the opportunistic infections found at 74 autopsies of pediatric HIV/AIDS patients included 53 cases fungal infections, 31 cases viral infections, and additional opportunistic infections were due to toxoplasmosis and tuberculosis (Drut, et al., 1997).

III. Causes and pathogenesis of AIDS in hemophiliac:

The medical evidence suggests that AIDS in hemophiliac patients is probably caused by the treatment with immunosuppressive agents (cyclophosphamide and glucocorticoids) which have been used to prevent the development of antibodies to factors VIII and XI in patients with hemophilia (Al-Bayati, 1999). The development of antibodies against factors VIII and IX and the use of corticosteroids by the hemophilia patients were also described by Fauci et al. (1998). They described the health problems in hemophilia patients, such as the formation inhibitors for factors VIII and XI, the joint problems, and the use of immunosuppressive agent in the treatment regimen of these patients. Patients with severe hemophilia have serious chronic joint problems resulting from bleeding inside the joints. This is also treated with glucocorticoids (Al-Bayati, 1999). AIDS has been reported in HIV negative and HIV positive hemophiliac patients. Duseberg, 1992a presented the result of 17 studies showing that a total of 717 hemophiliac patients had T4/T8 ratios less than or equal to one: 329 patients (46%) of them were HIV-negative (Al-Bayati, 1999).

IV. Causes and pathogenesis of AIDS in organ transplant and/or blood transfusion patients:

As of January 1, 1997, the number of patients who received blood transfusions, blood components or tissues then subsequently developed AIDS in USA is 7,888 (Al-Bayati, 1999). The list of adverse reactions to blood transfusion is present and the standard treatment used to prevent or cure these reactions is glucocorticoid as stated by Fauci et., (1998). For example, the risk of getting an allergic reaction from a blood transfusion is 1-4 per 100. The risk for delayed hemolytic reaction is 1 per 1,500. In contrast, the risk of infection with HIV from blood transfusion is 1 per 490,000 (Fauci, et. al., 1998). However, immune suppression as a result of the use of glucocorticoids in these patients was not investigated. Furthermore, glucocorticoids and other immunosuppressive agents are also used to prevent tissue rejection in organ transplant patients. The complications from these treatment and the list of opportunistic diseases are also described by Fauci et al., (1998). The list of opportunistic diseases in organ transplant patient receiving immunosuppressive agents are identical to the list of opportunistic diseases listed in Fauci et al., (1998) in people with AIDS.

V. Causes and pathogenesis of AIDS in Africa:

As of November 1996, the number of AIDS cases reported in Africa by the World Health Organization was 553,291 (Fauci et al., 1998). Severe malnutrition has been very well known to cause immune dysfunction and other serious health effects and should be considered in the differential diagnosis in HIV infected patients with AIDS and suffering from severe malnutrition before implicating HIV as the cause of AIDS in Africa. Actually the finding of atrophy of lymphoid tissue in people suffering from malnutrition was observed as early as 1925. For example, Jackson’s review on this topic in 1925 noted that many investigators had found a pronounced tendency of atrophy of lymphoid tissue in all conditions of malnutrition. Thymus weight was exquisitely sensitive to malnutrition and was earlier designated as the "barometer of nutrition" (Woodruff, 1972).

There is extensive literature describing the impact of malnutrition on the function and the structure of the immune system in people in Africa (Al-Bayati, 1999). This information clearly demonstrates that AIDS in Africa is more likely to be caused by starvation than by HIV. The function of the immune system, especially the cellular immunity, are impaired in malnutrition cases. The severity of the impairment is dependent on the degree of malnutrition in both human and animals. In studies of 345 malnourished children and two experimental models show the impact of food deprivation on the size of the thymus and the lymphoid organs. For example, the size of the thymus of 42 malnourished children was reduced by 90% as compared with a case-match normal controls (Parent et al., 1994). In a second study involving 110 malnourished children, the thymic area was found to be 20% of the size in healthy children (Chevalier et al., 1998). The result of studies that included 493 malnourished children who showed impairment in the function of the immune system; especially the cellular immunity (Al-Bayati, 1999).

