Destruction of the arrector pili muscle and fat infiltration in androgenic alopecia

Abstract
Background
Androgenic alopecia (AGA) is the most common hair loss condition in men and women. Hair loss is caused by follicle miniaturization, which is largely irreversible beyond a certain degree of follicular regression. In contrast, hair loss in telogen effluvium (TE) is readily reversible. The arrector pili muscle (APM) connects the follicle to the surrounding skin.

Objectives
To compare histopathological features of the APM in AGA and TE.

Methods
Archival blocks of 4 mm scalp punch biopsies from 8 patients with AGA and 5 with TE were obtained. New 4 mm biopsies from 5 normal cases were used as controls. Serial 7 μm sections were stained with a modified Mason's trichrome. “Reconstruct” software was used to construct and evaluate three-dimensional images of the follicle and APM.

Results
The APM degenerated and was replaced by adipose tissue in all AGA specimens. Remnants of the APM remained attached to the hair follicle. There was no fat in the normal skin specimens. Fat was seen in 2 of 5 TE specimens, but could be attributed to these patients also showing evidence of AGA. Quantitative analysis showed that muscle volume decreased and fat volume increased significantly (P<0.05) in AGA compared to controls.

Conclusions
APM degeneration and replacement with fat in AGA has not previously been described. The underlying mechanism remains to be determined. However we speculate that this phenomenon might be related to depletion of stem or progenitor cells from the follicle mesenchyme, explaining why AGA is treatment resistant.

http://onlinelibrary.wiley.com/doi/10.1111/bjd.12921/abstract


It looks like the whole picture are clear now...
There is a kind of fat accumulation in arrector pili muscle. From my view, this must be ectopic fat deposition.

Ectopic fat has to do with metabolic syndrome and insulin resistance. That's why AGA connected with diabetes and heart diseases.

The ectopic fat accumulation is the source of androgens via 5ar enzyme, estrogens via aromatase, insulin resistance and inflammatory and this source is connected in every follicle as ectopic fat.

any way to reduce this fat and enlarge the APM?

scalp fasting and steroids lol

bananasinpajamas wrote:any way to reduce this fat and enlarge the APM?

Exercise the muscle? Towling seems to do this. So does derma-rolling. Maybe the violet ray does it too? I haven't used one yet.

sounds like insulin problems.. insulin going to fat stores instead of muscle stores. how to fix.. not sure how to work those muscles.. maybe correcting insulin problems will auto help it..

Hmmm... this is interesting. The arrector pili muscle's principle function is to provide insulation, as it causes the hair to stand on end so it can trap air. The fact that the pili muscle and hair both degenerate may suggest that they interfere with evaporative cooling from the scalp, so both pili units and matrix cells are targeted for destruction. To simplify it; if heat is constantly being released through the scalp, then the pili and terminal hair would no longer be required for insulation, so may degenerate accordingly.

Once again, this ties in with the heat theory... you'd think that cold air would cause the arrector pili muscle and terminal hair to grow bigger so that they can help the scalp stay warm.

sanderson wrote:sounds like insulin problems.. insulin going to fat stores instead of muscle stores. how to fix.. not sure how to work those muscles.. maybe correcting insulin problems will auto help it..

Insulin management is the most important, but i wonder if there is any supplement to reduce ectopic fat, if that is the case.

Xenon wrote:Hmmm... this is interesting. The arrector pili muscle's principle function is to provide insulation, as it causes the hair to stand on end so it can trap air. The fact that the pili muscle and hair both degenerate may suggest that they interfere with evaporative cooling from the scalp, so both pili units and matrix cells are targeted for destruction. To simplify it; if heat is constantly being released through the scalp, then the pili and terminal hair would no longer be required for insulation, so may degenerate accordingly.

Once again, this ties in with the heat theory... you'd think that cold air would cause the arrector pili muscle and terminal hair to grow bigger so that they can help the scalp stay warm.

Interesting theory, but how would you explain the fact of fat accumulation around the pili muscle?

TNT wrote:

Xenon wrote:Hmmm... this is interesting. The arrector pili muscle's principle function is to provide insulation, as it causes the hair to stand on end so it can trap air. The fact that the pili muscle and hair both degenerate may suggest that they interfere with evaporative cooling from the scalp, so both pili units and matrix cells are targeted for destruction. To simplify it; if heat is constantly being released through the scalp, then the pili and terminal hair would no longer be required for insulation, so may degenerate accordingly.

Once again, this ties in with the heat theory... you'd think that cold air would cause the arrector pili muscle and terminal hair to grow bigger so that they can help the scalp stay warm.

Interesting theory, but how would you explain the fact of fat accumulation around the pili muscle?

