> Hair regrew thicker in mice treated with a novel microneedle patch (seen on right) compared to mice treated with testosterone as a control
They treated the control group with testosterone? I.e., the hormone most linked to baldness?
They treated the control group with testosterone? I.e., the hormone most linked to baldness?
1 - Higher testosterone, generally correlated with higher amounts of DHT as testosterone is metabolized into DHT. This obviously depends on some intermediary metabolic process and all of the dependencies involved there.
2 - Certain hair follicles are DHT resistant. Why does MPB follow a M-shaped pattern and devolve into common patterns across those afflicted?
3 - https://pubmed.ncbi.nlm.nih.gov/26622151/ Mechanical stress points on the scalp seems to map injectively to the areas that see hair recede.
Takeaway: mechanical stress induces chronic inflammation on the scalp, localized in areas that correspond to MPB hairloss areas. Chronic inflammation begets androgen binding and those with high amounts of systemic DHT/vulnerable follicles develop MPB.
What if the stress points simply cause lack of blood flow, leading to sebum buildup?
This seems measurable (inflammation markers in titers), testable (A/B test with NSAIDs), and amenable to preexisting population studies without tracking patients over time (eg. find patients with long hair, that wear hats, etc.)
> Nine mice were randomly assigned to one of three groups: negative control (testosterone), experimental (testosterone + MnMNP), and positive control (testosterone + minoxidil).
Different people have variable ratios, and genetics certainly play a role in the variability.
What it fails to explain is why, if testosterone is the culprit, hair grows in other places later in life.
A much more compelling theory is that hair loss is due to the stretching of the scalp as the muscles and bones in the face grow in aging. It also explains why men have more hair loss then women. The force diagrams match male pattern baldness perfectly. (yes, also correlation)
Also the current understanding is that it's specifically DHT (a second order type of testosterone) that causes head hair follicles, and hormone treatments that modulate conversion of T into DHT one way or the other have fairly predictable effects on hair loss patterns.
There probably isn't just one single cause here, but hormones are definitely a big part of it.
If MPB were due to a tension mechanism, transplants wouldn't work. But they do. If MPB were due to a tension mechanism, surgical intervention would be simpler than transplanting thousands of follicles. But it isn't. If MPB is due to an endocrine mechanism, which it is, transplanted hair would behave differently than adjacent "native" hair against the progression of balding. It does.
Billions of transplanted follicles on millions of balding heads testify to the fact that rubicon33 is way off base.
He simply says it the theory is based on correlation which you agree to in your first sentence.
(please Google for the studies and data, I don't have links ready but have reviewed them in the past, there are tons by different groups of researchers across many countries)
At this point, rejecting as main culprit for AGA either too much DHT or a DHT sensitivity that is to high or, worst case, both at once in one man, is nothing but crazy fringe science.
To stress this out, the vast majority of men will keep their hair forever with oral minoxodil and oral finasteride and someone not keeping it on oral dutasteride instead of finasteride is a freak of nature.
If follicles transplanted to these areas also failed, then the mechanical explanation would hold more water, but they empirically don't...so something is obviously different at the follicle level.