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Exposure to Chemical Pollutants Increases Fat



 
 
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  #11  
Old July 11th, 2011, 04:28 AM posted to sci.med.nutrition,alt.support.diabetes,alt.support.diet.low-carb
jay[_2_]
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Posts: 68
Default Exposure to Chemical Pollutants Increases Fat

citation for the above?

Dioxin: a review of its environmental effects and its aryl hydrocarbon
receptor biology.
A highly persistent trace environmental contaminant and one of the
most potent toxicants known is dioxin (2,3,7,8-tetrachlorodibenzo-para-
dioxin or TCDD). TCDD induces a broad spectrum of biological
responses, including induction of cytochrome P-450 1A1 (CYP1A1),
disruption of normal hormone signaling pathways, reproductive and
developmental defects, immunotoxicity, liver damage, wasting syndrome,
and cancer. Its classification was upgraded from "possible human
carcinogen" (group 2B) to "human carcinogen" (group 1) by the
International Agency for Research on Cancer (IARC) in 1997. Exposure
to TCDD may also cause changes in sex ratio, and tumor promotion in
other animals. Because of the growing public and scientific concern,
toxicological studies have been initiated to analyze the short- and
long-term effects of dioxin. TCDD brings about a wide variety of toxic
and biochemical effects via aryl hydrocarbon receptor (AhR)-mediated
signaling pathways. Essential steps in this adaptive mechanism include
AhR binding of ligand in the cytoplasm of cells associated with two
molecules of chaperone heatshock protein (Hsp90) and AhR interactive
protein, translocation of the receptor to the nucleus, dimerization
with the Ah receptor nuclear translocator, and binding of this
heterodimeric transcription factor (present in CYP1A) to dioxin-
responsive elements upstream of promoters that regulate the expression
of genes involved in xenobiotic metabolism. PMID: 15900503
  #12  
Old July 11th, 2011, 04:32 AM posted to sci.med.nutrition,alt.support.diabetes,alt.support.diet.low-carb
jay[_2_]
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Posts: 68
Default Exposure to Chemical Pollutants Increases Fat

Do you have a citation for the above?

2,3,7,8-Tetrachlorodibenzo-p-dioxin induces apoptotic cell death and
cytochrome P4501A expression in developing Fundulus heteroclitus
embryos.
Fundulus heteroclitus embryos were exposed to 2,3,7,8-
tetrachlorodibenzo-p-dioxin (TCDD) during early development using
nanoinjection or water bath exposure. TCDD caused developmental
abnormalities that included hemorrhaging, loss of vascular integrity,
edema, stunted development and death. The LC(50) and LD(50) of TCDD
for Fundulus embryos were approximately 19.7+/-9.5 pg TCDD/microl
(water bath) and 0.25+/-0.09 ng TCDD/g embryo (nanoinjection). To
identify a possible cause for these developmental abnormalities we
analyzed the effects of TCDD on apoptotic cell death and cytochrome
P4501A (CYP1A) expression in the embryos. TCDD exposure increased
apoptotic cell death in several tissues including brain, eye, gill,
kidney, tail, intestine, heart, and vascular tissue. CYP1A expression
was also increased in the TCDD-exposed embryos predominantly in liver,
kidney, gill, heart, intestine, and in vascular tissues throughout the
embryo. There was co-occurrence of TCDD-induced apoptosis and CYP1A
expression in some, but not all, cell types. In addition the dose
response relationships for apoptosis and mortality were similar, while
CYP1A expression appeared more sensitive to TCDD induction. PMID:
11311389
  #13  
Old July 11th, 2011, 04:37 AM posted to sci.med.nutrition,alt.support.diabetes,alt.support.diet.low-carb
jay[_2_]
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Posts: 68
Default Exposure to Chemical Pollutants Increases Fat

... citation for the above?

