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Systematic review and meta-analysis of evidence for increasing numbers of drugs in antiretroviral combination therapy

BMJ 2002; 324 doi: https://doi.org/10.1136/bmj.324.7340.757 (Published 30 March 2002) Cite this as: BMJ 2002;324:757

Rapid Response:

Stop Giving People Toxic Drugs: HIV Does Not Cause AIDS

Important editorial notice for readers: This is a rapid response (online comment by a third party) and not an article in The BMJ. It is attributed in a misleading way on certain websites and social media. The Editor, 06/12/2021.

 

Individuals with AIDS and HIV-positive asymptomatic individuals,
including pregnant women, have long been treated with toxic antiviral
drugs (AZT, Protease Inhibitors, as well as Nevirapine) that can cause
serious systemic injuries and even death. This is erroneously based on the
assumption that HIV is the cause of AIDS. Furthermore, the long-term
effects of these drugs on the composition of the human genomes have not
been determined. Prior to October of 1997, I believed that HIV was the
cause of AIDS based solely on the information that had been reported by
the United States Center for Diseases Control and Prevention (CDC) and the
AIDS establishment. However, my view was unquestionably changed when I
evaluated the medical evidence on the worldwide AIDS epidemic. My findings
clearly show: 1) The HIV-hypothesis is not supported by any medical fact
and AIDS is caused by agents and factors other than HIV. 2) The proponents
of the HIV-hypothesis have long overlooked crucial and essential medical
evidence that clearly describes the real causes of AIDS. 3) The results of
clinical studies on AZT, protease inhibitors, and nevirapine indicate that
these agents can cause severe systemic damage, AIDS, and death. However,
it is my opinion that the US Federal Drug Administration inappropriately
approved these drugs to be given to pregnant women and individuals with
serious health problems. My in-depth research findings are described in my
book "Get All the Facts: HIV Does Not Cause AIDS" in addition to my other
articles [1-7]. Below are examples that were selected from a large body of
evidence to illustrate my points.

Causes and pathogenesis of AIDS in drug users and homosexual men:

In the USA, about 90% of AIDS cases were male homosexuals and
heterosexuals and homosexual drug users [8]. 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 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; 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 homosexual men [1]. Furthermore, the approval of antiviral
drugs (AZT and protease inhibitors) and the corticosteroids by the US FDA
to treat patients with AIDS and asymptomatic patients infected with HIV
has exacerbated the problem [1,8].

It has been stated that the use of alkyl nitrites to relax the anal
muscle and facilitate anal sex permeated the gay life by 1977 [1].
Duesberg cited studies that show the significant use of alkyl nitrites and
illicit drugs by homosexuals [9, 10]. 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.

The regular uses of alcohol, heroin, cocaine, amphetamines, and alkyl
nitrite cause acute and 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 typically
diagnosed as “idiopathic” and currently treated with high doses of
glucocorticoids and/or cytotoxic drugs. In addition, some homosexual men
use rectal glucocorticoids as a treatment for chronic injuries [1, 8].
The treatment of a patient with prednisone at 60 mg per day for about
three months can actually cause AIDS [1]. This treatment and doses often
given to patients suffering from lung fibrosis, thrombocytopenia, or other
chemically induced chronic illnesses. For example, Fauci et al. described
the treatment for patient with lung fibrosis as follows: “A trial of oral
prednisone is begun at a dose of 1mg/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/µL should be maintained” [8,
page 1463]. At this dose levels, the CD4+T cells count in the peripheral
blood of the treated individual is expected to be <300/µL which meets
the definition for AIDS set by the US Center For Diseases Control and
Prevention (CDC).

The following is HIV-negative drug user woman who developed AIDS
following a few months of treatment with immunossuprassants. A 33-year-old
previously healthy female developed acute bilateral pulmonary infiltrates
after 18 hours of intense rock cocaine (crack) smoking. Ten months later,
she developed progressive dyspnea and interstitial pneumonia. She was
unsuccessfully treated with high doses of prednisone (1 mg/kg/day for
eight weeks) followed by a trial of cyclophosphamide. She died due to
respiratory failure with a superimposed mycobacterial infection. The time
from her first admission to the hospital with interstitial pneumonia and
her death with AIDS was about 21 months [11].