The results of autopsy of 118 malnourished children showed: 1) both thymus and peripheral lymphoid tissues are reduced in bulk in states of protein-calorie malnutrition (PCM), this reduction being disproportionately greater than the loss of body weight.; and 2) Severe thymic atrophy was presented in 70% of marasmus cases and 85% of Kwashiorkor cases. 59.3% of the children had marasmic and Kwashiorkor symptoms (Schonland, 1972). Fakhir et al., 1989 evaluated 100 severely malnourished children and found that these children had a significant

reduction in the absolute lymphocytes count, T cells count, and in the skin reaction to dinitrochloro benzene. The lymphocyte function of 30 black children with PCM as assessed by the delayed hypersensitivity reaction and morphology of lymphocyte transformation was found to be impaired and serum cortisol level was elevated. The function of lymphocyte and cortisol level returned to normal after 30 days of feeding (Zeng et al., 1991).

The levels of endogenous cortisol (a natural hormone) in plasma and urine have been found to be abnormally elevated in malnourished patients. Studies that included 159 malnourished children and 148 AIDS patients who showed significant increases in cortisol levels (Membreno et al., 1987; Piedrola, et al., 1996; Aref, et al., 1982; Schonland, et al., 1972; Laditan, 1983; Zeng, et al., 1991).

Atrophy in the lymphoid organs in malnourished people is caused by increased levels of cortisol as well as by protein and vitamin deficiency. The reduction in the thymus and the lymphoid tissue size and the reduction in the function of the immune system of malnourished children and animals were reversed after proper feeding. For example, the size of the thymus increased from 20% of normal in a malnourished child to 107% of normal following 9 weeks of proper feeding. The reversal of the reduction in CD4+T cell count in HIV+ pregnant women following proper feeding was also reported by Fawzi et al., (1998). Briefly, the influence of diet on T cells counts in peripheral blood in 1,075 HIV-infected pregnant women who had poor nutritional status were studied. The CD4+ T cell counts of the women who received multivitamin increased from 424/µL to 596/µL during six months of proper feeding.

The incidence of starvation, parasitic diseases, septicemia, and low birth weight are very high in Africa and other developing countries. As shown in eleven studies that include the prevalence of malnutrition and diseases in 1,425 infants and 5,834 children surveyed in nine countries (Al-Bayati, 1999). For example, the mortality among 299 severely malnourished children in Zambia was 25.8% (Gernaat et al., 1998). Pneumonia and diarrhea were the major causes of death.

In India, 49% of 183 cases of lymphadenopathy in children were found to be due to tuberculosis (Sheikh, et al., 1981).

In 1983 the World Health Organization estimated that 300 million children had growth retardation secondary to malnutrition (Fauci et al., (1998). High prevalence of malnutrition and disease in Africa and other developing countries is also reported by Fauci et al., 1998 who stated that insufficient consumption of protein and energy causes loss of both body mass and adipose tissue. Protein energy malnutrition (PEM) occurs in developing nations and it may be present in endemic form. Under famine conditions, the prevalence of PEM may approach 25 percent. In children of developing nations two syndromes of PEM have been distinguished:(1) maramus, manifested by stunted growth, loss of adipose tissue, generalized wasting of protein mass; and (2) kwashiorkor, manifested by growth failure, edema, and hypoalbuminemia, fatty liver, and preservation of subcutaneous. Mixed forms are common in both children and adults (Fauci et al., 1998).

In PEM cell-mediated immunity is impaired as indicated by all standard tests (Fauci et al., 1998; Al-Bayati, 1999). Further more, all wounds and incisions heal more slowly in PEM and wound dehiscence is common. In woman with PEM, nearly every aspect of reproduction is impaired, including implantation, fetal growth, lactation, and parturition. The infants are stunted in size and may have cognitive impairment if they survive (Fauci et al., 1998).

Gastrointestinal infections frequently precipitate clinical PEM because of the associated diarrhea, associated anorexia, vomiting, increased metabolic needs, and decreased intestinal absorption. Parasitic infections play a major role in many parts of the world. Common infections and opportunistic infections can lead to increased morbidity and mortality. Pneumonia is common (Fauci et al., 1998).