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) alters the mRNA expression
of critical genes associated with cholesterol metabolism, bile acid
biosynthesis, and bile transport in rat liver: a microarray study.
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent hepatotoxin
that exerts its toxicity through binding to the aryl hydrocarbon
receptor (AhR) and the subsequent induction or repression of gene
transcription. In order to further identify novel genes and pathways
that may be associated with TCDD-induced hepatotoxicity, we
investigated gene changes in rat liver following exposure to single
oral doses of TCDD. Male Sprague-Dawley rats were administered single
doses of 0.4 microg/kg bw or 40 microg/kg bw TCDD and killed at 6 h,
24 h, or 7 days, for global analyses of gene expression. In general,
low-dose TCDD exposure resulted in greater than 2-fold induction of
genes coding for a battery of phase I and phase II metabolizing
enzymes including CYP1A1, CYP1A2, NADPH quinone oxidoreductase,
UGT1A6/7, and metallothionein 1. However, 0.4 microg/kg bw TCDD also
altered the expression of Gadd45a and Cyclin D1, suggesting that even
low-dose TCDD exposure can alter the expression of genes indicative of
cellular stress or DNA damage and associated with cell cycle control.
At the high-dose, widespread changes were observed for genes encoding
cellular signaling proteins, cellular adhesion, cytoskeletal and
membrane transport proteins as well as transcripts coding for lipid,
carbohydrate and nitrogen metabolism. In addition, decreased
expression of cytochrome P450 7A1, short heterodimer partner (SHP;
gene designation nr0b2), farnesyl X receptor (FXR), Ntcp, and Slc21a5
(oatp2) were observed and confirmed by RT-PCR analyses in independent
rat liver samples. Altered expression of these genes implies major
deregulation of cholesterol metabolism and bile acid synthesis and
transport. We suggest that these early and novel changes have the
potential to contribute significantly to TCDD induced hepatotoxicity
and hypercholesterolemia. PMID: 16054898
  #14  
Old July 11th, 2011, 04:42 AM posted to sci.med.nutrition,alt.support.diabetes,alt.support.diet.low-carb
jay[_2_]
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Posts: 68
Default Exposure to Chemical Pollutants Increases Fat

... citation for the above?

Iron deficiency prevents liver toxicity of 2,3,7,8-tetrachlorodibenzo-
p-dioxin.
The compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes
hepatocellular damage and porphyria in C57B1/6J mice, among a wide
range of toxic effects. We compared the effect of TCDD toxicity in
iron-deficient mice with that in mice receiving a normal diet.
Porphyria did not develop in the iron-deficient animals, and these
animals were also protected from hepatocellular damage and certain
other toxic effects of TCDD. PMID: 432648
  #15  
Old July 11th, 2011, 05:18 AM posted to sci.med.nutrition,alt.support.diabetes,alt.support.diet.low-carb
jay[_2_]
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Posts: 68
Default Exposure to Chemical Pollutants Increases Fat

Some POPs alter cells via a non-ROS mechanisms ...
Do you have a citation for the above?


2,3,7,8-tetrachlorobenzo-p-dioxin inhibits proliferation of SK-N-SH
human neuronal cells through decreased production of reactive oxygen
species.
Oxidative stress has been known to be involved in the mechanism of
toxic effects of various agents on many cellular systems. In this
study we investigated the role of reactive oxygen species (ROS) in
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced neuronal cell
toxicity using SK-N-SH human neuroblastoma cells. TCDD inhibited
proliferation of the cells in a dose-dependent manner, which was
revealed by MTT staining, counting of cells stained with trypan blue
and [3H]thymidine uptake assay. TCDD also suppressed the basal
generation of ROS in a time- and concentration-dependent manner
assessed by 2',7'-dichlorofluorescein fluorescence. In addition, TCDD
induced a dose-dependent inhibition of lipid peroxidation, a biomarker
of oxidative stress, whereas it significantly increased the level of
glutathione (GSH), an intracellular free radical scavenger in the
cells. Moreover, TCDD altered the activities of major antioxidant
enzymes; increase in superoxide dismutase (SOD) and catalase, but
decrease in glutathione peroxidase (GSH-Px) and glutathione reductase
(GSH-Red). Pretreatment with L-buthionine-S,R-sulfoximine (BSO, 50
microM), an inhibitor of GSH synthesis, significantly prevented the
TCDD-induced reduction in lipid peroxidation and cell proliferation.
Interestingly, exogenous application of an oxidant, H2O2 (50 microM)
markedly restored the inhibited cell proliferation induced by TCDD.
Taken together, these results suggest that alteration of cellular
redox balance may mediate the TCDD-induced inhibition of proliferation
in human neuronal cells. PMID: 12607819
  #16  
Old July 11th, 2011, 05:25 AM posted to sci.med.nutrition,alt.support.diabetes,alt.support.diet.low-carb
jay[_2_]
external usenet poster
 
Posts: 68
Default Exposure to Chemical Pollutants Increases Fat

citation for the above?