In addition, I reviewed 7 selected studies that included 736 patients
(97% of them were homosexual or bisexual men) who were infected with HIV
and/or had AIDS. I found that these individuals suffered from extensive
rectal and gastrointestinal problems that dictate the chronic use of
therapeutic rectal corticosteroids [1].

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. In
1975 and 1976, Fauci and Fauci et al. described in detail the effects of
corticosteroids on the immune system [12,13]. 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. in 1998 [8]. For instance, in 1976, Fauci et al. 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. Studies of bronchial
aerosols showed that with higher doses of steroid in the aerosol, Candida
infections of the larynx and pharynx occurred more often” [13].

The reversal of CD4+ T cells depletion in the peripheral blood was
reported in HIV-positive homosexual men after the termination of their
treatment with glucocorticoids [14, 15]. Sharpstone et al. reported that
eight HIV-positive 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 [14]. Four of them underwent coloectomy that eliminated
the need for the steroid and their CD4+ T cells increased 4 cells/µL per
year. Eight HIV-positive men used as match control 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. In addition, investigators from George
Washington University and the National Institutes of Health reported a
case of HIV-positive homosexual man with ulcerative colitis who developed
a severe reduction in CD4+ T cells counts following 9 days treatment with
corticosteroids and the depletion in CD4+ T cells number was reversed
following the cessation of the treatment [15]. Briefly, approximately 3
weeks prior to surgery for ulcerative colitis that was unresponsive to
corticosteroids, the patient's CD4+ T cell count was 930 cells/µL of blood
and the count fell to 313 cells/µL within 10 days of treatment with
corticosteroids. Five days postoperatively, the patient become
asymptomatic and was discharged on tapering prednisone without the use of
antiretroviral agents. After surgery, the patient's CD4+ T cells counts
progressively rose. The CD4+ T cells counts were 622 cells/µL and 843
cells/µL at 3 and 6 weeks following the operation, respectively.

Kaposi’s sarcoma (KS), an AIDS-indicator disease also developed in
HIV-negative patients chronically treated with glucocorticoids [1, 16].
For example, KS developed eight months after initiation of prednisone
treatment (40 mg per day for three months) in HIV-negative man. He also
had lymphocytopenia (896/µL), reduction of T4 (CD4+) cells (215/µL), and
T4/ T8 ratio of 0.7. [16]. In addition, there are many cases who
developed KS following treatment with glucocorticoids and they had
reversal of their KS after the termination of the treatment [1].

My investigation also revealed that the majority of AIDS patients
suffer from metabolic and endocrine abnormalities [1]. The high
prevalence of adrenal insufficiency observed among AIDS patients provides
very strong evidence that AIDS in these patients is caused by the use of
corticosteroids. Fauci et al. 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
[8]. The most common abnormality seen in HIV infected individuals is
hyponatremia, seen in up to 30 percents of patients. They also stated in
the same book 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 [8]. However; the use
of corticosteroids by AIDS patients was not considered by Fauci and his
colleagues.

The HIV-hypothesis states that HIV cause AIDS by killing the CD4+ T
cells directly or indirectly [8]. 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. observed no evidence of
death in T cells infected with HIV in tissue culture [17]. These cells
continued to produce virus particles for more than four months after
inoculation with the virus. Many reports described 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-positive patients who were asymptomatic or had AIDS demonstrate three
distinct stages [1]. 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 which states HIV
destroys infected T cells [8].

The proponents of the HIV-hypothesis provide further elucidation.
Muro-Cacho, Pantaleo, and, Fauci examined 29 HIV-positive 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 [18]. They stated that “apoptosis was not restricted only to
CD4+ T cells; both B cells and CD8+ T cells were found to undergo
apoptosis. They also stated 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 [1].

