What makes you hair at the back and sides DHT resistant?
- Thread starter SayifDoit
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So wouldnt getting some botox injected in your head hypothetically create some pseudo fat helping to keep your hair? I mean you'd have to start young, which I would have but really thats a dumb theory. Its the same as body hair being resistant. It just is.
Also perhaps its not so resistant as there are more levels of DHT in the top portion of the scalp for certain people since your head and feet are supposedly the pinnacle of where blood pumps the hardest.
Its not gravity, but its rather the tightness of the scalp and the decrease in fat content that will both put pressure on the follicles.
Not only does this put pressure on the follicles, but also crushes the vascular system in those areas, causing a decrease in blood flow, and a decrease in O2 saturation.
A decrease in O2 saturation promotes the creation of DHT from free-testosterone. DHT promotes bone expansion.
So you are right, there are differnet areas of the scalp that have more levels of DHT, since the back and side of the heads don't get "pulled" and crushed, and so there is no O2 saturation depletion in comparison to normal.
Botox doesn't create a layer of fat, but the reason it works is that it relaxes the muscles of the scalp (not the actual galea, but hte muslce tendons that run underneath the scalp across the front and back). By releasing this tension, they increase blood flow, and the hair begins to grow again.
This is significant evidence as to why male pattern baldness happens in its specific pattern, and why it only happens in this particular region. It also explains "male pattern baldness itch."
To think that 2 hairs, divided by 1 mm are expressing different genes is ridiculous. There are no cells in the body that are like that. Its obvious it has to do with location, and is a side effect of the area in that location.
Not only does this put pressure on the follicles, but also crushes the vascular system in those areas, causing a decrease in blood flow, and a decrease in O2 saturation.
A decrease in O2 saturation promotes the creation of DHT from free-testosterone. DHT promotes bone expansion.
So you are right, there are differnet areas of the scalp that have more levels of DHT, since the back and side of the heads don't get "pulled" and crushed, and so there is no O2 saturation depletion in comparison to normal.
Botox doesn't create a layer of fat, but the reason it works is that it relaxes the muscles of the scalp (not the actual galea, but hte muslce tendons that run underneath the scalp across the front and back). By releasing this tension, they increase blood flow, and the hair begins to grow again.
This is significant evidence as to why male pattern baldness happens in its specific pattern, and why it only happens in this particular region. It also explains "male pattern baldness itch."
To think that 2 hairs, divided by 1 mm are expressing different genes is ridiculous. There are no cells in the body that are like that. Its obvious it has to do with location, and is a side effect of the area in that location.
Spanishlad
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It has absolutely nothing to do with fat, gravity or location as stated above... if that was the case then hair transplants would be useless.
The hair in the horse shoe pattern is DHT resistant just like all the hair on the head of a non balding person..
As for why this hair remains resistant to DHT that is the million dollar question.
The hair in the horse shoe pattern is DHT resistant just like all the hair on the head of a non balding person..
As for why this hair remains resistant to DHT that is the million dollar question.
http://www.top-hair-loss-remedy.com/skull-expansion.html
If it weren't so fishy of that guy trying to sell me his book, I'd actually be inclined to believe this.
But if we take those claims to be real then that would mean that DHT blockers would lead to skull bone decrease, which makes it sound all the more bull****ty.
Still, I do find it really strange for those horse shoe hairs to be immune to male pattern baldness.
If it weren't so fishy of that guy trying to sell me his book, I'd actually be inclined to believe this.
But if we take those claims to be real then that would mean that DHT blockers would lead to skull bone decrease, which makes it sound all the more bull****ty.
Still, I do find it really strange for those horse shoe hairs to be immune to male pattern baldness.
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Please don't ever post another link from Daily Mail. That site is pure trash.
No, the above doesn't seem to be the case at all. There are many new studies that say it has everything to do with the galea, and more importantly, blood flow to the scalp.
We know this to be the case because if you inject botox into a bald person's scalp, they grow hair:
http://www.jwatch.org/jd201111100000001/2011/11/10/growing-hair-with-botox
The only reason this would work is if baldness had something to do with the scalp muscles, which in turn reduces blood flow when tensed. This simple fact is the nail in the coffin for the idea that some hairs are DHT resistant, and other hairs are not DHT resistant.
If you take two hairs, one on the galea, and one not on the galea, they will contain the same genetic code. The only way they would express different traits, are if there was an environmental component that changed. This environmental component is DHT, which is excessive in the galea when it becomes tight or blood flow gets restricted.
DHT causes the skull to expand, which further exacerbates this problem in a circular fasion.
As for why hair transplants work, the simple truth of the matter is that it is not true that hair restoration is permanent. People who have hair restoration usually continue to take DHT inhibitors like finasteride and vasodiolators like minoxidil even after their hair restoration. If they didn't, we would likely see the miniaturization process in these follicles over time as well.
