Quick paranoia post (just started brushing): Could vigorous brushing cause permanent damage to follicles, or is it pretty much decided to be beneficial?

Hey guys, was just reading that thread "grow new hair" and a poster who was experiencing a ton of shedding posted this as a concern:

"I saw a post by someone called Xenon yesterday that talked about how producing heat on the scalp is detrimental to hair and actually increases hair loss....his rationale seemed quite plausible, but I cannot find it now....was it pulled? Did anybody else see it?"


I wouldnt have a problem with vigorous (ferox) brushing causing shedding and knocking out hairs that were already doomed, but the thought of doing permanent damage to the follicles suddenly popped into my head and its causing me a lot of apprehension.

Thoughts guys?

I think it might depend on what Norwood you are if your like NW1 you prob won't lose as much some people can lose a lot though and they probably won't grow back unless you stick with it for years. Internal is definitely safer imo as far as sheds go even stimulating topicals like garlic, onion, cinnamon, cayenne, msm etc. and internal gingkoa and other spices including curcumin.

I think a little brushing helps hair but too much might be bad. If this heat theory is correct are manuals/massages bad for the hair too?

I can see the maze of confusion this forum is getting itself into. "We need to increase circulation. The follicles have been cut off...they're not getting oxygen or nutrients." But wait: "Its the heat that's the problem. Increasing circulation is out the window. Exercise is out the window. Now we need to cool the scalp and slow down the metabolism there."

Which side are you on? Pick a side now for the battle royale.

Brushing seems positive but yeah don't go wildly overboard

Sizzling hairs, I am not entirely certain why my hair sheds if my scalp overheats, even though I can provide a number of possible reasons, but what I do know is, inflammation is the common denominator in most, if not all factors in hairloss.

The elevated scalp temp / inflammation may not be applicable to your circumstance, but I can understand your confusion, esp. if you are relatively new to this subject. I, personally, determine the cause/s of my hairloss by being in tune with my body and remaining aware of specific patterns which cause my scalp to inflame. IMO, introspection is a key factor in recognizing inflammatory pathways.

So, why is the scalp - in balding men - so susceptible to inflammation and increased shedding? First off, the hormone estrogen in females causes an increase in progenitor cells to scalp hair follicles. Without going in to too much scientific detail, progenitor cells basically cause an increase in matrix cells -- these cells are responsible for terminal hair growth, and if there is an increased number of them, then the hair will grow thicker and healthier. So, because progenitor cells continually cause new matrix cells to grow - when inflammation destroys old cells, new ones soon replace them.

After menopause, when there is a decline in estrogen, cell division is adversely affected, and this is why so many older women tend to start experiencing thinner hair. The regenerative properties are not as strong as they once were, and it leaves follicles susceptible to deterioration from various forms of inflammation.

DHT on the otherhand seems to cause an increase in progenitor cells within androgenic follicles, especially the beard, hence the reason beard hair grows so thick and fast under the influence of this hormone. So, I think that DHT causes most progenitor cells to migrate to androgenic hair follicles and away from the scalp. This would likely lead to decreased cell division and premature atrophy within scalp follicles -- especially when they are subjected to various forms of inflammation because their ability to regenerate is compromised, so they gradually deteriorate, until they stop producing hair completely.

I can't provide definitive proof on this, but it may well be true, that there may be innate lack of testosterone receptors within scalp follicles. My reasoning for this possibility is, testosterone / DHT are both growth factors, so both hormones should technically promote increased cell division within head hair follicles (as they do in androgenic hair follicles). And the anabolic effects of these steroid hormones should be even more marked than those of estrogen.

As for the boar brushing method... growth factors such as steroid hormones or cytokines cause an increase in progenitor cells in tissue subjected to injury, and this is likely how it works. In fact, boar brushing may cause an upregulation in steroid receptors, within sites of injury, but I don't know for certain. Ferox and Drex have had some pretty decent regrowth from boar brushing, but some others have reported no signs of growth. Maybe there is a particular method to how it's done? IDK. Maybe Ferox and Drex could provide better insights into this.

Estrogen induces endothelial progenitor cells proliferation and migration by estrogen receptors and PI3K-dependent pathways.

