NLRP3 Inflammasome Cause Of Male Pattern Baldness

[LeeLemonoil]

Although I lack the understanding you guys have, I was digging around tonight trying to find things that induce autophagy because I feel like it's the keystone and also possibly the way estrogen works.

I think I found something you need to read

DEFINE_ME

This is indeed required and essentila reading for anyboy interested in truly understanding hairloss.

It's also a strong indication and lends credibility to what Pnbecker found out.

With regards to Estrogen/Fina, this would indicate that neither migth be necessary for achieveing regrowth - or that guys like @ChemHead need to determine if Finasteride use migt alter steroids or bring about steroids and signaling that for a short term increase autophagy in such a substantial way as laid out in th epublication. This is, imo, the most plausible explainatin for hat Chemhead experienced.

In combination with things that show limited regrowth effects and additional topicas and systemic maintenace with polyphenols or aspirin and the like, this is the best bet to achieve regrowth. Things like regular Dermarolling would hasten and improve the process.

Also, you should find ut if Ketaconazole, in addition to blocking nlrp3, would also influence autophagy, like oligomycin used here


This gives other hints, Estrogen won't work I think. It has sotrt of regulatory, homeostatic effects on Autophgay. Maybe high dose Fina shortly provoked very strong autophagy-onset but get reigned in by Estrogen shortly after.

How does estrogen work on autophagy? - PubMed

Macroautophagy/autophagy is vital for intracellular quality control and homeostasis. Therefore, careful regulation of autophagy is very important. In the past 10 years, a number of studies have reported that estrogenic effectors affect autophagy. However, some results, especially those regarding...

pubmed.ncbi.nlm.nih.gov

More to find that Est can inhibit Autophagy.

 

[LeeLemonoil]

In addition, are there options to obtain both alpha-ketoglutarate and aöpha-ketobutyrate in bulk?

 

[benjt]

Just dropping a few papers that might be relevant:
"Thyroid hormones directly alter human hair follicle functions"
Money quote:

Studying microdissected, organ-cultured normal human scalp HFs, we show here that T4 up-regulates the proliferation of hair matrix keratinocytes, whereas their apoptosis is down-regulated by T3 and T4. T4 also prolongs the duration of the hair growth phase (anagen) in vitro, possibly due to the down-regulation of TGF-beta2, the key anagen-inhibitory growth factor. [...] Thus, we present the first evidence that human HFs are direct targets of thyroid hormones and demonstrate that T3 and/or T4 modulate multiple hair biology parameters, ranging from HF cycling to pigmentation.

Thyroid hormones are known in at least two locations to be necessary for autophagy:
- Liver (1, 2)
- Skeletal muscle (3)

I am wondering if thyroid function and/or hormones might play a role here.


Additionally, hypothyroidism is associated with low systemic testosterone. This may influence a lack of local hormones (local in the scalp or hair follicle) produced from testosterone, or it may lead to upregulation of 5AR to produce DHT in order to counteract a lack of T.

 

[fathom]

I am taking a shot at this. I picked up what things I needed yesterday. Today was day 1. My goal is to strengthen thyroid, lower DHT while raising autophagy. I am doing this through supplements and two topicals, grouped by what they target, one in the morning, one in the evening.

Topical 1) zinc and B6(commonly known as Zix) with added rosemary for DHT in an alcohol/water base
Topical 2) melatonin, olive leaf extract and caffeine for increased autophagy and wnt signaling in an alcohol/water base

Supplementing a thyroid booster. Stinging nettle for DHT. Curcumin, taurine, quercetin for autophagy

 

[keytothecity]

I am taking a shot at this. I picked up what things I needed yesterday. Today was day 1. My goal is to strengthen thyroid, lower DHT while raising autophagy. I am doing this through supplements and two topicals, grouped by what they target, one in the morning, one in the evening.

Topical 1) zinc and B6(commonly known as Zix) with added rosemary for DHT in an alcohol/water base
Topical 2) melatonin, olive leaf extract and caffeine for increased autophagy and wnt signaling in an alcohol/water base

Supplementing a thyroid booster. Stinging nettle for DHT. Curcumin, taurine, quercetin for autophagy

sounds pretty good, I will likely start something similar with bi-estro and systemic anti-estrogens soon

keep us updated and if any1 has further recommendations, especially in regards to autophagy and thyroid, I'm all ears.

 

[keytothecity]

Guys there are studies that bald men do worse when Covid infected, I‘m sure you have heard about them.
2 explanations I am seeing:
•bald men are unhealthier
•bald men have stronger immune responses

Here is a haidut quote on covid response unrelated to hair loss/

All viruses can do that, including the flu. If a person dies from the "flu" (or other viral infections), the cytokine storm and multi-organ failure is what usually does them in. There is nothing special/unique in regards to COVID-19 when it comes to causing it.
Inside a Cytokine Storm: When Your Immune System is Too Strong | Breakthroughs
The cytokine storm of severe influenza and development of immunomodulatory therapy
New fronts emerge in the influenza cytokine storm

Some public health authorities have said things like "well, some viruses (like Ebola) cause severe bleeding and those effects are unique". Nope, pretty much any virus can cause the same bleeding when the infection is severe enough. Including the "flu".
How a mild influenza B infection can kill: A case of pulmonary hemorrhage
Novel H1N1 influenza A viral infection complicated by alveolar hemorrhage - PubMed
A case of hemorrhagic colitis after influenza A infection - ScienceDirect
https://journal.chestnet.org/article/S0012-3692(18)31296-0/fulltext

I think it has been theorized that mpb (maybe due to funghi, or bacteria?) is the immune system attacking your follicles
Cortisone can work against hair loss, suppresses immune system
Cushing disease sufferers tend to have great hairlines and weak immune systems
It has recently been theorized that fin upregulates a corticosteroid

So imo this is making the overactive immune system-mpb link more plausible

there is also a study claiming covid survivors experience reversable hair loss

65% of COVID-19 survivors surveyed report experiencing hair loss, among other long-term effects

A recent survey conducted by Survivor Corps, a COVID-19 nonprofit, and Dr. Natalie Lambert from Indiana University School of Medicine found that 65% of coronavirus survivors reported hair loss.

www.foxla.com

 

[LeeLemonoil]

Bald men aren’t less „healthy“ in general. That’s a myth stemming from the obsession of the affected. Health is always context-dependent and mpb can or may not be a selective disadvantage or signal of good or poorer health in any given context.

