Pathogenesis Of Male Pattern Baldness New Theory

Pathogenesis Of Male Pattern Baldness
New Theory

In this post I will try to make a connection between Insulin resistance, inflammation, free fatty acids, prostaglandin D2 and sebum production. I will also propose a simple experiment that can prove this theory.

I will quote articles and studies that I think are important. Please read them before commenting. I am using articles rather that studies because they are more understandable to a wider range people. If you doubt the credibility of those articles, they also have references, so I suggest to check out those studies also.

What Causes Insulin Resistance?

http://wholehealthsource.blogspot.com/2011/11/what-causes-insulin-resistance-part-i.html

a variety of lines of evidence suggest that insulin resistance, in large part, is a cellular defense mechanism against energy excess. Cellular energy excess is caused primarily by the chronic consumption of energy in excess of what is expended. Fat tissue can mop up the excess energy for a while, but if the excess is chronic and fat tissue enlarges (particularly abdominal fat), other tissues will be exposed to progressively more energy (fatty acids and glucose), and cells will act to protect themselves by reducing insulin sensitivity.

The chemical pathology of insulin resistance and the metabolic syndrome
by Neil S. Harris, William E. Winter
How does body-fat content produce insulin resistance? First, it appears that it is particularly intra-abdominal fat (also termed visceral fat) that is the culprit here. Intra-abdominal fat is adipose tissue associated with the abdominal viscera. Subcutaneous fat is much less of a problem. One hypothesis suggests that a process that is central to the pathogenesis of insulin resistance is fat ectopia. (6,7) In the simplest terms, adipose tissue can only hold a certain amount of fat, and if excessively loaded with fat, there is a spillover or redistribution of lipid to ectopic sites, including liver and skeletal muscle(Figures 2-5). In support of this, hepatic steatosis ( is frequently observed in individuals with the metabolic syndrome. Nonalcoholic fatty liver disease has a prevalence of 57% to 74% in obese individuals.

Inflamation

http://wholehealthsource.blogspot.com/2011/11/what-causes-insulin-resistance-part-ii.html

Inflammation and energy excess are tightly interlinked. Flipping the calendar back to 1993, Dr. Gokhan Hotamisligil and colleagues showed in another landmark paper that blocking an inflammatory signal prevents the insulin resistance caused by obesity (, and similar findings have been reported many times since then (5, 6, 7). This suggests that energy excess causes insulin resistance in part by engaging inflammatory pathways in the body. The concept has received additional support from studies showing that salicylate can block the insulin resistance caused by acute energy excess due to infusing fatty acids into the circulation (9). Since insulin resistance is a protective mechanism against cellular energy excess, suppressing it with anti-inflammatory drugs may not be the greatest idea.

Energy excess causes inflammation, and inflammation causes insulin resistance. However, inflammation can be caused by other factors, and this can also contribute to insulin resistance. For example, inflammatory substances that mimic infection can cause insulin resistance (10). The digestive tract is full of these substances, and normally the gut barrier does a good job of keeping them out of circulation. However, under certain conditions these can enter the circulation in larger amounts, and this is thought to contribute to insulin resistance (11). It's worth emphasizing that the type of inflammation linked with insulin resistance is not the same powerful, acute inflammation that you might get at the site of a physical injury. It is a low-grade, chronic type of inflammation.

FFA and insulin resistance

http://edrv.endojournals.org/content/21/6/585.full
„It is widely accepted that increased availability and utilization of FFA contribute to the development of skeletal muscle insulin resistance (38, 39,40). Moreover, FFA have been shown to increase endogenous glucose production both by stimulating key enzymes and by providing energy for gluconeogenesis (41). Finally, the glycerol released during triglyceride hydrolysis serves as a gluconeogenic substrate (42). Consequently, resistance to the antilipolytic action of insulin in adipose tissue resulting in excessive release of FFA and glycerol would have deleterious effects on glucose homeostasis.“

Glucose fatty acid interactions and the regulation of glucose disposal.
Randle PJ, Priestman DA, Mistry SC, Halsall A.
Source
Nuffield Department of Clinical Biochemistry, John Radcliffe Hospital, Oxford, England.
Abstract
Glucose is essential for the energy metabolism of some cells and conservation of glucose is obligatory for survival during starvation. The principal site of this glucose conservation is the mitochondrial pyruvate dehydrogenase (PDH) complex, which is regulated by reversible phosphorylation (phosphorylation is inactivating). In cells in which glucose oxidation is switched off during starvation, fatty acids are used as fuel, and acetyl CoA and NADH formed by beta-oxidation promote phosphorylation of PDH complex by activation of PDH kinase. A longer-term mechanism further increases PDH kinase activity in response to cAMP and products of beta-oxidation of fatty acids. Coordinated inhibition of glycolytic flux mediated by effects of citrate on PFK1 and PFK2 in muscles and liver results in an associated inhibition of glucose uptake. Similar mechanisms lead to impaired glucose oxidation in diabetes.