Estrogen induces endothelial progenitor cells (EPCs) migration and proliferation, which may serve as a potential target for coronary artery disease, but the mechanisms are unclear. We hypothesized that estrogen receptors (ERs) and phosphatidylinositol 3-kinase (PI3K) signaling pathway, which represent particularly important roles of action for estrogen, may contribute to estrogen-induced EPCs migration and proliferation. Bone marrow mononuclear cells (MNCs) were cultured in Dulbecco's modified Eagle's medium (DMEM) supplemented with growth factors as previously described. A total of 87.32+/-5.13% of adherent cells showed uptake of acetylated low-density lipoprotein and lectin binding. Immunostaining and fluorescence activated cell sorting confirmed the endothelial progenitor phenotype. RT-PCR, immunocytochemistry staining and Western blot demonstrated expression of ERs. Exposure to 17beta-estradiol significantly improved EPCs migration and proliferation. Those effects were blocked by pretreatment with the pharmacological PI3K blockers LY294002 (1 h, 10 micromol/L) and ICI-182780 (1 h, 10 micromol/L), a specific estrogen receptor antagonist, which show involvement of estrogen receptors and PI3K pathway. These results suggest that estrogen induces EPCs migration and proliferation via ERs and PI3K pathway which provided a novel insight and treatment strategy of vascular biology.

http://www.ncbi.nlm.nih.gov/pubmed/17524430

^^Additionally, men generate more metabolic heat than women, and, so, sweat more. DHT assists in increasing adenosine trisphosphate levels. This results in increased metabolic heat generation within cells, so it may explain why increased DHT is implicated in higher sweat production. In other words, when cells overheat, the body will sweat in equal measure in order to cool down.

It's a general maxim, that a third of body heat is released from the scalp, yet this may be escalated even moreso if heat cannot escape from other sweat pores elsewhere upon the body. For instance, if antiperspirants are blocking sweat pores in the arm pits, then the heat has to escape somewhere else, and this will usually be the head. Also, wearing thick clothing or too many blankets in bed will cause the skin to retain heat, absorb any sweat it produces and cause overheating. Again, this heat will move to the sweat glands of the scalp because it is the most efficient place for heat to escape from. But if there is a thick build up of sebaceous oil covering the sweat pores of the scalp, then this heat will become trapped.

I once saw a medical program on TV, which documented the effects of increased temperatures upon cells. It said that if cells are exposed to temperatures beyond 98F, then cell division is drastically reduced. So, everytime I experienced inflammation and further shedding from elevated scalp temperatures, I believed that cell division was being affected because of this.

Also, sweat releases toxins, so I further surmised, that there was an overload of toxins (and other pro-inflammatory substances) within the cells of the scalp when too much heat migrates there. Yet if too much sebum is clogging sweat pores (perhaps also dead skin), then not all of these toxins can escape and they can contaminate cells.

Additionally, when the scalp is tighter, or becomes too compressed by our pillows during sleep, it has problems releasing these waste byproducts byway of venules; they then build up and cause heightened inflammation.

And as I mentioned in the previous post, lack of progenitor cells means even slower wound healing and cell renewal. This then leads to follicular atrophy.

It's an arbitrarily complex issue because we know for certain that inflammation leads to shedding, yet constant inflammation caused by boar brushing can - in some cases - lead to an increase in progenitor cells, which then can lead to hair regrowth.

I think that this maybe because friction from boar brushing mainly causes inflammation to the epidermis and not so much the underlying dermis and papilla. Consequently, PC's migrate to the epidermis in an effort to strengthen it, yet some might also migrate to the hair bulge, which then causes hair regrowth.

I'm not an expert on brushing, however a chronic irritation to the scalp could do more harm than good. If the brushing is more than just massage and causes some irritation, a break of some days is warranted to allow the healing process. The wounding effect does help hair growth, however a short break should be taken.

Concerning sweating, I wonder about mineral homeostasis.

Arch Environ Health. 2001 May-Jun;56(3):271-7.
Electrolyte loss in sweat and iodine deficiency in a hot environment.
Mao IF, Chen ML, Ko YC.

Institute of Environmental Health Sciences, College of Medicine, National Yang-Ming University, Taipei, Taiwan.

