blood circultion in bald men study

S Foote.

Experienced Member
Reaction score
66
Of course there are genetic differences in cellular aging. Like I said before, cellular aging is heavily influenced by the environment. Did you know metabolism is one of the main causes of cellular aging? You can adjust your metabolism via calorie intake. Caloric deficits are proven to extend life. At the same time, chronic caloric surplus decreases lifespan by increasing cell division and also increasing metabolism byproducts. Reactive oxygen species are a byproduct of metabolism, which can lead to increased oxidative stress. Intake of antioxidants via diet can help alleviate this. Of course, the natural base antioxidant capacity differs from people to people, but it is also heavily influenced by diet.

Inflammation and toxins will also result in premature cellular aging. Again, this is environmental. Of course nothing will stop the natural aging process, but to say environmental factors have an insignificant impact is erroneous.

There is increasing evidence that gut flora imbalance and western diets play a large role in the increase in autoimmune diseases and allergies. Again, this is environmental. Your gut health is heavily related to mental health and also the immune system. Gut flora is all environmental, and not genetic.


In addition, the evidence for the correlation between metabolic syndrome, CVD, and Androgenetic Alopecia is undeniable now. It is not some small studies drawing vague correlations. You can look up the large amount of studies from accredited journals yourself.

If there is a problem to be solved, then you ask questions; you don't keep denying things or you will get nowhere. The DHT theory is in no way complete; that is why you have keep investigating. Going back to the CVD relation, your can either say "correlation not causation" and abandon the research right there and just wait for an answer, or you can continue investigating.


What if I told you there are studies showing those with Androgenetic Alopecia are more likely to have hypertension? Just a correlation? What if I tell you that studies show those with hypertension have higher serum IL-6 and inflammation, and that IL-6 is the main inflammatory cytokine involved in the hair loss cascade? What if I also tell you that in vitro studies show that IL-6 upregulates androgen receptors? Still just an insignificant correlation?

How about in vitro study demonstrating a greater sensitivity to oxidative stress in balding scalp derma papilla cells vs nonbalding cells? No significance? How about an in vitro study demonstrating that oxidative stress can upregulate TGF-beta, the cytokine responsible for fibrosis? TGF-beta is also part of the androgen cascade, and suppresses hair growth.

If you look into the biochemical implications of this blood flow study, then you will see why this is significant. Optionally, you can continue to dismiss it.

The point is, hair follicle miniaturisation by the normal spatial growth controls, explains all this. It gives order and logic to these subsequent events, and indicates what is or is not relevant.
 

Armando Jose

Senior Member
My Regimen
Reaction score
977
This external pressure of the cast on the skin for a period of time, squeezes more fluid out of the tissue reducing the pressure around the follicles

In the study you cited:
"Our case is unusual be because the hairy area is just limited to the right back hand where the plaster cast and internal fixation surgery was performed instead of the whole cast applied area"

And in a similar study
http://www.hkmj.org/abstracts/v21n4/369.htm

"Complete resolution of hypertrichosis 3 months after
removal of cast"
 
Last edited:

S Foote.

Experienced Member
Reaction score
66

I don't think so Armando.

If anyone wants to propose how DHT effects hair growth, you have to explain it according to the scientific rules. This means you have to explain all the known effects of DHT on hair growth, in the most simple way possible. External pressure changes explain both how DHT increases body hair and beard growth, whilst having the opposite effect of reducing scalp growth in some people.

We have to consider why hair evolved in mammals in the first place, and this was all about body temperature control.

From the structural viewpoint, hair follicles are superbly adapted to have the hair production area adjusted by small changes in external tissue fluid pressures. This applies both to enlarging anagen follicles, and to those follicles already in full anagen size. This adaptation allows hair production in early mammals, to be adjusted in line with environmental temperature changes. Hot conditions increase surface blood flow, increasing local tissue fluid pressures, and reducing hair growth. Cold conditions reduce surface blood flow, reducing tissue fluid pressures and increasing hair growth.

