How male pattern balding actually works

Just jump on fin. (How old are you? If 21+ jump on fin.)
I'm 24 and noticed hair loss at 22, it had receded to a widow's peak but still look alright and I had great density. I just waited it out and now I'm noticing major density loss in the front, I can see my pattern now and I'm definitely going full Jude Law mode.
Couple days ago I jumped in the shower to use Nizoral for the first time (cope buy in my case but major recommend, it completely nuked my dandruff which has been a lifelong problem and after 1 use of Niz I didn't have a single flake, and i haven't felt scalp itch since I used it) and while I washing my hair I noticed hair covering my hands. That was my last straw, I'm setting up an appointment this Saturday to get a fin prescip and I will start taking it Monday.
Thing is if you think you will probably use it at some point then START NOW. That's my conclusion anyway, I should've just decided to get on at 22 instead of coping around. I've done a fuckload of research on this, less than 1% of men experience permanent sides. If you or I are that 1% life will certainly get 100x more hellish for us, but IMO that's worth a roll of the dice to maintain your hair. I plan on jumping on fin and then applying the protocol outlined here
as well as a few other things I've picked up from obsessively researching hair loss for 2 years to cope that I had control over it
tl;dr TAKE ACTION NOW PRESERVE HAIR
Stuff like Nizoral and Minox without fin/dut is like putting a bandage on a knife wound - You are bleeding out and need serious medical attention, a bandage can't save you unless you take care of the root of the problem. I also waited 2 years to take fin because I was scared of the side effects (took minox/saw palmetto and other stuff instead), but my hair continued to recede. Currently I'm only taking 0.5mg of fin each night (for 2 years and haven't been on anything else, not even minox, nizoral or anything of this nature), and my hair has never looked better. It was the only thing that saved my hair. As long as you take care to control the estradiol boost that occurs when you start taking it, the side effects you experience will be non-existent/minimal unless you know what you are looking for.
 
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Stuff like Nizoral and Minox without fin/dut is like putting a bandage on a knife wound - You are bleeding out and need serious medical attention, a bandage can't save you unless you take care of the root of the problem. I also waited 2 years to take fin because I was scared of the side effects (took minox/saw palmetto and other stuff instead), but my hair continued to recede. Currently I'm only taking 0.5mg of fin each night (for 2 years and haven't been on anything else, not even minox, nizoral or anything of this nature), and my hair has never looked better. It was the only thing that saved my hair. As long as you take care to control the estradiol boost that occurs when you start taking it, the side effects you experience will be non-existent/minimal unless you know what you are looking for.
Damn dude how old are you and how old were you when you started taking fin? Did density return?
I totally agree that those things without a potent anti-androgen are copes, I've resolute to start taking fin now. Although Nizoral seems to have nuked my scalp inflammation from orbit I know that alone will probably do nothing, if I cope with that in six months my scalp top will look like a fucking bombed out Iraqi village JFL
How do I control the estradiol boost?
 
Damn dude how old are you and how old were you when you started taking fin? Did density return?
I totally agree that those things without a potent anti-androgen are copes, I've resolute to start taking fin now. Although Nizoral seems to have nuked my scalp inflammation from orbit I know that alone will probably do nothing, if I cope with that in six months my scalp top will look like a fucking bombed out Iraqi village JFL
How do I control the estradiol boost?
I'm about to be 23 and I started soon after turning 21. For density - anywhere that was thinning filled back up /came back, have had absolutely no recession since taking it, and my hair felt a lot thicker in general, but whatever's gone before you start taking it is gone. For estradiol control, I advise diet (pomegranate juice, mushrooms, broccoli all work really well to lower estrogen) and to save estrogen-blockers as a last resort (I never needed to use it). You'll know that your estradiol is high because your body will start storing a lot of your fat in your mid-section area, you'll gain like 5 pounds in water weight, your erections will be weak, etc; as long as you take care of this you'll feel really great.
 
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I'm about to be 23 and I started soon after turning 21. For density - anywhere that was thinning filled back up /came back, have had absolutely no recession since taking it, and my hair felt a lot thicker in general, but whatever's gone before you start taking it is gone. For estradiol control, I advise diet (pomegranate juice, mushrooms, broccoli all work really well to lower estrogen) and to save estrogen-blockers as a last resort (I never needed to use it). You'll know that your estradiol is high because your body will start storing a lot of your fat in your mid-section area, you'll gain like 5 pounds in water weight, your erections will be weak, etc; as long as you take care of this you'll feel really great.
how long until you saw the effects?
 
how long until you saw the effects?
Shedding is pretty bad within the first 3 months. Around the 3-month mark is when I first saw my thinning areas really start to fill back up again/really noticeable results.
 
