NLRP3 Inflammasome Cause Of Male Pattern Baldness

emac

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So far I haven't really seen any profound regrowth stories on this forum (eg returning to dense nw1).

I think Danny and Ray are correct, though I wonder if someone who has a better understanding of biochemistry than i do could possibly integrate this guys theory into our bioenergetic view:

(i imagine its the subtle piece of the puzzle that allows some of us to revert multiple norwoods. maybe not idrk lol)

here's a really interesting comment on a Danny Roddy video:

1:
Mark Panbecker:
"It only took me 17 years and and about 50K pubmed abstracts to find out the SAME mechanism that causes gout ALSO is the same mechanism that causes male pattern baldness. Castration prevents both gout and mpb. The mechanism or VERY close is: NLRP3 inflammasome activation which involves casp1 activation(which is higher in mpb scalp). Problem with too much casp1 is that it cleaves(chews up) the glucocorticoid receptor. Inflammation and autoimmunity are well known with NLRP3 activation. Without glucorticoid receptor function(I believe) you get AR upreg stepping in as a surrogate for a dysfunctional GC receptor. Glucocorticoid resistance is THEE major problem in hair loss. Autophagy prevents the NLRP3 cascade. That's why you see also babies sometimes born like a mpb shape even in girls because sometimes the mother has high GC levels in late term."

- I saw in a Peat facebook group a woman claiming her husband growing his hairline back after fasting

- casp1 in aga scalps study Caspase-1 level is higher in the scalp in androgenetic alopecia - PubMed

- this may explain some of the finasteride/ mtf transition successful regrowth

- its been mentioned on this forum that a finasteride user kept great hair but aged poorly in other ways

- could this mean there is a very specific type of inflammation cascade occuring in the scalps of balding men?

- some hypothyroid people maintain really great hair. Some people recover their stress/thyroid health to ideal / hyper yet struggle to gain significant regrowth

- in other words, could this make sense of how some unhealthy people can keep great hair?

2:
"Mark Panbecker4 years ago
Read this link about lyme disease(activates NLRP3) and male pattern baldness initiation. https://www.nczonline.net/blog/2014/04/02/i-have-lyme-disease/ Also immortal hair has some college guys suddenly develop mpb in their mold filled apartment. NLRP3 activated by microbes, cholesterol crystals, low PH, numerous things."


- a possible connection with Danny - genetically some have stress physiology that is susceptible to this "NLRP3 cascade"

- btw im not suggesting castration as a solution lmao, maybe there is some peaty method that should be doubled down on in particular to allow sufficient / youth like autophagy of "NLRP3 inflammasome" (?)

3:
"Mark Panbecker3 years ago
I never said GOUT was the cause of mpb. NLRP3 is the key pathway to look at for gout and mpb.Castration cures both. Autophagy (lack of it) it the real problem because dht downregulates it thru microRNA 221. Autophagy stops the nlrp3 from firing. Look at all drugs that cause hair growth just "happen" to increase autophagy."

possibly related forum thread?: Hair Regrowth After Glucocorticoids - Any Ideas Why?

dafaq?
Autophagy is essential for maintaining the growth of a human (mini-)organ: Evidence from scalp hair follicle organ culture
Autophagy is essential for maintaining the growth of a human (mini-)organ: Evidence from scalp hair follicle organ culture


link to the Danny Roddy video where you can find the discussion towards the bottom of the comment section:


(sorry if my writing is scattered)

surely we can solve MPB completely and for good. (Btw i like to imagine that if the Ray Peat / pro metabolic community can legitimately surpass the mainstream big 3 'treatments' - itd lead to a huge awakening in the masses view of mainstream pharmaceuticals/thyroid/scientism)

id love to hear what you folks think of this.
 

LeeLemonoil

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sounds intriguing

for sakes sake
Natural Compounds as Regulators of NLRP3 Inflammasome-Mediated IL-1β Production

Soemthing that might be of interest, it's curious at the least.

For years and by various circmstances I am involved in research that tries to discover the pathomechanisms of a certain eye disease, corneal disease to be more precise.

I've encountered curious cases with the following situations that might be of intersest here in the nlrp3/Alopecia topic.

I've get to known three different pairs of brothers where in each pair both brothers developed said eye-disease. But in each pair one developed alopecia and one did not.

