Studies that help confirm my theory that balding = low oxygen + DHT

Slow, did the botox injections help promote hairline regrowth or mainly around the crown?

The only times I have ever suffered inflammation and a little thinning around the crown is when I have done too many sit ups / crunches. I think that this might have something to do with the trapezius muscles pulling tightly on the back of the scalp, but IDK to be exact.

Ya know, I'm willing to buy this. My only problem is this, as I don't have the original study: the participants are injected with botox and the hair counts are tracked over the course of a year. The results are there, I can't argue that. But aren't the study proctors making some conceptual leaps in their discussion of the results? Did the study methods actually provide any of the data to prove this was a result of increased blood-flow and oxygenation? I don't think they did. They are looking at the results and making some assumptions about what the botox could be doing, but that isn't necessarily what is going on.

http://www.nature.com/srep/2012/120528/srep00424/full/srep00424.html?WT..

Finally, we investigated the piloerection ability of the bioengineered hair follicles in the skin. Acetylcholine (Ach; 1 µg/site) was administered intradermally in the vicinity of the engrafted follicles, and the angles of the hair shafts before and after treatment were calculated (Fig. 4b). ACh injection led to a significantly increased angle of piloerection in the bioengineered pelage compared to a control (Fig. 4b and c). In contrast, an anti-cholinergic agent, atropine (AT), inhibited this effect (Fig. 4c).

I can't go through the following two studies to select the important snippets right now, overall they both should be read in their entirety because they are really interesting.

http://www.nature.com/jid/journal/v44/n2/pdf/jid196517a.pdf
http://www.nature.com/jid/journal/v30/n3/pdf/jid195823a.pdf
http://www.ncbi.nlm.nih.gov/pubmed/12269872

With the botox study, we've got to consider the actual actions of botox. It essentially blocks ACh receptors at the neuromuscular synapse, lowering contraction of the muscle. But what muscles
is botox acting on in the scalp? To me, the obvious would be arrector pili. But why would this necessarily cause an increase in hair growth?

Could it be that reducing the action of the arrector pili is lowering sebum output? After all, the hair follicle tends to release sebum when the angle increases. We also know things like stress (which increases adrenergic and ACh signalling) increases sebum output and we intuitively know stress increases hair loss. DHT increases the size and activity of sebaceous glands. Could it really all come back to sebum? Maybe its a combination of androgens and overexcitation of the the arrector pili muscles.

See what I'm saying? There are other possibilities here besides a tight galea. The things I just suggested, I have no idea if there is any truth to that idea. I'm just saying there are other things we can explore here too without jumping to the conclusion that the galea is tight. Again, I'm not saying the galea theory is wrong either. I just don't think we should put all of our eggs in one basket and we should continue to re-assess as more evidence accumulates.

I would totally agree that oxygen plays a major role in our overall health, and that a lack of the appropriate amounts of oxygen has an impact on our overall health. I recently came across the idea of ingesting hydrogen peroxide. You don't want to ingest just any hydrogen peroxide, but instead want to locate the type that is acceptable for humans to consume. The argument was that ingesting H2O2 on a regular basis will prevent cancer. I can't speak for whether or not that is a true statement, but I can see the logic behind increasing the amount of oxygen into my body.

AS54 wrote:Ya know, I'm willing to buy this. My only problem is this, as I don't have the original study: the participants are injected with botox and the hair counts are tracked over the course of a year. The results are there, I can't argue that. But aren't the study proctors making some conceptual leaps in their discussion of the results? Did the study methods actually provide any of the data to prove this was a result of increased blood-flow and oxygenation? I don't think they did. They are looking at the results and making some assumptions about what the botox could be doing, but that isn't necessarily what is going on.

http://www.nature.com/srep/2012/120528/srep00424/full/srep00424.html?WT..

Finally, we investigated the piloerection ability of the bioengineered hair follicles in the skin. Acetylcholine (Ach; 1 µg/site) was administered intradermally in the vicinity of the engrafted follicles, and the angles of the hair shafts before and after treatment were calculated (Fig. 4b). ACh injection led to a significantly increased angle of piloerection in the bioengineered pelage compared to a control (Fig. 4b and c). In contrast, an anti-cholinergic agent, atropine (AT), inhibited this effect (Fig. 4c).