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 in 187 patients and atrophy in 28 patients,
and 15 lymph nodes showed Kaposi’s sarcoma and lymphoma [1]. US CDC
considers these changes as AIDS-indicator illnesses, yet the subjects were
HIV-negative.

In addition to the information presented above that demonstrates the
invalidity of the HIV-hypothesis, the rates of T cells infection by HIV,
and the rates of the thymus and the lymphoid tissue regeneration also
conflict with the HIV-hypothesis. Duesberg 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 [9]. 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 [19]. Baltimore and Feinberg also
stated that, in the late stage of AIDS disease, HIV infects 1 in 100 CD4+
T cells or 1 in 400 mononuclear cells [20]. Furthermore, Al-Bayati et al.
found that the rates of regeneration in the damaged thymus and lymphoid
tissue of mice treated with a lymphotoxic agent (vanadate) are very high
[21]. A total of 120 mice were treated with metavanadate solution (15.5
mg/kg). Severe necrosis in the thymus of treated mice was observed at 2
days following treatment and the thymus healed completely in about 10
days.

Some studies show increases in CD4+ T cells in HIV-positive
individual after treatment with the antiviral drugs [1]. 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 [1]. In addition
to the failure of the antiviral drugs, AIDS patients suffering from immune
deficiency are treated with glucocorticoids [8]. This practice is not
supported by any known biomedical mechanism of action.

The causes of AIDS in infants and children:

In the United States of America, ninety percent of infants and
children who developed AIDS had mothers who were drug users [8]. The
prevalence of cocaine use among pregnant women in the USA is relatively
high as shown by countless studies [1,8]. Cocaine-positive urine was found
in 15.3% of 411 pregnant women surveyed in hospitals at the time of
delivery. During 1993, 12.8% (361 of 2810) of all live singleton infants
born at Harem Hospital in New York were identified as cocaine exposed. The
impact of illicit drug and alcohol abuse during pregnancy on infant health
is extremely serious. Nine studies that included 1,295 drug-using mothers
and 4,293 nonusers showed that cocaine use during pregnancy led to a high
prevalence of premature births and low birth weights [1].

A mother expected to have a premature birth is treated with
glucocorticoids prior to delivery to facilitate the development of the
lungs and to reduce the incidence of necrotizing enterocolitis in a
premature infant. Drug exposed infants usually have serious health
problems that are treated with glucocorticoids [1]. In addition, the
natural cortisol levels in plasma and urine of the cocaine-exposed preterm
neonates was also found to be significantly higher than in normal infants
[22]. Therapeutic glucocorticoids and endogenous cortisol can cause severe
reduction in T cells and B cells numbers and their functions. The long-
term use of corticosteroids at the therapeutic levels causes atrophy of
the thymus and lymphoid tissue of infants, children, and adults and
increases the incidence of infections [1, 8, 23].

The histology of the thymus of HIV-infected infants and children
showed changes such as atrophy of the lymphoid tissue, Hassall's
corpuscles, and connective tissue. These changes are consistent with those
observed in the lymphoid organs of HIV-negative individuals suffering from
severe malnutrition or treated with high doses of corticosteroids.
Moreover, HIV-positive infants and children who died with AIDS suffered
from opportunistic infections (tuberculosis, fungal, yeast, and viral
infections) similar to those reported in HIV-negative infants and children
suffering from malnutrition or treated with high doses of corticosteroids
[1, 8, 23, 24]. However, the proponents of the HIV-hypothesis have not
considered corticosteroids as a factor of causing AIDS in the risk groups
who are receiving high doses of these agents. On the contrary,
corticosteroids are used to treat people with AIDS who suffer from
tuberculosis, thrombocytopenia, peripheral neuropathy, lung fibrosis, and
other chronic diseases. This approach is unscientific and should be
evaluated.

Anthony Fauci and the proponents of the HIV-hypothesis have long been
aware of the use of illicit drugs among pregnant women and the impact of
drug use on the health of mothers and their infants as shown in their
literature. For instance, Fauci et al. explained the impact of illicit
drugs on the pregnant mothers and their infants as follows: 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 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 [8].

