DHEA Has Very Similar Anabolic Activity To DHT

[kineticz]

The prolactin is caused by ACTH/Adrenal suppression. You spiked preg and/or DHEA higher than your basal metabolic rate will allow. This will make TRH and TSH rise.

Take some thyroid hormone instead for a while.

Hey kineticz, sorry for posting this to this thread but I could not find your other post that I was looking for. Didn't you say that DHEA suppresss the HPA axis? What do you think of this study?
http://www.ncbi.nlm.nih.gov/pubmed/17928160

That confirms what I have been saying, that in the conditions of hypothyroidism, excess adrenal steroids will spike your preg, dhea, cortisol, resulting in net adrenal suppression.

If I am reading this study right it says that the adrenal steroids like DHEA will spike ACTH and cortisol. How is that "adrenal suppression"? Am I missing something?
I do agree that DHEA and pregnenolone can make matters worse for hypothyroid people but I suspect that it would be due to this stimulation of ACTH and cortisol, not due to suppressing ACTH/cortisol. Also DHEA and maybe pregnenoloone can convert into estrogen and for hypo people that would be bad b/c estrogen directly suppresses the thyroid and induces fatty acid oxidation, which is bad in Peat-land.
In what capacity do you think estrogen can be good in such situation? I saw you said that with high estrogen you felt better and low estrogen made you tired and depressed, so I am wondering what mechanism you think is at play.
Thanks in advance.

In hypothyroidism, and in advanced stages of cortisol deficiency, norephiprene stimulates the adrenals via ACTH. My view is that it is much preferable to have norephiprene stimulate ACTH than to have serotonin and catabolism stimulate ACTH, because norephiprene activates all systems ready to absorb preg in small doses, and serotonin and catabolism will just result in excess free floating adrenal hormones that downregulate multiple metabolic pathways. Excess cortisol resulting from the addition of a spike in adrenal hormones and increased cortisol shown in the study will downregulate this protective norephiprene mechanism (cortisol has a negative feedback mechanism on norephiprene), leading to lower metabolic rate and increased fatty acid suffocation of the adrenal mitochondria, which results in depersonalisation as I have experienced.

Norephiprene as we know is a TRH and ACTH potentiator, which extracts deficient energy from the adrenal mitochondria which has the effect of minimising the risk of fatty acid and serotonin suffocation of the adrenal intake of LDL to form steroids. Due to norephiprene downregulation via excess adrenal hormones in hypothyroidism, serotonin will increase as a ratio of the stimulatory neurotransmitters, further exacerbating the issue of mitochondrial respiration.

The study also doesn't mention the thyroid or metabolic state of the test subjects. In a normal person, pregnenolone sparing will occur leading to increased DHEA, preg-s, and cortisol, which are all beneficial IF your cellular metabolic capacity is efficient and respiring clearly enough, since DHEA makes the sex hormones for gender vitality, and T3 requires sufficient cortisol aside from cortisol's many functions such as anti-inflammation.

My theory on the use of E2 to protect pregnenolone and therefore avoid depression and increased adrenaline is here:

viewtopic.php?f=3&t=6177&p=74169#p74401

In blood tests, my TSH would go down when my E2 went up, indicating a positive correlation between E2 and effective thyroid.

I have recently boosted estrogen using pueraria mirifica and licorice. My personality and zest for life are showing new signs I've never felt before.

In hypothyroidism, Peat shows that E2 raises ACTH. Other studies show E2 protects ACTH from responsiveness to stress, resulting in increased pregnenolone storage in the mitochondria, despite using fatty acids for this purpose. I am sure Peat also says E2 increases glycolysis somewhere, so not just lipolysis. So this combination of stimulating ACTH but modulating pregnenolone exhaustion and prolonging neurotransmitter synapse residue via MAO-I, I believe is crucial to my recovery.

So my theory is that E2, while not metabolically optimum or efficient, can have a protective role in adrenal mitochondria, because it helps to keep the ball in the adrenal's court, and through it's slowing of active thyroid hormone will reduce or slow the need for fatty acid liberation. Excess fatty acid liberation is the crux of aging and stress in the modern day.

 

[narouz]

I'm enjoying this thread. :)

 

[haidut]

The prolactin is caused by ACTH/Adrenal suppression. You spiked preg and/or DHEA higher than your basal metabolic rate will allow. This will make TRH and TSH rise.

Take some thyroid hormone instead for a while.

