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Author Topic: Yep, Estradiol Raises Stress Hormones ACTH, NE, and Cortisol  (Read 4522 times)

Kierkegaard

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Yep, Estradiol Raises Stress Hormones ACTH, NE, and Cortisol
« on: December 24, 2015, 09:16:23 am »
Well, it seems like estradiol increases ACTH, cortisol, and NE in males, at least when it comes to stressors (as opposed to resting levels, which are addressed below). ACTH is the pituitary hormone stimulated by CRH in the hypothalamus which in turn stimulates the adrenals to release pregnenolone, progesterone, DHEA, testosterone, estrogen, etc.

This is pretty important stuff (especially the somewhat complicated stuff about dampening of cortisol-mediated negative feedback mentioned below), as this basically means that estradiol is basically a big stimulator of stress hormones.

  • Evidence from animal studies and clinical observations suggest that the activity of the pituitary-adrenal axis is under significant influence of sex steroids. [Stop and read that one again -- K] The present study investigated how a short term elevation of estradiol levels affects ACTH, cortisol, norepinephrine, and heart rate responses to mental stress in healthy men. In a double blind study, 16 men received a patch delivering 0.1 mg estradiol/day transdermally, and age- and body mass index-matched control subjects received a placebo patch. Twenty-four to 48 h later, they were exposed to a brief psychosocial stressor (free speech and mental arithmetic in front of an audience). In response to the psychosocial stressor, ACTH, cortisol, norepinephrine, and heart rate were increased in both experimental groups (all P < 0.0001). However, the estradiol-treated subjects showed exaggerated peak ACTH (P < 0.001) and cortisol (P < 0.002) responses compared to the placebo group. Also, the norepinephrine area under the response curve was greater in the estradiol group (P < 0.05). Although heart rate responses differences failed to reach statistical significance, they, too, tended to be larger in the estradiol group. Neither mood ratings before or after the stressor, nor ratings of the perception of the stressor could explain the observed endocrine response differences. In conclusion, short term estradiol administration resulted in hyperresponses of the pituitary-adrenal axis and norepinephrine to psychosocial stress in healthy young men independent of psychological effects, as assessed in this study.

Full study: https://www.researchgate.net/publication/14349263_Short-term_estradiol_treatment_enhances_pituitary-adrenal_axis_and_sympathetic_responses_to_psychosocial_stress_in_healthy_young_men

So whereas both experimental and control (no idea why the study refers to "both experimental groups," a little confusing) show elevations in ACTH, cortisol, NE, and heart rate, the estradiol group shows much higher ACTH and cortisol responses, with ACTH 80% higher, cortisol 50% higher, and NE 20% higher (I don't know if the higher response by ACTH than cortisol means anything, i.e., if the ratio of increase should be 1:1).  Important to note that the estradiol levels for control were 38.5+/-5.7 pg/ml, and 61.9+/-5.2 in the estradiol group; this is a modestly elevated estradiol level for the control to use as a baseline, so perhaps the increases in ACTH, cortisol, and NE would have been more pronounced if they were at a healthier low-20s pg/ml level for the control and 10 or so points higher for the experimental group.

Also important to note that there were psychological measures to compare anxiety for control and experimental groups that showed no statistically significant difference between results.  This means that although there were clear statistically significant differences between groups physiologically, there weren't any differences between psychological evaluations of stress and anxiety.  This could be explained by the already relatively high level of E2 for control groups compared to experimental groups.  At the end of the day, perhaps it means that it's not really estradiol by itself that causes noticeable or significant increases in anxiety in response to stressors, but other things that interact with estradiol, such as too-low cortisol or thyroid problems.  So even though estradiol by itself doesn't caused psychological problems, it could cause an interaction effect with another variable wonky hormonal variable.  This psychological part, to me, is the most interesting. 

This doesn't say anything about resting levels of ACTH, cortisol, or NE, but if you look closely on the chart on p. 3641, you see that there is a difference in resting ACTH levels of about 50% experimental compared to control; NE and cortisol are basically the same.  This could mean something: higher ACTH with equal cortisol means a slightly decreased cortisol:ACTH ratio, which could add up (especially with other wonky hormones) and create resting psychological problems, such as generalized anxiety. 

