Silly Question: Doesn't Taking Hormones Suppress Your Hormone Production?

[FinnRooney]

I know the answer is 'no' because of the way people talk about it on this forum but I've been unable to find an explanation. I originally thought this because of hearing that taking testosterone suppresses your test production (whether that's true or not or only applies to testosterone as opposed to progesterone or thyroid, I don't know).
Any explanations as to why that myth is there, and why it is wrong would be greatly appreciated as I'm struggling to find information on the Peat forum debunking this.

 

[sladerunner69]

I think the people ont his forum generally accept that taking hormones does suppress production, but there is more nuance to that. Hormones that are more upstream, such as pregnenlone or thyroid, seem to be much less prone to long term suppression, like testosterone seems to be.

 

[DaveFoster]

I know the answer is 'no' because of the way people talk about it on this forum but I've been unable to find an explanation. I originally thought this because of hearing that taking testosterone suppresses your test production (whether that's true or not or only applies to testosterone as opposed to progesterone or thyroid, I don't know).
Any explanations as to why that myth is there, and why it is wrong would be greatly appreciated as I'm struggling to find information on the Peat forum debunking this.

I think the people ont his forum generally accept that taking hormones does suppress production, but there is more nuance to that. Hormones that are more upstream, such as pregnenlone or thyroid, seem to be much less prone to long term suppression, like testosterone seems to be.

From thyroid hormone, any suppression of the hypothalamic-pituitary-adrenal-axis (HPA) recovers within one week. DHEA and progesterone do not suppress the hypothalamic-pituitary-testes-axis (HPTA), and pregnenolone, as well metabolites of progesterone actually stimulate the HPTA and help it to recover from suppression similar to human chorionic gonadotropin hormone (hCG). If a hormone stimulates GnRH secretion, then researchers consider that hormone to not suppress the hypothalamus' activation of the HPTA.

REFERENCES

el-Etr M, Akwa Y, Fiddes RJ, Robel P, Baulieu EE. A progesterone metabolite stimulates the release of gonadotropin-releasing hormone from GT1-1 hypothalamic neurons via the gamma-aminobutyric acid type A receptor. Proc Natl Acad Sci USA. 1995 Apr 25;92(9):3769–73. The reduced progesterone metabolite tetrahydroprogesterone (3 alpha-hydroxy-5 alpha-pregnan-20-one; 3 alpha,5 alpha-THP) is a positive modulator of the gamma-aminobutyric acid type A (GABAA) receptor. Experiments performed in vitro with hypothalamic fragments have previously shown that GABA could modulate the release of gonadotropin-releasing hormone (GnRH)...3 alpha,5 alpha-THP not only modulated muscimol-induced secretion but also stimulated GnRH release when administered alone.

Brown GA, Vukovich MD, Sharp RL, Reifenrath TA, Parsons KA, King DS. Effect of oral DHEA on serum testosterone and adaptations to resistance training in young men. Journal of Applied Physiology. 1999 Dec 1;87(6):2274–83. The findings of the present study are similar to those of Mortola and Yen (29), demonstrating that DHEA ingestion has no effect on serum FSH or LH concentrations and suggesting that the hypothalamic-pituitary-adrenal regulation of testosterone production is not altered by DHEA intake.

El-Etr M, Akwa Y, Baulieu E-E, Schumacher M. The neuroactive steroid pregnenolone sulfate stimulates the release of gonadotropin-releasing hormone from GT1-7 hypothalamic neurons, through N-methyl-D-aspartate receptors. Endocrinology. 2006 Jun;147(6):2737–43. HYPOTHALAMIC GnRH NEURONS are central regulators of reproduction; the pulsatile secretion of GnRH is required for fertility and drives the synthesis and release of gonadotropins from the pituitary, which control gametogenesis and steroidogenesis. GnRH neurons, in turn, receive information from several steroid feedback mechanisms and particularly from estrogens, which may act as positive or negative signals, as well as from progesterone and testosterone...Immortalized hypothalamic GT1-7 neurons represent a good model system to investigate the control of GnRH secretion. Using these cells, we observed that the neuroactive steroid, pregnenolone sulfate (PREGS), is able to stimulate the release of GnRH in a dose-dependent manner through N-methyl-D-aspartate (NMDA) receptors, because its action is completely blocked by a specific NMDA receptor antagonist and magnesium.

Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, et al. Patterns off recovery of the hypothalamic-pituitary-thyroid axis in patients taken of chronic thyroid therapy. J Clin Endocrinol Metab. 1975 Jul;41(1):70–80. Following prolonged thyroid therapy in euthyroid patients, recovery of normal TSH responsiveness to TRH preceded recovery of the normal T3 and T4 response to TRH by 3 to 6 days.

Sim JA, Skynner MJ, Herbison AE. Direct regulation of postnatal GnRH neurons by the progesterone derivative allopregnanolone in the mouse. Endocrinology. 2001 Oct;142(10):4448–53. The mechanisms through which gonadal steroids exert critical feedback actions upon the activity of the GnRH neurons are not understood. We have examined here whether progesterone may modulate the electrical activity of the GnRH neurons following its rapid metabolism to the neuroactive steroid allopregnanolone within the brain. Progesterone (1 microM) was not observed to have any actions (up to 5 min exposure) upon GnRH neurons. However, allopregnanolone (500 nM-1 microM) exerted rapid (<1 min) effects upon the baseline membrane potential of all GnRH neurons and also significantly (P < 0.01) enhanced their GABA responses by up to 4-fold.

 

[FinnRooney]

From thyroid hormone, any suppression of the hypothalamic-pituitary-adrenal-axis (HPA) recovers within one week. DHEA and progesterone do not suppress the hypothalamic-pituitary-testes-axis (HPTA), and pregnenolone, as well metabolites of progesterone actually stimulate the HPTA and help it to recover from suppression similar to human chorionic gonadotropin hormone (hCG). If a hormone stimulates GnRH secretion, then researchers consider that hormone to not suppress the hypothalamus' activation of the HPTA.

REFERENCES

el-Etr M, Akwa Y, Fiddes RJ, Robel P, Baulieu EE. A progesterone metabolite stimulates the release of gonadotropin-releasing hormone from GT1-1 hypothalamic neurons via the gamma-aminobutyric acid type A receptor. Proc Natl Acad Sci USA. 1995 Apr 25;92(9):3769–73. The reduced progesterone metabolite tetrahydroprogesterone (3 alpha-hydroxy-5 alpha-pregnan-20-one; 3 alpha,5 alpha-THP) is a positive modulator of the gamma-aminobutyric acid type A (GABAA) receptor. Experiments performed in vitro with hypothalamic fragments have previously shown that GABA could modulate the release of gonadotropin-releasing hormone (GnRH)...3 alpha,5 alpha-THP not only modulated muscimol-induced secretion but also stimulated GnRH release when administered alone.

Brown GA, Vukovich MD, Sharp RL, Reifenrath TA, Parsons KA, King DS. Effect of oral DHEA on serum testosterone and adaptations to resistance training in young men. Journal of Applied Physiology. 1999 Dec 1;87(6):2274–83. The findings of the present study are similar to those of Mortola and Yen (29), demonstrating that DHEA ingestion has no effect on serum FSH or LH concentrations and suggesting that the hypothalamic-pituitary-adrenal regulation of testosterone production is not altered by DHEA intake.

El-Etr M, Akwa Y, Baulieu E-E, Schumacher M. The neuroactive steroid pregnenolone sulfate stimulates the release of gonadotropin-releasing hormone from GT1-7 hypothalamic neurons, through N-methyl-D-aspartate receptors. Endocrinology. 2006 Jun;147(6):2737–43. HYPOTHALAMIC GnRH NEURONS are central regulators of reproduction; the pulsatile secretion of GnRH is required for fertility and drives the synthesis and release of gonadotropins from the pituitary, which control gametogenesis and steroidogenesis. GnRH neurons, in turn, receive information from several steroid feedback mechanisms and particularly from estrogens, which may act as positive or negative signals, as well as from progesterone and testosterone...Immortalized hypothalamic GT1-7 neurons represent a good model system to investigate the control of GnRH secretion. Using these cells, we observed that the neuroactive steroid, pregnenolone sulfate (PREGS), is able to stimulate the release of GnRH in a dose-dependent manner through N-methyl-D-aspartate (NMDA) receptors, because its action is completely blocked by a specific NMDA receptor antagonist and magnesium.

Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, et al. Patterns off recovery of the hypothalamic-pituitary-thyroid axis in patients taken of chronic thyroid therapy. J Clin Endocrinol Metab. 1975 Jul;41(1):70–80. Following prolonged thyroid therapy in euthyroid patients, recovery of normal TSH responsiveness to TRH preceded recovery of the normal T3 and T4 response to TRH by 3 to 6 days.

Sim JA, Skynner MJ, Herbison AE. Direct regulation of postnatal GnRH neurons by the progesterone derivative allopregnanolone in the mouse. Endocrinology. 2001 Oct;142(10):4448–53. The mechanisms through which gonadal steroids exert critical feedback actions upon the activity of the GnRH neurons are not understood. We have examined here whether progesterone may modulate the electrical activity of the GnRH neurons following its rapid metabolism to the neuroactive steroid allopregnanolone within the brain. Progesterone (1 microM) was not observed to have any actions (up to 5 min exposure) upon GnRH neurons. However, allopregnanolone (500 nM-1 microM) exerted rapid (<1 min) effects upon the baseline membrane potential of all GnRH neurons and also significantly (P < 0.01) enhanced their GABA responses by up to 4-fold.

Thank you so much!

 

[sladerunner69]

From thyroid hormone, any suppression of the hypothalamic-pituitary-adrenal-axis (HPA) recovers within one week. DHEA and progesterone do not suppress the hypothalamic-pituitary-testes-axis (HPTA), and pregnenolone, as well metabolites of progesterone actually stimulate the HPTA and help it to recover from suppression similar to human chorionic gonadotropin hormone (hCG). If a hormone stimulates GnRH secretion, then researchers consider that hormone to not suppress the hypothalamus' activation of the HPTA.

REFERENCES

el-Etr M, Akwa Y, Fiddes RJ, Robel P, Baulieu EE. A progesterone metabolite stimulates the release of gonadotropin-releasing hormone from GT1-1 hypothalamic neurons via the gamma-aminobutyric acid type A receptor. Proc Natl Acad Sci USA. 1995 Apr 25;92(9):3769–73. The reduced progesterone metabolite tetrahydroprogesterone (3 alpha-hydroxy-5 alpha-pregnan-20-one; 3 alpha,5 alpha-THP) is a positive modulator of the gamma-aminobutyric acid type A (GABAA) receptor. Experiments performed in vitro with hypothalamic fragments have previously shown that GABA could modulate the release of gonadotropin-releasing hormone (GnRH)...3 alpha,5 alpha-THP not only modulated muscimol-induced secretion but also stimulated GnRH release when administered alone.

Brown GA, Vukovich MD, Sharp RL, Reifenrath TA, Parsons KA, King DS. Effect of oral DHEA on serum testosterone and adaptations to resistance training in young men. Journal of Applied Physiology. 1999 Dec 1;87(6):2274–83. The findings of the present study are similar to those of Mortola and Yen (29), demonstrating that DHEA ingestion has no effect on serum FSH or LH concentrations and suggesting that the hypothalamic-pituitary-adrenal regulation of testosterone production is not altered by DHEA intake.

El-Etr M, Akwa Y, Baulieu E-E, Schumacher M. The neuroactive steroid pregnenolone sulfate stimulates the release of gonadotropin-releasing hormone from GT1-7 hypothalamic neurons, through N-methyl-D-aspartate receptors. Endocrinology. 2006 Jun;147(6):2737–43. HYPOTHALAMIC GnRH NEURONS are central regulators of reproduction; the pulsatile secretion of GnRH is required for fertility and drives the synthesis and release of gonadotropins from the pituitary, which control gametogenesis and steroidogenesis. GnRH neurons, in turn, receive information from several steroid feedback mechanisms and particularly from estrogens, which may act as positive or negative signals, as well as from progesterone and testosterone...Immortalized hypothalamic GT1-7 neurons represent a good model system to investigate the control of GnRH secretion. Using these cells, we observed that the neuroactive steroid, pregnenolone sulfate (PREGS), is able to stimulate the release of GnRH in a dose-dependent manner through N-methyl-D-aspartate (NMDA) receptors, because its action is completely blocked by a specific NMDA receptor antagonist and magnesium.

Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, et al. Patterns off recovery of the hypothalamic-pituitary-thyroid axis in patients taken of chronic thyroid therapy. J Clin Endocrinol Metab. 1975 Jul;41(1):70–80. Following prolonged thyroid therapy in euthyroid patients, recovery of normal TSH responsiveness to TRH preceded recovery of the normal T3 and T4 response to TRH by 3 to 6 days.

Sim JA, Skynner MJ, Herbison AE. Direct regulation of postnatal GnRH neurons by the progesterone derivative allopregnanolone in the mouse. Endocrinology. 2001 Oct;142(10):4448–53. The mechanisms through which gonadal steroids exert critical feedback actions upon the activity of the GnRH neurons are not understood. We have examined here whether progesterone may modulate the electrical activity of the GnRH neurons following its rapid metabolism to the neuroactive steroid allopregnanolone within the brain. Progesterone (1 microM) was not observed to have any actions (up to 5 min exposure) upon GnRH neurons. However, allopregnanolone (500 nM-1 microM) exerted rapid (<1 min) effects upon the baseline membrane potential of all GnRH neurons and also significantly (P < 0.01) enhanced their GABA responses by up to 4-fold.

Well thanks for the references, Mr. Foster. And nice to still see you active on here.

Interesting about allopregnanolone, as it seems to be a downstream hormone (after 5-ar enzyme) and therefore (I would think) more suspressive. I am not sure if GnRH are great surrogate measurements of gonadal steroids.

 

[Cameron]

Trace or small amounts of hormones are found in eggs raw milk and blood (if you consume fresh animal blood) organ meats problem is taking upstream hormones in amounts more than what your body is daily producing using small amounts works more as a raw material for the body especially in stress or need. pregnenolone with sufficient sugar seems to be very beneficial even in high amounts

 

[DaveFoster]

Thank you so much!

Well thanks for the references, Mr. Foster. And nice to still see you active on here.

Interesting about allopregnanolone, as it seems to be a downstream hormone (after 5-ar enzyme) and therefore (I would think) more suspressive. I am not sure if GnRH are great surrogate measurements of gonadal steroids.

No problem. Likewise. I check my inbox frequently, but I rarely lurk. The effects seem to be complicated, where GnRH might have a biphasic effect on steroid production in the testes:

From a 2010 study by Padmasana and Amitabh:

"GnRH agonist treatment produced significant changes in ovarian mass, circulating steroids level and ovarian follicular development, steroidogenesis and apoptosis in the mice. GnRH agonist also caused dose dependent histological changes in follicular development and luteinization. The mice treated with different doses of GnRH agonist showed biphasic effects on steroid synthesis due to its effects on ovarian expression of LH-receptor, StAR, and 3β -hydroxysteroid dehydrogenase proteins. The high dose showed stimulatory effect, whereas pharmacological dose showed inhibitory effect on ovarian follicular development and steroidogenesis. The in vitro study generally showed inhibitory effects of GnRH agonist on ovarian activities, which may be reversed by the presence of LH.

Both inhibitory and stimulatory effects found in the present study suggest that GnRH agonist is a versatile tool in the therapy of a variety of gynecological and non-gynecological conditions. This study suggests that the outcome of direct effect of GnRH-ag on ovary depends on LH-responsiveness."
​

Generally, the downstream steroids from the GnRH, the gonadotropins, such as follicle-stimulating hormone (FSH), luteinizing hormone (LH) and human chorionic gonadotropin (hCG), stimulate sex steroid production, as they control growth and sexual maturation in the mammalian life cycle. That's why bodybuilders take hCG when they want to restart their suppressed HPTA. However, Dr. Peat focuses extensively on the harm of these pituitary hormones when secreted in excess. He believes that they partly drive the aging process. hCG itself has been linked to cancer.