Hey kineticz, sorry for posting this to this thread but I could not find your other post that I was looking for. Didn't you say that DHEA suppresss the HPA axis? What do you think of this study?
http://www.ncbi.nlm.nih.gov/pubmed/17928160

That confirms what I have been saying, that in the conditions of hypothyroidism, excess adrenal steroids will spike your preg, dhea, cortisol, resulting in net adrenal suppression.

If I am reading this study right it says that the adrenal steroids like DHEA will spike ACTH and cortisol. How is that "adrenal suppression"? Am I missing something?
I do agree that DHEA and pregnenolone can make matters worse for hypothyroid people but I suspect that it would be due to this stimulation of ACTH and cortisol, not due to suppressing ACTH/cortisol. Also DHEA and maybe pregnenoloone can convert into estrogen and for hypo people that would be bad b/c estrogen directly suppresses the thyroid and induces fatty acid oxidation, which is bad in Peat-land.
In what capacity do you think estrogen can be good in such situation? I saw you said that with high estrogen you felt better and low estrogen made you tired and depressed, so I am wondering what mechanism you think is at play.
Thanks in advance.

In hypothyroidism, and in advanced stages of cortisol deficiency, norephiprene stimulates the adrenals via ACTH. My view is that it is much preferable to have norephiprene stimulate ACTH than to have serotonin and catabolism stimulate ACTH, because norephiprene activates all systems ready to absorb preg in small doses, and serotonin and catabolism will just result in excess free floating adrenal hormones that downregulate multiple metabolic pathways. Excess cortisol resulting from the addition of a spike in adrenal hormones and increased cortisol shown in the study will downregulate this protective norephiprene mechanism (cortisol has a negative feedback mechanism on norephiprene), leading to lower metabolic rate and increased fatty acid suffocation of the adrenal mitochondria, which results in depersonalisation as I have experienced.

Norephiprene as we know is a TRH and ACTH potentiator, which extracts deficient energy from the adrenal mitochondria which has the effect of minimising the risk of fatty acid and serotonin suffocation of the adrenal intake of LDL to form steroids. Due to norephiprene downregulation via excess adrenal hormones in hypothyroidism, serotonin will increase as a ratio of the stimulatory neurotransmitters, further exacerbating the issue of mitochondrial respiration.

The study also doesn't mention the thyroid or metabolic state of the test subjects. In a normal person, pregnenolone sparing will occur leading to increased DHEA, preg-s, and cortisol, which are all beneficial IF your cellular metabolic capacity is efficient and respiring clearly enough, since DHEA makes the sex hormones for gender vitality, and T3 requires sufficient cortisol aside from cortisol's many functions such as anti-inflammation.

My theory on the use of E2 to protect pregnenolone and therefore avoid depression and increased adrenaline is here:

viewtopic.php?f=3&t=6177&p=74169#p74401

In blood tests, my TSH would go down when my E2 went up, indicating a positive correlation between E2 and effective thyroid.

I have recently boosted estrogen using pueraria mirifica and licorice. My personality and zest for life are showing new signs I've never felt before.

In hypothyroidism, Peat shows that E2 raises ACTH. Other studies show E2 protects ACTH from responsiveness to stress, resulting in increased pregnenolone storage in the mitochondria, despite using fatty acids for this purpose. I am sure Peat also says E2 increases glycolysis somewhere, so not just lipolysis. So this combination of stimulating ACTH but modulating pregnenolone exhaustion and prolonging neurotransmitter synapse residue via MAO-I, I believe is crucial to my recovery.

So my theory is that E2, while not metabolically optimum or efficient, can have a protective role in adrenal mitochondria, because it helps to keep the ball in the adrenal's court, and through it's slowing of active thyroid hormone will reduce or slow the need for fatty acid liberation. Excess fatty acid liberation is the crux of aging and stress in the modern day.

If excessive fatty acids are the main problem then why not just suppress them with aspirin/niacinamice and take T3 to oxidize the sugar? No need to get estrogen involved. As long as estrogen is high it will shuttle most of the sugar you ingest to fatty acid synthesis, so you could end up getting fat and more metabolically deranged even on a very low calorie/fat diet consisting of sugar and protein. The inverse correlation between E2 and thyroid you saw in your results can be protective response - i.e. the body ups thyroid synthesis when it senses increase in metabolic poisons like estrogen. Not everybody will have a good enough thyroid response like you and get end up with just high estrogen, which sucks. Also, higher estrogen will raise prolactin in virtually 100% of people, so not sure that's beneficial either. Have you had your prolactin tested btw?
Thoughts?