My hypothesis:

In the simplest terms, adipose tissue can only hold a certain amount of fat, and if excessively loaded with fat, there is a spillover or redistribution of lipid to ectopic sites, including liver and skeletal muscle

I believe that sebaceous glands and skin are also one of the ectopic sites (just like liver or skeletal muscle) that get overload with fat once that adipose tissue is full.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835893/
Sebaceous gland lipids
There is evidence indicating that dietary factors alter sebaceous gland output. It has been demonstrated that sebum production can be increased by the consumption of dietary fat or carbohydrate.27 Variations in carbohydrates can also affect sebum composition.28,29 In turn caloric restriction has been shown to dramatically decrease the sebum secretion rate.30,31 All these findings suggest that dietary habits, supplying substrates for the sebaceous lipid synthesis, can be involved in the sebum production mechanism.32 Considering that increased sebum production is a primary component in acne, dietary factors have long been implicated in its pathogenesis. So far data concerning this issue are still controversial.

Diet and triglyceride metabolism
IAN MACDONALD
From the Department ofPhysiology, Guy's Hospital Medical School, London

The skin is another site of triglyceride metabolism
that can be influenced by the diet. It used to be taught
that alteration in the level of carbohydrate in the
diet could influence the 'greasiness' of the skin.
Some evidence for this is the finding that the amount
of lipid on the surface of the skin is partly dependent
on the type of carbohydrate consumed. A high
intake of sucrose in men raised the triglyceride on
the surface of the skin, whereas dietary starch had
the reverse effect

According to this theory any condition that will increase circulating fatty acids will lead to insulin resistance (in susceptible individuals), which will lead to ectopic fat distribution (liver , muscle and if I am right also skin and sebaceous glands).

http://www.ncbi.nlm.nih.gov/pubmed/19171470
CONCLUSION:
„All the conditions that increase circulating fatty acids and cause lipid overloading (obesity, lipoatrophy, lipodystrophy, catabolic states, etc.) induce a lipotoxic state in non-adipose tissues that gives rise to insulin resistance.“

Once the fat or sebum gets redistributed to the skin it starts the inflammatory processes in the scalp that causes hair loss probably through the action of Prostaglandin D2 and sebaceous gland hyperplasia.

Prostaglandin D2 inhibits hair growth and is elevated in bald scalp of men with androgenetic alopecia.
Garza LA, Liu Y, Yang Z, Alagesan B, Lawson JA, Norberg SM, Loy DE, Zhao T, Blatt HB, Stanton DC, Carrasco L, Ahluwalia G, Fischer SM, FitzGerald GA, Cotsarelis G.
Furthermore, we find that a transgenic mouse, K14-Ptgs2, which targets prostaglandin-endoperoxide synthase 2 expression to the skin, demonstrates elevated levels of PGD(2) in the skin and develops alopecia, follicular miniaturization, and sebaceous gland hyperplasia, which are all hallmarks of human AGA. These results define PGD(2) as an inhibitor of hair growth in AGA and suggest the PGD(2)-GPR44 pathway as a potential target for treatment.

How to test this ?

After starvation, overnight fast, physical (exercise) or psychical stress, circulating fatty acids will increase. This will cause increased delivery of FFA to ectopic sites (liver, muscle, sebacues glands and skin). In simplest words sebum production will increase and your hair should become oilier.
The best way to test this is to try not to eat for 48h. Starvation would cause very high FFA concentration and if I am right your sebum production should be very high.

After breaking the fast and normalizing nutrition your insulin level should increase, your FFA level will drop and sebum production should slow down.
Your hair should look even better than before because insulin sensitivity should increase after a small weight loss during 48h fast. When you break a fast you should eat a large meal that will increase you insulin levels. (high insulin levels will suppress FFA in the blood.) If you eat a high fat meal than your insulin levels would be low, and circulating FFA would remain high.

Michael Roden
First Medical Department, Hanusch Hospital, A-1140 Vienna, Austria

TABLE 1. Plasma free fatty acid concentrations in humans under physiological and pathological conditions
Condition Plasma Free Fatty Acids, mmol/l
Physiological conditions
Fasting overnight, 1012 h ~0.10.5
Low-carbohydrate/high-fat diet ~0.8
Exercise, ~2 h, trained subjects ~1.0
Exercise, ~2.5 h, moderately trained subjects ~1.6
Starvation, 69 h ~1.8
Epinephrine, intravenous ~1.8
Pathological conditions
Lean insulin-resistant offspring of type 2 diabetic parents ~0.6
Obese nondiabetic humans ~0.60.8
Overt type 2 diabetes mellitus ~0.70.9
Nonalcoholic fatty liver disease ~0.7
Lipoprotein lipase defect ~1.0
Oral fat loading in familial combined hyperlipidemia ~1.2
Type A insulin resistance ~3.3

Physical exercise is also one way to test this theory. High intensity training is a little specific because hiit would at first decrease FFA and then increase them a few hours after. So if you are doing high intensity training your sebum production should be lower during training and then higher a few hours later.