The authors studied electrolyte loss from profuse sweating in soccer-team players and evaluated the relationship between this source of iodine loss and iodine deficiency. Thirteen male soccer-team players and 100 sedentary students from the same high school were evaluated for 8 d, during which the players were training. The authors analyzed 208 sweat samples to determine losses of iodine, sodium, potassium, and calcium in sweat. Excretion of urinary electrolytes by the subjects was also measured. The mean losses of iodine, sodium, potassium, and calcium in sweat following a 1-hr game were 52 microg, 1,896 mg, 248 mg, and 20 mg, respectively; the ratios of sweat loss to urinary daily loss of the four electrolytes were 0.75, 0.2, 1.88, and 0.92, respectively. Urinary iodine was significantly (p < .02) lower than the normal level of 50 microg/gm creatinine in 38.5% of the soccer players, compared with 2% of the sedentary students. Forty-six percent of the players had Grade I goiter, compared with a mere 1% of the sedentary students (p < .01). The results of the study suggest that loss of iodine through profuse sweating may lead to iodine deficiency, and loss of electrolytes through sweating may have a dietary significance for heat-stressed individuals or for individuals who perform heavy workloads.

Yeah Immortal, that does seem to make sense. Although ferox said he does it everyday and has seemed to get results. Also there are others I have heard of that have seemed to get results from everyday.


In terms of a break, do you mean like 1 day vigorous brushing/1 day off? Or would 3 days on 1 day off be more along the lines of what you were thinking?

I was thinking that because it is just somewhat vigorous brushing and not actually dermarolling that, lets say roughly, 16-18 hour (speaking of daily brushing) period before each brushing session might be sufficient?

Well ask yourself, what is the purpose of brushing, what are you mechanically trying to do?
Increase blood flow, exfoliate the scalp a bit, stimulate? Then simply do that, don't brush until you are damaging the skin and existing hair, its pointless. Brushing slightly/temporarily helps keep fluids moving along within a stagnant scalp, just as massage does, but there are so many other methods that would systemically give better results to this action especially when every method is used consistently in conjuntion. Just brush sensibly with dedication to your cause, but don't over do it because you are relying on this to grow your hair back. You didnt loose your hair due to a deficiency of scalp brushing...

Xenon I no longer believe dht does anything negative to the actual hair follicles themselves as we've been told it does. I think its completely pro hair as long as the environment isn't low flow and hypoxic. Hair isnt even really that hard to grow if you think about it, hair grows unchallenged all over your whole body, Terminal hair grows easily when theres adequate fatty tissue and capillary support. Hair only has trouble generally growing in a specific area, your scalp, due to numerous variables that bring about its stagnancy as we progress with age...

The authors analyzed 208 sweat samples to determine losses of iodine, sodium, potassium, and calcium in sweat. Excretion of urinary electrolytes by the subjects was also measured.

Interesting, Symmetry. I wonder also, if continuous calcium excretion from sweat glands within the temples can contribute to calcification in those specific areas?

Xenon wrote:

The authors analyzed 208 sweat samples to determine losses of iodine, sodium, potassium, and calcium in sweat. Excretion of urinary electrolytes by the subjects was also measured.

Interesting, Symmetry. I wonder also, if continuous calcium excretion from sweat glands within the temples can contribute to calcification in those specific areas?

Another over complication imo. If that were true then everyone who sweats would have thinning temples sooner or later, which isnt the case...I think over heating is negative when there's inflammation present, I used to itch really bad right before I started to sweat back when I had a lot of inflammation on my scalp, but if we go to the beginning of the chain of this problem it will have nothing to do with sweat. Its as simple as understanding what caused the inflammation, and the effects of that chronic inflammation, and how it negatively changes the area of conversation...

Another over complication imo. If that were true then everyone who sweats would have thinning temples sooner or later, which isnt the case...I think over heating is negative when there's inflammation present, I used to itch really bad right before I started to sweat back when I had a lot of inflammation on my scalp, but if we go to the beginning of the chain of this problem it will have nothing to do with sweat. Its as simple as understanding what caused the inflammation, and the effects of that chronic inflammation, and how it negatively changes the area of conversation...

I understand your point, but this is an extremely complicated problem, hence the fact that it has been prevalent since the dawn of man. As you are aware, inflammation occurs in several ways, and if the cell has poor renewal capabilities, i.e., a low yield of progenitors / growth factors, then it will begin deteriorate when inflammation strikes.

Some men are immune to the detrimental effects of inflammation because of the high numbers of progenitors contained in their follicles, so any destroyed cells are soon replaced. This is why women are generally immune to follicle atrophy because estrogen promotes an increase in progenitors within follicles.