 

[kineticz]

If excessive fatty acids are the main problem then why not just suppress them with aspirin/niacinamice and take T3 to oxidize the sugar? No need to get estrogen involved. As long as estrogen is high it will shuttle most of the sugar you ingest to fatty acid synthesis, so you could end up getting fat and more metabolically deranged even on a very low calorie/fat diet consisting of sugar and protein. The inverse correlation between E2 and thyroid you saw in your results can be protective response - i.e. the body ups thyroid synthesis when it senses increase in metabolic poisons like estrogen. Not everybody will have a good enough thyroid response like you and get end up with just high estrogen, which sucks. Also, higher estrogen will raise prolactin in virtually 100% of people, so not sure that's beneficial either. Have you had your prolactin tested btw?
Thoughts?

I had my prolactin tested before and after aromatase inhibitors. After it was 3 times as high with high TSH 3.0 and zero E2, almost 1000 on a scale 15-360. With E2 at 36, the only things that changed was prolactin was only 395, and TSH was only 1.25 or so.

I didn't see an inverse correlation, I saw a direct correlation. As E2 went up, so did thyroid absorption. The body lowers thyroid synthesis via TSH because more T3 is entering cells.

This tells me E2 has a protective compensatory role in improving adrenal/thyroid axis. I am glad you agree that I have said E2 is protective a few times.

I said that E2 is not metabolically optimum but is far better than having no E2 and high LH sequestering pregnenolone from the adrenals.

My point with E2 is it has been proven to do you all the things you say, but it is superior because in my instance I was ACTH, thyroid and adrenal deficient. E2 tilts the balance back to adrenal activity. The adrenals are more important than the gonads.

What is worse than simply high E2, is high LH, high prolactin, high progesterone, low E2, low adrenal respiration. This is what I've endured, and am trying to warn people from blindly reducing E2.

It is also an issue of norephiprene versus serotonin. The two compete blindly for compensatory energy, and serotonin will not promote the synthesis of exogenous pregnenolone, but norephiprene does. Furthermore, I believe estrone is less active but is a silent blocker of metabolism.

Your suggestion regarding niacinamide and aspirin and T3 are correct, but not in the context of my theories. I am talking about more advanced stages of adrenal exhaustion and the protective role of E2 to restore balance. I am not saying E2 alone is going to truly solve people's metabolism, but I am giving my opinion on my experiences and blood results regarding estrogen blockers.

High prog/E2 ratio attenuates ACTH depleting pregnenolone and cortisol. High LH diverts LDL away from adrenals rendering adrenals in low respiration. Dopamine converts significantly to adrenaline. Not a pleasant scenario. E2 underpins all these processes.

If you lower E2 but don't have the resources to maintain your adrenals, you will progressively worsen.

 

[haidut]

If excessive fatty acids are the main problem then why not just suppress them with aspirin/niacinamice and take T3 to oxidize the sugar? No need to get estrogen involved. As long as estrogen is high it will shuttle most of the sugar you ingest to fatty acid synthesis, so you could end up getting fat and more metabolically deranged even on a very low calorie/fat diet consisting of sugar and protein. The inverse correlation between E2 and thyroid you saw in your results can be protective response - i.e. the body ups thyroid synthesis when it senses increase in metabolic poisons like estrogen. Not everybody will have a good enough thyroid response like you and get end up with just high estrogen, which sucks. Also, higher estrogen will raise prolactin in virtually 100% of people, so not sure that's beneficial either. Have you had your prolactin tested btw?
Thoughts?

I had my prolactin tested before and after aromatase inhibitors. After it was 3 times as high with high TSH 3.0 and zero E2, almost 1000 on a scale 15-360. With E2 at 36, the only things that changed was prolactin was only 395, and TSH was only 1.25 or so.

I didn't see an inverse correlation, I saw a direct correlation. As E2 went up, so did thyroid absorption. The body lowers thyroid synthesis via TSH because more T3 is entering cells.

This tells me E2 has a protective compensatory role in improving adrenal/thyroid axis. I am glad you agree that I have said E2 is protective a few times.

I said that E2 is not metabolically optimum but is far better than having no E2 and high LH sequestering pregnenolone from the adrenals.

My point with E2 is it has been proven to do you all the things you say, but it is superior because in my instance I was ACTH, thyroid and adrenal deficient. E2 tilts the balance back to adrenal activity. The adrenals are more important than the gonads.

What is worse than simply high E2, is high LH, high prolactin, high progesterone, low E2, low adrenal respiration. This is what I've endured, and am trying to warn people from blindly reducing E2.

It is also an issue of norephiprene versus serotonin. The two compete blindly for compensatory energy, and serotonin will not promote the synthesis of exogenous pregnenolone, but norephiprene does. Furthermore, I believe estrone is less active but is a silent blocker of metabolism.

