Back to the roots: Causes and effects of elevated DHT

LayZ

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dht in puberty has already created beard follicles, theres nothing you can do about it.
BUT nofappers including me report slower rate of beard growth.
I get in 4weeks the beard length I used to get in one week.

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how the **** is local production not effected when systemic levels change? are you willing to explain that?!?!

"After 3 months without sex, testosterone drop to levels close to children's levels ."
http://prezi.com/7psnqtet-oom/how-sexual-activity-effects-sports-competition/

After looking over the complete stain of an article you linked to as evidence for your claims:

I can only conclude that you're sneaking in some fapping if that beard of yours is still a growing...

Practice What You Preach!!!!
 

Hairbackpls

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Ive been no fap for a month now. Cant see any results yet. I plan to continue no fap and start finasteride so if i get good results, no fap might have some effect. Will see in couple months. Im also planning to use cetrizine 20mg a day while on finasteride.. Just for science.
 

uncomfortable man

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No fap is so last month. It's all about holding your shiat now. Pooping causes hairloss so it's time to put a cork in it!

(I know I said this before but I think it deserved an encore, no?)
 

Hairbackpls

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No fap is so last month. It's all about holding your shiat now. Pooping causes hairloss so it's time to put a cork in it!

(I know I said this before but I think it deserved an encore, no?)

Yeah it is, but im not doing it because of hairloss. I do believe it has some effect on hairloss tho (theres studies too). Id say its not the Cure, nor as powerful as dht blockers, but its an extra topping on ur treatment. Better than drinking tea atleast...
 

dps

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what do you mean by no results? no regrowth?
by one month you should have decreased shedding, and I believe you do.
 

Hairbackpls

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what do you mean by no results? no regrowth?
by one month you should have decreased shedding, and I believe you do.

Well.. My hair shed have just gotten worse in this month and i need to hurry up getting on finasteride. No regrowth either.
 

bushbush

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when you study few years of ancient alchemical hocus-pocus

ftfy.

semen production starts in the brain, I don't know what the produced substance is called, but it then travels down the spine to the prostate and tests to become the semen that you carelessly love to waste.

Do you have any evidence to back up such a wild claim?
 

inbrugge

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I think Sexual Activity in general increases overall DHT in body, which also affects the scalp. It's as simple as that. No fap won't be a cure, but I believe increased sexual activity will help accelerate hair loss.
 

Ventures

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Testosterone is primarily anabolic steroid which strongly binds to androgen receptors in muscle cells and increases muscle protein synthesis. DHT is produced locally in sex organ cells and also in dermal papilla cells of scalp and body hair and strongly binds to androgen receptors in those tissues. DHT has fairly short half life time (2-3 hours ?) meaning there is low probability DHT generated in your testis will float freely in bloodstream and reach scalp and DP unless it by some magic way not get absorbed or attached to androgen receptors on its way. This all means that DHT generated inside scalp hair follicles and in close proximity causes DP miniaturisation.

Of course, high sexual activity (sexual intercourse, masturbation) may rise systemic T which in turn causes more T to be delivered in scalp since testosterone is systematically distributed in the whole body. And more T may cause higher probability for conversion to DHT by 5ard. So, indeed more T due to masturbation could mean more DHT production but only if there is presence of 5adr enzymes in target locations.


On the other hand I am not informed what is relation between sexual activity and 5ard production. Can masturbation increase 5ard type I or II production ? I don't think so ? But this is only my opinion. We should find research papers which analyse that.
 

Hairbackpls

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DHT is inactivated to 3α-androstanediol and 3β-androstanediol by the enzymes 3α-hydroxysteroid dehydrogenase and 3β-hydroxysteroid dehydrogenase, respectively.
Source:Wikipedia dht

Just wondering if its possible to use these a & b-hydroxysteroid dehydrogenases as topical to inactivate dht in scalp somehow??
 

Ventures

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I wondered, well It is known that there is more DHT generated in balding regions compared to the occipital region (both inside follicles and in sebaceous glands). But what if hair follicles from donor region (occipital hair) were transplanted to the front. Do they start to produce more DHT inside dermal papilla or does the level of DHT generated inside DP remain the same ? That is the question; because modern Male pattern baldness theory considers that resistance lies within follicles rather than in its surrounding/tissue location where they were transplanted.


