Fascinating New Paper On Hair Loss

Pablo Cruise

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There is simply no real evidence that DHT causes hair loss. The entire hypothesis is null and void.
What do you base that on? Are you saying DHT is an inocent bystander? I might have to re read the article but DHT and other hormones play a role in the author's hypothesis of scalp tension.
 

Pablo Cruise

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Many authorities on the matter do doubt and/or minimize the role that DHT plays in contributing to hair loss, but comparatively few completely exclude DHT as even a partial cause of hair loss.

I disagree. When I was a younger man and hysterical about hair loss, I took Finasteride 10mg/day. My scalp hair flourished. I had so much more hair. No question about it but it also shrunk my testicles and took all my libido so I had to quit.
The author said DHT is found in higher amounts in the scalp of AGA sufferers and DHT/Estrogen play a role muscle tension so if I reduce the microflora of the scalp, the sebum, that reduces DHT and its affects----with a anti dandruff shampoo? What a thought?
 

Dhair

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What do you base that on? Are you saying DHT is an inocent bystander? I might have to re read the article but DHT and other hormones play a role in the author's hypothesis of scalp tension.
I'm basing that on the total lack of evidence.
With all due respect to Rob, I would say that Danny Roddy has a much more nuanced and interesting approach to the hair loss problem and he draws logical conclusions about what the research is actually saying. As Danny has said, the mechanical approach has not yielded significant results and has been tried for decades now. With that being said, some people swear by Rob's approach. It just depends on what makes sense to you.
 

Pablo Cruise

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Nope. Not at all. The DHT in the balding scalp is probably an adaptive change to stress. T and DHT make hair grow thicker and stronger. The original research on the pseudohermaphrodites was conducted by incompetent scientists. High progesterone and youth steroids (including DHT) = no hair loss. No trials involving DHT have had patients drop out due to sudden hair loss. Hair Like a Fox should be required reading for every moron in the medical community. Elevated prolactin is probably the number one cause of hair loss. Doctors rarely check prolactin for any reason. My primary asked, "Are you lactating?" and laughed at me when I asked for the test. These people are not to be taken seriously.

Thanks for mentioning the "Fox".
 

LCohen

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Instead of fighting about DHT and estrogen, I think we should focus more on;

- Inflammation
- Fibrosis
- Prolactin
- Cortisol
- Aldosterone
- Serotonin
- Histamines

Since they are all linked with hair loss at %100 with no doub
 

mangoes

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He's right. Valerie Randall proved that DHT when applied directly actually stimulated hair growth.

I read it, and the article first starts out with a summary of nearly all observations regarding hair loss. He ends up concentrating on scalp tension, fibrosis, and calcification—with calcification being induced by androgens more‐or‐less directly:

'In mice, dose-dependent DHT and testosterone injections increase arterial calcification lesions by 300–400% [47].' ―Robert English

The mechanisms linking androgens to fibrosis are not very straightforward, and his final conculsion seems most centered around scalp tension. He does note that physical tension can induce cyclooxygenase‐2, and explains the prostaglandin D₂ in this manner, but I will point out that Garza had also found increased ptgds to match—this is the enzyme which creates prostaglandin D₂ from prostaglandin H₂; this enzyme is induced by cortisol, a steroid Robert English mentions not once.

Since the evidence linking prostaglandin D₂ to hair loss is so strong, I like to focus on that. I think the patterning is just as well explained by the microcirculation: The steroid transfer rate from blood binding proteins—such as cortisol transferred from albumin—has been proven to increase in microcirculatory regions. I think the ptgds gradient observed by Garza, and others, would be superimposable over the cortisol gradient since cortisol is the only thing shown to induce ptgds.


But since he focuses on fibrosis, calcification, and tension, the fundamental final pathway is more‐or‐less reduced blood flow. Prostaglandin D₂ has been shown in dozens of experiments to constrict the lungs, and also to constrict the blood vessels in a few others. One good thing about having reduced blood flow as the final mechanism, besides it being logical, is that it includes nearly all observations. As long reduced blood flow can be logically explained somehow, then most alternative explanations could have merit—disagreement coming only from the relative contributions of each particular one.

I think the two best explanations not touched on in the article for how androgens cause hair loss is through interferon-γ from the thymus and cortisol from the adrenals. In humans, androgens increase both of these and both can cause hair loss (as seen in mice overexpressing either interferon-γ or the mineralocorticoid receptor on the skin—both are nearly completely hairless).

