Why Do Older Guys Lose Hair If Testosterone/dht Decreases With Age?

RatherGoBlindThanSeeItGo

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This is completely anecdotal, but my brother's father is in his sixties and he looks like his baldness has barely progressed in the last 10 years. I doubt he's on finasteride because it's too far gone to save, and it doesn't look like he cares, but I could be wrong (he could have prostate issues, I wouldn't know). Same goes for when I compare my pictures of my grandfather. The difference between when he was 28 and 55 is huge. Between 55 and 85 there is barely any difference. And he was 55 in the late sixties so I doubt finasteride or any drug had much to do with that. Neither of them are/were completely slick bald. Just very, very diffuse (lost 90% of hair).
 

Swoop

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I agree the observation by Hamilton defies the cumulative damage idea and the idea of a "switch" is more logical.

Furthermore looking from a broad view at Androgenetic Alopecia I believe that one component to it is "stress". Inflammation is often present that can even lead to fibrosis. Furthermore there are supporting studies for ROS, DNA damage and such that may have implications in Androgenetic Alopecia.

Since aging is a progressive decline to withstand stress and damage it is logical to assume that older (stem)cells would have more troubles coping with stress/damage than young ones.

Aubrey de Grey called hair loss a cell loss problem:

"Hair loss and grey hair are mostly a cell loss problem, and rejuvenating the epidermal stem cell population (as well as melanocytes specifically) is something a lot of people are making good progress on; check out the work of Elaine Fuchs and Fiona Watt and Colin Jahoda especially."

RepleniSens:

Every day, our cells are damaged by both tiny molecular-level insults and by obvious trauma. Some of these damaged cells are repaired, but others are either destroyed, or forced into a dysfunctional ‘senescent’ state where they can no longer divide, or commit ‘cellular suicide’ (apoptosis) for the greater good of the body. Some of the lost cells are replaced by the pools of specialized, tissue-specific stem cells, but the degenerative aging process makes these stem cell pools less effective at repair over time.
 

buckthorn

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I agree the observation by Hamilton defies the cumulative damage idea and the idea of a "switch" is more logical.

Furthermore looking from a broad view at Androgenetic Alopecia I believe that one component to it is "stress". Inflammation is often present that can even lead to fibrosis. Furthermore there are supporting studies for ROS, DNA damage and such that may have implications in Androgenetic Alopecia.

Since aging is a progressive decline to withstand stress and damage it is logical to assume that older (stem)cells would have more troubles coping with stress/damage than young ones.

Aubrey de Grey called hair loss a cell loss problem:

"Hair loss and grey hair are mostly a cell loss problem, and rejuvenating the epidermal stem cell population (as well as melanocytes specifically) is something a lot of people are making good progress on; check out the work of Elaine Fuchs and Fiona Watt and Colin Jahoda especially."

RepleniSens:

Every day, our cells are damaged by both tiny molecular-level insults and by obvious trauma. Some of these damaged cells are repaired, but others are either destroyed, or forced into a dysfunctional ‘senescent’ state where they can no longer divide, or commit ‘cellular suicide’ (apoptosis) for the greater good of the body. Some of the lost cells are replaced by the pools of specialized, tissue-specific stem cells, but the degenerative aging process makes these stem cell pools less effective at repair over time.

very hopeful yet depressing at the same time. f*** aging. and f*** you swoop for playing with my emotions, you beautiful bastard. :p
 

Swoop

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very hopeful yet depressing at the same time. f*** aging. and f*** you swoop for playing with my emotions, you beautiful bastard. :p

Yes, Androgenetic Alopecia is very depressing buckie. I mean it's basically comparable to aging. Highly likely irreversible too from a certain timepoint.

Constant damage/stress to these cells over time just is never a good thing. Those brittle beautiful healthy hair follicles basically get raped to death.

May god Tsuji create new ones out of our healthy ones. That's all I hope for.
 

buckthorn

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hair follicles basically get raped to death.

couldn't have said it better. every night my scalp feels like it's getting raped to death.
 

itsover

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Aubrey de Grey called hair loss a cell loss problem:

"Hair loss and grey hair are mostly a cell loss problem, and rejuvenating the epidermal stem cell population (as well as melanocytes specifically) is something a lot of people are making good progress on; check out the work of Elaine Fuchs and Fiona Watt and Colin Jahoda especially."