Then you have this interesting observation in the discussion section:
  • Although ACTH levels in the estradiol group followed the time course of the control group (on a higher level, however), the cortisol time course appeared to be altered in the estradiol-treated volunteers. Their cortisol concentrations continued to rise for another 10 min until they reached a peak 20 min after the cessation of stress. This is rather unusual because in numerous studies we observed that our stress protocol induces peak salivary cor- tisol levels 10 min after completion. The prolonged increase in the estradiol group is in accord with findings by Burgess and Handa (lo), who reported that corticosterone levels rose over a prolonged time in ovariectomized rats treated with estradiol. Along with data from in vitro receptor studies, the researchers concluded that estradiol may cause an impairment of the glucocorticoid-receptor mediated slow negative feedback. This appears to be a possible explanation for the observed cortisol effect in the present study, too.

"Impairment of the glucocorticoid-receptor-mediated slow negative feedback."  Translation: estradiol slows down the process of cortisol "cooling down" the stress response by looping back up to the hyopthalamus and telling it to chill out and reduce CRH and (from the pituitary) ACTH.  This might be evident from the increased percentage response of ACTH between groups (80%) compared to cortisol (50%).  The control group was able to "cool down" its stress response faster by cortisol doing its thing faster through negative feedback on ACTH.  This is a pretty important detail, because you want the cortisol-mediated feedback to be as crisp and quick as reasonably possible so you can recover from stress faster. 

And the reverse is also important: if estradiol raises ACTH, cortisol, and NE, too little estradiol will result in less ACTH, cortisol, and NE than the body needs.  What happens with low ACTH?  Pregnenolone, progesterone, DHEA, etc., are all reduced, and that can make you feel bad.  This low ACTH effect is even worse news for guys like me who have low cortisol; if you lower ACTH further, you lower cortisol even more, making you feel even worse.
« Last Edit: January 01, 2016, 08:22:45 am by Kierkegaard »
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Kierkegaard

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Re: Yep, Estradiol Raises Stress Hormones ACTH, NE, and Cortisol
« Reply #1 on: December 24, 2015, 11:09:41 pm »
Obnoxious bump.  This is big news, fellas!
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Re: Yep, Estradiol Raises Stress Hormones ACTH, NE, and Cortisol
« Reply #1 on: December 24, 2015, 11:09:41 pm »


Kierkegaard

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Re: Yep, Estradiol Raises Stress Hormones ACTH, NE, and Cortisol
« Reply #2 on: December 27, 2015, 12:45:44 am »
I've been thinking a lot about this one the last few days.  What if something like this happens?

High estradiol means increased cortisol but even higher increased ACTH, meaning there's a slight reduction in the cortisol:ACTH ratio, meaning the body isn't producing enough cortisol relative to ACTH, resulting in increased ACTH even at the resting level as the hypothalamus picks up on slightly insufficient cortisol and pumps out more CRH and therefore the pituitary pumps out more ACTH -- which, aha, is exactly what you see if you look at the figures in the thread for ACTH: even before the stressor their ACTH is considerably different, which is the only hormone measured in the study where baseline (non-stressed) levels were different (cortisol and NE didn't show these differences).

You also have to wonder if there's a sort of at least slight estrogen dominance that's going on with this picture: as estrogen gets high and cortisol lags behind ACTH, is part of the reason cortisol is lagging because progesterone is also lagging or can't keep up with the demands for cortisol?  Lower progesterone and higher estrogen = estrogen dominance.  This makes you wonder what would happen if a person supplemented with pregnenolone or progesterone when dealing with high estradiol, and it might be safer to supplement with progesterone because pregnenolone has the risk of increasing estradiol even more.  Maybe all cases of "high estrogen" causing problems is really because of estrogen dominance!  This could explain why so many guys can have somewhat or just downright high levels of E2 and feel fine, compared to other guys who barely push through 30 pg/ml and feel awful.

So the higher a person's (well, male's at least) estradiol, the more he's putting himself in a semi-adrenally unresponsive situation with regard to cortisol lagging behind ACTH.  Perhaps this is why people feel so terrible when estradiol is so high?  And maybe this is why people feel awful on low estradiol as well, such as through too much anastrozole: low estradiol means lower ACTH stimulation, meaning lower cortisol and other adrenal hormones such as pregnenolone, progesterone, etc.

