The Cause Of Baldness

Luckytype

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Its absolutey multifaceted.

I lowered my already completely fine hairline with massage techniques WITHOUT any change in shedding rate.

In other words i improved my hairline by massage right after i began shedding last year, but to this day continue to shed but maintain a killer hairline that hides it
 

Luckytype

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As another data point to this: i am a man of few expressions, i was born with quite a poker face and have been accused of lacking affect many times. I have my smiling bouts but i largely operate with minimal movement of my facial expression and with no movement of my forehead like this furled brow "look at me on instagram" type of face.


That video shows how he decided to "startle" his forehead to give something to the photo...just like every other idiot on social media trying to get attention for a self portrait
 
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CLASH

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@Thoushant @Mossy

Effect of dihydrotestosterone on cultured human tenocytes from intact supraspinatus tendon. - PubMed - NCBI

"Cell morphology assessment and cell proliferation tests were performed 48, 72 and 96 h after DHT treatment. DHT-treated tenocytes showed an increased proliferation rate at DHT concentration higher than 10(-8) M."

"In conclusion, in vitro, progressive increasing concentration of DHT at doses greater than 10(-8) M had direct effects on male human tenocytes, increasing cell number after 48 and 72 h of treatment, and leading to a dedifferentiated phenotype after 48 h of treatment."


This can possibly explain the difference between men and women balding. Men have more DHT expression in general, so with less hypoxia DHT is upregulated to higher levels in men. With higher levels of DHT you can see increase in number of tenocytes in the scalp and thus increase fibrosis with inflammatory stimulus. So it takes less hypoxia, i.e. less fibrosis in men to see hairloss compared to women due to the increased expression of 5AR.

simple logical pathway to explain it easier visually:

inflammation (endotoxin I think in this case)-> fibrosis- > hypoxia-> increased 5AR (easier to increase in men, i.e. it takes less hypoxia to induce**)-> increased DHT-> increased tenocyte proliferation-> inflammation-> fibrosis-> cycle continues.

**check this link to see Hair Loss Help Forums - The real reason why balding scalps have more DHT

Its a feed forward pathway. It exponentiates itself as you can see above. Gotta break the cycle. Also, explains why reversal is so difficult, once hypoxia is set in with fibrosis, DHT is very hard to down regulate until the fibrosis abates and blood vessels can supply O2.

Also, if DHT is present to stimulate repair of damage as suggested by the article then DHT isn't negative. Its actually a protective factor, which goes along with peat, haidut and Roddy who i personally subscribe to in most general thought process. It seems DHT is a bystander in the process, being upregulated to heal and protect but in excessive amounts leading to symptomatology.

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@Thoushant
Haha I know you mean well, no worries. The questioning is good, it allows us to find the truth. I don't care about being right for the sake of being right, I just want to know what the truth is. I had a lot of messages to reply to so perhaps I came off short. Not my intention. Just wanted to reach everyone haha.
 
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REOSIRENS

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I'm not sure about raw dairy. My brother drinks a lot of milk ( straight from the cow, since my grandmother has one ) and he is still balding heavily.
Dairy is pro Cholesterol (and cholesterol is pro testosterone/dht) so best way to normalize things is by checking thyroid... Triiodothyronine stops baldness from high cholesterol diet by converting cholesterol into protective steroids like Pregnenolone and Progesterone
 
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CLASH

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Heres some references supporting the adrenal up regulation piece:

1) Hormonal parameters in androgenetic hair loss in the male. - PubMed - NCBI

"Significant differences in serum levels of androstenedione, cortisol, 17 beta-estradiol and luteinizing hormone were noted between hair loss patients and control subjects. Suprarenal stimulation as well as hypophyseal feedback mechanisms therefore seem to be involved in male pattern alopecia."


2) Hormone studies in females with androgenic hairloss. - PubMed - NCBI
"The results of the study show no significant elevation of androgens in females with androgenic hairloss, but a more complex condition with involvement of the glandula suprarenalis and the hypophyseal level"
(this was in women, the study also shows with up regulation of the HPA axis, the Thyroid is down regulated, this is evidenced by the increased TSH in the women.)

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3) Hormonal profile of men with premature balding. - PubMed - NCBI
"The frequency of subnormal values in SHBG, FSH, testosterone and epitestosterone (but not in free androgen index) was significant in the balding men. A borderline significant trend was recorded with respect to increased levels in 17OH-P and prolactin."


