INTRODUCTION:
In the last two years, I reviewed the medical records of several individuals (male and female) who were diagnosed with idiopathic illnesses of the nervous system, respiratory system, kidneys, and
liver or asthma. They were treated chronically with glucocorticoids or with glucocorticoids and cytotoxic drugs at moderate to high therapeutic doses. These people lived in different states within
the United States. They consulted with me to find out if their exposure to chemicals at the workplace and/or the use of medications triggered and/or contributed to their illnesses. The
review of their medical files showed that all of them suffered from various degrees of lymphocytopenia. One of these cases was a 60 year-old-white male who developed Immunodeficiency syndrome
similar to those described in patients with Acquired Immune Deficiency Syndrome (AIDS) and Idiopathic CD4+ T cells lymphocytopenia (ICL) (1) after treatment with a two months course
of prednisone (60 mg per day) and two weeks course of azathioprine (50-100 mg per day) for lung fibrosis. His blood analysis revealed a CD4+ T cells count of 255/無 (normal range
542 to 1595/無) and a CD4+T cells /CD8+ T cells ratio of 0.6 (normal range 1.0-3.5). He was suffering from a severe lymphocytopenia (peripheral blood lymphocytes count was 483/無).
Prior to his treatment with prednisone, his lymphocytes count was normal (1513/無). In addition, he suffered from pneumonia and developed a severe fungal infection on the skin of various regions
of his body and very painful sores in his mouth (gum and cheeks which looked like white cottage cheese). He was not infected with the Human Immune Deficiency Virus (HIV) as determined by three
tests at various clinics.
This man was diagnosed as having Idiopathic Pulmonary Fibrosis (IPF) in June of 1997 at Kaiser Permanente Medical Center in
Vallejo, California. My review of the work history of this man revealed that he had been working at Travis Air Force Base in Fairfield, California since 1979 as a flight engineer. He had been
exposed chronically at his workplace to organic solvents and aviation jet fuels (JP-8 in particular which is composed of 99% kerosene (2)). The review of his medical records revealed that he had
pulmonary fibrosis and changes in the upper respiratory airways (hyperplasia and metaplasia of the epithelial layers and hyperplasia of the smooth muscle cells) that were consistent with
the changes resulting from long term exposure to toxic levels of kerosene and aviation fuel by inhalation. (3-7)
The treating physician at Kaiser Permanente changed the course
of treatment for this man in November of 1997 based on the diagnosis and the recommendation that I provided. He showed significant improvements in his general health condition and in his
immune system. His physician stopped the treatment with azathioprine, tapered the treatment with prednisone and treated the patient with anitihistamine (Chlorpheninamine, 24 mg/day) to
relax the muscle of the airways. On May 19, 1998, 22 days after the last dose of prednisone, his CD4+ T cells and CD8+ T cells counts were 657 cells/無 and 659 cells/無, respectively. These
counts were 247% and 153% of the values during the tapering of prednisone for the CD4+ T cells (T4) and the CD8+ T cells (T8), respectively. In addition, his fungal infection and pneumonia were
resolved following treatment with short course of antibiotic (Doxycycline 200mg per day for 2 weeks) and topical antifungal agent (Loprox). In June of 1998, this man was treated with
colchicine (0.6-1.2 mg/daily) for two weeks for a minor joint problem. On September 30, 1998, his CD4+ T cells count was 516/無, 21% lower than the count on May 19, 1998 prior to
treatment with colchicine. It took four more months to bring CD4+ T cells count to 719/無. It is clear that prednisone, azathioprine and colchicine were all responsible for lowering CD4+ T cells in this patient.