I also have to go back to another study*, which references another study in saying that "Studies have shown that estrogen inhibits cortisol synthesis by specific interference with enzyme activity,13 thereby exacerbating a cortisol deficiency and initiating hormonal imbalances."  I can't find a free version of the study using the databases I have access to, but I really wonder what enzyme we're talking about here.  Could it be something around the 17-hydroxyprogesterone or 11-deoxycortisol areas, such that increasing estrogen clogs up cortisol-line hormones?

*http://drplechner.com/pdf/elestrogen.pdf
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electrify

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Re: Yep, Estradiol Raises Stress Hormones ACTH, NE, and Cortisol
« Reply #3 on: December 27, 2015, 01:29:30 am »
Could this be one reason why Clomid increases Cortisol? Other than the LH/FSH/p450 stuff? As even HCG should theoretically but some people see a decrease in cortisol with that. But with Clomid I always see cortisol increase consistantly...
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Re: Yep, Estradiol Raises Stress Hormones ACTH, NE, and Cortisol
« Reply #3 on: December 27, 2015, 01:29:30 am »


Kierkegaard

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Re: Yep, Estradiol Raises Stress Hormones ACTH, NE, and Cortisol
« Reply #4 on: December 27, 2015, 02:23:28 am »
Could this be one reason why Clomid increases Cortisol? Other than the LH/FSH/p450 stuff? As even HCG should theoretically but some people see a decrease in cortisol with that. But with Clomid I always see cortisol increase consistantly...

Could what be a reason why clomid increases cortisol?
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PeakT

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Re: Yep, Estradiol Raises Stress Hormones ACTH, NE, and Cortisol
« Reply #5 on: December 27, 2015, 04:57:17 am »
Well, it seems like estradiol increases ACTH, cortisol, and NE in males, at least when it comes to stressors (as opposed to resting levels, which are addressed below). ACTH is the pituitary hormone stimulated by CRH in the hypothalamus which in turn stimulates the adrenals to release pregnenolone, progesterone, DHEA, testosterone, estrogen, etc.

This is pretty important stuff (especially the somewhat complicated stuff about dampening of cortisol-mediated negative feedback mentioned below), as this basically means that estradiol is basically a big stimulator of stress hormones.

  • Evidence from animal studies and clinical observations suggest that the activity of the pituitary-adrenal axis is under significant influence of sex steroids. [Stop and read that one again -- K] The present study investigated how a short term elevation of estradiol levels affects ACTH, cortisol, norepinephrine, and heart rate responses to mental stress in healthy men. In a double blind study, 16 men received a patch delivering 0.1 mg estradiol/day transdermally, and age- and body mass index-matched control subjects received a placebo patch. Twenty-four to 48 h later, they were exposed to a brief psychosocial stressor (free speech and mental arithmetic in front of an audience). In response to the psychosocial stressor, ACTH, cortisol, norepinephrine, and heart rate were increased in both experimental groups (all P < 0.0001). However, the estradiol-treated subjects showed exaggerated peak ACTH (P < 0.001) and cortisol (P < 0.002) responses compared to the placebo group. Also, the norepinephrine area under the response curve was greater in the estradiol group (P < 0.05). Although heart rate responses differences failed to reach statistical significance, they, too, tended to be larger in the estradiol group. Neither mood ratings before or after the stressor, nor ratings of the perception of the stressor could explain the observed endocrine response differences. In conclusion, short term estradiol administration resulted in hyperresponses of the pituitary-adrenal axis and norepinephrine to psychosocial stress in healthy young men independent of psychological effects, as assessed in this study.

