SCIENTIFIC DATA AGAINST THE USE OF NEVIRAPINE
In Pregnant Women, Infants, Children, and Anybody Else

By Roberto Giraldo

Oct. 2001

This primary intention of this paper is to provide technical assistance to
the lawyers of
the Ministry of Health of the Republic of South Africa in a court trial
initiated by a lawsuit
brought by the non-governmental organization Treatment Action Campaign
against
the Government of South Africa "for not providing Nevirapine to every HIV
positive pregnant
woman and babies born to HIV positive mothers."

The following data support the sensible intention of the Department of
Health of South
Africa to perform clinical trials at two research sites in all nine
Provinces for a period of two
years before deciding what is the best course for the prevention of what
is known as
"mother to child transmission of HIV (MTCT)" in South Africa (Ministry of
Health 2001).

The information provided herein should be carefully analyzed, particularly
now that the
Government of Uganda has decided to make Nevirapine compulsory to all
unmarried pregnant
woman in that country, irrespective of their "HIV status" (Mohamend
2001).

1. Avoidance of toxic substances during pregnancy and infanthood.

There are numerous scientific findings supporting the internationally
accepted practice
of avoiding as much as possible any potential toxic exposure of pregnant
women, infants,
and children (Needlemann & Bellinger 1994; Holmes 1994; Kavlock & Daston
1997a, b;
Schardein 2000; Koren 2001).

1.1 Nevirapine is a non-nucleoside reverse transcriptase inhibitor that
belongs to
the dipyridodiazepinone chemical class of compounds (PDR 2001).

"Nevirapine binds directly to reverse transcriptase and blocks the
RNA-dependent and
DNA-dependent DNA polymerase activities by causing disruption of the
enzyme’s catalytic site"
(PDR 2001).

Reverse transcriptase is an enzyme earlier thought to be unique to
retroviruses. However,
currently it is known than many different human cells have and use reverse
transcriptase for
very important chemical reactions (Temin et al 1972; Temin 1985). Once in
the body systems,
Nevirapine can inhibit reverse transcription in normal human cells. This
is why Nevirapine is a
very toxic substance especially for the growing cells of fetuses and
infants.

"Animal studies have shown that nevirapine is widely distributed to nearly
all tissues and
readily crosses the blood-brain barrier" (PDR 2001). Also, "Nevirapine is
widely distributed in
humans, readily crosses the placenta and is found in breast milk" (PDR
2001).

1.2. Long-term effects of Nevirapine are unknown.

Clinical trials with Nevirapine to prevent MTCT have been conducted only
recently (Guay
et al 1999; Marseille et al 1999). It is too early to evaluate the
potential long-term side effects
of this chemical on the tissues and organs of the mothers and children who
received it.

The PDR states "The long term effects of Viramune are unknown at this
time" (PDR 2001).

"There are no adequate and well-controlled studies in pregnant women.
Viramune should
be used during pregnancy only if the potential benefit justifies the
potential risk to the fetus"
(PDR 2001).

However, it is known that Nevirapine "produces significant decrease in
fetal body weight"
(PDR 2001), which researchers have found can be "the origin of several
adult cardiovascular
and metabolic diseases" (McDade et al 2001a,b). "Interest in the fetal and
infant origins of
many adult chronic, degenerative diseases is currently high, and evidence
is mounting for an
association between intrauterine growth retardation (IUGR) and adult
hypertension, abnormal
blood lipid profiles, coronary artery disease, and diabetes" (Barker 1992,
1994, 1998a,b; Leon
1998; McDade et al 2001a,b).

It is disturbing to note that the use of Nevirapine in infants is being
recommended when
the "evaluation of the pharmacokinetics of nevirapine in neonates is
ongoing" and "the safety
profile of Viramune in neonates has not been established" (PDR 2001).
Additionally, three
clinical trials with Nevirapine in pediatric patients reported an overall
incidence of related
adverse events in 46% of the children (PDR 2001). Insisting on prescribing
Nevirapine to
babies is akin to "putting the cart before the horse," similar to soldiers
commencing firing
while awaiting confirmation of their superior’s orders.