Your suggestion regarding niacinamide and aspirin and T3 are correct, but not in the context of my theories. I am talking about more advanced stages of adrenal exhaustion and the protective role of E2 to restore balance. I am not saying E2 alone is going to truly solve people's metabolism, but I am giving my opinion on my experiences and blood results regarding estrogen blockers.

High prog/E2 ratio attenuates ACTH depleting pregnenolone and cortisol. High LH diverts LDL away from adrenals rendering adrenals in low respiration. Dopamine converts significantly to adrenaline. Not a pleasant scenario. E2 underpins all these processes.

If you lower E2 but don't have the resources to maintain your adrenals, you will progressively worsen.

So, what you are saying is:

1. That your personal experience shows that adrenal fatigue is a very real condition.
2. If severe enough you may have to trade temporary estrogen buildup for basic metabolic functionality.
3. Pregnenolone and DHEA are counterproductive in such a state due to inhibiting ACTH and cortisol/adrenalin, which you do need to function if thyroid is not working.

Am I getting this right? I agree that if you are adapted to run on adrenalin/cortisol and just blindly suppress the HPA axis without providing thyroid support then you will suffer. However, I don't understand why would not direct supplementation with T3 and suppressing the fatty acids work in such cases. Are you saying that if adrenal depletion is severe enough the cells won't react to T3? Like some sort of T3 resistance, similar to insulin resistance? Also, there are studies that show the body is pretty smart about using supplemental progesterone and pregnenolone into the pathways that are deficient. So, if your cortisol is low and you take progesterone or pregnenolone then you'll get a "cortisol steal" and you will synthesize cortisol from those hormones. Yes, you will suppress ACTH but you will have enough cortisol.

 

[kineticz]

So, what you are saying is:

1. That your personal experience shows that adrenal fatigue is a very real condition.
2. If severe enough you may have to trade temporary estrogen buildup for basic metabolic functionality.
3. Pregnenolone and DHEA are counterproductive in such a state due to inhibiting ACTH and cortisol/adrenalin, which you do need to function if thyroid is not working.

Am I getting this right? I agree that if you are adapted to run on adrenalin/cortisol and just blindly suppress the HPA axis without providing thyroid support then you will suffer. However, I don't understand why would not direct supplementation with T3 and suppressing the fatty acids work in such cases. Are you saying that if adrenal depletion is severe enough the cells won't react to T3? Like some sort of T3 resistance, similar to insulin resistance? Also, there are studies that show the body is pretty smart about using supplemental progesterone and pregnenolone into the pathways that are deficient. So, if your cortisol is low and you take progesterone or pregnenolone then you'll get a "cortisol steal" and you will synthesize cortisol from those hormones. Yes, you will suppress ACTH but you will have enough cortisol.

You're a clever dude haidut. That summary is exactly what I'm saying.

And yes, I am saying T3 resistance. On both blood tests, my free T3 was very high, but so was my TSH on the second one. It was because of this high FT3 that I neglected external thyroid treatment. I assumed that applying pregnenolone and reducing estrogen would team up with this free T3 and solve all ills. It didn't end well, hence I'm on Ray Peat's forum warning people not to take his approach of estrogen is bad and pregnenolone is good literally. The adrenals need to respire and people should always start with serotonin. Serotonin's restrictive effects are mainly from muscle catabolism, not strictly limited to E2 levels.

And no, the body is not smart in using pregnenolone and progesterone, from my extensive experience.

My experience of progesterone and pregnenolone is worlds apart. Progesterone has the clear effect of dry joints and skin, excess muscle tension, all the symptoms of low E2. Pregnenolone depends on form. Cream is safest but not guaranteed to be effective. Pill form can be disastrous for people.

With E2, I must state I get different results with different estrogen blockers. DIM can make me feel very bad, zoned out. But a potent bodybuilding AI can make me feel very tense and assertive as you would expect. So there is an unknown mechanism there. But the common aspect is that after I reduce E2, my adrenals struggle to recover, therefore my thyroid struggles to uptake T3 in cells.

E2 stimulates cortisol, slows down thyroid hormone reducing thyroid resistance, and seems to increase pregnenolone due to it's calming neurotransmitters, but can also boost norephiprene resulting in TRH and ACTH going up together for a boost in basal metabolic rate. The key is to reduce the serotonin in favour of norephiprene for better mitochondrial respiration and therefore better likelihood of accepting external pregnenolone without side effects.