In regards to the sweat issue, I believe that if it is not released efficiently enough (due to excess sebum blocking sweat pores), then the toxins it is carrying can become trapped in tissue. Given the close proximity between the sweat gland and the follicle, it is plausible IMO, that toxins / bacteria can leak into follicles and contaminate them.

This IMO is just one of many inflammatory triggers...

Its an interesting hypothesis, given the proximity of the sweat glands to the hair follicle. But what is the exact mechanism causing the blockage of sweat? There doesn't seem to me to be anything plausible for that to occur. Even hyperexcretion of sebum on the skin surface shouldn't cause that. As someone who has always had excess sebum on the scalp, I can tell you I've never had a problem sweating from the same tissues.

Now I do think we can contribute some pathological processes to occurring within the sebaceous glands, and I think the big culprit here is proliferation of keratinocytes. I also suffer from pretty bad keratosis pilaris, with oveproduction on the arms, legs, in the cheeks (rosy appearance), and I'd hypothesize in the scalp tissues. An overproduction of keratin has the potential to negatively impact sebaceous glands and sebum motility. This could cause an overgrowth of commensal bacteria in the dermis, and incite the immune attack.

Not only this but the deposition of keratin can also create an inflammatory situation that could lead to further deposition of other GAGs and collagen, slowly causing each successive hair to thin as the shaft narrows.

As an example; I put coconut oil on my scalp a few weeks ago (when it was a really hot day), as I sat in the sun, I noticed that I wasn't producing an ounce of sweat - which is highly unusual, as it's normally my temples that sweat immensely on a hot day. My scalp began to inflame very quickly under the hot sun, and I could not understand what was happening, until I realized, that I'd applied coconut oil to my scalp. I washed it off, then two things happened; my scalp began to sweat and the inflammation began to disappear.

So, I'm in no doubt that the coconut oil was covering the sweat pores and preventing the scalp from cooling. For this reason, I also think that sebum can also have the same effect if it is allowed to build up on the scalp.

I think that toxin induced inflammation only really occurs if too much sweat is produced, and has problems being released. I'm not saying that sebum completely prevents sweating, rather it may slow the process down (as the coconut oil did), which then may cause an accumulation of toxins within underlying tissues.

However, I think that the main inflammatory factor (regarding sebum build up) is too much heat building up inside the scalp, and not having any efficient means of escape.

When Sanderson was exposing his scalp to too much hot water from the shower, he noticed that his scalp was inflamed as soon as he got out of the shower (this has happened to me too, and as I have also learned, many others). Yet, when he switched to using lukewarm water, he noticed that there was no inflammation.

Even though sebum is removed when showering with hot water, the scalp cannot cool down because very hot water is constantly heating it. Even if it is sweating during this process, the elevated water temperature will override the cooling effects of perspiration. Inflammation then results.

I don't know the precise underlying mechanism behind this... perhaps H2 histamine, heat shock proteins, but I know that cells cannot function if they are exposed to temperatures exceeding their normal core temperature for too long. So, I imagine, that this would be the reason why inflammation occurs.

The idea of sebum compromising the ability to sweat make sense to me.

Another thing is (and it's a controversial point to conventional medicine) is that the amount of iodine and sodium lost can affect this as well.

For example, when there is an anxious feeling or of stress, sweat can be produced. I wrote a recent article on the effects of sodium loss and its effects on anxiety increases.

Sodium losses can increase angiotensin and likely elevates aldosterone levels, which in turn increases the reabsorption of sodium.

This is a recipe for higher anxiety if these salts are not replaced.

My only problem with sweat being a factor in this is it doesn't provide a very easy avenue for how to get to the sex distribution and the general population distribution of pattern hair loss. Everyone possesses sweat glands. So where would be the causal link explaining why males suffer the preponderance of hair loss? And mineral imbalance from sweating excessively? Then wouldn't we expect to see people with hyperhydrosis (both male and female) suffering from hair loss?

There are two types of sweat glands, apocrine and eccrine. Apocrine sweat glands terminate in a hair follicle. The only problem is these are not found on the head. They are located primarily around the genitals and armpits and a couple other small regions. On the scalp, the sweat gland tubule has no contact/communication with a sebaceous gland at all. So does this sweat theory hold that the sweat gland is being blocked at the terminal opening at the skin's surface? This would more than likely require some type of plugging/hardening of sebum on the surface of skin and we'd find these plugs all over the scalp. But I don't think most of us do. Where I find plugs is on fallen hair.