4) 17-Hydroxyprogesterone in children, adolescents and adults. - PubMed - NCBI

"An inherited deficiency of 21-hydroxylase leads to greatly increased serum concentrations of 17-OHP, while the absence of cortisol synthesis causes an increase in adrenocorticotrophic hormone. The classical congenital adrenal hyperplasia (CAH) presents usually with virilisation of a girl at birth."

"A non-classical form of congenital adrenal hyperplasia (NC-CAH) presents later in life usually with androgen excess. Moderately raised or normal 17-OHP concentrations can be seen basally but, if normal and clinical suspicion is high, an ACTH stimulation test will show 17-OHP concentrations (typically >30 nmol/L) above the normal response."

#3 and #4 are together. #3 shows increase in hypophyseal activation with FSH test and epitest but also shows increased 170H-P and prolactin. As shown earlier Prolactin is indicative of tissue estrogen and serotonin (look at original post). Also, prolactin shows an increase In hypophyseal activation. The 17OH-P is often elevated in congenital adrenal hyperplasia as shown in #4 hence the grouping of these two together, which as shown above is also elevated in balding men. What do you know, babies with congenital adrenal hyperplasia also show virilisation at birth (increased body hairiness) which is similar to the hirsutism seen in balding men and also the hirsutism seen in cushings syndrome. I don' think these are coincidences. All of these disorders show adrenal up regulation clearly and all have similar side effects. Also, shows why PCOS and balding are related. They are the same diseases just in different genders. PCOS is adrenal up regulation in females leading to high androgens from DHEA. Also, PCOS presents with insulin resistance, and obesity which are side effects of excess cortisol, i.e. adrenal up regulation.

adrenal androgens PCOS:
The adrenal and polycystic ovary syndrome. - PubMed - NCBI

PCOS, IR, Obesity:
https://www.hindawi.com/journals/ijrmed/2014/719050/

adrenal gland volume in PCOS:
Adrenal gland volume assessed by magnetic resonance imaging in women with polycystic ovary syndrome - ScienceDirect
 

RedStaR

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Just because milk has IGF1 doesn't mean it will adjust the ratio. I think this is dependent on many different things in the body. I think its a little reductionistic to think like that in this situation and may get you in trouble logically, especially when the study is correlational at best and there are numerous controls on IGF1 in the body.

I highly doubt skull expansion is a direct issue for hair growth. It only becomes an issue when the galea is fibrosed and thus inelastic. The direct issues, I think, are fibrosis of the galea and decreased O2 to the scalp which effect the follicle chemically with DHT and all these other inflammatory mediators and responders (signals of the hypoxia and inflammation). Trying to understand baldness globally by looking at it street by street is just not going to work i.e. the map is not the territory to some extent. The perspective and thought process is just as important as the information.
I'm sure there is a study out there that measures dairy consumption (or milk to be specific) with serum IGF and IGFBP levels. That would be a step closer to finding out whether is it bad for hair or not.

Skull expansion is not a direct issue, but it's a contributor. Skull expansion is way up there on the pathway to a fibrosed galea, not the other way round.
 
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@RedStaR
I apologize I meant to say "in my opinion" after everything. I dont like the tone i responded to you.

Check these out for your IGF1:IGFBP:

Milk intake, circulating levels of insulin-like growth factor-I, and risk of colorectal cancer in men. - PubMed - NCBI

“Associations of Serum Insulin-like Growth Factor (IGF-I) and IGFBP-3 Levels Biomarker-Calibrated Protein, Dairy, and Milk Intake in the Women's Health Initiative”

Yes, it is a contributor, but i dont think its something to focus on. I would focus on loosening the galea to deal with the expansion as opposed to trying to stop the expansion. I think fibrosis of galea is the issue.
 

RedStaR

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@RedStaR
I apologize I meant to say "in my opinion" after everything. I dont like the tone i responded to you.

Check these out for your IGF1:IGFBP:

Milk intake, circulating levels of insulin-like growth factor-I, and risk of colorectal cancer in men. - PubMed - NCBI

“Associations of Serum Insulin-like Growth Factor (IGF-I) and IGFBP-3 Levels Biomarker-Calibrated Protein, Dairy, and Milk Intake in the Women's Health Initiative”

Yes, it is a contributor, but i dont think its something to focus on. I would focus on loosening the galea to deal with the expansion as opposed to trying to stop the expansion. I think fibrosis of galea is the issue.
I had no problems with the tone.

You can deal directly with the issue of fibrosis, like some people deal with hair loss using finasteride, but that still doesn't address some of the root issues. Skull expansion may not be an important variable, but it exists nonetheless, AND high IGF-1 levels may be an indicator to a more severe underlying issue. Long story short, if milk raises IGF levels, then it may well be inflammatory.
 
