Prostate Size And Male Pattern Baldness

Haircraft

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835896/
"Human sebaceous glands and hair follicles are equipped with all the necessary enzymes for biosynthesis and metabolism of androgens"

And take note: Even before puberty.
Alright, thank you. So, sebaceous glands are found all over our skin except from the palms on the hands and the soles of the feet. Sebaceous glands are more numerous on the face and on the scalp. I educated myself on this with the help of Wikipedia and here's an image of how sebaceous glands are attached to hair follicles:

310px-Hair_follicle-en.svg.png


As the NCBI article says, the sebaceous gland is the main factory within the skin that produces hormones. Your quote is from the fifth paragraph, which also includes:

The classical androgen-dependent dermatoses, acne, androgenetic alopecia (Androgenetic Alopecia), seborrhea and hirsutism are among the most common skin disorders. Human sebaceous glands and hair follicles are equipped with all the necessary enzymes for biosynthesis and metabolism of androgens.​

So from what I understand, the sebaceous glands can produce the androgens responsible for the development of male pattern baldness. But then the question is if sebaceous glands alone can produce the amount required to actually trigger the process. We also know that testosterone made elsewhere in the body, such as the testes which stand for more than 95% of the production in men, are responsible for male pattern baldness. Otherwise men wouldn't halt their hair loss entirely through castration. Please correct me if I'm wrong, but I suppose this has to do with that testosterone can be delivered through the bloodstream from the testes to the sebaceous glands which leads to an increase of dihydrotestosterone production. With this in mind it sounds plausible that dihydrotestosterone produced, in the prostate for example, could also seek its way through the bloodstream directly to the hair follicles and trigger male pattern baldness.
 

Haircraft

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We also know that testosterone made elsewhere in the body, such as the testes which stand for more than 95% of the production in men, are responsible for male pattern baldness. Otherwise men wouldn't halt their hair loss entirely through castration. Please correct me if I'm wrong, but I suppose this has to do with that testosterone can be delivered through the bloodstream from the testes to the sebaceous glands which leads to an increase of dihydrotestosterone production. With this in mind it sounds plausible that dihydrotestosterone produced, in the prostate for example, could also seek its way through the bloodstream directly to the hair follicles and trigger male pattern baldness.
Of course, with my theory that a bigger prostate produces more dihydrotestosterone than a smaller one, it could also be that with castration the prostate shrinks drastically which could lead to a significant decrease in dihydrotestosterone production. If this stands true, and also that dihydrotestosterone can be delivered from the prostate to the hair follicles, this decrease in dihydrotestosterone production in the prostate could explain why men stop developing male pattern baldness upon castration.
 

Haircraft

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Black men get prostate cancer the most, i assume they have the biggest prostate due to testosterone levels...i wouldn't say they have the highest balding rates.

All to do with DHT sensitivity.
The study I found compares Caucasians with African Americans and it concludes that there's a 2.2 times higher prevalence of prostate cancer in African Americans. (http://onlinelibrary.wiley.com/doi/10.1111/j.1464-410X.2010.09991.x/full#t1n1)

What I found interesting about this study is about how they were medicated. African Americans were more likely to be medicated with alpha-blockers (42.0%) than Caucasians (33.5%) but they were less likely to be medicated with 5-alpha-reductase inhibitors (5.8%) compared to Caucasians (7.2%). That's a 1.4% difference. It's also interesting that out of the 5.8% of African Americans that were medicated with 5-alpha-reductase inhibitors, 4.3% of them medicated with alpha-blockers simultaneously whereas in the Caucasian group 3.5% medicated with them simultaneously. This means that if 5-alpha-reductase inhibitors are more efficient than alpha-blockers at fighting prostate cancer, then the African Americans were generally worse off when they begun their treatments. Also, apparently alpha-blockers have no impact on prostate volume. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2213889/) But as we know, 5-alpha-reductase inhibitors such as finasteride, do shrink the prostate.
 

bridgeburn

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Sure, polycystic ovary syndrome is a medical condition, but it's actually very common. This study doesn't study the prevalence of the condition but it concludes its prevalence with someone else's data which says that between 15 and 20 percent of women meet the criteria for the condition:

The prevalence of PCOS varies depending on which criteria are used to make the diagnosis, but is as high as 15%–20% when the European Society for Human Reproduction and Embryology/American Society for Reproductive Medicine criteria are used. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3872139/)​

Do you have any study that concludes that women have lower dihydrotestosterone levels than men? It'd be interesting to compare. Unfortunately, I haven't even found any information regarding the amount of 5-alpha-reductase that any of the organs stand for.

