What are some potential theories for why the NW7 "horseshoe" remains? I'm unable to think of any evolutionary explanation for it. What is strange is that the horseshoe is, invariably, very clearly defined in terms of its outline, its shape, and also its exact location. What are some theories for why the hair in this area of the scalp is never lost?
From an evolutionary standpoint, why does the clearly defined "horseshoe" remain?
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SayifDoit
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I think because of it's position being so low down the face it is comparable to facial hair and so for whatever reason not effected by DHT unlike the hair on the top. male pattern baldness is a horrible trait will never die out due to how unpredictable and dorment it can be and think when we living in caves and never bothered to cut our hair, the baldies probably looked no different. + Rape
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Like blue eyes, just consider it a random mutation. It has no evolutionary benefit, there is no rhyme or reason. A random group of genes mutated, and the result was the horseshoe. There must have been a population bottleneck at some point for it to be so prevalent... Actually the baldness gene is present in apes too, so the bottle neck must have happened to them rather than us, to be so common in human populations and ape populations. Most apes and humans bread at younger ages, before male pattern baldness kicked in, so the ugliness thing never got to be a factor until now. Also most breeding was done by rape or by instinct, not dating, romance, physical attraction or mutually consenting sex.
To understand why it is the shape that it is, if there is any reason, you'd best look at apes, not humans. Didn't start with us.
Like all of natures **** ups, it's just random, and like all persistent **** ups, it stick around because it doesn't kick in until later in life. A disease that doesn't kick in until several years after sexual maturity is essentially shielded from natural selection in evolutionary history
To understand why it is the shape that it is, if there is any reason, you'd best look at apes, not humans. Didn't start with us.
Like all of natures **** ups, it's just random, and like all persistent **** ups, it stick around because it doesn't kick in until later in life. A disease that doesn't kick in until several years after sexual maturity is essentially shielded from natural selection in evolutionary history
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I would have thought that it has less to do with the enzyme and DHT and more due to follicular susceptibility. Many people have high DHT levels but no hair loss. DHT is half of the equation. Fighting DHT creation is one approach. the other approach I suppose would be introducing something that competes with DHT for the binding sites in the hair follicle. I don't think male pattern baldness prone individuals simply have more DHT in their balding zone than normal folks, I think they just have more susceptible follicles, and that DHT inhibition is just one way to counter it.
I'm surprised no treatment is on the market that acts as a DHT competitor. Or maybe it is, I suppose that's what spironolacetone does, right?
I'm surprised no treatment is on the market that acts as a DHT competitor. Or maybe it is, I suppose that's what spironolacetone does, right?
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Do you noticed that the no balding areas in elevated Norwood exhibit always the same pattern? Curiously are the same zones that have no problems to eliminate the sebum produced by the hair (pilosebaceos unit), there is not acumulation and degeneration of hair fat.
It could be a posible explanation. Also the acumulation of sebum is correlated with the DHT levels.
I dont think in a simpe genetic of common baldness gene,
It could be a posible explanation. Also the acumulation of sebum is correlated with the DHT levels.
I dont think in a simpe genetic of common baldness gene,
Androgenetic Alopecia is a sebaceous gland disorder just like acne and other skin disorders, that's true . What I dont understand is if it's caused by overactive sebumproduction like you said , why is it that women and Some guys have diffuse thinning and others have only balding on the top?
They are not resistant to DHT, they just have lower levels of it.
[B said:
maybe, it is level of intrafollicular DHT in donor hair follicles which remain same after transplantations to balding regions. So, it is the intrafollicular DHT wich remain same and lower in donor hair follicles after hair transplant.
Anyway, presence of hors-shoe pattern is due to several raesons:
- less androgen sensitivity
- less 5ard activity in occipital area
- and maybe increased blood supply
Are there any studies which show this, follicular DHT levels of transplanted donor hair follicles before/after in hair transplant ?
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It is not an overcative sebum production but a flow problem with this hair fat. The time between production and elimination is very important due oxidation and degeneration of this biological product. In a few words, it is necesary produce and eliminate it at the same rate. The differences between women and men lies in this point. The elimination need a physic contact with the outside or with the same neighbourg hair shaft fiber, then the density, spatial pattern and lenght of the hair is important. People with dense, curly and thick hair are less prone to this malatie. The lengh of hair can aid to eliminate the sebum because there is tangential movement of it along the hair shaft. Men, generally, wore a short scalp hair lenght. An interesting zone is the whorl of the hair, where the direction of the hair shaft change abruptly with the angle.
This is my idea, but I can be wrong.
Transplanted hair from affected follicles will miniaturize when planted on your arms. The hair produces it's own DHT, every body tissue that can, does so.
I always thought of hair in the male pattern baldness areas as having much higher expression of androgen receptors compared to say the horshoe shape where the hair is more resistant just simply doesnt have the receptor counts and then is less affected by circulating local DHT. Men with male pattern baldness in general have much higher androgen receptor expression than men without.
Not really, no. DHT has little endocrine activity. Not all men with high androgen receptor densities have male pattern baldness. It's a little more complicated than that. Generally, the intrafollicular levels of DHT is higher in miniaturizing hair, irregardless of the person housing it.
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And, what about men without male pattern baldness? identical expression of AR in all areas, verdad?