I know you don't personally believe in this explanation for hair loss. However, I don't think anything you've said refutes the principle of the galea being the underlying cause of hair loss or the recent studies that have been published to support this explanation.
Not "personal belief", but a conclusion based on mountains of evidence, and a finding that all real researchers in hair follicle biology also accept (as far as I know).
Nordstom's findings were reflected upon
here, in the study where they analyzed expected galeal stress patterns and found them to match the Norwood hair loss pattern exactly:
The involvement of mechanical stress in Androgenetic Alopecia implies that hair follicles do not have genetically preprogramed androgen sensitivity. It is imperative at this point to mention the ingenious experiment by Nordstrom, who transplanted hair follicles from both balding and occipital scalp to the forearm. The result was the loss of hair from the balding scalp whereas the occipital hair continued growing.
[32] This study is considered a proof of genetic follicle preprograming, but according to the approach of the present paper, it would be necessary to know the strain supported by the forearm skin and to realize that the hair follicles close to receding hairline have already started a countdown toward the miniaturization, but not the occipital follicles. In hair transplantation, the grafted follicles start a new "balding clock," but hair growth would be guaranteed for many years even without preventive pharmacotherapy.
And one of the experiments I already posted debunks this - the one where they transplanted occipital hair to frontal scalp in stump-tailed macaques and they survived for
eight years, twice as long as the macaques had even been alive up to that point, and like 100 times longer than native frontal hair takes to start miniaturizing in response to androgens at puberty.
How do you explain that balding matches the expected tension distribution of the galea?
Does it? It looks to me like it only matches some patterns, but not others. Let's see the same analysis done on men with different balding patterns. Also, let's see the same analysis done on balding non-human primates like macaques, uakaris, chimpanzees, bonobos, and orangutans to rule out coincidence.
How do you explain that Botox therapy to the scalp can increase hair growth significantly?
Imagine the Botox study was done before any of these hair transplant studies. You could then hypothesize: "Well, maybe tension explains the pattern of hair loss." And then you could do the transplantation studies and you would find this hypothesis to be wrong. As for the mechanism, I don't know because it hasn't been investigated (and I sort of agree with the things d3nt3dsh0v3l said
here, but ultimately it's irrelevant because the conclusions you try to pull from it are already known to be false.
Here is the conventional explanation for the effectiveness of Botox for hair growth, which also recognizes tension as a primary mediator of androgenic hair loss:
The proposed mechanism for hair growth in androgenic alopecia after botulinum toxin A treatment is that paralysis of the scalp muscles enhances blood flow to the scalp by reducing the tension on the scalp skin. Because the conversion to dihydrotestosterone (DHT) is enhanced in a low-oxygen environment, oxygenated blood reduces this conversion and increases conversion to estradiol. This might be the same mechanism by which minoxidil affects androgenic alopecia.
The 18% increase in hair count is similar to that achieved with finasteride. How injecting BTX A into scalp muscles could be protected as intellectual property is difficult to see.
https://www.jwatch.org/jd201111100000001/2011/11/10/growing-hair-with-botox
This explanation as a whole suggests that the galea likely causes epigenetic changes to the hair follicles, by inducing specific genes to upregulate (androgen production and androgen sensitivity) in response to tension during development and lifespan.
Now you're contradicting yourself. I thought you said that once miniaturization started, due to a positive feedback loop, miniaturization would continue even after transplantation to a different site??? That's how you explained away the Nordstrom study. But according to what you're
now saying, Botox has the same effect as anti-androgens (i.e. stops and partially reverses hair loss). In other words, maintaining this tension is critical for continuing hair loss just as androgens are, and we should expect that once (like androgens) we remove this tension, hair loss should stop. And according to you, regional muscle tension on the galea is where this tension comes from. But AGAIN, the Nordstrom study contradicts this contradictory claim of yours, and I already posted yet another experiment that shows this is wrong: The experiment where they transplanted frontal hair to occipital scalp in ovariectomized macaques before giving them testosterone.
Transplantation is a difficult thing to speculate on in the context of this model, because we don't know how long it would take to reverse the positive genetic switches that the occipital scalp turns on and replace them with the negative switches the galea would turn on.
Not after at least 15 years in humans, and not after at least 8 years in macaques. None of these studies has ever found evidence for what you're claiming.
We also don't know how much of the mechanical stress from the galea will transmit to transplanted hair compared to native hair over time to change these switches.
Dermis associated with native hair in balding prone scalp is considered to be "fused" to the galea. What about dermis associated with transplanted hair? Transplantation is an artificial surgical process. Would the same "fusion" occur to equally transmit mechanical stress?
Now AGAIN you're ignoring the frontal-to-occipital transplant study done in ovariectomized macaques. I posted those studies for a reason, FFS.
If transplanted hair truly does survive very well (decades) even in young balding men in the absence of anti-androgens like finasteride (and I am highly skeptical this is the case as I have seen disastrous examples of guys who have had transplants and not taken their meds after),
Any links to studies comparing transplant survival rates in men who take finasteride vs. those who don't?
it would suggest primarily that either the epigenetics induced by developing in the occipital scalp are resistant to change or that the mechanical process of transplantation keeps the transplanted hair "unloaded" from the galea.
And AGAIN (how many times do I have to say this), you're ignoring the frontal-to-occipital transplant study done in ovariectomized macaques. This nullifies all this muscletensionpatternexplainshairloss conjecture. Why do you keep ignoring this?
So I don't think anything you're saying undermines the basic principle of this model. This model still best explains the distribution of hair loss that is seen with male pattern baldness. It just suggests we don't really know how transplanted hair reacts to relocation in the context of this model.
Only in Fantasyland is a failed hypothesis the "best explanation" for anything. Meanwhile, the exact same principles that guide biological pattern formation in most other contexts, and which ARE consistent with REALITY - nah, that's not the best explanation.