NLRP3 Inflammasome Cause Of Male Pattern Baldness

LeeLemonoil

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@Mauritio

Dont wsste ur time. Wont do anything. There is a master regulator of whats going on in mpb. Unless the root os addressed. Very few things can hijack the process
That’s wrong in regards to Klotho.
If one were to fictively modulate Klotho and what it influences in MPB tissue there would be various up- and downstream effects that you can’t judge are sufficient or not to remedy the situation. Klotho-signaling is a powerful pathway.

But name the master regulater if you please. I will help you to shake down your hypothesis
 

GorillaHead

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That’s wrong in regards to Klotho.
If one were to fictively modulate Klotho and what it influences in MPB tissue there would be various up- and downstream effects that you can’t judge are sufficient or not to remedy the situation. Klotho-signaling is a powerful pathway.

But name the master regulater if you please. I will help you to shake down your hypothesis
Twist1.

All i am saying is u can increase klotho all u want u wont see it halting AGA. Because the body regulates whats happening differently locally depending whats happening locally and because of genes. People are losing hair because kf two reasons an instigator and an accelerator. The instigator is tied to the genetics and is the progression of age.
The accelerator is things like endotoxin. Excess androgens, endocrine disruptors and more.

If you take an old rat and young rat and you inject both prostates with the same test levels. The young rays prostate will not grow but the old one will. (this is proven btw in a study). Essentially as we age the androgenic expressions are increasing leading to an imbalance. Androgens regulate things like fibrosis they arent direct causes or mpb but are needed to fuel the fire. Even if u cut off systemic androgens if you live long enougb they will be made locally and expressed locally just like if u cut off a prostate from androgens in some cases it will make its own expression. Its a very interesting and frustrating body response.

Take it from somebody who has spent the past 4-5 years obsessing over hair-loss. Unless u can directly increase klotho directly where u need it and LONG enough to make a difference in the follicle it wont do anything. Ur just better off using minoxidil or adenosine.

Cancer. Twist1. Local Prolactin Receptor, aldosterone expression. There are the big players of AGA. Ultimately many different things can accelerate AGA.
 

Ras

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I still think the answer lies in how that many, if not most, babies are born with male pattern baldness. There is something about the maternal hormone environment that causes most babies to be born not only bald, but pattern bald, and to retain that baldness for many months. Regarding that, Panbecker's GC theory was given in the first post of this thread. Until we understand why babies are born with balding patterns that are often identical to those of post-pubescent males, we will not cure male pattern baldness.
 

GorillaHead

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@Ras
Alot of good theories already exist. But the pattern has to do with a specific gene i forgot. The pattern doesnt really mean that much in grand scheme of things. But even in advanced aga. They will bald everywherre at the nape and even the so called immune zones. Ive seen it. Many surgeons have talked about it. Anyways prolactin may be a big player but not serum prolactin. This forum is light years behind on AGA. Some of the discord groups i am in. Are legit trialing ***t no human has ever been recorded to trial. Crazy ***t is happening. But look up HMI hope medcine prolactin antibody. In monkeys who bald it fully reverses hairloss with one injection and apparently side effect free. Of course no telling how the monkeys really feel
 

jondoeuk

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@Ras
Alot of good theories already exist. But the pattern has to do with a specific gene i forgot. The pattern doesnt really mean that much in grand scheme of things. But even in advanced aga. They will bald everywherre at the nape and even the so called immune zones. Ive seen it. Many surgeons have talked about it. Anyways prolactin may be a big player but not serum prolactin. This forum is light years behind on AGA. Some of the discord groups i am in. Are legit trialing ***t no human has ever been recorded to trial. Crazy ***t is happening. But look up HMI hope medcine prolactin antibody. In monkeys who bald it fully reverses hairloss with one injection and apparently side effect free. Of course no telling how the monkeys really feel

I would be very cautious about preclinical data, as almost everything that works in non-humans fails to do so when tested in humans https://www.bio.org/sites/default/f...6-2015 - BIO, Biomedtracker, Amplion 2016.pdf Estimation of clinical trial success rates and related parameters
 

GorillaHead

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Fun fact we have insider info its working with humans already. Rats to humans. Ya that really doesn't work. But monkeys to humans studies translate often. Thats how they discovered finasteride works, it was done on monkeys.
 