There are conditions in which the sweat gland can become blocked, and these vary depending on the type of sweat gland. But if you take a look at the presentation of these conditions, I think it also lends evidence to the fact that this is not the process occurring in the scalp of pattern hair loss sufferers.

Miliaria rubra is an infection of the eccrine sweat glands. Some type of dermatitis (allergic skin reaction) usually precedes this condition, and the dermatitis causes the damage that blocks the sweat gland w/ excess keratin. This promotes an infection in the sweat gland that can spread and causes a rash. See below. If this was what was occurring in the scalp, we'd expect to see it. If surface sebum was somehow (and this is a huge stretch) blocking the opening of a sweat gland, I guess it could create the conditions. The big problem here is there are men who wash their hair multiple times a day and this hasn't impacted hair loss.


Hydradenitis Suppurativa is an infection of the apocrine sweat glands, which due to their location really close the follicle release a different kind of sweat with more triglycerides in it. Blockage here can occur too for the same reason, usually excess keratin deposition. The result is shown below.


I think there is ALOT more evidence that the problem here is with the sebaceous glands, NOT the sweat glands and not due to excess heat in the scalp. I think there is a lot of confusion here about heat too. The eccrine sweat glands release heat from the body in an even manner. Heat is not just release through the scalp. Wouldn't we be losing hair in other areas like the genitals or armpits if this weren't the case? And heat shock proteins require heat shock for activation, not usually temperatures we'd get from exercising or taking a warm shower. They CAN be activated as part of the normal stress response however, and in that capacity they are protective.

If we actually take a look at the pilosebaceous unit in the scalp follicles. The sebaceous gland has a direct communication with the follicle. It is vulnerable to hyperkeratosis and hyperplasia. There is direct evidence for hyperplasia of the sebaceous gland induced by DHT and steroid hormones and DHT's effects on proliferation of keratinocytes. These can and do block the sebaceous glands and lead to low sebum motility. This does promote an overgrowth of bacteria in the follicle and can cause an immune attack. I just don't think the sweat glands in the scalp have a major role to play here, at least not even close to how big of a role the sebaceous glands do. I mean, look at acne. It is the result of infections from sebaceous glands, also sensitive to androgens. Male pattern hair loss is a variant of this in my belief.

As someone with pretty advanced keratosis pilaris and way above average sebum production, I can tell you by looking at all of the lost hairs that keratinized sebum plugs were present on most of the fallen hairs. My scalp was incredibly oily after a night's sleep. Despite this, I never had a problem sweating and never had any type of sweat gland infection. In fact I sweat quite a bit, including from the scalp. Given that I'm slick bald now and shave almost daily, you'd think clearing all of that excess sebum away with a razor might help regrow some hair if the sweat theory was correct.

Xenon wrote:
I understand your point, but this is an extremely complicated problem, hence the fact that it has been prevalent since the dawn of man. As you are aware, inflammation occurs in several ways, and if the cell has poor renewal capabilities, i.e., a low yield of progenitors / growth factors, then it will begin deteriorate when inflammation strikes.

Well the shape of the Earth was once complicated also, so...
What is causing this low yield of growth factors ( in the scalp only) that ARE present in the body...
Yes inflammation leads to the rest of this process. And yes we must address why cells inflame...

Some men are immune to the detrimental effects of inflammation because of the high numbers of progenitors contained in their follicles, so any destroyed cells are soon replaced. This is why women are generally immune to follicle atrophy because estrogen promotes an increase in progenitors within follicles.

I assure you no one is immune to inflammation. As far as mpb, It doesn't happen in some men because their scalps don't go as hypoxic as others. This is simply the main factor imo. So many variables determine this outcome person to person, the flow of one river is different from another.. Most of CS supplement recommendations are indirect responses to this...

In regards to the sweat issue, I believe that if it is not released efficiently enough (due to excess sebum blocking sweat pores), then the toxins it is carrying can become trapped in tissue. Given the close proximity between the sweat gland and the follicle, it is plausible IMO, that toxins / bacteria can leak into follicles and contaminate them.

This IMO is just one of many inflammatory triggers...