In addition, Fauci et al. stated 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 hiccupping in 30%. The child usually has a low
birth weight and may be otherwise unremarkable until the second day, when
symptoms are likely to begin [8].

O'Shea et al. evaluated the outcome of pregnancy of 95 HIV-positive
pregnant women and found that there was little variation in plasma viral
load occurred during pregnancy. However, there was an association between
viral load and prematurity; the mean gestation at delivery decreasing by
1.3 weeks for every 10-fold increase in maternal HIV RNA [25]. We know
that HIV does not induce labor but premature delivery is a good indicator
for drug use as described above and in Fauci's book and my book [1,8]. The
findings of this study and others indicate that HIV is a good marker for
drug use, practicing unsafe sex, in addition to poor hygiene.

I reviewed the designs and the results of numerous AZT and protease
inhibitors clinical trials and found that AZT and protease inhibitors are
very toxic drugs and the conclusions of these studies do not support the
claims that these drugs can be used to cure people with AIDS [1]. On the
contrary, AZT causes severe bone marrow depression and reduces white blood
cells counts including T cells. It is very toxic to the stem cells in bone
marrow (the source of T and B lymphocytes) and to fast growing tissues
such as embryonic and fetal tissues. For example, Fischl et al. treated
145 AIDS patients treated with AZT for up to 24 weeks. The CD4+ T cell
counts of these patients were reduced from baseline of 66/µL to 37/µL
[26]. Some patients felt very sick and treatment was terminated early.

In a second study, Fischl et al. gave AZT to 524 subjects who had a
first episode of Pneumocystis carinii pneumonia [27]. These subjects
received AZT in either a dose of 250 mg taken orally every four hours
(n=262) or a dose of 200 mg taken orally every four hours for four weeks
and thereafter 100 mg taken every four hours (n=262). In this study,
additional AIDS-defining opportunistic infections developed in 429
subjects (82%) in the AZT treated groups. Furthermore, the neutrophil
counts declined to less than 34% of baseline in 230 subjects; the
hemoglobin levels declined to less than 66% of baseline in 178 subjects;
and one hundred thirty-four subjects received red-cell transfusions. One
hundred eighty-three subjects (35%) were withdrawn from AZT therapy
because of toxic reactions such as severe anemia and neutropenia. At 24
months of treatment, the mortality rates were 66% and 73% in the low and
standard AZT doses, respectively.

Besides, the following is a list of some of the serious adverse
reactions to AZT that have been reported in infants, children, and adults
as stated in the drug information book for physicians and other databases
to illustrate the danger of AZT [1, 8, 23]. These reactions may include,
neutropenia, granulocytopenia, anemia, thrombocytopenia, myopathy and
myositis, hepatomegaly with steatosis, hepatitis, pancreatitis, lactic
acidosis, sensitization reactions, hyperbilirubinemia, vasculitis,
abdominal pain, back pain, body odor, chest pain, chills, edema of the
lip, fever, flu syndrome, hyperalgesia, syncope, vasodilation, bleeding
gums, constipation, diarrhea, dysphagia, edema of the tongue, eructation,
flatulence, mouth ulcer, rectal hemorrhage, lymphadenopathy, arthralgia,
muscle spasm, tremor, twitch, anxiety, confusion, depression, dizziness,
emotional lability, loss of mental acuity, nervousness, paresthesia,
somnolence, vertigo, cough, dyspnea, epistaxis, hoarseness, pharyngitis,
rhinitis, sinusitis, acne, changes in skin and nail pigmentation,
pruritus, rash, sweat, urticaria, amblyopia, hearing loss, photophobia,
taste perversion, dysuria, polyuria, urinary frequency, and urinary
hesitancy.

