Tweet
http://www.*******************/forum...d-prostate-101 (and links at the end of it)
What in the world? Addressing root cause? Normalizing hormones? If this isn't complete madness then it feels to me like we are all quite stupid!
I can't even see any flaw in the science of it yet, and i'm a biotech student...
Edit: tch, link deleted, pasting below:
"THE DETAILED CAUSES OF MALE PATTERN BALDNESS AND PROSTATE GROWTH
Overview:
when systemic progesterone and systemic cortisol levels are too low, this causes too high DHT metabolism in hair follicles which in turn causes excess free radical damage to the hair follicles on our head in areas where the blood flow is restricted ("due to genetic predisposition"). The additional lack of blood flow to hair follicles means the free radical damage to hair follicles cannot be repaired adequately.
The same excess-free-radical-damage-due-to-excess-DHT-metabolism occurs in our prostate, inflaming our prostate causing either pain and / or constricting the urethra thus reducing urine flow.
This overview omits a lot of important details, so you MUST also read the following detailed explanation before discounting the above info.
Details:
Relatively high levels of progesterone are necessary to compete with DHT for DHT receptors. When progesterone triggers a DHT receptor, then DHT cannot trigger that receptor, and the progesterone which enters the cell triggers progesterone's actions not DHT's actions.
Relatively high levels of progesterone are necessary to upregulate the p53 tumor suppressor protein, which is postulated as one of the primary means of minimizing prostate tumors.
Relatively high levels of cortisol are necessary to oppose / downregulate DHT metabolism. Cortisol acts directly on our genes to limit the ability of T and DHT to trigger their own genetic effects.
When the cortisol-production-line hormones progesterone and cortisol are too downregulated, then cells will aromatase T into E2, and use the E2 to oppose T metabolism and DHT metabolism. To our cells, this is "Plan B". "Plan A" is to use progesterone and cortisol to oppose / downregulate T and DHT metabolism.
While using E2 to oppose T metabolism and DHT metabolism works well in cells which absorb DHT from serum, it works very poorly in cells which manufacture their own DHT (eg: prostate, and hair follicles, ie: all cells with plenty of 5α reductase). Hence these cells continue to experience too high DHT metabolism even in the presence of too high E2.
At the onset of male pattern baldness, our progesterone and our cortisol have gone too low, which would allow T metabolism and DHT metabolism to go too high, so our cells invoke their secondary defence mechanism and increase E2, and they then use E2 to oppose T metabolism and DHT metabolism.
When progesterone is relatively too low, this spells that all of the cortisol-production-line hormones (eg: preg, prog, cortisol) are downregulated to below optimum, and this is why the solution is to restore the optimal hormone levels in the cortisol-production-line.
HALTING AND POSSIBLY REVERSING MALE PATTERN BALDNESS
Addressing The Root Cause
Addressing the root cause requires boosting systemic progesterone (not necessarily by supplementating with progesterone) and boosting systemic cortisol (not necessarily by supplementing with HC, which is man made bioidentical cortisol), up to the level which balances systemic DHT metabolism.
Unfortunately for most males, boosting the cortisol-production-line also requires boosting thyroid hormones T3 and T4, because once the cortisol-production-line hormones are lowered, our cells automatically downregulate our T3 to match our reduced cortisol levels, which creates an excess of T4 (T3 is made from T4). When our hypothalamus detects excess T4, it downregulates the synthesis of T4 in the thyroid gland.
Unfortunately once our hypothalamus downregulates our T4, our body enters a very stable state with a reduced resting metabolic rate. When this occurs, boosting the cortisol-production-line hormones requires boosting our resting metabolic rate, and that requires a three phased solution approach, ie:
Phase 1: Restore preg, prog and cortisol, via supplementary transdermal pregnenolone (or prog), to as good as can be achieved without thyroid hormones.
Phase 2: Restore thyroid hormones, pref via supplementary slow-release-compounded T3 (not yet T4) and adjust both preg and T3 thyroid hormones together to achieve optimum balance as well as optimum levels of all cortisol-production-line hormones as well as optimum levels of thyroid hormones.
Phase 3: Swap out as much T3 with T4 as possible (definitely possible) and swap out as much pregnenolone with dietary cholesterol as possile (less effective with increasing age)."
