The Real Cause Of Hairloss ? Dht Still Bad. Its Not What You Think.

[Pixie]

I was doing research on HRT for hair loss a few weeks ago, and this article claimed regrowth is actually the result of reduced tension via muscular atrophy in the scalp.

https://perfecthairhealth.com/trans-hormone-replacement-therapy-hair-regrowth/

After reading that and seeing all the talk about skull size, scalp tightness and their effect on blood-flow, I made an observation on my own head:

I have much better muscular control on the left side of my scalp. I can flex it, move it forward, back and wiggle my ear. This also happens to be the side where my hair is more receded.

Maybe this is the case for some of you guys?

 

[jiggo]

This theory can easy be proven. Just take som follicles of balding areas and implant them in the back of the head, your arm or on your tits if it makes fun. If the hair still falls out, the theory is bullshit.

 

[Charlie Foxtrot]

I was doing research on HRT for hair loss a few weeks ago, and this article claimed regrowth is actually the result of reduced tension via muscular atrophy in the scalp.

https://perfecthairhealth.com/trans-hormone-replacement-therapy-hair-regrowth/

After reading that and seeing all the talk about skull size, scalp tightness and their effect on blood-flow, I made an observation on my own head:

I have much better muscular control on the left side of my scalp. I can flex it, move it forward, back and wiggle my ear. This also happens to be the side where my hair is more receded.

Maybe this is the case for some of you guys?

That’s interesting stuff man, although I must say it sounds a bit weird to me

For as long as I can remember, I’ve always been able to flex some parts of my head a little bit and wiggle my ears. I can’t flex the top part though.

I’m no medical genius but for me it would make more sense if it was the other way around. Like, if I had a really tight scalp it would be the reason of poor blood circulation to the follicle cause it’s so tight it’s being cut off a little.

And if this theory is true, any idea how to explain how people get results from blocking DHT alone?

 

[Jakejr]

The original post has a lot of theories. The twins observation I don’t fully comprehend. One on propecia on left has fuller hair, and healthier skin. The head shapes could be same. When you recede from hairline more skull is exposed, so it may only appear more oval. I dunno.. The fat loss or retention in the face is what kind of fat? DHT is a fat burner so cutting DHT does what again..
I noticed when I took anti-androgen supplements. My adult acne definitely improved. This is no joke. I surmise from less sebum production. Which some companies say is a contributing factor in hair loss..Anyways good discussion!

 

[EndlessPossibilities]

Thanks everyone who was open to my post with respective arguments and contributions

 

[Jakejr]

As I’ve said before I don’t know the exact cause or cure, but I said in another forum topic where the subject was microneedling & stiff scalp, that for me one thing I also noticed is my scalp on sides is flexible, but forehead & top is stiff/ tight as Fu$k. To nead & pinch that part of scalp I almost jam/dislocate my fingers. So maybe there is a calcification/fibrosis in those parts. So I read a researchers thoights in reversing this per medical studies. To summarize there are 4 ways to do this: 1) magnesium, I have a magnesium roll on and I roll it on my forehead & top. 2) Aspirin cuts inflammation
3Grapefruit Juice 4) Grapefruit peel.
I took a grapefruit & juiced it, then took juice and pulp & blended it for my drink. The studies didn’t reference grapefruit juice per se, just things like aspirigin, but the grapefruit is the source on bottles of specific supplements. So cheaper to make your own.
I can get more specific, but that’s the gist.
So you can try to break up fibrosis/ calcification with magnesium, grapefruit & peel,aspirin & one other thing after shampoo spray some white vinegar.
Massage, microneedling if you want.
Also BAT brown fat to increase..
Holy Basil, basil, oregano, ginger, Citrulline, Arginine. Also cold pads to scalp if you want.Whew that’s s lot. Trial & error

 

[Bigbone]

The original post has a lot of theories. The twins observation I don’t fully comprehend. One on propecia on left has fuller hair, and healthier skin. The head shapes could be same. When you recede from hairline more skull is exposed, so it may only appear more oval. I dunno.. The fat loss or retention in the face is what kind of fat? DHT is a fat burner so cutting DHT does what again..
I noticed when I took anti-androgen supplements. My adult acne definitely improved. This is no joke. I surmise from less sebum production. Which some companies say is a contributing factor in hair loss..Anyways good discussion!

Yeah, just because they're twins it doesn't mean that they will look exactly the same. There are other factors at play too, like body fat%. However, I won't deny a rise in estrogen might make it harder to lose weight or maybe even cause more water retention.