The adverse reactions of the second drugs (Nevirapine) that have also
been given to HIV-pregnant women may include severe and life-threatening
skin reactions (stevens-johnson syndrome, toxic epidermal necrolysis),
severe and life-threatening hepatotoxicity, skin rash, maculopapular
erythematous cutaneous eruptions, fever, nausea, headache, and
granulocytopenia [23]. In addition, the safety profile of this drug in the
neonates has not been established.

The information presented above describing the toxicities of AZT and
nevirapine tells the horrifying stories about the suffering of pregnant
women, infants, and children who are given these toxins based on a false
assumption that HIV is a killer virus. Some of these people are forced to
ingest these toxins. This is heartbreaking!

Causes and pathogenesis of AIDS in hemophiliacs:

The medical evidence shows that AIDS in hemophiliac patients is
caused by the treatment with immunosuppressive agents (cyclophosphamide
and/or glucocorticoids) to prevent the development of antibodies to
factors VIII and XI. Fauci et al. also described the development of
antibodies against factors VIII and IX and the use of corticosteroids in
the hemophilia patients [8]. Patients with severe hemophilia usually have
serious chronic joint problems resulting from bleeding inside the joints
and this is also treated with glucocorticoids. Low CD4+ T cells counts
have been observed in both HIV- negative and HIV-positive hemophiliac
patients. Duseberg presented the results of 17 studies showing that a
total of 717 hemophiliac patients had T4/T8 ratios less than or equal to
one and 46% of them (329 patients) were HIV-negative [9].

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

As of January 1, 1997, the number of patients in the USA who received
blood transfusions, blood components or tissues then subsequently
developed AIDS was 7,888 [8]. Adverse reactions to blood transfusion have
been frequently reported and the standard treatment used to prevent or
cure these reactions is glucocorticoid as stated by Fauci et al. [8]. 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 [8]. 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 treatments and the list of opportunistic diseases are also
described by Fauci et al [8]. The list of opportunistic diseases in organ
transplant patients receiving immunosuppressive agents is identical to the
list of opportunistic diseases listed in people with AIDS [8].

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 [8]. Severe malnutrition has
been very well known to cause immune dysfunction and other serious health
effects. It 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” [28].

The functions 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 animal. The size
of the thymus of 42 malnourished children was reduced by 90% as compared
with the size in the normal children of the same age [29]. In a second
study involving 110 malnourished children, the thymic area was found to be
20% of the size in healthy children [30]. The results of autopsy of 118
malnourished children showed: 1) both thymus and peripheral lymphoid
tissues were reduced in bulk in 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 and 59.3% of the children had marasmic and
Kwashiorkor symptoms [31]. Fakhir et al. evaluated 100 severely
malnourished children and found that these children had a significant
reduction in the absolute lymphocytes counts, T cells counts, and in the
skin reaction to dinitrochlorobenzene [32]. The lymphocyte functions of 30
black children with PCM as assessed by the delayed hypersensitivity
reaction and morphology of lymphocyte transformation were found to be
impaired and serum cortisol level was elevated [33]. The functions of
lymphocytes and cortisol levels in these patients were returned to normal
after 30 days of feeding.

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 functions 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 [30]. The levels of endogenous
cortisol in plasma and urine have been found to be abnormally elevated in
malnourished patients as shown by studies included 159 malnourished
children and 148 AIDS patients [1].

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
[1]. For example, the mortality rate among 299 severely malnourished
children in Zambia was 25.8% [34]. 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 [35].

The prevalence of KS and lymphoma, lymphadenitis, and tuberculosis in
Africa are similar to those reported in the male homosexuals AIDS patients
in US and Europe and even higher [1]. However, AIDS in Africa occurs
almost equally in males and females because starvation affects both sexes
equally. Sibanda and Stanczuk reviewed all lymph nodes histopathology
reports of lymph nodes biopsies submitted to the Histopathology unit in
Harare, Zimbabwe, in the period of January 1988 to June 1990. They found
that 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
[36]. In children, the prevalence of KS was higher in children under 5
years than in 6-15 year bracket. In adults, approximately two thirds (65%)
of all patients with KS were aged between 20 and 40 years.