On the other hand, it is not even accepted that Nevirapine can prevent the
transmission
of HIV. This is why the PDR warns: "Patients should be informed that
Viramune therapy has
not been shown to reduce the risk of transmission of HIV-1 to others
through sexual contact
or blood contamination" (PDR 2001).

1.3. Nevirapine is a very toxic compound.

Roxane, the pharmaceutical company that produces and commercializes
Nevirapine with
the commercial name of Viramune, recognized its toxicity in the
Physicians’ Desk Reference
(PDR 2001), considered the best available source of information on the
safety of medications
for humans.

They write in capital letters:

"WARNING: SEVERE LIFE-THREATENING SKIN REACTIONS, INCLUDING FATAL CASES,
HAVE
OCCURRED IN PATIENTS TREATED WITH VIRAMUNE. THESE HAVE INCLUDED CASES OF
STEVEN-
JOHNSON SYNDROME, TOXIC EPIDERMAL NECROLYSIS, AND HYPERSENSITIVITY
REACTIONS
CHARACTERIZED BY RASH, CONSTITUTIONAL FINDINGS, AND ORGAN DYSFUNCTION.
PATIENTS
DEVELOPING SIGNS OR SYMPTOMS OF SEVERE SKIN REACTIONS OR HYPERSENSITIVITY
REACTIONS
MUST DISCONTINUE VIRAMUNE AS SOON AS POSSIBLE. SEVERE AND LIFE-THREATENING

HEPATOTOXICITY, INCLUDING FATAL HEPATIC NECROSIS, HAS OCCURRED IN PATIENTS
TREATED
WITH VIRAMUNE. RESISTANT VIRUS EMERGES RAPIDLY AND UNIFORMLY WHEN VIRAMUNE
IS
ADMINISTERED AS MONOTHERAPY, THEREFORE, VIRAMUNE SHOULD ALWAYS BE
ADMINISTERED
IN COMBINATION WITH ANTIRETROVIRAL AGENTS" (PDR 2001).

I strongly recommend that any government or institution regulating the use
of Nevirapine
in pregnant women and children at very least first carefully study the
information from the PDR
regarding this medication.

1.4. Nevirapine can be toxic for the immune system.

The potential long-term immunotoxic effects of Nevirapine have not been
evaluated. However,
it is very probable that Nevirapine can be toxic for the growing and
dividing cells of the immune
system. It could therefore be a risk factor for acquired immune deficiency
rather than protecting
against AIDS.

Nevirapine is known to be active in "peripheral blood mononuclear cells,
monocyte derived
macrophages, and lymphoblastoid cell lines" (PDR 2001), which are all
cells of the immune
system.

Nevirapine causes anemia, trombocytopenia and granulocytopenia, especially
in pediatric
patients (PDR 2001). It should be remembered that granulocytes also play
an important role in
the immune system.

Similarly, Nevirapine is known to increment oxidative metabolism in humans
(PDR 2001).
Interestingly, a growing body of scientific research supports the belief
that oxidative stress
has a crucial role in the pathogenesis of AIDS (Papadopulos-Eleopulos
1988, 1998/1999;
Fuchs et al 1991; Papadopulos-Eleopulos et al 1992; Salvain & Mark 1992;
Baruchel &
Wainberg 1992; Favier 1994; Giraldo 1997). This is why antioxidants are
effectively and
widely used in the treatment and prevention of AIDS (Javier et al 1990;
Turner 1990;
Greenspan 1993; Zhang et al 1997; Giraldo 2000a,b). The increment of
oxidative metabolism
by Nevirapine is therefore one of the ways Nevirapine can contribute to
immunosuppression and AIDS.

Viramune tablets, in addition to Nevirapine, contain cellulose, lactose
monohydrate,
povidone, sodium starch glycolate, colloidal silicon dioxide, and
magnesium stearate. The
oral suspension contains carbomer 934P, methylparaben, propylparaben,
sorbitol, sucrose,
polysorbate 80, sodium hydroxide, and water. (PDR 2001). Several of these
compounds are
known to be toxic for the cells and chemical reactions of the immune
system. For example,
silicon, methylparaben and propylparaben are well known to be immunotoxic
(Descotes 1988a).
This is yet another way in which Nevirapine could cause immunosuppression
and AIDS.

