DWAT: Dermal White Adipose Tissue Hypothesis

[balda]

There is a hypothesis that hairloss (or better say hairfreeze) caused by surrounding dermal white adipose tissue (dwat) issues.

Possible adipose tissue issues are:
- fibrosis of adipose tissue: adipocyte-myofibroblasts transitions (amt), check the illustration
- regression of adipose tissue: over-lipolysis of adipocytes
- under-production of adiponectin

What do you think about this?
Do you know any scientists who work on dwat-related therapies?

PS.
more details and references to scientific sources could could be found on reddit:

https://www.reddit.com/r/tressless/comments/kh7gn5

 

[TheHawk]

Reminds me of the pig lard study:

https://cltri.gov.in/Pugazhendan/Beneficial%20Effect%20of%20Lard%20in%20Androgenic%20Alopecia.pdf

I’m gonna put organic pig lard on my scalp. I did a night ago. Again tonight.

I just to need to get in a rhythm.

I have a lot in my regimen topical and internal right now.

 

[balda]

@TheHawk that's funny )

if it's legit, would be nice to know how it works.
basically, the "dwat" hypothesis assumes, that remedies are supposed to have any of these properties:
- adipogenic
- antifibrotic
- antiandrogenic (optional)

so, which one is present in the "lard"?

 

[TurboFixer]

@pegasus2 care to comment on this?

 

[TheHawk]

@TheHawk that's funny )

if it's legit, would be nice to know how it works.
basically, the "dwat" hypothesis assumes, that remedies are supposed to have any of these properties:
- adipogenic
- antifibrotic
- antiandrogenic (optional)

so, which one is present in the "lard"?

Gotta be adipogenesis right?


No more lipolysis.

I’m reading on brown fat in the scalp too.

Beta-lapachone may help brown the fat.

Beta-lapachone activates brown fat cells - Beta-Lapachone.com

What is brown fat (brown adipose tissue) ? Beta-lapachone and brown fat cell targeting offers great hope for those struggling with age related diseases. The adipose organ in mammals is composed of both white and brown adipose tissue. Brown adipose tissue, or BAT, is especially present in newborn...

www.beta-lapachone.com

 

[pegasus2]

@pegasus2 care to comment on this?

This is not a new theory. Even though women have more estrogen they still have skin atrophy as they age and adipose degeneration. It impacts hair quality, but doesn't cause hair loss as you can see on women and occipital scalp. The reason hair on the top of the head loses more adipose tissue than occipital scalp is because it doesn't have hair, not vice versa. A healthy cycling hair promotes adipogenesis. After your hair is gone or miniaturized the adipose layer stops regenerating as before.

 

[balda]

@pegasus2
about what goes first "dwat" or "follicles":

That's basically the key point of the hypothesis, proposing "opposite" causation: "Meanwhile some of the latest research findings indicate that DWAT plays a very important role in skin properties and that hairs depend on it, not vice versa."

Imho, approach to treat hair follicles is a dead end! To continue that way we can only expect to postpone (with anti-androgens) the loss and temporarily pump (minoxidil, etc) the growth.

So the new hypothesis says, that no reason to stimulate or to recreate hair follicles. They will not grow without proper environment - healthy dermal adipose tissue, DWAT. Yes, it fluctuates with hair cycles, but if it's damaged enough, ie fibrotic or diminished, the cycling stops. Androgens and some other factors damage adipose tissue, not hair follicles.

 

[balda]

@pegasus2
about women alopecia:

Women can experience Androgenetic Alopecia. I saw it by myself, for old women (75+ yo) with specific hormonal profile. It's kind of mild Androgenetic Alopecia. It's not like more common type of women alopecia caused by thyroid or adrenal issues.

Lack of oestrogens or some other factors lead to DWAT thinning, not fibrosing. Important! Potentially only androgens, in case of high level of androgen receptor expression in the dermal adipose tissue, able to cause fibrosis. In contrast to thinning (lipolysis), scarring (fibrosis, see adipocytes myofibroblast transition) cannot be reverted easily with hormonal correction or other DWAT stimulation (adipogenic remedies, oral or topical). It hypothetically requires myofibroblast reverting stuff (antifibrotic remedies, topical). Scientists says it's possible to (see iinks in the original post).