I can't go through the following two studies to select the important snippets right now, overall they both should be read in their entirety because they are really interesting.

http://www.nature.com/jid/journal/v44/n2/pdf/jid196517a.pdf
http://www.nature.com/jid/journal/v30/n3/pdf/jid195823a.pdf
http://www.ncbi.nlm.nih.gov/pubmed/12269872

With the botox study, we've got to consider the actual actions of botox. It essentially blocks ACh receptors at the neuromuscular synapse, lowering contraction of the muscle. But what muscles
is botox acting on in the scalp? To me, the obvious would be arrector pili. But why would this necessarily cause an increase in hair growth?

Could it be that reducing the action of the arrector pili is lowering sebum output? After all, the hair follicle tends to release sebum when the angle increases. We also know things like stress (which increases adrenergic and ACh signalling) increases sebum output and we intuitively know stress increases hair loss. DHT increases the size and activity of sebaceous glands. Could it really all come back to sebum? Maybe its a combination of androgens and overexcitation of the the arrector pili muscles.

See what I'm saying? There are other possibilities here besides a tight galea. The things I just suggested, I have no idea if there is any truth to that idea. I'm just saying there are other things we can explore here too without jumping to the conclusion that the galea is tight. Again, I'm not saying the galea theory is wrong either. I just don't think we should put all of our eggs in one basket and we should continue to re-assess as more evidence accumulates.

Botox was not injected into the areas of balding. It was injected into the muscles that bind the galea (the balding region) to the skull. When they contract, they pull the galea down like pulling a sheet draped over a bowling ball; the arteries that geeed the scalp are below the galea "sheet" and are pinched between the galea and the skull.

The injections are placed in the temporalis, occipital and temporalis muscles; away from areas of hair loss. They are paralyzed, and pressure on the arteries, from the tight galea, is removed.




Comprising five layers, the scalp is bound by the face anteriorly and the neck laterally and posteriorly. The skin is the first layer. The second layer is connective tissue, which is a thin layer of fat and fibrous tissue with a thickness of 4-7 mm. [11] The third layer is the galea aponeurotica, which exists as a tough layer of dense fibrous tissue that extends between the frontalis and occipitalis muscles. [18] Deep to these layers, the loose areolar connective tissue comprises collagen bundles and houses the major blood vessels of the scalp. This layer is laterally attached to the zygomatic arch and mastoid processes and posteriorly attached to the superior nuchal line. This layer provides the separation plane for surgical flaps and traumatic avulsions. [11] The final layer is the pericranium, which is the periosteum of the skull. This layer ends laterally with the origin of the temporalis fascia along the superior temporal line and provides nutrient supply to the bone

Hey Slow,

I missed that part when reading through your last post. That's my bad.

That does make things interesting. But what makes you (and I'm assuming the study authors) certain this is a restriction of blood flow? It seems to me the arteries that actually supply the dermis-epidermis of the scalp don't really interact much with the galea. Of course they do to some degree just from proximity, but what I'm wondering is why would a change in the forces on the galea effect the blood supply when the arteries/veins are not inserting through the galea, but sit overtop of it?

What I'm wondering is if the forces on the galea are somehow straining it, actually effecting the basal lamina that connects the dermis to the epidermis. If that were the case you would get a big effect on the hair follicles, which sit right at the border.



All of the vessels sit in the subcutaneous tissue. The galea is basically sitting right on top of the skull bone. Why would tension in the galea inhibit blood flow. I have to imagine the only way is due to some cellular adhesion between the galea and the tissue above it. But why does MPB happen in such an uneven pattern then (usually) where there is frontal recession and thinning at the crown, rather than just diffusely everywhere up top?

AS54 wrote:Hey Slow,

I missed that part when reading through your last post. That's my bad.

That does make things interesting. But what makes you (and I'm assuming the study authors) certain this is a restriction of blood flow? It seems to me the arteries that actually supply the dermis-epidermis of the scalp don't really interact much with the galea. Of course they do to some degree just from proximity, but what I'm wondering is why would a change in the forces on the galea effect the blood supply when the arteries/veins are not inserting through the galea, but sit overtop of it?