I believe the controversy over the definition of adrenal fatigue is trivial and all amounts to the same issues:

Catabolic destruction of cells
High serotonin relative to norephiprene (norephiprene sensitivity goes up when effective thyroid goes up, according to Peat. Norephiprene stimulates the LDL to preg conversion in the adrenals, serotonin does not)
High reliance on fatty acids without adrenal mitochondrial respiration
Low thyroid sensitivity
Nutrient deficiency due to reliance on adrenaline
Switch from high quality HDL cholesterol to LDL and triglycerides
A western civilisation designed to divide and rule


Cheers

 

[aquaman]

Now is the high prolactin also caused by too high dose of pregnenolone or DHEA? I'm going to skip both for now until the headache and the racing hearbeat disappear then lower the dose to 30mg preg and 15 DHEA daily. But I wonder if I should lower DHEA, too if it's also the culprit for high andrenaline and prolactin.

To me your symptoms sound like classical Raypeatforum "too much too soon" dosing

60mg preg and 15 of DHEA? I'm sure Peat says 10mg of preg and a few mg of DHEA are enough in an interview

 

[kineticz]

Any reduction in adrenal cortex signalling and increase in helplessness signalling will result in exogenous adminstration being rejected by your body's complex metabolic structure.

In this manner, deficient cortisol is more willing to accept preg than excess cortisol, so long as norephiprene signalling is higher than serotonin.

 

[haidut]

So, what you are saying is:

1. That your personal experience shows that adrenal fatigue is a very real condition.
2. If severe enough you may have to trade temporary estrogen buildup for basic metabolic functionality.
3. Pregnenolone and DHEA are counterproductive in such a state due to inhibiting ACTH and cortisol/adrenalin, which you do need to function if thyroid is not working.

Am I getting this right? I agree that if you are adapted to run on adrenalin/cortisol and just blindly suppress the HPA axis without providing thyroid support then you will suffer. However, I don't understand why would not direct supplementation with T3 and suppressing the fatty acids work in such cases. Are you saying that if adrenal depletion is severe enough the cells won't react to T3? Like some sort of T3 resistance, similar to insulin resistance? Also, there are studies that show the body is pretty smart about using supplemental progesterone and pregnenolone into the pathways that are deficient. So, if your cortisol is low and you take progesterone or pregnenolone then you'll get a "cortisol steal" and you will synthesize cortisol from those hormones. Yes, you will suppress ACTH but you will have enough cortisol.

You're a clever dude haidut. That summary is exactly what I'm saying.

And yes, I am saying T3 resistance. On both blood tests, my free T3 was very high, but so was my TSH on the second one. It was because of this high FT3 that I neglected external thyroid treatment. I assumed that applying pregnenolone and reducing estrogen would team up with this free T3 and solve all ills. It didn't end well, hence I'm on Ray Peat's forum warning people not to take his approach of estrogen is bad and pregnenolone is good literally. The adrenals need to respire and people should always start with serotonin. Serotonin's restrictive effects are mainly from muscle catabolism, not strictly limited to E2 levels.

And no, the body is not smart in using pregnenolone and progesterone, from my extensive experience.

My experience of progesterone and pregnenolone is worlds apart. Progesterone has the clear effect of dry joints and skin, excess muscle tension, all the symptoms of low E2. Pregnenolone depends on form. Cream is safest but not guaranteed to be effective. Pill form can be disastrous for people.

With E2, I must state I get different results with different estrogen blockers. DIM can make me feel very bad, zoned out. But a potent bodybuilding AI can make me feel very tense and assertive as you would expect. So there is an unknown mechanism there. But the common aspect is that after I reduce E2, my adrenals struggle to recover, therefore my thyroid struggles to uptake T3 in cells.

E2 stimulates cortisol, slows down thyroid hormone reducing thyroid resistance, and seems to increase pregnenolone due to it's calming neurotransmitters, but can also boost norephiprene resulting in TRH and ACTH going up together for a boost in basal metabolic rate. The key is to reduce the serotonin in favour of norephiprene for better mitochondrial respiration and therefore better likelihood of accepting external pregnenolone without side effects.

