Will there be a cure for baldness by 2030 according to you?

[pegasus2]

Women don't lose hair at the temples. They lose it in the center. So much for proximity theory

 

[farnsworth]

Women don't lose hair at the temples. They lose it in the center. So much for proximity theory

The proximity theory has been seen in all animal and human models. It is not a theory but the empirical observation on transplants and regrowth patterns which requires significant coordination of hair cycles, this is the efficacy of prolactin. There is a recent study where they attempt a single human hair stem cell transplant in a murine model without success. But the minimum addition of 3 produces growth.

I have a theory to women hairloss which explains that but I’m not interested enough in the research to verify it. What is true is that 5AR inhibition is far less effective with Androgenetic Alopecia in women than men. Additionally, unlike men, the dht levels of women experiencing Androgenetic Alopecia is not significantly different than those without.

 

[farnsworth]

MPC inhibition causes a build up of Pyruvate in the cell. What do you think about using Pyruvate topically?

Will not work. MPC or lack thereof is an intracellular process. The goal is to prevent the conversion into glucose and instead allow lactate production.

 

[pegasus2]

Your theory was already tried by Follicum without success. Do you have any sources for anything you say? You're making a lot of factual assertions with nothing to back them up. I'll humor you and pretend you actually addressed the point about fphl. What about men? Why does our hair on the side not recede from front to back also, and why do some men not recede? According to your theory Androgenetic Alopecia should be nothing but straightline recession, and bald spots should not exist

while murine pelage HFs synchronize their cycles and grow in coordinated domains (Plikus et al., 2011; Plikus et al., 2008), human scalp HFs cycle asynchronously

A guide to studying human hair follicle cycling in vivo

Hair follicles (HFs) undergo life-long cyclical transformations, progressing through stages of rapid growth (anagen), regression (catagen), and relative “quiescence” (telogen). Since HF cycling abnormalities underlie many human hair growth ...

www.ncbi.nlm.nih.gov

 

[farnsworth]

Your theory was already tried by Follicum without success. Do you have any sources for anything you say? You're making a lot of factual assertions with nothing to back them up. I'll humor you and pretend you actually addressed the point about fphl. What about men? Why does our hair on the side not recede from front to back also, and why do some men not recede? According to your theory Androgenetic Alopecia should be nothing but straightline recession, and bald spots should not exist

A guide to studying human hair follicle cycling in vivo

Hair follicles (HFs) undergo life-long cyclical transformations, progressing through stages of rapid growth (anagen), regression (catagen), and relative “quiescence” (telogen). Since HF cycling abnormalities underlie many human hair growth ...

www.ncbi.nlm.nih.gov

I do! I cannot post links as described in my original post. If you notice I kept my footnote indications, I did so to provide them in the future.

Men have higher follicular density on the center forehead than the lateral. Please read the original post. Hair should recede in the temples first and then around those areas as follicular density diminishes. Hair loss should also be an accelerating process. Follicular density is less on the crown than it is on the center forehead.

As per Follicum, osteopontin has nothing to do with Androgenetic Alopecia or any of the mechanisms I’ve described.

My background is Cellular Control Theory. Cellular processes are messy and economic. Nonetheless we see that despite being independently driven:

the vast majority of asynchronously cycling HFs in healthy human scalp are considered to be in anagen (80–90%)

 

[Dar]

So you're on this forum just to tell the rest of us we have nothing to hope for?

There is always hope. But people also need to have REALISTIC expectations.

 

[coolio]

According to your theory Androgenetic Alopecia should be nothing but straightline recession, and bald spots should not exist

His theory incorporates the follicles having a genetic susceptibility to 5ar. The inherited patterns & severity of loss would be rooted in that.

 

[farnsworth]

I don't know about you, but I've always had lower density around the ears yet it never receded there. Men also have higher follicular density at the crown than the hairline, yet I lost my crown before my hairline. Hmm..

You might want to learn what osteopontin does. The whole point is to increase pyruvate uptake to the cell. Anyways, you're not first with this theory, it's been around forever so I'm not wasting more time on it. Just going to tell you unequivocally that it won't reverse Androgenetic Alopecia.

Increasing pyruvate uptake to the cell should exacerbate hairloss or at best do nothing.

Male side burns are usually androgenetic.

Skeptical on the non-novelty considering the research to have this theory in ensemble came out in 2021.

Alright good luck.

 

[ChemHead]

yet I lost my crown before my hairline. Hmm..

Hmmmmmmmmm

 

[Baeyer]

Increasing pyruvate uptake to the cell should exacerbate hairloss or at best do nothing.

Male side burns are usually androgenetic.

Skeptical on the non-novelty considering the research to have this theory in ensemble came out in 2021.

Alright good luck.

Pls respond to my pm sir.

 

[pegasus2]

Increasing pyruvate uptake to the cell should exacerbate hairloss or at best do nothing.

Male side burns are usually androgenetic.

Skeptical on the non-novelty considering the research to have this theory in ensemble came out in 2021.

Alright good luck.

I'm not talking about sideburns wtf?

 

[farnsworth]

That's not his theory. His theory is proximity, but whatever. I don't have time for this half-baked sh*t. Another moronic theory that is going to get all the suckers drooling. What a wasteland this website has become.

No that is my theory, proximity is your strawman. It’s an ensemble theory the majority of the mechanism of hairloss has nothing to do with proximity.

 

[pegasus2]

No that is my theory, proximity is your strawman. It’s an ensemble theory the majority of the mechanism of hairloss has nothing to do with proximity.

So your theory is dht causes hair loss? Great! What an incredible breakthrough you've discovered. I can't believe nobody ever noticed this before

 

[Baeyer]

So your theory is dht causes hair loss? Great! What an incredible breakthrough you've discovered. I can't believe nobody ever noticed this before

Strongest of argument bro.