What I'm wondering is if the forces on the galea are somehow straining it, actually effecting the basal lamina that connects the dermis to the epidermis. If that were the case you would get a big effect on the hair follicles, which sit right at the border.



All of the vessels sit in the subcutaneous tissue. The galea is basically sitting right on top of the skull bone. Why would tension in the galea inhibit blood flow. I have to imagine the only way is due to some cellular adhesion between the galea and the tissue above it. But why does MPB happen in such an uneven pattern then (usually) where there is frontal recession and thinning at the crown, rather than just diffusely everywhere up top?

That picture is not accurate. There is a layer of connective tissue BENEATH the galea, and it houses the MAJOR arteries of the scalp. The minor arteries pass through the galea to get to the hair follicles:

Comprising five layers, the scalp is bound by the face anteriorly and the neck laterally and posteriorly. The skin is the first layer. The second layer is connective tissue, which is a thin layer of fat and fibrous tissue with a thickness of 4-7 mm. [11] The third layer is the galea aponeurotica, which exists as a tough layer of dense fibrous tissue that extends between the frontalis and occipitalis muscles. [18] Deep to these layers, the loose areolar connective tissue comprises collagen bundles and houses the major blood vessels of the scalp. This layer is laterally attached to the zygomatic arch and mastoid processes and posteriorly attached to the superior nuchal line. This layer provides the separation plane for surgical flaps and traumatic avulsions. [11] The final layer is the pericranium, which is the periosteum of the skull. This layer ends laterally with the origin of the temporalis fascia along the superior temporal line and provides nutrient supply to the bone

http://www.surgicalneurologyint.com/article.asp?issn=2152-7806;year=2011;volume=2;issue=1;spage=178;epage=178;aulast=Kemp

I'd say Slowmoe makes some plausible points here, esp considering the fact that these arteries exist beneath the galea.

It's interesting to note that pattern baldness is in the pattern of the galea, yet beneath it, hairloss never occurs. Although if oxygen loss is playing a role here I wouldn't entirely pin it on the scalp muscles pulling on the galea; I'd say that an expanded skull + pillow compression is causing further pressure on capillaries.

We saw that pillow pressure in the case of pressure alopecia can cause hairloss, so it could be a combination of these things.

Definitely some connection with the galea.
Nice variables pointed out by as45.

Something that doesn't sit right with me, say this works...Botox use long term surely isn't good??
What sides could you expect?

Since the arteries are housed in loose connective tissue, I wonder if the tissue is somehow being depleted/ weakened to allow compression of the blood vessels..... Hmmm

Live forever wrote:Definitely some connection with the galea.
Nice variables pointed out by as45.

Something that doesn't sit right with me, say this works...Botox use long term surely isn't good??
What sides could you expect?

Increased sexiness would be one side effect.

Yeah but anything with "toxin" in its name can't be too geat for you. IDK There are topical botox alternatives like snap 8 and argeline (sp?)

It is a thought, because we've seen evidence presented here before that fat is depleted in the area. All of that subcutaneous tissue that houses the cutaneous arteries/veins is mostly fat.

Perhaps there is something being triggered in the region that is favoring the metabolism of the fats there. Hypoxia might be that trigger. Its a really interesting possibility.

If the fat is being preferentially metabolized due to the hypoxic conditions, depending on the lipids that make it up, you could have a lot of inflammatory products being formed too. Thats all in addition to the sebum-androgen connection.


As far as botox goes, I really do think its quite safe if used moderately and only locally. The only side effect is on the muscle, which with the muscles we're talking about, I don't think we'd miss it if we lost some contractile ability there. To my knowledge it isn't systemmic, otherwise we'd see bigger problems, i.e. heart failure   

When I hear about Oxygen being the main problem my
gut instinct is to look to getting my body in as best
a condition as possible.
I see manuals and botox as secondary to that.

The insulin thing really makes sense now, AS did you mention
something about insulin increasing receptor sensitivity? and it's
something passed on from our fathers?

Xenon the pillow compression thing... I almost always wake up
sleeping on my right temple... and it's that side that has always
been further back compared to the left.... this has been for way
over 6-7 years though... before i even considered it hair loss.