Full study: https://www.researchgate.net/publication/14349263_Short-term_estradiol_treatment_enhances_pituitary-adrenal_axis_and_sympathetic_responses_to_psychosocial_stress_in_healthy_young_men

So whereas both experimental and control (no idea why the study refers to "both experimental groups," a little confusing) show elevations in ACTH, cortisol, NE, and heart rate, the estradiol group shows much higher ACTH and cortisol responses, with ACTH 80% higher, cortisol 50% higher, and NE 20% higher (I don't know if the higher response by ACTH than cortisol means anything, i.e., if the ratio of increase should be 1:1).  Important to note that the estradiol levels for control were 38.5+/-5.7 pg/ml, and 61.9+/-5.2 in the estradiol group; this is a modestly elevated estradiol level for the control to use as a baseline, so perhaps the increases in ACTH, cortisol, and NE would have been more pronounced if they were at a healthier low-20s pg/ml level for the control and 10 or so points higher for the experimental group.

Also important to note that there were psychological measures to compare anxiety for control and experimental groups that showed no statistically significant difference between results.  This means that although there were clear statistically significant differences between groups physiologically, there weren't any differences between psychological evaluations of stress and anxiety.  This could be explained by the already relatively high level of E2 for control groups compared to experimental groups.  At the end of the day, perhaps it means that it's not really estradiol by itself that causes noticeable or significant increases in anxiety in response to stressors, but other things that interact with estradiol, such as too-low cortisol or thyroid problems.  So even though estradiol by itself doesn't caused psychological problems, it could cause an interaction effect with another variable wonky hormonal variable.  This psychological part, to me, is the most interesting. 

This doesn't say anything about resting levels of ACTH, cortisol, or NE, but if you look closely on the chart on p. 3641, you see that there is a difference in resting ACTH levels of about 50% experimental compared to control; NE and cortisol are basically the same.  This could mean something: higher ACTH with equal cortisol means a slightly decreased cortisol:ACTH ratio, which could add up (especially with other wonky hormones) and create resting psychological problems, such as generalized anxiety. 

Then you have this interesting observation in the discussion section:
  • Although ACTH levels in the estradiol group followed the time course of the control group (on a higher level, however), the cortisol time course appeared to be altered in the estradiol-treated volunteers. Their cortisol concentrations continued to rise for another 10 min until they reached a peak 20 min after the cessation of stress. This is rather unusual because in numerous studies we observed that our stress protocol induces peak salivary cor- tisol levels 10 min after completion. The prolonged increase in the estradiol group is in accord with findings by Burgess and Handa (lo), who reported that corticosterone levels rose over a prolonged time in ovariectomized rats treated with estradiol. Along with data from in vitro receptor studies, the researchers concluded that estradiol may cause an impairment of the glucocorticoid-receptor mediated slow negative feedback. This appears to be a possible explanation for the observed cortisol effect in the present study, too.

"Impairment of the glucocorticoid-receptor-mediated slow negative feedback."  Translation: estradiol slows down the process of cortisol "cooling down" the stress response by looping back up to the hyopthalamus and telling it to chill out and reduce CRH and (from the pituitary) ACTH.  This might be evident from the increased percentage response of ACTH between groups (80%) compared to cortisol (50%).  The control group was able to "cool down" its stress response faster by cortisol doing its thing faster through negative feedback on ACTH.  This is a pretty important detail, because you want the cortisol-mediated feedback to be as crisp and quick as reasonably possible so you can recover from stress faster. 

And the reverse is also important: if estradiol raises ACTH, cortisol, and NE, too little estradiol will result in less ACTH, cortisol, and NE than the body needs.  What happens with low ACTH?  Pregnenolone, progesterone, DHEA, etc., are all reduced, and that can make you feel bad.  This low ACTH effect is even worse news for guys like me who have low cortisol; if you lower ACTH further, you lower cortisol even more, making you feel even worse.

Incredible find K.  Haven't been able to do much reading the last few days - lots of (good) family stuff.

Obviously, most men would experience a negative impact from E2 going up with all things being equal.  Also, looking at it from another angle, low estradiol men - and we have a few on here - should probably check the above hormones.
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Kierkegaard

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Re: Yep, Estradiol Raises Stress Hormones ACTH, NE, and Cortisol
« Reply #6 on: December 27, 2015, 05:18:02 am »
Well, it seems like estradiol increases ACTH, cortisol, and NE in males, at least when it comes to stressors (as opposed to resting levels, which are addressed below). ACTH is the pituitary hormone stimulated by CRH in the hypothalamus which in turn stimulates the adrenals to release pregnenolone, progesterone, DHEA, testosterone, estrogen, etc.