Nevirapine "produces significant decrease in fetal body weight" (PDR
2001), and it is
scientifically recognized that "prenatal undernutrition has been linked to
deficits in several
aspects of cell-mediated immunity, to involution of lymphoid tissues such
as the thymus, and
to suppression of antibody responses to vaccination" and that "These
deficits persist for weeks
or, in some cases, even years" (Chandra 1975a,b, 1981; Moscatelli et al
1976; Ferguson 1978;
Lewis & Wilson 1995; Hasselbach et al 1999; McDade et al 2000. 2001a,b).
On the other hand,
"murine models have documented impairments in immunity after maternal
undernutrition that
last through adulthood and into the next generation, despite ad libitum
feeding of both F1 and
F2 generations" (Chandra 1975c; Beach et al 1982). Therefore, it is
probable that in this
manner Nevirapine could also cause long-term damage to the immune system
and contribute
to the development of AIDS.

In this time of AIDS it must be emphasized that there is a growing number
of chemicals that
are immunotoxic, cause immunosuppression, and that therefore play
significant roles in the
pathogenesis of AIDS (Descotes 1988a,b; Dean & Luster 1994; Holladay &
Luster 1994).

1.5. Nevirapine is known to be toxic for many organs and systems.

"In vivo studies in humans and in vitro studies with human liver
microsomes have shown
that nevirapine is extensively biotransformed via cytocrome P450
(oxidative) metabolism to
several hydroxylated metabolites" (PDR 2001).

It is well known that "Nevirapine is extensively metabolized by the liver
and nevirapine
metabolites are extensively eliminated by the kidneys. However, the
pharmacokinetics of
nevirapine has not been evaluated with either hepatic or renal
dysfunction" (PDR 2001).

"Severe or life-threatening hepatotoxicity, including fatal fulminant
hepatitis (trasaminases
elevations, with or without hyperbilirubinemia, prolonged partial
thromboplastin time, or
eosinophilia), has occurred in patients treated with Viramune" (PDR 2001).
This is why
"Clinical chemistry tests, which include liver function tests, should be
performed prior to
initiating Viramune" (PDR 2001).

The CDC of the United States has issued a warning: "The drug, nevirapine,
can produce
liver damage severe enough to require liver transplants, and has caused
death in such use,
the Centers for Disease Control and Prevention said in its weekly report"
(Altman 2001c).

It has been shown that Nevirapine can impair fertility in rats treated
with it, and it produces
a significant decrease in fetal body weight (PDR 2001).

Also, there are a growing number of substances with neurotoxic effects on
fetuses and
children (Rodier et al 1994). Many have toxic effects in the developing
bone marrow, heart,
lungs, kidneys, liver, endocrine glands, etc. (Lau & Kavlock 1994; Koren
2001), Nevirapine
could be one of them.

2. Nevirapine cannot prevent or cure AIDS.

The relationship between in vitro susceptibility of HIV-1 to nevirapine
and the inhibition
of HIV-1 replication in humans has not been established" (PDR 2001).

"At present, there are no results from controlled clinical trials
evaluating the effect of
Viramune in combination with other antiretroviral agents on the clinical
progression of HIV-1
infection, such as the incidence of opportunistic infections or survival"
(PDR 2001). On the
other hand, "Resistant virus emerges rapidly and uniformly when Viramune
is administered
as monotherapy. Therefore, Viramune should always be administered in
combination with
at least one additional antiretroviral agent" (PDR 2001).

"Patients receiving Viramune or any other antiretroviral therapy may
continue to develop
opportunistic infections and other complications of HIV infection, and
therefore, should remain
under close clinical observation by physicians" (PDR 2001).

" Viramune is not a cure for HIV-1 infection; patients may continue to
experience illnesses
associated with advanced HIV-1 infection, including opportunistic
infections" (PDR 2001).