I wonder if lightly stimulating lymphs and body massages
would help in all of this.

Live Forever,

I was mentioning the androgen paradox. For some reason, still not understood, DHT promotes hair growth in places like the face while it depletes it on the scalp. Overall, everything we've been discussing here is attempting to solve this problem, and there have been some interesting things tossed around in this thread.

One thing that has been put out there is that the connection is IGF-1. There is a series of three nucleotide repeats on the X-chromosome (from mom) that makes the front scalp follicles much more sensitive to androgens than on other parts of the body. DHT is growth inhibitory there. IGF-1 is growth promoting, except on the frontal/crown area of the scalp.

It could be that both insulin and DHT are changing the effects of IGF-1. A hypoxic environment, and anything that would promote higher serum insulin (I'd almost guarantee some correlation between MPB and insulin resistance), are now blocking the good effects of other molecules.

And lymph flow is always important, without it the immune system is all out of whack. Massage and exercise are good for this.

AS54 wrote:
One thing that has been put out there is that the connection is IGF-1. There is a series of three nucleotide repeats on the X-chromosome (from mom) that makes the front scalp follicles much more sensitive to androgens than on other parts of the body. DHT is growth inhibitory there. IGF-1 is growth promoting, except on the frontal/crown area of the scalp.

Sorry if I sound like a noob but does this mean that IGF-1 is bad for frontal/crown hair if you have mpb but positive if you don't?

Xenon the pillow compression thing... I almost always wake up
sleeping on my right temple... and it's that side that has always
been further back compared to the left.... this has been for way
over 6-7 years though... before i even considered it hair loss.

Well, Live Forever, the pics shown the effects of pillow compression on hair growth, so I don't think it's out of the question to suggest that pillow compression may be involved in MPB. I mean if we don't sleep with the temples pressed against a pillow, then we sleep with the crown pressed against it, and these, incidentally, are the places where baldness usually occurs.

7 - 8 hours on average of pillow compression - on an already tightened area of tissue - would surely cause worse probs.

But if hypoxia and poor lymph drainage are involved in this, then other hypoxia inducing factors are probably at play here, such as an extremely sedentary lifestyle, poorly ventilated living quarters, + tight hats / scalp, etc.  

From what I've gathered, the scalp muscles / adipose tissue of the lower back and sides of the head are partially designed for sleeping on, as they act as a form of padding when we rest our heads. it seems that we are not supposed to have the galea compressed against a pillow as the vessels there readily compress against the skull.

I was thinking of making a head rest, so that only the scalp muscles make contact with it during sleep. This may decompress the galea blood vessels and improve lymph drainage.

AS54 wrote:Live Forever,

I was mentioning the androgen paradox. For some reason, still not understood, DHT promotes hair growth in places like the face while it depletes it on the scalp. Overall, everything we've been discussing here is attempting to solve this problem, and there have been some interesting things tossed around in this thread.

One thing that has been put out there is that the connection is IGF-1. There is a series of three nucleotide repeats on the X-chromosome (from mom) that makes the front scalp follicles much more sensitive to androgens than on other parts of the body. DHT is growth inhibitory there. IGF-1 is growth promoting, except on the frontal/crown area of the scalp.

It could be that both insulin and DHT are changing the effects of IGF-1. A hypoxic environment, and anything that would promote higher serum insulin (I'd almost guarantee some correlation between MPB and insulin resistance), are now blocking the good effects of other molecules.

And lymph flow is always important, without it the immune system is all out of whack. Massage and exercise are good for this.

Personally I think the simple answer is androgens are good for hair, but the tissues get overwhelmed by them if the blood supply/ waste removal isn't up to par. I think trying to gontrol growth factors specifically and this and that isn't getting to the root of the problem; bad irrigation caused by inflammation, tight galea, poor circulation etc.

I'd also like to pipe in about head muscle tension; the temporalis muscles are involved in elevation of the mandible bone and help us clench our teeth when chewing. if you clench your teeth now and touch the temporalis muscles you'll feel them contract. The frontalis muscles assist in facial expressions and allow us to frown / scowl. The occipitalis muscle assists in retracting the scalp backwards, but that's about as much info as I have on the occipitalis muscles, other than it and the temporalis acting as natural cushions when we lay on a hard surface.