Neural precursor cell proliferation is disrupted through activation of
the aryl hydrocarbon receptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin.
Neurogenesis involves the proliferation of multipotent neuroepithelial
stem cells followed by differentiation into lineage-restricted neural
precursor cells (NPCs) during the embryonic period. Interestingly,
these progenitor cells express robust levels of the aryl hydrocarbon
receptor (AhR), a ligand-activated transcription factor that regulates
expression of genes important for growth regulation, and xenobiotic
metabolism. Upon binding 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a
pervasive environmental contaminant and potent AhR ligand, AhR, is
activated and disrupts gene expression patterns to produce cellular
toxicity. Because of its widespread distribution in the brain during
critical proliferative phases of neurogenesis, it is conceivable that
AhR participates in NPC expansion. Therefore, this study tested the
hypothesis that AhR activation by TCDD disrupts signaling events that
regulate NPC proliferation. The C17.2 NPC line served as a model
system to (1) assess whether NPCs are targets for TCDD-induced
neurotoxicity and (2) characterize the effects of TCDD on NPC
proliferation. We demonstrated that C17.2 NPCs express an intact AhR
signaling pathway that becomes transcriptionally active after TCDD
exposure. (3)H-thymidine and alamar blue reduction assays indicated
that TCDD suppresses NPC proliferation in a concentration-dependent
manner without the loss of cell viability. Cell cycle distribution
analysis by flow cytometry revealed that TCDD-induced growth arrest
results from an impaired G1 to S cell cycle transition. Moreover, TCDD
exposure altered p27( kip1) and cyclin D1 cell cycle regulatory
protein expression levels consistent with a G1 phase arrest. Initial
studies in primary NPCs isolated from the ventral forebrain of
embryonic mice demonstrated that TCDD reduced cell proliferation
through a G1 phase arrest, corroborating our findings in the C17.2
cell line. Together, these observations suggest that the inappropriate
or sustained activation of AhR by TCDD during neurogenesis can
interfere with signaling pathways that regulate neuroepithelial stem
cell/NPC proliferation, which could adversely impact final cell number
in the brain and lead to functional impairments. PMID: 20486776
  #17  
Old July 11th, 2011, 05:59 PM posted to sci.med.nutrition,alt.support.diabetes,alt.support.diet.low-carb
Billy[_4_]
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Posts: 215
Default Exposure to Chemical Pollutants Increases Fat

In article
,
jay wrote:

... citation for the above?


Receptor- and reactive intermediate-mediated mechanisms of
teratogenesis.
Drugs and environmental chemicals can adversely alter the development
of the fetus at critical periods during pregnancy, resulting in death,
or in structural and functional birth defects in the surviving
offspring. This process of teratogenesis may not be evident until a
decade or more after birth. Postnatal functional abnormalities include
deficits in brain function, a variety of metabolic diseases, and
cancer. Due to the high degree of fetal cellular division and
differentiation, and to differences from the adult in many biochemical
pathways, the fetus is highly susceptible to teratogens, typically at
low exposure levels that do not harm the mother. Insights into the
mechanisms of teratogenesis come primarily from animal models and in
vitro systems, and involve either receptor-mediated or reactive
intermediate-mediated processes. Receptor-mediated mechanisms
involving the reversible binding of xenobiotic substrates to a
specific receptor are exemplified herein by the interaction of the
environmental chemical 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or
"dioxin") with the cytosolic aryl hydrocarbon receptor (AHR), which
translocates to the nucleus and, in association with other proteins,
binds to AH-responsive elements (AHREs) in numerous genes, initiating
changes in gene transcription that can perturb development.
Alternatively, many xenobiotics are bioactivated by fetal enzymes like
the cytochromes P450 (CYPs) and prostaglandin H synthases (PHSs) to
highly unstable electrophilic or free radical reactive intermediates.
Electrophilic reactive intermediates can covalently (irreversibly)
bind to and alter the function of essential cellular macromolecules
(proteins, DNA), causing developmental anomalies. Free radical
reactive intermediates can enhance the formation of reactive oxygen
species (ROS), resulting in oxidative damage to cellular
macromolecules and/or altered signal transduction. The teratogenicity
of reactive intermediates is determined to a large extent by the
balance among embryonic and fetal pathways of xenobiotic
bioactivation, detoxification of the xenobiotic reactive intermediate,
detoxification of ROS, and repair of oxidative macromolecular damage.
PMID: 20020262