Wow, nice to see there are people on hairloss forum interested in Aubrey de Grey and SENS, this guy is great, he wants to cure aging, imagine if we could enjoy our NW0 for hundreds of years.
 

Pavi

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This is pretty simple.

Men become hypersensitive to testosterone as they age. Once again, it is not the level of androgens present that is important, it is the responsiveness of the hair to DHT that is important.

I started balding at 16. I almost clinically have low DHT. Yet I have body hair everywhere and I build muscle with ease. My body is clearly hypersensitive to testosterone/DHT

It's the sensitivity.
 

coolio

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Wow, nice to see there are people on hairloss forum interested in Aubrey de Grey and SENS, this guy is great, he wants to cure aging, imagine if we could enjoy our NW0 for hundreds of years.

Norwood#0 is the rounded female hairline. Norwood#1 is the straight-across teenage boy hairline.


Men become hypersensitive to testosterone as they age. Once again, it is not the level of androgens present that is important, it is the responsiveness of the hair to DHT that is important.

It's both, levels and sensitivity.

But sensitivity is by far the bigger player. It's also the only one we should be messing with for hair purposes.
 

InBeforeTheCure

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I agree the observation by Hamilton defies the cumulative damage idea and the idea of a "switch" is more logical.

Furthermore looking from a broad view at Androgenetic Alopecia I believe that one component to it is "stress". Inflammation is often present that can even lead to fibrosis. Furthermore there are supporting studies for ROS, DNA damage and such that may have implications in Androgenetic Alopecia.

Since aging is a progressive decline to withstand stress and damage it is logical to assume that older (stem)cells would have more troubles coping with stress/damage than young ones.

Aubrey de Grey called hair loss a cell loss problem:

"Hair loss and grey hair are mostly a cell loss problem, and rejuvenating the epidermal stem cell population (as well as melanocytes specifically) is something a lot of people are making good progress on; check out the work of Elaine Fuchs and Fiona Watt and Colin Jahoda especially."

RepleniSens:

Every day, our cells are damaged by both tiny molecular-level insults and by obvious trauma. Some of these damaged cells are repaired, but others are either destroyed, or forced into a dysfunctional ‘senescent’ state where they can no longer divide, or commit ‘cellular suicide’ (apoptosis) for the greater good of the body. Some of the lost cells are replaced by the pools of specialized, tissue-specific stem cells, but the degenerative aging process makes these stem cell pools less effective at repair over time.

Check out Steve Horvath's paper: DNA methylation age of human tissues and cell types

He found a set of 353 CpG sites, which he calls an "epigenetic clock", that correlate almost perfectly (correl = 0.96 in testing set) with age across many cell types. Some highlights:

- both embryonic stem cells and iPS cells have an "age" of about 0
- cells get "older" with each passage in culture
- genes around these CpG sites are enriched for cell death/survival, organismal/tissue development, and cancer
- rate of aging measured by the clock is highly heritable, but less so later in life (likely non-genetic effects in play)
- Aging is highly accelerated before adulthood; afterwards, it's approximately linear:

horvath1.png

- DNAm age (clock age) is not related to mitotic age or cellular senescence
- DNAm age is accelerated in cancer cells
- He hypothesizes that DNAm aging is accelerated by an "epigenetic maintenance system" (EMS), which works to maintain epigenetic stability.
Predictions of this model:
- Cancer cells should show signs of accelerated aging, reflecting the protective actions of the EMS.
- Mitogens, genomic aberrations, and oncogenes, which trigger EMS, should accelerate DNAm aging.
- High age acceleration of cancer tissue should be associated with fewer somatic mutations given the
protective role of the EMS.
- Mutations in p53 should decrease age acceleration of cancer tissue, assuming p53 signaling helps trigger
the EMS.
He shows that all these predictions turn out to be true.

In another paper, Horvat et al. also demonstrated that in the offspring of semi-supercentenarians, DNAm age is lower than expected based on actual age.