3. Drastic changes in regulations to prescribe antiretroviral
medications.

Since the middle of the 1980’s, researchers have developed 15 drugs to
combat HIV.
"Nevertheless, HIV is so wily that the drugs are still failing thousands
of infected people,
including many who have taken each of the 15 at one time or another."
"New, safer drugs
are urgently needed" (Altman 2001b).

During the summer 1996 at the 11th International AIDS Conference in
Vancouver, the central orientation upon prevention and treatment of AIDS
was "hit HIV early,
hit hard." David Ho, the Director of the Aaron Diamond AIDS Research
Center of New York
University, is still remembered for disseminating that slogan across the
globe. It entitled
him to be named "Man of the Year" by TIME magazine. This marked the
beginning of the
simultaneous use of several antiretrovirals, combinations which came to be
called
"cocktails", also known as "highly active antiretroviral therapy" or HAART
(Altman 1996;
Gorman 1996).

Only a few years later, at the 13th International AIDS Conference in
Durban in 2000, due to the high number and severity of side effects
manifested by
individuals on these cocktail therapies, many of the side effects being
life-threatening,
there was a shift in gears: it was ordered that "intermittent therapy" or
"therapy with
holidays" be instituted (Easterbrook et al 2000; Havlir et al 2000).

However, the toxicity of antiretrovirals continued, with incrementing
numbers and
severity. On February 6, 2001, the Eighth Annual Retrovirus Meeting in
Chicago, together
with the USA Department of Health and Human Services, again shifted gears:
Do not
initiate any antiretroviral treatment in HIV positive individuals until
the appearance of
symptoms of AIDS. "The new approach calls for waiting until the immune
system shows
serious signs of weakening" (Altman 2001a).

"Concern has grown over nerve damage, weakened bones, unusual accumulation

of fat in the neck and abdomen, diabetes and a number of other serious
sides effects
of therapy." "Many people have developed dangerous high levels of
cholesterol and
other lipids in the blood" (Altman 2001a).

"Among the most troubling side effects seen in people taking the HAART
cocktails
are death of hip bone tissue, increase in blood cholesterol levels,
neuropathy or loss
of nerve sensations, kidney failure, radical alterations of liver
metabolism, diabetes,
skin rashes, pancreas failure, severe anemia, liver dysfunctions so acute
as to require
transplants and near-instantaneous death due to buildup of lactic acid"
(Garrett 2001).

"The fundamental issue in the field right now is the toxicity of our
drugs," explained
Dr. Diane Havlir of the University of California in San Francisco,
speaking in Chicago
(Altman 2001b).

"Altering a long-held policy, federal health officials are now
recommending that
treatment for the AIDS virus be delayed as long as possible for people
without symptoms
because of increased concerns over toxic effects of the therapies" (Altman
2001a).

Pharmaceutical companies like Glaxo-Smith-Kline are very disappointed with
the new
directions (Lews 2001).

Beginning in early January officials started announcing the changed
course: "The shift,
NIH scientists will explain at the annual Conference on Human Retroviruses
in Chicago, is
prompted by an emerging consensus on three factors. First, the
cocktails-called highly
active anti-retroviral therapy, or HAART-can’t wipe out all viruses in a
person’s body, so
patients must take these drugs every day, probably for the rest of their
lives. That
prompts the second and third factors: toxicity and resistance. The longer
people take
HAART cocktails, the greater the number of side effects they experience"
(Garrett 2001).

In December 2000, in a speech to the Royal Society of Medicine in London,
prominent
AIDS physician Charles Carpenter of Brown University, a member of the AIDS
advisory
committee to the NIH, signaled plans to change the treatment guidelines.
"In retrospect,"
he said, "we now realize the risk of drug toxicity is greatly enhanced by
taking these drugs
early" (Garret 2001). Antony Fauci, Director of the United States National
Institute of Allergy
and Infectious Diseases, commented: "We are starting to see a greater and
greater realization
of accumulation of toxic side effects." (Garrett 2001).

The new guidelines can be viewed at www.hivatis.org (Altman 2001a).