Huh? That's all you got? ;O)
--
- Billy

Mad dog Republicans to the right. Democratic spider webs to the left. True conservatives, and liberals not to be found anywhere in the phantasmagoria
of the American political landscape.

America is not broke. The country is awash in wealth and cash.
It's just that it's not in your hands. It has been transferred, in the
greatest heist in history, from the workers and consumers to the banks
and the portfolios of the uber-rich.
http://www.politifact.com/wisconsin/.../michael-moore
/michael-moore-says-400-americans-have-more-wealth-/
  #18  
Old July 12th, 2011, 06:15 PM posted to sci.med.nutrition,alt.support.diabetes,alt.support.diet.low-carb
Billy[_4_]
external usenet poster
 
Posts: 215
Default Exposure to Chemical Pollutants Increases Fat

In article
,
Billy wrote:

In article
,
jay wrote:

... citation for the above?


Receptor- and reactive intermediate-mediated mechanisms of
teratogenesis.
Drugs and environmental chemicals can adversely alter the development
of the fetus at critical periods during pregnancy, resulting in death,
or in structural and functional birth defects in the surviving
offspring. This process of teratogenesis may not be evident until a
decade or more after birth. Postnatal functional abnormalities include
deficits in brain function, a variety of metabolic diseases, and
cancer. Due to the high degree of fetal cellular division and
differentiation, and to differences from the adult in many biochemical
pathways, the fetus is highly susceptible to teratogens, typically at
low exposure levels that do not harm the mother. Insights into the
mechanisms of teratogenesis come primarily from animal models and in
vitro systems, and involve either receptor-mediated or reactive
intermediate-mediated processes. Receptor-mediated mechanisms
involving the reversible binding of xenobiotic substrates to a
specific receptor are exemplified herein by the interaction of the
environmental chemical 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or
"dioxin") with the cytosolic aryl hydrocarbon receptor (AHR), which
translocates to the nucleus and, in association with other proteins,
binds to AH-responsive elements (AHREs) in numerous genes, initiating
changes in gene transcription that can perturb development.
Alternatively, many xenobiotics are bioactivated by fetal enzymes like
the cytochromes P450 (CYPs) and prostaglandin H synthases (PHSs) to
highly unstable electrophilic or free radical reactive intermediates.
Electrophilic reactive intermediates can covalently (irreversibly)
bind to and alter the function of essential cellular macromolecules
(proteins, DNA), causing developmental anomalies. Free radical
reactive intermediates can enhance the formation of reactive oxygen
species (ROS), resulting in oxidative damage to cellular
macromolecules and/or altered signal transduction. The teratogenicity
of reactive intermediates is determined to a large extent by the
balance among embryonic and fetal pathways of xenobiotic
bioactivation, detoxification of the xenobiotic reactive intermediate,
detoxification of ROS, and repair of oxidative macromolecular damage.
PMID: 20020262


Huh? That's all you got? ;O)


http://www.scientificamerican.com/article.cfm?id=chemical-controls
April 2010, Scientific American
p. 30
Chemical Controls

Seriously of the more than 80,000 chemicals in use in the U.S., only
five have been either restricted or banned. Not 5 percent, five. The
EPA has been able to force health and safety testing for only around
200.
--
- Billy
America is not broke. The country is awash in wealth and cash.
It's just that it's not in your hands. It has been transferred, in the
greatest heist in history, from the workers and consumers to the banks
and the portfolios of the uber-rich.
http://www.politifact.com/wisconsin/.../michael-moore
/michael-moore-says-400-americans-have-more-wealth-/