So lets say this is true, we shouldn't end a presentation with a statement that's not seeking the beginning of our problem. So why is the sweat *no longer* being released efficiently enough versus someone elses head who can do this (and whatever else that is needed) to grow hair sufficiently. Some of Slowmoe's posts comes to mind, which are also indeed a consequence of other causes, thyroid comes to mind.. When I think of toxins, bacteria I think low flow/ph...

Many people live in doors,work in doors, even exercise indoors, but also sit on our ass a large amount of time ( like right now) We probably sweat significantly less than earlier man did, who physically worked much harder than we did, and likely was also significantly more stressed on a regular basis due to the requirements of his survival... Without being able to prove this I have zero doubt that all forms of hair loss are dramatically increased in all ages, races, and sexes in modern man, just like all the other ailments and diseases.
Well of course, because they all tend to have common denominators and self perpetrating actions...

Therefore how could sweating/sebum be an inflammatory trigger? Any malfunction in those areas are also likely due themselves to inflammation which was already silently present. Actually this applies to most of the theories ive read from you, they all could be plausible in someone whose already been chronically inflamed. I'm not saying your wrong by any means, I'm sure you can tell when you have more noticeable inflammation going on since your so tuned into it, but what I am saying is I don't believe that any of what your saying is actually a cause or should be focal area. Consider that your thoughts are somewhere way later in the chain, but by all means keep discussing every angle...

Btw when I had my worst bout of inflammation, itching and bad shedding is when I experienced those white sebum plugs and waxy greesy scalp. I haven't had any significant inflammation in a long time now, thus the other scalp problems haven't reappeared.

"Well the shape of the Earth was once complicated also, so...
What is causing this low yield of growth factors ( in the scalp only) that ARE present in the body...
Yes inflammation leads to the rest of this process. And yes we must address why cells inflame..."

Well, it's interesting to note that estrogen causes hair to become really thick and to grow faster, whereas DHT has the opposite effect. Estrogen promotes an increase in progenitor cells to follicles, whereas, it would seem DHT causes them to decrease. Yet, DHT causes an increase in growth factors in other androgenic hair follicles (most notably the beard). So, maybe, the hormone causes the majority of progenitor cells to migrate to these follicles (and other binding sites) and away from the scalp.

Many fin users also report thinner body / facial hair when their head hair begins to regrow. So this must indicate, that DHT must cause vastly increased protein synthesis / cell division in target sites.

Perhaps we need to find a natural way of increasing the yield of progenitors, so that there is 'enough to go around', so to speak.

"I assure you no one is immune to inflammation. As far as mpb, It doesn't happen in some men because their scalps don't go as hypoxic as others. This is simply the main factor imo. So many variables determine this outcome person to person, the flow of one river is different from another.. Most of CS supplement recommendations are indirect responses to this..."

What I meant was, those who have good growth factors have better cell renewal capabilities. And I also agree with you about the hypoxia issue. This is an inflammatory pathway in some - if the not the majority - of balding men -- absolutely no doubt about it. And it would seem that the tight scalp is the issue here. My point is, it doesn't matter what is causing the inflammation in the scalp, it is the fact that cells cannot regenrate effectively enough.

"So lets say this is true, we shouldn't end a presentation with a statement that's not seeking the beginning of our problem. So why is the sweat *no longer* being released efficiently enough versus someone elses head who can do this (and whatever else that is needed) to grow hair sufficiently. Some of Slowmoe's posts comes to mind, which are also indeed a consequence of other causes, thyroid comes to mind.. When I think of toxins, bacteria I think low flow/ph... "

Because DHT is implicated in higher sebum and sweat production. Sweat evaporates, but sebum builds up on the scalp and eventually clogs sweat pores -- especially if the hair is cut really short -- long hair can absorb it moreso and alleviate it building up on the scalp. Women generally have longer hair and produce less sebum and sweat, so this is far less of an issue to them.

"Many people live in doors,work in doors, even exercise indoors, but also sit on our ass a large amount of time ( like right now) We probably sweat significantly less than earlier man did, who physically worked much harder than we did, and likely was also significantly more stressed on a regular basis due to the requirements of his survival"

And earlier man also suffered from hairloss. In fact, it may have been all of these extreme stresses which gradually caused MPB to develop into a transgenerational genetic condition. Some men may have not been so stressed out because they had slaves running all of their errands for them. But I guess we could go on and on with this, yet wont come to anything resolute, as we just don't know precisely where or when MPB originated.

