2016 Study On Alpha Lipoic Acids Effects On Thyroid

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I think all antioxidants would do that...
 

thegiantess

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I'm not sure he would be against it if you are "pretreated with H2O2" :ss
 
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Drareg

Drareg

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It's interesting that the h2o2 could be increasing to fend off virus/bacteria/ stress.
I'm more concerned with the epigentics of it, if your predisposed to react strongly to any stressor. When we look at from this angle it's just as plausible that ALA will increase rt3?

The DIO3 enzyme is really interesting.
 
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Well vitamin E, taurine... sounds like there would be plenty of free radical breakers that are Ray Peat... of course he would tell you that without PUFA you shouldn't have to worry in the first place.
 

Nighteyes

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Yes the idea is to efficiently deal with free radicals and keep the cell in an oxidized state through vitamin E, Ascorbic acid as mentioned by Such, not bombard it with anti-oxidants which are not beneficial. One of the most reduced states the cell can be in is in cancer where the NAD to NADH ratio is almost 1:1... in normal cells this ratio is hundreds of times in favor of the oxidized state.
 

Koveras

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Older study shower the opposite (although I can't access the full text, and it doesn't specify humans - only assuming)

Effect of alpha-lipoic acid on the peripheral conversion of thyroxine to triiodothyronine and on serum lipid-, protein- and glucose levels. - PubMed - NCBI

Then this study in pigs does support a positive effect on thyroid function

Effects of Dietary L-carnosine and Alpha-lipoic Acid on Growth Performance, Blood Thyroid Hormones and Lipid Profiles in Finishing Pigs. - PubMed - NCBI

This discussion also brings up again whether serum levels are correlates of tissues levels
 
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They didn't use hydrogen peroxide. It's different things.
 

Koveras

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They didn't use hydrogen peroxide. It's different things.

Cells are regularly exposed to hydrogen peroxide.

"In a biological context, ROS are formed as a natural byproduct of the normal metabolism of oxygen.

The reduction of molecular oxygen (O2) produces superoxide (·O2−) and is the precursor of most other reactive oxygen species

O2 + e− → ·O2−

Dismutation of superoxide produces hydrogen peroxide (H2O2)

2H+ + ·O2− + ·O2− → H2O2 + O2"
 
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Cells are regularly exposed to hydrogen peroxide.

"In a biological context, ROS are formed as a natural byproduct of the normal metabolism of oxygen.

The reduction of molecular oxygen (O2) produces superoxide (·O2−) and is the precursor of most other reactive oxygen species

O2 + e− → ·O2−

Dismutation of superoxide produces hydrogen peroxide (H2O2)

2H+ + ·O2− + ·O2− → H2O2 + O2"

Yeah but oxidative stress to the point of blocking deiodinase isn't exactly physiological. Hence the pretreatment to bring it about experimentally.
 

Koveras

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Yeah but oxidative stress to the point of blocking deiodinase isn't exactly physiological. Hence the pretreatment to bring it about experimentally.

Figured it had more to do with it being a cell culture rather than a living being (although to your point the relevance/transfer is still open ended).

Could be physiological depending on an individuals overall oxidative status/stress, or maybe for individuals with impaired SOD activity or production.
 

Koveras

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Figured it had more to do with it being a cell culture rather than a living being (although to your point the relevance/transfer is still open ended).

Could be physiological depending on an individuals overall oxidative status/stress, or maybe for individuals with impaired SOD activity or production.

For example:

" Many studies have shown that diabetes mellitus (type 1 and 2) is associated with increased formation of free radicals and decreased antioxidant potential, leading to oxidative damage of cell components [10]. Direct evidence of oxidative stress in diabetes is provided by the measurement of oxidative stress markers such as plasma and urinary F2-isoprostane as well as plasma and tissue levels of nitrotyrosine and superoxide radicals (O2•–) [11–13]. There are multiple sources of oxidative stress in diabetes, including nonenzymatic, enzymatic and mitochondrial pathways."
 

Koveras

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"In the thyroid gland, H2O2 is generated in response to thyrotropin (TSH) stimulation and is necessary for thyroglobulin iodination by the enzyme thyroid peroxidase and thus for thyroxine (T4) synthesis [247]. However, excess H2O2 has been shown to inactivate thyroid peroxidase [248] and leads to an increased rate of thyroid cell necrosis and invasion of macrophages [249,250]."
 

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