 

[balda]

Fibrosis is a separate issue

New researches say it's probably the issue too. There are two issues: lipolysis and fibrosis. The references could be checked in my original post: "The Big Fat Layer" on reddit.

 

[pegasus2]

Lipolysis isn't an issue. Fibrosis isn't causal, but might be involved in limiting the ability of hairs to fully regenerate after they are long gone.

 

[balda]

There is no such thing as "follicle regeneration". Follicles structure isn't affected during balding. They are just "blocked", not getting metabolites. Cause of "lipolysed" and "fibrosed" environment, ie damaged dermal adipose tissue.

Stimulating hair, instead of restoring/preserving the environment is a dead end. That's why even good "conventional treatment" responders get so crappy results.

Well, will not repeat it again, just wanted to clarify the key points of the hypothesis.


PS.
By the way, one more observation. Children hairs usually "spread" with speed and pattern related to its quality in adulthood. Children with prone to agressive balding genes have pretty slowly popping up hairs. Usually with the pattern reminding future hair loss. Why? Hypothetically, that's because of genetically predisposed dermal white adipose tissue properties.

PPS.
Frequently mentioned WNTb has potential too, as It modulates dwat (not sure it has antifibrotic properties, but adipogenic properties for sure ). Check a research: "When the Wnt pathway was activated in the embryonic epidermis, there was a dramatic and premature increase in adipocytes in the absence of hair follicle formation, demonstrating that Wnt activation, rather than mature hair follicles, is required for adipocyte generation.

 

[pegasus2]

There is not such thing as "follicle regeneration". Follicles structure isn't affected during balding. They are just "blocked", not getting metabolites. Cause of "lipolysed" and "fibrosed" environment, ie damaged dermal adipose tissue.

This is simply not true.

 

[balda]

Gotta be adipogenesis right?


No more lipolysis.

I’m reading on brown fat in the scalp too.

Beta-lapachone may help brown the fat.

Thanks. Would be interesting to find researches on how it affects dermal adipose tissue specifically. If i get it right, brown fat located deeper and relates to subcutaneous layer or hypodermis. Which is good for skin elasitcity, but seems doesn't helpful for hair follicles.

 

[balda]

Going to post scientific statements and possible remedies related to dermal white adipose tissue here in this thread.

"Functional analysis of adipocyte lineage cells in mice with defects in adipogenesis and in transplantation experiments revealed that intradermal adipocyte lineage cells are NECESSARY and SUFFICIENT to drive follicular stem cell activation."

 

[balda]

The second part of the "The Big Fat Layer" hypothesis description. Some possible remedies are listed there:

https://www.reddit.com/r/tressless/comments/knzj2j

 

[balda]

"Dermal adipocytes and their progenitors actively signal to neighbouring skin cell types, including hair follicle cells, and become important MODULATORS of their growth activities."
https://www.nature.com/articles/nrendo.2017.162

 

[balda]

Some hair transplantologists think in the right direction too (not just cashing out the hair trans hype):
"It presents the question of whether it is possible to INDUCE follicle entry into ANAGEN (growth phase) BY transplanting ADIPOSE derived stem cells into bald scalp."

 

[balda]

No healthy adipose tissue -> No metabolites (incl. adiponectin) -> No hair cycling/growth:

"Adiponectin (APN), released mainly from adipose tissue, is a well-known homeostatic factor for regulating glucose levels, lipid metabolism, and insulin sensitivity. A recent study showed that human hair follicles express APN receptors and the presence of APN-mediated hair growth signaling, thereby suggesting that APN is a potent hair growth-promoting adipokine."

 

[Armando Jose]

"follicle regeneration". Follicles structure isn't affected during balding

"follicle regeneration" and follicles structure is affected during each natural hair follicle cycle.

In your opinion, have DWAT relation to sebaceous gland?

 

[balda]

@Armando Jose
Follicles structure: if it changes irreversibly (!) during balding, would be interesting to check such researches. Temporal changes, like resizing or adding/removing some cell types, during specific hair growth stage is not a point. As it could be healthy, not pathogenic, process for follicles. Such fluctuations are not supposed to be linked to balding issues.

Sebaceous gland: haven't investigated yet. Just haven't came across possible glands issues affecting DWAT or HF functioning.