Addressing root cause of male pattern baldness: a well known approach? - BaldTruthTalk.com
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  1. #1
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    Default Addressing root cause of male pattern baldness: a well known approach?

    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)."
    Last edited by Aston; 05-26-2012 at 03:58 PM. Reason: link obfuscated, pasting text

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    yeah this was already posted on HLH back in 2011:
    http://www.hairlosshelp.com/forums/m...threadid=95933


    do you really want to mess with your thyroid?

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    I'm already messing with my testicles and prostate with finasteride. I believe in cold science, and these guys are the first ones to use it since i started looking into male pattern baldness. Furthermore, more than the therapy itself, it's isolating the cause that is always the most important step, something which they seem to have done. There may be other ways to correct leptin resistance than those they propose as well...

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    Quote Originally Posted by 2020 View Post
    yeah this was already posted on HLH back in 2011:
    http://www.hairlosshelp.com/forums/m...threadid=95933


    do you really want to mess with your thyroid?
    I dont hear you knocking this guys clear cut science that decreased blood flow is a factor.

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    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.
    again with the bloodflow... god damnit reading stupid theories like that is making me lose hair....

    IT HAS BEEN ALREADY PROVEN DECADES AND DECADES AGO THAT BLOODFLOW IS NOT A FACTOR IN MPB!!!

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    Quote Originally Posted by 2020 View Post
    again with the bloodflow... god damnit reading stupid theories like that is making me lose hair....

    IT HAS BEEN ALREADY PROVEN DECADES AND DECADES AGO THAT BLOODFLOW IS NOT A FACTOR IN MPB!!!
    Are you blind or dumb? It suggest that decreased blood flow allows this hair loss....

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    I didn't even notice that detail. Can anyone link me to a study debunking inherent impaired blood flow in follicular capillaries? (Since 2020 says it has been proven.) The only studies i find are old, but confirm it instead.

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    Quote Originally Posted by Aston View Post
    I didn't even notice that detail. Can anyone link me to a study debunking inherent impaired blood flow in follicular capillaries? (Since 2020 says it has been proven.) The only studies i find are old, but confirm it instead.
    You just opened a can of worms you didn’t want to open. All that I have ever seen confirms lack of blood flow in balding areas and also that a tight scalp restricts blood flow thus rendering the top of your head the most blood flow stationary part in your body also explaining why you only lose hair and debunking this hole “single hair genetic predisposition”. But like I said the can of worms you just opened is now where 2020 tells you that facts says blood flow has nothing to do with it and then follows with studies regarding very few people and having less then reliable results to say the least. Good luck, watch out for the name calling the bald guys on this topic get rather feisty 

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    Quote Originally Posted by Aston View Post
    I didn't even notice that detail. Can anyone link me to a study debunking inherent impaired blood flow in follicular capillaries? (Since 2020 says it has been proven.) The only studies i find are old, but confirm it instead.
    Botox clearly states why there product works and how it applies to releiving pressure....
    http://journals.lww.com/plasreconsur...ulinum.79.aspx

    Study shows that blood flow is decreased in areas balding and not in men with no MPB. remember this is cappilary blood flow not affected by hair count what so ever....btw I got in contact with this Docotor and he was amazed nobody did follow up studies and confirmed his findings with me.
    http://www.ncbi.nlm.nih.gov/pubmed/8628793

    Minoxodil is a vasodilater more specific to certain areas luckily for balding people it works well on the scalp... well kind of well

    http://cardiovascres.oxfordjournals....2/120.abstract

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    Yeah, my point is this isn't open for discussion... inflammation constricts arteries. As we all know, hair loss is an inflammatory state caused by excess DHT (which my first post info links elegantly to a metabolic "insufficiency"). There is clear empirical data proving circulation is impeded in the balding areas of the scalp, just as there is evidence confirming the presence of inflammatory prostaglandins. I am really interested in what proof 2020 has for denying this.

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