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Setipiprant Does Work, But Only On Really Really High Doses.
- Thread starter westonci
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Yeah, like I said in the other thread where you mentioned that, thanks for the update, and that really speaks for itself.
Stick to proven approaches. That whole "private forum" seems like a cult. Thousands of dollars over there everyone's pouring into things with zero or minimal evidence for results that look worse than a lot of minoxidil users.
Even Allergan's now backing down on this one. What does that say?
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I agree that cost is ridiculous.
But you're wrong with results. Westonci brings results here : hair loss completely stopped and a lot of vellus hair/little regrowth.
People who can afford 2g/day on private forum had much success than him.
I think Seti is too much for an oral or topical use. 2g/day is too much against 0.5/1.5mg Fina.
150mg Fevi/day will be way better.
This + Daorlutamide should stop hair loss forever and offers real maintenance.
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At the 2015 hair congress, Cots et al. presented data showing that:
- PGD2 inhibits hair growth in mouse and human follicles (known already).
- Hair follicles from some people don't respond to PGD2.
- There are three SNPs (all in high linkage disequilibrium) around the PTGDR2 gene (also known as DP2, CRTH2, or GPR44) associated with response to PGD2 (rs545659, rs634681, rs7167). One of these SNPs -- rs545659 -- is known to affect PTGDR2 mRNA stability. The T allele at rs545659 results in lower mRNA stability and is associated with a lower risk of asthma and non-response to PGD2 in hair follicles.
Here's what Cotsarelis et al. say in one of his patents:
So here we have genetic variants with a large biological effect. Cots says we can use these variants to infer who is likely to prevent A.G.A using DP2 antagonists. So...What effect do these SNPs have on risk of A.G.A? If Cots is right we should expect these SNPs, which have a large biological effect, to also have a large effect on risk of A.G.A (and for DP2 to be a good drug target). Fortunately, after Cots et al. published this information, Hagenaars et al. published a genome-wide association study (GWAS) on A.G.A with a cohort of 52,000 men. They made their summary data available, so we can check those SNPs and see what effect they have on one's chances of going bald.
Yeah, zero effect on A.G.A risk. p = 0.17-0.2 (not significant even without multiple testing correction). SNPs associated with PGD2 sensitivity are irrelevant for A.G.A risk, and DP2 is likely to be a lousy drug target.
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sh*t, why are they even testing it then ?
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How do you know that Daorlutamide will not go systemic ?
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Only 3% max of metabolites goes systemic and it doesn't cross BBB.
"I doubt 99% of guys would notice any side effects with even 15 mg darolutamide twice a day topically and that in theory should be pretty strong."
Don't throw statistics like this, it's based on nothing haha
But I understand your excitement it's may be a good ally against MBP.
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It's tested on 52k people.
Only few people have PGD2 hair sensitivity. If some takes Seti and Fevi,it's not for CRTH2 sensitivity but if you follow Cots theory, there is too much of it in a bald scalp which prevent hair growth and hairs induced by dermaneedling or anything can't grow without a PGD2 antagonist.
DHT is necessary for hair at good dose. PGD2 isn't. But both are important to the body.
And CRTH2 antagnist also take care of DHT by chain reaction if I understand it well.
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60 percent had it.
I don't think you understood my point. Consider people with androgen insensitivity syndrome - they have loss-of-function in AR and don't go bald. Large biological effect (loss of function), large difference in outcome. Therefore, AR plays an important role in A.G.A and is a good drug target for preventing baldness. Same goes for SRD5A2, the gene encoding 5-alpha reductase type II. Pseudo-hermaphrodites have loss of function in this gene and don't go bald. This is another case of a large biological effect with a large difference in outcome, and 5ar type II inhibitors like finasteride usually prevent baldness.
Even variants with small effects can be associated with disease risk as long as they control genes that play some role in causing the disease. For example, the T allele at rs7349332 is associated with a slightly lower expression of WNT10A in hair follicles and is associated with a slightly increased risk of A.G.A (source). Small biological effect, small but significant effect on A.G.A risk. Contrast this with rs545659, which has a major effect on PTGDR2 mRNA stability and is highly associated with hair follicle sensitivity to PGD2 (with an odds ratio of 5.0). According to Cots' hypothesis, PGD2/PTGDR2 is a major node in the network that causes baldness. But large differences in the level of signaling through this node have zero effect on baldness risk? Doesn't check out.