There have been no studies of hair restoration and users not continuing propecia/minoxidil that I can find. This makes the claim that hair restoration is permanent very fragile in my opinion, and after seeing the 75% effectiveness of botox injections in male pattern baldness, it literally destroys the claim that some hairs are DHT resistant and others are not. Rather, it has to do with the amount of DHT in a region, which has been found to be higher in the scalp for balding men due to an 18% difference in the O2 saturation of their scalps.
DHT/free T ratios sway towards DHT in lower oxygen environments.
I wrote more here: http://www.gourmetstylewellness.com/interac...rs-Old-was-in-denial-shaved-my-head-yesterday
If you have any comments/questions I would love to hear them.
DHT doesn't signal skull bone decrease though, but signals bone expansion (skeletal remodeling). If you take away DHT, it doesn't mean you have a decrease in bone size.
As I mentioned in other threads, horseshoe is also susceptible to balding, but reasons why it doesn't fall out even in old age are:
There is interesting article which suggests that androgen receptors become active under low oxygen environments, which is a much more logical explanation than extra androgen receptors being located ONLY in the EXACT shape of the galea.
http://www.ncbi.nlm.nih.gov/pubmed/22266320
- less AR sites located in donor hair follicles
- less DHT follicular production compared to hair follicles located at front and top of the head
- increased blood flow/nutrient and oxygen supply due to occipital muscle
- other yet unknown factors obviulsy connected to its location on scalp, I found paper that suggests that even sebaceous glands on top of the head are bigger than those located at donor region. Sebaceous glands squeeze hair follicles and shafts causing mechanical degradation/miniaturisation
There is interesting article which suggests that androgen receptors become active under low oxygen environments, which is a much more logical explanation than extra androgen receptors being located ONLY in the EXACT shape of the galea.
http://www.ncbi.nlm.nih.gov/pubmed/22266320
Ah if we only had the answers. Why do androgens cause body hair to grow but have the opposite effect on head hair? Been waiting for the answers for about 20 years. Never seen it but they are important questions for sure. Doing something with the answers though wouldnt be much easier.
As we see from the variety of answers there are theories abound with many intricate parts. I have my doubts we will see a definite answer to these questions sometime soon
As we see from the variety of answers there are theories abound with many intricate parts. I have my doubts we will see a definite answer to these questions sometime soon
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Hairs on sides of head don't suffer from hair fat acumulation inside the pilosebaceous unit. Several hours at day/night are in full contact with an absorbent surface, ..., problems with sebum is the trigger in my opinion, ..., later, passing the time, other harder biological process are implicated.
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Because when we sleep the back and sides of our head gets massage and more blood flow and nutrients.
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Is there even any evidence for DHT resistance? I was always of the thinking that there is simply less 5AR and receptor sites in the occipital portion, after all a genetic disposition or not to Androgenetic Alopecia subjecting a HF to vast amounts of androgens will result in apoptosis.
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I have a really complicated well thought out answer to this question. We dont know. No one knows why this happens. Every answer here is just a guess based off the little bit we know.
We dont know anything about why hair is even sensitive to androgens in the first place. This is partly why male pattern baldness has such poor treatments. No one understands anything about this problem. How do you fix or cure a problem no one understands?
We dont know anything about why hair is even sensitive to androgens in the first place. This is partly why male pattern baldness has such poor treatments. No one understands anything about this problem. How do you fix or cure a problem no one understands?
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Time to take in account the Occam's razor.
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Nobody knows. How can we know when we advocate the use of primitive medications such as Minoxidil and Finasteride? We have chosen a false path from the start. All we can do is look at it realistically.
Questions: A. What is the hereditary gene supposedly responsible for alopecia and found more than twenty years ago called? B. What is truly the role of dihydrotestosterone?
Answers: A. Nobody has a clue and B. Nobody has a clue
But let us hypothesize based on data we have.
A. It appears to be a gene from your mother’s side that supposedly makes you sensitive to dihydrotestosterone in the follicles. Why only in scalp? Why only in the galea region? Why not in the entire body? How does one determine that?
B. Dihydrotestosterone is the man’s hormone. Facts: if one significantly reduces it, it has an impact on skin, bone, muscle and brain. So we obviously need it. My hypothesis lies with the amount of testosterone and dihydrotestosterone receptors and the ability of some people to endure the drug better than others and have increased libido. Because anyone who responds well to it as far as side effects are concerned states an increased libido is noticeable from day one.
But now here is the thing: all theories are shut down by everyday examples.
Big skull theory: tons of people out there with big skulls of all sizes and shapes that have zero hair loss anywhere, even their massive temples are not hit.
Galea theory: diffuse pattern alopecia, global alopecia, some lose hair in the front only, some lose in the vertex only, people with huge galeas don’t lose a single hair.