IDK perhaps due to lack of muscular contractions (or lack of energy use), the muscle begins to atrophy and accumulates fat? Doesn't the same process occur in skeletal muscle tissue when we don't exercise them enough?

I guess so, but on the other hand, muscle tissues supposed that they shouldn't store fat, including the liver or heart muscle. When that happen, this kind of fat, referred as ectopic fat and is one of the reasons for metabolic syndrome development.

But you are right. Muscle movement, could help to reduced fat accumulation...

TNT wrote:I guess so, but on the other hand, muscle tissues supposed that they shouldn't store fat, including the liver or heart muscle. When that happen, this kind of fat, referred as ectopic fat and is one of the reasons for metabolic syndrome development.

But you are right. Muscle movement, could help to reduced fat accumulation...

As Sanderson mentioned in regards to insulin resistance, this study states that lack of muscular exercise can contribute to insulin resistance and fat accumulation.


Skeletal muscle lipid deposition and insulin resistance: effect of dietary fatty acids and exercise1,2,3
Michael P Corcoran, Stefania Lamon-Fava, and Roger A Fielding
+ Author Affiliations

1From the Lipid Metabolism Laboratory (MPC and SL-F) and the Nutrition, Exercise Physiology, and Sarcopenia Laboratory (RAF), Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA
Abstract

Mounting evidence indicates that elevated intramyocellular triacylglycerol concentrations are associated with diminished insulin sensitivity in skeletal muscle. This lipid accumulation is most likely due to enhanced fatty acid uptake into the muscle coupled with diminished mitochondrial lipid oxidation. The excess fatty acids are esterified and either stored or metabolized to various molecules that may participate or interfere with normal cellular signaling, particularly insulin-mediated signal transduction, thus altering cellular and, subsequently, whole-body glucose metabolism. Impaired insulin responsiveness, if not managed, can further progress to type 2 diabetes mellitus, an all too common condition. For most of the human population this is avoidable, given that causes of intramyocellular lipid deposition are predominantly lifestyle-mediated. Chronic overconsumption of calories coupled with deleterious intakes of saturated or trans-unsaturated fatty acids inconsistent with the recommendations outlined in the Dietary Guidelines for Americans have been shown to increase the risk of insulin resistance. Furthermore, lack of exercise, which can have a profound effect on skeletal muscle lipid turnover, is implicated in this lipid-induced insulin resistance. This review summarizes the current understanding of the effects of elevated intramyocellular lipids on insulin signaling and how these effects may be altered by varying dietary fat composition and exercise.

http://www.ncbi.nlm.nih.gov/pubmed/18625114

Thx xenon. Maybe the same thing happens and in peripheral head muscles, but those muscles are moved often, as we eat, talk, etc. so fat storage is management.

TNT wrote:Thx xenon. Maybe the same thing happens and in peripheral head muscles, but those muscles are moved often, as we eat, talk, etc. so fat storage is management.

Yes the peripheral head muscles are exercised often, but the tiny arrector pili muscles attached to follicles relax under hot conditions because this allows heat to escape better. This is what I found particularly interesting about the information you posted because muscles atrophy if they are not exercised, so it made me wonder if hot temperatures were causing the arrector pili muscles to enter into a permanently relaxed state, which then causes atrophy and perhaps insulin resistance.

What I also find interesting; the two units which assist in heat retention (hair and the pili muscle) are the ones which degenerate, whereas the sweat glands, which assist in cooling, become more active.

Anyway, I'd prefer not to delve too heavily into the heat theory at this point, as the cooling experiments seemed to cause worse hairloss for me, even though I thought that they would have had the opposite effect.

yeap, i know what you mean, cold water makes my hair worse, but maybe this is logical if arrector pill has degenerated.

Cold, fear etc. may stimulate the sympathetic nervous system and thus cause contraction of this muscle.
So under extremely cold conditions, ar.pili can not respond to this impulse , and inflammatory goes up.

TNT wrote:yeap, i know what you mean, cold water makes my hair worse, but maybe this is logical  if arrector pill has degenerated.

Cold, fear etc. may stimulate the sympathetic nervous system and thus cause contraction of this muscle.
So under extremely cold conditions, ar.pili can not respond to this impulse , and inflammatory goes up.

That's an excellent point. It seems that the scalp loses it's natural defenses against cold, which then give rise to inflammatory cytokines. It's also interesting that there is very little BAT within the scalp, and BAT also aids in insulation. So there's three insulating mechanisms which are lost in the scalp. To add to this, we find that BAT seems to increase in cold stressed tissue and decrease due to too much heat.