The striking similarity between the immunodeficiency syndrome observed in this case and those described by Fauci et al.and Galloin patients with AIDS and ICL, combined with the wide use of
immunosuppressive agents in modern medicinal practice to treat a variety of chronic illnesses (thrombocytopenia, pulmonary fibrosis, chronic joints disease, peripheral neuropathy, etc.) gave me the
incentive to review the medical literature to evaluate the HIV-hypothesis and the contribution of the illicit drugs, alcohol, and therapeutic agents, and malnutrition to the pathogenesis of AIDS. (1,8-11)
The HIV-hypothesis states that HIV cause AIDS by killing the CD4+ T cells directly or indirectly and after long incubation times (about 10 years), the number of these cells will reach very low
levels which lead to severe immune deficiency. Patients with severe immune deficiency (CD4+ T cells < 200/無) 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 inhibitors of reverse trascriptase (AZT) or protease
inhibitors can delay the progression of AIDS by preventing HIV replication in the cells. (1,8)
My initial review of the medical literature revealed that the short
and the long term use of glucocorticoids at therapeutic doses, resulted independently of HIV 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. (1,9,12-29) Table 1 contains a list of the wide range effects of glucocorticoids on the immune system, respiratory system, and other tissues.
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. (30) He also had lymphocytopenia (896/無), reduction of T4 cells (215/無), and T4/ T8 ratio of 0.7.
This man was HIV-negative as tested by western blot. 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. Table 2 contains a brief description of 16 such cases.
The reversal of CD4+ T cells depletion in the peripheral blood was
also reported in HIV+ homosexual men after the termination of their treatment with glucocorticoids (Table 2). Sharpstone et al., 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/無 per year. Four of them underwent colectomy that eliminated the need for the steroid and their CD4+
T cells increased 4 cells/無 per year. Eight case-matched controls who did not have surgery continued to have a decline of 47 cells/無 per year. (31) This shows the importance of measuring CD4+
T and CD8+ T cells in patients chronically treated with moderate or high therapeutic doses of glucocorticoids.
Nineteen years have passed since the first cases of AIDS were
reported in the United States, and the leaders of the HIV-hypothesis still are uncertain about the pathogenesis of AIDS. (32) They continue to contradict each other on the ways that
HIV is purported to destroy CD4+ T cells. In 1987, Robert Gallo stated that "many T4 cells are infected in the lymph node during contact with a macrophage. After a variable latency, the infected
lymphocyte may be killed by viral replication. Clearly the T4 population is reduced by the death of infected cells". (8) In 1998, Fauci et al. stated that "apoptosis is strictly dependent on cellular
activation. Direct infection of CD4+ T cells with HIV is not required for apoptosis to occur". They also stated that "it is difficult to explain completely the profound immunodeficiency noted in
HIV-infected individuals solely on the basis of direct infection and quantitative depletion of CD4+ T cells". (1)
I have found no scientific evidence to indicate 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. (1,8) In 1985, Hoxie et al. 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. (33) I reviewed many reports describing the changes in the lymph nodes of patients infected with HIV and have found that the changes range from extensive
cellular hyperplasia of T and B lymphocytes and the supporting stroma to severe atrophy of the glands. (34-42) Table 3 lists the changes in the lymph nodes of 505 HIV infected patients who
were asymptomatic or had AIDS. Three distinct stages of changes in lymph nodes are evident. These are hyperplasia (245 patients), atrophy (117 patients), and mixed stage (172 patients). The
presence of hyperplasia in the infected lymph nodes contradicts the HIV-hypothesis that states that HIV destroys infected T cells. (1,8)
My conclusions are also supported by the findings reported by the leaders of the HIV-hypothesis. In 1995, Muro-Cacho, Pantaleo, and, Fauci 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 disease and the levels of viral load". (42) HIV provirus was also found in CD4+ T cells, CD8+ T cells, and B cells lymphocytes in the lymph nodes
of HIV infected patients (43) and its ability to infect cells is not restricted to cells that have CD4 receptor as predicted by the HIV-hypothesis. (1,8)
Furthermore, in Tanzania, Fawzi et al. studied the influence of multivitamin supplements in the diet on T cells counts in peripheral blood in 1,075 HIV infected pregnant women who had
