Re: This negative aricle about Antioxidants appeared in the Lancet

From: Robert (RobertJ_at_hotmail.com)
Date: 10/23/04 

Date: Fri, 22 Oct 2004 23:53:37 -0700

"peterb" <peterb@mytrashmail.com> wrote in message
news:a25cdd6c.0410222049.26e727e7@posting.google.com...
> "Dr. Zarkov" <Ming@Mongo.com> wrote in message
news:<kLydndNzOPQk-uTcRVn-rQ@rcn.net>...
> > "peterb" <peterb@mytrashmail.com> wrote...
> > > "Dr. Zarkov" <Ming@Mongo.com> wrote>...
> > > > "peterb" <peterb@mytrashmail.com> wrote...
> > > > > "Michael C Price" <michaelEXCISESPAMprice@ntlworld.com> wrote >...
> > > > > > "peterb" <peterb@mytrashmail.com> wrote in message
> > > > > >
> > ...
> > > > > Can you name any synthetic chemicals that are beneficial to human
> > > > > health? A few are indeed useful in short-term, crisis health
care,
> > > > > however I'm not referring to short-term exposures during medical
> > > > > interventions that might forestall death. Rather, I'm referring
to
> > > > > long-term effects that I believe are linked to disease progression
> > > > > over a lifetime of exposure. Examples are food additives,
fluoride,
> > > > > hydrocarbons, pesticides, PFOAS, pcbs, and phlalates.
Consequently, I
> > > > > don't accept that these are variably "good" or "bad" depending on
> > > > > levels of exposure. They are *ALL* bad, all the time, simply less
so
> > > > > in minimal doses.
> > > >
> > > >
> > > > Medications administered for chronic conditions like hypertension
are
> > often
> > > > if not usually synthetic. And some synthetic food additives may
well be
> > > > beneficial. Some syntheitic antioxidants extend lifespan in
animals.
> > It
> > > > depends on the dose and the substance.
> > > >
> > > >
> > > > > > Look at selenium -- it has good effects at some levels and is
also
> > > > > > toxic at other levels *and* these levels probably overlap.
> > > > >
> > > > > I think education is so absent on this subject that you have to
start
> > > > > with what *IS* simple. Very few people think like chemists. One
> > > > > reason I responded to your earlier comments was because I wanted
you
> > > > > to clarify how you implicated nutrients in cancer. I don't think
> > > > > anyone has been particularly confused by any comments I've made
about
> > > > > the toxic affects of man-made chemicals. The only detractors I've
had
> > > > > so far are industry goons riding shotgun.
> > ...
> > > > > A summary of my thinking, in case it helps:
> > > > >
> > > > > 1. All synthetic chemicals are foreign to human physiology and
> > > > > therefore toxic.
> > > > > 2. No human has an evolved metabolic response to synthetic
chemicals.
> > > > ...
> > > >
> > > > That simply is not true. Humans have evolved a number of defense
and
> > > > detoxification mechanisms for foreign (including many synthetic)
> > chemicals.
> > >
> > > You are confusing immunology with metabolization. In that regard, the
> > > response is a direct attempt to prevent metabolic errors in the first
> > > place.
> >
> >
> > You are changing the point from your assertion that "All synthetic
chemicals
> > are foreign to human physiology and therefore toxic."
>
> No, I'm saying that an evolved metabolic response that breaks down
> nutrients for energy is different than an immune response that
> attempts to neutralize a foreign agent. It's the fact that the
> initial response fails that metabolic errors can then occur.
>
> > For that matter,
> > detoxification is not the same as an immune response.
>
> > Any response to neutralize an antigen, even a synthetic one, is an
immune response.
>
> > But the point is the
> > same: foreign chemicals (including synthetics) are neutralized and
> > eliminated.
>
> Like the body neutralizes tobacco so that smokers don't get lung
> cancer any more often than the rest of us? Don't be a fool.
>
> > Not every single type, of course, natural or synthetic.
>
> Not *ANY* single type with 100% success unless exposure is short term.
>
> > But synthetic substances do not have a chemistry from another
universe...
>
> Your body has no concept for "another universe"; it only knows the
> difference between a toxin and a nutrient. Your genes are the genes of
> ancestors one million years old; as far as "they" are concerned,
> man-made chemicals are as foreign as a microbe from another planet.
>
> > they share the same chemical groups as natural substances.
>
> Human physiology does not recognize synthetic chemicals simply because
> they are recombinations of existing molecules. Otherwise, Vioxx would
> have been utilized as a nutrient rather than resisted as a poison.