This is why it has left me puzzled why I lost more hair during the cooling experiments. BAT should increase, the arrector pili muscle should grow larger, terminal hair should grow. Who knows though? Maybe the tissue needs to suffer from cold induced inflammation before it says, 'Enough is enough, something needs to be done here'. Then hair and the pili muscle might regrow again, but it might get much worse before it gets better. I guess you could liken this to skeletal muscles... when they are stressed from heavy workouts, they need to grow in order to deal with extra pressure, but first they must go through the inflammatory process. 'No pain, no gain', as they say.

Miniaturized hairs maintain contact with the arrector pili muscle in alopecia areata but not in androgenetic alopecia: A model for reversible miniaturization and potential for hair regrowth

Background: Hair follicle miniaturization is the hallmark of male pattern hair loss (MPHL), female pattern hair loss (FPHL), and alopecia areata (AA). AA has the potential for complete hair regrowth and reversal of miniaturization. MPHL and FPHL are either irreversible or show only partial regrowth and minimal reversal of miniaturization. Hypothesis: The arrector pili muscle (APM) attachment to the hair follicle bulge, a recognized repository of stem cells may be necessary for reversal of hair follicle miniaturization. Materials and Methods: Sequential histological sections from MPHL, FPHL, AA, and telogen effluvium were used to create three-dimensional images to compare the relationship between the APM and bulge. Results: In AA, contact was maintained between the APM and the bulge of miniaturized follicles while in MPHL and FPHL contact was lost. Discussion: Contact between the APM and the bulge in AA may be required for reversal of hair follicle miniaturization. Maintenance of contact between miniaturized follicles in AA could explain the complete hair regrowth while loss of contact between the APM and the bulge in MPHL and FPHL may explain why the hair loss is largely irreversible. This loss of contact may reflect changes in stem cell biology that also underlie irreversible miniaturization.

http://www.ijtrichology.com/article.asp?issn=0974-7753;year=2012;volume=4;issue=3;spage=154;epage=157;aulast=Yazdabadi

Well, xenon, i guess losing contact with arrector pili, this is a point of no return..? But i think in transplanted hair arrector pili is absent also

Well, IDK... Drex has had pretty good regrowth in areas which were slick bald for many years, so I wouldn't give up all hope. Although I agree that regrowing hair is very difficult.

This is a little OT, but I took my dog for a very long walk before, it's cold outside today so I put on lots of thick clothing, including a thick jacket. I walked very fast and I noticed that I started sweating heavily from my temples. I normally don't sweat from my temples anymore, but the thick fabric was preventing my body from cooling, so the heat moved to my scalp to escape.

When I got back in before, I felt my scalp starting to inflame and I suspected the cause was metabolic byproducts in sweat (possibly lactic acid or uric acid), so I cleaned the scalp with some cool water and the inflammation immediately went away.

Maybe an electric head pulse device...? something like this but for another purpose.

A pilomotor effect stimulating device is designed to electrically stimulate the arrector pili muscles of the skin to cause a pilomotor reaction in which goosebumps are formed in the affected area and the hairs are raised away from the skin. The device has a handle and a head at one end of the handle carrying electrodes for skin application. An electronic control unit in the handle is connected to the handles and includes a pulse generator configured to produce a pulsed electrical signal at the electrodes which is designed to stimulate the arrector pili muscles in the vicinity when the electrodes are applied to the skin. The device may be used as a shaving aid to raise the hairs in an area to be shaved, making it easier to cut the hairs closer to the skin when shaving.

http://www.google.co.uk/patents/WO2013119307A1?cl=en

Interesting. Doesn't the violet ray emit an electrical current over the skin? I'm not too savvy on the violet ray, but I heard that it does something like that.

Dalesandar wrote:https://immortalhair.forumotion.com/t7541-pathogenesis-of-male-pattern-baldness-new-theory

That thread covers almost everything...thx Dalesandar...
Looks like lipotoxicity, so fat consuming must be limited. From the other hand, my endo says to eat more fat, for boosting my low testosterone, because i was already in a low fat diet and high carb. Great.... 

This is a study about a canadian lynx whose thyroid had atrophied. The thyroid cells were replaced by fat cells.

http://www.scitechnol.com/2325-9590/2325-9590-2-108.php

Xenon Omicron Draconis wrote:Interesting. Doesn't the violet ray emit an electrical current over the skin? I'm not too savvy on the violet ray, but I heard that it does something like that.

Good question. I think that violet ray + Tom Hagerty scalp exercise is the way to go.

TNT wrote:

Dalesandar wrote:https://immortalhair.forumotion.com/t7541-pathogenesis-of-male-pattern-baldness-new-theory

That thread covers almost everything...thx Dalesandar...
Looks like lipotoxicity, so fat consuming must be limited. From the other hand, my endo says to eat more fat, for boosting my low testosterone, because i was already in a low fat diet and high carb. Great.... 

