It gives a possible cause and cure and gives the definetly way to test our 5AR2 activity!
Baldness and Prostate 101
by
chilln
Published on 01-30-2011 01:36 PM Number of Views: 1247
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 (âdue to genetic predispositionâ). 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 progesteroneâs actions not DHTâs 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 âPlan Bâ. âPlan Aâ 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 5? 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).
This is explained in Hormone Modulation Therapy 101 (HMT101) scroll down to âWhat process should my doctor followâŚâ, and the details re pregnenolone supplementation are explained in Cortisol Boost 101 (CB101), scroll down to âFinding the pregnenolone and progesterone âtop upâ sweet spotsâ. The details re thyroid hormone supplementation are explained in Thyroid Boost 101 (TB101), scroll down to âDosing suggestions for T3-only, and T4-onlyâ.
HALTING AND POSSIBLY REVERSING MALE PATTERN BALDNESS
Leaving The Root Cause In Place By Reducing Hair Follicle DHT Metabolism
Option 1: Infra Red or Laser Thermal Treatment of Hair Follicles.
This increases the metabolic rate of the hair follicle cells, so they absorb more hormones including progesterone, and they allow the free radical damage to be repaired.
Option 2: Localized DHT Metabolism Reduction: Hair Follicles Only
Only Big Pharma drugs are available to achieve this, and the best of these are topical low concentration ketoconazole (eg: Nizoral) and spironolactone (eg: Aldactone)
Provided you keep the concentration low, then these do have mild systemic effects, however in many cases a small degree of systemic DHT suppression is required to help keep DHT metabolism in the prostate in check, and some people have discovered that ceasing their ketoconazole and / or spironolactone treatement results in mild prostate inflammation.
Option 3: Systemic Reduction Of DHT Metabolism: Only Use This If Systemic DHT Metabolism Is High
WARNINGS:
- A little suppression of systemic DHT metabolism may reduce libido.
- Too much suppression of systemic DHT metabolism will definitely reduce libido.
- If your cortisol-production-line is too downregulated while youâre undergoing systemic DHT suppression therapy, then this can âtip you over the edgeâ and strongly suppress your entire cortisol-production-line (the âfinasteride effectâ). This can happen after a week if your cortisol-production-line is too downregulated when you start systemic DHT suppression therapy, or it can occur after several years as aging will eventually downregulate your cortisol-production-line hormones over time.
How to measure systemic DHT metabolism is explained here (hint: 24 hr urinalysis of several specific metabolites is necessary):
musclechatroom.com/forum/showâŚ36&postcount=4
The Big Pharma drugs available to specifically reduce DHT metabolism, without directly reacting with other hormones, are dutasteride (eg: Avodart) and finasteride (eg: Proscar, Propecia)
The natural substance isolates / extracts which specifically reduce DHT metabolism are saw palmetto (not sure if there are any others).
Of these three substances, low dose dutasteride (eg: Avodart) is able to be managed much more reliably than both finasteride and saw palmetto (more on this below), and when finasteride or saw palmetto are not managed adequately in some people, those people have experienced a severe crash of the cortisol-production-line hormones - and these people have formed self-help groups such as propeciahelp.com, mypropeciasideeffects.com, etcâŚ
NB: all these people need to do is restore their cortisol-production-line hormones to optimum, but:
a) they donât understand what their cortisol-production-line hormones are,
b) theyâre prepared to undergo âquick fixâ hormone modulation therapy using finasteride or saw palmetto, but theyâre usually not prepared to undergo the much slower but much more reliable process of boosting their cortisol-production-line hormones.
HALTING AND POSSIBLY REVERSING MALE PATTERN BALDNESS
Recovering Libido
The only option to maintain hair and recover libido is to boost the cortisol-production-line hormones (eg: preg, prog, cortisol) as much as possible, and in addition boost thyroid hormones T4 and T3 up to the limit imposed by the maximum cortisol levels.
Determining the max boost to the cortisol-production-line hormones and thyroid hormones as an iterative process (boost preg/prog/cortiso, then boost T4/T3, boost preg/prog/cortisol a little more, boost T4/T3 a little more, etcâŚ) This will boost overall metabolism, which includes boosting systemic T and systemic DHT, yet the DHT metabolism boost within hair follicles and the prostate is kept manageable, ie: there is no excessive free radical damage to these tissues so hair follicles stay healthy and the prostate remains normal size.
WHAT SPECIFICALLY ABOUT FINASTERIDE AND SAW PALMETTO CAUSES THIS HORMONE CRASH ?
