Low Dht And Balding... finasteride Or Not Recommended ?
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Ask for a hormonal blood test. You would have to ask for DHT to be screened for too as most blood teats don't include it.
To OP I've never had my DHT levels tested but I believe mine is low too due to very little body hair, extreme difficulty building muscle and a patchy beard.. I'm on finasteride with no side effects from it.
But does that really mean anything? I'm like the only un-hairy guy among my friends (maybe 1 more). And I have some minor recession going. My friends are hairy as gorillas and all have the perfect juvenile helmet hairline haha.
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Its all due to follicle androgen sensitivity. You can have low DHT and low follicle sensitivity which means you will probably bald slower and later in life. You can also have high DHT and even lower sensitivity or just complete immunity to DHT which means lots of body hair and perfect hair. Its not as black and white as I'm explaining but its the general idea.
Yeah, but if male pattern baldness does kick in later in life their male pattern baldness will probably be fast and hard. The more androgens you have the more likely the male pattern baldness is fast and rough once it does kick in.
Nothing in male pattern baldness is absolute when no one knows anything really how it works in different people, but id take the bet that more very hair men go bald and bald worse than much less hairy men.
Judging from the women with santa beards I see I would say androgens do cause facial hair and body hair for men. Not a lot of other explanations which is why its hard to understand how very hairy men dont have higher DHT or T than their counterparts.
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Just as head hairs can be more or less sensitive to DHT, so can body hair. Some guys become a lot hairier as they age, while others don't. It's really the same effect. It may hold true in general for body hair(no one has really studied it), but we do see that the testosterone levels of NW5s are basically random distributions with no significant lean towards higher testosterone levels. Men with higher testosterone having more body hair and balding more often/sooner seems like a logical assumption to me, but it doesn't seem to bear out once examined.
I do wish more was done to explore what causes increases in DHT sensitivity rather than just saying "Well, if we nuke DHT, it solves the problem". It's like... yeah, but it's a really drastic solution. I'd prefer to figure out why some scalp hairs become more sensitive to DHT over time, and if there are other ways to deal with it than just knocking down DHT levels with cancer drugs.
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How much DHT do you have? Is it actually LOW or is it in range but on the lower end? Serum DHT unfortunately does not play a huge role unless it is really high or really low. The reason why Finasteride works is because it inhibits the enzyme inside the follicle. Not necessarily that it reduces DHT in the body.
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I've never seen this before. Every discussion I've seen of Finasteride's effect on DHT has always been its systemic effect. Do you have any research papers that discuss activity inside of the follicle?
Well this is a roundabout way of saying that DHT local to the hair is what causes male pattern baldness. That is why finasteride works it inhibits the enzyme in the follicle preventing DHT from forming and effecting the hair. It is DHT that causes male pattern baldness, but its just the local DHT in the hairs. You dont need to nuke DHT in your entire body to fix hair loss its just what we are stuck doing right now.
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Where do you think systemic DHT comes from? DHT is produced in tissues and act locally on those tissues (scalp, hair, skin, prostate, etc.). It does not get produced in the prostate and then goes to act elsewhere in the body like endogenous hormones such as Testosterone, Estrogen and Progesterone. Men who bald do not necessarily have higher DHT in the blood, the activity of the 5AR2 enzyme in the scalp/hair follicle leads to the issues (or at least plays a major role). Testosterone gets converted into DHT in the hair follicle and then the DHT acts on that specific tissue.
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I understood this is what you were saying. I'm interested in reading a more detailed explanation of this, because I've never seen it stated that a hair follicle has a 5AR2 enzyme dangling off of it, and it attracts free testosterone, which then converts to DHT right there in the follicle(and presumably attaches immediately to the androgen receptor in the follicle).
My understanding of how it works is basically that free testosterone in the bloodstream regularly produces DHT - not in relation to any contact with hair follicles. And that the free floating DHT attaches to the AR in the hair follicle. And that some hairs are either more sensitive to DHT, or may even have a stronger affinity for DHT(I've never seen this explained clearly either).
I would like you to be correct in your statement. Because if it works like that, topical dutasteride would be almost perfectly effective. That just doesn't match my current understanding of how and when DHT is produced. So if you do have any research papers which describe the process of DHT being created by 5AR2 enzymes in the follicle, I would like to read about it. My approach to hair loss prevention is based on a different premise that is far from ideal if what you say is correct.
