Thyroid hormone increases anti-oxidant enzymes, glucocorticoids lower them

[Mauritio]

In this study they looked at the influence of certain hormones (thyroid hormone, insulin and glucocorticoids) on certain anti-oxidant enzymes (SOD, catalase, glutathione peroxidase).

They showed that thyroid increased catalase and superoxide dismutase, while glucocorticoids lower them.

Thyroid did not increase glutathione peroxidase.Insulin on the other hand increased glutathione (and the other antioxidants as well), but it also caused more hydrogen peroxide production.

Thyroid also caused the rats to produce less h2o2 to begin with , which of course requires less antioxidants and causes less oxidative damage.

Basically: peat right again. Thyroid lowers the bad stuff and increases the good stuff, while cortisol does the opposite.

Interestingly one of those enzymes, catalase , is correlated with life expectancy and in a study in mice the overexpression of that enzyme caused an increase of about 20% in median and maximum life expectancy.
(Overexpression of catalase targeted to mitochondria attenuates murine cardiac aging)




"Insulin increased the activities of CuZn-SOD, catalase, and GPX and reduced that of Mn-SOD. Thyroid hormones raised the activities of CuZn- and Mn-SOD and decreased that of GPX, whereas glucocorticoids reduced both Mn-SOD and GPX. The removal of the adrenal medulla caused a decrease of Mn-SOD and GPX activities in the macrophages. Hydrogen peroxide production was increased by insulin and reduced by thyroid hormones and glucocorticoids. The changes in antioxidant enzyme activities caused by these hormones in macrophages may indicate important mechanisms for the establishment of impaired immune function in endocrine pathologies."
- Hormonal regulation of superoxide dismutase, catalase, and glutathione peroxidase activities in rat macrophages - PubMed

 

[Mauritio]

Ray Peat on thyroid as an anti-oxidant.


View: https://youtu.be/DAmdFDWjkVM

 

[NewACC]

In this study they looked at the influence of certain hormones (thyroid hormone, insulin and glucocorticoids) on certain anti-oxidant enzymes (SOD, catalase, glutathione peroxidase).

They showed that thyroid increased catalase and superoxide dismutase, while glucocorticoids lower them.

Thyroid did not increase glutathione peroxidase.Insulin on the other hand increased glutathione (and the other antioxidants as well), but it also caused more hydrogen peroxide production.

Thyroid also caused the rats to produce less h2o2 to begin with , which of course requires less antioxidants and causes less oxidative damage.

Basically: peat right again. Thyroid lowers the bad stuff and increases the good stuff, while cortisol does the opposite.

Interestingly one of those enzymes, catalase , is correlated with life expectancy and in a study in mice the overexpression of that enzyme caused an increase of about 20% in median and maximum life expectancy.
(Overexpression of catalase targeted to mitochondria attenuates murine cardiac aging)




"Insulin increased the activities of CuZn-SOD, catalase, and GPX and reduced that of Mn-SOD. Thyroid hormones raised the activities of CuZn- and Mn-SOD and decreased that of GPX, whereas glucocorticoids reduced both Mn-SOD and GPX. The removal of the adrenal medulla caused a decrease of Mn-SOD and GPX activities in the macrophages. Hydrogen peroxide production was increased by insulin and reduced by thyroid hormones and glucocorticoids. The changes in antioxidant enzyme activities caused by these hormones in macrophages may indicate important mechanisms for the establishment of impaired immune function in endocrine pathologies."
- Hormonal regulation of superoxide dismutase, catalase, and glutathione peroxidase activities in rat macrophages - PubMed

although the full range of effects of liothyronine is simply shocking, the properties of caffeine are no less surprising. Thus, isolated caffeine has a twofold greater antioxidant effect against the formation of iron and PUFA peroxides, PUFA and oxygen peroxides and an increase in antioxidant enzymes in the liver and brain equivalent to the thyroid gland in humans. Also, a medium dose of caffeine can increase RMR by 10-12%, which is also twice as high as the thyroid in eutheriods. Although the key may be that studies are not conducted with isolated t3 and in truly hypothyroid people, and if a person is euthyroid, then caffeine is the preferred to thyroid supplement.

 

[Mauritio]

although the full range of effects of liothyronine is simply shocking, the properties of caffeine are no less surprising. Thus, isolated caffeine has a twofold greater antioxidant effect against the formation of iron and PUFA peroxides, PUFA and oxygen peroxides and an increase in antioxidant enzymes in the liver and brain equivalent to the thyroid gland in humans. Also, a medium dose of caffeine can increase RMR by 10-12%, which is also twice as high as the thyroid in eutheriods. Although the key may be that studies are not conducted with isolated t3 and in truly hypothyroid people, and if a person is euthyroid, then caffeine is the preferred to thyroid supplement.