Here it comes. The 3 different guys that did not develp alopecia although their brothers did (and male ancestors too mostly) took either minocycline alone or together with isotretinoin to treat acne (which the brothers did not have). It's puzzling but it is true.

Minocycline alleviates or suppresses NLRP3 activation. All of said cases took it longterm. 1-3 years. Much longer that usual and recommended.

I've come acroos studies that sho that Isotretinoin not directly inhibt nlrp3 but by causing aptostosis to pro-inflammatory sebocytes which's sebum would normally trigger nlrp3 ativation.

Those guys that see succes in hairloss treatment with Retinic acid might do so by helping reducig nlrp3.

here is that study:
Error - Cookies Turned Off


here are moe substances that inhibit nlrp activation (coming from the acne angle)

baicalin (plant derived, available)
Baicalin suppresses Propionibacterium acnes-induced skin inflammation by downregulating the NF-κB/MAPK signaling pathway and inhibiting activation of NLRP3 inflammasome


aurafonin (pharmacon)
Repurposing Auranofin, an Anti-Rheumatic Gold Compound, to Treat Acne Vulgaris by Targeting the NLRP3 Inflammasome













But let's be clear here, the guy you quote does not ay that inhibition of nlrp3 alone stops mpb.
He sais nlrp3 leads to overexpressio of that casp1 which in turn leads to disfunctiong of GC-receptors (in scalp cells) so ARs get expressed as a compensation.

He then kind of implicates that AR activation by DHT supresses autophagy somewhere where it leads to nlrp3 activation.
A vicious circel or negative feddback loop, reinforcing negativity. That's not s seldom in physiology.
Still it is both a bit "cheap" and a nit inconsistent in recommending treatment
 
Last edited:

LLight

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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.
 

LeeLemonoil

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"cheap" becuase it comes back to the AR/DHT-angle that gets purported by decades for mpb-cause (albeit on a new fundamental base) and what is the rationale for AR compenastng for Glucocrticoid action? The immune-suppressive effects of androgens? Not impossible but he bases his theory on this bit that is not proven.

Thnaks @LLight
Travis thouht that Isotretinon might be a ligand of LXR. Maybe that too explains Isotretinois effects heretofore undescribed.

So assuming the guy is correct a sufferer of mpb should:

Stop nlrp3 by topical and systemic means (possible)
Inhibit DHR action on ARs in the scalp still (possible)

and thus steer himself to a state of homestatic, normal low grade nlrp3 - this would the some time also lead to the stop of autophagy inhibition by AR.

You could assist that procss by topical nd systmical substamces that mimic autophagy too
(Olive leaf extract, Rapamycin and similar stuff)
 

LeeLemonoil

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nlrp3 would also corrobate a bit the "genetic" aspect of mpb. The differing response by various means of inflammation to xenobiotics is one of the crucial default playforms of evolution in existing, highyl evolved orgnaisms too. It's the big wheel of fortune of evolution, the lottery. Reacting to tressors makes and breaks organisms. Highly evoved ogainisms did survive becuase they have a wide variety of possible reactions to various stressors thus securing survival. So yes, mpb is "genetic" partially in that sense. Allthough Peaters dont like to hear that

I now realize that neither "he" the 50k-abstract guy nor I adressed the purported "glucocorticoid-resistance is the major problem in mpb"-problem.
How to solve that once these Receptors are cuttd of? Refunctioning autophagy might only go so far if at all
 

LLight

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Well, the differences between sex are not really that important:
upload_2020-11-30_18-0-35.png
 

emac

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nlrp3 would also corrobate a bit the "genetic" aspect of mpb. The differing response by various means of inflammation to xenobiotics is one of the crucial default playforms of evolution in existing, highyl evolved orgnaisms too. It's the big wheel of fortune of evolution, the lottery. Reacting to tressors makes and breaks organisms. Highly evoved ogainisms did survive becuase they have a wide variety of possible reactions to various stressors thus securing survival. So yes, mpb is "genetic" partially in that sense. Allthough Peaters dont like to hear that