The prevalence of KS and lymphoma, lymphadenitis, tuberculosis in Africa is similar to the male homosexuals AIDS patients in US and Europe and even higher (Al-Bayati, 1999). However, AIDS in Africa occurs almost equally in males and females because starvation affects both sexes equally. Sibanda and Stanczuk, (1993) reviewed all lymph node histopathology reports of lymph node biopsy submitted to the Histopathology unit in Harare, Zimbabwe in the period of January 1988 to June 1990. The commonest diseases in the 2,194 lymph node specimens were: non specific hyperplasia (33%), tuberculous lymphadenitis (27%); metastases (12%), Kaposi’s sarcoma (9%); and lymphomas (7%). Kaposi’s sarcoma (KS) involving the lymph nodes was reported in 176 (9%) of the lymph nodes. In children, the prevalence of KS was higher in children under 5 years than in 6-15 year bracket. Approximately two thirds (65%) of all patients with KS were aged between 20 and 40 years.

Furthermore, the large study of Fawzi et al., 1998 clearly demonstrated HIV is not implicated and the impairment of the immune system in a mother (HIV-positive) who suffers from malnutrition can be reversed by feeding the mother proper nutrition. This treatment also improved the outcome of pregnancy. In Tanzania, 1,075 HIV-infected pregnant women between 12 and 27 weeks’ gestation received vitamin A (n=269), multivitamins excluding vitamin A (n=269), multivitamins including vitamin A (n=270), or a placebo (n=267). In this study, malnutrition supplementation decreased the risk of low birth weight (<2500 g) by 44%, severe preterm birth (<34 weeks of gestation) by 39% and small size for gestational age at birth by 43%. During pregnancy, all T-cells subsets (CD4+, CD8+, and CD3+) increased in all groups between base-line (mean 18 week’s gestation and 6 weeks postpartum). There was a significantly larger increase in the CD4+ T cell counts and percentage of CD4+ T cells among women assigned multivitamins. The mean increases between base-line and 6 weeks postpartum were 167 cells/µL and 112 cells/µL among women on multivitamins and those on no vitamins, respectively. If HIV were the cause of AIDS as the HIV-hypothesis claim, then improved nutrition alone will never reverse the decline of T cells in these HIV-positive women.

VI. Evidence that invalidate the HIV-hypothesis.

The following is a list of medical facts that invalidate the HIV-hypothesis’ claim which states that HIV selectively kills CD4+T cells and cause AIDS: 1) the reduction of CD4+ T cells in HIV positive homosexual men who used rectal steroid was reversed after the cessation of the treatment with corticosteroids (Sharpstone et al., 1996). If the HIV is the cause of AIDS in these patients then the cessation of the steroids will not reverse the disease. 2)The reversal of the reduction of CD4+ T cells in HIV-positive pregnant women following the feeding multivitamin and provided balanced diet disprove the idea that HIV is the cause of AIDS. The average CD4+ T cells increase in these patients from 426/ul to 576/ul (Fawzi, et al. 1998). 3) The lymph nodes of majority of the 505 HIV-infected individuals showed lymphoid hyperplasia that include T and B cells (Al-Bayati, 1999). 4) The lymphoid atrophy observed in HIV-infected patients include reduction in T cells (CD4+ and CD+8), B cells, and stroma (Al-Bayati, 1999; Muro-Cacho, et al., 1995). 5) HIV particles were found in CD4+, CD8+ T cells, B cells, and other cells indicating HIV do not need specific receptors as the HIV-hypothesis predict (Al-Bayati, 1999). 6) 90% of AIDS cases were reported to be in drugs users and homosexuals and the changes in the lymphoid organs of HIV-negative drug users or homosexuals were similar to those described in HIV-positive drug users and/or homosexual men ( Fauci, et al., 1998; Al-Bayati, 1999). 7) There are numerous diseases caused by the use of drugs by inhalation such as lung fibrosis, thrombocytopenia and these diseases are chronically treated with high therapeutic doses of corticosteroids ( Fauci, et al., 1998; Al-Bayati, 1999). The long term use of corticosteroids (3-6 months) at dose levels of 60 mg per day can cause AIDS in HIV negative patients (Al-Bayati, 1999). 8) The hemophilia patients are chronically treated with immunosuppressive agents to prevent the development of antibodies to factor VIII and IX and reductions in T cells have been observed in HIV-positive and HIV negative hemophilia patients on corticosteroids ( Fauci, et al., 1998; Al-Bayati, 1999). 9) Blood transfusion patients and people with organ transplants develop AIDS after being treated with corticosteroids and the list of opportunistic diseases described in these groups are similar to those described in people with AIDS ( Fauci, et al., 1998). 10) Patients described with idiopathic CD4+ T cells lymphocytopenia have identical changes in the lymph node to those in people with AIDS, yet these people were HIV negative( Fauci, et al., 1998; Al-Bayati, 1999). 11) HIV-negative people with severe malnutrition have AIDS and show severe atrophy of thymus( Fauci, et al., 1998; Al-Bayati, 1999). 12) The majority (77%) of the cases (2349) in the four AZT clinical trials with AIDS or reduce immunity were HIV-negative (Fischl, et al., 1987 and 1990; Volberding , et al., 1990; Hamilton, et al., 1992; Al-Bayati, 1999). 13) The incubation of HIV with T cells in vitro did not kill any cells for about 4 months (Hoxie, et al., 1985). 14) There are thousands of cases infected with the HIV and did not show any symptoms for more than 10 years( Fauci, et al., 1998; Al-Bayati, 1999).