 

[sladerunner69]

No problem. Likewise. I check my inbox frequently, but I rarely lurk. The effects seem to be complicated, where GnRH might have a biphasic effect on steroid production in the testes:

From a 2010 study by Padmasana and Amitabh:

"GnRH agonist treatment produced significant changes in ovarian mass, circulating steroids level and ovarian follicular development, steroidogenesis and apoptosis in the mice. GnRH agonist also caused dose dependent histological changes in follicular development and luteinization. The mice treated with different doses of GnRH agonist showed biphasic effects on steroid synthesis due to its effects on ovarian expression of LH-receptor, StAR, and 3β -hydroxysteroid dehydrogenase proteins. The high dose showed stimulatory effect, whereas pharmacological dose showed inhibitory effect on ovarian follicular development and steroidogenesis. The in vitro study generally showed inhibitory effects of GnRH agonist on ovarian activities, which may be reversed by the presence of LH.

Both inhibitory and stimulatory effects found in the present study suggest that GnRH agonist is a versatile tool in the therapy of a variety of gynecological and non-gynecological conditions. This study suggests that the outcome of direct effect of GnRH-ag on ovary depends on LH-responsiveness."
​

Generally, the downstream steroids from the GnRH, the gonadotropins, such as follicle-stimulating hormone (FSH), luteinizing hormone (LH) and human chorionic gonadotropin (hCG), stimulate sex steroid production, as they control growth and sexual maturation in the mammalian life cycle. That's why bodybuilders take hCG when they want to restart their suppressed HPTA. However, Dr. Peat focuses extensively on the harm of these pituitary hormones when secreted in excess. He believes that they partly drive the aging process. hCG itself has been linked to cancer.

Perhaps hCG could help restart the 5-ar pathway, increasing DHT and allopregnenlone. The dosage of hCG would be high, but only held for a few days or a week. This could kick the 5ar pathway back into gear.

 

[tommyg130]

No problem. Likewise. I check my inbox frequently, but I rarely lurk. The effects seem to be complicated, where GnRH might have a biphasic effect on steroid production in the testes:

From a 2010 study by Padmasana and Amitabh:

"GnRH agonist treatment produced significant changes in ovarian mass, circulating steroids level and ovarian follicular development, steroidogenesis and apoptosis in the mice. GnRH agonist also caused dose dependent histological changes in follicular development and luteinization. The mice treated with different doses of GnRH agonist showed biphasic effects on steroid synthesis due to its effects on ovarian expression of LH-receptor, StAR, and 3β -hydroxysteroid dehydrogenase proteins. The high dose showed stimulatory effect, whereas pharmacological dose showed inhibitory effect on ovarian follicular development and steroidogenesis. The in vitro study generally showed inhibitory effects of GnRH agonist on ovarian activities, which may be reversed by the presence of LH.​

​

Both inhibitory and stimulatory effects found in the present study suggest that GnRH agonist is a versatile tool in the therapy of a variety of gynecological and non-gynecological conditions. This study suggests that the outcome of direct effect of GnRH-ag on ovary depends on LH-responsiveness."​

​

Generally, the downstream steroids from the GnRH, the gonadotropins, such as follicle-stimulating hormone (FSH), luteinizing hormone (LH) and human chorionic gonadotropin (hCG), stimulate sex steroid production, as they control growth and sexual maturation in the mammalian life cycle. That's why bodybuilders take hCG when they want to restart their suppressed HPTA. However, Dr. Peat focuses extensively on the harm of these pituitary hormones when secreted in excess. He believes that they partly drive the aging process. hCG itself has been linked to cancer.

So how would you or Dr peat suggest restarting after taking trt for a year. Skip the hcg and use prog, thyroid, preg, dhea , cholesterol vitamin A rich foods ?! Appreciate any thoughts !

 

[DaveFoster]

So how would you or Dr peat suggest restarting after taking trt for a year. Skip the hcg and use prog, thyroid, preg, dhea , cholesterol vitamin A rich foods ?! Appreciate any thoughts !

Ask him.