Studies On Thyroid Suppression By PUFA

EndAllDisease

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Dr. Peat has said, “Unsaturated oils block thyroid hormone secretion, its movement in the circulatory system, and the response of tissues to the hormone.”

I'm having difficulty finding evidence for these effects.
Does anybody have any evidence showing:
1. PUFA blocks thyroid secretion
2. PUFA blocks thyroid circulation
3. PUFA blocks tissues responses to thyroid
 
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EndAllDisease

EndAllDisease

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I've found the most efficient way to look for studies is to go to a search engine and try searches like 'pufa thyroid secretion', 'ala thyroid secretion,' 'unsaturated fat thyroid' but I haven't been able to find anything on this.

I've also searched Ray's articles where he speaks of this, and read through the fantastic collection of info on functionalps, but nobody talking about this seems to have ever referenced it.
 

livesimply

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I don't know if there are any other articles here ray peat articles that are NOT at functionalps, but it's worth a try!
 
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EndAllDisease

EndAllDisease

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You're right Ray Peat article's aren't there, but he's assembled one hell of a database of quotes from Ray and included many studies to back up his assertions at the bottom of each page; for example: http://www.functionalps.com/blog/2012/04/22/fatty-acid-composition-of-diet-reflected-in-fat-tissue/

Anyway, anybody have any evidence of pufa suppressing thyroid production, transport and utilization? I'm beginning to think the only way to evidence this is indirectly by looking at the high metabolisms of efa deficient animals.
 
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EndAllDisease

EndAllDisease

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YES!!!! Thank you so much that forefront health article has scientific evidence for all three steps! I appreciate both of your links thanks again guys.
 

marteagal

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A few weeks ago, I, like you, was in desperate need of those references, and the forefronthealth site was a good starting point! During my search, I found additionally references. Some are taken from bibliographies of other RP-inspired websites.

"Safflower oil was more effective than tallow as a repressor of T3 action. The effect of dietary fat, particularly safflower oil, was to increase the amount of T3 required to induce the activity of lipogenic enzymes. [...] These data support the hypothesis that polyunsaturated fats uniquely suppress the gene expression of lipogenic enzymes by functioning as competitive inhibitors of T3 action, possibly at the nuclear receptor level." (Clarke & Hembree (1990) Inhibition of triiodothyronine's induction of rat liver lipogenic enzymes by dietary fat)

"The increased serum level of rT3, which is a metabolically inactive degradation product of T4, may result from a preferential conversion of T4 to rT3 due to its metabolic changes in some tissues in the fish oil-fed group. This may be supported by our previous finding of increaed biliary excretion of rT3 during the infusion of linoleic acid.25 Such findings might be related to the decreased activity of malic enzyme (Table 5) and decreased T3 binding to the liver nuclear receptors (Figures 2 and 4)." (Knopp et al. (1992) Triiodothyronine receptors and malic enzyme activity in liver of rats fed fish oil or cooca butter)

"We have recently demonstrated that unsaturated fatty acids are potent inhibitors of nuclear T3 binding [3]. The aim of the present study was to elucidate further the mechanism by which unsaturated fatty acids inhibit the binding of T3 to its nuclear receptor. Oleic acid was used as a representative fatty acid [3]. [...] The competitive nature of the binding inhibition by oleic acid suggests that the fatty acid competes directly with T3 for the same binding site on the nuclear receptor. However, competitive inhibition is also compatible with an allosteric hindrance of the ligand-receptor binding [8]. Because the inhibitory effect of unsaturated fatty acids is not limited to the T3 receptor, we consider an allosteric hindrance of nuclear T3 binding by oleic acid as the most likely explanation." (van der Klis et al. (1989) Studies on the mechanism of inhibition of nuclear triiodothyronine binding by fatty acids)

"We have previously shown that unsaturated fatty acids are potent inhibitors of nuclear T, binding in vitro by decreasing the affinity constant of the binding of T3 to its receptors (Wiersinga et al., 1988). [...] The potency of unsaturated fatty acids for INB [Inhibition of Nuclear T3 Binding] was greater than of saturated fatty acids, and increased with the number of double bonds. This again is similar to the greater inhibitory effect of unsaturated than of saturated fatty acids on the binding of angiotensin II, tamoxifen and estradiol to their specific receptors (Goodfriend and Ball, 1986; Hwang, 1986; Vallette et al., 1988). [...] It can be hypothesized that fatty acids interact with receptor hydrophobic sites, resulting in conformational changes of the nuclear T3 receptor and a lower affinity for T3. (Wiersinga & Schiphorst (1990) Inhibition of nuclear T3, binding by fatty acids - Dependence on chain length, unsaturated bonds, Cis-trans configuration and esterification)

"The effects of selected fatty acids (linoleic, oleic, and palmitic) on triiodothyronine (T3)-receptor binding were compared in isolated rat hepatocytes, rat liver nuclei, and receptor protein. Scatchard analysis indicated that the inhibition of T3-receptor binding by fatty acids was characterized by an increase in Kd and no change in maximum binding capacity (MBC). In isolated receptors, the rank order of potency for inhibition was linoleic acid greater than oleic acid greater than palmitic acid." (Mazzachi (1992) Effect of Fatty Acids on Rat Liver Nuclear T3-Receptor Binding) But the authors also say: "However, in vivo it seems unlikely that fatty acids will have access to the nuclear receptors in sufficiently high concentrations to affect T3-receptor binding in liver cells."

Well, I hope this helps.
 
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