That's debatable.
Caffeine simply doesn't work for everybody ,even Peat said that and it increases adrenergic tone, while thyroid does the opposite. And who said you can't use both ? I think they're synergistic.

 

[NewACC]

That's debatable.
Caffeine simply doesn't work for everybody ,even Peat said that and it increases adrenergic tone, while thyroid does the opposite. And who said you can't use both ? I think they're synergistic.

Yeah, and I wanted to comment that caffeine is in many ways similar to the thyroid gland and each of them has unique and amazing properties and for each person their effectiveness will vary greatly, for example, I have always tolerated caffeine much worse than the thyroid supplement and, in addition to liver health, I haven't felt most of the effects that t3 has. In any case, caffeine is definitely not an indispensable substance, albeit with a huge track record of well-studied effects, while it never cured my hypothyroidism and I always found the thyroid to be a much more active and useful supplement, although, as you said, nothing cancels their simultaneous use

 

[NewACC]

That's debatable.
Caffeine simply doesn't work for everybody ,even Peat said that and it increases adrenergic tone, while thyroid does the opposite. And who said you can't use both ? I think they're synergistic.

Also, @haidut suggested that caffeine could help transport T3 even into cells full of polyunsaturated fatty acids, and aspirin also works. By the way, it would be pretty good if @haidut added some caffeine to the transdermal t3. Moreover, thyroid hormones are very important regulators of the level of PUFA in cellular lipids and the higher they (thyroid hormones) are, the lower the level of n-6 and n-3 and the higher the level of monounsaturated fatty acids and the synthesis of Mead's acid in membrane lipids is. Quite similar to the effect of androgens, zinc and vitamin b6 - they are all POWERFUL negative regulators of PUFA in cellular lipids (that is, they reduce the level of n-6 and n-3), well, vitamin E, but it can only saturate PUFA's in adipose tissue only when applied topically or saturate PUFA's in plasma and intestines when administered orally

 

[Mauritio]

Also, @haidut suggested that caffeine could help transport T3 even into cells full of polyunsaturated fatty acids, and aspirin also works. By the way, it would be pretty good if @haidut added some caffeine to the transdermal t3. Moreover, thyroid hormones are very important regulators of the level of PUFA in cellular lipids and the higher they (thyroid hormones) are, the lower the level of n-6 and n-3 and the higher the level of monounsaturated fatty acids and the synthesis of Mead's acid in membrane lipids is. Quite similar to the effect of androgens, zinc and vitamin b6 - they are all POWERFUL negative regulators of PUFA in cellular lipids (that is, they reduce the level of n-6 and n-3), well, vitamin E, but it can only saturate PUFA's in adipose tissue only when applied topically or saturate PUFA's in plasma and intestines when administered orally

You can just add some caffeine to your t3 yourself .

Do you have any sources on those compounds effects on membrane saturation ?

 

[NewACC]

You can just add some caffeine to your t3 yourself .

Do you have any sources on those compounds effects on membrane saturation ?

Yeah, here they are:

Administration of dehydroepiandrosterone enanthate to oophorectomized women--effects on sex hormones and lipid metabolism - PubMed

Eight bilaterally oophorectomized women were given a depot injection of 200 mg DHEA-enanthate to study the effect on endocrine and lipid metabolism. A decrease in sex-hormone binding globulin (SHBG) and an increase in androstenedione was found 14 and 30 days after the injection. No changes could...

www.ncbi.nlm.nih.gov

"...More marked changes were found in the relative fatty acid composition of cholesterol esters, with a decrease in the essential fatty acids linoleic and arachidonic and an increase in non-essential palmitic and oleic acids. In a comparative study between post-menopausal and amenorrhoeic women, women with amenorrhoea were found to have higher levels of testosterone and androstenedione and lower SHBG compared to post menopausal women. Also in this study the essential fatty acids were lower (G. Samsioe and L. Hamberger, to be published). It is therefore suggested that androgens induce changes mainly in the fatty acid composition of cholesterol esters."

Contribution of Brain Tissue Oxidative Damage in Hypothyroidism-associated Learning and Memory Impairments

The brain is a critical target organ for thyroid hormones, and modifications in memory and cognition happen with thyroid dysfunction. The exact mechanisms underlying learning and memory impairments due to hypothyroidism have not been understood yet. Therefore, ...

www.ncbi.nlm.nih.gov

"Hypothyroidism increases the levels of polyunsaturated n − 3 and n − 6 series (e.g., 22: 6n − 3 and 18: 2n − 6) and decreases the levels of monosaturated n − 7 and n − 9 fatty acids.[31] In addition, the change in plasma membrane composition could, in turn, modify the activity of the Na+/K+-ATPase as well as other transmembrane ion exchangers.[103] In fact, it has been described as the reduction of Na+/K+-ATPase activity in the hippocampus of hypothyroid rats.[104,105] The decrease in enzymatic activity might alter the sodium/potassium transmembranal gradient and diminish the uptake of the neurotransmitter glutamate[106] or stimulate the reversed uptake of glutamate.[107] This increase could, in turn, produce mitochondrial calcium overload, decline ATP production, and activate calcium-dependent phospholipases, proteases, and endonucleases.[108] Those biochemical events may increase ROS production and as a result, the lipid peroxidation.[109]”