You put Lloyd Blankfein in pound-me-in-the-ass prison for one six-month term, and all this bull**** would stop, all over Wall Street. That's all it would take. Just once.
  #19  
Old July 13th, 2011, 05:01 AM posted to sci.med.nutrition,alt.support.diabetes,alt.support.diet.low-carb
jay[_2_]
external usenet poster
 
Posts: 68
Default Exposure to Chemical Pollutants Increases Fat

Study Finds Exposure to Chemical Pollutants Increases Fat
Rats exposed to high levels of chemical pollutants in fish oil could
not regulate fat properly


Links to original paper:

http://ehp03.niehs.nih.gov/article/f...89/ehp.0901321
or
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854721/

"In this study, we demonstrate for the first time a causal
relationship between POPs and insulin resistance in rats. In vivo,
chronic exposure to low doses of POPs commonly found in food chains
induced severe impairment of whole-body insulin action and contributed
to the development of abdominal obesity and hepatosteatosis. Treatment
in vitro of differentiated adipocytes with nanomolar concentrations of
POP mixtures mimicking those found in crude salmon oil induced a
significant inhibition of insulin-dependent glucose uptake. These data
provide compelling evidence that exposure to POPs increases the risk
of developing insulin resistance and metabolic disorders.
Despite intense investigations and establishment of both preventive
and therapeutic strategies, insulin resistance–associated metabolic
diseases such as type 2 diabetes, obesity, and nonalcoholic fatty
liver disease have reached alarming proportions worldwide (Angulo
2002; Ford et al. 2004; Zimmet et al. 2001). By 2015, the World Health
Organization (WHO) estimates that 1.5 billion people will be
overweight and that 338 million people will die from chronic diseases
such as diabetes and heart disease (WHO 2005). Although physical
inactivity and regular intake of high-energy diets are recognized
contributors (Hill and Peters 1998; Roberts and Barnard 2005), these
lifestyle factors can only partially explain the explosive and
uncontrolled global increase in metabolic diseases. Recently, the
development of insulin resistance and inflammation was found to be
exacerbated in humans and animals exposed to air pollution (Kelishadi
et al. 2009; Sun et al. 2009). Furthermore, the widespread
environmental contaminant bisphenol A was reported to impair
pancreatic beta cells and trigger insulin resistance (Alonso-Magdalena
et al. 2006). Our data, together with the finding that type 2
diabetics accumulate significant body burdens of POPs (Lee et al.
2006), provide additional evidence that global environmental pollution
contributes to the epidemic of insulin resistance–associated metabolic
diseases.
Although rats chronically fed the HFC diet for 28 days were exposed to
a relatively high intake of organic pollutants, the concentrations of
PCDDs/PCDFs and indicator PCBs in adipose tissue of these animals did
not exceed those observed in Northern Europeans 40–50 years of age
(Kiviranta et al. 2005), thereby indicating that doses of POP exposure
sufficient to induce detrimental health effects were not excessive.
Whether the exposure to lower levels of POPs would induce similar
detrimental effects as those observed in the present study remains to
be investigated.
Dietary interventions are current strategies to prevent or treat
metabolic diseases, and nutritional guidelines are usually based on
energy density and glycemic index of the diet; however, the levels of
POPs present in food has received less attention. Given that POPs are
ubiquitous in food chains (Fisher 1999), such underestimation may
interfere with the expected beneficial effects of some dietary
recommendations and lead to poor outcomes. For instance, the presence
of POPs in food products may, to some extent, explain the conflicting
results regarding the protective effects of n-3 polyunsaturated fatty
acids against the incidence of myocardial infarction (Guallar et al.
1999; Rissanen et al. 2000). Overall, better understanding of the
interactions between POPs and nutrients will help improve nutritional
education of patients with insulin resistance syndrome.
To protect consumer health, the presence of contaminants in food is
internationally regulated. In the European Union legislation, certain
POPs including dioxins and dioxin-like PCBs are regulated in
foodstuffs (European Union 2006). Risk assessment of these organic
pollutants is based on the ability of individual compounds to produce
heterogeneous toxic and biological effects through the binding of the
aryl hydrocarbon receptor. Interestingly, we found that cultured
adipocytes exposed to a PCDF or PCDD mixture have normal insulin
action, even though the TEQ of these mixtures could be up to 3,500
times higher than the TEQ of the non-ortho-substituted and mono-ortho-
substituted PCB mixtures that impaired insulin action. These findings
demonstrate that risk assessment based on WHO TEQs assigned to dioxins
and dioxin-like PCBs is unlikely to reflect the risk of insulin
resistance and the possible development of metabolic disorders.
Although the production of organochlorine pesticides has been
restricted since the 1970s, the global production and use of
pesticides are poorly controlled (Jorgenson 2001; Nweke and Sanders
2009), and the presence of these environmental chemicals in seafood
still remains unregulated in European countries (European Union 2008).
Of the POP mixtures tested in vitro, organochlorine pesticides were
the most potent disruptors of insulin action. This powerful inhibitory
effect of pesticides on insulin action likely explains the common
finding emerging from several independent cross-sectional studies
reporting an association between type 2 diabetes and the body burdens
of p,p′-DDE, oxychlordane, or trans-nonachlor (Lee et al. 2006;
Rignell-Hydbom et al. 2007; Turyk et al. 2009). Therefore, widespread
pesticide exposure to humans appears to be of particular global
concern in relation to public health.
We draw two main conclusions from these observations. First, exposure
to POPs present in the environment and food chains are capable of
causing insulin resistance and impair both lipid and glucose
metabolism, thus supporting the notion that these chemicals are
potential contributors to the rise in prevalence of insulin resistance
and associated disorders (Figure 4). Second, although beneficial, the
presence of n-3 polyunsaturated fatty acids in crude salmon oil (in
the HFC diet) could not counteract the deleterious metabolic effects
induced by POP exposure. Altogether, our data provide novel insights
regarding the ability of POPs to mediate insulin resistance–
associated metabolic abnormalities and provide solid evidence
reinforcing the importance of international agreements to limit the
release of POPs to minimize public health risks."
  #20  
Old July 22nd, 2011, 10:56 PM posted to sci.med.nutrition,alt.support.diabetes,alt.support.diet.low-carb
mrbrklyn
external usenet poster
 