"... Without being able to prove this I have zero doubt that all forms of hair loss are dramatically increased in all ages, races, and sexes in modern man, just like all the other ailments and diseases.
Well of course, because they all tend to have common denominators and self perpetrating actions.."

I completely concur with your statement. Growth factors naturally decrease with age, so cell division within follicles would also decrease. But the problem is largely accelerated by inflammation. Progenitors can only divide a certain number of times before the cell atrophies. Yet, this is generally not the case if growth factors cause new progenitors to migrate to target sites, cue the effects of estrogen in the follicles, for example.

"Therefore how could sweating/sebum be an inflammatory trigger? Any malfunction in those areas are also likely due themselves to inflammation which was already silently present. Actually this applies to most of the theories ive read from you, they all could be plausible in someone whose already been chronically inflamed. I'm not saying your wrong by any means, I'm sure you can tell when you have more noticeable inflammation going on since your so tuned into it, but what I am saying is I don't believe that any of what your saying is actually a cause or should be focal area. Consider that your thoughts are somewhere way later in the chain, but by all means keep discussing every angle...

Btw when I had my worst bout of inflammation, itching and bad shedding is when I experienced those white sebum plugs and waxy greesy scalp. I haven't had any significant inflammation in a long time now, thus the other scalp problems haven't reappeared."

I always have inflammation if I allow sebum to build up on my scalp for a day or so. So what exactly gives? Is it because sebum is covering sweat pores and inhibiting the release of heat and toxins? Or is it because sebum contains pro-inflammatory acids? Perhaps both. As I explained to Anthony in my previous post; when my scalp was laced with a film of coconut oil, I noticed that my scalp stopped sweating under the hot sun, and it began to inflame very badly. When I washed the coconut oil off my scalp, it began to sweat, cool down and inflammation disappeared.

More examples that extremes of heat can lead to inflammation; exposing the scalp to very hot water under the shower for too long. I mentioned that regular shampoo doesn't do a good job of removing scalp sebum, so sweat pores are likely still covered with it during showering. When extremes of heat build up inside the scalp, the scalp cannot perspire well enough, then inflammation arises. If I've been exercising too intensely and for too long, my scalp will also inflame. Incidentally, it is after intense exercise that I produce more sebum (and sweat)... likely because of increased bloodflow.

But you also have a great point; it seems that there may also be an upregulation of inflammatory receptors in the scalp, which then causes the condition to occur more frequently in others. I suppose this is comparable to the heightened autoimmune response in alopecia areata sufferers. This, in MPB sufferers, may be caused by a number of factors; 1) the tight scalp slows down the release of toxins, which then contaminate cells 2) too much heat to the scalp may cause an increase in histamine H2 receptors and so on and so on.

Also understand that I don't have a dogma to defend. I'm just merely reporting my observations on inflammation. This may not be an issue for you, and I'm not doubting at all that hypoxia is another major cause of inflammation (I have created many threads on this in the past).

"My only problem with sweat being a factor in this is it doesn't provide a very easy avenue for how to get to the sex distribution and the general population distribution of pattern hair loss. Everyone possesses sweat glands. So where would be the causal link explaining why males suffer the preponderance of hair loss? And mineral imbalance from sweating excessively? Then wouldn't we expect to see people with hyperhydrosis (both male and female) suffering from hair loss?"

DHT causes higher sweat and sebum production. This is one of the fundamental differences. And let's also take into account that estrogens promote quicker wound healing in scalp follicles.

"the sweat gland tubule has no contact/communication with a sebaceous gland at all. So does this sweat theory hold that the sweat gland is being blocked at the terminal opening at the skin's surface? This would more than likely require some type of plugging/hardening of sebum on the surface of skin and we'd find these plugs all over the scalp. But I don't think most of us do. Where I find plugs is on fallen hair."

As I mentioned before; it is sebum covering sweat pores or terminal openings. Regular shampoo doesn't remove sebaceous residue and this is how layers of it can cover these pores and cause heat to become trapped, especially in the temples and crown, as it's here where heat is released.

Also, the plugging may somewhat be caused when we press our temples / crowns against our pillows during sleep and wearing tight hats / helmets. In other words, pressure forces these oils further into the sweat shaft. Oils are water insoluble, so likely build up and cause narrowing of the shaft - causing a build up of heat in underlying tissues, i.e. the follicle. incidentally, it's morning time that i generally notice a huge build up of sebum, but not anymore.