What in the world? Addressing root cause? Normalizing hormones? If this isn't complete madness then it feels to me like we are all quite stupid!
I can't even see any flaw in the science of it yet, and i'm a biotech student...
Edit: tch, link deleted, pasting below:
"THE DETAILED CAUSES OF MALE PATTERN BALDNESS AND PROSTATE GROWTH
Overview:
when systemic progesterone and systemic cortisol levels are too low, this causes too high DHT metabolism in hair follicles which in turn causes excess free radical damage to the hair follicles on our head in areas where the blood flow is restricted ("due to genetic predisposition"). The additional lack of blood flow to hair follicles means the free radical damage to hair follicles cannot be repaired adequately.
The same excess-free-radical-damage-due-to-excess-DHT-metabolism occurs in our prostate, inflaming our prostate causing either pain and / or constricting the urethra thus reducing urine flow.
This overview omits a lot of important details, so you MUST also read the following detailed explanation before discounting the above info.
Details:
Relatively high levels of progesterone are necessary to compete with DHT for DHT receptors. When progesterone triggers a DHT receptor, then DHT cannot trigger that receptor, and the progesterone which enters the cell triggers progesterone's actions not DHT's actions.
Relatively high levels of progesterone are necessary to upregulate the p53 tumor suppressor protein, which is postulated as one of the primary means of minimizing prostate tumors.
Relatively high levels of cortisol are necessary to oppose / downregulate DHT metabolism. Cortisol acts directly on our genes to limit the ability of T and DHT to trigger their own genetic effects.
When the cortisol-production-line hormones progesterone and cortisol are too downregulated, then cells will aromatase T into E2, and use the E2 to oppose T metabolism and DHT metabolism. To our cells, this is "Plan B". "Plan A" is to use progesterone and cortisol to oppose / downregulate T and DHT metabolism.
While using E2 to oppose T metabolism and DHT metabolism works well in cells which absorb DHT from serum, it works very poorly in cells which manufacture their own DHT (eg: prostate, and hair follicles, ie: all cells with plenty of 5α reductase). Hence these cells continue to experience too high DHT metabolism even in the presence of too high E2.
At the onset of male pattern baldness, our progesterone and our cortisol have gone too low, which would allow T metabolism and DHT metabolism to go too high, so our cells invoke their secondary defence mechanism and increase E2, and they then use E2 to oppose T metabolism and DHT metabolism.
When progesterone is relatively too low, this spells that all of the cortisol-production-line hormones (eg: preg, prog, cortisol) are downregulated to below optimum, and this is why the solution is to restore the optimal hormone levels in the cortisol-production-line.
HALTING AND POSSIBLY REVERSING MALE PATTERN BALDNESS
Addressing The Root Cause
Addressing the root cause requires boosting systemic progesterone (not necessarily by supplementating with progesterone) and boosting systemic cortisol (not necessarily by supplementing with HC, which is man made bioidentical cortisol), up to the level which balances systemic DHT metabolism.
Unfortunately for most males, boosting the cortisol-production-line also requires boosting thyroid hormones T3 and T4, because once the cortisol-production-line hormones are lowered, our cells automatically downregulate our T3 to match our reduced cortisol levels, which creates an excess of T4 (T3 is made from T4). When our hypothalamus detects excess T4, it downregulates the synthesis of T4 in the thyroid gland.
Unfortunately once our hypothalamus downregulates our T4, our body enters a very stable state with a reduced resting metabolic rate. When this occurs, boosting the cortisol-production-line hormones requires boosting our resting metabolic rate, and that requires a three phased solution approach, ie:
Phase 1: Restore preg, prog and cortisol, via supplementary transdermal pregnenolone (or prog), to as good as can be achieved without thyroid hormones.
Phase 2: Restore thyroid hormones, pref via supplementary slow-release-compounded T3 (not yet T4) and adjust both preg and T3 thyroid hormones together to achieve optimum balance as well as optimum levels of all cortisol-production-line hormones as well as optimum levels of thyroid hormones.
Phase 3: Swap out as much T3 with T4 as possible (definitely possible) and swap out as much pregnenolone with dietary cholesterol as possile (less effective with increasing age)."
Comment