But even if calcium plays only a minor role, people should get enough vitamin K and vitamin D to keep their arteries from calcifying. Warfarin, a vitamin K antagonist, causes rapid calcification of the arteries. Vitamin K is used as a cofactor for the enzyme which creates the γ-carboxyglutamate domain on proteins; this domain strongly binds Ca²⁺ ions and keeps them from precipitating in the blood (with phosphate).

Wow, really informative and interesting. So is that why some trans guys get MPB from hormone therapy? Testosterone > inteferon-y/cortisol > balding?

--
I know some women get MPB too, like the singer Sia, who shows a typical frontal recession, interestingly she's been diagnosed as hyperthyroid which I never really understood
 

Travis

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Hey guys I see how knowledgeable you all are on hair loss, if you could please check out my thread and help me/give me some advice I'd really appreciate it. Thank you.
Wow, really informative and interesting. So is that why some trans guys get MPB from hormone therapy? Testosterone > inteferon-y/cortisol > balding?

--
I know some women get MPB too, like the singer Sia, who shows a typical frontal recession, interestingly she's been diagnosed as hyperthyroid which I never really understood
Of course DHT cannot cause hair loss directly; this is anabolic everywhere, especially on beard follicles.

But it does cause a shift in immunity; there is a 'gender gap in immunity' characterized by a differential TH₁/TH₂ ratio. There are sex hormone receptors in the thymus thought responsible for this, but also in the adrenals where castration at an early age changes the corticosteroid profile.

So androgens are involved in hair loss, but the most indirectly. Next in line, and closer to the real action, are cytokines and cortisol—followed by enzymes, prostaglandins, and then their receptors. Louis Garza leaves off at the PGD₂–receptor interaction, but one could go further yet and attempt to explain how this binding event perhaps leads to muscle contraction of the vascular wall. Obviously there are many factors involved, but I like to focus on PGD₂ because the evidence is so powerful; nothing seems to correlate quite as well, not even or interferon-γ or cortisol.
 
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mangoes

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Of course DHT cannot cause hair loss directly; this is anabolic everywhere, especially on beard follicles.

But it does cause a shift in immunity; there is a 'gender gap in immunity' characterized by a differential TH₁/TH₂ ratio. There are sex hormone receptors in the thymus thought responsible for this, but also in the adrenals where castration at an early age changes the corticosteroid profile.

So androgens are involved in hair loss, but the most indirectly. Next in line, and closer to the real action, are cytokines and cortisol—followed by enzymes, prostaglandins, and then their receptors. Louis Garza leaves off at the PGD₂–receptor interaction, but one could go further yet and attempt to explain how this binding event perhaps leads to muscle contraction of the vascular wall. Obviously there are many factors involved, but I like to focus on PGD₂ because the evidence is so powerful; nothing seems to correlate quite as well, not even or interferon-γ or cortisol.

Oh wow, thanks I understand. I'll look into Louis Garza and PGD2.

Can someone rich please fund Travis to cure baldness? You'll become a billionaire :b lol
 

Scenes

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Of course DHT cannot cause hair loss directly; this is anabolic everywhere, especially on beard follicles.

But it does cause a shift in immunity; there is a 'gender gap in immunity' characterized by a differential TH₁/TH₂ ratio. There are sex hormone receptors in the thymus thought responsible for this, but also in the adrenals where castration at an early age changes the corticosteroid profile.

So androgens are involved in hair loss, but the most indirectly. Next in line, and closer to the real action, are cytokines and cortisol—followed by enzymes, prostaglandins, and then their receptors. Louis Garza leaves off at the PGD₂–receptor interaction, but one could go further yet and attempt to explain how this binding event perhaps leads to muscle contraction of the vascular wall. Obviously there are many factors involved, but I like to focus on PGD₂ because the evidence is so powerful; nothing seems to correlate quite as well, not even or interferon-γ or cortisol.

You said you were familiar or had at least looked at swisstemples’ blog on hairloss/regrowth? Basically his entire theory was pgd2 causes loss, pge2 causes growth.

Block pgd2 with setipripant (I think you even mentioned this as a pgd2 blocker) and raise pge2 (he applied this directly or used castor oil topically) and you should have hair back.

Not sure how successful this was for anyone...certainly news of it hasn’t boomed and it’s at least 2-3 years old, had a lot of traction at the time he was writing.