Accumulation of linoleic and gamma-linolenic acids in tissue lipids of pyridoxine-deficient rats - PubMed

Young male Sprague-Dawley rats were fed diets containing added pyridoxine . HCl at 22 mg/kg (control), 0 mg/kg or 88 mg/kg for 6 weeks. In comparison with control or pyridoxine-supplemented (+PN) rats, growth of the pyridoxine-deficient (-PN) rats was significantly less after 2 weeks. After 6...

pubmed.ncbi.nlm.nih.gov

"...In -PN rats, phospholipid levels of linoleic and gamma-linolenic acids were increased, but arachidonic acid was decreased compared to controls in plasma, liver, thymus and skin. In liver triglycerides from -PN rats, all essential fatty acids (n3 and n6) were increased compared to both control and +PN rats. The n3 essential fatty acids were significantly increased in plasma, liver, and thymus phospholipids in the +PN compared to control rats. These results support previous reports of an effect of pyridoxine on essential fatty acid metabolism and suggest that both linoleic desaturation and gamma-linolenic acid elongation may be impaired in -PN rats. In addition, the accumulation of essential fatty acids in the liver triglycerides of -PN rats suggests that essential fatty acid turnover between triglyceride and phospholipid may be influenced by pyridoxine."

Essential fatty acids in tissue phospholipids and triglycerides of the zinc-deficient rat - PubMed

This study addressed the possibility that zinc deficiency has different effects on the fatty acid composition of triglyceride compared to total phospholipid. Male weanling Sprague-Dawley rats were maintained for 6 weeks on a semisynthetic diet deficient in zinc (3 mg/kg zinc). Control rats (40...

pubmed.ncbi.nlm.nih.gov

"In zinc-deficient rats, the percentage of linoleic acid was increased or that of arachidonic acid was decreased in total phospholipids of plasma, liver, and testis, and in skin total lipids. Saturated and monounsaturated fatty acids were increased in the triglyceride of liver but decreased in the triglyceride of epididymal fat of zinc deficient rats. Essential fatty acids, as a proportion of total fatty acids, were decreased in triglyceride of liver but increased in triglyceride of epididymal fat of zinc-deficient rats."

Dietary fat influences the effect of zinc deficiency on liver lipids and fatty acids in rats force-fed equal quantities of diet - PubMed

Previous studies showed that zinc deficiency influences the fatty acid composition of rat tissues, but the influence of dietary fat on the effects of zinc deficiency was not considered at that time. The present study was therefore conducted to investigate the effect of zinc deficiency on lipid...

pubmed.ncbi.nlm.nih.gov

"The zinc-deficient rats fed the coconut oil diet developed fatty livers, whereas zinc-deficient animals fed the fish oil diet did not. The zinc-deficient rats in both dietary fat groups had lower levels of linoleic acid, arachidonic acid and total (n-6) fatty acids in the liver phospholipids, especially in the phosphatidylcholine, but greater concentrations of (n-3) fatty acids compared with zinc-adequate controls. We conjecture that zinc deficiency influences incorporation of polyunsaturated fatty acids into phosphatidylcholine. The lower levels of arachidonic acid are replaced in the zinc-deficient animals fed a coconut oil diet by docosapentaenoic and docosahexaenoic acids and in the zinc-deficient animals fed a fish oil diet by eicosapentaenoic acid. The replacement of arachidonic acid by other fatty acids in the phospholipids is likely to have implications for prostaglandin synthesis"

 

[Mauritio]

Yeah, here they are:

Administration of dehydroepiandrosterone enanthate to oophorectomized women--effects on sex hormones and lipid metabolism - PubMed

Eight bilaterally oophorectomized women were given a depot injection of 200 mg DHEA-enanthate to study the effect on endocrine and lipid metabolism. A decrease in sex-hormone binding globulin (SHBG) and an increase in androstenedione was found 14 and 30 days after the injection. No changes could...

www.ncbi.nlm.nih.gov

"...More marked changes were found in the relative fatty acid composition of cholesterol esters, with a decrease in the essential fatty acids linoleic and arachidonic and an increase in non-essential palmitic and oleic acids. In a comparative study between post-menopausal and amenorrhoeic women, women with amenorrhoea were found to have higher levels of testosterone and androstenedione and lower SHBG compared to post menopausal women. Also in this study the essential fatty acids were lower (G. Samsioe and L. Hamberger, to be published). It is therefore suggested that androgens induce changes mainly in the fatty acid composition of cholesterol esters."