 

[pegasus2]

I'm supposed to believe that a guy who can't figure out how to get around a link ban solved male pattern baldness

 

[scientist_0005]

The proximity theory has been seen in all animal and human models. It is not a theory but the empirical observation on transplants and regrowth patterns which requires significant coordination of hair cycles, this is the efficacy of prolactin. There is a recent study where they attempt a single human hair stem cell transplant in a murine model without success. But the minimum addition of 3 produces growth.

I have a theory to women hairloss which explains that but I’m not interested enough in the research to verify it. What is true is that 5AR inhibition is far less effective with Androgenetic Alopecia in women than men. Additionally, unlike men, the dht levels of women experiencing Androgenetic Alopecia is not significantly different than those without.

you mean something like paracrine signaling from nearby healthy populations is required to secure survival and inductivity?

 

[scientist_0005]

i wonder if there is some grand unified theory of male pattern baldness. of course there is many things we do not know but some pathways have been indentified but other things about the nature of it are really hard to grasp and the current literature does not give too much insight on that at all.

 

[DuncanOP]

Note: It looks like I can't post sources or post a separate thread. I'm not going to wait for a moderator to provide that permission.

This is a quick discussion, I am a very busy person. I will post some of my research but not all of it in the interest of time. I have almost cured my Androgenetic Alopecia to baseline, I will not recommend the materials to do so because of legal precariousness, but they've each been discussed throughout the forums at least in a speculative capacity. It is this ensemble of these materials which cures Androgenetic Alopecia.

Anything you do is at your own risk and this is in no way a recommendation.

The explanation anticipates all and every symptomatic facet of Androgenetic Alopecia hairloss.

There are two major causes of the symptoms of Androgenetic Alopecia, the first is namely 5AR sensitivity about the follicles, and the hormones which are aromatized into DHT. DHT kills follicles by triggering Mitochondrial Pyruvate conversion (MPC) [6]. Lack of lactate production has recently been shown to determine the quiescence of the stem cells (note: the mere addition of lactate will not help Androgenetic Alopecia).

This quiescence of the stem cells leads to the eventual demise of the follicle by preventing replenishment of the follicle by a mechanism discussed below.

The second is evinced by the question which remains, why does a 5AR-inhibitor or otherwise DHT removal not trigger complete rejuvenation of the follicle given that the stem cell exists quiescently? The answer is that a single stem cell follicle itself is unable to signal strongly enough to receive the prolactin/17b-estradiol and other chemicals to participate in the hair cycle, which on trigger switches on MPC inhibition. What is needed is a collection (read density) of follicles (even if fully miniaturized!) to be fully synchronized, this can only happen if each stem cell remains in cycle with each other, where they solicit participation of the next hair cycle [1,2,3,4].

This is why single hair follicle transplants fail and why a minimum density of follicles is required. Additionally, this is why grafts only succeed in adjacency to healthy hair, while regrowth will always occur starting from the adjacent hairs.

Finally, this is why hairloss often begins at the temple which has half the density of follicles than everywhere else on the head [7]. As stem cells become dysfunctional, it becomes more difficult for adjacent cells to participate in the next hair cycle. That is, hairloss is an exponential process, accelerating on each new cycle.

The goal of Androgenetic Alopecia prevention and rejuvenation of quiescent cells is to then allow hairs to synchronously begin and maintain a hair cycle. This is where the efficacy of lactate hydrogenase medicine (e.g. minoxidil, but it should be clear though that this is not enough if the follicle is DHT treated or otherwise not in cycle) and 5AR inhibition occurs.

Cool. I will wait for your post with more details about it in the future.
I don't see any reason or logic to this explanation be fake. It is too much work to mean nothing.

You've earned a vote of confidence. And I think other people too.

Thanks.

 

[pegasus2]

No that is my theory, proximity is your strawman. It’s an ensemble theory the majority of the mechanism of hairloss has nothing to do with proximity.

Proximity theory is the only thing I see here that is new, and it's complete bunk, but if that's a strawman let's move on. LDH theory of stem cell activation has been around for years https://www.nature.com/articles/ncb3575 The problem is this isn't where the defect lies in Androgenetic Alopecia, stem cells don't need to be activated they have to be converted to progenitor cells and they aren't. How does modulating lactate and/or pyruvate accomplish this? https://www.jci.org/articles/view/44478

This drug you're using for Pelage will probably increase the rate of hair growth by increasing the efficiency of the progenitor cells that you do have, but it won't replenish the population of progenitor cells, and thus won't reverse hair loss to a large degree. I can't even how many threads I've seen on here for new ways to activate HFSCs. None of them worked to reverse Androgenetic Alopecia.

" CD34+ (CD34 antigen) stem cells activate inflammatory response programs and start dividing. Pharmacological attenuation of inflammation inhibits CD34+ cell proliferation. Subsequently, the Wnt pathway controls the recovery of Lgr5+ cells and inhibition of Wnt signalling prevents Lgr5+ cell and hair germ recovery. Thus, our study uncovers a compensatory relationship between two stem cell populations and the underlying molecular mechanisms that enable hair follicle regeneration."

Stem cell plasticity enables hair regeneration following Lgr5+ cell loss - PubMed

Under injury conditions, dedicated stem cell populations govern tissue regeneration. However, the molecular mechanisms that induce stem cell regeneration and enable plasticity are poorly understood. Here, we investigate stem cell recovery in the context of the hair follicle to understand how two...

pubmed.ncbi.nlm.nih.gov

 

[Janks16]

Let's hope that something good happens for all of us.