LOL. You truly are ignorant of much!

Try Coxsackie virus. Relatively harmless--but known as Keshan's
disease in the context of selenium deficiency. Keshan is a province in
China where the disease has been seen rather commonly.

However, HIV disease can result in AIDS in nutrient replete
individuals. A multi is NOT a cure--but a good part of therapy that
may well delay the need for ARV for some time in people with higher
CD4+ counts.

Most diseases can take a more severe course in the context of
malnutrition. This is not news. Nor is it particularly news (though it
may be to many physicians) that nutritional interventions can help in
disease management.

But again, the issue is that while this is one CRITICALLY important
and far too often ignored aspect, multis don't represent a cure,
unfortunately.

By all means, Paul. Take a multi.

        George M. Carter

Good Nutrition Benefits All--

It's well known that a nutritional deficiency can weaken one's
defenses against microbes. But what does it do to the actual microbes?

Seven years ago, Melinda A. Beck, a virologist at the University of
North Carolina, addressed this question with Agricultural Research
Service nutritionist Orville A. Levander. According to Levander, who
helped establish the first Recommended Dietary Allowance for selenium,
Chinese scientists had noticed that a serious heart muscle
inflammation attributed to selenium deficiency in their country
fluctuated from season to season and year to year.

This suggested that an infectious agent--possibly a virus--might be
involved in the disease, which hits infants and children. So the
Chinese scientists looked for and found a virus in those patients. It
was a virulent strain of coxsackievirus--named after Coxsackie, New
York, where it was first isolated.

Levander teamed up with Beck's laboratory to learn how selenium
deficiency and coxsackievirus interacted. They showed that a normally
innocuous strain of coxsackievirus--the B3/0 strain--mutated into a
heart-damaging pathogen in mice raised without any selenium added to
their diets. The same thing occurred if the mouse diets lacked vitamin
E, also an antioxidant. Theirs was the first report showing that a
host nutritional deficiency could turn a harmless microbe into a
pathogen. (See "Nutrient Deficiency Unleashes Jekyll-Hyde Virus,"
Agricultural Research, August 1994, p. 14.)

Such mutations could have global implications. According to Levander,
who is with ARS' Nutrient Requirements and Functions Laboratory in
Beltsville, Maryland, Americans get the recommended levels of selenium
in their diets. But there are pockets of selenium deficiency around
the world that might be generating mutated viruses.

Levander says, "The association between famine and epidemics has been
noted throughout history. However, scientists have always focused on
the effects of nutritional deficiencies on the people themselves,
never on the invading pathogen."

Beck and Levander wondered whether other viruses were susceptible to
changes in the oxidative environment of their host cells. Together
with researchers at the Nestle Research Center in Lausanne,
Switzerland, Beck and her co-workers challenged mice with a normally
mild form of influenza virus--an influenza A strain that originated in
Bangkok in 1979. Like coxsackieviruses, the genome of influenza
viruses is composed of RNA, rather than the more stable DNA common to
bacteria and all higher organisms.

Earlier this year, the group reported that this mild influenza strain
caused more severe flu in mice raised on a selenium-deficient diet
than in animals fed adequate amounts of this essential trace element.
What's more, a careful look at the genome of the virus taken from the
lungs of the selenium-deficient mice showed that 29 of the bases had
mutated in a gene segment thought to affect virulence. By contrast, no
mutations were found in the same gene segment of the virus taken from
mice raised on a selenium-adequate diet. The selenium level in the
deficient diet was only about 1/60 that of the adequate diet.

"Our work points to the importance of antioxidant protection against
viral disease," says Beck. She speculates that increased oxidative
stress in the mice--due to selenium deficiency--may have caused
oxidative damage to the virus' genome, making the virus more virulent.

Beck says that new strains of flu viruses arise each year because the
genes tend to shuffle places, and those that code for the viral
antigens are highly susceptible to mutation.

"But the mutations resulting from selenium deficiency occurred in a
normally stable part of the genome, making them all the more
remarkable," Beck notes.

More Viral Vagaries

Even before the influenza studies began, Argentine microbiologist
Ricardo M. Gomez, at the University of Buenos Aires, wondered if
selenium deficiency would alter the effect of a variety of human
viruses from unrelated families on mice hearts. He and Levander tested
two other coxsackieviruses--B1 and A9--an echovirus, and a herpes
simplex virus. The herpesvirus is potentially more stable, since it's
a DNA virus. Ten days after exposing the animals, Gomez inspected
their hearts--with mixed results.

Selenium-deficient mice had more heart damage from the echovirus and
the B1 coxsackievirus than the animals getting ample selenium. But it
was the reverse in animals infected with the DNA herpes simplex virus:
The selenium-deficient mice fared better. In the animals infected with
the A9 strain of coxsackievirus, selenium status had no effect.
Whether or not any of the viruses mutated under the strain of selenium
deficiency is a subject for further research.

These results, concludes Gomez, indicate that selenium status
selectively influences the degree of virus-induced heart damage. They
also demonstrate that a nutrient deficiency can affect a range of
viruses and may have important implications for public health, says
Levander. He adds that the phenomenon might also apply to certain
animal and plant viruses.