poor nutritional status. These women received regular diet (n=267), vitamin A (n=269), multivitamins excluding vitamin A (n=269), or multivitamins including vitamin A (n=270) in a
randomized, double-blind, placebo-controlled trial between 12 and 27 weeks of gestation. The T cells (CD4+ , CD8+, and CD3+) increased in all groups between baseline (mean =18 weeks
gestation) and 6 weeks postpartum. The average CD4+ T cells at baseline were 423 and 424/無 for the placebo and multivitamins group, respectively. At 6 weeks postpartum, the average CD4+ T
cells count were 520/無 (123% of baseline) for the placebo and 596/無 (141% of baseline) for the multivitamins group. (44) This large study showed very clearly that not only is there is no killing
of T cells by HIV in vivo, but on the contrary, significant increases of T cells had occurred for 20 weeks in the presence of HIV. These findings are also supported by the observation of the leaders of
the HIV-hypothesis. Fauci et al. reported that there are thousands of HIV+ individuals living in the United Stated of America without any health problem since their infection with HIV approximately ten
years previously. They estimated their number to be about 5% of the HIV infected cases in USA (28,690 individuals as of 1/1/1997). They labeled these unexplained HIV+ healthy individuals, "
long-term nonprogressors." (1)
My investigation also revealed an astonishing result: the majority of AIDS patients who participated in the four major Zidovudine
(AZT) clinical trials were HIV-negative prior to their treatment with AZT. (45-8) These studies cumulated in the approval of AZT by the USA FDA to treat AIDS and aymptomatic HIV+ patients. Therefore,
it is sadly ironic that the conclusions of these studies stating that AZT prolongs the lives of patients with AIDS or prevents the development of AIDS in asymptomatic HIV infected individuals are
false. 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: 1) 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); 2) 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; 3) Volberding et al., 1990: 1338 subjects participated;
only 117 patients (9%) had detectable levels of HIV p24 antigen at baseline; and 4) Hamilton et al., 1992: 321 AIDS patients received AZT but only 63 patients (20%) had detectable level of
p24 antigen at base-line. The findings of these studies clearly demonstrate that AIDS in 77% of these patients was caused by agent(s) or processes other than HIV. Moreover, the treatment of
very sick people with a very toxic drug, AZT was not beneficial.
Fauci et al. stated, "in 1983, human immunodeficiency virus (HIV) was isolated from a patient with lymphadenopathy, and by 1984 it
was demonstrated clearly to be the causative agent of AIDS". ( 1(p.1791)) My review of the literature did not lead to any medical facts that link HIV as the cause of AIDS. It did reveal that
approximately 90% of AIDS cases in the USA and Europe are observed in homosexual men and drug users. (1,49,50) 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. (1,9-11, 32,51-93) Homosexual men are usually heavy user of illicit drugs, alcohol, and rectal
glucocorticoids. (1,49,50) The treatment of a patient with prednisone at 60 mg per day for about three months can actually cause AIDS as described above. This dose is usually given to patients
suffering from lung fibrosis, thrombocytopenia, and other chemically induced chronic illnessess. (1)
The medical evidence described above indicated that the
HIV-hypothesis ignores many crucial pieces of evidence that are important in the pathogenesis of AIDS, the programs designed to treat the patients with AIDS, and to solve the AIDS crisis. P. H.
Duesberg also came to the same conclusionin 1987. (49,50) He has challenged the HIV-hypotheses since 1987 and has presented overwhelming evidence in his publications indicating that the use
of the illicit drugs and alcohol by the risk groups may have important roles in the pathogenesis of AIDS in America and Europe and should be evaluated.
For these reasons, I reviewed more than one thousand published articles and several standard medical text books in many medical subjects (pathology, toxicology, pharmacology, immunology,
nutrition, endocrinology, infectious diseases, and human medicine) to evaluate the role of drugs, malnutrition, and infectious agents in the pathogenesis of AIDS. My goals were to pin-point the causes
of AIDS, to explain the pathogenesis of the AIDS syndrome, and, hopefully, to suggest an appropriate approach to cure this disease. I am very happy to state that my major objectives have
been achieved. The next sections contain detailed description of the pathogenesis of AIDS in America, Europe, Africa, and other countries for all risk groups. It also contains a list of
recommendations for treating patients with AIDS and preventing the occurrence of AIDS in patients within each risk group.
