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Starting to really wonder if elevated DHT levels in the scalps of balding men is anything more than a symptom of the real underlying problem with male pattern baldness.
Firstly, I do believe it plays a part, and ACCELERATES the condition, but maybe isn't part of the real equation.
Also, I've read all the studies, etc. This is just a theory.
-Finasteride, Dutasteride, DHT blockers, help. However, they are extremely limited in how much they are able to help, let alone they cannot reverse the condition.
-HRT, estrogen has not only stopped male pattern baldness, and or regrew hair......it has completely reversed male pattern baldness in many patients.
-Classic male pattern baldness nearly always follows the same exact pattern. Either one of 2 things has to be true.
A) Every man with Androgenic Alopecia is born with an over sensitivity to Androgens.....only on the male pattern baldness hairs though. DHT is essential to body and beard hair growth. DHT does not affect the hair on the rest of head not in the male pattern baldness area. Why does the same androgen affect hair follicles, on the same person positively except for the male pattern baldness areas on the head?
Or
B) There is another cause.
That leads me to scalp tension, bone structure, and circulation. I know this isn't a new "theory" , but it makes total sense.
-The hair loss is always in the same pattern.
-Studies have shown that the balding areas on the scalp are the highest tension areas on the scalp.
What if this was the chain of events:
1) Scalp tension, bone structure, or some other underlying cause created an environment where certain areas of male scalps begin to be starved for blood flow oxygen (true, has been shown in studies).
2) As a result of the starvation, inflammation occurs in the follicles.
2) The Body sends, creates, more whatever..... DHT to the scalp, because its normally essential in hair growth, and has anti-inflammatory qualities.
3) DHT creates some kind of fibrosis in the follicle, shrinking it. The follicle is now being fed reduced oxygen, blood, and is getting pounded by DHT which is having a negative affect instead of the usual positive one.
Again, this isn't very technical, but here are some things I think that support this kind of possibility.
-Women make way more estrogen, less T then men. Women have smaller skulls. Women usually do not have deterioration of the fat tissue under the scalp until after menopause.
-Finasteride can slow, halt, and sometimes have a minor regrowth effect. But, it cannot reverse male pattern baldness like has been seen in HRT many times.
Maybe this explains the huge difference of results between people. Perhaps the finasteride "super responders" only had a minor circulation/scalp tension issue. Blocking DHT in this person may stop the negative affect DHT is having on the oxygen/blood starved follicles, and allow them to somewhat recover. But it does not address the root underlying cause that caused the inflammation in the first place.
-Minixodil is a vasodialator, and it's effects are limited to religious application, and the results are lost very quickly after stopping it. EVEN if Finasteride is used in combination with it, blocking DHT. This makes 0 logical sense. If minixodil grows a hair, through a follicle, which goes terminal......and you are blocking DHT with finasteride from the underside, it makes no logical sense that finasteride would not maintain that hair.....unless circulation is the underlying cause.
-Maybe this is why microneedling is effective. It stimulates blood flow to the area, helping starved follicles get more oxygen/nutrients.
Is it possible male pattern baldness can be cured 100%, by simply removing any underlying circulation/oxygen problem, even surgically if needed? Perhaps our skulls grow, or we age, and it creates more tension on the scalp over time. As the fat layer deteriorates, the follicle derm pap is being crushed by increased downward pressure from the skull, and from the "cushion" being deteriorated from underneath?
Maybe estrogen, along with some androgenic effects, restores the fat layer under the scalp, and the scalp is well nutritioned again, and this is why some HRT patients have completely reversed male pattern baldness and went from NW6 to NW1 in studies?
Sorry for the long rant, just made a lot of sense to me and wanted to share. Again, its not very technical, but its based on a LOT of reading, studying etc. There are many other phenomenons, that kind of further this train of thought.
Maybe the study on those guys with a total 5ar deficiency only tells part of the story? Yes, they don't ever get AA. However, maybe its not because of the lack of DHT, maybe its because of their increased estrogen (I dont know if this was a by-product of the condition or not, correct me if I'm wrong).
Maybe this explains various stages of baldness in newborns? Maybe as the skull moves, or whatever, it causes small, temporary circulation issues.
Maybe males who do not suffer from AA, just have a better hormonal balance between E and T? Has there ever been a study done to see if AA males have MORE androgen receptors than those without AA in the male pattern baldness areas of the scalp?
Maybe in those who do not have AA, their estrogen level, or balance creates a stable fat layer under their scalp so the follicles never become starved (regardless of head shape).