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@RedStaR
Thats why I recommend stopping the fibrosis by dealing with the cause of inflammation which I believe is in the gut. TLR4 activation directly leads to fibrosis. This is also why I recommeded changing the microbiome as opposed to inhibiting TLR4 with a drug and avoiding alcohol. As both endotoxin and alcohol are agonists. Did you read the initial post?

Both those studies show milk isnt raising the inflammation, atleast through the IGF-1 pathway (A1 milk in some people does increase inflammation tho, but not through IGF-1). Just because ice cream and shark attaks are correlated doesnt mean that eating ice cream directly leads to being attacked by a shark, the long and short story in the case u presented arent the same story. They are two completely differenr stories in my opinion.
 
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johnwester130

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There is no "cause" and "cure".

It's like cancer, a gradual decline in health and deterioration of the whole body.
 
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@johnwester130
There is a "cause" or impedus for that decline. Regardless, the definition and terminology in this respect isn't the importance of the thread. The importance is understanding the process or the "gradual decline" in order to stop it and reverse it.
 

johnwester130

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@johnwester130
There is a "cause" or impedus for that decline. Regardless, the definition and terminology in this respect isn't the importance of the thread. The importance is understanding the process or the "gradual decline" in order to stop it and reverse it.

so the cause of balding is............aging ?
 

RedStaR

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@RedStaR
Thats why I recommend stopping the fibrosis by dealing with the cause of inflammation which I believe is in the gut. TLR4 activation directly leads to fibrosis. This is also why I recommeded changing the microbiome as opposed to inhibiting TLR4 with a drug and avoiding alcohol. As both endotoxin and alcohol are agonists. Did you read the initial post?

Both those studies show milk isnt raising the inflammation, atleast through the IGF-1 pathway (A1 milk in some people does increase inflammation tho, but not through IGF-1). Just because ice cream and shark attaks are correlated doesnt mean that eating ice cream directly leads to being attacked by a shark, the long and short story in the case u presented arent the same story. They are two completely differenr stories in my opinion.
No I didn't. The studies didn't observe inflammation if I understand correctly. Circulating IGF-1 is lower in chronic inflammatory diseases, but I do not know if there is a correlation between inflammation and IGF ratios or free indices. I understand the logic, but if milk is raising IGF in blood, then either it's an inflammatory response, or simply from normal protein/mineral intake (depending on the significance of its magnitude). IGF-1 in tissue is good, but usually the opposite in serum, especially unbound.
 
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CLASH

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Depends on your definition, for me atleast.
Aging meaning increasing your time alive, then no.

Aging meaning increasing your bodies deterioration, then yes.

Increasing the amount of time you have been alive is not directly the same as increasing the amount of deterioration of the body. They are related but they are not the same.

Baldness is increasing the bodies deterioration rate which has a cause. The goal is to find out that cause, stop it and reverse it. I have presented hypothesis here. If you believe that baldness is directly caused just because you increase your time alive then I dont know if youll enjoy this thread.
 

REOSIRENS

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"By suppressing the thyroid and stimulating the pituitary's secretion
of prolactin, estrogen can have a variety of complex effects on hair growth;
usually, thinning of the hair on the head is a consequence of
hypothyroidism. In both men and women, loss of hair from the scalp is
associated with low thyroid, but "male pattern baldness" has been held to
be produced by a male hormone; but even the male hormones can be
turned into estrogen by enzymes in the skin, and experiments show that it
is estrogen which causes the hair follicle to become inactive, while an
estrogen-blacker can stimulate the renewal of hair. (R. C. Smart, et al.,
Proc. Nail. Acad. of Sciences, Oct. 29, 1996.)"

From pms to menopause book
Dr Raymond Peat
 

RedStaR

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"By suppressing the thyroid and stimulating the pituitary's secretion
of prolactin, estrogen can have a variety of complex effects on hair growth;
usually, thinning of the hair on the head is a consequence of
hypothyroidism. In both men and women, loss of hair from the scalp is
associated with low thyroid, but "male pattern baldness" has been held to
be produced by a male hormone; but even the male hormones can be
turned into estrogen by enzymes in the skin, and experiments show that it
is estrogen which causes the hair follicle to become inactive, while an
estrogen-blacker can stimulate the renewal of hair. (R. C. Smart, et al.,
Proc. Nail. Acad. of Sciences, Oct. 29, 1996.)"

From pms to menopause book
Dr Raymond Peat
That's flat-out wrong.
 
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