Posts: 2
Default Exposure to Chemical Pollutants Increases Fat

On Jul 9, 6:08*pm, montygraham wrote:
Another instance where they should have had two other groups of rats,
both of which would be fed coconut oil rather than fish oil, one would
get the POPs and one would not. *My guess is that they are not
familiar with the relevant literature, because it suggests that
coconut oil and POPs might not present any major problem, unlike fish
oil and POPs. *If so, it would have been yet another good
demonstration of the apparent dangers of fish oil.



quack quack

Warning::: Monty1945 is a certified nut case pretending to have
medical credentials. He posts across the Internet, trolling for
victims and recommends a diet high saturated fat content for a
healthy lifestyle, and as a cure for disease. He denies the
existence of AID's. In addition, "Dr Monty" by admission in usenet,
uses his body for experimental purposes, the results, being as
they are, a completely dysfunctional brain pattern, probably
secondary to the stoke he has acquired by following his own medical
advice. He's also been know to have two way conversations with his
AM/FM radio and to hound professional athletes.
Anything he posts needs to be viewed as the rantings of a brain
damaged adult limited to 24/7 skill nursing care.
thus speakith Monty the troll:

QUOTE
Did you read my recent post here, "Using basic logic to understand
"HIV/AIDS."" ?

They have abandoned logic, even at the most basic level. We are
beyond
the Emperor's New Clothes now. In this case, the "Emperor" has no
kingdom, aside from the asylum and his fellow inmates, whom he calls
his
"subjects." Like all periods of fanaticism, this one will come to an
end
at some point, and historians like myself will write about it in very
similar terms as they do now the witchcraft fears of the sixteenth and
seventeenth centuries in Europe. Being heavily "invested" in a notion
is quite similar to insanity, and many of us realize this in politics
these days, but when it comes to what is considered "science," it is
much easier to convince the public that "white is black" and "black is
white." Thus, it will take longer for the deadly "HIV=AIDS=DEATH"
house
of cards to crumble than it does for incompetent, ideological-minded
politicians to be voted out of office. If you have yet to do so, I
explain what the best explanation for "HIV/AIDS" is on my web site:
http://groups.msn.com/TheScientificDebateForum-/ I quote the "virus
hunters" directly, and I also cite numerous studies from the
scientific
literature.
/QUOTE



 




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