Not scalp hair.
Doesn't seem likely.
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DHT can induce (which roughly translates as "indirectly generate" -- as in to generate by some roundabout or multi-step pathway) PGD2 Synthase, and, by extension, PGD2 itself
https://www.ncbi.nlm.nih.gov/pubmed/24548754
Yeah I know that and understand your point,but the main point is : keeping hair,brain and dick at the same time. 5-Ar are essential to the brain so it won't be a good solution at the end.
Yeah so nothing scientifically proved on bald scalp as yourself say.
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Are you a biochemischst?
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You can do your own research and I try to be the most clear as possible by presenting ncbi paper etc
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I'm sorry. I probably shouldn't be baited by this but I don't understand what you are saying. Do you deny finasteride can cause regrowth in >~80% of men? That is not my "opinion". It has been shown objectively in scientific research.
How do you explain this?
I will not reply further if your response does not properly address what I'm asking as it's wasting everyone's time and cluttering the thread.
mowingdown
Member
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Let it go. He is either trolling or doubling down when he knows he is wrong. It's a total waste of time.
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I don't mean to butt in but after seeing you repeatedly post, I feel the need to pay you the courtesy of a tip. I mean this in the nicest way possible - you are either not as knowledgeable as you claim, or you have done an extremely poor job of demonstrating your competency on the subject thus far.
Consider the irony of claiming that your statements are backed by the one or two studies you posted. My friend, have you any idea how much literature exists on the role of androgens in androgenetic alopecia? Now I think I understand the point you are attempting to make, which is that androgens initiate a cascade and it is peripheral processes that ultimately influence hair growth or lack thereof. But saying that androgens play a minor role is a very poor way of transmitting that message and frankly demonstrates a gross misunderstanding of male pattern baldness.
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Every part where you continue to both demonstrate your misunderstanding of the literature and insist that your interpretation is correct demonstrate the mismatch between how well versed you appear to believe are on the subject versus how accurate your posts are.
So in short, most of your recent posts.
It's not my job to win an arguement with you. It's your job to get it right. We are likely not deceiving you when we take issue with you stating that androgens play a minor role in androgenetic alopecia. It's not exactly up for debate and continuing to argue with you about it while you insist otherwise is an especially unappealing activity to partake in, given that we are already heading the way of personal attacks, with you so humbly calling me someone else's "conniver"
I speak only for myself, thank you very much for making me clarify that.
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The mechanism he proposes doesn't work since A.G.A is AR-dependent. And that's in prostate, not hair follicles. The pathways controlling PTGDS expression in HFs aren't well understood. Yes, PTGDS is a downstream target of DHT somehow, but we don't know how, and it could be (and probably is) secondary to more important factors.
Well, if you want to keep your hair by targeting downstream components, you have to figure out what those downstream components are first. Or you could just a topical AR inhibitor to maintain hair, though understanding the downstream components might help with reversal.
Nope.
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So other than you parroting back to me the very same thing I just told you, I actually agree with that last part.
Indeed it is time for me to move on. It is not time for me to wonder what you are still doing here if you will let everyone make their own judgements - it's apparent that they have, just as you have. And it is especially not time to try to understand why in the world you would assume that I meant it was your actual paid job to do anything in this forum; in context, it obviously meant your problem, burden, or responsibility, and it was referring to you being responsible for knowing what you are talking about, if indeed you care about reading the literature and talking about it, not that you were somehow responsible for convincing others of this viewpoint or that - that isn't what I said. And it's not time for me to explain the difference between an ad hominum attack and an objective observation, albeit an unpleasant one.
No it is certainly time to move on to the next thing. Please enjoy the camraderie and civil discussion that this place has to offer - I'm sure you'll fit right in.
He IS using anti-androgens, Dutasteride no less. I know this as a fact, this isn't the only forum that he frequents.
Based on your regimen, it's pretty evident that you don't care about your sexual function - However most of us do value our penis.
You can squeal all you want about how you're still getting boners like a 15 year old, a user on HLH thought the exact same thing; even going as far as to make a thread entitled "Is my dick a superhero?" and boast about his erection quality despite using 100mg Androcur.
Nowadays, his penis has shrunk, doesn't work anymore, has been cheated on/cuckolded, and his hair looks like sh*t on top of that.
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LOL, 15 posts on 3 years, but you shoot, you score