The answer to insulin resistance is not to consume less fat, necessarily. Both an excess of fat or carbohydrate can induce insulin resistance. Its really a matter of energy flux and oxidative signalling, imo. A diet high in carbohydrate, without adequate utilization, and adequate O2 consumption will lead to higher levels of lipid products in the cell also. Insulin resistance is probably a densensitization mechanism similar to that the brain experiences when it get's higher than normal levels of nt stimulation. The cell's are saying, "K...yup...had enough". Obviously it isn't conscious, its a built in fail safe probably relying on the level of ROS.

The things is, fat metabolism at the mitochondria itself causes a lot less ROS to be generated. To me, the problem is probably related more closely to the rise in consumption of high-energy-density-to-volume carbohydrate combined with unsaturated plant oils. This is asking for insulin resistance.

Now, a diet balancing intake with output and getting the right balance of saturated fats to carbs (total carbs probably 40% of total dietary calories or less), is how to do things. And if I had to guess, the timing of carbohydrate intake is probably paramount also, because the problem of insulin resistance starts at the liver and someone trying to throw energy at a glycogen-replete liver (here's looking at you HFCS) is asking for hepatic insulin resistance.

AS54 wrote:

TNT wrote:

Dalesandar wrote:https://immortalhair.forumotion.com/t7541-pathogenesis-of-male-pattern-baldness-new-theory

That thread covers almost everything...thx Dalesandar...
Looks like lipotoxicity, so fat consuming must be limited. From the other hand, my endo says to eat more fat, for boosting my low testosterone, because i was already in a low fat diet and high carb. Great.... 

The answer to insulin resistance is not to consume less fat, necessarily. Both an excess of fat or carbohydrate can induce insulin resistance. Its really a matter of energy flux and oxidative signalling, imo. A diet high in carbohydrate, without adequate utilization, and adequate O2 consumption will lead to higher levels of lipid products in the cell also. Insulin resistance is probably a densensitization mechanism similar to that the brain experiences when it get's higher than normal levels of nt stimulation. The cell's are saying, "K...yup...had enough". Obviously it isn't conscious, its a built in fail safe probably relying on the level of ROS.

The things is, fat metabolism at the mitochondria itself causes a lot less ROS to be generated. To me, the problem is probably related more closely to the rise in consumption of high-energy-density-to-volume carbohydrate combined with unsaturated plant oils. This is asking for insulin resistance.

Now, a diet balancing intake with output and getting the right balance of saturated fats to carbs (total carbs probably 40% of total dietary calories or less), is how to do things. And if I had to guess, the timing of carbohydrate intake is probably paramount also, because the problem of insulin resistance starts at the liver and someone trying to throw energy at a glycogen-replete liver (here's looking at you HFCS) is asking for hepatic insulin resistance.

+1

fat isn't going to cause insulin resistance.. fat can be used into insta energy by your body. carbs are what is causing insulin to spike in your body.. hence the more insulin, the more "insulin resistant" you become. but insulin is not always bad. insulin makes your muscle grow. it also makes your fat grow. you want it to grow your muscle. so what you have to do is get onto a very frequent exercise routine. you want your muscles to make use of the insulin as best as possible.. so start lifting heavy and grabbing most of your carbs post workout. also, yoga as much as possible.. i go every morning (srs). exercise = your best friend. i never knew how important it was until i start researching into insulin resistance.

since i've started carb backloading (ONLY eating carbs after heavy weight lifting), i've had no itch with eating the highest GI carbs.. let's see.. i worked out today after not eating carbs for 2 days (only veggies, fat, and protein) and then post workout i ate about 10 bananas, chocolate gluten free brownies (5 of them), pizza from whole foods. and guess what? absolutely no itch from any of these foods. for real. 30 minutes post workout.. literally no high GI food you eat gets turned into fat.. it all gets turned into muscle. your muscles open up what's called GLUT4 and all insulin gets shoved into your muscles.. that's why high GI foods work so well  because it spikes your insulin fast and your muscles absorb all of it. i gained about 7 lbs in a week from doing this and no itch after eating the food. really the only thing that gives me itch now is if masturbate then it will come.. but i really believe this has to do with my post fin issues that are still being worked out. this has helped me feel close to normal libido wise.. but my body is flucuating a lot. if you want more info on this.. search "carb backloading" on google and find all the articles by kiefer.. it's pretty amazing stuff. i'm going to be making a post on this.. but school is seriously messing with me now.

i think with a few hacks and optimizing everything.. this could really be the healthiest diet for both lifespan and hairloss.. imagine if every carb you ate.. it all went to your muscle and you never had to deal with insulin issues.. it all just built muscle? get your BF% down as much as possible.. that's what i'm trying to do.. to cut all visceral fat as i believe it is contributing to some of my problems