I now realize that neither "he" the 50k-abstract guy nor I adressed the purported "glucocorticoid-resistance is the major problem in mpb"-problem.
How to solve that once these Receptors are cuttd of? Refunctioning autophagy might only go so far if at all


i appreciate ur contributions so much. thank you.
i think there is no denying there is a blatant "genetic" component to this whole baldness thing. The real tragedy is the notion of learned helplessness genetic determinism which dominates tressless and all those other communities.
If a person has had thick hair earlier in their life, and trans people are able to recover hair in once bald regions (in other words: the follicles in bald areas on the scalp are not truely gone), then i see no reason why a person cannot recover norwoods while still maintaining a great low stress metabolic health.

if anything, the factor thats causing baldness implies there is still a little bit more a person who is 'Peating' etc can do to truely optimise their health / inflammtion that needs to be eliminated.
 

emac

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The plot thickens. Some more studies etc that may piece things together.



How does estrogen work on autophagy?
https://www.tandfonline.com/doi/full/10.1080/15548627.2018.1520549


Man With Male Pattern Baldness Regrows Hair With Methylene Blue
Man With Male Pattern Baldness Regrows Hair With Methylene Blue


Reciprocal Crosstalk Between Autophagic and Endocrine Signaling in Metabolic Homeostasis
https://academic.oup.com/edrv/article/38/1/69/2959894


Emerging role of glucocorticoid receptor in castration resistant prostate cancer: A potential therapeutic target
Emerging role of glucocorticoid receptor in castration resistant prostate cancer: A potential therapeutic target


α-Viniferin activates autophagic apoptosis and cell death by reducing glucocorticoid receptor expression in castration-resistant prostate cancer cells
α-Viniferin activates autophagic apoptosis and cell death by reducing glucocorticoid receptor expression in castration-resistant prostate cancer cells - PubMed


Role of Autophagy in Glucocorticoid-Induced BAT Whitening
Role of Autophagy in Glucocorticoid-Induced BAT Whitening


Glucocorticoids Suppress Antimicrobial Autophagy and Nitric Oxide Production and Facilitate Mycobacterial Survival in Macrophages
https://www.nature.com/articles/s41598-017-01174-9


Inhibition of autophagy overcomes glucocorticoid resistance in lymphoid malignant cells
https://pubmed.ncbi.nlm.nih.gov/25778879/


Lack of Genetic Mutation May Still Indicate Glucocorticoid Resistance Syndrome, Case Study Suggests
https://cushingsdiseasenews.com/2019/03/14/patients-with-high-cortisol-levels-but-no-clinical-signs-of-cushings-syndrome-may-instead-have-glucocorticoid-resistance-syndrome/


Do the interactions between glucocorticoids and sex hormones regulate the development of the metabolic syndrome?
https://www.frontiersin.org/articles/10.3389/fendo.2012.00027/full


Does increased expression of glucocorticoid receptor support application of antagonists to this receptor for the treatment of castration resistant prostate cancer?
https://amj.amegroups.com/article/view/4506/5248


Glucocorticoid Receptor Confers Resistance to Anti-Androgens by Bypassing Androgen Receptor Blockade
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3932525/


Comparing the rules of engagement of androgen and glucocorticoid receptors
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5425506/


Light induces NLRP3 inflammasome activation in retinal pigment epithelial cells via lipofuscin-mediated photooxidative damage
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4510924/
 

baccheion

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MPB is one symptom of progesterone deficiency.

Sustained-release melatonin after growth years (minimum amount) likely helps slow/prevent, especially the steadily accumulating version (ie, more with each passing decade).

Many things happen as a result of melatonin: hGH/IGF-1 release due to lowered insulin, opposed cortisol, increased T4 to T3 and pushing into cells (may also lead to more progesterone and IGF-1), less inflammation, suppressed adrenal/thyroidal activity, etc. Balanced by vitamin D3 in the morning. Unsure if it would reverse existing balding.
 

emac

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MPB is one symptom of progesterone deficiency.

Sustained-release melatonin after growth years (minimum amount) likely helps slow/prevent, especially the steadily accumulating version (ie, more with each passing decade).

Many things happen as a result of melatonin: hGH/IGF-1 release due to lowered insulin, opposed cortisol, increased T4 to T3 and pushing into cells (may also lead to more progesterone and IGF-1), less inflammation, suppressed adrenal/thyroidal activity, etc. Balanced by vitamin D3 in the morning. Unsure if it would reverse existing balding.


