Hair Steroid Profiling Reveals Differences In Male Pattern Baldness Between Korean & Caucas. Men

FredSonoma

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Jun 23, 2015
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I find it hard to believe that Koreans have higher testosterone and DHT than Caucasians. Smaller bone structure, much less body hair, and typically less much less muscle mass. Something smells fishy.

I think the bone structure part is wrong. Koreans have some of the most massive, broad, well-developed bone structures out of any people I have ever seen, even compared to other Asians. Definitely less body hair, maybe less muscle mass. But I've known plenty of Koreans that most definitely do not exercise or lift regularly and they are very naturally muscular, not huge, but very strong and lean.
 
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Dante

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Sep 9, 2016
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correct.

I think that Hairloss could be mitigated by increasing the activity of 3ß-HSD in those tissues. DHT must breakdown into 3ß-diol is my very simple theory. I don't "suffer" MPB so I never looked into that field but I've seen an interesting thread in some forums about some believe that increasing DHT breakdown into 3alpha-diol is the way to go. Don't think so, it's beta becuase it does only marginally convert back into DHT and it occupies both ERs so it's protective against Estrogens on the hair follicle.
Look at this intriguing article on 3ß-diol and prostate cancer:
The Anticancer Testosterone Metabolite 3β-Adiol - Meridian Valley Lab

don't know how valid the info is but the author provides references. What is really interesting frm a Peat-Point of view ist that the supplements and pathways he identified for increasing 3ß-HSD are very very "peatish" as far as I can tell. I'm not a Peater per se and only here for the cool info around, but this looks good.
I wonder if it is not partially by this mechanism that DHT is such a favourable substance, taht it breaks down into an estrogenic substance that exerts all kind of protective effects and so keeping the "real" estrogens at bay.
Someone willing to ask R.P. himself about this substance? @Dante
I have seen that meridian valley research a few months ago and yes i agree that 3-beta diol is a protective substance even though it happens to act via "estrogen receptor beta" .I won't call it an estrogen as it produces potent neurosteroid benefits just like DHT and unlike estradiol( but i am guessing you already know these). I think reduction of 3-beta-diol by strong inhibition of DHT via fin/dut can cause aggressive prostate cancer as seen in PCPT trials( though the trials have been reanalyzed statistically and they said improved detection in the fin group caused more screening of prostate cancer,lol) . I agree with 3beta-HSD part (though i am neither white nor korean so i am not sure what would apply to me ,lol)

I wanted to ask ray about this DHT metabolite but haven't got his email address
 

lvysaur

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Mar 15, 2014
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I think the bone structure part is wrong. Koreans have some of the most massive, broad, well-developed bone structures out of any people I have ever seen

I agree with this. The "short legs long torso" phenotype that some whites seem to have is even more predominant in northern Asians. Wide jaws as well.
 

cats

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May 4, 2016
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Regarding the 5β-DHP "paradox," I'll offer some speculation: Perhaps both the Koreans and Caucasians have low scalp progesterone levels. The balding Koreans are losing progesterone via excessive conversion to 5β-DHP (which, according to Wikipedia, is not a progestogen), while the low levels of 5β-DHP in the balding Caucasians is the result of having very little substrate in the first place.
 

Art Vandelay

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Jul 1, 2016
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I might be completely wrong here but i think it's the skin around the hair produces hormones (along with the stuff that the incoming capillaries bring) and the hair follicles are the target tissues for it.

Yep, that seems to be the case. After doing some research on the matter I came across this interesting article: The Hair Follicle as an Estrogen Target and Source

I haven't finished reading it all yet but here are some notes I've taken from the article:

17β-estradiol (E2) also modifies androgen metabolism within distinct subunits of the pilosebaceous unit (i.e., hair follicle and sebaceous gland). The latter displays prominent aromatase activity, the key enzyme for androgen conversion to E2, and is both an estrogen source and target.

because in clipped guinea pigs the regrowth of the hair was faster in spayed than in breeding females

Oh and Smart (26) in 1996, who showed that the prototypic ER agonist, E2, after topical application, is a very potent hair growth inhibitor in mice, thus calling our attention to similar effects that had already been reported many decades ago in several mammalian species.This hair growth-inhibitory activity reported in mice strikingly contrasted with the supposedly hair growth-stimulatory topical E2 therapy long practiced in many countries for the treatment of female pattern androgenetic alopecia (29, 30) and the hair loss induced by therapy with aromatase inhibitors, which lower serum and tissue E2 levels

Estrogens are able to modify androgen metabolism within distinct subunits of the hair follicle (e.g., in the dermal papilla), diminishing the amount of 5α-dihydrotestosterone formed after incubation with testosterone

Because aromatase, the enzyme that converts testosterone to E2 is also found at many of the sites of ER and androgen receptor expression (39), the local balance between E2 and androgen levels may serve to fine-tune E2 and androgen action in their target cells

Also, many of the growth and transcription factors, cytokines, and hormones that are currently recognized to control hair growth (21, 34, 35, 36) are themselves modulated by estrogens. Thus, it will be far from easy to clearly distinguish direct from indirect E2 effects on hair growth, even when ER-null mice are used, because nonclassical E2 effects could still alter the expression of many genes that have not previously been shown to have an estrogen response element

The hair follicle cycle is associated with a dramatically altered cutaneous blood vessel supply. It has been shown that in species with a synchronized hair cycle, anagen development is accompanied by an increase in skin perfusion due to a rearrangement of the skin vasculature and a genuine, substantial angiogenesis (65). Therefore, the hair follicle represents an unusually attractive model for studying how physiological angiogenesis is controlled by a complex epidermal-mesenchymal interacting system in vivo. We still do not know exactly what cellular or molecular mechanisms control these vascular changes. Besides the two major recognized angiogenesis stimulators, vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) (65, 66, 67), processes of angiogenesis can generally be modulated by hormonal changes, including changes in estrogen levels (68). In fact, E2 reportedly even stimulates human hair follicle synthesis of VEGF (69).
 

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