This is pretty important stuff (especially the somewhat complicated stuff about dampening of cortisol-mediated negative feedback mentioned below), as this basically means that estradiol is basically a big stimulator of stress hormones.

  • Evidence from animal studies and clinical observations suggest that the activity of the pituitary-adrenal axis is under significant influence of sex steroids. [Stop and read that one again -- K] The present study investigated how a short term elevation of estradiol levels affects ACTH, cortisol, norepinephrine, and heart rate responses to mental stress in healthy men. In a double blind study, 16 men received a patch delivering 0.1 mg estradiol/day transdermally, and age- and body mass index-matched control subjects received a placebo patch. Twenty-four to 48 h later, they were exposed to a brief psychosocial stressor (free speech and mental arithmetic in front of an audience). In response to the psychosocial stressor, ACTH, cortisol, norepinephrine, and heart rate were increased in both experimental groups (all P < 0.0001). However, the estradiol-treated subjects showed exaggerated peak ACTH (P < 0.001) and cortisol (P < 0.002) responses compared to the placebo group. Also, the norepinephrine area under the response curve was greater in the estradiol group (P < 0.05). Although heart rate responses differences failed to reach statistical significance, they, too, tended to be larger in the estradiol group. Neither mood ratings before or after the stressor, nor ratings of the perception of the stressor could explain the observed endocrine response differences. In conclusion, short term estradiol administration resulted in hyperresponses of the pituitary-adrenal axis and norepinephrine to psychosocial stress in healthy young men independent of psychological effects, as assessed in this study.

Full study: https://www.researchgate.net/publication/14349263_Short-term_estradiol_treatment_enhances_pituitary-adrenal_axis_and_sympathetic_responses_to_psychosocial_stress_in_healthy_young_men

So whereas both experimental and control (no idea why the study refers to "both experimental groups," a little confusing) show elevations in ACTH, cortisol, NE, and heart rate, the estradiol group shows much higher ACTH and cortisol responses, with ACTH 80% higher, cortisol 50% higher, and NE 20% higher (I don't know if the higher response by ACTH than cortisol means anything, i.e., if the ratio of increase should be 1:1).  Important to note that the estradiol levels for control were 38.5+/-5.7 pg/ml, and 61.9+/-5.2 in the estradiol group; this is a modestly elevated estradiol level for the control to use as a baseline, so perhaps the increases in ACTH, cortisol, and NE would have been more pronounced if they were at a healthier low-20s pg/ml level for the control and 10 or so points higher for the experimental group.

Also important to note that there were psychological measures to compare anxiety for control and experimental groups that showed no statistically significant difference between results.  This means that although there were clear statistically significant differences between groups physiologically, there weren't any differences between psychological evaluations of stress and anxiety.  This could be explained by the already relatively high level of E2 for control groups compared to experimental groups.  At the end of the day, perhaps it means that it's not really estradiol by itself that causes noticeable or significant increases in anxiety in response to stressors, but other things that interact with estradiol, such as too-low cortisol or thyroid problems.  So even though estradiol by itself doesn't caused psychological problems, it could cause an interaction effect with another variable wonky hormonal variable.  This psychological part, to me, is the most interesting. 

This doesn't say anything about resting levels of ACTH, cortisol, or NE, but if you look closely on the chart on p. 3641, you see that there is a difference in resting ACTH levels of about 50% experimental compared to control; NE and cortisol are basically the same.  This could mean something: higher ACTH with equal cortisol means a slightly decreased cortisol:ACTH ratio, which could add up (especially with other wonky hormones) and create resting psychological problems, such as generalized anxiety. 

Then you have this interesting observation in the discussion section:
  • Although ACTH levels in the estradiol group followed the time course of the control group (on a higher level, however), the cortisol time course appeared to be altered in the estradiol-treated volunteers. Their cortisol concentrations continued to rise for another 10 min until they reached a peak 20 min after the cessation of stress. This is rather unusual because in numerous studies we observed that our stress protocol induces peak salivary cor- tisol levels 10 min after completion. The prolonged increase in the estradiol group is in accord with findings by Burgess and Handa (lo), who reported that corticosterone levels rose over a prolonged time in ovariectomized rats treated with estradiol. Along with data from in vitro receptor studies, the researchers concluded that estradiol may cause an impairment of the glucocorticoid-receptor mediated slow negative feedback. This appears to be a possible explanation for the observed cortisol effect in the present study, too.