 

[igamblesowhat]

To increase brown fat in body there are many methods. Like exposure to cold... showers/temperature for extended periods. As I was writing this post, I came across an idea, I haven’t tried: putting a cooling ban/ pad on the scalp, as opposed to standing out in cold. Again I’m not an expert, but I would start with Citrulline. Citrulline is often paired with Arginine. So I have both. Bodybuilders take up to 20 grams Arginine. I started with 250 mg Citrulline & 750 mg Arginine. Since upped Citrulline to 2 grams. Arginine to 1.5 grams. One thing for sure my body is getting tighter. Excess white fat seems to be being replaced with some brown. My body looks more healthy & ripped rather than pudgy.
Also spices that increase brown fat: black pepper, basil, cinnamon, Holy Basil, oregano, because they increase Ursolic acid.
Apple peels also if you eat apples & blueberries.
Hope it helps

I believe there is a study floating around about staying in 63F ambient temp for ~6h a day is enough to induce ones body to produce a measurable increase in brown fat. Don't quote me on that, but it is what I recall from Wim Hof aka, The Iceman. He has broken damn near every world record for withstanding cold, climbed mountains in just a pair of shorts, swam under the ice in the Arctic until his retinas froze, etc. And unfortunately, he still suffers from a male pattern baldness

 

[Mandar kumthekar]

Brown fat induces angiogenesis means new blood vessels. So increasing brown fat is good for hair. The whole approach should be reducing scalp tension, draining clogged dht and taking nutrition rich to hair.

 

[Arrade]

Brown fat induces angiogenesis means new blood vessels. So increasing brown fat is good for hair. The whole approach should be reducing scalp tension, draining clogged dht and taking nutrition rich to hair.

DHT doesnt get clogged it's a hormone

 

[Mandar kumthekar]

DHT doesnt get clogged it's a hormone

I mean excess dht that is waiting in hair bulb.

 

[igamblesowhat]

I believe there is a study floating around about staying in 63F ambient temp for ~6h a day is enough to induce ones body to produce a measurable increase in brown fat. Don't quote me on that, but it is what I recall from Wim Hof aka, The Iceman. He has broken damn near every world record for withstanding cold, climbed mountains in just a pair of shorts, swam under the ice in the Arctic until his retinas froze, etc. And unfortunately, he still suffers from a male pattern baldness

Found a study from 1961: http://jap.physiology.org/content/16/6/1011

Synopsis:

Month-long study, a U.S. Army researcher exposed 10 nude men to temperatures in the low 50s for eight hours a day. Not surprisingly, the poor study subjects did a lot of shivering—which is the body’s quick-fix way to generate heat. But by day 14, the men had mostly stopped shivering, and their bodies seemed to be making heat some other way.

Today, experts understand that special heat-producing fat cells—known as “brown fat”—deserve the credit for our ability to acclimatize.

 

[Arrade]

I was doing research on HRT for hair loss a few weeks ago, and this article claimed regrowth is actually the result of reduced tension via muscular atrophy in the scalp.

https://perfecthairhealth.com/trans-hormone-replacement-therapy-hair-regrowth/

After reading that and seeing all the talk about skull size, scalp tightness and their effect on blood-flow, I made an observation on my own head:

I have much better muscular control on the left side of my scalp. I can flex it, move it forward, back and wiggle my ear. This also happens to be the side where my hair is more receded.

Maybe this is the case for some of you guys?

Perhaps instead of loosening the muscle it is loosening the calcium deposits in the scalp?

"“baldness occurred in people where calcification of the skull bones apparently not only firmly knitted the cranial sutures but also closed or narrowed various small foramens through which blood vessels pass“. He thought this would also explain why men suffer baldness more than women, since bone growth or calcification is generally greater in males than females"

https://tmdocclusion.com/home/connection-to-other-diseases-and-syndromes/hair-loss/

 

[Arrade]

The confirmation of this explanation for hair loss can be found in several studies:

• Bald subjects had a positive response when injected with Botox into the muscles surrounding the scalp, including frontalis, temporalis, periauricular, and occipitalis muscles. Conceptually, Botox “loosens” the scalp, reducing pressure on the perforating vasculature, thereby increasing blood flow and oxygen concentration. This leads to reduced hair loss and new hair growth [21].
• The subcutaneous blood flow in the scalp of patients with early male pattern baldness is much lower than the values found in the normal individuals [22].
• Men suffering from androgenic alopecia have significantly lower oxygen partial pressure (meaning microvascular insufficiency and hypoxia) in the areas of their scalp affected by balding (frontal and vertex regions) versus unaffected areas (temporal and occipital regions). Moreover, balding men have significantly lower oxygen partial pressure in the areas of balding scalp than the same areas of non-bald people [23].
• It has been found that Minoxidil solution stimulates the microcirculation of the bald scalp, effectively promoting hair growth [24].
• By relieving tension at the vertex in the scalp, cutaneous blood flow rate increases, promoting hair regrowth [25].
• Minoxidil is less effective in subjects with significant inflammation in the scalp than in subjects with no significant inflammation [26].
• In women, significant degrees of inflammation and fibrosis is present in cases of androgenetic alopecia. Even if less significant, inflammation and fibrosis is present also in chronic telogen effluvium cases[27].
• Dr. Frederick Hoelzel of Chicago reported the observations he made in 1916-17 while he served as a technician in gross anatomy at the College of Medicine of the University of Illinois. During that time, he removed the brains of around 80 cadavers and noticed an obvious relation between the blood vessel supply to the scalp and the quantity of hair: “baldness occurred in people where calcification of the skull bones apparently not only firmly knitted the cranial sutures but also closed or narrowed various small foramens through which blood vessels pass“. He thought this would also explain why men suffer baldness more than women, since bone growth or calcification is generally greater in males than females [28].

 

[Arrade]

The confirmation of this explanation for hair loss can be found in several studies:

• Bald subjects had a positive response when injected with Botox into the muscles surrounding the scalp, including frontalis, temporalis, periauricular, and occipitalis muscles. Conceptually, Botox “loosens” the scalp, reducing pressure on the perforating vasculature, thereby increasing blood flow and oxygen concentration. This leads to reduced hair loss and new hair growth [21].
• The subcutaneous blood flow in the scalp of patients with early male pattern baldness is much lower than the values found in the normal individuals [22].
• Men suffering from androgenic alopecia have significantly lower oxygen partial pressure (meaning microvascular insufficiency and hypoxia) in the areas of their scalp affected by balding (frontal and vertex regions) versus unaffected areas (temporal and occipital regions). Moreover, balding men have significantly lower oxygen partial pressure in the areas of balding scalp than the same areas of non-bald people [23].
• It has been found that Minoxidil solution stimulates the microcirculation of the bald scalp, effectively promoting hair growth [24].
• By relieving tension at the vertex in the scalp, cutaneous blood flow rate increases, promoting hair regrowth [25].
• Minoxidil is less effective in subjects with significant inflammation in the scalp than in subjects with no significant inflammation [26].
• In women, significant degrees of inflammation and fibrosis is present in cases of androgenetic alopecia. Even if less significant, inflammation and fibrosis is present also in chronic telogen effluvium cases[27].
• Dr. Frederick Hoelzel of Chicago reported the observations he made in 1916-17 while he served as a technician in gross anatomy at the College of Medicine of the University of Illinois. During that time, he removed the brains of around 80 cadavers and noticed an obvious relation between the blood vessel supply to the scalp and the quantity of hair: “baldness occurred in people where calcification of the skull bones apparently not only firmly knitted the cranial sutures but also closed or narrowed various small foramens through which blood vessels pass“. He thought this would also explain why men suffer baldness more than women, since bone growth or calcification is generally greater in males than females [28].

 

[BalderBaldyBald]

How did this concept evolve?

The understanding of the hair follicle biology over the last 20 years established the fundamental role of the mesenchyme derived dermal papillae in the maintenance of the hair growth, with the multipotent epithelial stem cells at the bulge giving rise to proliferation and differentiation. [14],[15],[16],[17] Other autocrine, paracrine factors and signaling pathways are also involved in this cross-talk between the dermal papillae and the hair follicle stem cells. [16],[18],[19]

Testosterone and other weaker androgens such as dehydroepiandrosterone and androstenedione are metabolized in many skin tissues. Testosterone can freely penetrate the cell membrane and is converted in the cytoplasm to dihydrotestosterone (DHT) by 5 α reductase (mainly Type II). The DHT strongly binds to androgen receptor (AR) and this complex is translocated to the nucleus, helped by the AR co activators. This results in target gene transcription and finally translation into genes which exert biological activity. [20],[21],[22]

The cross-talk between the dermal papillae and the hair follicle cells which unfolds under the influence of androgens result from the secretion of many factors from the dermal papillae. These have autocrine effect on the dermal papillae itself and paracrine effect on the hair follicle epithelial cells. [23] These factors include growth factors like Insulin like growth factor (IGF-1), basic fibroblast factor (bFGF), vascular endothelial growth factor (VEGF); and cytokines like transforming growth factor beta 1 (TGFβ 1), interleukin 1 alpha (IL -1α) and tumor necrosis factor alpha (TNF α). [24],[25],[26]

Why do people go bald in Androgenetic Alopecia?