Regarding the new shift in gears at the Chicago meeting, it was said:
"Experts did not
predict most toxicities of the available drugs, and they poorly understand
why they develop"
(Altman 2001b). However, this is not true; for almost a decade now,
scientist Peter Duesberg,
from the Department of Molecular Biology at the University of California
in Berkeley, has been
warning about the toxicity of all antirretroviral medications, as well as
the certainty that those
medications cause the very AIDS that they are supposed to prevent or cure
(Duesberg 1992a,b,
1996; Duesberg & Rasnick 1997, 1998). Many have died because they, their
physicians, and
the official institutions, did not heed this warning.

Researchers meeting in Chicago were shaken by the fact that: "Some
infected people are
known as long-term nonprogressors because they have controlled HIV without
therapy for
as long as 20 years" (Altman 2001b).

Since pharmaceutical companies continued advertising the "great benefits"
of antiretrovirals,
on April 27, 2001, the Food and Drug Administration (FDA) of the Federal
Government of the
United States ordered pharmaceutical companies to stop printing lies about
the benefits of
their antiretroviral products.

4. Alternative non-toxic measures to prevent MTCT.

The Department of Health of the Republic of South Africa is aware of
alternative non-toxic
means to avoid what is known as "MTCT of HIV", means which will be tested
and compared to
Nevirapine during the projected protocol (Ministry of Health 2001).

Scientific studies support the contention that the use of vitamins by
themselves could be
enough to avoid what is known as mother to child transmission of HIV
(Stiehm 1995; Landers
1995; Fawzi & Hunter 1998). If this is the case, as many clinical trials
and scientific papers
contend, it would constitute a very inexpensive and non-toxic practice for
South Africa and
other countries.

Regarding vitamins in HIV disease progression and vertical transmission,
researchers
from the Harvard School of Public Health state: "The higher rates of HIV
progression and
vertical transmission in developing countries coincide with similarly
higher rates of malnutrition
and vitamin deficiencies, indicating that HIV infection, may be modified
by nutritional status."
"Numerous observational studies report inverse association between vitamin
status,
measured bio-chemically or as levels of dietary intake, and the risk of
disease progression
or vertical transmission." "Adequate vitamin status may also reduce
vertical transmission
through the intra-partum and breastfeeding routes by reducing HIV viral
load in lower
genital secretions and breast milk" and "Vitamin supplements may be one of
the few
potential treatments that are inexpensive enough to be made available to
HIV-infected
persons in developing countries" (Fawzi & Hunter 1998).

"A growing body of data suggests that low serum levels of vitamin A among
HIV-infected
pregnant women is associated with higher risk of vertical transmission of
HIV" (Fawzi &
Hunter 1998).

"Mean vitamin A concentration in 74 mothers who transmitted HIV to their
infants was
lower than that in 264 mothers who did not transmit HIV to their infants"
(Semba et al
1994a).

"In Malawi, higher serum retinol of HIV-infected pregnant women was
associated
with a reduced risk of vertical transmission" (Semba et al 1994a; Fawzi &
Hunter 1998).

" Women who had increasing serum retinol levels over time, however were at
a lower risk,
whereas women who had declining serum retinol were at a higher risk of
transmitting the virus"
(Landesman 1996; Fawzi & Hunter 1998).

"Vitamin A supplementation to a population of HIV-infected pregnant women,
many of
whom had low vitamin A levels, was associated with a decreased number of
preterm births
and with reduced mother-to-child transmission of HIV in preterm babies,
but was not associated
with a reduction in HIV transmission overall. Vitamin A decreased HIV
transmission in the preterm
babies by 47%" (Coutsoudis et al 1999).

"Detection of vaginal HIV-1 DNA was associated with abnormal vaginal
discharge, lower
absolute CD4 cell count, and severe vitamin A deficiency" (John et al
1997).

"Women with CD4 cell depletion, especially those with vitamin A
deficiency, may be at
increased risk of transmitting HIV-1 to their infants through breast milk"
(Nduati et al 1995).

"Increased risk of maternal-infant transmission was associated with severe
vitamin A
deficiency among non-breastfeeding women" in the United States (Greenberg
et al 1997).