Contribution of Brain Tissue Oxidative Damage in Hypothyroidism-associated Learning and Memory Impairments

The brain is a critical target organ for thyroid hormones, and modifications in memory and cognition happen with thyroid dysfunction. The exact mechanisms underlying learning and memory impairments due to hypothyroidism have not been understood yet. Therefore, ...

www.ncbi.nlm.nih.gov

"Hypothyroidism increases the levels of polyunsaturated n − 3 and n − 6 series (e.g., 22: 6n − 3 and 18: 2n − 6) and decreases the levels of monosaturated n − 7 and n − 9 fatty acids.[31] In addition, the change in plasma membrane composition could, in turn, modify the activity of the Na+/K+-ATPase as well as other transmembrane ion exchangers.[103] In fact, it has been described as the reduction of Na+/K+-ATPase activity in the hippocampus of hypothyroid rats.[104,105] The decrease in enzymatic activity might alter the sodium/potassium transmembranal gradient and diminish the uptake of the neurotransmitter glutamate[106] or stimulate the reversed uptake of glutamate.[107] This increase could, in turn, produce mitochondrial calcium overload, decline ATP production, and activate calcium-dependent phospholipases, proteases, and endonucleases.[108] Those biochemical events may increase ROS production and as a result, the lipid peroxidation.[109]”

Accumulation of linoleic and gamma-linolenic acids in tissue lipids of pyridoxine-deficient rats - PubMed

Young male Sprague-Dawley rats were fed diets containing added pyridoxine . HCl at 22 mg/kg (control), 0 mg/kg or 88 mg/kg for 6 weeks. In comparison with control or pyridoxine-supplemented (+PN) rats, growth of the pyridoxine-deficient (-PN) rats was significantly less after 2 weeks. After 6...

pubmed.ncbi.nlm.nih.gov

"...In -PN rats, phospholipid levels of linoleic and gamma-linolenic acids were increased, but arachidonic acid was decreased compared to controls in plasma, liver, thymus and skin. In liver triglycerides from -PN rats, all essential fatty acids (n3 and n6) were increased compared to both control and +PN rats. The n3 essential fatty acids were significantly increased in plasma, liver, and thymus phospholipids in the +PN compared to control rats. These results support previous reports of an effect of pyridoxine on essential fatty acid metabolism and suggest that both linoleic desaturation and gamma-linolenic acid elongation may be impaired in -PN rats. In addition, the accumulation of essential fatty acids in the liver triglycerides of -PN rats suggests that essential fatty acid turnover between triglyceride and phospholipid may be influenced by pyridoxine."

Essential fatty acids in tissue phospholipids and triglycerides of the zinc-deficient rat - PubMed

This study addressed the possibility that zinc deficiency has different effects on the fatty acid composition of triglyceride compared to total phospholipid. Male weanling Sprague-Dawley rats were maintained for 6 weeks on a semisynthetic diet deficient in zinc (3 mg/kg zinc). Control rats (40...

pubmed.ncbi.nlm.nih.gov

"In zinc-deficient rats, the percentage of linoleic acid was increased or that of arachidonic acid was decreased in total phospholipids of plasma, liver, and testis, and in skin total lipids. Saturated and monounsaturated fatty acids were increased in the triglyceride of liver but decreased in the triglyceride of epididymal fat of zinc deficient rats. Essential fatty acids, as a proportion of total fatty acids, were decreased in triglyceride of liver but increased in triglyceride of epididymal fat of zinc-deficient rats."

Dietary fat influences the effect of zinc deficiency on liver lipids and fatty acids in rats force-fed equal quantities of diet - PubMed

Previous studies showed that zinc deficiency influences the fatty acid composition of rat tissues, but the influence of dietary fat on the effects of zinc deficiency was not considered at that time. The present study was therefore conducted to investigate the effect of zinc deficiency on lipid...

pubmed.ncbi.nlm.nih.gov

"The zinc-deficient rats fed the coconut oil diet developed fatty livers, whereas zinc-deficient animals fed the fish oil diet did not. The zinc-deficient rats in both dietary fat groups had lower levels of linoleic acid, arachidonic acid and total (n-6) fatty acids in the liver phospholipids, especially in the phosphatidylcholine, but greater concentrations of (n-3) fatty acids compared with zinc-adequate controls. We conjecture that zinc deficiency influences incorporation of polyunsaturated fatty acids into phosphatidylcholine. The lower levels of arachidonic acid are replaced in the zinc-deficient animals fed a coconut oil diet by docosapentaenoic and docosahexaenoic acids and in the zinc-deficient animals fed a fish oil diet by eicosapentaenoic acid. The replacement of arachidonic acid by other fatty acids in the phospholipids is likely to have implications for prostaglandin synthesis"

Thanks very interesting!