Many of the studies have accepted the role of androgens and the interplay between the dermal papillae and hair follicle as the critical processes involved in miniaturization of hair follicles.

The concentration of DHT along with 5 α reductase and androgen receptors are increased in the balding scalp. [27],[28] The other enzymes involved in conversion of weak androgens to potent androgens are 3 β hydroxysteroid dehydrogenase (3 β HSD) and 17 β hydroxysteroid dehydrogenase (17 β HSD) also show increased activity in Androgenetic Alopecia. [29] The higher the concentration of androgen and androgen receptor, more the effect on expression of genes which control follicular cycling.

The signaling which follows at the dermal papillae and hair follicle interface in balding person results in premature termination of anagen associated with premature entry into catagen. Catagen occurs as a consequence of decreased expression of anagen maintaining factors, such as the growth factors- IGF-1, bFGF and VEGF. Also, an increased expression of cytokines (TGFβ 1, IL -1α and TNF α) promotes apoptosis. [30] Recently, DKK-1 is found to be up regulated gene by DHT, resulting in inhibition of outer root sheath cells and triggering apoptosis. [31]

Another recent advance is identification of the critical role of Wnt/β catenin signaling pathway in the maintenance of the DPC inductive properties required for hair follicle regeneration and growth of the hair shaft. [32] The androgens and ligand activated AR can negatively influence the Wnt/β catenin signaling pathway. [33] The androgens hamper the pathway by increasing the glycogen synthase kinase (GSK 3β) expression. [34]

The exact roles and processes related to hair follicle stems cells in Androgenetic Alopecia are not clear. It is considered that while KRT15(hi) stem cells are maintained in bald scalp, there is a defect in conversion of hair follicle stem cells to CD200-rich and CD34-positive progenitor cells, both of which are needed to maintain proper follicular activity. [35]

When do people go bald?

Androgenetic alopecia (Androgenetic Alopecia) is a multifactorial disorder caused by interactions between several genes and environmental factors.

Genes involved in Androgenetic Alopecia: A polygenic mode of inheritance is established due to the high prevalence and the wide range of expressed phenotypes in Androgenetic Alopecia. The genes influence predisposition through DNA sequence variations- single nucleotide polymorphisms, microsatellite repeats, insertion mutations, deletion mutations and copy number variations; or epigenetic modifications such as X chromosome inactivation, hypermethylation (switch off gene expression) or hypomethylation (switch on gene expression) of DNA in gene promoter regions. [36],[37]

The two major genetic risk loci are the X chromosome AR/EDA2R locus and the PAX1/FOX A2 locus on chromosome 20. Recent studies indicate HAD C9 locus on chromosome 7 as a new susceptibility locus. [38],[39],[40],[41]

The androgen receptor gene: The androgen receptor determines the sensitivity of cells to androgen. The AR gene regulates the potency of androgen available to the hair follicle. Of the many AR gene polymorphisms known, the Stu 1 polymorphism has the most significant association with Androgenetic Alopecia. [42]

Several other genes where associations could not be proved conclusively include 5α reductase, aromatase, estrogen receptor α and IGF-2 genes. The role of Y chromosome needs further comprehensive examination of the genome. [43]

Hair follicle inflammation and environmental factors: The implication of follicular inflammation has been brought out by several studies. The process is slow, subtle and indolent unlike the inflammatory and destructive process in the classical scarring alopecia. Microbial toxins related to Propionibacterium sp., Staphylococcus sp., Malassezia sp., or Demodex could be involved in generation of inflammatory response. [44] Alternatively, keratinocytes may respond to chemical stress from irritants in cosmetics and grooming agents, pollutants and actinic damage as in UV irradiation by producing radical oxygen species and nitric oxide. [45]

 

[BalderBaldyBald]

Medical Treatment


Minoxidil

The exact mechanism of action of minoxidil has not been elucidated. Minoxidil is converted to minoxidil sulphate, the active form of the drug which opens ATP-sensitive potassium channels in cell membranes, leading to a vasodilatory effect. While vasodilatation could be one of the possible mechanisms of action, other more important actions of minoxidil on the hair follicles have been suggested including - increased expression of vascular endothelial growth factor (VEGF) mRNA in the dermal papillae, activation of cytoprotective prostaglandin synthase-1, an enzyme that stimulates hair growth and increased expression of hepatocyte growth factor (HGF) m-RNA which is another hair growth promoter. Important recommendations stemming from the meta-analysis by Blumeyer et al., [69] included: Topical 2% and 5% minoxidil solution, 1 ml applied twice daily is effective to prevent progression and improve Androgenetic Alopecia in males above 18 years. The 5% solution is more effective and the standard formulation (with propylene glycol) is preferred as there is no sufficient evidence for other preparations like the foam preparation or higher concentrations. The response to treatment should be assessed ideally at the end of six months. In female patients there is no sufficient data to recommend the 5% minoxidil solution instead of the 2% solution. Patients should be informed of telogen shedding which is usually seen in the first 8 weeks of therapy. [69] Different studies have shown conflicting results with combination therapy of minoxidil with tretinoin. [70],[71] The most common side effect of topical minoxidil is hypertrichosis. Irritant and allergic contact dermatitis may also occur. Irritation is more common with the 5% solution due to its higher propylene glycol content. [69]