Discussion

The proponents of the HIV-hypothesis must be aware of the impact of illicit drug and alcohol abuse on health. However, they choose to discount the AIDS connection. Fauci et al. (1998) stated, "a markedly higher age-specific mortality rate among injection drug users in the general population was documented even before the epidemic of infection with HIV and AIDS. For example, in New York City between 1965 and 1972, the death rate among relatively young (20 to 54-year-olds) adult heroin addicts not involved in drug-treatment programs was estimated to be five time greater than that among age-matched non-heroin-addicted adults (28.2 per 1000 versus 5.6 per 1000). A substantial portion of this excess mortality was the result of infectious complications of injection drug use". At least 25 percent of such opiate abusers are likely to die within 10 to 20 years of active abuse". The same period (10-20 years) is also given by A. Fauci and the leaders of the HIV-hypothesis as the incubation time for HIV in the drug users (Fauci et al., 1998 and Al-Bayati, 1999).

The list of health problems induced by drug and alcohol abuse and those resulting from practicing receptive anal sex that required treatment with steroid is extensive. The chronic use of high doses of steroid (40-60 mg per day for several months) can cause AIDS as described in this report. I also stated above that the chronic use of rectal steroid reduced the CD4+ T cells by 47-85/µL per year in HIV positive homosexuals. Suppose that a homosexual man has a 1000 CD4+ T cells/µL prior to using rectal steroids to treat the wide range of chronic health problems. In 10 years, he may lose a total of 470-850 cells/µL from the use of rectal steroids leaving him with 150-530 CD4+ T cells/µL. If a homosexual man inhaling cocaine and has respiratory problems that also requires the use of glucocorticoids, the period needed for the CD4+ T cells count to reach to a level of 150/µL may be cut into half. This explains very well the high prevalence and the severity of AIDS among HIV-positive and HIV-negative homosexual men without any contribution from the HIV.

Alpha lipoic acid is a powerful antioxidant that has been used to prevent injury caused by chemicals in vivo and in vitro and injuries in diabetic patients for the last two decades (Al-Bayati, 1999). It has been used in Europe to reverse peripheral neuropathy in diabetic patients and has been shown to be effective and safe in several clinical trials. This drug is very effective in preventing and reversing injuries resulting from metabolic changes and/or exposure to chemicals that induce lipid peroxidation . This medication should be given to people with AIDS to boost the immune system and to heal tissue injury (Al-Bayati, 1999).