You are way overstating human physiology as somehow being able to discern a
poison from non poison or useful metabolite. Enzyme systems are stupid and
act on substrates with similar chemical structures. Ethanol is deadly only
with large volumes while methanol can cause blindness and toxicity far
beyond ethanol.
You can have harmless natural plant compounds converted via CytoC Oxyd P450
into a deadly oxidized metabolite as in mushrooms.
The biochemistry is to eliminate chemicals through biotransformation into
water soluble forms ie urine and sweat or bile form ie GI. It can take a
harmless chemical and convert it into a deadly compound because it is trying
to eliminate it.
It's not the body utilizing nutrient versus a poison but enzyme systems
acting on substrates of what ever is out there.
Don't ingest a toxin and expect the body to know the difference.
Synthetics such as mannitol which is non metabolized can be hung IV and
cause a diuresis to maintain the renal tubules open and prevent renal
failure or maintain a high osmotic gradient for brain injuries to minimize
brain swelling.

Semin Cancer Biol. 2004 Dec;14(6):473-86. Related Articles, Links

Environmental and chemical carcinogenesis.

Wogan GN, Hecht SS, Felton JS, Conney AH, Loeb LA.
Biological Engineering Division, Massachusetts Institute of Technology, Room
26-009, Cambridge, MA 02139, USA.

Excerpt
This approach can be applied to evaluation of other environmental
carcinogens, and the evaluations would be markedly facilitated by
prospective epidemiologic studies incorporating phenotypic
carcinogen-specific biomarkers. Heterocyclic amines represent an important
class of carcinogens in foods. They are mutagens and carcinogens at numerous
organ sites in experimental animals, are produced when meats are heated
above 180 degrees C for long periods. Four of these compounds can
consistently be identified in well-done meat products from the North
American diet, and although a causal linkage has not been established, a
majority of epidemiology studies have linked consumption of well-done meat
products to cancer of the colon, breast and stomach. Studies employing
molecular biomarkers suggest that individuals may differ in their
susceptibility to these carcinogens, and genetic polymorphisms may
contribute to this variability. Heterocyclic amines, like most other
chemical carcinogens, are not carcinogenic per se but must be metabolized by
a family of cytochrome P450 enzymes to chemically reactive electrophiles
prior to reacting with DNA to initiate a carcinogenic response. These same
cytochrome P450 enzymes-as well as enzymes that act on the metabolic
products of the cytochromes P450 (e.g. glucuronyl transferase, glutathione
S-transferase and others)-also metabolize chemicals by inactivation
pathways, and the relative amounts of activation and detoxification will
determine whether a chemical is carcinogenic. Because both genetic and
environmental factors influence the levels of enzymes that metabolically
activate and detoxify chemicals, they can also influence carcinogenic risk.
Many of the phenotypes of cancer cells can be the result of mutations, i.e.,
changes in the nucleotide sequence of DNA that accumulate as tumors
progress. These can arise as a result of DNA damage or by the incorporation
of non-complementary nucleotides during DNA synthetic processes. Based upon
the disparity between the infrequency of spontaneous mutations and the large
numbers of mutations reported in human tumors, it has been postulated that
cancers must exhibit a mutator phenotype, which would represent an early
event in cancer progression. A mutator phenotype could be generated by
mutations in genes that normally function to guarantee genetic stability.
These mutations presumably arise via DNA damage by environmental or
endogenous agents, but it remains to be determined whether the acquisition
of a mutator phenotype is a necessary event during tumor progression.

PMID: 15489140 [PubMed - in process]

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