I believe the controversy over the definition of adrenal fatigue is trivial and all amounts to the same issues:

Catabolic destruction of cells
High serotonin relative to norephiprene (norephiprene sensitivity goes up when effective thyroid goes up, according to Peat. Norephiprene stimulates the LDL to preg conversion in the adrenals, serotonin does not)
High reliance on fatty acids without adrenal mitochondrial respiration
Low thyroid sensitivity
Nutrient deficiency due to reliance on adrenaline
Switch from high quality HDL cholesterol to LDL and triglycerides
A western civilisation designed to divide and rule


Cheers

Yeah, I think I get your point. It doesn't matter if you call it adrenal fatigue or whatnot, but suppressing adrenals while hypothyroid and not supporting thyroid, can be very bad.
What do you think of this study I posted long time ago?
viewtopic.php?f=75&t=3594

So, it seem that prolactin is a very good surrogate for serotonin (and estrogen). If suppressing prolactin also suppresses serotonin, this would explain all the beneficial metabolic effects seen with prolactin inhibitors. Here are some studies showing lowering prolactin improved a number of metabolic parameters.
http://www.ncbi.nlm.nih.gov/pubmed/22074059
http://www.ncbi.nlm.nih.gov/pubmed/23233277
http://www.ncbi.nlm.nih.gov/pubmed/23082447
http://www.ncbi.nlm.nih.gov/pubmed/25123447
http://www.ncbi.nlm.nih.gov/pubmed/24355865
http://www.ncbi.nlm.nih.gov/pubmed/25592453
http://www.ncbi.nlm.nih.gov/pubmed/23506485
http://www.ncbi.nlm.nih.gov/pubmed/16584506
http://www.ncbi.nlm.nih.gov/pubmed/21128120
http://www.ncbi.nlm.nih.gov/pubmed/20559294

I also posted a study showing that reducing peripheral serotonin by inhibiting TPH2 reverses obesity and restores youthful metabolism without any thyroid supplementation. Since we both agree that serotonin is a cardinal metabolic poison do you think lowering serotonin and prolactin (or maybe just prolactin it they are so tightly correlated) would be the best approach, maybe even before (or instead) of supplementing with thyroid?
If you believe the studies above (all human) everybody's metabolism and gonadal function normalized after bringing prolactin down, which presumably also lowers serotonin and estrogen.
As a specific protocol, taking a low dose cabergoline together with cyproheptadine will not only attack both prolactin and serotonin but the cyproheptadine will also prevent the side effects of cabergoline on the heart valves. Cabergoline is an agonis of the 5-HT2b "receptor" and in some people that causes pulmonary and cardiac fibrosis. Cyproheptadine is an antagonist on the 5-HT2b "receptor" (as well as other serotonin receptors) and will prevent that bad effect, plus it will bring overall serotonin levels under control.
Other valid combinations are lisuride (on its own), pramipexole + cyproheptadine, etc.
What problems do you see with this approach, if any?

P.S. Some people do convert supplemental pregnenolone and progesterone into cortisol. In fact, this method is used in people who cannot tolerate oral medrol or IV cortisone infusions. Why it does not work in you I don't know, but I suspect the high prolactin has something to do with it and most of the progesterone you take probably goes towards suppressing that rather than convert into cortisol.

 

[kineticz]

Yeah, I think I get your point. It doesn't matter if you call it adrenal fatigue or whatnot, but suppressing adrenals while hypothyroid and not supporting thyroid, can be very bad.
What do you think of this study I posted long time ago?
viewtopic.php?f=75&t=3594

So, it seem that prolactin is a very good surrogate for serotonin (and estrogen). If suppressing prolactin also suppresses serotonin, this would explain all the beneficial metabolic effects seen with prolactin inhibitors. Here are some studies showing lowering prolactin improved a number of metabolic parameters.
http://www.ncbi.nlm.nih.gov/pubmed/22074059
http://www.ncbi.nlm.nih.gov/pubmed/23233277
http://www.ncbi.nlm.nih.gov/pubmed/23082447
http://www.ncbi.nlm.nih.gov/pubmed/25123447
http://www.ncbi.nlm.nih.gov/pubmed/24355865
http://www.ncbi.nlm.nih.gov/pubmed/25592453
http://www.ncbi.nlm.nih.gov/pubmed/23506485
http://www.ncbi.nlm.nih.gov/pubmed/16584506
http://www.ncbi.nlm.nih.gov/pubmed/21128120
http://www.ncbi.nlm.nih.gov/pubmed/20559294

I also posted a study showing that reducing peripheral serotonin by inhibiting TPH2 reverses obesity and restores youthful metabolism without any thyroid supplementation. Since we both agree that serotonin is a cardinal metabolic poison do you think lowering serotonin and prolactin (or maybe just prolactin it they are so tightly correlated) would be the best approach, maybe even before (or instead) of supplementing with thyroid?
If you believe the studies above (all human) everybody's metabolism and gonadal function normalized after bringing prolactin down, which presumably also lowers serotonin and estrogen.
As a specific protocol, taking a low dose cabergoline together with cyproheptadine will not only attack both prolactin and serotonin but the cyproheptadine will also prevent the side effects of cabergoline on the heart valves. Cabergoline is an agonis of the 5-HT2b "receptor" and in some people that causes pulmonary and cardiac fibrosis. Cyproheptadine is an antagonist on the 5-HT2b "receptor" (as well as other serotonin receptors) and will prevent that bad effect, plus it will bring overall serotonin levels under control.
Other valid combinations are lisuride (on its own), pramipexole + cyproheptadine, etc.
What problems do you see with this approach, if any?

