Hypothyroidism Dramatically Increases Estrogen Synthesis

haidut

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I posted a study some time ago showing the effects of thyroid hormone on synthesis/metabolism of various steroids. Hyperthyroidism increased androgen production several-fold, but the effects on estrogen synthesis were less clear. This study shows that hypothyroidism increases estrogen (estradiol) synthesis several fold. Some people on this forum expressed opinion that estrogen rises in HYPER-thyroidism as a mechanism to suppress thyroid activity - i.e. in a way to rule thyroid in. Well, this study shows otherwise and agrees with Peat. Giving T3 supplement quickly normalized the elevated estrogen levels and brought its synthesis down to normal levels. The increased estrogen synthesis was likely due to increased aromatase in hypothyroidism. The HED dose of T3 that reversed the increase in estrogen was quite high - 5mcg/kg, so way beyond the 100mcg Ray things should be the upper limit of T3 intake.

Influence of thyroid hormone on androgen metabolism in peripuberal rat Sertoli cells. - PubMed - NCBI

"...Testosterone metabolism in Sertoli cells isolated from 3- and 4-week-old hypothyroid rats was mainly expressed by the lowering of 5α-dihydrotestosterone + androstane 3α, 17β–diol and an enhanced formation of 5α-reduced steroids with poor androgenic properties (e.g. 5α–androstane, 3, 17α-dione (androstanedione), 5α–androstan, 3-ol-17-one (androsterone)). Treatment of the same group of animals with T3 in vivo and in vitro did not influence the pattern of 5α–reductase steroids substantially. The most striking finding in the Sertoli cells of 3-week-old hypothyroid rats was the dramatic enhancement of oestradiol formation which persisted to a lesser extent 1 week later. Oestradiol formation was greatly decreased by the addition of T3 in vivo and in vitro in hypothyroid animals. These results suggest that T3 might influence androgen metabolism during the functional maturation of Sertoli cells."

"...Since the period in which Sertoli cells multiply corre¬ sponds with the ability of these cells to produce oestradiol (Armstrong & Dorrington 1977), it is possible to specu¬ late that the enhanced and prolonged aromatase activity observed in hypothyroid rats may be associated with increased and sustained mitogenic activity of Sertoli cells. For instance, it has been found that induced neonatal hypothyroidism retards the morphological differentiation of Sertoli cells and prolongs the proliferation of these cells up to day 30 when it ceases almost completely at 20 days in controls (van Haaster et al. 1992)."
 
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charlie

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encerent

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Hyperthyroidism also dramatically increases stress hormones. The study you posted a while back specifically showed that cortisol went from 20 mg/day to 70 mg/day, when hyperthyroidism was induced in normal people. Though the clearance of it was also dramatically increased.

It was a good study for me to remind me not to overdo it with the thyroid sups. Producing so much more hormones (both the stress and adaptive ones) doesn't seem to be very healthy. Hyperthyroidism seems like a generally more stressful state, with these hormones being made and cleared too fast. Seems like a wired state of being.
 
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I posted a study some time ago showing the effects of thyroid hormone on synthesis/metabolism of various steroids. Hyperthyroidism increased androgen production several-fold, but the effects on estrogen synthesis were less clear. This study shows that hypothyroidism increases estrogen (estradiol) synthesis several fold. Some people on this forum expressed opinion that estrogen rises in HYPER-thyroidism as a mechanism to suppress thyroid activity - i.e. in a way to rule thyroid in. Well, this study shows otherwise and agrees with Peat. Giving T3 supplement quickly normalized the elevated estrogen levels and brought its synthesis down to normal levels. The increased estrogen synthesis was likely due to increased aromatase in hypothyroidism. The HED dose of T3 that reversed the increase in estrogen was quite high - 5mcg/kg, so way beyond the 100mcg Ray things should be the upper limit of T3 intake."

I agree with @encerent that we shouldn't take the fact that estrogen is raised in hypothyroidism as evidence that it's necessarily lowered in hyperthyroidism. How then would you explain the following study that clearly shows an increase in estrogen (albeit estrone rather than estradiol) in hyperthyroidism?

The Conversion of Androgens to Estrogens in Hyperthyroidism

"To investigate the mechanism of the increased plasma estradiol levels in spontaneous hyperthyroidism, the contribution, by peripheral conversion, of androstenedione and testosterone to the circulating estrogens was determined. The conversion ratio of androstenedione to estrone was significantly increased in both males and females (0.0396 and 0.0256, respectively). The conversion ratio of androstenedione to estradiol was increased in the male (0.0094) but not in the female (0.0051) patients. The conversion ratio of testosterone to estrone was increased in both males (0.0072) and females (0.0070). The conversion of testosterone to estradiol, however, was not increased in either sex. The plasma concentration of androstenedione was significantly increased (0.34 μg/100 ml) in the male patients with hyperthyroidism. However, the production rate of androstenedione was increased in both sexes (8.59 and 6.72 mg/day). The contribution of testosterone and androstenedione to plasma estrone and estradiol (product of conversion ratio and plasma concentration of precursor) was significantly increased in the men and women with hyperthyroidism. Thus, the increased estrogen levels in spontaneous hyperthyroidism results in large part, from increased peripheral conversion rather than by direct glandular secretion. The pharmacologic induction of hyperthyroidism in a patient with panhypopituitarism suggests that the increased androgen-estrogen conversion is a direct effect of thyroid hormone manifested mainly by the increased conversion of androstenedione to the estrogens."

