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From: jay on 12 Aug 2008 18:26
> Many pesticides are removed from the body via
> metallothionein (MT), which also removes mercury and other heavy metals ...

Induction of metallothionein in the livers of female Sprague-Dawley
rats treated with TCDD.
Metallothioneins (MTs) are cysteine-rich metal-binding proteins that
exert cytoprotective effects against metal toxicity and external
stimuli including ionizing or ultraviolet B irradiation. Since 2,3,7,8-
tetrachlorodibenzo-p-dioxin (TCDD) is known to cause an exaggerated
oxidative stress response in animals and in different organs, we have
studied possible involvement of MT in the oxidative responses induced
by TCDD. Female Sprague-Dawley (SD) rats (6-week old) were
administered a single oral dose of TCDD that varied from 1.0 to 4.0
microg/kg body weight. The serum and tissues were collected 7 days
after dosing. Indicators of oxidative damage were assessed.
Significant increases in serum 8-hydroxydeoxyguanosine (8-OHdG) levels
were observed in the rats dosed with 2.0 and 4.0 microg TCDD/kg bw.
Only 4.0 microg TCDD/kg bw produced a decrease in reduced glutathione
concentration in the liver. Immunohistochemical staining revealed a
TCDD-induced increase in heme oxygenase-1 (HO-1) expression in the
hepatic macrophages (Kupffer cells). Under these conditions, MT
protein as well as the mRNAs of MT-I and MT-II, were dose-dependently
induced in the liver by TCDD doses from 1.0 microg/kg bw. TCDD-induced
MT was found to localize in the parenchymal cells of the liver. Serum
concentrations of cytokines (TNF-alpha, IL-1beta and IL-6) were not
affected by TCDD. The hepatic concentrations of Cu, Zn and Fe were all
increased significantly by TCDD administration. Our results suggest
that MT levels are increased in the liver upon exposure to TCDD,
perhaps by TCDD-generated reactive oxygen species, and that it may
play a protective role in TCDD-induced oxidative stress responses as
an antioxidant. PMID: 11521753
From: Kofi on 16 Aug 2008 13:40

> 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).
>

FYI, the aryl hydrocarbon receptor is also activated by low-dose
aspirin, so avoid it. You also don't want to eat much BBQ with that
problem (or smoke, for that matter).

> 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.

Yup.

> And of all the vegetarian foods, soy and soy-containing
> foods causes me the most nerve inflammation/irritation. Soy has
> phytoestrogens.

Also might be an antibody to a lectin or something else in it.

> 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.

I don't know. I'd suspect maltodextrin or another common allergen in
the probiotic mix first.

> 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.

#3 is certainly true. It's also possible an infection or low vitamin D3
knocks down your gut detoxification first and then the ambient exposure
becomes problematic.
From: Kofi on 16 Aug 2008 13:42
Forgot to say that deliberately inducing your detoxification pathways
like you're doing via supplementation can lead to a temporary increase
in the toxin burden as it moves out of your system and hits your liver
and kidneys. You really need to monitor that.

Also, don't forget the carnitine/betaine and butyrate/vitamin D3.
They're also important for cell cycle arrest and limiting cancer
development.
From: jay on 16 Aug 2008 16:11
> FYI, the aryl hydrocarbon receptor is also activated by low-dose
> aspirin, so avoid it.

I haven't found an abstract where aspirin activates AhR (and more
importantly is detrimental with TCDD exposure). Are you referring to
the following one? (Only CYP1's are triggered by AhR)

Isozyme-specific induction of low-dose aspirin on cytochrome P450 in
healthy subjects.
The effect of low-dose aspirin on CYPs was enzyme-specific. Both 7-day
and 14-day low-dose aspirin induced the in vivo activities of CYP2C19
but did not affect the activities of CYP1A2, CYP2D6, and CYP2E1. The
effect of low-dose aspirin on CYP3A activity awaits further
confirmation. When low-dose aspirin is used in combination with drugs
that are substrates of CYP2C19, doses of the latter should be adjusted
to ensure their efficacy. PMID: 12621391
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