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You got me looking into this, and while I didn't find anything proving that DHT is ever synthesized inside the follicle, I did find this very comprehensive paper "Androgen actions on the human hair follicle: perspectives"
https://onlinelibrary.wiley.com/doi/pdf/10.1111/exd.12024
Highlights:
Aromatase activity is detectable in hair follicles, and its expression in the outer root sheath of anagen hair
follicles and in sebaceous glands, suggesting the presence of a
local balance system for androgens and oestrogens and that hair
follicles function as oestrogen targets and sources. A comparison
of aromatase content in frontal hair follicles from men and
women with pattern baldness has shown that it is six times greater
in women, which has led to speculation that this difference
may account for the difference in clinical presentations of pattern
baldness
it was reported that an inhibitor of 5aR1 and 5aR1/2 can suppress endogenous
5a-reductase activity in plucked hairs from females but selective
5aR2 inhibitors cannot. These observations seem to indicate
that 5aR1 may be dominant in hair follicles. Another more recent
study detected activity of both 5aR1 and 5aR2 in microdissected
hair follicles and found that it was higher in balding hair follicles
than occipital(bottom of head) hair follicles from both men and women
beard and Androgenetic Alopecia formation is dependent on 5aR2 activity but not 5aR1. As for
gender differences, 5aR1 and 5aR2 contents in female frontal hair
follicles were 3 and 3.5 times less than in male frontal follicles
AR expression is significantly higher in beard and Androgenetic Alopecia DP than in
non-bald occipital scalp cells (36,50,52–55), indicating that AR is
one of the key molecules which regulate androgen sensitivity in
DP
AR content in female frontal hair follicles was found to be approximately 40% lower than in
male frontal follicles
prostaglandin D2 synthase (PTGDS) is elevated at the mRNA and protein levels in bald scalp compared with haired scalp of men with Androgenetic Alopecia and the product of PTGDS enzyme activity, prostaglandin D2 is similarly elevated in bald scalp (82), suggesting that pathogenic mechanisms beyond androgen pathway play important roles in Androgenetic Alopecia. Alternatively, there may be any linkage between AR and prostaglandin D2
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So we do indeed have 5aR1 and 5aR2 enzymes in hair follicles, and there are far more in the front, than at the bottom of the head.
I wonder why systemic reduction of DHT is so effective for hair follicles if they have their own 5aR2 enzymes, because I know that lowering systemic DHT had no impact on sebum production. Very odd and something I can't explain right now.
Though the most interesting thing in the entire paper may be this
https://onlinelibrary.wiley.com/doi/pdf/10.1111/exd.12024
Highlights:
Aromatase activity is detectable in hair follicles, and its expression in the outer root sheath of anagen hair
follicles and in sebaceous glands, suggesting the presence of a
local balance system for androgens and oestrogens and that hair
follicles function as oestrogen targets and sources. A comparison
of aromatase content in frontal hair follicles from men and
women with pattern baldness has shown that it is six times greater
in women, which has led to speculation that this difference
may account for the difference in clinical presentations of pattern
baldness
it was reported that an inhibitor of 5aR1 and 5aR1/2 can suppress endogenous
5a-reductase activity in plucked hairs from females but selective
5aR2 inhibitors cannot. These observations seem to indicate
that 5aR1 may be dominant in hair follicles. Another more recent
study detected activity of both 5aR1 and 5aR2 in microdissected
hair follicles and found that it was higher in balding hair follicles
than occipital(bottom of head) hair follicles from both men and women
beard and Androgenetic Alopecia formation is dependent on 5aR2 activity but not 5aR1. As for
gender differences, 5aR1 and 5aR2 contents in female frontal hair
follicles were 3 and 3.5 times less than in male frontal follicles
AR expression is significantly higher in beard and Androgenetic Alopecia DP than in
non-bald occipital scalp cells (36,50,52–55), indicating that AR is
one of the key molecules which regulate androgen sensitivity in
DP
AR content in female frontal hair follicles was found to be approximately 40% lower than in
male frontal follicles
prostaglandin D2 synthase (PTGDS) is elevated at the mRNA and protein levels in bald scalp compared with haired scalp of men with Androgenetic Alopecia and the product of PTGDS enzyme activity, prostaglandin D2 is similarly elevated in bald scalp (82), suggesting that pathogenic mechanisms beyond androgen pathway play important roles in Androgenetic Alopecia. Alternatively, there may be any linkage between AR and prostaglandin D2
--------------
So we do indeed have 5aR1 and 5aR2 enzymes in hair follicles, and there are far more in the front, than at the bottom of the head.
I wonder why systemic reduction of DHT is so effective for hair follicles if they have their own 5aR2 enzymes, because I know that lowering systemic DHT had no impact on sebum production. Very odd and something I can't explain right now.
Though the most interesting thing in the entire paper may be this
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So serum DHT once again is essentially a spill over from DHT produced in tissues (prostate for example). When you take a 5AR inhibitor it is inhibiting the enzyme in these tissues which causes less of a spill over. 5AR inhibitors reduce hair loss not so much because it reduces overall serum DHT (though this probably helps) but because it is reducing the actual enzyme activity in the follicle which is where the DHT accelerating baldness comes from MAINLY. Also, the actual enzyme itself, with an increase in activity could also cause increased oxidative stress and immune reaction in the follicle.
Once again, DHT is not a hormone where it is produced in one area of the body and then is circulated to act in other areas (like Testosterone being produced in the testicles mainly and acts on multiple tissues). It is converted inside the tissue and locally acts on that tissue.
While DHT seems to be the main driver in male pattern baldness for female pattern baldness it does not seem to be the main driver. For them it seems to be an imbalance from healthy estrogen balance to either an unfavorable estrogen imbalance and/or Androgen dominance. This could be caused by many things.
For men, testosterone alone does not cause male pattern baldness. The main driver is the increased production of DHT inside the hair follices leading to a host of issues. Why this starts--there are many theories and there are probably many causes.