The study of Fawzi et al. in Tanzania clearly demonstrated that HIV
is a harmless virus. Feeding HIV-positive malnourished pregnant women
proper nutrition reversed the impairments of the immune system functions.
This measure also improved the outcome of their pregnancy [37]. They gave
1,075 HIV-infected pregnant women between 12 and 27 weeks' gestation
vitamin A (n=269), multivitamins excluding vitamin A (n=269),
multivitamins including vitamin A (n=270), or a placebo (n=267). All T-
cells subsets (CD4+, CD8+, and CD3+) increased in all treatment groups
from baseline levels during pregnancy and 6 weeks following delivery.
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 baseline and 6 weeks postpartum were 167 cells/µL and
112 cells/µL among women on multivitamins and those on no vitamins,
respectively. Vitamin supplementation also 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%.

Summary of findings:

1) HIV is a harmless virus, both in vivo and in vitro. The HIV-
hypothesis is not supported.

2) AIDS in drug users and homosexuals in the U.S. and in Europe
results from heavy ancillary use of glucocorticoids and other
immunosuppressive agents. Physicians prescribe these drugs to treat a wide
range of chronic illnesses of the respiratory and gastrointestinal
systems, and other organs.

3) The appearance of AIDS in the U.S. and Europe coincided with the
approval of glucocorticoid aerosol use in 1976, the introduction of crack
cocaine, the use of heroin by inhalation, and the use of alkyl nitrites by
homosexuals to enhance anal sex.

4) AIDS in hemophiliacs relates to the use of corticosteroids and
other immunosuppressive agents to prevent development of antibodies for
factors VIII and IX, and used to treat other chronic illnesses such as
joint disease.

5) AIDS in people receiving blood and/or tissue follows use of
glucocorticoids to prevent transfusion and tissue rejection, and to treat
other illnesses.

6) AIDS in infants and children is caused by their exposure to drugs
and corticosteroids in utero, and to corticosteroids used after birth to
treat their chronic illnesses.

7) AIDS in Africa results from malnutrition, the consequent release
of endogenous cortisol, and opportunistic diseases. Atrophy in the thymus
and lymphoid tissue in people suffering from malnutrition has been known
since 1925; malnutrition also impairs T cells function. Feeding an
adequate diet reverses these changes. It cures AIDS! Thymus size in
malnourished children increased from 20% of normal to 107% of normal,
after nine weeks of feeding.

8) Kaposi's sarcoma (KS) and lymphoma result from the use of steroids
and drugs, and the release of endogenous cortisol. They are not caused by
a slow virus. Stopping treatment with immunosuppressive agents prior to
metastasis reverses KS in some cases.

9) The medications currently used to treat patients with AIDS, such
as AZT, protease inhibitors, and glucocorticoids are highly toxic. They
can cause AIDS in asymptomatic patients; they worsen the condition of AIDS
patients and even lead to their death. These drugs have no therapeutic
value; their use should stop forthwith.

10) Damage to the immune system is rapidly reversible after removal
of the true insulting agent or treatment of the true causes. Examples: a)
The CD4+ T cells of 1,075 HIV-positive pregnant women increased from
426/uL to 596/uL in six months on a balanced diet. This also improved the
outcome of their pregnancies; and b) In HIV-positive homosexuals, stopping
treatment with glucocorticoids reversed a fall in CD4+ T cells.

Urgent actions are needed to correct the problem:

I hope that the medical evidence presented in this article along with
the cited references will alert you to the facts that unfortunately we are
moving in the wrong direction concerning the war on AIDS. It is
incredibly difficult to imagine that A. Fauci, the director of the AIDS
program at the National Institute of Health, has spent billions of dollars
to find a cure for AIDS, yet the solutions for the AIDS crisis are
presented in his very own publications. We have a large body of medical
evidence that clearly shows HIV does not cause AIDS. I urge each and every
government, including all individuals, to review the evidence. The AIDS
establishment's unscientific, costly, and risky approach needs to be re-
examined to save the world population from an imminent tragic consequences
from the wide use of toxic drugs and to save important resources.