While finasteride (eg: Proscar, Propecia) lowers systemic DHT metabolism similar to dutasteride, the fact that the half life of finasteride is anywhere from 4 hours (in fast metabolizers) to as high as 12 hours (in slow metabolizers), which means the effective life of the finasteride or saw palmetto can be anywhere from 6 hours to 18 hours. This means that the amount of suppression / downregulation of DHT metabolism can be much greater than anticipated.
The problem with excessive DHT suppression / downregulation is that DHT triggers many of the same gene expression actions as T (not 100% overlap) and therefore suppression / downregulation of DHT results in downregulation of our testosterone metabolism.
Since one of progesteroneâs and cortisolâs critical functions is to oppose T and DHT metabolism, therefore when T and DHT metabolism activity declines (includes genetic expression effects), then cells downregulate their cortisol and progesterone receptors and absorb less cortisol and less progesterone. This is because they need less âoppositionâ or âdownregulationâ of T and DHT.
The way the body achieves this negative feedback loop is by downregulating the entire cortisol-production-line (eg: preg, prog, cortisol). But 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. Once weâve entered this very stable state with a lowered resting metabolic rate, most males who then back out their finasteride or saw palmetto can only recover their previous hormone levels (along with their previous high resting metabolic rate) very very slowly, and some will never recover their previous high hormone levels without intervention.
Once weâve entered this very stable state with a lowered resting metabolic rate, the intervention required is to boost the cortisol-production-line hormones by boosting resting metabolic rate, and that requires the three phased solution approach, explained in the previous section âAddressing the root causeâ.
HOW DO I PREVENT MY HORMONES CRASHING WHEN SUPPRESSING DHT ?
While itâs simple to explain at a high level, itâs a complex process when implemented: You need to initially monitor your sex hormones and your cortisol-production-line hormones (eg: preg, prog, cortisol) and if these are too low initially then you will need to either abstain from using DHT suppressants / downregulators, or you must first optimize at least your cortisol-production-line hormones (eg: preg, prog, cortisol) until your E2 is lowered, before commencing to suppress DHT.
This process is described in the Cortisol boost 101 primer, and you can access that from the links in the Hormones 101 primer, which is a sticky on the front page of this AllThingsMale forum.
WHAT IF INCREASED SERUM PROGESTERONE DOESNâT REVERSE MALE PATTERN BALDNESS ?
Thatâs usually because the progesterone isnât being absorbed by cells, which is usually because those cells have an overall metabolic rate which is too low.
Since the progesterone is synthesizing into some cortisol (just not enough) the reason for the too low metabolic rate in these cells is not due to inadequate cortisol. In this case itâs due to inadequate thyroid hormone T4.
Once T4 levels are restored to optimum, the cells will absorb both the T4 (which gets enythesized into T3) and extra cortisol, and they will boost their overall metabolic rate to optimum, and thatâs when theyâll start absorbing more progesterone.
WHY IS THE DHT METABOLISM IN MY HAIR FOLLICLES HIGH, YET I DONT HAVE EXCESSIVE LIBIDO, AND / OR MY ERECTION PERFORMANCE IS BELOW PAR ?
Since libido and erection performance are promoted by DHT which originates from cells which absorb DHT from serum (ie: not the prostate, not hair follicles), and since these cells are using relatively high E2 to oppose / downregulate their DHT metabolism, therefore the cells which promote libido and erection performance are doing a poor job of triggering adequate libido, and theyâre doing a poor job of triggering adequate erection performance.
When these cells use increased levels of progesterone and cortisol to oppose / downregulate T metabolism and DHT metabolism, then IF your thyroid hormone T4 levels rise to match the increase in your cortisol (more likely in younger males, less likely in older males), then your overall metabolic rate will increase, and this includes your systemic T and DHT metabolism but NOT your hair follicle or your prostate DHT metabolism ! Thus your libido and erection performance will remain unchanged, yet your hair will stay put, and your prostate will shrink to normal size.
HOWEVER (WARNING!) When these cells use increased levels of progesterone and cortisol to oppose / downregulate T metabolism and DHT metabolism, then IF your thyroid hormone T4 levels do not rise to match the increase in your cortisol (more likely in older males, less likely in younger males), then your overall metabolic rate will not increase, so your systemic T and DHT metabolism will not increase. Thus your libido and erection performance will decrease. In this case you must boost your thyroid hormones too. This is explained in the Thyroid boost 101 primer, which has a link in the Hormones 101 âstickyâ on the first page of this AllThingsMale subforum.
