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From: Kofi on 5 Aug 2008 06:40
I haven't had a chance to read through all of this, but I'll chip in
what I know. Many pesticides are removed from the body via
metallothionein (MT), which also removes mercury and other heavy metals.
Constant chronic mercury poisoning depletes MT and also depletes
molybdenum, given how much of the mineral winds up in MT. MT expression
is also regulated by histone acetylation. More butyrate=more
metallothionein - both because butyrate shares a common chemical
backbone with MT and because butyrate is a histone acetylator.
Butyrate, in turn, cannot be metabolized without adequate levels of
carnitine (which may account for the reason men appear more resilient to
autoimmune diseases; they have greater carnitine levels). If you've
read my previous postings on these threads, you know that certain
viruses can downregulate MT. Problems with OCTN1 (the ergothioneine
transporter) or OCTN2 (the carnitine transporter) - due to either
genetics or injury - can also affect components in MT and are associated
with inflammatory bowel problems. To make things worse, mercury is an
antibiotic and friendly gut bacteria produce butyrate.

Metallothionein is produced at the end of a pathway triggered by
gut-protective HIF-1a. Innate antimicrobials/antiinflammatory factors
like cathelicidin can be found along this pathway and vitamin D3
activates HIF-1a, making it crucial for gut detoxification.
Cathelicidin, EPO, metallothionein and sometimes VEGF all lie downstream
of HIF-1. Vitamin D3 and butyrate also activate regulatory T-cells and
synergystically stimulate innate immunity.

Notice how often the methylator betaine (trimethylglycine) comes up in
this network:

+ carnitine is gamma-trimethyl-beta-hydroxybutyrobetaine; transported
via OCTN2

+ ergothioneine - the betaine of a sulfur-containing derivative of
histidine; also known as thiolhistidylbetaine
(2-thiol-L-histidine-betaine) and thioneine/thionein; transported via
OCTN1

+ thionein is the apoprotein of metallothionein; an apoprotein is a
polypeptide chain that has not yet formed a complex with the prosthetic
group (non-amino acid compound attached to a protein) required to form
the active holoprotein; MT is made of a prosthetic group attached to
ergothioneine (aka thioneine/thionein)

With regards to pesticide toxicity, what comes first? Does overexposure
to toxins tax the detox pathway causing IBD or do preexisting defects in
gut detoxification trigger an over-reaction to pesticides that results
in IBD? If it's the former, then anyone can be pushed into getting IBD.
If it's the later, then only certain vulnerable individuals will be
adversely affected from a given level of exposure - which is what you
see among veterans developing Gulf War syndrome.

Since viruses can cause some of these detox defects (see my posts on
heart failure), do you get the toxic exposure first which weakens the
network leading to an opportunistic viral infection or does the viral
infection happen first, depressing the detox pathways and leading to the
toxin accumulation? Why choose one versus the other? Once you've got
the problem, you've got to tackle all ends of it at once.
From: Beez on 5 Aug 2008 13:34
Hey, Kofi, do you supplement with carnitine? I think I've read before
that you do supplement with butyrate...

Thanks,
Dave
From: Kofi on 6 Aug 2008 09:54
> Hey, Kofi, do you supplement with carnitine? I think I've read before
> that you do supplement with butyrate...

Yeah. You have to use the two together. Lately I've found that glycine
Proprionyl-l-carnitine ("Mitocarnitine") works better than plain old
L-carnitine.
From: Beez on 6 Aug 2008 12:44
Thanks!
From: jay on 10 Aug 2008 00:30
> I haven't had a chance to read through all of this,
> but I'll chip in what I know.

Thanks Kofi. Your prior suggestions have been helpful.

> Many pesticides are removed from the body via metallothionein (MT),
> which also removes mercury and other heavy metals.

Per your earlier suggestion, I take NAC(w/ molybdenum) along with DMSA
and other supplements.

While pesticides and heavy metals are probably involved, as they
frequently go hand-in-hand (ie as in farm-raised Atlantic Salmon),
dioxins may be the primary factor in my case since I have chloracne.

Pubmed articles indicates dioxin's detrimental effects are produced
moslty by activating the Aryl Hydrocarbon Receptor mediated pathways.
The same pathways may cause my parent, sibling, cousin and uncle's
health issues (breast cancer, chronic bronchitis, CD with ielostomy,
polyneuropathy).

According to pubmed, the continuously activated detoxification enyzmes
can interact with endo/exogenous chemicals including estrogens and
other POPs to produce intermediates that, in some cases are more toxic
than the original, causing cellular stress and DNA damage. Some people
are more susceptible due to genetic polymorphisms.

I have noticed that barbequed meats, but not steamed/cooked meats,
cause significant gut, colon and nerve inflammation. Combustion of
matter (wood, charcoal, diesel, waste, plastics, meat) are strong AhR
activators. And of all the vegetarian foods, soy and soy-containing
foods causes me the most nerve inflammation/irritation. Soy has
phytoestrogens. My past super sensativity to foods and probiotics
could suggest that hyperactive detox causes cellular stress/
inflammation even to healthy foods and beneficial gut bacteria.
Cruciferous veggies are detoxed by same pathway, but dioxins are
thousands of times more potent and persistent.

Below factors may be involved in a wide range of ailments including
Crohn's Disease:
1) POP (esp TCDD) hyperactivates AhR-Mediated Pathways. TCDD has many
other effects including immune modulation.
2) Resulting detox enzymes convert POPs, endo/exogenous estrogens, etc
into toxic intermediates that can cause increased cellular stress to
DNA damage.
3) Some people are more susceptible due to genetic polymorphism in AhR-
mediated pathways.

Is above reasonable?
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