Implementing effective preventives measures can solve the problem of
AIDS. These include: 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 health 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 a significant time; 4)
discontinue the treatment of patients with AIDS and asymptomatic HIV-
positive patients with AZT and protease inhibitors immediately since these
are very toxic medications and have no therapeutic values; 5) provide
proper clinical support and nutrition to patients with AIDS based on their
medical needs

References

[1] Al-Bayati, MA. Get All The Facts: HIV does not cause AIDS. Toxi-
Health International, Dixon, CA 1999 [http://www.toxi-health.com].

[2] Al-Bayati, MA. The Real Cause of AIDS. Mecola's health
newsletter, Issue 236, July 11, 2001
[http://www.mercola.com/2001/jul/11/aids3.htm].

[3] Al-Bayati, MA. Is there proof that HIV-positive persons
consistently develop illnesses that are rare or never occur in HIV
negative persons? Virusmyth.net, September 2001
[http://www.virusmyth.net/aids/data/mabcdc.htm].

[4] Al-Bayati, MA. HIV Does Not Cause AIDS. The British Medical
Journal, January 30, 2002
[http://bmj.com/cgi/eletters/324/7331/237].

[5] Al-Bayati, MA. Keep The Dentist Working: HIV Does Not Cause AIDS.
The British Medical Journal, March 15, 2002
[http://bmj.com/cgi/eletters/324/7337/564#20541].

[6] Al-Bayati, MA. AIDS in Africa is caused by Starvation and
Medications. The British Medical Journal, March 7, 2002
[http://bmj.com/cgi/eletters/324/7335/446/a#20389].

[7] Al-Bayati, MA, Flores JJ, Hosbein LM, Maggiore C. Resolution of
AIDS in HIV Positive Patients: A Clinical Study of Non-HIV Causes and
Treatments for AIDS Illnesses, 2000 [www.aliveandwell.org/index.php?
page=study].

[8] Fauci AS, Braunwald E, Isslbacher KJ, Wilson, JD, Martin JB,
Kasper DL, Hauser SL, Longo DL. Harrison's Principles of Internal
Medicine. McGraw-Hill Companies, Inc. New York USA, ed. 14, 1998

[9] Duesberg PH. AIDS Acquired by drug consumption and other
noncontagious Risk Factors. Pharmac. Ther. 1992; 55: 201-277

[10] Duesberg PH. The role of drugs in the origin of AIDS. Biomed
Pharmacother 1992; 46:3-15

[11] O’Donnell AE, Mappin FG, Sebo TJ, Tazelaar H.: Interstitial
pneumonitis associated with “crack” cocaine abuse. Chest 100(4):1155-7,
1991

[12] Fauci AS. Mechanisms of Corticosteroid Action on lymphocyte
subpopulations I. Redistribution of circulating T and B lymphocytes to the
bone marrow. Immunology 1975; 28: 669-679

[13] Fauci AS, Dale DC, Balow JE. Glucocorticosteroid therapy:
Mechanisms of Action and Clinical Considerations. Annals of Internal
Medicine 1976; 84:304-15

[14] Srpstone DR, Duggal A, Gazzard BG. Inflammatory bowel disease in
individuals seropositive for the human immunodeficiency virus. Eur. J.
Gastroentrol. Hepatol 1996; 8:575-8

[15] Silver S, Wahl SM, Orkin BA, Orenstein JM. Changes in
circulating levels of HIV, CD4, and tissue expression of HIV in a patient
with recent-onset ulcerative colitis treated by surgery, Case report.
Journal of Human Virology 1999; 2:52-7

[16] Schottstaedt MW, Hurd ER, Stone MJ. Kaposi’s sarcoma in
rheumatoid arthritis. Am J Med 1987; 82:1021-6

[17] Hoxie JA, Haggarty BS, Rackowski JL, Pillsury N, Levy JA.
Persistent Noncytopathic Infection of Normal Human T lymphocytes with
AIDS-Associated Retrovirus. Science 1985; 229(4720):1400.

