Bayer Prolactin Receptor Antibody For Male And Female Pattern Hair Loss
- Thread starter Ollie
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I don't know jack sh*t about these things but does prolactin only affect the catagen-anagen cycle or actually cause miniaturization?
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Orgasm 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.
I don't know about "routinely", but estrogen and cortisol both can stimulate prolactin release, so it would make sense.
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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 ?
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yeah 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
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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
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.
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so you DO believe nofap will help keeping your hair?
thats the oldest myth in male pattern baldness broscience
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I think we're getting a bit ahead of ourselves with the no fap business. The fact that jerking off or having sex will increase your prolactin doesn't necessarily mean it will speed up your hairloss. It's possible that the prolaction->hairloss response is very dose dependant and any prolactin beyond what's produced in the HF makes little or no difference. Of course, it's possible that it WILL, but I'm saying just knowing that orgasming increases prolactin doesn't necessarily also tell you it will speed up hairloss.
I mean look at the monkey study. After they got off the antibody and prolactin started activating the receptor again it didn't do sh*t. Well, maybe it started the long cascade of hairloss, but in that case it prolly means that once it's activated it moves at a glacial pace, so would jerking off every day really make a noticeable difference?
Is there any evidence that more DHT will speed up hairloss to a significant degree?
I mean look at the monkey study. After they got off the antibody and prolactin started activating the receptor again it didn't do sh*t. Well, maybe it started the long cascade of hairloss, but in that case it prolly means that once it's activated it moves at a glacial pace, so would jerking off every day really make a noticeable difference?
Is there any evidence that more DHT will speed up hairloss to a significant degree?
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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).
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.
This is a table from the mouse study linked above showing that only full inactivation of the PRLR enlarged hair shafts. Also from this you can see that silencing the PRLR enlarges male follicles more than female. This aligns with the hair counts from the macaque study that found males responded better than females to the PRLR antibody, and studies showing that catagen genes are downregulated by prolactin in human female frontotemporal hair, and blocking prolactin causes apoptosis in those hairs while adding prolactin elongates them. This is the opposite of what has been observed in human male scalp follicles. This might partially explain the different patterns in female and male pattern hair loss. PRLR antagonism will likely only work on the vertex in women while working everywhere in men.
Prolactin: an emerging force along the cutaneous–endocrine axis
In mice the PRLR is not expressed in the HM, while in humans it's expressed in the HM only during catagen. The HM sits on top of the DP and contains the cells that produce the hair shaft. Androgenetic Alopecia pathogenesis might involve aberrant PRLR signaling in the matrix reducing proliferation during anagen. Silencing the PRLR for long enough might return the hair follicle to its normal state where PRLR is only expressed in the matrix during catagen, and that could explain why the macaque regrowth lasted for years after discontinuing treatment. When DP cell numbers drop below a minimum threshold cell proliferation stops. So my question, does the DP cell number dropping below this threshold cause the matrix to express PRLR and enter catagen
This is a handy but not up-to-date chart showing known regulators of prolactin. There was a Japanese twin study which found there might be a link between smoking and severity of hair loss, but it was a weak link. The only known significant promoters here of ePRL are estrogen and TRH, but neither appears to be the major promoter of prolactin in the HF, and TRH downregulated PRLR immunoreactivity in the outer root sheath.
When looking at prolactin's biological effects it's important to remember that they are both site- and sex-specific. There are multiple PRL and PRLR variants with differing biological actions. For instance, PRL induces cell proliferation in breast cancer, but stops it in the HF.
I believe 3 more have been found since this review was published.
This study found a role for PRLR in the pathogenesis of alopecia areata, independent of serum prolactin. Two additional studies found similar results, but two others found significantly increased serum prolactin levels in patients with AA. They all found a role for prolactin signaling in AA. From this study, "a significant positive correlation was found between the prolactin receptor and the SALT[severity of alopecia] score".