Also, you're right about the size of the testes. For example, those injecting anabolic steroids will shrink their testes. If you inject anabolic steroids, your testes will no longer need to produce testosterone due to the body already receiving its demands from the injections. If you've been injecting for a prolonged amount of time, your testes will have lost their former ability to produce testosterone.

However, the testes don't constantly grow as is the case with the prostate. The ovaries on the other hand risk developing cysts with age. Thus we could have a similarity between the prostate in men and the ovaries in women. My theory is that an increase in size of the prostate leads to an increase in 5-alpha-reductase, just like cysts in the ovaries do.
Women have high estrogen which helps reduce Dht, not sure if it actually reduces 5ar directly but it does increase SHBG which keeps Dht less bioavailable. Also, women have less T production itself, and premenopausal women have higher progesterone levels and progesterone combines with 5ar to produce allopregnanedione.

ok but the ovaries aren't really a counterpart to the prostate and i doubt cystic growth is the same type of enlargement the prostate goes through. Skene's glands are often reffered to as thr "female prostate". the size could just be a byproduct or correalation of the real problem.
 

Armando Jose

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Alright, thank you. So, sebaceous glands are found all over our skin except from the palms on the hands and the soles of the feet. Sebaceous glands are more numerous on the face and on the scalp. I educated myself on this with the help of Wikipedia and here's an image of how sebaceous glands are attached to hair follicles:

View attachment 76746

As the NCBI article says, the sebaceous gland is the main factory within the skin that produces hormones. Your quote is from the fifth paragraph, which also includes:

The classical androgen-dependent dermatoses, acne, androgenetic alopecia (Androgenetic Alopecia), seborrhea and hirsutism are among the most common skin disorders. Human sebaceous glands and hair follicles are equipped with all the necessary enzymes for biosynthesis and metabolism of androgens.​

So from what I understand, the sebaceous glands can produce the androgens responsible for the development of male pattern baldness. But then the question is if sebaceous glands alone can produce the amount required to actually trigger the process. We also know that testosterone made elsewhere in the body, such as the testes which stand for more than 95% of the production in men, are responsible for male pattern baldness. Otherwise men wouldn't halt their hair loss entirely through castration. Please correct me if I'm wrong, but I suppose this has to do with that testosterone can be delivered through the bloodstream from the testes to the sebaceous glands which leads to an increase of dihydrotestosterone production. With this in mind it sounds plausible that dihydrotestosterone produced, in the prostate for example, could also seek its way through the bloodstream directly to the hair follicles and trigger male pattern baldness.


More than 10 years ago, in this forum. A post of Mr. Bryan Shelton:
"There are a few separate lines of evidence which, taken together, strongly suggest that it's follicular DHT which is the much more important factor, and that DHT itself doesn't have much of a role as an endocrine hormone in the body:

1) I read in a medical journal article (I wished I had saved it, so I could cite it) that most molecules of DHT formed within cells go on to bind to androgen receptors within that same cell. If that's true, then the implications are obvious.

2) Serum DHT is eliminated fairly rapidly, so it obviously can't hang around long enough to have much of an endocrine effect.

3) The animal experiments (and at least one small human experiment) with topical 5a-reductase inhibitors (for example, the hamster study with the topical fatty acids) show an effect only where they're actually applied, strongly implying once again that serum DHT isn't doing anything to keep those hamster flank organs going. Reducing only the local DHT was sufficient to sharply inhibit their growth. So if that's the case with sebaceous glands which are exquisitely sensitive to androgenic stimulation, is it really so difficult to believe that it's also the case with hair follicles?

4) Conversely, sharply reducing serum DHT with finasteride had no effect on sebum production in humans in Imperato-McGinley's study which I posted about recently, again showing that serum DHT doesn't seem to have any detectable effect on sebaceous glands. Why would one expect it to have much effect on hair follicles?

5) Dr. Proctor has said numerous times on alt.baldspot that endocrinologists have traditionally been taught that DHT only has an effect where it's actually produced (which is to say, it again doesn't have much of a role as an endocrine hormone).

Bryan"

https://www.hairlosstalk.com/interact/threads/is-5ar-type-2-produced-inside-the-hair-follicle.27870/
 
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