As noted earlier the stage of hyperplasia in the lymph nodes in drug users and in homosexuals HIV-positive or HIV-negative is usually followed by a stage of mixed stage (hyperplasia and atrophy) and then by a state of atrophy. These lympholytic stages resulted from the chronic use of massive therapeutic doses of steroids to treat the wide range of chronic health condition and from the releases of endogenous steroids (cortisol) induced by the stage of infections and malnutrition. Fauci et al. (998) warned about the use of glucocorticoids in patients with lymphoadenopathy . They stated that "glucocorticoids should not be used to treat lymphadenopathy because of it’s lympholytic effect. They contribute to delay in healing or activation of underlying infections ". Fauci et al.(1998) also reported that glucocorticoids produce a depletion of lymphoid tissue, especially T cells and impairs cell mediated immunity. Furthermore, Fauci et al. (1998) provided a long list of opportunistic infections (viral, fungal, bacteria parasitic agents) in organs transplant patients who were treated with steroid and/or other immunosuppressive agents. This list of infections is very similar to the list of opportunistic infections also reported by Fauci et al. (1998) in patients with AIDS.

Hyperplasia in the thymus and in the lymphoid organs of the drug users explains the result of Kreek’s study cited by Cohen, (1994) who observed increases in CD4+ T cells of heroin addicts. Kreek reported that 11 long-term heroin users had a mean of 1500 CD4+ T cells/µL which is a significant elevation from normal (normal range of 600 to 1200/µL) and the opposite of what is seen in AIDS, "Heroin is a blessedly untoxic drug: concludes Kreek". Cohen (1994) cited the result of Kreek’s study an argument against Duesberg’s suggestion that the use of illicit drugs is responsible for AIDS and not HIV (Duesberg, 1992a and 1992b). The observations of Kreek and Duesberg are both somewhat correct. The observations by Kreek supports Duesberg’s observation that the use of drugs is the cause of the problem in people having AIDS after treatment with corticosteroids. The true problem is that the leaders of the HIV-hypothesis and the CDC do not understand the sequence of events that leads to AIDS in patients in each risk groups. They have been ignoring important medical facts related to this subject, including the information presented in their own publications, and are blindly attributing AIDS to the HIV virus.

The medical evidence describing the effect of malnutrition on lymphoid tissues is extensive (Fauci et al., 1998). Fauci et al. (1998) also described the health problems in hemophilia patients, such as the formation of inhibitors for factors VIII and XI, the joint problems, and the use of immunosuppressive agent in the treatment regimen of these patients. Yet, they ignored all these facts and claimed that the problems in these patients is caused by HIV leading to the treatment of these very sick people with extremely toxic drugs (AZT and protease inhibitors).

AIDS patients have been treated with antiviral medications based on the assumption that the HIV causes AIDS. However, decreasing the plasma viral load does not restore the immune system (Al-Bayati, 1999). The thymus and the lymphoid tissues have very high rates of regeneration. A 50% destruction of the thymus by a chemical agent was restored within 10 days after cessation of exposure. If the cause of AIDS is HIV and the antiviral drugs are reducing the viral load, then the patients would recover within days.

Furthermore, according to the clinical trial results of the major four studies on the AZT conducted in the USA between 1987-1992, at least 77% of the patients were HIV-negative prior to their treatment with AZT. However, they claimed that AZT prolonged lives. The antiviral medications and the glucocorticoids not only fail to cure AIDS but they cause severe damage to sick people. The proponents of the HIV hypothesis failed to anticipate this disaster.

The proponents of HIV causation are unable to explain medical events in patients with AIDS using the HIV-hypothesis such as the changes in the lymphoid organs and the other medical information. They describe the disease by giving names to conditions to fit their hypothesis. For example, "long-term nonprogressors" is a name given to a large number of healthy people who have been infected with HIV for more than 10 years but are without AIDS symptom. The number of these people living in USA as of January of 1997 was 28,690. The proponents of the HIV-hypothesis cannot explain why people are living in perfect health 10 years and more with HIV if HIV kills T cells. The second very obvious example is the people with AIDS but who remain HIV-negative. These are described by the leaders of the HIV-hypothesis as having idiopathic CD4+ T cells lymphocytopenia (ICL). Fauci et al. (1998) stated that this condition is different from AIDS because the ICL patient shows low CD8+ T cells and B cells counts. However, in the same book, they stated that people with AIDS also have low B cells and CD8+ T cells counts. These findings seems contradictory.