There's good reason to believe that prolactin plays an important role in the pathogenesis of Androgenetic Alopecia as well. The gene for PRL is next to an Androgenetic Alopecia risk locus, indicating a potential causal relationship. The remarkable regrowth of hair in bald stump-tailed macaques confirms that this is an area requiring further attention. I believe that PRLR antagonists will become part of the big 3. To fight Androgenetic Alopecia in the future people will antagonize the androgen receptor, upregulate the canonical Wnt pathway, and antagonize the prolactin receptor.
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.
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7 years of attempting to treat hair loss summed up in a single sentence. Beautiful, and sad.
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thoughts on minitherapy approach?
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There is a suspicion that Minoxidil, a potassium channel opener, may be related to the development of this disease. A two year test with Minoxidil, under normal dosing parameters, was carried out on rats which caused pheochromocytomas in both males and females, and preputial gland adenomas in males[1].
Two-year carcinogenicity studies of Minoxidil have been conducted by the dermal and oral (dietary) routes of administration in mice and rats. There were no positive findings with the oral (dietary) route of administration in rats.
In the two-year dermal study in mice, an increased incidence of mammary adenomas and adenocarcinomas in the females at all dose levels (8, 25 and 80 mg/kg/day) was attributed to increased prolactin activity. Hyperprolactinemia is a well-known mechanism in the enhancement of mouse mammary tumors, but has not been associated with mammary tumorigenesis in women.
However:
Additionally, topical Minoxidil has not been shown to cause hyperprolactinemia in women on clinical trials.
What about men?
Two-year carcinogenicity studies of Minoxidil have been conducted by the dermal and oral (dietary) routes of administration in mice and rats. There were no positive findings with the oral (dietary) route of administration in rats.
In the two-year dermal study in mice, an increased incidence of mammary adenomas and adenocarcinomas in the females at all dose levels (8, 25 and 80 mg/kg/day) was attributed to increased prolactin activity. Hyperprolactinemia is a well-known mechanism in the enhancement of mouse mammary tumors, but has not been associated with mammary tumorigenesis in women.
However:
Additionally, topical Minoxidil has not been shown to cause hyperprolactinemia in women on clinical trials.
What about men?
This approach is better. This peptide will supposedly silence prolactinogenic activity even if prolactin binds PRLR along with the peptide and, because of that, it's easier to gain more useful information if you know you can reliably silence all prolactinogenic activity sytemically. With the other approach, if it doesn't work, it's difficult to tell why exactly it didn't work. At least if this doesn't work, you'll know that the PRLR doesn't play a significant role.
Other than the side effects to look out for due to the obvious inhibition of PRLR, the other factors that have to be considered are receptor-independent effects of prolactin. Based on the research, it seems like it's probably not very likely that prolactin has PRLR-independent effects that are responsible for hair loss, but it could still be possible that prolactin may have receptor-independent side effects. Just something to look out for. There's not a whole lot of clinical research out there on these hormones that are typically and criminally labeled "female" hormones. I wish that estrogens and progestagens and other hormones like this weren't casually thrown into a "female" category. It obfuscates real research. These hormones have a purpose in both males and females and this "labeling" has caused decades of ignoring their potential roles in various diseases and disorders (imo).
I'm very pleased to see research into other hormones rather than continuing to beat a dead horse with the androgen receptor and DHT. They're all likely interconnected in the pathogenesis of Androgenetic Alopecia, but the industry's obsession over only this one element has been a source of disappointment to me for awhile.
finasteride and dutasteride will cause a dramatic spike in prolactin if it has affected your Estrogen enough - Estrogen being the primary precursor to Prolactin. My E goes up 50% on finasteride and as a result my Prolactin absolutely sky rockets. If i control my E with an AI it normalises.
EDIT: Which is actually super f*****g weird now i think about it as Estrogen is the one hormone that allows for the greatest amount of regrowth - perhaps as long as Prolactin doesn't increase disproportionately greater than the increase of E.
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