PAPERS / REFERENCES
- Confirmation of ability of progesterone to inhibit DHT in hair follicles:
Journal: European Journal of Dermatology. Volume 11, Number 3, 195-8, May - June 2001, Revues
Title: âInfluence of estrogens on the androgen metabolism in different subunits of human hair folliclesâ
URL full text
- Confirmation of cortisolâs ability to downregulate T
Journal: JCEM
Title: Acute Suppression of Circulating Testosterone Levels by Cortisol in Men
URL abstract
and
Journal: Journal of Molecular Endocrinology, 41, 165-175.
Title: Glucocorticoids antagonize cAMP-induced Star transcription in Leydig cells through the orphan nuclear receptor NR4A1
URL full text
3A) Confirmation that hair follicles which have their own 5? reductase absorb serum T to manufacture most of their own DHT.
Journal: Archives of Dermatological Research. 1998 Mar;290(3):126-32.
Title: 5 alpha-reductase activity in the human hair follicle concentrates in the dermal papilla.
URL abstract
3B) Corrolary: Since increasing cortisol downregulates T synthesis, therefore increasing cortisol also downregulates the synthesis of DHT within hair follicle cells.
Thatâs because hair follicle cells donât absorb much DHT directly, but instead they absorb T from serum and synthesize that into DHT via the action of 5? reductase.
4A) Confirmation that upregulation of serum DHT levels follows upregulation of hair follicle DHT levels (not to the same extent):
I donât have an obvious demonstration of this.
4B) Confirmation that downregulation of serum DHT levels follows downregulation of hair follicle DHT levels (not to the same extent):
Journal: Journal of the American Academy of Dermatology Volume 55, Issue 6 , Pages 1014-1023, December 2006
Title: The importance of dual 5?-reductase inhibition in the treatment of male pattern hair loss: Results of a randomized placebo-controlled study of dutasteride versus finasteride
URL abstract
URL detailed summary
4C) Assumption with high likelihood of being correct: Since the downregulation of serum DHT levels follows downregulation of hair follicle DHT levels (but not to the the same extent), that the upregulation of serum DHT levels follows downregulation of hair follicle DHT levels (but not to the the same extent).
While you might choose to be pedantic and dispute this assumption, if you rejected the hard fact that both progesterone and cortisol downregulate DHT in hair follicles, just because you chose to dispute this assumption, then youâd be throwing the baby out with the bathwater.
5A) Confirmation that E2 does not suppress DHT metabolism adequately in cells which manufacture their own DHT
[TO DO]
ACCURATE MONITORING OF DHT METABOLISM
Unfortunately serum DHT levels get high when DHT gets âbacked upâ and DHT is not being used up (ie: when DHT metabolism is low). This is quite unlike testosterone, which does not get âbacked upâ when T is not being used.
When DHT is being used up, more DHT needs to be synthesized, ie:
testosterone â5? reductaseâ> DHT
Therefore any biomarker which can indicate the activity of 5? reductase enzymes also indicates the rate of synthesis of DHT from testosterone, and thus indicates DHT metabolism.
Via experimental research, several research teams have confirmed that the synthesis of tetrahydrocortisol â5? reductaseâ> 5? tetrahydrocortisol (5?THF)
âŚcan be monitored using 24hr urinary analysis, and the ratio of 5?THF to THF follows the 5? reductase activity, ie:
high ( 5?THF / THF ) shows high 5? reductase activity
low ( 5?THF / THF ) shows low 5? reductase activity
Taken together, these are good indicators of 5? reductase acitivity, and thus DHT metabolism. Dr Crisler seems to agree.
The following research teams confirmed that the ratio of 5?THF to THF follows the 5? reductase activity, and thus DHT metabolic activity, eg:
Title: Diagnosis of 5alpha-reductase 2 deficiency: a local experience
Journal:
Author(s):
URL Full Text
NB: 5a THF/THF normal ratio range is between 0.5 and 2.5 quoted in âDiagnosis of 5alpha-reductase 2 deficiency: a local experienceâ.
Title: The Diagnosis of 5{alpha}-Reductase Deficiency in Infancy
Journal: blah
Author(s): blah
URL Full Text
Title: A Case of 5 alpha-reductase Deficiency in Infancy
Journal: blah
Author(s): blah
URL Full Text
Title: Early diagnosis and management of 5 alpha-reductase deficiency
Journal: blah
Author(s): blah
URL Full Text
Title: Increased 5{alpha}-Reductase Activity and Adrenocortical Drive in Women with Polycystic Ovary Syndrome
Journal: blah
Author(s): blah
URL Full Text
Copyright is retained by chilln, 2008, 2009, 2010, 2011
So, now i can go back to suicide plans 