How sensitive the tissue is to this particular blood flow change, depends on another factor. This is the natural toughness of the tissue. Soft weak tissue will allow the fluid pressure changes to make more of a difference. In most hairy mammals I think this is the dermal characteristic. I think in general, modern Human tissue is tougher, and this cold response doesn't work well. But there have been anecdotes on the forums about the old time ice carriers, developing increased hair growth on their backs caused by carrying the ice sacks.

I think there is also an example of this tissue hardness relationship in modern Humans. If you feel the tissue beneath your eyebrows, you can feel how this is softer than the surrounding tissue.. Less external resistance to follicle enlargement, bigger follicles, more hair growth. So where does DHT come into this?

Androgens play a major role in tissue building and performance. To get the maximum effect, you need to increase the nutrient supply and waste removal around the tissue cells. Increasing lymphatic drainage efficiency would do this well, and I think this is what DHT does. This also explains why people on the forums complain about loss of gym performance and results, whilst on Finasteride.

DHT induced body hair and beard growth, are clearly related to areas rich in superficial lymphatic vessels. I go into more detail about this, and how this can cause the opposite effect in the scalp in my article here.
https://www.academia.edu/17570665/A...nt_Hair_Research_and_an_Overlooked_Connection.

There are two other factors this explains. Normally when there is local high tissue fluid pressure, this naturally tries to disperse into the surrounding lower pressure areas. The male pattern baldness area has been linked to the same area as the galea membrane. This membrane would hinder this drainage into lower tissues, and whilst not causal in male pattern baldness, this could play a part in making treatments harder.

The other thing noted in male pattern baldness is the increased androgen receptor sensitivity, linked to increased local DHT production. This could be the bodies attempt to try and increase the local lymphatic drainage, in response to the edema. But the problem is the drains are effectively being blocked, by too much DHT activity lower down the lymph vessels.

According to this situation, taking Finasteride may take care of the blocked drain, but it will also reduce DHT where it is really needed according to this scenario.. This is in the bald scalp itself. This leads to what many people may think is a crazy idea.

According to this, people using an oral dose of Finasteride, should also apply topical DHT to the balding area. There are such creams available. This shift in the local distribution of DHT, should in theory boost the effects of oral Finasteride significantly. If it does it opens up the possibility of using much reduced doses of Finasteride, and so reduced side effects. But if anyone wants to try this, Its your decision and the usual disclaimers apply.
 

S Foote.

Experienced Member
Reaction score
66
In the study you cited:
"Our case is unusual be because the hairy area is just limited to the right back hand where the plaster cast and internal fixation surgery was performed instead of the whole cast applied area"

And in a similar study
http://www.hkmj.org/abstracts/v21n4/369.htm

"Complete resolution of hypertrichosis 3 months after
removal of cast"

There are many cases of where there was no surgery to confuse the issue, and hair growth was linked to the areas of increased cast pressure on the skin.
 

Armando Jose

Senior Member
My Regimen
Reaction score
977
DHT induced body hair and beard growth
Yes, you are right. And the same for healthy scalp hair.

All you say is well, but my question is related to the posibles changes in the viscosity of sebum. Sebum is a fluid and all people know that in the neighbourgh of root hair exist a sebaceous gland secreting a type of hair fat, and it could take part in the external resistance to follicle enlargement, is it possible?
 

RatherLurk

Member
My Regimen
Reaction score
50
According to this, people using an oral dose of Finasteride, should also apply topical DHT to the balding area. There are such creams available. This shift in the local distribution of DHT, should in theory boost the effects of oral Finasteride significantly. If it does it opens up the possibility of using much reduced doses of Finasteride, and so reduced side effects. But if anyone wants to try this, Its your decision and the usual disclaimers apply.

I actually tried this. 1,25 mg ED with Topical Finasteride Liposomal 1,5%. I have only regrets, my hairline lost half an inch since januari when I started the topical. Quit after 4 months as my hairline seemed to be getting worse rapidly.
 