Can you explain why perhaps this didn’t work out for many?
 

Travis

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You said you were familiar or had at least looked at swisstemples’ blog on hairloss/regrowth? Basically his entire theory was pgd2 causes loss, pge2 causes growth.

Block pgd2 with setipripant (I think you even mentioned this as a pgd2 blocker) and raise pge2 (he applied this directly or used castor oil topically) and you should have hair back.

Not sure how successful this was for anyone...certainly news of it hasn’t boomed and it’s at least 2-3 years old, had a lot of traction at the time he was writing.

Can you explain why perhaps this didn’t work out for many?
Ramatroban is also an inhibitor of the prostaglandin D₂ receptor GPR44. There are three receptors for this prostaglandin, and two specifically for PGD₂ alone. Louis Garza's studies had suggested that GPR44 was the target, but I don't think this is 100% conclusive. But what is certain is that prostaglandin D₂ inhibits hair growth when applied directly to the skin, and so can basically anything which creates prostaglandins. So even if Garza is wrong about the specific target, it would still have to cause hair loss somewhere.

Ramatroban and Setipiprant work specifically on the GPR44 receptor.

Prostaglandin D₂ also becomes prostaglandin J₂ spontaneously upon loss of a molecule of water, and prostaglandin J₂ has two unique functions: it binds the strongest out of any prostaglandin to PPARγ, and it also is the only one which releases p53. The first function—binding to PPARγ—should actually stimulate growth, but the second function causes apoptosis of the cell. This is an alternate pathway that could have some relevance, and the ability of prostaglandin D₂ to cause hair loss is indisputable whether or not Setipiprant works or not. But you'd think it ought to, since indomethacin has been shown to cause hair loss—paradoxically—despite being an inhibitor of cyclooxygenase‐2. A little known fact is that indomethacin is actually the classic ligand for this prostaglandin D₂ receptor, and its molecular structure—along with Ramatroban—was actually used to design Setipiprant. Indomethacin doesn't bind nearly as strongly as prostaglandin D₂, Ramatroban, or Setipiprant, but it does bind and is actually known for this.

Ramatroban has been used to inhibit prostaglandin D₂ in asthma patients in Japan—for decades. This is available online and could perhaps work, although you won't find any studies on this. It wasn't until 2012 that Garza had published his first article, and new drugs are also more profitable than generic ones.. .
 

JDreamer

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Rob focuses on scalp tension, fibrosis and calcification because he has a mechanical approach to the hair loss problem focusing mostly on scalp massage. I have talked to him directly, and he is aware of both Ray Peat and Danny Roddy and he agrees that limiting PUFA is necessary for stopping hair loss. Speaking of vitamins D and K - have you read any literature regarding what an optimal ratio might be for daily supplementation?

How does one alleviate scalp tension?

One of my largest complaints is the tension I feel in my forehead and front part of my scalp. It's also no surprise my hair is receding there and accompanied by diffused thinning.
 

Ras

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Travis
Forgive me if you've already said this somewhere, but what exactly does Prostaglandin D₂ do to a hair follicle to cause it to stop producing terminal hairs?
 

Travis

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Travis
Forgive me if you've already said this somewhere, but what exactly does Prostaglandin D₂ do to a hair follicle to cause it to stop producing terminal hairs?
The downstream effects of prostaglandin D₂ need to be explored further, but it could be enough to say that it acts as a pressor agent in blood vessels and a bronchoconstrictor in the lungs. Prostaglandin E₂ has opposite effects in the arteries, in the airways, and on hair growth—lending support to the idea that the final downstream mechanism could simply be hypoxia. But again, you're on your own here; nobody really has explored these depths and the case against prostaglandin D₂ is epidemiological mostly, although it has been shown to decrease hair growth when applied directly.

I think it's either the pressor effect on the vessel walls or the Ca²⁺ influx, but these two events are inseparable because it's the Ca²⁺ ion which ultimately causes vasoconstriction through myosin light chain on the vessel wall.
 

Ras

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The downstream effects of prostaglandin D₂ need to be explored further, but it could be enough to say that it acts as a pressor agent in blood vessels and a bronchoconstrictor in the lungs. Prostaglandin E₂ has opposite effects in the arteries, in the airways, and on hair growth—lending support to the idea that the final downstream mechanism could simply be hypoxia. But again, you're on your own here; nobody really has explored these depths and the case against prostaglandin D₂ is epidemiological mostly, although it has been shown to decrease hair growth when applied directly.