"The eccrine sweat glands release heat from the body in an even manner. Heat is not just release through the scalp. Wouldn't we be losing hair in other areas like the genitals or armpits if this weren't the case? And heat shock proteins require heat shock for activation, not usually temperatures we'd get from exercising or taking a warm shower. They CAN be activated as part of the normal stress response however, and in that capacity they are protective."

This is not the case for me, I can resolutely assure you. Whenever I sweat profusely, it is always from the temples (and the crown - to a slightly lesser extent). The amount of heat I generate within my scalp is tremendous. Yet, since I've been keeping my scalp clean I don't generate as much heat as I once did. Further testimony that excess sebum disrupts perspiration.

Sweat is also released from the sweat glands all over the body, yet the temples are a major area of perspiration. A third of body heat is sweated out of the scalp, due to the large number of sweat glands located there. When we wear thicker clothing, the fabric can absorb sweat and slow down heat release, so it then builds up and migrates to the scalp. For this reason, it may be true, that sweat glands of the temples are mass produced, as this is the area where it can be released more easily.

There was someone on here who mentioned that he wore a beanie hat during exercise and began to experience severe inflammation and temple recession. This is likely because the beanie was absorbing sweat from his scalp and prevented it from cooling.

But I don't know if everyone sweats primarily from their scalps in order to cool down. I guess you can determine this when you exercise and monitor what area of your body sweats the most -- not to mention produces the most heat.

Also i didn't say a warm shower, I said a hot shower. I actually recommended to Sanderson that he reduced the temperature of water to his scalp, which helped reduce his inflammation.

And finally; the core temperature for cells is 37C / 98F. If they remain a few degrees above or below for too long, they cannot function effectively. So, IMO, this prolonged temperature disturbance triggers inflammation.

I'm not saying that this heat issue is causing all hairloss in men. This may not be applicable to you, and I can understand that it may be causing confusion for some people, as some say hypoxia is the problem, then this, then that. If this problem was so straightforward, it would have been cured by now, but this is testimony to how complex it in fact is. I'm just merely reporting what I've so far observed.

I still find most of that over complication to all of this, but cool. I may just start a thread one day laying out what I believe, and where I see it now, its simpler than all of that when you go to the root..

987 wrote:I still find most of that over complication to all of this, but cool. I may just start a thread one day laying out what I believe, and where I see it now, its simpler than all of that when you go to the root..

Well, that's OK, I'm not forcing my opinion on anyone. If people disagree with any of it, then that's fine. At least you and Anthony provide a good argument, unlike the other ignorant asshole who just tried to regularly shoot me down without having anything to back him up. This is where the freshmen always fall short and left red faced -- they're new to this subject and think they know everything. I've been studying this for 14 years and it still amazes me how complicated it all is.

Might disagree on some things, but couldn't agree more with your last point.

I thought I'd also add a particularly important piece to the puzzle; if it's true (as that science program stated) that elevated temperatures slow down cell division, then this would further suggest the reason why scalp follicles don't regenerate so well when exposed to heat. Elevated temperatures would likely counteract the effects of growth factors. So, this may cause a premature decrease in progenitors.

The fact that I've got some new temple hairs growing, must be down to the fact that thermoregulation is now balanced within the temples because the build up of sebum has been removed from the sweat pores. This means that heat is no longer building up en masse in my scalp, rather it is being released easier, hence the reason the scalp is now cooler than it has ever been.

So, if we remove the heat problem, then growth factors will promote greater cell division.

Xenon wrote:I thought I'd also add a particularly important piece to the puzzle; if it's true (as that science program stated) that elevated temperatures slow down cell division, then this would further suggest the reason why scalp follicles don't regenerate so well when exposed to heat. Elevated temperatures would likely counteract the effects of growth factors. So, this may cause a premature decrease in progenitors.

The fact that I've got some new temple hairs growing, must be down to the fact that thermoregulation is now balanced within the temples because the build up of sebum has been removed from the sweat pores. This means that heat is no longer building up en masse in my scalp, rather it is being released easier, hence the reason the scalp is now cooler than it has ever been.

So, if we remove the heat problem, then growth factors will promote greater cell division.

To understand your 'position clearly, so will a person not experiencing hair loss loose hair due to elevated scalp temperature? If not then why not? Why was thermoregulation unbalanced? The heat problem is a product of what? What do you think you did that removed the heat problem?