Last edited:

abcdefg

Senior Member
Reaction score
782
Of course there are genetic differences in cellular aging. Like I said before, cellular aging is heavily influenced by the environment. Did you know metabolism is one of the main causes of cellular aging? You can adjust your metabolism via calorie intake. Caloric deficits are proven to extend life. At the same time, chronic caloric surplus decreases lifespan by increasing cell division and also increasing metabolism byproducts. Reactive oxygen species are a byproduct of metabolism, which can lead to increased oxidative stress. Intake of antioxidants via diet can help alleviate this. Of course, the natural base antioxidant capacity differs from people to people, but it is also heavily influenced by diet.

Inflammation and toxins will also result in premature cellular aging. Again, this is environmental. Of course nothing will stop the natural aging process, but to say environmental factors have an insignificant impact is erroneous.

There is increasing evidence that gut flora imbalance and western diets play a large role in the increase in autoimmune diseases and allergies. Again, this is environmental. Your gut health is heavily related to mental health and also the immune system. Gut flora is all environmental, and not genetic.


In addition, the evidence for the correlation between metabolic syndrome, CVD, and Androgenetic Alopecia is undeniable now. It is not some small studies drawing vague correlations. You can look up the large amount of studies from accredited journals yourself.

If there is a problem to be solved, then you ask questions; you don't keep denying things or you will get nowhere. The DHT theory is in no way complete; that is why you have keep investigating. Going back to the CVD relation, your can either say "correlation not causation" and abandon the research right there and just wait for an answer, or you can continue investigating.


What if I told you there are studies showing those with Androgenetic Alopecia are more likely to have hypertension? Just a correlation? What if I tell you that studies show those with hypertension have higher serum IL-6 and inflammation, and that IL-6 is the main inflammatory cytokine involved in the hair loss cascade? What if I also tell you that in vitro studies show that IL-6 upregulates androgen receptors? Still just an insignificant correlation?

How about in vitro study demonstrating a greater sensitivity to oxidative stress in balding scalp derma papilla cells vs nonbalding cells? No significance? How about an in vitro study demonstrating that oxidative stress can upregulate TGF-beta, the cytokine responsible for fibrosis? TGF-beta is also part of the androgen cascade, and suppresses hair growth.

If you look into the biochemical implications of this blood flow study, then you will see why this is significant. Optionally, you can continue to dismiss it.

Why dont women go bald, but men do despite all these same factors you speak of? Why would women not be going bald in the same numbers as men when all the same factors you want all apply to them? Doesnt make much sense.
I agree with you that some of those things might play some role. Its a question of how much.
 
Last edited:

Thebaldcel

Member
My Regimen
Reaction score
39
Why dont women go bald, but men do despite all these same factors you speak of? Why would women not be going bald in the same numbers as men when all the same factors you want all apply to them? Doesnt make much sense.
I agree with you that some of those things might play some role. Its a question of how much.

But women do go bald, and there are women that suffer from Androgenetic Alopecia. The fact that women suffer from Androgenetic Alopecia shows that androgen receptor transcriptional activity is much more important than concentration of androgens. The reasonable research move is to observe what can cause increased immune response in the scalp and androgen receptor transcription activity, and that is what I've discussed.

The reason women go bald less than men is because androgens. Androgens play a vital role in the immune response while at the same time having some hair growth inhibiting properties in the scalp. It is because males have higher levels of androgens plus lower aromatase that they bald more than women. With low levels of androgen, it takes much more androgen receptor upregulation in females than men to cause any sort of hair loss cascade.

Androgens do a play a vital role, but I believe they are only a vital piece of the puzzle, and not the full puzzle. PGD2 plays an important role in the immune response, and has anti-inflammatory properties in some tissues with inflammatory properties in others. Unfortunately, it has a negative effect on hair growth. Regardless, they are involved in the immune response to an insult, and is downstream of the cascade. What we want to know is the insult that causes AR upregulation in the first place.