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jondoeuk

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Fun fact we have insider info its working with humans already. Rats to humans. Ya that really doesn't work. But monkeys to humans studies translate often. Thats how they discovered finasteride works, it was done on monkeys.

No, we don't, as those are anecdotes. The real evidence will come from large, multi-central, randomised and placebo controlled trials. As for NHPs, that doesn't change things. Finally, here is a link which talks of the history of discovery (though it leaves out human observational data going back to the 40s) The extraordinary case of the Guevedoces
 

Jamsey

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Not trying to detract from current discussion and not sure if this has been posted before, but I though this was interesting and relevant to this threads topic.
 

Jamsey

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Not trying to detract from current discussion and not sure if this has been posted before, but I though this was interesting and relevant to this threads topic.
Also interesting
 

Mauritio

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Not trying to detract from current discussion and not sure if this has been posted before, but I though this was interesting and relevant to this threads topic.
Thanks for posting i noticed that everything anti-candida/fungal drastically lowers my hair loss.

Thymol lowers NLRP3 and is anti-fungal.

- Thymol Alleviates LPS-Induced Liver Inflammation and Apoptosis by Inhibiting NLRP3 Inflammasome Activation and the AMPK-mTOR-Autophagy Pathway - PubMed
 

Mauritio

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I don't know if your theory is correct but:

The LXR seems to inhibit NLRP3:
Liver X receptors agonists suppress NLRP3 inflammasome activation - PubMed
"In this study, LXRs agonists inhibited the induction of IL-1β production, caspase-1 cleavage and ASC oligomerization by NLRP3 inflammasome. The agonists also inhibited inflammasome-associated mtROS production. Importantly, the agonists inhibited the priming of inflammasome activation. In vivo data also showed that LXRs agonist prevented NLRP3-dependent peritonitis. In conclusion, LXRs agonists are identified to potently suppress NLRP3 inflammasome and the regulation of LXRs signaling is a potential therapeutic for inflammasome-driven diseases."​
LXR ligands are oxysterols (among potential other). 4β-Hydroxycholesterol is one of them.
This oxysterol seems to be found in higher quantity in women:
4β-Hydroxycholesterol, an endogenous marker of CYP3A4/5 activity in humans - PubMed
"The concentration of 4β-OHC was higher in women than in men, confirming previous studies indicating a gender difference in CYP3A4/5-activity."​

By the way, the LXR seems to be involved in cardiovascular diseases, while they are associated with hair loss.
Oh that is so interesting!
I have been noticing for a while that things that agonize LXR/ FXR really help with my hair loss. For example 5aDHP or emodin. I saw the pattern emerging, but I just couldn't figure out what the mechanism was. I thought it had to do with bile, but it might very well be the inhibition of NLRP3, so thanks for sharing.
 

Mauritio

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This study is interesting because B2 was the only B vitamin that inhibited the inflammatory response through IL1b and NLRP3.

"Murine bone marrow-derived macrophages (BMDMs) were primed with lipopolysaccharide (LPS) and subjected to a nigericin (NG) treatment to trigger the NLRP3 inflammasome assembly in the presence of vitamin B1, B2, B3, B5, B6 (pyridoxine), and C, as shown in Fig. 1A. The secretion of IL-1β, an indicator of inflammasome activation, was increased by the NG treatment, as expected (Fig. 1B). Interestingly, the releases of IL-1β were attenuated by vitamin B2 (riboflavin) in a dose-dependent manner, whereas the other B vitamins had little effect."
- Riboflavin, vitamin B2, attenuates NLRP3, NLRC4, AIM2, and non-canonical inflammasomes by the inhibition of caspase-1 activity - Scientific Reports
 

Mauritio

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Mauritio

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