T h e dynamics of plasma free fatty acid
metabolism during exercise*
S A M U E L J. F R I E D B E R G , ? PAUL B. SHER, MonToN D. BOGDONOFF, and E. HARVEY ESTES, JR.

I n recent years it has become evident t h a t plasma free f a t t y acids (FFA) serve directly, along with glucose, a s a major fuel for muscular contraction (1-9). Concomitants of FFA utilization by muscle are a change in concentration of plasma FFA and in turnover r a t e of F FA (5, 6 , 0 ) . Earlier work (6) has shown t h a t vigorous exercise of relatively short duration (15 min) lowers t h e concentration of plasma FFA and t h a t this lowering is accompanied by a n increase in the turn- over r a t e of plasma FFA. A t t h e conclusion of exer- tion, the F FA concentration rises abruptly t o higher than resting values. Further observations provided additional information ; during more prolonged and less vigorous exercise, the initial F FA fall was less marked, and a gradual rise then took place'

Psychical stress, chronic stress, sleep deprivation will also have similar effect on insulin sensitivity. This is probably why chronic stress and sleep are associated with hair loss.

I would like to hear your opinion. Thank you.

This is probably why chronic stress and sleep are associated with hair loss.

Do you mean lack of sleep? I don't see how sleep could be associated with hair loss.

perhaps melatonin, which is involved in ur body clock, and HGH and other hormones are produced while u sleep.

Anxious1 wrote:perhaps melatonin, which is involved in ur body clock, and HGH and other hormones are produced while u sleep.

HGH being produced while you sleep is a great reason to get a good nights sleep.

While a lot of what you said is true, theres too many fat diabetics with NW1s. The correlation between MPB and metabolic syndrome has conflicting results. If you have some type of metabolic dysfunction by all means, correct it but I think we should be looking at this from other angles.

One thing i have been thinking into is a gluten intolerance, and how it affects the way certain people absorb minerals and vitamins, leading to problems gaining weight etc.

I have always been told i eat alot, but i have never been able to gain much weight...looking back on my diet, it was very high in gluten and wheat.

I'm really taking a shot in the dark here, but perhaps all the NW1's that are obese do not suffer from any food intolerances and can digest and absorb all the minerals they consume, meaning that despite their poor diets, the fact that they consume so much, means that their hair and scalp is fed adequately.

Please be kind if i'm the biggest idiot ( or second biggest after 2020 )

This doesn't seem to address the gender issue why men only go bald, and not women.

Perhaps it could be a simple as the fact that women pay a lot more attention to their hair and thus keep the circulation to the scalp strong through regulary brushing and maintenance.

Women also have a lot more subcutaneous fat, and therefore the adipose tissue in the scalp may not get depleted as easily as in men.

Dalesandar, this is a very nice theory...

Well, i work at night's for 2 days in the week. From 22.00 until 06.00 in the morning. When i finish my shift, and i go home, i face in the mirror an awful - oily hair. When i sleep for a 5-6 hours and wake up, my hair looks a lot better. In my night shift i don't eat anything...(except insomnia)
And another thing.
In the gym, after weight's workout, i used to run for 20 min. of a hiit training.
This year, i only drink a protein shake when i finish, after the shower, and usually when i go home my hair they do not have the looks that they have before training.
They just seems more weak...Today i notice exactly the same thing, and i was thinking about it before i read your post.
I mention the above example, because, last year, i used to drink with the protein shake and a carbohydrate shake, mixing together and my hair looks stronger, especially the training days....(i guess because of the insulin spike from simple carb's????)

Anyway...is there any solutions about this theory?

2020_the_time_traveler wrote:yeah you forgot one thing: sebaceous glands enlarged WHEN exposed to PGD2 and not the other way around....

I didn't forget. I don't see how this disprove my theory.

Cellular energy excess and high circulating FFA > Inflammation > Insulin resistance > fat ectopia (there is a spillover or redistribution of lipid to ectopic sites, including liver and skeletal muscle and if I am right sebaceous glands and skin.) Once the body start inflammation processes it is quite possible that PGD2 increases.

Do you mean lack of sleep? I don't see how sleep could be associated with hair loss.

I meant lack of sleep, of course.

This doesn't seem to address the gender issue why men only go bald, and not women.