Ep. 46 Interview with Travis Burch: Sick Buildings and the Pillars of Health

check this out at around 44 minutes in.

he mentions at how for some people taking the Peat approach - simply hormone supplementation is all it takes however there may be other factors at play that inhibit other people from recovering fully (in this case im implying that true metabolic health etc should reverse the scalps calcification and recover scalp hair etc)

he mentions things like mold, emf, circadian rythm, gut health

i think the peat approach is getting us around 80% there, but there are other subtle environmental factors that we need to consider that may be inhibiting the effectiveness of mere hormones / hormonal supplementation which in theory we think will balance everything out - think about it, in theory there should be no reason why maintaining a temp at 37, having a calm and proactive mindset, keeping the stress hormones low etc (the usual peat protocol) wouldnt solve pretty much all of our health issues.

there must be something else yet to be corrected.
 

emac

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some resources that may be helpful in understanding how a lack of autophagy is involved in chronic inflammation.
 

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Kenny

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i wonder how estrogen actually plays into this process.
Trans people seem to often regrow very much of their air when they undergo HRT to become more feminine. It seems that estrogen can play a positive role in hair growth? I suppose the Haiduts and roddys might say the opposite. I'm not quite sure what to make if this
 

LeeLemonoil

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@Kenny
Estrogen might according the hypothesis developed in this thread prevent AR expression or simply block DHT from the AR.

Autophagy is here meant at the follicle (here dubbed mini-organ) I assume. It’s very vague how that plays in.

@emac
On a first glance some of the studies you provided corroborate the hypothesis, but some seem to contradict the purported pathomechansism.
I’ll have a closer look when I find time and comment what I think
 

emac

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@Kenny

while its true the estrogen is a dangerous stress hormone, there must be something about it that goes against the casp1 / nlrp3 inflammation cascade and thus allows the scalp to regrow hair. (despite the fact the estrogen also does kill off hair). this effect can also be said for spiro etc

"Autophagy (lack of it) it the real problem because dht downregulates it thru microRNA 221. Autophagy stops the nlrp3 from firing. Look at all drugs that cause hair growth just "happen" to increase autophagy." - Mark Panbecker

At first glance this may seem like im trying to counter the Peaty view the estrogen etc is bad - yes it is bad for hair health and many other things, however in the scalps of balding man it probably works to increase autophagy

"The huge signaling network downstream of estrogen can promote autophagy and reduce overstimulated autophagy at the same time, which allows autophagy to be regulated by estrogen in a restricted range" - https://www.tandfonline.com/doi/full/10.1080/15548627.2018.1520549

we notice how there are blatantly unhealthy / eg estrogenic / hypo people who still retain hair and vice versa - this probably accounts for it. (i imagine that these hypothetical estrogen people who retain hair would nonetheless experience in improvement in hair colour / thickness upon peating etc)

In transitioning people its necessary for them to take progesterone or some kind of inferior or synthetic progesterone derivative to protect from the cancerous effects of estrogen. That estrogen that they do consume allows them to reap the desireable effects eg - breast growth, feminine/ youthful hair

Ep. 46 Interview with Travis Burch: Sick Buildings and the Pillars of Health
if you check out this podcast at around 44 mins in, Travis makes a point that emf is a new mordern factor that interferes with blood sugar, so i imagine perhaps years ago a man with adequate thyroid and progesterone would regrow hair, when today he might not.

the emf for example is the extra stressor that prevents full regeneration.

a more relevant example mentioned by Travis is Mould:

as we can see earlier in the thread, its claimed that the NLRP3 cascade can be induced by mould, lymes disease, microbes etc.
place a woman in this scenario - her higher estrogen (for example) - may prevent the vicious cycle of casp1 and nlrp3 inflmation leading to glutocorditcoid resistance in the scalp and so the metabolism of her hair follicles are restored.

a man on the other hand would start to go bald because is dht would perpetuate the inflammatory cycle.

side notes:

ive heard of red light helmets being effective for more regrowth:
Light induces NLRP3 inflammasome activation in retinal pigment epithelial cells via lipofuscin-mediated photooxidative damage - this could have something to do with it