"Impairment of the glucocorticoid-receptor-mediated slow negative feedback."  Translation: estradiol slows down the process of cortisol "cooling down" the stress response by looping back up to the hyopthalamus and telling it to chill out and reduce CRH and (from the pituitary) ACTH.  This might be evident from the increased percentage response of ACTH between groups (80%) compared to cortisol (50%).  The control group was able to "cool down" its stress response faster by cortisol doing its thing faster through negative feedback on ACTH.  This is a pretty important detail, because you want the cortisol-mediated feedback to be as crisp and quick as reasonably possible so you can recover from stress faster. 

And the reverse is also important: if estradiol raises ACTH, cortisol, and NE, too little estradiol will result in less ACTH, cortisol, and NE than the body needs.  What happens with low ACTH?  Pregnenolone, progesterone, DHEA, etc., are all reduced, and that can make you feel bad.  This low ACTH effect is even worse news for guys like me who have low cortisol; if you lower ACTH further, you lower cortisol even more, making you feel even worse.

Incredible find K.  Haven't been able to do much reading the last few days - lots of (good) family stuff.

Obviously, most men would experience a negative impact from E2 going up with all things being equal.  Also, looking at it from another angle, low estradiol men - and we have a few on here - should probably check the above hormones.

Yes, my thinking exactly.

People should feel worse on too-high or too-low E2 depending on the type of adrenal insufficiency they have.  If you have secondary AI, your body doesn't produce enough ACTH, so increasing estradiol probably won't increase ACTH (but it might increase CRH, the levels of which are already high in secondary AI folks, causing higher levels of NE and other hormones) and therefore won't increase cortisol -- which with the increase in NE and other hormones would make you feel worse and probably more anxious big time.  Primary AI guys would see an ever-widening of their already too-small/wide cortisol:ACTH ratio, making them feel even worse, likely exacerbating the "glucocorticoid-receptor mediated slow negative feedback" mentioned in the article. 
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Re: Yep, Estradiol Raises Stress Hormones ACTH, NE, and Cortisol
« Reply #7 on: December 27, 2015, 05:23:15 am »
All of this shows how grossly old school just measuring T is or even T and E2. 

What is interesting is that you have studies like the above that essentially change on hormone at a time and see what happens.  However, then you have Dzugan's approach where he ramps up everything to youthful levels.  I wonder which one works better.  In the case of Dzugan, I see considerable variability in how guys do at different levels, so I don't know how he would determine "youthful" levels for each individual...
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Re: Yep, Estradiol Raises Stress Hormones ACTH, NE, and Cortisol
« Reply #8 on: December 27, 2015, 05:36:54 am »
All of this shows how grossly old school just measuring T is or even T and E2. 

What is interesting is that you have studies like the above that essentially change on hormone at a time and see what happens.  However, then you have Dzugan's approach where he ramps up everything to youthful levels.  I wonder which one works better.  In the case of Dzugan, I see considerable variability in how guys do at different levels, so I don't know how he would determine "youthful" levels for each individual...

I'd imagine because Dzugan increases so much simultaneously that he has a bigger chance for really big effects or problems from one or two hormones getting out of whack as he raises them. 
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Re: Yep, Estradiol Raises Stress Hormones ACTH, NE, and Cortisol
« Reply #9 on: December 27, 2015, 08:54:51 pm »
Interesting stuff.  There is research showing that activation of estrogen receptors in the amygdala causes anxiety, so that may be where estradiol exerts its effect.  There is also a study showing that blocking estrogen receptors in the amygdala caused the lab rodents to become more interested in "novel females."  I looked up estrogen in the amygdala, when I noticed that (even with normal T), weight gain seemed to give me slight anxiety, social inhibition and a slightly exaggerated startle response.
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Re: Yep, Estradiol Raises Stress Hormones ACTH, NE, and Cortisol
« Reply #9 on: December 27, 2015, 08:54:51 pm »