The logical steps that should be taken to prevent AIDS and to cure people with AIDS are: 1) prevent the causes of AIDS by educating the public about the toxic effects of the illicit drugs and alcohol; 2) limit the use of glucocorticoids in the treatment of chronic conditions and in the treatment of people with AIDS; 3) monitor the levels of CD4+ T cells and CD8+ T cells in the blood of patients who are receiving medium or high therapeutic doses of glucocorticoids for significant times; 4) discontinue the treatment of patients with AIDS and asymptomatic patients with AZT and protease inhibitors immediately. These are very toxic medications; 5) provide proper clinical support and nutrition to patients with AIDS based on their medical needs. Prior to the development of full blown AIDS in drug users and homosexuals, the damage is caused by the use of drugs.

Acknowledgements

I am very grateful to Professor Otto G. Raabe from the University of California Davis for spending a great deal of time for reviewing this complicated manuscript and for his valuable input.

Mohammed Ali Al-Bayati, Ph.D., DABT, DABVT
(Toxicologist and Pathologist)
Toxi-Health International
150 Bloom Dr.
Dixon, CA 95620
Phone: (707) 678-4484
Fax: (707) 678-8505
Email: maalbayati@toxi-health.com
Copyright © 2001 by Mohammed Ali Al-Bayati & Toxi-Health International

References

Al-Bayati, M.A. (1999). Get All The Facts: HIV does not Cause AIDS. Toxi-health International, Dixon, California.

Al-Bayati, M.A., Culbertson, R.M., Schreider, J.P., Rosenblatt, L.S., and Raabe, O.G. (1992). The Lymphotoxic Action of Vanadate. Journal of Environmental Toxicology and Oncology, 11(2):19-27.

Aref, G.H., Abdel-Aziz, A., Elaraby II, et al. (1982). A post-mortem study of the thymolymphatic system in protein energy malnutrition. J Trop Med Hyg 85 (3):109-14.

Baltimore, D., Feinberg, M.B. (1989). HIV revealed: Toward a natural history of infection. The New England Journal of Medicine. 321(24), 1673-4.

Booth W. (1988). A rebel without a cause of AIDS. Science 239(4847):1485-1488

Chevalier, P., Sevilla, R., Sejas, E., et al. (1998). Immune recovery of malnourished children takes longer than nutritional recovery: implications for treatment and discharge. J. Trop Perdiatr 44(5):304-7

Cohen, J. (1994). Could drugs, rather than a virus, be the cause of AIDS? Science 266(5191), 1648-9.

Duesberg, P.H. (1992a). AIDS Acquired by drug consumption and other noncontagious Risk Factors. Pharmac. Ther. Vol.55, 201-277.

Duesberg, P.H. (1992b). The role of drugs in the origin of AIDS. Biomed Pharmacother 46(1):3-15.

Drut, R., Anderson, V., Greco, M.A., et al.(1997). Opportunistic infections in pediatric HIV infection: a study of 74 autopsy cases from Latin America. The Latin American AIDS pathology study group. Pediatr Pathol Lab Med 17(4):569-76

Fakhir, S., Ahmad, P., Faridi, M.A., and Rattan, A. (1989). Cell-Mediated immune responses in malnourished host. J. Trop. Pediatr. 35(4):175-8.

Fauci, A.S. (1975). Mechanisms of Corticosteroid Action on lymphocyte Subpopulations I. Redistribution of circulating T and B lymphocytes to the bone marrow. Immunology 28: 669-679.

Fauci, A.S., Dale, D.C., and Balow, J.E. (1976). Glucocorticosteroid therapy: Mechanisms of Action and Clinical Considerations. Annals of Internal Medicine 84: 304-15.

Fauci A.S., Braunwald, E., Isslbacher, K.J., et al. Harrison’s. Principles of Internal Medicine. (McGraw-Hill Companies, Inc. New York USA, ed. 14, 1998).

Fawzi, W.W., Msamanga, G.I., Spiegelman, D., et al. (1998). Randomized trial effects of vitamin supplements on pregnancy outcomes and T cell counts in HIV-1-infected women in Tanzania. The Lancet 351:1447-1482.

Fischl, M.A., Richman, D.D., Grieco, M.H., et al. (1987): The efficacy of Azidothymmidine (AZT) in the treatment of patients with AIDS and AIDS-related complex. A double-blind, Placebo-Controlled Trial. The New England Journal of Medicine. Volume 317, number 4 (185-191).