A conclusion im coming to and i fear to announce it to this forum despite how vastly open minded we are compared to the rest of society:

there is something legit about fasting / autophagy in achieving youthfulness

- something i think about (and im stating the obvious here): balding men had a point once in their lives at which they

a: had a thick full head of growing hair
b: had a youthful metabolism
c: had functional mitochondria
d: simultaneously had a high sex drive and a functional / growing penis

and so from that i reason that it must be possible though some kind of healing for a man to reach that state again.

idk much about fasting etc though i wonder it somehow its possible to produce the desirable autophagy that new agers / mainstream people promote as the secret to youth etc with out the destructive metabolic effects that Ray describes in this video

 

emac

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okay so ive been doing some research:

caffeine induces autophagy

so we dont need to starve ourselves lol

topical caffeine is legit. im gonna post a bunch on studies to kinda guide my reasoning.

also ive checked out the other recent topical caffeine thread: @johnwester130 mentions fungus involved in hair loss:

i think its all coming together

this candidalysin (probs the mould i was talking about earlier) probs comes from our modern environment - cadidalysin is probably what keeps the inflammation cascade going on in male scalps. antifungals and caffeine + the rest of the danny roddy pyamid protocol should in theory (both ours and the mainstreams are in fact one) be the cure.
 

emac

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On stress, longevity and autophagy

How Did We Evolve To Live Longer?



“Even in older animals, autophagy can be robustly increased through, for example, fasting and exercise, two interventions that have nothing to do with aging in itself.” -

How to Increase Autophagy for Lifespan Extension - Rogue Health and Fitness



Essential role for autophagy in life span extension

Essential role for autophagy in life span extension - PubMed

“Life and health span can be prolonged by calorie limitation or by pharmacologic agents that mimic the effects of caloric restriction. Both starvation and the genetic inactivation of nutrient signaling converge on the induction of autophagy, a cytoplasmic recycling process that counteracts the age-associated accumulation of damaged organelles and proteins as it improves the metabolic fitness of cells.” - Caffeine can be this agent that mimics starvation, minus the ffa metabolic damage of fasting



Autophagy and aging

Autophagy and aging - PubMed



Towards an understanding of the anti-aging mechanism of caloric restriction

Towards an understanding of the anti-aging mechanism of caloric restriction - PubMed

“Accumulation of oxidatively altered cell components may play a role in the age-related cell deterioration and associated diseases.”



“1. The function of autophagy declines with increasing age; 2. The temporal pattern of the decline parallels the changes in biomarkers of membrane aging and in amino acid and hormone signalling. 3. These age-dependent changes in autophagy are prevented by calorie restriction. 4. The prevention of the changes in autophagy and biomarkers of aging co-varies with the effects of calorie restriction on life-span. 5. A long-lasting inhibition of autophagy accelerates the process of aging. 6. A long-lasting stimulation of autophagy retards the process of aging in rats. 7. Stimulation of autophagy may rescue older cells from accumulation of altered mtDNA.”





The Link Between Autophagy And Hair Health:

The Link Between Autophagy And Hair Health.



Tom Hagerty claims he has retained his hair and hair colour (and also has a forum with other testimonials) using his scalp exercise







Autophagy and Thyroid Disease

Autophagy and Thyroid Disease.





Thyroid Hormone Stimulation of Autophagy Is Essential for Mitochondrial Biogenesis and Activity in Skeletal Muscle

Thyroid Hormone Stimulation of Autophagy Is Essential for Mitochondrial Biogenesis and Activity in Skeletal Muscle - PubMed



Intermittent fasting, your thyroid, and your immune system

https://www.boostthyroid.com/blog/2...t-fasting-your-thyroid-and-your-immune-system

(Perhaps a flawed article)



https://raypeatforum.com/community/threads/caffeine-increases-autophagy.6080/



NathanK “Interesting article. Sounds like the "hack" to increasing autophagy is to increase stress. Hypoxia is another way of increasing autophagy along with resveratrol, metformin, and a ketogenic diet (I believe).



I wonder if keeping your mitochondria healthy in the first place then you might be able to allay autophagy decline as we age and not need any "hacks". Not sure what comes first, the decline of autophagy or energy. They probably go hand in hand.



I wonder if this is what Ray meant when he said many of the benefits of fasting/calorie restriction can be found by limiting methyl donors. Maybe by limiting those it increases autophagy as well.