Actually there is a study which http://www.ncbi.nlm.nih.gov/pubmed/16931898 showed that high concentrations of T and 5alpha-DHT were needed to induce apoptotic effects in dermal papilla cells (DPC) from nonbalding scalp regions of healthy volunteers.


So this indicates that donor hair is also
vulnerable to DHT but it's threshold is greater, probably due to much less number of AR in dermal papilla cells, compared to the hair from balding regions.
 

Python

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25 pages and still the same questions and answers are brought up over and over again. It's like no one even bothers to read the first pages.
 

xRedStaRx

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I wondered, well It is known that there is more DHT generated in balding regions compared to the occipital region (both inside follicles and in sebaceous glands). But what if hair follicles from donor region (occipital hair) were transplanted to the front. Do they start to produce more DHT inside dermal papilla or does the level of DHT generated inside DP remain the same ? That is the question; because modern Male pattern baldness theory considers that resistance lies within follicles rather than in its surrounding/tissue location where they were transplanted.


Actually there is a study which http://www.ncbi.nlm.nih.gov/pubmed/16931898 showed that high concentrations of T and 5alpha-DHT were needed to induce apoptotic effects in dermal papilla cells (DPC) from nonbalding scalp regions of healthy volunteers.


So this indicates that donor hair is also
vulnerable to DHT but it's threshold is greater, probably due to much less number of AR in dermal papilla cells, compared to the hair from balding regions.

They also have less 5-AR II activity, so transplanted hair on bald regions stay that way, because their own internal environment is not predisposed to miniaturization. Just as like how you find some anomaly hair strands that do no really miniaturize on bald scalps.
 

I.D WALKER

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To your fine point: It really is remarkable how transplanted and/or non affected follicles are resistant to miniaturization at such environmentally small and microscopic level(s). Survival of the fittest prevails even in some of the most finite and hostile areas.
 

Ventures

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So reasons why hair follicle transplanted from donor region doesn't miniaturise (and fall out) is:

a. ) it produces less follicular DHT (inside Dermal papilla) and of course;

b.) it is less genetically predisposed to DHT miniaturisation, because it contains less androgen receptors


Do you agree that both factors contribute to its resistance and permanent life cycle, and which factor is more important ? Another question, how many times is donor hair "more resistant" to DHT level than balding hair in the same individual. What I wanted to ask you, if a threshold for miniaturisation of balding hair is, lets say, 5 pmol/g, than what level of DHT concentration inside follicles can harm donor hair in the same person. Is this level two or three times greater than 5 pmol/g ? Apparently it seems that people with aggressive hair loss often tend to have thinning donor zone which means even 10-20% or even more of hair in that donor zone also miniaturise latter in life.
 

I.D WALKER

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I don't mean to regress to rhetorical circumlocution, but do we know then: That the levels of T and 5alpha-DHT are measured proportionately (+/-) and consistently throughout the entire scalp region of every Androgenetic Alopecia "sufferer"? That is, are these levels consistent or not between balding hair region and "safe zone" or occipital? Thanks.
 

xRedStaRx

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So reasons why hair follicle transplanted from donor region doesn't miniaturise (and fall out) is:

a. ) it produces less follicular DHT (inside Dermal papilla) and of course;

b.) it is less genetically predisposed to DHT miniaturisation, because it contains less androgen receptors


Do you agree that both factors contribute to its resistance and permanent life cycle, and which factor is more important ? Another question, how many times is donor hair "more resistant" to DHT level than balding hair in the same individual. What I wanted to ask you, if a threshold for miniaturisation of balding hair is, lets say, 5 pmol/g, than what level of DHT concentration inside follicles can harm donor hair in the same person. Is this level two or three times greater than 5 pmol/g ? Apparently it seems that people with aggressive hair loss often tend to have thinning donor zone which means even 10-20% or even more of hair in that donor zone also miniaturise latter in life.

I'd say a mixture of both.

http://www.ncbi.nlm.nih.gov/pubmed/9284093

Balding follicles had around 80% more DHT than non-balding follicles.
 

I.D WALKER

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I have to wonder whether this is found to be accumulative or not? (5alpha DHT or T build up so to speak)
 
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