Does Competition Boost Virulence?

Selenium confers its antioxidant protection mainly through two enzymes
that contain it--glutathione peroxidase and thioredoxin reductase. So
Levander and his co-workers wondered whether other metals that compete
for the selenium site in these enzymes might worsen infection. They
chose to work with the innocuous coxsackievirus B3/0 strain used in
Beck's earliest studies.

Levander and food scientist Paul K. South, now with the Food and Drug
Administration, chose mercury--a prevalent environmental
contaminant--as the competitor. The metal is known to reduce activity
of both antioxidant enzymes in test animals, and it increases
oxidative stress.

South says 90 percent of the mice given the highest dose of mercury
alone--right at their limit of tolerance--survived. But the survival
rate plunged to 36 percent of the mice exposed to both mercury and the
innocuous coxsackievirus. About one-third of the infected mice given
the highest dose of mercury had more severe heart damage, and their
hearts had higher numbers of virus.

Gold is another selenium competitor, known to reduce the activity of
one of the antioxidant enzymes. That prompted virologist Allen D.
Smith and Levander to test two gold-containing compounds,
aurothiomalate and aurothioglucose. Both are prescribed to treat
rheumatoid arthritis in people.

Smith saw similar pathological trends in the mice he injected with
aurothiomalate but not in the animals given aurothioglucose. He says
both compounds inhibited the activity of the antioxidant enzyme
thioredoxin reductase to about the same extent. So aurothiomalate is
producing its lethal effect through some route other than as a
selenium competitor. "It's probably affecting the immune system
directly," he says.

Ditto for mercury. While the high dose did reduce the activity of both
selenium-containing antioxidant enzymes in different organs to
different degrees, "it's more likely that mercury has some effect on
immune function," says South. He suspects the toxic stress of the
mercury allowed the virus to replicate at a higher rate.

This research is part of Human Nutrition, an ARS National Program
(#107) described on the World Wide Web at http

Orville A. Levander and Allen D. Smith are with the USDA-ARS Nutrient
Requirements and Functions Laboratory, 10300 Baltimore Ave., Bldg.
307, Beltsville, MD 20705-2350; phone (301) 504-8504 [Levander], (301)
504-8577 [Smith], fax (301) 504-9062, e-mail
levander-at-307.bhnrc.usda.gov smitha-at-307.bhnrc.usda.gov.

COPYRIGHT 2001 U.S. Government Printing Office
COPYRIGHT 2001 Gale Group

Citation? Sure. Drugs will suppress immunity--as well as inhibitions
as far as using condoms. They don't cause AIDS.

May be true--but also use of poppers does not correlate with AIDS. HIV
infection does tho. So of the 60-70%, most were not infected and did
not develop AIDS, despite use of poppers.

It's caused by both. Toxins and other agents, except maybe
cyclosporin, do NOT cause a chronic decline in CD4 count.

The "drugs cause AIDS" theory is just ridiculous.

        George M. Carter

**
Ostrow DG, Beltran ED, Joseph JG, DiFranceisco W, Wesch J, Chmiel JS.
Recreational drugs and sexual behavior in the Chicago MACS/CCS cohort
of homosexually active men. Chicago Multicenter AIDS Cohort Study
(MACS)/Coping and Change Study. J Subst Abuse. 1993;5(4):311-325.

University of Michigan.

Since initial reports emerged of an association between recreational
drug use and high-risk sexual behaviors in gay men, there has been
interest in studying this relationship for its relevance to behavioral
interventions. Reported here are the longitudinal patterns of alcohol
and recreational drug use in the Chicago Multicenter AIDS Cohort Study
(MACS)/Coping and Change Study (CCS) of gay men. A pattern of
decreasing drug use over 6 years was observed that paralleled a
decline in high-risk sexual behavior (i.e., unprotected anal
intercourse). In contrast, alcohol consumption tended to be more
stable over time, and to show no relationship to sexual behavior
change. Men who combined volatile nitrite (popper) use with other
recreational drugs were at highest risk both behaviorally and in terms
of human immunodeficiency virus-1 (HIV) seroconversion throughout the
study. Popper use also was associated independently with lapse from
safer sexual behaviors (failure to use a condom during receptive anal
sex). Use of other recreational substances showed no relationship to
sexual behavior change patterns, and stopping popper use was unrelated
to improvement in safer sexual behavior. When popper use and lapse
from safer sex were reanalyzed, controlling for primary relationship
status, popper use was associated with failure to use condoms during
receptive anal sex among nonmonogamous men only. These findings
suggest an association between popper use and high-risk sexual
behavior among members of the Chicago MACS/CCS cohort that has
relevance to HIV prevention intervention efforts.

**
Erratum in: Am J Epidemiol 1996 Jan 1;143(1):104.

Ostrow DG, DiFranceisco WJ, Chmiel JS, Wagstaff DA, Wesch J. A
case-control study of human immunodeficiency virus type 1
seroconversion and risk-related behaviors in the Chicago MACS/CCS
Cohort, 1984-1992. Multicenter AIDS Cohort Study. Coping and Change
Study. Am J Epidemiol. 1995 Oct 15;142(8):875-883.