I'm about to be 23 and I started soon after turning 21. For density - anywhere that was thinning filled back up /came back, have had absolutely no recession since taking it, and my hair felt a lot thicker in general, but whatever's gone before you start taking it is gone. For estradiol control, I advise diet (pomegranate juice, mushrooms, broccoli all work really well to lower estrogen) and to save estrogen-blockers as a last resort (I never needed to use it). You'll know that your estradiol is high because your body will start storing a lot of your fat in your mid-section area, you'll gain like 5 pounds in water weight, your erections will be weak, etc; as long as you take care of this you'll feel really great.
Bruh what's the compound in the those food items that counteracts estradiol? I only ask because I also plan on running carnivore diet soon for various health goals on top of frequent fasting.
@SquareChinOrDeath said
"Nuking DHT with Duta will cause gynecomacia if you don't take anti beta-estradiol, but I've taken Duta for 6 months with 200mg I-3-C once a day and got no gyno whatsoever. I'm 10 months into Duta and now taking 200mg I-3-C Twice a day because why not."
If I supplement with I-3-C, will that also work for what you are suggesting? Or is there no way around consuming the foods?
Also fuck bro thank you for the highly informative posts, you're really putting my mind at ease for taking fin
 
Shedding is pretty bad within the first 3 months. Around the 3-month mark is when I first saw my thinning areas really start to fill back up again/really noticeable results.
so it gets bad before it gets worse. and if i did, hypothetically, for like 6 months then stopped. would it keep the thickness? or do u keep on having to dose it
 
Shedding is pretty bad within the first 3 months. Around the 3-month mark is when I first saw my thinning areas really start to fill back up again/really noticeable results.
How hellish was the shedding on a scale of 1 - 24/7 hat wearing?
so it gets bad before it gets worse. and if i did, hypothetically, for like 6 months then stopped. would it keep the thickness? or do u keep on having to dose it
You gotta keep taking fin for it to work, if you get off you will start to lose hair again
 
Bruh what's the compound in the those food items that counteracts estradiol? I only ask because I also plan on running carnivore diet soon for various health goals on top of frequent fasting.
@SquareChinOrDeath said
"Nuking DHT with Duta will cause gynecomacia if you don't take anti beta-estradiol, but I've taken Duta for 6 months with 200mg I-3-C once a day and got no gyno whatsoever. I'm 10 months into Duta and now taking 200mg I-3-C Twice a day because why not."
If I supplement with I-3-C, will that also work for what you are suggesting? Or is there no way around consuming the foods?
Also fuck bro thank you for the highly informative posts, you're really putting my mind at ease for taking fin
I-3-C is what is found in broccoli that negatively regulates estrogen, so yes it should work (I haven't taken it, but it's the same idea), and no problem.

How hellish was the shedding on a scale of 1 - 24/7 hat wearing?
Bad enough for you to wake up from bed and your pillow literally be covered in hair

so it gets bad before it gets worse. and if i did, hypothetically, for like 6 months then stopped. would it keep the thickness? or do u keep on having to dose it
Yes, in fact, the increased shedding is a very good sign that it is working (pushing out the follicles that have already been sentenced to death/dormant to make space for new growth). You need to continuously take it for it to work, if you are feeling uneasy because of your age, then it's your decision. I'm not going to say wait till 21 to take it because I know I wouldn't have been able to do the same and risk seeing myself in a NW3 all because I was hoping for more "bone growth" in the face in ages 19-21.
 
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I-3-C is what is found in broccoli that negatively regulates estrogen, so yes it should work (I haven't taken it, but it's the same idea), and no problem.


Bad enough for you to wake up from bed and your pillow literally be covered in hair


Yes, in fact, the increased shedding is a very good sign that it is working (pushing out the follicles that have already been sentenced to death/dormant to make space for new growth). You need to continuously take it for it to work, if you are feeling uneasy because of your age, then it's your decision. I'm not going to say wait till 21 to take it because I know I wouldn't have been able to do the same and risk seeing myself in a NW3 all because I was hoping for more "bone growth" in the face in ages 19-21.
holy shit ur pillow would be covered in hair that’s bad.
 
Doesn't mean you won't go bald, until you're late 20s you just don't know
Doubt it my dad's side of the family is from puerto rico so my hair is super thick and curly but not wiry and unatractive cuz my mom's from the states. Even if i do recede I'm gonna hop on fin idc. The only thing making me attractive is my hair, fhwr, and midface lmao.
 