EDIT: I see now. His foundation of anti aging can be summed up in this quote. He wants stress. But not to the point of excess distress. I think there's definitely something to be said about it" "...“Longevity is correlated with having and meeting a healthy level of challenge – not too little and not too much stress.” A later 2009 blog entry Hormesis and age retardation started out by saying “An important approach to retarding aging that I have not discussed explicitly so far is hormesis, challenging cells and body systems by mild stress resulting in them becoming stronger and resistant to aging(ref). The stress can be physical, chemical and even possibly psychological.”"



It's also an interesting article and explains more the rationale of hypoxia, etc: http://www.anti-agingfirewalls.com/2012 ... longevity/. “





https://raypeatforum.com/community/...rks-its-not-what-you-think.36262/#post-557897

Fruit fasting may be legit?



Really great article on autophagy

Caffeine activates Autophagy – Caffeine can activate autophagy via an mTOR-dependent mechanism”

http://www.anti-agingfirewalls.com/...ousekeeper-in-every-cell-that-fights-aging-2/



“Caffeine induces apoptosis by enhancement of autophagy via PI3K/Akt/mTOR/p70S6K inhibition”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3039768/





https://raypeatforum.com/community/...oiled-water-and-then-apply-on-my-scalp.37424/
 

LeeLemonoil

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a more relevant example mentioned by Travis is Mould:

as we can see earlier in the thread, its claimed that the NLRP3 cascade can be induced by mould, lymes disease, microbes etc.
place a woman in this scenario - her higher estrogen (for example) - may prevent the vicious cycle of casp1 and nlrp3 inflmation leading to glutocorditcoid resistance in the scalp and so the metabolism of her hair follicles are restored.

a man on the other hand would start to go bald because is dht would perpetuate the inflammatory cycle.


That’s a good passage, making the mechanism more precise.

So we assume that some effects of estrogen (which estrogens?) prevent hairloss by inducing autophagy, halting the nlrp3 cascade.
This would explain lots of effects and the „paradox“ we sometimes see discussed in RPF that „estrogenic“ guys have good hair or the claims that bald guys are androgen-dominant but somewhat suboptimal.

Or that poor aging males have sometimes full hair despite being a mess with lots of health and energy concerns.

It might be interesting to look into what is known about women with hairloss problems or unusual hair growth patterns like hirsutidm, if that gives additional hints.

And absolutely, autophagy can be helped along with various means, it needn’t estrogen or castration.

The mould/xenobiotic angle is highly interesting but there will be more reasons and causes while some guys lose and other keep hair despite being exposed to mould or others causrs. Nlrp3 can be activated by many things.


It’s also promising to look at all substances known to slow down hairloss and determine if they directly or indirectly modulate nlrp3 or the cascade.


It’s a good hypothesis, I like hat i potentially unifies many pathways and seems to offer answers to the described hormonal paradoxes.
Let’s never forget that the big hormones are all part of the highest level of evolved immunity. Everything evolved from communication and struggle among cells and microorganisms

If the hypothesis here is right or broadly right than it’s absolutely feasible that hairloss can be treated rather „easily“ and maybe even reversed with more benign substances than finasteride.


Also Nlrp3 overactivation chronically by mold would cause a lot of problems apart from hairloss or no. It would be good to collect substances and ways to mitigate the effects
 

emac

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my basic understanding is that many stressors are coming together. hypothyroidism + chronic fungus

men with aga are genetically predisposed to a lack of autophagy in their ar response to these stressors - leading to chronic inflammation / insufficient energy metabolism.


The fungal peptide toxin Candidalysin activates the NLRP3 inflammasome and causes cytolysis in mononuclear phagocytes
The fungal peptide toxin Candidalysin activates the NLRP3 inflammasome and causes cytolysis in mononuclear phagocytes | Nature Communications


An essential role for the NLRP3 inflammasome in host defense against the human fungal pathogen, Candida albicans
An essential role for the NLRP3 inflammasome in host defense against the human fungal pathogen, Candida albicans


Turning Up the Heat: Inflammasome Activation by Fungal Pathogens

Turning Up the Heat: Inflammasome Activation by Fungal Pathogens


Candidalysin Crucially Contributes to Nlrp3 Inflammasome Activation by Candida albicans Hyphae
Candidalysin Crucially Contributes to Nlrp3 Inflammasome Activation by Candida albicans Hyphae


Candidalysin - Wikipedia


Candida albicans and candidalysin in inflammatory disorders and cancer
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Interaction of the Glucocorticoid and Androgen Receptors in Adipogenesis

Author links open overlay panel
https://www.sciencedirect.com/science/article/pii/S1074552112003328

“Recent studies have shown that glucocorticoids may also interact with androgen signaling and/or metabolism in adipose tissues (Zhu et al., 2010; Veilleux et al., 2012).”

