How can Dr Ustuner explain the Hair Transplant patient Wesley?

How can Dr Ustuner explain situations like Wesley, the HT patient who is being treated by Dr Nigam, and has been treated elsewhere by HT surgeons in Belgium and Turkey? Look at his before and after photos, posted on this forum. The photos show the back and sides of his scalp are severely affected by AGA, almost to the point if being denuded of hair. How would Dr Ustuner’s “gravity” theory explain cases like this? According to Dr Ustuner’s own criteria, follicles in those areas are not affected by gravity.

???

in his theory, gravity affects the fat layer, not the follicles. The follicles are affected by the lack of fat, not gravity.

At least, that was my interpretation

Actually his theory is pretty complex… Men start losing the fat layer that cushions the hair follicles. This makes the follicles susceptible to pressure exerted by gravity. Pressure on the follicle sends a signal to produce DHT locally (he doesn’t explain how he knows this). The DHT causes further fat loss, in a vicious cycle. The more fat lost, the more pressure on the follicle, which causes follicles to shrink via some unexplained or not very well explained means. What he also hasn’t explained is why some people are much more predisposed to this whole thing, while most people are completely unaffected. He keeps on avoiding the issue of hairloss on the sides and back in some people (e.g., Wesley), female pattern baldness, and other “exceptions” to his theory.

He also maintains AGA is not a genetically inherited disorder, because a single responsible gene hasn’t been isolated. The fact is, we know that the condition is genetic, since it clearly runs in families. The mode of genetic inheritance however is a bit complex, with probably multiple genes responsible, acting in combinations which can affect the severity of the phenotype.

[quote][postedby]Originally Posted by roger_that[/postedby]
Actually his theory is pretty complex… Men start losing the fat layer that cushions the hair follicles. This makes the follicles susceptible to pressure exerted by gravity. Pressure on the follicle sends a signal to produce DHT locally (he doesn’t explain how he knows this). The DHT causes further fat loss, in a vicious cycle. The more fat lost, the more pressure on the follicle, which causes follicles to shrink via some unexplained or not very well explained means. What he also hasn’t explained is why some people are much more predisposed to this whole thing, while most people are completely unaffected. He keeps on avoiding the issue of hairloss on the sides and back in some people (e.g., Wesley), female pattern baldness, and other “exceptions” to his theory.

He also maintains AGA is not a genetically inherited disorder, because a single responsible gene hasn’t been isolated. The fact is, we know that the condition is genetic, since it clearly runs in families. The mode of genetic inheritance however is a bit complex, with probably multiple genes responsible, acting in combinations which can affect the severity of the phenotype.[/quote]

I like your synopsis, but even if there are a couple of unexplained “fill-in-the-blanks” in the article, respectfully, that’s why it’s just a theory and not a blue print of the cause of AGA. Also, I don’t think Dr. U is saying that AGA is not genetic, just that no one specific gene which causes AGA has been discovered. This is consistent with your own posts on the subject over the years, RT.

Perhaps the genetic condition at issue involves the applicable derm layer that is or becomes susceptible to the damage caused by the DHT in the vicious cycle which ends up choking the follicle, or perhaps it involves a handful of other genetic conditions not directly related to the hair follicle itself. Candidly, I’m not even remotely qualified to render an opinion on it, but so far, nothing I’ve read (which I’ve been able to understand) debunks Dr. Ustuner’s theory. A lot of us who disagree may have a bias that favors the ongoing traditional belief that the solution lies in focusing on the hair follicle itself, and figuring out what is different about AGA susceptible follicles so they can be replaced in a one-time, permanent solution (eg., HM). Dr. U’s theory shoots this traditional belief down pretty hard, so we don’t want him to be right. Not that it means much, but I have a feeling he is.

Maybe the solution is to find a way to recreate the environment (ie., a palpable scalp with the right layers of fat) for susceptible follicles to continue to cycle, and not so much how to create new hair in an environment that cannot sustain it anyway. The concept of a realistic HM treatment is close to 20 years old. What’ve we got so far?