I believe it is a culmination of things upregulating the AR, that eventually causes a positive feedback loop. The same inflammatory cytokine that is upregulated by AR can also be upregulated by AR activation. In cancer cell line studies (https://www.ncbi.nlm.nih.gov/pubmed/17617741) (https://www.ncbi.nlm.nih.gov/pubmed/11410519), even without androgens, IL-6 and IL-8 were able to significantly enhance androgen expression and promoter activation. It is very significant. Inflammation will upregulate AR, even without AR. Inhibiting IL-6 in castration resistant cancer increases the effectiveness of targeted anti-cancer drugs.

Castration resistant prostate cancer shows how other pathways can express local AR to a level where castration does not stop it.

edit: bald less not more
 
Last edited:

Arrade

Senior Member
My Regimen
Reaction score
1,253
I think age reduced circulation certainly wont help.
The older you are, the worse your circulation.
At around 40 estrogen starts rising in men which creates inflammation and exponential growth of conditions like atherosclerosis.
Fibrosis also starts to rapidly occur
 

Arrade

Senior Member
My Regimen
Reaction score
1,253
Why dont women go bald, but men do despite all these same factors you speak of? Why would women not be going bald in the same numbers as men when all the same factors you want all apply to them? Doesnt make much sense.
I agree with you that some of those things might play some role. Its a question of how much.
Women are far less susceptible of circulation or heart issues because they have higher levels of estrogen and progesterone, which is protective of the cardiovascular system.
They also have 6xtimes the amount of estrogen in the skin (I think I read this somewhere, could be wrong) but this would also negate skin tissue interaction of androgen.
 

abcdefg

Senior Member
Reaction score
782
Women are far less susceptible of circulation or heart issues because they have higher levels of estrogen and progesterone, which is protective of the cardiovascular system.
They also have 6xtimes the amount of estrogen in the skin (I think I read this somewhere, could be wrong) but this would also negate skin tissue interaction of androgen.

You might be right, but my point was that the amount of women with major hair loss at 50+ years old compared to men is much much much less. I mean most women I see, and I think the numbers would agree also, do not lose almost any hair whatsoever most of their lives. Why? Its exactly what your saying its a difference in hormones. The major difference, and major cause of male pattern baldness in men is male hormones.

"The reason women go bald more than men is because androgens. "
Women go bald way way way less often than men do, and to way less a degree at ages like 50+. Its because of hormones like estrogen maybe others, but its largely male hormones that account for this difference between genders. That is my point male pattern baldness is mostly a hormone driven problem well initially. DHT should be at the top of list on things to stop.
Anyways I agree with everything your saying. I just dont know how much I agree with the effects of hypoxia, and environmental factors how much of a role these play in male pattern baldness verse those other things your mentioning like PGD 2. I think male pattern baldness is largely not environmental factors, but time will tell. I dont think we know enough to say. They play a role, but maybe minor.
 
Last edited:

abcdefg

Senior Member
Reaction score
782
The older you are, the worse your circulation.
At around 40 estrogen starts rising in men which creates inflammation and exponential growth of conditions like atherosclerosis.
Fibrosis also starts to rapidly occur

Maybe so, but estrogen is good for hair.
 

Jimm

Experienced Member
My Regimen
Reaction score
679
When @S Foote. speaks of external pressure factors as it applies to favorable growth environment and massage to increase circulation, would a device that creates negative pressure to the scalp achieve what he advocates? Perhaps in the most base of terminology, basically a penis pump for your head, but the effect is the same. Decrease external pressure, draw blood into the area. Might be impossible as maintenance if you have hair but on a balding crown, cupping or some other pump means might be possible.


OR: https://www.amazon.com/gp/product/B072Q6RS6J/ref=oh_aui_search_detailpage?ie=UTF8&psc=1

Tie a shirt or some thin fabric over your hair so you avoid all the friction, and use this. Your girlfriend will appreciate you having one, also (be sure to wash it in that case). You're not going to get the same effect using your fingers as you do with this. I try to do 10 mins twice a day over the scalp and around the neck, but I've never been consistent. Trying consistent derma rolling once a week and this twice a day, hopefully. I can tell you one thing for sure: It scratches the male pattern baldness itch in a way that is both refreshing, relieving and novel.
 