You may note that excessive teeth clenching and frowning are typical stress reactions, so too much of this may well cause tightness of the galea. Perhaps less scowling and teeth clenching may alleviate galea tension.

I have to admit, that I always have a semi scowl on my face and have done for years. Perhaps this has played a part in causing galea tightness around the temples and may have also played a part in temple recession.

Xenon wrote:I'd also like to pipe in about head muscle tension; the temporalis muscles are involved in elevation of the mandible bone and help us clench our teeth when chewing. if you clench your teeth now and touch the temporalis muscles you'll feel them contract. The frontalis muscles assist in facial expressions and allow us to frown / scowl. The occipitalis muscle assists in retracting the scalp backwards, but that's about as much info as I have on the occipitalis muscles, other than it and the temporalis acting as natural cushions when we lay on a hard surface.

You may note that excessive teeth clenching and frowning are typical stress reactions, so too much of this may well cause tightness of the galea. Perhaps less scowling and teeth clenching may alleviate galea tension.

I have to admit, that I always have a semi scowl on my face and have done for years. Perhaps this has played a part in causing galea tightness around the temples and may have also played a part in temple recession.

Yeah I have a bad habbit of clenching my teeth, and my temporalis muscle is usually the one that is chronically active; I notice this when I scrunch my scalp..

I never actually put that together, but holy cow. I have pretty bad apnea which by definition means I'm in a hypoxic state for the better part of the night. Not only that, but I clench my teeth during all of these episodes and I have had a dentist tell me that I have one of the worst teeth clenching problems he's seen. I am trying to get fitted for a bite splint to help stop this.

But its interesting to think, especially given how fast my hair went when the apnea set in, that part of the the problem could be the teeth clenching. My temporalis muscle is very pronounced especially when biting and appears to have experienced hypertrophy (its bigger than most peoples) and my masseter muscles are both much bigger.

Could be that the teeth clenching is adding to the overall apnea issue for the same reasons that stress does by creating tension in the muscles of the upper back/neck.

theseeker86 wrote:

AS54 wrote:
One thing that has been put out there is that the connection is IGF-1. There is a series of three nucleotide repeats on the X-chromosome (from mom) that makes the front scalp follicles much more sensitive to androgens than on other parts of the body. DHT is growth inhibitory there. IGF-1 is growth promoting, except on the frontal/crown area of the scalp.

Sorry if I sound like a noob but does this mean that IGF-1 is bad for frontal/crown hair if you have mpb but positive if you don't?

That is an interesting thought but I'm not sure if there are studies out there that show this or not. There is evidence out there that shows the paradox of IGF-1 being growth-positive for facial/body hair but negative for the scalp. I wonder though if in non-balding men, IGF-1 is acting differently in the scalp. It could very well be.

I think at the end of the day though, insulin and androgens are the big modulators of this relationship. Androgen are hard to control, insulin is more in our control.

As far as androgens being good for hair, I think I probably am on board with that one half-way. To me, things in the body can be both good and bad in certain contexts. I think one thing Slowmoe has demonstrated to me is that DHT is protective cellularly in hypoxia so in that sense its probably increased in the scalp as a protective mechanism. But that doesn't mean that those same androgens can't be promoting bad things at the very same time. Through other pathways, well documented ones, the androgens are promoting inflammation in other cell lines. So where it might be a white knight in one context, it can be bi-polar.

SlowMoe wrote:

Xenon wrote:I'd also like to pipe in about head muscle tension; the temporalis muscles are involved in elevation of the mandible bone and help us clench our teeth when chewing. if you clench your teeth now and touch the temporalis muscles you'll feel them contract. The frontalis muscles assist in facial expressions and allow us to frown / scowl. The occipitalis muscle assists in retracting the scalp backwards, but that's about as much info as I have on the occipitalis muscles, other than it and the temporalis acting as natural cushions when we lay on a hard surface.

You may note that excessive teeth clenching and frowning are typical stress reactions, so too much of this may well cause tightness of the galea. Perhaps less scowling and teeth clenching may alleviate galea tension.

I have to admit, that I always have a semi scowl on my face and have done for years. Perhaps this has played a part in causing galea tightness around the temples and may have also played a part in temple recession.