Anyway, I wonder if the mechanism of the A.G.A "switch" could also maybe involve some interaction between genetics and age-associated epigenetic changes such as these.
 

Feelsbadman.jpg

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Has no one considered the very simple fact that levels of 5 alpha reductase and aromatase eznyme levels increase with aging?

I think people get way too carried away with "sensitivity". Hamilton's experiments most likely have a far more simpler explanation. The younger enuch had lower levels of 5 AR in his hair follices than the older eunuch. The older enuch, had high levels of 5AR, but the lack of testosterone prevented this enzyme from forming large quantities of DHT. As soon as T was injected, the enzyme had the substrate it needed and copious amounts of DHT were produced very quickly. Hence his rapid balding.

DHT and 5 AR operate off of a "feed forward" mechanism. That is, the more DHT present, the more 5AR is made and vice versa. Androgen receptor expression is influenced by the typing of androgen binding to the receptor. Marty Sawaya's finasteride experiments showed that there were two types of androgen receptors (just like there are two types of estrogen alpha and beta) and that finasteride use caused an upregulation of a the more beneficial kind. To me, this sounds like androgens that are more anabolic, like T, stimulate androgen receptors in a way that increses the expression of the more beneficial/less damaging receptor type and hormones that are more androgenic, like DHT, do the exact opposite.

In other words, hormone receptor expression can change simply by modifying the hormones that interact w/ the receptors. This can be seen with SERMs and breast cancer. Estrogen receptor beta is protective agaisnt breast cancer while estrogen recptor alpha stmulation seems to increase it. Estrogen receptor beta can be increased by taking hormones/drugs that interact w/ estrogen receptor beta. I imagine Androgenetic Alopecia is at least somewhat similar as finasteride seems to increase beneficial androgen receptor expression.


It would be interesting to see what would have happened to the older eunuch if he had been placed on finasteride for a year prior to T administration. Not that this would have been possible, but my guess would be he would have balded at a rate slower than the young eunuch or not at all.

Just some food for thought. I'm not going to bother to reference or cite anything because I'm kind of lazy and it's not worth my time so take it all w/ a grain of salt.
 

plisk

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Yep, the steroid thing is also true. It's also probably worth looking into what happens to SHBG as you age. Free androgens may also play a role...

I want to point out something of interest anecdotally

Im an experienced steroid user, been in many of those communities for years. Many of them, especially the older guys, use finasteride to prevent hair loss on cycle.

the clever-silly in me suggests to them that this is pointless as most of the steroids they use do not go under 5AR conversion, and are potent androgens in and of themselves, and therefore finasteride has no protective mechanism (other than the protection it might offer while they are using large doses of testosterone specifically)...

however, in practice, for many it does seem to work to varying degrees despite this "on paper" fact. It leads to me to believe there is some unexplained mechanism that finasteride is beneficial to hair, perhaps upregulating some other enzyme despite the massive presence of androgens, some significantly more powerful than testosterone or even DHT. This "uneducated" or "dumb" practice actually ends up being beneficial.

Danny roddy who seems confused on a number of topics, so i take his word with a large fistful of salt, suggests that propecia works because it is somehow similar to progesterone. This doesnt make sense on the surface, but trying to research a connection, 5AR is also responsible for the conversion of progesterone to allopregnanolone. In theory then, the prevention of this conversion allows for higher circulating levels of progesterone, much the same as the reduction of 5AR allows for higher levels of testosterone and estradiol.
 

abcdefg

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Since aging is a progressive decline to withstand stress and damage it is logical to assume that older (stem)cells would have more troubles coping with stress/damage than young ones.

I agree, but I think the role of aging is still yet to be understood. Does aging control 80 percent of male pattern baldness or is it 5? A lot of things no one understands tend to go under the generic terms like aging until someone figures out the real cause.
You might need the male pattern baldness triggers for aging to actually carry through its processes to put hair into the damaged dead state. Most men are suspectible to male pattern baldness and maybe even all men if injected with enough T would get male pattern baldness who knows maybe genetics has some upper tolerance level.
Men do exist that are 50 even 60+ years old that have teenage almost zero hair loss. Its very very rare compared to women but they exist which almost alone proves aging does not directly cause male pattern baldness by itself unless your susceptible to male pattern baldness to begin with
What triggers hair to become sensitive? We always wondered that and still dont know
 

mr_robot

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I agree the observation by Hamilton defies the cumulative damage idea and the idea of a "switch" is more logical.