[18] Muro-Cacho CA, Pantaleo G, Fauci AS. 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 1995; 154:5555-66

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

[20] Baltimore D, Feinberg MB. HIV revealed: Toward a natural
history of infection. The New England Journal of Medicine 1989; 321:1673-4

[21] Al-Bayati MA, Culbertson RM, Schreider JP, Rosenblatt LS, Raabe
O.G. The Lymphotoxic Action of Vanadate. Journal of Environmental
Toxicology and Oncology 1992; 11:19-27

[22] Scafidi FA, Field TM, Wheeden A, et al. Cocaine-exposed preterm
neonates show Behavioral and hormonal differences. Pediatrics 97(6 Pt
1):851-5, 1996

[23] USPDI. Drug Information for the health care professional. Volume
1, 21st Edition, Published & Distributed by Micromedex, Englewood, Co,
USA

[24] Drut R, Anderson V, Greco MA, et al.: 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, 1997

[25] O'Shea S, Newell ML, Dunn DT, et al.: Maternal viral load, CD4
cell count and vertical transmission of HIV-1. J. Med. Virol 54(2):113-7,
1998

[26] Fischl MA, Richman DD, Grieco MH, et al.: 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), 1987

[27] Fischl, MA, Corette BP, Pettinelli C, et al. A randomized
controlled trial of a reduced daily dose of zidovudine in patients with
the acquired immunodeficiency syndrome. The New England Journal of
Medicine 1990; 323:1009-14

[28] Woodruff JF. Thymolymphatic deficiency and depression of cell-
mediated immunity in protein-calorie malnutrition. Lancet 1972;
1(7741):92-3.

[29] Parent G, Chevalier P, Zalles L, Sevilla R, Bustos M, Dhenin JM,
Jambson B. In vitro lymphocyte-differentiating effects of thymulin (Zn-
FTS) on lymphocyte subpopulation of severely malnourished children. Am.
J. Clin. Nutr 1994; 60:274-8

[30] Chevalier P, Sevilla R, Sejas E, zalles L, Belmonte G, Parent,
G. Immune recovery of malnourished children takes longer than nutritional
recovery: implications for treatment and discharge. J. Trop Perdiatr 1998;
44:304-7

[31] Schonland M. Depression of immunity in protein-calorie
malnutrition:a post-mortem study. J. Trop Pediatr Environ Child Health
1972; 18:217-24

[32] Fakhir S, Ahmad P, Faridi MA, Rattan A. Cell-Mediated immune
responses in malnourished host. J. Trop. Pediatr 1989; 35:175-8

[33] Zeng B, Qian Y, Zheng D, Wu K, Zhou M, Gong Q. Change of T
lymphocyte subsets in peripheral blood of children with malnutrition and
zinc deficiency. Hua His. I Ko. Ta. Hsueh Pao 1991; 22:337-9

[34] Gernaat HB, Dechering WH,Voorhoeve HW. Mortality in severe
protein-energy malnutrition at Nchelenge Zambia. J Trop. Pediatr 1998;
44:211-7

[35] Sheikh MM, Ansari Z, Ahmad P, Tyagi SP. Tuberculous
lymphadenopathy in children. Indian Pediatrics 1981; 18: 293-297

[36] Sibanda EN, Stanczuk G. Lymph node pathology in Zimbabwe: a
review of 2194 specimens. Q. J. Med. 1993; 86:811-7

[37] Fawzi WW, Msamanga GI, Spiegelman D, et al. Randomized trial
effects of vitamin supplements on pregnancy outcomes and T cell counts in
HIV-1-infected women in Tanzania. The Lancet 1998; 351:1447-1482

Competing interests: No competing interests

05 April 2002
Mohammed Ali Al-Bayati
President, Toxicologist, and Pathologist
Toxi-Health International, 150 Bloom Dr., Dixon, California 95620, USA