Department of Psychiatry and Behavioral Medicine, Medical College of
Wisconsin, Milwaukee 53202, USA.

This paper focuses on 76 human immunodeficiency virus type 1 (HIV-1)
seroconverters who concurrently participated in the Chicago, Illinois,
component of the Multicenter AIDS Cohort Study (MACS) and the Coping
and Change Study (CCS) of homosexual/bisexual men between 1984 and
1992. A nested case-control analysis was performed to assess the
critical behavioral risk factors associated with incident HIV-1
infection and the consistency of these relations in early (1984-1988)
versus later (1989-1992) phases of the study. Univariate results
revealed strong early period associations between seroconversion and
various measures of receptive anal intercourse (RAI) that became
considerably weaker in the study's later period. The weaker
associations reflected the overall decline in levels of RAI among the
cohort during the 9 years of observation. In contrast, univariate
results revealed stronger later period associations between
seroconversion and measures of receptive oral intercourse and
insertive anal intercourse. Subsequent multivariate testing did not
support the hypothesis that receptive oral intercourse and/or
insertive anal intercourse have replaced unprotected RAI as important
risk behaviours in the homosexual transmission of HIV-1. In
conditional logistic regression models combining intercourse measures
with indices of drug and condom use, only the latter variables were
consistently associated with HIV-1 seroconversion in both early and
later study periods. Adjusted odds ratios (ORs) for nonuse of condoms
during RAI were consistently significant throughout the study (ORs =
3.7-4.8), while adjusted odds ratios for recreational drug use
variables rose dramatically during the latter half of the study (e.g.,
for use of cocaine, OR = 81.3 (95% confidence interval 8-824)
[corrected], and for use of nitrite "poppers," OR = 9.1 (95%
confidence interval 1.8-45.5)). The behavioral intervention
applications of these findings, as well as their relation to data from
other recent cohort studies of HIV-1 seroconversion among
homosexual/bisexual men, are discussed.

Here's the abstract of the study in Tanzania below. These data, in a
more rigorous trial design, are in line with other studies of multis
done over the years. A multivitamin is not a cure, but it is certainly
an important part of treating people living with HIV and efforts
should be made to get a good multi to everyone who needs it.

It is extremely inexpensive. Extremely doable.

Unfortunately, don't count on the US. We're too busy killing Iraqis to
the tune of $300 billion. No time, money, resources or effort to spend
on multis for Africans and Asians!! Nope! Gotta murder some more kids
for oil.

        George M. Carter

**
N Engl J Med. 2004 Jul 1;351(1):23-32.  Related Articles, Links  

Comment in:
N Engl J Med. 2004 Jul 1;351(1):78-80.
 
A randomized trial of multivitamin supplements and HIV disease
progression and mortality.

Fawzi WW, Msamanga GI, Spiegelman D, Wei R, Kapiga S, Villamor E,
Mwakagile D, Mugusi F, Hertzmark E, Essex M, Hunter DJ.

Department of Nutrition, Harvard School of Public Health, Boston, MA
02115, USA. mina@hsph.harvard.edu

BACKGROUND: Results from observational studies suggest that
micronutrient status is a determinant of the progression of human
immunodeficiency virus (HIV) disease. METHODS: We enrolled 1078
pregnant women infected with HIV in a double-blind, placebo-controlled
trial in Dar es Salaam, Tanzania, to examine the effects of daily
supplements of vitamin A (preformed vitamin A and beta carotene),
multivitamins (vitamins B, C, and E), or both on progression of HIV
disease, using survival models. The median follow-up with respect to
survival was 71 months (interquartile range, 46 to 80). RESULTS: Of
271 women who received multivitamins, 67 had progression to World
Health Organization (WHO) stage 4 disease or died--the primary
outcome--as compared with 83 of 267 women who received placebo (24.7
percent vs. 31.1 percent; relative risk, 0.71; 95 percent confidence
interval, 0.51 to 0.98; P=0.04). This regimen was also associated with
reductions in the relative risk of death related to the acquired
immunodeficiency syndrome (0.73; 95 percent confidence interval, 0.51
to 1.04; P=0.09), progression to WHO stage 4 (0.50; 95 percent
confidence interval, 0.28 to 0.90; P=0.02), or progression to stage 3
or higher (0.72; 95 percent confidence interval, 0.58 to 0.90;
P=0.003). Multivitamins also resulted in significantly higher CD4+ and
CD8+ cell counts and significantly lower viral loads. The effects of
receiving vitamin A alone were smaller and for the most part not
significantly different from those produced by placebo. Adding vitamin
A to the multivitamin regimen reduced the benefit with regard to some
of the end points examined. CONCLUSIONS: Multivitamin supplements
delay the progression of HIV disease and provide an effective,
low-cost means of delaying the initiation of antiretroviral therapy in
HIV-infected women. Copyright 2004 Massachusetts Medical Society