Something to keep in mind is that vitamin A could be teratogenic and WHO
recommends
that pregnant women should not take more than 10,000 IU of Vitamin A per
day (Shah et al
1987; Fawzi & Hunter 1998).

5. Optimal nutritional status to treat and prevent AIDS.

The Government of South Africa is doing its best to treat and prevent AIDS
using all the
tools provided by the scientific community. In this regard, besides
looking at antiretroviral
medications, the Department of Health is implementing different measures
to guarantee, as
much as possible, a good nutritional status to people at risk for AIDS,
and to all South Africans
at large, as an effective means of dealing with AIDS.

Since the beginning of the AIDS epidemic well recognized researchers in
the field of nutrition
and immunology, such as Dr. Ranjit Kumar Chandra, noticed that: "There is
an uncanny similarity
between the immunological findings in nutritional deficiencies and those
seen in acquired
immunodeficiency syndrome, AIDS" (Jain & Chandra 1984).

"There is a similarity between the immune deficiency, multiple infections,
and severe weigh
loss seen in AIDS patients, and the association of protein calorie
malnutrition (PCM) with
reduced resistance to infection observed in malnourished children,
particularly in the Third
World." "It is also possible that nutritional deficiency may play a
significant role in the clinical
course of the immunodeficient state." "These similarities between AIDS and
PCM suggest that
nutrition may contribute to the immunodeficient state. The
immunodeficiency in children with
PCM can be reversed by nutritional rehabilitation, which suggest that
restoration of nutritional
state may be a useful adjunct to therapy for AIDS patients" (Gray 1983).

The immunological alterations found in protein energy malnutrition (PEM)
are practically
identical to those of AIDS: impaired delayed cutaneous hypersensitivity,
lymphocyte proliferation
response to mitogens, complement activity and secondary response to
antigens. There is also
a reduced number of rosetting T lymphocytes, increased deoxynucleotidyl
transferase activity,
decreased serum thymic factor, fewer helper T cells, impaired production
of interferon gamma
and interleukins 1 and 2, reduced antibody affinity, impaired secretory
immunoglobulin A (IgA)
antibody response and phagocyte dysfunction. The proportion of
helper/inducer T lymphocytes
recognized by the presence of CD4 positive antigen on the cell surface is
markedly decreased.
The ratio Cd4/CD8 is significantly decreased. Lymphoid atrophy is a
prominent feature of
nutritional deprivation. Serum antibody responses are generally intact in
PEM. Most complement
components are decreased, especially C3, C5, factor B and total haemolytic
activity
(Chandra1993).

On the other hand, "Nutritional problems have been a part of the clinical
aspects of AIDS
from its earliest recognition as a new disease" (Keusch & Thea 1993). "In
fact, in many AIDS
patients, death seams to be determined more by the individual’s
nutritional status than by any
particular opportunistic infection. This is, when wasting of lean body
mass approaches 55% of
normal for age, sex, and height, death is imminent regardless of the
forces resulting is such
profound malnutrition" (Keusch & Thea 1993).

As explained above, it is scientifically known that "prenatal
undernutrition have been linked
to deficits in several aspects of cell-mediated immunity, to involution of
lymphoid tissues such as
the thymus, and to suppression of antibody responses to vaccination."
These deficits persist for
weeks or, in some cases, even years (Chandra 1975a,b, 1981; Moscatelli et
al 1976; Ferguson
1978; Lewis & Wilson 1995; Hasselbach et al 1999; McDade et al 2000,
2001a,b).

Similarly, there is a growing scientific data showing that many chronic
diseases of adulthood
have their origin at " in utero programming" (Barker 1998a,b). This
includes illnesses
such as coronary heart disease and stroke, hypertension, type II diabetes
and other endocrine
alterations (Naeye et al 1971; Barker 1992, 1994, 1998a,b), as well as
several immunological
disturbances (Chjandra 1975a,b; Ferguson 1978; Beach et al 1982; McDade
2000, 2001a,b).
Therefore, it appears that whatever happens during embryonic and fetal
times will be remembered
by cells, tissues, organs, and systems throughout a lifetime.