Also, what about the "well-known" association between gynecomastia and hyperthyroidism?
 

haidut

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I agree with @encerent that we shouldn't take the fact that estrogen is raised in hypothyroidism as evidence that it's necessarily lowered in hyperthyroidism. How then would you explain the following study that clearly shows an increase in estrogen (albeit estrone rather than estradiol) in hyperthyroidism?

The Conversion of Androgens to Estrogens in Hyperthyroidism

"To investigate the mechanism of the increased plasma estradiol levels in spontaneous hyperthyroidism, the contribution, by peripheral conversion, of androstenedione and testosterone to the circulating estrogens was determined. The conversion ratio of androstenedione to estrone was significantly increased in both males and females (0.0396 and 0.0256, respectively). The conversion ratio of androstenedione to estradiol was increased in the male (0.0094) but not in the female (0.0051) patients. The conversion ratio of testosterone to estrone was increased in both males (0.0072) and females (0.0070). The conversion of testosterone to estradiol, however, was not increased in either sex. The plasma concentration of androstenedione was significantly increased (0.34 μg/100 ml) in the male patients with hyperthyroidism. However, the production rate of androstenedione was increased in both sexes (8.59 and 6.72 mg/day). The contribution of testosterone and androstenedione to plasma estrone and estradiol (product of conversion ratio and plasma concentration of precursor) was significantly increased in the men and women with hyperthyroidism. Thus, the increased estrogen levels in spontaneous hyperthyroidism results in large part, from increased peripheral conversion rather than by direct glandular secretion. The pharmacologic induction of hyperthyroidism in a patient with panhypopituitarism suggests that the increased androgen-estrogen conversion is a direct effect of thyroid hormone manifested mainly by the increased conversion of androstenedione to the estrogens."

Also, what about the "well-known" association between gynecomastia and hyperthyroidism?

The study I posted did not make the rats HYPER-thyroid. It made them hypothyroid, noted the increase in estrogen formation, and then made them euthyroid again using T3 to bring estrogen down.
 

superhuman

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@haidut was that in one dosage? how do you think this can be applied in humans. Just follow the RP guildelines in terms of nibbling small amount of t3?

Since i know its popular in bodybuilding circles to take t3 in somewhat bigger dosages like 50-150mcg a day. They usually take 50 mcg 3x a day or 25mcg 3x a day. They also show different views in terms of T3 half life. Alot of thyroid doctors say the t3 half life is like 24-36 hours so you dont need to dose that often.
 

haidut

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@haidut was that in one dosage? how do you think this can be applied in humans. Just follow the RP guildelines in terms of nibbling small amount of t3?

Since i know its popular in bodybuilding circles to take t3 in somewhat bigger dosages like 50-150mcg a day. They usually take 50 mcg 3x a day or 25mcg 3x a day. They also show different views in terms of T3 half life. Alot of thyroid doctors say the t3 half life is like 24-36 hours so you dont need to dose that often.

No, it was not in one dosage but a 7 day treatment to reverse the hypothyroidism.
 

nullredvector

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oh so it was just 5mcg/kg divided by 7 days?
"T3 3 micrograms/100 g body weight"
(3 mcg) / (100 g) = 30 mcg / kg
HED = dose (30mcg/kg) x rat (6) / human (37)
HED = 4.86mcg/kg
right?
so @5mcg/kg thats 350mcg/kg for a 70kg person, then divide that by 7 days? 50mcg/day, thats not over 100mcg per day though
I c, but how was the dosages done then? how many times a day etc
I cant imagine the researchers gave more than one injection per day
 

haidut

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oh so it was just 5mcg/kg divided by 7 days?
"T3 3 micrograms/100 g body weight"
(3 mcg) / (100 g) = 30 mcg / kg
HED = dose (30mcg/kg) x rat (6) / human (37)
HED = 4.86mcg/kg
right?
so @5mcg/kg thats 350mcg/kg for a 70kg person, then divide that by 7 days? 50mcg/day, thats not over 100mcg per day though

I cant imagine the researchers gave more than one injection per day

No, it was 5mg/kg per day, every day, for 7 days.
 

haidut

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umm ok... then my original question... is that lethal? ahhhh! haha, I guess I'll look it up!

I don't hink 200mcg - 300mcg would be lethal for most people. Many bodybuilders use such doses to lose weight without dieting. That does not mean it is advisable though.
Not sure why you think the dose of thyroid in this study is so important. I would not take it to mean to use 5mcg/kg daily and decrease estrogen as a result. The study was meant to show that hypothyroidism increases estrogen and restoring metabolism lowers it to normal values. The high doses T3 were probably done to achieve normalization of estrogen and thyroid activity in just 7 days. Nobody wants to wait 6 months for these rats to regain metabolism on say 1 grain NDT daily.
 

nullredvector

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I don't hink 200mcg - 300mcg would be lethal for most people. Many bodybuilders use such doses to lose weight without dieting. That does not mean it is advisable though.
Not sure why you think the dose of thyroid in this study is so important. I would not take it to mean to use 5mcg/kg daily and decrease estrogen as a result. The study was meant to show that hypothyroidism increases estrogen and restoring metabolism lowers it to normal values. The high doses T3 were probably done to achieve normalization of estrogen and thyroid activity in just 7 days. Nobody wants to wait 6 months for these rats to regain metabolism on say 1 grain NDT daily.
I suppose I was thinking too reductionistic or linearly, and not about the side effects of that abrupt change.
 
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