You are right. I still think that DHT is part of the equation, but I am not sure how (at least not on a molecular level). However we all know that sex hormones are influenced by insulin resistance and metabolic disturbances.

While a lot of what you said is true, theres too many fat diabetics with NW1s. The correlation between MPB and metabolic syndrome has conflicting results.

You are right, there are many factors we don't understand, and I can't explain them.

I am just trying to say that:

Insulin resistance correlates with high circulating FFA and redistribution of lipid to ectopic sites.

Insulin resistance correlates with hair loss

Sebum correlates with hair loss

From my personal observation I found a correlation between circulating FFA and sebum output, and I would like others to test this. A already wrote what causes increased FFA availability in my first post.

I don't say that this will stop or cure hair loss. I am just saying that there is a correlation.

Steve_Gr wrote:Dalesandar, this is a very nice theory...

Anyway...is there any solutions about this theory?

There are many solutions, but I don't really want to start that debate right now.

Basically if I am right and there is a correlation between sebum and circulating FFA in susceptible individuals then any behavior aimed at lowering serum FFA would be beneficial for reducing sebum.

schpiloch123 wrote:Perhaps it could be a simple as the fact that women pay a lot more attention to their hair and thus keep the circulation to the scalp strong through regulary brushing and maintenance.

Women also have a lot more subcutaneous fat, and therefore the adipose tissue in the scalp may not get depleted as easily as in men.

^ these extreme and dumb theories is why I stopped taking this forum seriously

here_comes_the_sun wrote:

schpiloch123 wrote:Perhaps it could be a simple as the fact that women pay a lot more attention to their hair and thus keep the circulation to the scalp strong through regulary brushing and maintenance.

Women also have a lot more subcutaneous fat, and therefore the adipose tissue in the scalp may not get depleted as easily as in men.

^ these extreme and dumb theories is why I stopped taking this forum seriously

yet you are still posting on "this" forum???

P.S. schpiloch123's post is in fact extremely absurd but that does not give you the right to bash this forum as a whole.

i dont think anyones denying genetics plays a role.i mean genetics codes for every protein in the body and epigenetics (methylation, acetylation and micro RNA) regulates the expression probably above 90% of genetics. but u must also realise the environmental influences changes ur epigenetics thereby changing ur genetics.

so wats so wrong about trying to alter the environmental influences. It may not alter our genetics but it alters the expression thru epigenetics, and it least its something, better than surrenedering to our genetics.

Mike Peter wrote:We all know what male pattern baldness can do to us. Whether your hair loss is genetically related or induced due to other factors, it is important to get to the toot cause of the problem and find a solution. First of all, find out what causes your hair loss. Is it due to:

bad genes
poor diet
wrong lifestyle
underlying disease such as thyroid
wrong use of hair products
medications etc.

You can reverse hair loss by bringing about positive changes in your lifestyle, improving your diet, avoiding chemical based products and using safe and effective natural treatments that include Saw palmetto and He Shou Wu. Check this video to find a free recipe for natural hair growth shampoo - https://youtu.be/FstLYoC5MSE

http://fullheadhair.com/

talking about product promotion. you have no manners or respect for the forum?

Mike,

Please tell me that isn't your blog that was linked to. Pretty shameless self-promotion on forum whose creators are already offering better information than you're providing, and doing it for free. Not to mention their information is backed up by relevant research, not a lot of pop science that is years behind.

Just from your description of hair loss causes, its obvious you don't have a very clear concept of genetics. You are adding "bad genes" as a bullet point in the list as if it is a separate cause from the others, when all of the causes you listed exert their negative effects because of their effects on genes and gene transcription. Not to mention, there really isn't such a thing as a "bad" gene (unless you count blatant mutations that are known to cause disease). A gene simply produces a protein. An effect of those proteins may be "unwanted" based on the entire concurrent metabolic milieu but to say there is a bad gene that causes hair loss is just misguided, as if its only point for existence is to cause hair loss. Hair loss is an ancillary effect of localized inflammation. That inflammation has a purpose in the human body as do all of the associated hormones and other proteins.

If you want to have a successful hair related site, take a hint from this forum. Ditch the blatant e-marketing tools that should just die: big highlighted red words and fake testimonials all leading you to the secure purchase form at the bottom.

Some years I ago I made the following thread:

https://immortalhair.forumotion.com/t1129-hypothesis-of-male-pattern-hair-loss

I believe this hypothesis to be correct and much information has been updated since that time.

Simply stated, thyroid function dictates energy metabolism and/or energy metabolism suffers from
what negatively affects the the thyroid. The above thread will explain most of the points.

I can show an animal or human with a certain genetic expression and I can show the same animals
or humans with a different genetic expression. Yes, the genes are the same, but one is expressed
and other pair is not. Altering the stasis of the thyroid.