Yeah I have a bad habbit of clenching my teeth, and my temporalis muscle is usually the one that is chronically active; I notice this when I scrunch my scalp..

Yeah, I quoted myself lol.

Just to add to this, the tension on my temporal muscle from teeth clenching.... Is directly in line with the portion of my hairline that has receeded. Hmmmmm

Although, upon further evaluation, when I scrunch my scalp up, and clench my teeth, I notice no downward pull on my galea. The strongest contractions are when I raise my eyebrows or wiggle my ears. Try it, put a palm on each temple, push the scalp upwards and then see what causes the downward pull.

My temporalis muscle is very pronounced especially when biting and appears to have experienced hypertrophy

i read about some woman who had a habit of clenching her teeth which resulted in her masseter muscles overgrowing and she developed a very masculine square jaw. She went to see a doctor and he injected her masseter muscles with botulin to relax them. About a year or so later her masseter muscles began to shrink, which then gave her face a more feminine appearance.

Interestingly, though, I have seen many guys with very developed temporalis muscles and they all had a receded hairline (my older brother is one of them). I used to wonder if this was because the overgrown muscle was pulling at the connective tissue and choking off blood. But IDK if that is true or not.

ETA: I think that this capillary compression problem causes heat retention when the heart rate increases. Perhaps capillaries are too constricted to allow enough heat to be released from the sweat glands and so it builds up and causes that burning sensation i so often feel when undergoing high intensity training.

i guess this could be compared to a pressure cooker whereby a compressed capillary network slows down heat transportation to the sweat glands, which then results in cellular hyperthermia. It could be paradoxical in the respect that a) under normal heart rate constricted capillaries slow down oxygen delivery to cells b) when heart rate increases - via too much high intensity training - scalp capillaries are resistant to vasodilation which then may lead to metabolic heat being trapped.

Maybe the scalp loosening exercises as well as other countermeasures would gradually solve both of these problems.

Xenon wrote:

Xenon the pillow compression thing... I almost always wake up
sleeping on my right temple... and it's that side that has always
been further back compared to the left.... this has been for way
over 6-7 years though... before i even considered it hair loss.

Well, Live Forever, the pics shown the effects of pillow compression on hair growth, so I don't think it's out of the question to suggest that pillow compression may be involved in MPB. I mean if we don't sleep with the temples pressed against a pillow, then we sleep with the crown pressed against it, and these, incidentally, are the places where baldness usually occurs.

7 - 8 hours on average of pillow compression - on an already tightened area of tissue - would surely cause worse probs.

But if hypoxia and poor lymph drainage are involved in this, then other hypoxia inducing factors are probably at play here, such as an extremely sedentary lifestyle, poorly ventilated living quarters, + tight hats / scalp, etc.  

From what I've gathered, the scalp muscles / adipose tissue of the lower back and sides of the head are partially designed for sleeping on, as they act as a form of padding when we rest our heads. it seems that we are not supposed to have the galea compressed against a pillow as the vessels there readily compress against the skull.

I was thinking of making a head rest, so that only the scalp muscles make contact with it during sleep. This may decompress the galea blood vessels and improve lymph drainage.

Live Forever, I woke up this morning on left temple, it was inflamed and so was the left side of my crown but the crown to a slightly lesser extent. Normally I try to position my pillows in an convex arc shape so that my galea doesn't press against it, but it somehow was back in it's usual position when i woke up. Now that my head is away from the pillow the inflammation has  gone.

There is definitely something in this. Perhaps you should observe your temples for signs of inflammation upon awakening. This may be ongoing throughout the night.

AS54 wrote:Live Forever,

I was mentioning the androgen paradox. For some reason, still not understood, DHT promotes hair growth in places like the face while it depletes it on the scalp. Overall, everything we've been discussing here is attempting to solve this problem, and there have been some interesting things tossed around in this thread.

One thing that has been put out there is that the connection is IGF-1. There is a series of three nucleotide repeats on the X-chromosome (from mom) that makes the front scalp follicles much more sensitive to androgens than on other parts of the body. DHT is growth inhibitory there. IGF-1 is growth promoting, except on the frontal/crown area of the scalp.