I think it's either the pressor effect on the vessel walls or the Ca²⁺ influx, but these two events are inseparable because it's the Ca²⁺ ion which ultimately causes vasoconstriction through myosin light chain on the vessel wall.
Thanks
 

Lokzo

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Nope. Not at all. The DHT in the balding scalp is probably an adaptive change to stress. T and DHT make hair grow thicker and stronger. The original research on the pseudohermaphrodites was conducted by incompetent scientists. High progesterone and youth steroids (including DHT) = no hair loss. No trials involving DHT have had patients drop out due to sudden hair loss. Hair Like a Fox should be required reading for every moron in the medical community. Elevated prolactin is probably the number one cause of hair loss. Doctors rarely check prolactin for any reason. My primary asked, "Are you lactating?" and laughed at me when I asked for the test. These people are not to be taken seriously.

Then what are your thoughts on using Royal Jelly (A known prolactin reducer).
 

CoolTweetPete

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This very much jives with my experience restoring my hair. Last year I was introduced to the concept of Anatomy Trains, or myofascial meridians which seem to the principle drivers of motion, acting like puppet strings directing something that Dr. Peat wrote about in a recent newsletter -- Buckminster Fuller's concept of tensile integrity or "tensegrity".

Within this concept, we can see that the tensile forces in the complex myofascial network (which extends down to collaginous cellular pockets of the extracellular matrix wherein the cells live) influence the nervous & circulatory systems with tensile signaling that is essentially the backbone of our nervous systems' communication.

If the collaginous tissue of the scalp is tense, distribution of nutrients & nervous system impulses will be altered. The thick myofascial line, which can be traced from the front of the scalp to the back of the head, out to the shoulder, and finally terminating in each finger except the thumb, can become dysfunctional along any point and contribute to distorted position, again altering circulatory & nervous function through altered tensile integrity.

As I have taken measures to improve the position & symmetry of these lines (with soft tissue work (foam rollers, golf balls, and devices appearing suited for medieval torture) and targeted stretching) I have actually been able to sense my pulse more in regions of my body that seemed "isolated", for lack of a better word, particularly the front of my scalp, my lower scapula, hips, and ligamentous areas of my toes.

Needless to say, these tissues seem to have improved plasticity, elasticity, & functionality.

This is a fascinating topic with much fruit to bear it seems.

qxot55.jpg
 
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Philjay

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Honestly, no, I can't put it into layman's terms, as it's a long research paper with certain technical language that I don't fully grasp. Basically, the author is saying there are various inter-related factors at play in men's hair loss and that MPB cannot be primarily caused by DHT (the testosterone derivative that is often blamed as the main cause of MPB).

This has been known for a long time Aa is entirely different from mpb.

Studies were concluded in the 80s showing some individuals with very low dht follicle binding were still prone to mpb.
Personally having worked in this field for a while now I would suggest its more to do with the amount of androgen receptors in the scalp as opposed to the amount of dht produced by the individual.
 

Hairfedup

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This has been known for a long time Aa is entirely different from mpb.

Studies were concluded in the 80s showing some individuals with very low dht follicle binding were still prone to mpb.
Personally having worked in this field for a while now I would suggest its more to do with the amount of androgen receptors in the scalp as opposed to the amount of dht produced by the individual.

I've been thinking that the way to tackle AA would be very different from MPB...as someone with AA is the hormonal rebalancing more important than deficiencies, massage etc?
 

Philjay

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I've been thinking that the way to tackle AA would be very different from MPB...as someone with AA is the hormonal rebalancing more important than deficiencies, massage etc?

I would suggest that Aa its going to be vital as you say to first locate the hormonal issue , is it too much testosterone converting to dht , or is it perhaps far to much 5 alpha reductase activity? These are the issues that are going to be most likely key .
As an example,
Person 1' uses steroids to build muscle, his skin clears up but his hair starts to fall out.
Person 2. Uses steroids to build muscle, his skin becomes very spotty and oily but his hair is perfectly fine.

Person 1 sees a huge amount of 5alpha reductase activity in the scalp.
Person 2 in the skin.

Another example, John is in his mid 20s and starts seeing a rapidly shedding crown, however he has no other markers for Aa, this is most likely mpb as it seems to be more visible at the crown , and its likely treatment would be through invasive tactics.
In my opinion Aa can be treated, mpb can be covered either with surgery or dna retranscription.
 
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