Blood flow theory: tons of people into gymnastics, hanging upside down, having strong neck muscles, inversion tables, you name it. They are still bald. Cold? Heat? Modern way of life? Many folks from ancient times in North America were bald. Eskimos has bald ones. Black people had bald ones. Their blood flow was fine.
Race theory: bald people everywhere, nobody escapes.
We know that estrogen and testosterone blockers regrow hair (pay attention, not dht blockers but t blockers). We know that vasodilators promote hair regrowth. We know that Botox and scalp massages promote regrowth. We know that micro needling/damaging the skin promotes regrowth.
In my opinion, everyone gets hit the same. The start is the same for everyone. All the rest, the blood flow, the scalp size, the scalp pressure, the dht accumulation, the experiments, these all come later and fighting them does not fight the root cause so you’re still losing.
The root cause lies in the gene, in the testosterone itself, maybe even before that. Or perhaps @Retinoid suggestion is correct. We need to shift our eyes there instead of talking about castration and total destruction of our manhood and brain. It’s almost 2020, it’s time to evolve.
This is why Tsuji is the only solution. He doesn’t fight anything, he provides you with an extended solution to cover the damage. He doesn’t prevent any damage. Those who do, will lose. Because unless you fight the root cause, you’re just beating around the bush.
@hemingway_the_mercenary @Tommybommy1363
Let’s hear your thoughts on this.
Questions: A. What is the hereditary gene supposedly responsible for alopecia and found more than twenty years ago called? B. What is truly the role of dihydrotestosterone?
Answers: A. Nobody has a clue and B. Nobody has a clue
But let us hypothesize based on data we have.
A. It appears to be a gene from your mother’s side that supposedly makes you sensitive to dihydrotestosterone in the follicles. Why only in scalp? Why only in the galea region? Why not in the entire body? How does one determine that?
B. Dihydrotestosterone is the man’s hormone. Facts: if one significantly reduces it, it has an impact on skin, bone, muscle and brain. So we obviously need it. My hypothesis lies with the amount of testosterone and dihydrotestosterone receptors and the ability of some people to endure the drug better than others and have increased libido. Because anyone who responds well to it as far as side effects are concerned states an increased libido is noticeable from day one.
But now here is the thing: all theories are shut down by everyday examples.
Big skull theory: tons of people out there with big skulls of all sizes and shapes that have zero hair loss anywhere, even their massive temples are not hit.
Galea theory: diffuse pattern alopecia, global alopecia, some lose hair in the front only, some lose in the vertex only, people with huge galeas don’t lose a single hair.
Blood flow theory: tons of people into gymnastics, hanging upside down, having strong neck muscles, inversion tables, you name it. They are still bald. Cold? Heat? Modern way of life? Many folks from ancient times in North America were bald. Eskimos has bald ones. Black people had bald ones. Their blood flow was fine.
Race theory: bald people everywhere, nobody escapes.
We know that estrogen and testosterone blockers regrow hair (pay attention, not dht blockers but t blockers). We know that vasodilators promote hair regrowth. We know that Botox and scalp massages promote regrowth. We know that micro needling/damaging the skin promotes regrowth.
In my opinion, everyone gets hit the same. The start is the same for everyone. All the rest, the blood flow, the scalp size, the scalp pressure, the dht accumulation, the experiments, these all come later and fighting them does not fight the root cause so you’re still losing.
The root cause lies in the gene, in the testosterone itself, maybe even before that. Or perhaps @Retinoid suggestion is correct. We need to shift our eyes there instead of talking about castration and total destruction of our manhood and brain. It’s almost 2020, it’s time to evolve.
This is why Tsuji is the only solution. He doesn’t fight anything, he provides you with an extended solution to cover the damage. He doesn’t prevent any damage. Those who do, will lose. Because unless you fight the root cause, you’re just beating around the bush.
@hemingway_the_mercenary @Tommybommy1363
Let’s hear your thoughts on this.
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A somewhat old hypothesis and more of an observation than theory but it was based on several observations made by researchers that skull shape correlates with baldness. Newborns, whose skull shapes often show similarities to Androgenetic Alopecia-affected skulls often have hair growing in reverse order of Androgenetic Alopecia as the cranium rapidly develops.
IMO the GA scalp tension theory is the best explanation atm, your dismissal of it is pretty weak in reality, in fact this theory is the only theory that I know of that can effectively explain why pattern baldness is patterned the way it is. BTW global alopecia has nothing to do with Androgenetic Alopecia.
Here is my problem with these skull shape or scalp tension theories. Why wont women go bald? Women have a variety of head shapes that mimics the variety in men yet men go bald, and 3/4 of women dont even less before menopause when their hormones go bonkers. If these theories were true we would see FPB at the same rates and same patterns on the scalp as men. We dont.