Tables 1-3 (Pages 8-13)
Table 1. Acute and chronic toxicity of glucocorticoids and their contribution to the pathogenesis of AIDS
Table 2. Cases of Kaposi's sarcoma and CD4+ T cells lymphocytopenia induced by the treatment of immunosuppressive drugs and reversed by termination of the treatment
Table 3. Histopathologic changes in lymph nodes of HIV + drug users, homosexuals, and hemophiliacs with persistent nonmalignant lymphadenopathies
Explanation of the information presented in Table 1
- The information presented in this Table shows the acute and chronic effects of glucocorticoids on the functions of the immune system and other several vital organs and tissues.
Glucocorticoids reduce the functions and the numbers of T and B cells lymphocytes and macrophages. They cause adrenal insufficiency and interfere with growth of bone, muscle, and
other peripheral tissues and delays wound healing. The chronic use of glucocorticoids cause atrophy of the lymph nodes and increase the incidence of infections by opportunistic
pathogens. They also increase the incidence of cancer. All lesions and the symptoms described in this Table were observed in patients with AIDS (weather HIV+ or
HIV-negative) and people suffering from severe malnutrition (weather HIV+ or HIV-negative). Malnutrition induces the release of endogenous cortisol that acts similarly to therapeutic corticocorticoids.
- Glucocorticoids are widely used currently in modern medicinal practices to treat many acute and chronic health conditions that result from the use of illicit drugs and alcohol such as
thrombocytopenia, pulmonary fibrosis, peripheral neuropathy, tuberculosis, etc. Rectal corticosteroids are also widely and chronically used by homosexual men to treated wide range of
chronic rectal and gastrointestinal diseases that result from practicing anal sex. Hemophiliacs are also use glucocorticoids and other immunosuppressive agents to prevent the
development of inhibitors for factors VIII and IX and to treat chronic joint illness. Patients receiving blood transfusions and/or transplanted tissues also use glucocorticoids to
prevent anaphylactic reactions and tissue rejection.
- Glucocorticoids are also used to treat respiratory illness and other illnesses in premature babies. The use of cocaine and other illicit drugs during pregnancy increases the incidence of premature delivery.
- Glucocorticoids are used by all risk groups prior and after their diagnosis with AIDS. Glucocorticoids cause the symptoms and lesions that are observed in patients with AIDS, not the HIV.
Table 1
Acute and chronic toxicity of glucocorticoids and their contribution to the pathogenesis of AIDS
Target cells, organs,and processes |
Effects (1,9,12-29) |
Lymph nodes |
Atrophy (fibrosis and fatty degeneration) (17) |
Lymphocytes (B and T cells) (01,9,12-16) |
Decrease numbers in circulation (B and T cells).Alters the migration patterns of lymphocytes. Suppress cutaneous delayed-type hypersensitivity
reaction to antigens and reduces expression of lymphocyte function. Decrease lymphoid cell access to antigens in inflammatory sites and antigen blastogenesis. |
B cells (1) |
Increase the incidence of lymphoma |
Monocyte and Macrophages (1,9,15,16) |
Reduce their release from bone marrow and their numbers in circulation. Reduce endocytosis and reticuloendothelial system clearance. Decrease
bactericidal and fungicidal clearance. Reduce effects of mediators on macrophage. |
Leukocyte |
Cause leukocytosis. (1,9) |
Adrenal glands |
Cause secondary adrenal insufficiency. (1,9) |
Respiratory system |
Inhalation of glucocorticoids aerosol (Beclovet) increases infections with Candida albicans and/or Aspergillus niger in the mouth and pharynx and
occasionally in the larynx. Positive culture for oral Candida may be present in up to 75% of patients. (9) |
Wound healing |
Both systemic and topical glucocorticoids cause a variety of skin changes, including acne-form eruptions, atrophy, striae. High doses can retard
wound healing and increases the risk for bacterial, yeast, and fungal skin infection. (1,9) |
Mesenchyma |
Increase the incidence of Kaposi's sarcoma. (1,9,17-29) |
Activation of infectious |
Increase the incidence of viral, bacterial, fungal, and parasitic infection. (1,9) |
Muscle and Bone |
Myopaties and bone disorders. (1) |
Explanation of the information presented in Table 2
Reduction in CD4+ T cells counts and appearance of Kaposi's sarcoma are considered as AIDS-indicator diseases by the U.S. Centers for
Disease Control and Prevention (CDC).