Fischl, M.A., Corette, B.P., Pettinelli, C., et al. (1990). A randomized controlled trial of a reduced daily dose of zidovudine in patients with the acquired immunodeficiency syndrome. The New England Journal of Medicine. Volume 323, number 15 (1009-14).

Gallo, R.C. (1987). The AIDS Virus. Scientific America. 256:46-56.

Gernaat, H.B., Dechering. W.H., Voorhoeve, H.W. (1998). Mortality in severe protein-energy malnutrition at Nchelenge Zambia. J Trop. Pediatr. 44(4):211-7

Hamilton, J.D., Hartigan, P.M., Simberkoff, M.S., et al. (1992). A controlled trial of early versus late treatment with Zidovudine in symptomatic human immunodeficiency virus infection. New England Journal of Medicine 326 (7):437-443.

Hoxie, J.A., Haggarty, B.S., Rackowski, J.L., et al. (1985). Persistent Noncytopathic Infection of Normal Human T lymphocytes with AIDS-Associated Retrovirus. Science 229(4720):1400.

Laditan, A.A. (1983). Hormonal changes in severely malnourished children. Afr. J Med Med Sci 12(3-4):125-32.

Membreno, L., Irony, I., Dere, W., et al. (1987). Adrenocortical function in acquired immnodeficiency syndrome. J. Clin. Endocrinol. Metab. 65 (3):482-7

Muro-Cacho, C. A., Pantaleo, G., Fauci, A.S. (1995). Analysis of apoptosis in lymph nodes of HIV-infected persons. Intensity of apoptosis correlates with the general state of activation of the lymphoid tissue and not with stage of disease or viral burden. J. Immunol 154 (10):5555-66.

Parent, G., Chevalier, P., Zalles, L., et al. (1994). In vitro lymphocyte-differentiating effects of thymulin (Zn-FTS) on lymphocyte subpopulation of severely malnourished children. Am. J. Clin. Nutr. 60(2):274-8

Piedrola, G., Casado, J.L., Lopez, E., et al. (1996). Clinical features of adrenal insufficiency in patients with acquired immunodeficiency syndrome. Clin. Endocrinol 45 (1):97-101.

Schonland, M. (1972). Depression of immunity in protein-calorie malnutrition: a post-mortem study. J. Trop Pediatr Environ Child Health 18(3):217-24.

Schonland, M.M., Shanley, B.C., Loening, W.E., et al. (1972). Plasma-cortisol and immuosuppression in protein-calorie malnutrition. Lancet 2 (7774):435-6.

Schottstaedt, M.W., Hurd, E.R., Stone, M.J. (1987). Kaposi’s sarcoma in rheumatoid arthritis. Am J Med 82(5):1021-6

Sharpstone, D.R., Duggal, A., Gazzard, B.G. (1996). Inflammatory bowel disease in individuals seropositive for the human immunodeficiency virus. Eur. J. Gastroentrol. Hepatol 8(6):575-8.

Sheikh, M.M., Ansari, Z., Ahmad, P., Tyagi, S.P. (1981). Tuberculous lymphadenopathy in children. Indian Pediatrics, Volume 18 (293-297)

Sibanda, E.N., Stanczuk, G. (1993). Lymph node pathology in Zimbabwe: a review of 2194 specimens. Q. J. Med. 1993; 86(12):811-7.

Volberding, P.A., Lagakos, S.W., Koch, M.A., et al. (1990). Zidovudine in asymptomatic human. immunodeficiency virus infection: A controlled trial in persons with fewer than 500 CD4+positive cells per cubic millimeter. The New England Journal of Medicine. Volume 322 (14):941-949.

Woodruff, J.F. (1972). Thymolymphatic deficiency and depression of cell-mediated immunity in protein-calorie malnutrition. Lancet 1(7741):92-3

Zeng, B., Qian, Y., Zheng, D., et al. (1991). Change of T lymphocyte subsets in peripheral blood of children with malnutrition and zinc deficiency. Hua His. I Ko. Ta. Hsueh Pao 22(3):337-9.