“ Then they documented the effects of glucocorticoid receptor (GR) stimulation on AR expression and activity. They demonstrate that the GR and corticosteroids positively regulate AR expression while simultaneously decreasing AR activity and altering androgen effects on adipogenesis. The impact of dihydrotestosterone (DHT) on androgen receptor conformation during adipogenesis is also investigated. These findings are supported by high content analysis and quantitative imaging assays that were used previously by this group to investigate estrogen receptor ligands (Ashcroft et al., 2011).”
 
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Soren Thyroid (t3) causes body odor change what is the cause? Should I stop? Thyroid and Hormones 11
M Will topical zinc cause grey hair ? Hair & Nails 3
Zpol 'SARS-CoV-2 Spike Protein Alone May Cause COVID-19 Lung Damage – Even Without the Presence of Intact Virus' Scientific Studies 15
C What mechanism of Phenibut would cause an increase in urine concentration? Health 2
R Dairy cause constipation? Dairy 4
Spartan300 Skin becomes muc drier when off T3 - what would cause this? Skin 4
Hans Hypo-intellectism: is hypothyroidism the cause? Articles & Scientific Studies 26
Mauritio Dutasteride / Finasteride cause fibrosis of the penis and prostate; decrease androgen receptors, increase estrogen receptors Scientific Studies 9
GelatinGoblin Can Thyroid supplementation cause Osteoporosis? Supplements, Pharmaceutical Drugs 1
bzmazu COVID-19 not the sole cause of excess U.S. deaths in 2020 Viruses, Parasites, Fungus, Vaccines 0
haidut Metabolic (energy) deficiency may be the cause of Parkinson Disease (PD) Scientific Studies 1
haidut Mitochondrial debris leaking in bloodstream may cause autoimmune disease Scientific Studies 0
md_a The spike protein alone can cause severe disease Scientific Studies 4
ecstatichamster Vaccines cause more dangerous strains to evolve and shed (from vaccinated hosts) Vaccines 37
haidut Endotoxin (LPS) as a cause of systemic inflammation seen in obesity Scientific Studies 0
haidut Even "non-carcinogenic" estrogens can cause cancer Scientific Studies 1
J Why do carbonated drinks cause me to cramp during exercise? Soda (Mexican Coke, Pepsi, etc.) 8
M Zinc, Copper, Ceruloplasmin is confusing / Hair loss reversible when the cause is solved? Ask For Help or Advice 6
Hgreen56 Milk cause Crohn disease & Rheumatoid Arthritis? Dairy 7
Soren Can Thyroid Medication Cause Swollen Lymph Nodes? Ask For Help or Advice 8
Hgreen56 High sugar consumption could cause the body to become unable to regulate androgen levels? Hormones 21
F Can high reverse T3 cause acummulation of the exogenous thyroid hormone in the body? Ask For Help or Advice 3
D Does B-50 cause anhedonia? Water-Soluble Vitamins 29
V Would Pyrucet cause diarrhea? Digestion 1
Drareg German Study: Laboratory Accident Most Likely Cause of Coronavirus Pandemic Society 38
yerrag Just Learned From Experience Bicarbonate Intake Isn't the Real Solution, May Even Cause Problems Supplements, Pharmaceutical Drugs 20
B What could be the cause of anxious feeling in the gut? Digestion 16
md_a COVID-19 spike proteins may cause neurological issues Scientific Studies 2
GorillaHead Could Zinc be the cause of arthritis and cartilage destruction ? Symptoms, Causes 18
S Chronic mental overwork (near burn out) + training cause AA deficiency Amino Acids 0
Xavage Cause of differences in peoples / civilisations Political Talk, Alternative World Theories 3
L Does a Moderna vaccinated person cause harm to a non vaccinated person? Vaccines 15
F ""Low Serum AM Cortisol The Cause Of My Problems?"" Doubts About Milk 70

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