P.S. Some people do convert supplemental pregnenolone and progesterone into cortisol. In fact, this method is used in people who cannot tolerate oral medrol or IV cortisone infusions. Why it does not work in you I don't know, but I suspect the high prolactin has something to do with it and most of the progesterone you take probably goes towards suppressing that rather than convert into cortisol.

Yep.

In my post on another thread, I stated that prolactin independently takes over the role of effective pregnenolone management via ACTH. This undermines and skews the use of cortisol.

I thought serotonin stimulates prolactin, are you saying prolactin stimulates serotonin? Or both?

How does progesterone suppress prolactin? My progesterone was high normal on bloods but my prolactin was extremely high.

Your knowledge on prolactin is far superior to mine. Please explain what metabolic parameters reducing prolactin achieves?

I have taken vitex in the past with very good results. I tried it recently with no effect though since lowering E2 so much. But recently I thought reducing serotonin and improving thyroid via adrenal replenishment would reduce prolactin via a reduction in TRH.

I think that if the ACTH signal is weak and prolactin is up, pregnenolone will further weaken this signal and increase TRH and prolactin further.

 

[haidut]

Serotonin and prolactin both stimulate each other. Peat has said that and I have seen rodent studies. So inhibiting one helps with the other. Cyproheptadine is a nice tool here since it inhibits both serotonin and prolactin.
Progesterone is supposed to inhibit prolactin by being anti-estrogenic. Estrogen stimulates porlactin and Peat thinks this proves that estrogen is bad for bone. Here is also a study that shows progesterone inhibits prolactin:
http://www.ncbi.nlm.nih.gov/pubmed/22697120
Finally, I would not trust blood tests for estrogen and/or progesterone. None of these tests is indicative of tissue levels.
http://jco.ascopubs.org/content/32/14/1396.full

So, your high blood estrogen could mean that your liver was doing its job and glucuronidating the estrogens released from fatty tissue and preparing them for excretion. In other words, your tissue levels were getting lower, and this could explain the better response to thyroid. I guess the only way to know for sure is to do a fatty tissue biopsy. Are you up for doing one?
It will help solve one of Peat's central claims - i.e. menopausal women show very low plasma estrogens but Peat claims they have very high tissue estrogens. This is leading doctors to believe that menopause is estrogen deficiency, while in fact Peat says it is estrogen excess and progesterone deficiency. I have seen enough studies and evidence to know that estrogen is carcinogenic (especially in menopausal women) so I think Peat is right on this one as well. But it would be nice to get an objective verification by a blood test.
Anyways, it looks like taking care of prolactin, serotonin, or estrogen takes care of the other two poisons. Vitamin E has been shown to lower both estrogen and prolactin and unsurprisingly I found studies showing it lowers serotonin as well (in the synapse). Combining vitamin E with something like cyproheptadine or cabergoline (or taking all 3 together) should give a major boost to metabolism/health.
Just my 2c.

 

[narouz]

Thanks haidut and kineticz for this exploration.
Fascinating stuff.

 

[schultz]

Finally, I would not trust blood tests for estrogen and/or progesterone. None of these tests is indicative of tissue levels.
http://jco.ascopubs.org/content/32/14/1396.full

So, your high blood estrogen could mean that your liver was doing its job and glucuronidating the estrogens released from fatty tissue and preparing them for excretion. In other words, your tissue levels were getting lower, and this could explain the better response to thyroid. I guess the only way to know for sure is to do a fatty tissue biopsy. Are you up for doing one?
It will help solve one of Peat's central claims - i.e. menopausal women show very low plasma estrogens but Peat claims they have very high tissue estrogens. This is leading doctors to believe that menopause is estrogen deficiency, while in fact Peat says it is estrogen excess and progesterone deficiency. I have seen enough studies and evidence to know that estrogen is carcinogenic (especially in menopausal women) so I think Peat is right on this one as well. But it would be nice to get an objective verification by a blood test.

I was thinking the same thing reading through this thread. Ray says progesterone can knock tissue bound estrogen out into the blood therefore raising blood levels. A menopausal woman has low blood levels of estrogen because she has a low progesterone. Without the progesterone, estrogen isn't being released into the blood stream to be excreted by the liver.