It could be that both insulin and DHT are changing the effects of IGF-1. A hypoxic environment, and anything that would promote higher serum insulin (I'd almost guarantee some correlation between MPB and insulin resistance), are now blocking the good effects of other molecules.

And lymph flow is always important, without it the immune system is all out of whack. Massage and exercise are good for this.

do you have study regarding igf1 being bad ? I think igf1 is good in order to make hair in anagen phase. Im really not sure there is negativ effect from it.

http://www.ncbi.nlm.nih.gov/pubmed/10025745

Men with higher levels of testosterone were more likely to have vertex baldness (odds ratio [OR] = 2.5, 95% confidence interval [CI: 0.9 to 7.8] per 194 ng/dL increment of testosterone). In addition, for each 59 ng/mL increase in IGF-1, the odds of having vertex baldness doubled (95% CI [1.0 to 4.6]). Those who were found to have higher circulating levels of SHBG were less likely to have dense hair on their chest (OR = 0.4, 95% CI [0.1 to 0.9] per 24 nmol/L increment in SHBG]).

Admittedly though, this was with older subjects so the situation with senescene could be much different than for a guy losing at 25.

http://www.ncbi.nlm.nih.gov/pubmed/10827403

Of the 431 men, 128 had vertex balding at age 45. Compared with men who were not balding, for a 1 standard deviation increase in plasma IGF-1 level (72.4 ng/mL), the OR for vertex balding was 1. 31 (95% CI, 0.95-1.81). For a 1 standard deviation increase in plasma IGFBP-3 (957 ng/mL), the OR for vertex balding was 0.62 (95% CI, 0.44-0.88).

Older men with vertex balding have lower circulating levels of IGFBP-3 and higher levels of IGF-1 when controlling for IGFBP-3 level.

Again, we're talking older men here, so it may be that I am extrapolating a bit by assuming the situation with MPB is the same between age groups.

http://www.ncbi.nlm.nih.gov/pubmed/12894070

IGF-1 was up-regulated by finasteride treatment in 4 of 9 patients. Among the patients with increased IGF-1 expression, 3 of them showed moderate clinical improvement after 12 months of treatment and another patient remained unchanged. In contrast, 3 patients with decreased IGF-1 expression in the balding scalp showed clinical worsening after 12 months. The other 2 patients without noticeable change in IGF-1 expression showed either slight improvement or no change in their hair condition.

In a small uncontrolled study of 9 patients with AGA, an increased expression of IGF-1 messenger RNA levels in the DP was associated with patient response to finasteride.

Now here's some evidence the other way. I realize the problem is I worded that in a stupid way in my former post. IGF-1 is growth promoting...the reason it isn't in the scalp is that DHT inhibits it. However, we do have evidence to show irrespective of DHT, IGF-1 is associated with vertex balding in older subjects. There is obviously something more complicated happening up there. Because despite this, we still have androgen promoting hair growth on the face body, but what would seem to be programmed androgen inhibition of hair on the scalp. What is the mediator that is causing DHT to either promote/inhibit growth factor in the scalp versus the face.

There are some dense journal articles out there about the IGF family and hair cycling. If I get a bit of time later on tonight I can post them, but they are a relatively easy find on Google. They'll for the most part confirm what you are saying. In any other context outside of the vertex of the scalp, IGF-1 is promoting growth. It just seems its signal isn't being heard in the scalp because of DHT.

If you look at the results of the study CS posted yesterday:
https://immortalhair.forumotion.com/t9882-a-prostaglandin-d-synthase-positive-mast-cell-gradient-characterizes-scalp-patterning#101418

These data indicate that scalp is spatially programmed via mast cell prostaglandin d-synthase distribution in a manner reminiscent of the pattern seen in androgenetic alopecia.

This suggests that the immune system is programming MPB. That might be stated a little exceptionally, but mast cells have to migrate from the lymph tissue. Why are mast cells targeting the MPB area directly? Is it a chemotaxic attraction? If so, to what? Either way, this study shows there is programmed process happening on the scalp, at least from the perspective of the immune system. Again, we're back at the problem of wondering what the antigen is though, or what the physical damage is that's attracting the mast cells, or whether it could just be a genetic thing (no outright damage).