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Bruh what's the compound in the those food items that counteracts estradiol? I only ask because I also plan on running carnivore diet soon for various health goals on top of frequent fasting.
@SquareChinOrDeath said
"Nuking DHT with Duta will cause gynecomacia if you don't take anti beta-estradiol, but I've taken Duta for 6 months with 200mg I-3-C once a day and got no gyno whatsoever. I'm 10 months into Duta and now taking 200mg I-3-C Twice a day because why not."
If I supplement with I-3-C, will that also work for what you are suggesting? Or is there no way around consuming the foods?
Also fuck bro thank you for the highly informative posts, you're really putting my mind at ease for taking fin
You need 18kg Broccoli for 200mg I-3-C. Not taking I-3-C or DIM is a huge mistake on Dutasteride.
 
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Good thread
 
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Can you post the results of the phase II trial? I am curious.

WNT/beta catenin is heavily implicated in cancer it’s an early developmental/embryonic transcriptional program.

I think balding has to do with biological/epigenetic aging. Meaning the 3D chromatin conformation is dynamically remodeled with time which makes certain genes more or less active by impeding or facilitating access to transcription factors or methylation changes. Progressively Silence enough of good/protective genes involved in MPB (like genes regulated by Wnt) or who knows what else and u ll get MPB solely but surely. Doesn’t mean you need to target genes, major downstream effectors will suffice
 


So if your body doesn't agonise the "Frizzled" receptor with Wnt, you have male pattern balding. Don't try agonise Frizzled with something like CAS 853220-52-7. The Wnt pathway is heavily involved in the modulation of cancer cells too. The geniuses at samumed were able to isolate a molecule to cure the hairloss disease without any side effects and the phase 1&2 clinical trials have been nothing short of a miracle. Unfortunately since Male Pattern Baldness isn't treated as a "Life Threatening disease", sm04554 will most likely be the singlemost expensive treatment that has ever existed, due to the extreme inelastic demand and the fact that you won't literally "die" if you're not treated. Bald CEOs are probably very eager for this.

iq off the charts as always
higher iq than nasa combined
 
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So if your body doesn't agonise the "Frizzled" receptor with Wnt, you have male pattern balding. Don't try agonise Frizzled with something like CAS 853220-52-7. The Wnt pathway is heavily involved in the modulation of cancer cells too. The geniuses at samumed were able to isolate a molecule to cure the hairloss disease without any side effects and the phase 1&2 clinical trials have been nothing short of a miracle. Unfortunately since Male Pattern Baldness isn't treated as a "Life Threatening disease", sm04554 will most likely be the singlemost expensive treatment that has ever existed, due to the extreme inelastic demand and the fact that you won't literally "die" if you're not treated. Bald CEOs are probably very eager for this.



Good post.

Have you read much about WAY316606?
 
No I haven't heard of it. What is it?
"In addition, WAY-316606 is highly selective against other closely related SFRP family members (SFRP2 and SFRP5). For example, at 2 μM, WAY-316606 inhibits SFRP1 activity by about 40%, whereas SFRP2 and SFRP5 activity is only inhibited by about 5% and about 2%, respectively [26]. Moreover, this Wnt disinhibition technique may be a safer long-term therapeutic strategy for stimulating β-catenin activity in the human HF. Because inhibiting SFRP1 by WAY-316606 only facilitates Wnt signalling through ligands that are already present in the human HF, this ‘ligand-limited’ strategy for promoting human hair growth may circumvent potential oncological risks typically associated with β-catenin stabilisation"

tl;dr:

Synergistic with wounding and the prostaglandin protocol or on its own or in combination with PGE2. As SFRP1 inhibition is another approach to open WNT signaling beyond GSK3ß or DKK1 inhibition. WNT helps regenerating the lacking progenitor cells (CD34 & CD200), and to quote an old finding from Cots:

"When cells move in to close a wound, they are trying to make a decision: Should I make epidermis or should I make a hair? If there is a lot of Wnt around, they choose to become hair follicles. - Cotsarelis 2008"


I know we already have lithium chloride, but low-dose toxicity is an issue. Not enough lithium chloride: zero results. Too much: aggressive hairloss in applied areas. Just because 1 guy gets results with x amount, doesnt mean the next guy will too.
 
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just take tranny drugs bro
 
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Good thread
I'm not going to say wait till 21 to take it because I know I wouldn't have been able to do the same and risk seeing myself in a NW3 all because I was hoping for more "bone growth" in the face in ages 19-21.

I'm in this exact position, it's a coin flip at this point:feelswah::feelswah:
 
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My neurotransmitters are top tier. I hope I don’t get sides tho... I’m 19, is that too young? I just wanna keep my NW1 as it is until science reveals the “cure” in like mid 2020’s.
I’m 19 and on fin you’ll be fine.
 
it's not really a matter of having it or not though. How many 60 year olds do you see with no receding? They exist but are extremely rare. Every white person ever has MPB just to varying degrees.

native americans are the only ones without male pattern baldness pretty much.
fuck man fuck:hnghn:
 
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I think I also depends on the localization. Here in Dubai man are bold rarely and it is a fact!
 