Rant off, flame if needed. Would love some dialogue or discussion though!
Firstly, I do believe it plays a part, and ACCELERATES the condition, but maybe isn't part of the real equation.
Also, I've read all the studies, etc. This is just a theory.
-Finasteride, Dutasteride, DHT blockers, help. However, they are extremely limited in how much they are able to help, let alone they cannot reverse the condition.
-HRT, estrogen has not only stopped male pattern baldness, and or regrew hair......it has completely reversed male pattern baldness in many patients.
-Classic male pattern baldness nearly always follows the same exact pattern. Either one of 2 things has to be true.
A) Every man with Androgenic Alopecia is born with an over sensitivity to Androgens.....only on the male pattern baldness hairs though. DHT is essential to body and beard hair growth. DHT does not affect the hair on the rest of head not in the male pattern baldness area. Why does the same androgen affect hair follicles, on the same person positively except for the male pattern baldness areas on the head?
Or
B) There is another cause.
That leads me to scalp tension, bone structure, and circulation. I know this isn't a new "theory" , but it makes total sense.
-The hair loss is always in the same pattern.
-Studies have shown that the balding areas on the scalp are the highest tension areas on the scalp.
What if this was the chain of events:
1) Scalp tension, bone structure, or some other underlying cause created an environment where certain areas of male scalps begin to be starved for blood flow oxygen (true, has been shown in studies).
2) As a result of the starvation, inflammation occurs in the follicles.
2) The Body sends, creates, more whatever..... DHT to the scalp, because its normally essential in hair growth, and has anti-inflammatory qualities.
3) DHT creates some kind of fibrosis in the follicle, shrinking it. The follicle is now being fed reduced oxygen, blood, and is getting pounded by DHT which is having a negative affect instead of the usual positive one.
Again, this isn't very technical, but here are some things I think that support this kind of possibility.
-Women make way more estrogen, less T then men. Women have smaller skulls. Women usually do not have deterioration of the fat tissue under the scalp until after menopause.
-Finasteride can slow, halt, and sometimes have a minor regrowth effect. But, it cannot reverse male pattern baldness like has been seen in HRT many times.
Maybe this explains the huge difference of results between people. Perhaps the finasteride "super responders" only had a minor circulation/scalp tension issue. Blocking DHT in this person may stop the negative affect DHT is having on the oxygen/blood starved follicles, and allow them to somewhat recover. But it does not address the root underlying cause that caused the inflammation in the first place.
-Minixodil is a vasodialator, and it's effects are limited to religious application, and the results are lost very quickly after stopping it. EVEN if Finasteride is used in combination with it, blocking DHT. This makes 0 logical sense. If minixodil grows a hair, through a follicle, which goes terminal......and you are blocking DHT with finasteride from the underside, it makes no logical sense that finasteride would not maintain that hair.....unless circulation is the underlying cause.
-Maybe this is why microneedling is effective. It stimulates blood flow to the area, helping starved follicles get more oxygen/nutrients.
Is it possible male pattern baldness can be cured 100%, by simply removing any underlying circulation/oxygen problem, even surgically if needed? Perhaps our skulls grow, or we age, and it creates more tension on the scalp over time. As the fat layer deteriorates, the follicle derm pap is being crushed by increased downward pressure from the skull, and from the "cushion" being deteriorated from underneath?
Maybe estrogen, along with some androgenic effects, restores the fat layer under the scalp, and the scalp is well nutritioned again, and this is why some HRT patients have completely reversed male pattern baldness and went from NW6 to NW1 in studies?
Sorry for the long rant, just made a lot of sense to me and wanted to share. Again, its not very technical, but its based on a LOT of reading, studying etc. There are many other phenomenons, that kind of further this train of thought.
Maybe the study on those guys with a total 5ar deficiency only tells part of the story? Yes, they don't ever get AA. However, maybe its not because of the lack of DHT, maybe its because of their increased estrogen (I dont know if this was a by-product of the condition or not, correct me if I'm wrong).
Maybe this explains various stages of baldness in newborns? Maybe as the skull moves, or whatever, it causes small, temporary circulation issues.
Maybe males who do not suffer from AA, just have a better hormonal balance between E and T? Has there ever been a study done to see if AA males have MORE androgen receptors than those without AA in the male pattern baldness areas of the scalp?
Maybe in those who do not have AA, their estrogen level, or balance creates a stable fat layer under their scalp so the follicles never become starved (regardless of head shape).
Rant off, flame if needed. Would love some dialogue or discussion though!