Thebaldcel

Member
My Regimen
Reaction score
39
You might be right, but my point was that the amount of women with major hair loss at 50+ years old compared to men is much much much less. I mean most women I see, and I think the numbers would agree also, do not lose almost any hair whatsoever most of their lives. Why? Its exactly what your saying its a difference in hormones. The major difference, and major cause of male pattern baldness in men is male hormones.

"The reason women go bald more than men is because androgens. "
Women go bald way way way less often than men do, and to way less a degree at ages like 50+. Its because of hormones like estrogen maybe others, but its largely male hormones that account for this difference between genders. That is my point male pattern baldness is mostly a hormone driven problem well initially. DHT should be at the top of list on things to stop.
Anyways I agree with everything your saying. I just dont know how much I agree with the effects of hypoxia, and environmental factors how much of a role these play in male pattern baldness verse those other things your mentioning like PGD 2. I think male pattern baldness is largely not environmental factors, but time will tell. I dont think we know enough to say. They play a role, but maybe minor.

I meant women bald less, bad typo. You are right there is not enough conclusive evidence to tell. It is just my theory obtained from many studies to explain the gap in the DHT theory. The strange thing has always been the question of why Androgenetic Alopecia can progress even with very low androgen levels, and the AR "sensitivity" being the cause. However, why does sensitivity seem to change? This implies that epigenetics play a large role in this, and sensitivity is mediated via an increase in androgen receptor levels and signal amplification. However, it is important to note that genetics can influence epigenetics too. People have different environmental thresholds before gene expression is altered enough to cause significant effects. If you look at old men, how many do you see are NW1 and not higher? Almost all old men have at least some levels of recession or thinning. Those of us with Androgenetic Alopecia just has this recession process progress faster than normal.

While ultimately hormone driven, the true direct cause is the immune system response, and the AR seems to be a strong mediator in the immune system. Certain environmental insults can cause an increase in AR signaling, because AR is a mediator of inflammation and immunity. So are androgens the messenger or the direct cause? I believe it's both.

The point is, hair follicle miniaturisation by the normal spatial growth controls, explains all this. It gives order and logic to these subsequent events, and indicates what is or is not relevant.

What is your take on the tight scalp theory (not expanding skull theory)?
 

Arrade

Senior Member
My Regimen
Reaction score
1,253
Maybe so, but estrogen is good for hair.
estrogen is good for hair in the scalp skin, and protectetive in women but higher levels in a man with normal androgens isn't good for hair.
If you're not castrated and have high estro it will raise dht in tissue as a stress response
 

NewUser

Experienced Member
Reaction score
305
Even *if you're castrated, you won't re-grow any hair. Big pharma's faulty hair follicles theory comes up short again.
 
Last edited:

justlol@you

Established Member
My Regimen
Reaction score
112
estrogen is good for hair in the scalp skin, and protectetive in women but higher levels in a man with normal androgens isn't good for hair.
If you're not castrated and have high estro it will raise dht in tissue as a stress response

I'm aware you're a member of the ray peat forum, and to me this smacks of typical contortionist thinking on that forum trying to shove everything into a ray peat paradigm. What evidence is there for the relationship you just described?
 

couldntthinkofaname

Established Member
My Regimen
Reaction score
223
do people who suffer from illness that affect blood vessels like vasculitis or diabetes lose more hair?
 

Trichosan

Senior Member
My Regimen
Reaction score
1,321
do people who suffer from illness that affect blood vessels like vasculitis or diabetes lose more hair?

I wouldn't put that as a "given". I've seen many diabetic men and women over a period of many years. Numerous full heads among the men with a distribution that parallels the incidence of male pattern baldness in the population. Thyroid and hormone deficiencies seem to impart the gradual thinning in women as a noticeable change.
 
Top