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The study is about sistemic prolaction not prolactin on the hair folicules
No, having more sex won't make you bald.
No, having more sex won't make you bald.
You think systemic prolactin doesn't reach the hair follicle too? What about systemic dht? If it's in the blood then it's going to hit the HF. Also, why wouldn't extrapituitary prolactin also be increased?The study is about sistemic prolaction not prolactin on the hair folicules
No, having more sex won't make you bald.
Why does dutasteride increase prolactin levels?You think systemic prolactin doesn't reach the hair follicle too? What about systemic dht? If it's in the blood then it's going to hit the HF. Also, why wouldn't extrapituitary prolactin also be increased?
It doesn't.Why does dutasteride increase prolactin levels?
I don't know jack sh*t about these things but does prolactin only affect the catagen-anagen cycle or actually cause miniaturization?Sex and masturbation both raise prolactin, so both are bad for your hair. According to that study sex is worse.
isnt prolactin routinely raised in bloods after people take finasteride? i could swear I have seen that half a dozen times
My theory is that these are two almost closed systems. Because taking cabergoline won’t help your hair afaik?. So, what’s the logic. I think the concentration of locally synthesized prolactin is almost always higher intracellularly, than the amount in the serum. So cell membrane osmosis will always happen from the cell to serum and not the opposite. But i’m not sure. What do you think @pegasus2 ?You think systemic prolactin doesn't reach the hair follicle too? What about systemic dht? If it's in the blood then it's going to hit the HF. Also, why wouldn't extrapituitary prolactin also be increased?
yeah thats why I think it's eitherOrgasm increasing prolactin may give some credibility to the people who claim their hair loss slowed down while doing nofap.
I don't know about "routinely", but estrogen and cortisol both can stimulate prolactin release, so it would make sense.
this would also mean that men who want to f*** and masturbate lose hair. not those that have no libido in the first place. whether actually doing the act or abstaining despite being horny matters would be another questionyeah thats why I think it's either
1. closed systems and it doesn't matter
2. high prolactin leading to low intrafollicular prolactin, because hair functions as a systemic endocrine balancer. if you look at what hyperprl. in men does it's less body hair, libido problems, gyno. I think this profile sounds pretty good to grow hair
No, I don't think so. It's the act itself that increases prolactin. Low prolactin is what makes your libido high, then prolactin is released after the act as a reward for procreating, and to suppress your sex drive allowing you to focus on other aspects of survival.this would also mean that men who want to f*** and masturbate lose hair. not those that have no libido in the first place. whether actually doing the act or abstaining despite being horny matters would be another question
It won't do anything. It's been tried. There's zero effect on extrapituitary prolactin and hair growth.I’m going to test Cabergoline. I have 2 bottles of it. See if it does anything.
My theory is that these are two almost closed systems. Because taking cabergoline won’t help your hair afaik?. So, what’s the logic. I think the concentration of locally synthesized prolactin is almost always higher intracellularly, than the amount in the serum. So cell membrane osmosis will always happen from the cell to serum and not the opposite. But i’m not sure. What do you think @pegasus2 ?
so you DO believe nofap will help keeping your hair?No, I don't think so. It's the act itself that increases prolactin. Low prolactin is what makes your libido high, then prolactin is released after the act as a reward for procreating, and to suppress your sex drive allowing you to focus on other aspects of survival.
It won't do anything. It's been tried. There's zero effect on extrapituitary prolactin and hair growth.
I don't think that it's closed. There's a bit of crossover regulation. I will get back to you with a more detailed post later.
I agree with you that autocrine/paracrine PRL has much more effect on the hair follicle than endocrine prolactin, but I don't think endocrine prolactin is closed off from HF cells. Look at hyperprolactinemia where scalp hair gets decimated. Either pituitary PRL is having a direct effect on the cells, or intrafollicular PRL is upregulated by serum PRL through the immune system, or upregulated by the same promoter as pituitary PRL. PRL research is still in its infancy, but it appears to me that all three of these are true. This is the first study confirming an autocrine PRL loop in breast tissue; in it they suggest targeting "both endocrine and autocrine/paracrine levels" to fight breast cancer. I would think the same strategy would be necessary for alopecia. BAY and SMI both do this, dopamine agonists obviously do not. (dopamine receptors have been found in adipocytes now, but they are not a promoter of PRL in the HF).My theory is that these are two almost closed systems. Because taking cabergoline won’t help your hair afaik?. So, what’s the logic. I think the concentration of locally synthesized prolactin is almost always higher intracellularly, than the amount in the serum. So cell membrane osmosis will always happen from the cell to serum and not the opposite. But i’m not sure. What do you think @pegasus2 ?
A key question is, how low does PRLR signaling have to be to reverse hair loss? Dopamine agonists don't tell us anything except that reducing endocrine PRL is insufficient. PRLR expression in the HF is different in mice, but this study shows that PRLR null mice grow significantly longer and thicker hair, whereas PRLR impaired mice do not. Unfortunately I don't know the level of PRLR signaling impairment in the heterozygote mice, but this tells us that, in mice, there is no benefit to partial PRLR antagonism. In order to improve hair growth it has to be complete inhibition or at least below a threshold that is lower than what is present in the PRLR +/- mice. Another factor is that the PRLR is also bound by growth hormone. Does GH have the same biological action on the receptor as PRL does in the HF? Pure speculation here, but I wonder if GH reverses hair loss through binding to the PRLR and preventing PRL from binding to it.
In humans, variants of PRL of 14–17 and 22 kDa have been identified, some with differing biological activities. For example, the 16 kDa variant exerts important antiangiogenic functions, in contrast to the classic 23 kDa PRL, which has proangiogenic properties....
I believe 3 more have been found since this review was published.PRLR isoforms, of which six have been identified to date [26], might elicit their distinct biological properties depending on their ability to activate specific signaling cascades
Why does dutasteride increase prolactin levels?
genetic expression of some enzyme or receptor is higher than it should be in the hair follicle, but normal in the rest of the body... and when you attempt to correct that with pharmaceuticals, you fix the problem in the hair follicle and cause other problems due to deficiency in the rest of the body.
I'm not sure why clinical research shows no changes in serum prolactin levels from dutasteride use. Finasteride caused hyperprolactinemia for me. As far as why a 5AR antagonist would increase prolactin levels: if DHT has a role in regulating PRLR expression, then lowering DHT synthesis will cause lowered overall prolactinogenic activity and will, thus, likely cause an upregulation in prolactin synthesis to compensate for the lowered PRLR expression.
If prolactinogenic activity turns out to play a significant role in Androgenetic Alopecia, this would also explain the loss of efficacy of 5AR antagonists over time. Eventually, the lowered PRLR expression (caused by lowered DHT synthesis) is negated by an increase in prolactin synthesis to normalize prolactinogenic activity (which would explain elevated PRL due to a 5AR antagonist). And all of this, of course, is because genetic expression of some enzyme or receptor is higher than it should be in the hair follicle, but normal in the rest of the body... and when you attempt to correct that with pharmaceuticals, you fix the problem in the hair follicle and cause other problems due to deficiency in the rest of the body.
thoughts on minitherapy approach?7 years of attempting to treat hair loss summed up in a single sentence. Beautiful, and sad.