Furthermore looking from a broad view at Androgenetic Alopecia I believe that one component to it is "stress". Inflammation is often present that can even lead to fibrosis. Furthermore there are supporting studies for ROS, DNA damage and such that may have implications in Androgenetic Alopecia.

This is n't entirely related but I thought I'd ask your opinion regardless. I've had slowly receding hairline for around 15 years, a couple of years ago after chronic fatigue and stress my crown which was slightly diffuse went full on diffuse. Now my particular regime which is mainly minoxidil/peppermint oil/stemox managed to regrow temple hair that I've lost over 10 years ago from around a NW3V to NW2 but other than thickening of existing hair the crown has not really responded as well.

The peculiar thing is the peppermint oil response, the cooling/tingling sensation from the peppermint oil is significantly dulled in the crown area, yet areas where there is regrowth the reaction is strong. I'm wondering why this would be the case? Lack of blood circulation? Fibrosis meaning the skin is not responsive? Simply lack of penetration due to clogged follicles?
 

Medina

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What if androgen receptors become more sensitive because testosterone levels have dropped. What do old men and young balding guys have in common? They have lower levels of T. So the body reacts by upregulating the receptors to harvest more testosterone in.
 

NewUser

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This is pretty simple.

Men become hypersensitive to testosterone as they age. Once again, it is not the level of androgens present that is important, it is the responsiveness of the hair to DHT that is important.

I started balding at 16. I almost clinically have low DHT. Yet I have body hair everywhere and I build muscle with ease. My body is clearly hypersensitive to testosterone/DHT

It's the sensitivity.

You wouldnt have body hair without increased DHT levels since puberty. DHT kickstarts proliferation of body hair in normal pubescence, but never does the reverse occur in either eunuchs or those of us taking DHT-inhibiting drugs.

The faulty hair follicle theory also fails to explain why pattern baldness is recently associated with:

coronary heart disease
polycistic ovarian cancer
prostate cancer
metabolic syndrome
insulin resistance
 
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resu

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Why older men have new body hair in areas where previously the follicles weren't producing hair? Probably same reason.
 

bigentries

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What about newborn males? Apparently male babies have ridiculous amounts of testosterone for a short while after they are born

A friend had a boy a few months ago and couldn't help but notice the kid had a terrible combination of diffuse thinning and recession, yet strong hair exactly in the horseshoe pattern. Kinda like the worst cases of baldness I've seen in grown men

I've read it has more to do with telogen effluvium, but there are too many coincidences to just brush off any connection

What if androgen receptors become more sensitive because testosterone levels have dropped. What do old men and young balding guys have in common? They have lower levels of T. So the body reacts by upregulating the receptors to harvest more testosterone in.

What about eunuchs, female-to-male transexuals or women who abuse testosterone for bodybuilding purposes?

Why older men have new body hair in areas where previously the follicles weren't producing hair? Probably same reason.

Yes, to me the same mechanism has to be involved. Which makes it more complicated. Why does DHT cause hair to die in a very specific area of the body while promoting hair growth anywhere else?
 
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abcdefg

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"however, in practice, for many it does seem to work to varying degrees despite this "on paper" fact. It leads to me to believe there is some unexplained mechanism that finasteride is beneficial to hair, perhaps upregulating some other enzyme despite the massive presence of androgens, some significantly more powerful than testosterone or even DHT. This "uneducated" or "dumb" practice actually ends up being beneficial."

This is partly why I never tried finasteride. This stuff is so complicated and poorly understood why are we even messing with it? No one has any idea what changing all these different hormone loops really ends up doing.
I have wondered how important are all the byproducts of lowering 5-ar 2 compared to the actual DHT level itself in terms of male pattern baldness.
This is why I cant see male pattern baldness being cured anytime soon. You could literally write a huge book full of open questions on male pattern baldness. Most have no answers yet even fundamentally important ones.
 
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