"Research in Gambia associated season of birth with infectious disease
mortality after the
age of 15 years, suggesting an association between prenatal
undernutrition, immune function,
and adult vulnerability to infectious disease" (More et al 1997, 1999).
Prenatal undernutrition
has been found to impair antibody responses to vaccination with Salmonella
thyfi
that last at least up to adolescent times (McDade et al 2001a). The
findings of these researchers
"suggest a role for fetal and early infant experience in programming the
immune system" which
may accompany the individual during its entire life (McDade et al
2001a,b).

In addition, "murine models have documented impairments in immunity after
maternal
undernutrition that last through adulthood and into the next generation,
despite ad libitum
feeding of both F1 and F2 generations" (Chandra 1975c). Also in mice,
deprivation of zinc
during pregnancy causes immunodeficiency that can last at least for three
generations
(Beach et al 1982).

It is therefore very probable that in Africa the consequences of poverty
and malnutrition
are being transmitted from generation to generation with a cumulative
effect and that AIDS
in Africa may be the topmost consequence of these cumulative effects of
poverty.

In this light, the crucial role of maternal undernutrition in the
pathogenesis of pediatric
AIDS has seriously been considered to be the case in developing countries
(Giraldo 1997).
This reasoning also concludes that malnutrition constitutes the main risk
factor for AIDS in
adults in developing countries (Giraldo 1997). Scientifically speaking,
there is no rational
for indicting sexual promiscuity as the cause of AIDS in Africa, while
underestimating the
role of poverty and malnutrition.

"It is not surprising, therefore, that dietary therapy for AIDS has been
proposed, debated,
and more importantly surreptitiously or overtly used from the early days
of the epidemic"
(Keusch & Thea 1993).

Twenty years later, researchers insist: "Because nutrient deficiencies may
play an
important role in the pathogenesis of HIV disease, medical nutrition
therapy and counseling
are critical aspects of treatment" (Mahan & Escott -Stump 2000).
Nutritional therapy is then
a must in AIDS (Gerrior & Wanke 2001).

5.1. Good nutrition as a mean to prevent AIDS.

An optimal nutritional status as well as adequate vitamin levels is known
to be by themselves
enough to prevent AIDS in people who react positively on the tests for
HIV. Let us examine some
scientific facts:

"All persons with HIV infection should be screened for nutritional
problems and concerns at
the time of their first contact with a health care professional, and
routine monitoring should be
performed on an ongoing basis" (Mahan & Escott -Stump 2000).

"The risk of death among HIV-infected subjects with adequate serum vitamin
A levels was
78% less, when compared with Vitamin A-deficient subjects" (Semba et al
1994a,b; Fawzi &
Hunter 1998).

"In a study carried out among HIV-positive homosexual men, development of
Vitamin A
deficiency over an 18-month period was associated with a decline in CD4
cell count, widely
used as a marker of HIV immune impairment. Normalization of vitamin A was
associated with
higher CD4 cell counts" (Baum et al 1995; Fawzi & Hunter 1998).

"Lower serum levels of vitamin A were associated with a faster rate of
progression among
men who participated in the Multicenter AIDS Cohort Study (MACS)" (Tang et
al 1997; Fawzi &
Hunter 1998).

"Among well nourished HIV- seropositive men who participated in the San
Francisco Men’s
Health Study, high energy-adjusted vitamin A intake at baseline was
associated with higher
CD4 cell count at baseline, as well as with lower risk of developing AIDS
during the 6 years
period follow up" (Abrams et al 1993; Fawzi & Hunter 1998).

"In a placebo-controlled trial in South Africa among children born to
HIV-positive women,
Vitamin A supplements resulted in approximately 50% reduction in diarrheal
morbidity among
HIV-infected children" (Coutsoudis et al 1995; Fawzi & Hunter 1998).

In Tanzania: "Multivitamin supplementation is a low-cost way of
substantially decreasing
adverse pregnancy outcomes and increasing T-cell counts in HIV-1 infected
women" (Fawzi et
al 1998).