1 The HIV-hypothesis states that HIV reduces the CD4+ T cells by killing the cells directly or
indirectly. The information presented in this Table shows medical evidence that proves these AIDS-indicator diseases can really be caused
by the use of corticosteroids:
1. The elimination of the use of glucocorticoids in HIV+ homosexuals men reverses the reduction of CD4+ T cells. If the HIV kills CD4+ T
cells as the HIVhypothesis predicts, then the T cells count should continue to go down following the elimination of corticosteroid use.
2. Kaposi's sarcoma developed in patients treated chronically with high therapeutic doses of glucocorticoids and/or other immunosuppressive
and complete regression of KS occurred following the cessation of treatment with immunosuppressive agents.
Table 2
Cases of Kaposi's sarcoma and CD4+ T cells lymphocytopenia induced by the treatment of immunosuppressive
drugs and reversed by termination of the treatment
Condition Number of Patients |
AIDS Indicator |
Description of 32 Cases (18-29,31) |
HIV+/16 |
Reduction of CD4+T cells |
Eight HIV+ males with inflammatory bowel disease who used rectal steroid preparations had a decline in their CD4+ T cells to 85 cells/無 per year.
Four of them underwent colectomy that eliminated the need for the steroid and their CD4+ T cells increased 4 cells/無 per year. Eight case matched controls had a decline of 47 cells/per year. (31)
|
KS/8 |
|
Eight patients developed KS after treatment with a steroid for chronic illness. The lesions regressed after the cessation of treatment. (18-25) |
HIV-negati ve KS/8 |
|
Eight organ transplant patients developed KS after treatment with cyclosporin and prednisone. Their lesions regressed after the cessation or
reduction of the treatments . (26-29) |
Explanation of the information presented in Table 3
- The information presented in this Table describing the pathology of the lymph nodes in HIV infected individuals who are asymptomatic or with AIDS. This medical evidence shows
the following facts that disapprove the claims of the HIV- hypothesis that HIV is the cause of AIDS.
- HIV was isolated from lymph nodes showing cellular hyperplasia (T and B cells) and this fact contradicts the claim of the HIV-hypothesis that HIV kills CD4+ T cells.
- HIV was isolated from lymph nodes showing severe atrophy (reduction in lymphocytes and stroma) and this contradicts the claim of the HIV- hypothesis that the HIV causes
selective T cells necrosis. It is believed that HIV kills only CD4+ T cells because these cells have CD4 receptor that binds with HIV protein. Actually, this type of atrophy in the
lymphoid organs is usually associated with chronic use of glucocorticoids and/or severe malnutrition.
- The information shows that the disease passes through three stages in the lymphoid tissues. These are hyperplasia, mixed phase (hyperplasia and atrophy), and atrophy. The symptoms
of AIDS are usually associated with development of atrophy.
Table 3
Histopathologic changes in lymph nodes of HIV+ drug users, homosexuals, and hemophiliacs with persistent nonmalignant lymphadenopathies
Lesions Type |
Description of changes in lymph nodes of 505 patients (34-42) |
Number of Patients |
(A) Follicular hyperplasia (34-42) |
Hyperplastic germinal center. Cellular regeneration with much mitosis. Hyperplasia of the T zone CD4+ T cells > CD8+ T cells. Immature sinus
histocytosis. Extensive cytolysis and phagocytosis. Scattered Multinucleated giant cells. Clusters of polymorphonuclear neutrophils. Multifocal hemorrhage. |
245 |
(B) Mixed type (34-6,39-41) |
Lesions are mixed between A and C |
172 |
C) Follicular Involution (34-7,39- 41) |
Lymph nodes with atrophic burnt-out follicles. Follicles are small and are depleted of lymphocytes. CD8+ T cells > CD4+ T cells. Follicles are
inconspicuous and focally hyalinized. Loss of lymphocytes from interfollicular cortex. Extensive diffuse vascular proliferation. Depletion of dendritic cells. Thickened capsule. |
117 |