5 alpha reductase inhibitors

The enzyme 5-alpha-reductase converts testosterone to its active form dihydrotestosterone (DHT) and inherited sensitivity of the hair follicles to DHT is one of the etiological factors in Androgenetic Alopecia. Two types of 5-alpha-reductase are seen in humans. Type I is seen mainly in the liver, skin and scalp while type II predominates in prostate, genitourinary tract and the hair follicle.

Two drugs inhibiting the 5-alpha-reductase used in Androgenetic Alopecia are finasteride which is a type II 5-alpha-reductase-inhibitor, and dutasteride, which inhibits both type I and type II 5-alpha-reductase.

Important recommendations based on the meta-analysis by Blumeyer et al., [69] include:

Oral finasteride 1 mg a day is recommended to improve or to prevent progression of Androgenetic Alopecia male patients above 18 years with mild to moderate Androgenetic Alopecia. The response to treatment should be assessed at 6 months, although in some men it may not become evident until 12 months. Oral dutasteride 0.5 mg a day is another option, but sufficient studies are not available which compare its efficacy to finasteride. There are fewer studies related to the use of finasteride in female patients. Finasteride is contraindicated in pregnancy. Rare adverse effects reported include gynecomastia, reduced libido and erectile dysfunction. Finasteride also reduces PSA level. If treatment is started after the age of 45 years, monitoring of PSA level should be considered. The PSA levels should be double to compensate the reduction due to finasteride, resulting in an interpretation of the test remaining accurate. [69]

Studies have shown that it is not effective in post-menopausal females. It is contraindicated in pregnancy. Topical finasteride is not effective for Androgenetic Alopecia. [69] Studies in both humans and animals have shown that the combination of minoxidil 2% and finasteride 1 mg is superior to finasteride or minoxidil mono-therapies. [72],[73] Combining hair transplant with finasteride is also considered more effective than hair transplant alone. [74]

 

[BalderBaldyBald]

Miscellaneous Treatments


Though not evidence based, a number of other treatment modalities have been tried in Androgenetic Alopecia. [69] Some of the mechanisms by which these alternative drugs work include: Promotion of hair regrowth by activation of the dermal papillae leading to induction of anagen hair re-growth (Iron supplements, millet seeds, Ginkgo Biloba, Aloe vera, hibiscus, retinoids, cyclosporine), improving the perifollicular vascularization (prostaglandin analogues like latanoprost, aminexil, mesotherapy, benzyl nicotinate, beta-sitosterol), hormonal effects like inhibition of 5-alpha-reductase (polysorbate, green tea, ketoconazole, saw palmetto extract), anti-inflammatory activity (zinc pyrithione, corticosteroids) and improvement of hair follicle nutrition (vitamin supplements, trace elements). [69]

Other topical applications which have been used in Androgenetic Alopecia, but are not supported by sufficient evidence include - carpronium chloride, t-flavanone, adenosine, Cytopurine/pentadecane and cepharanthine. [84]

 

[BalderBaldyBald]

In other words

NO

 

[Baldingbob123456]

Very interesting and logically supported... just not scientifically supported. There still needs to be studies but the logic i think warrants it. I also believe head shape has something to do with it. Not sure if youve noticed but balding people tend to have wider top of their heads. like wider from the eyes up. i believe this may stretch the skin and compress down down blood vessels (or brown fat) and cause them to atrophy and disappear from the constant pressure. It also makes sense that brown fat would cause hair growth in the sense that brown fat is used as a thermoregulator. You'd expect people who live in colder climates to have more brown fat and more body hair. You'd also expect them to have more brown fat on their scalp and thus more hair on their scalp (following your logic) as this would protect against harsh cold and heat loss from the scalp. Do cold showers actually have evidence to support brown fat production? Ive heard that they have benefits to hairloss but that might have been debunked. If not the two would support each other. More brown fat from cold showers =less hair loss