He says it in these two clips...

"So the only way you can really tell how much estrogen influence a person has when they're 50 years old is to take a snip of tissue and analyze its estrogen content."

So if you feel really your best with a high blood level of E2, you could actually just be lowering your tissue bound estrogen...

 

[haidut]

Finally, I would not trust blood tests for estrogen and/or progesterone. None of these tests is indicative of tissue levels.
http://jco.ascopubs.org/content/32/14/1396.full

So, your high blood estrogen could mean that your liver was doing its job and glucuronidating the estrogens released from fatty tissue and preparing them for excretion. In other words, your tissue levels were getting lower, and this could explain the better response to thyroid. I guess the only way to know for sure is to do a fatty tissue biopsy. Are you up for doing one?
It will help solve one of Peat's central claims - i.e. menopausal women show very low plasma estrogens but Peat claims they have very high tissue estrogens. This is leading doctors to believe that menopause is estrogen deficiency, while in fact Peat says it is estrogen excess and progesterone deficiency. I have seen enough studies and evidence to know that estrogen is carcinogenic (especially in menopausal women) so I think Peat is right on this one as well. But it would be nice to get an objective verification by a blood test.

I was thinking the same thing reading through this thread. Ray says progesterone can knock tissue bound estrogen out into the blood therefore raising blood levels. A menopausal woman has low blood levels of estrogen because she has a low progesterone. Without the progesterone, estrogen isn't being released into the blood stream to be excreted by the liver.

He says it in these two clips...

"So the only way you can really tell how much estrogen influence a person has when they're 50 years old is to take a snip of tissue and analyze its estrogen content."

So if you feel really your best with a high blood level of E2, you could actually just be lowering your tissue bound estrogen...

Do you know of a minimally invasive tissue test for estrogen? I am thinking that since doctors take cheek swabs and cervix swabs those should be usable as tissue samples to test for estrogen. Not sure, but hoping that it works. Now, even if these tissues are enough I still have to find a lab that would do such a test. Do you know of a lab that would do a tissue analysis for estrogen?

 

[RPDiciple]

gummybear; how much DHEA are u taking daily?

 

[docall18]

Well that was the DHEA trial over quickly, it's suppressing my ACTH again. Horrible lethargy and irritability. My basal metabolic rate has some ground to cover.

Have never heard that Dhea supresses ACTH.

Your symptoms sound to me like high Estradiol.

I found from labs that even small doses of Dhea or Pregnenolone can increase my E2 way over-range.

High E2 always gives me Heart-burn. Also, I get a good reaction from Indolplex DIM. This is how I can easily tell my E2 is high.

 

[kineticz]

Well that was the DHEA trial over quickly, it's suppressing my ACTH again. Horrible lethargy and irritability. My basal metabolic rate has some ground to cover.

Have never heard that Dhea supresses ACTH.

Your symptoms sound to me like high Estradiol.

I found from labs that even small doses of Dhea or Pregnenolone can increase my E2 way over-range.

High E2 always gives me Heart-burn. Also, I get a good reaction from Indolplex DIM. This is how I can easily tell my E2 is high.

My E2 was near zero.

DHEA will suppress ACTH if your liver cannot handle the low basal metabolic rate. This is why a good source of fructose is required.

 

[Peatit]

If conversion into estrogen is an issue one can combine DHEA with zinc to reduce any potential aromatization.

What is the usual zinc dosage to achieve anti-aromatase effect?

 

[IWishIWasRich]

Wait, so DHEA promotes hair loss, since it increases DHT?

This makes me nervous since I just bought MRM DHEA 25mg and Pure pregnenolone 30mg and plan to use these to make me a few inches taller and lift my face for anti-aging. But if DHEA makes my already thinning hair worse then I have to reconsider alternatives or at least use correct dosage.

So what is a good daily/weekly dosage for pregnenolone and DHEA that's very potent for the reasons above but without hair loss? I'm 35 yrs old, male, 5'9" (175cm), 160lbs (73kg). I will also take Vitamin A, D3, E, and K2 to compliment these. Do I also need to cycle the intake or no? Week on then off? 4 days on 3 days off?

How do you pretend to grow taller at age 35?
Try topical fin and minox for the thinning hair.

 

[FredSonoma]

Well that was the DHEA trial over quickly, it's suppressing my ACTH again. Horrible lethargy and irritability. My basal metabolic rate has some ground to cover.

How can I know when my basal metabolic rate is good enough that I can experiment with DHEA / preg? (any temp / pulse I should be hitting, or certain bloodwork) Or do I just need to experiment and see how I feel?