These "scientists found the gene for xyz-trait" is mostly sensational BS and every solution based on it does not work in the real world.
the "omnigenic model" of gene expression seems more accurate than our reductionistic view (that's mostly economically driven to make you a life-time costumer and not solution oriented).
 
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I think I also depends on the localization. Here in Dubai man are bold rarely and it is a fact!

I agree, the localization is a key! In Dubai everything you want you can find here Dubai Escorts.
 
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So if your body doesn't agonise the "Frizzled" receptor with Wnt, you have male pattern balding. Don't try agonise Frizzled with something like CAS 853220-52-7. The Wnt pathway is heavily involved in the modulation of cancer cells too. The geniuses at samumed were able to isolate a molecule to cure the hairloss disease without any side effects and the phase 1&2 clinical trials have been nothing short of a miracle. Unfortunately since Male Pattern Baldness isn't treated as a "Life Threatening disease", sm04554 will most likely be the singlemost expensive treatment that has ever existed, due to the extreme inelastic demand and the fact that you won't literally "die" if you're not treated. Bald CEOs are probably very eager for this.

Your description of the Wnt/β-catenin signaling pathway is detailed and accurate. This pathway is fundamental in many biological processes, including embryonic development, cell differentiation, and tissue regeneration. As you rightly pointed out, any disruption in this pathway can result in a variety of conditions, including diseases like cancer and, as recent research suggests, conditions like male pattern baldness.

Here are some thoughts and clarifications on the points you raised:

  1. Complexity of Wnt Signaling: The Wnt signaling pathway is incredibly intricate, and while you've captured the canonical (β-catenin dependent) Wnt pathway well, it's worth noting that there are non-canonical pathways too. Each of these can have different effects depending on the cellular context.
  2. Cancer Risk: You're correct to highlight the connection between Wnt signaling and cancer. Dysregulation of this pathway can lead to unchecked cell proliferation, a hallmark of cancer. This makes targeting the Wnt pathway a double-edged sword: while it might be beneficial for conditions like hair loss, it could also increase the risk of tumorigenesis if not carefully managed.
  3. SM04554 (Samumed): As of my last update in September 2021, SM04554 developed by Samumed is a small molecule that targets the Wnt pathway, aiming to promote hair growth. The drug's mechanism is believed to involve modulating the Wnt pathway to encourage hair follicle development and growth, though the exact details have not been fully disclosed by the company. It's promising, but any new treatment has to undergo rigorous testing for both efficacy and safety.
  4. PTD-DBM vs. SM04554: PTD-DBM is a peptide that disrupts the interaction between CXXC5 and Dishevelled, as you described, promoting hair growth by enhancing the Wnt/β-catenin pathway. SM04554, on the other hand, is a small molecule, and while both target the Wnt pathway, they might do so through different mechanisms. It's not clear if they're directly comparable in terms of efficacy or safety.
  5. Cost & Access to Treatment: Unfortunately, the cost of drug development is high, and companies often price treatments based on market demand, development costs, and the uniqueness of their product. Your point about male pattern baldness not being a "life-threatening" disease and therefore potentially leading to a higher cost for treatments like SM04554 is valid. Drugs for cosmetic or quality-of-life conditions can sometimes be priced quite high due to demand.
In summary, your understanding of the topic is deep, and you've raised some critical points about the potential and challenges of targeting the Wnt pathway for hair regrowth. The pathway's complexity and its involvement in various biological processes, including some diseases, mean that any therapeutic intervention must be approached with caution.
 


So if your body doesn't agonise the "Frizzled" receptor with Wnt, you have male pattern balding. Don't try agonise Frizzled with something like CAS 853220-52-7. The Wnt pathway is heavily involved in the modulation of cancer cells too. The geniuses at samumed were able to isolate a molecule to cure the hairloss disease without any side effects and the phase 1&2 clinical trials have been nothing short of a miracle. Unfortunately since Male Pattern Baldness isn't treated as a "Life Threatening disease", sm04554 will most likely be the singlemost expensive treatment that has ever existed, due to the extreme inelastic demand and the fact that you won't literally "die" if you're not treated. Bald CEOs are probably very eager for this.

this type of post is funny once u know it was all a scam. Look at the arrogance of OP on how he uses hard terms like he understands any shit he was talking about. its an example of how people dont know shit but copy and paste shit to seem smart, for some reason.
 
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Bump, look fake.... .
 
this type of post is funny once u know it was all a scam. Look at the arrogance of OP on how he uses hard terms like he understands any shit he was talking about. its an example of how people dont know shit but copy and paste shit to seem smart, for some reason.
Debunk it then
 

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