Now Covid and Mpb:

SarsCov2 infection activates the nlrp3 inflammasome.

I don’t know if there are any merits in the steroidal connections that were drawn.
If so, the most interesting data are that males with severe cases have as it seems significantly less testosterone.
Don’t know if they „have“ more DHT for it.

And there is also Data showing that 5-Ar inhibitor takers are worse off too when infected.

It’s hard to get a consistent picture from all that.

 

[BrianF]

Sebum production / Vitamin A deficiency are clearly a factor in this process. The funghi/bacteria are clearly a factor because they feed on the sebum and create PUFA or other cause for concern for the immune system. But why does the body immune system overreact in such a dramatic fashion? Let me remind you guys about the specific L-Reuteri ATCC PTA 6475 and its effect on hair. What this non-pathogenic microbe and other so called 'non-pathogenic' or 'friendly' gut bacteria do is to regulate the immune response and increase Tregs (whatevever the hell Tregs are?). Read this:

What are T Regulatory Cells (Tregs)?​

Tregs comprise ∼5% – 10% of T helper cells and can be identified by the DNA reading protein ‘Foxp3’ or a lot of CD25 proteins on its membrane/surface.

There are two types of Tregs: ‘natural’ (nTregs) or ‘induced’ (iTregs). Both types are anti-inflammatory. Natural means that they are part of the cells naturally found in our thymus gland. Induced means that they are created outside the thymus. (There are 2 kinds of induced Tregs: Tr1 and Th3) [1, 2].

Tregs produce TGF-B and interleukin IL-10, both of which mostly inhibit the immune system [3].

Tregs suppress the harmful/activated (effector) Th1, Th2, Th17 cells and their cytokines, eosinophils, mast cells, basophils, IgE’s (switches to IgG4), and the migration of inflammatory cells to tissues [4].

In addition, they suppress CD8+ T cells, dendritic cells (DCs), monocytes/macrophages, B cells, natural killer cells and natural killer T cells [5].

Tregs need to be ‘activated’ in order to have their suppressor functions [6].

Tregs inhibit immune activation by a direct cell to cell contact. This means that it doesn’t only work through cytokine intermediaries such as TGF-B and IL-10. These cells are directly anti-inflammatory [7]. For some reason, this information excites me.

The Good​

Treg cells help to restrain the immune system and prevent an excessive T Cell response [8].

Even in healthy people, immune cells can attack our own tissue. Tregs stop our immune cells from attacking our own tissue [9].

In particular, TGFb and IL-10 seem to be crucial for sustained tolerance induction by Treg [10]. On the other hand, TNF, IL-1, and IL-6 block the ability of Tregs to induce tolerance [10].

Tregs can also reverse food intolerances and allergies.

Probably the single most important reason we develop IgE-related allergies is that we aren’t creating Treg cells in the gut, but instead Th2 or Th17 cells [11].

This happens in 3 ways: by changing the type of dendritic cells that reside in our gut, by blocking Th2/mast cells/other immune cells, and by actually changing the tissue structure of our gut [11].

Our gut has dendritic cells that capture proteins from food and bring them to the lymph nodes. To produce Tregs, we need sufficient vitamin A, TGF-B, and the enzyme IDO [11].

If we produce Tregs, then they will tell the dendritic cells that the protein they carry is cool and there’s no need to ring the alarm bells [11].

For oral tolerance, immune cells (DCs) are told not to react to a protein in the gut tissue, and these cells circulate to other tissues, which trains the immune system [12].

Technical: Tregs produce inhibitory cytokines (eg, IL-10, TGFb, and IL-35), absorb inflammatory cytokines, kill target cells directly (secretion of granzymes, perforin), block important cellular functions (through CD25, 39, 73 and adenosine), increase cAMP (and therefore energy), decrease costimulatory molecules (CD80/CD86) and turn the dendritic cells off by activating surface proteins that inhibit immune function (CTLA-4, PD-1, or Histamine Receptor 2) [11, 12].

I’ve tried all different ways to induce tolerance, but I haven’t found this to be effective for lectin sensitivity at all. This works for probably most other food allergies.

Treg cells, surprisingly, can be important for clearing some infections. They are crucial for the establishment of a functional Th17 response after the infection in the gut (with the help of IL-2) [13].

Tregs can improve wound healing [14] and are neuroprotective in stroke models [15].

The Bottom Line: If you’ve got autoimmune or inflammatory problems, there’s a good chance that you’re deficient in Tregs or that they’re dysfunctional. Tregs can then be considered ‘good’.


So is it possible, that the single biggest factor (because lets face it there is more than one at play here) is that due to basic dysbiosis causing an autoimmune response and couldn't this explain why bald men are more likely to suffer other autoimmune conditions such as RA?

I'm not the first one to think this, many on here have raised this theory - I'm sure John Wester was one of them.

 

[LeeLemonoil]

Sebum production / Vitamin A deficiency are clearly a factor in this process. The funghi/bacteria are clearly a factor because they feed on the sebum and create PUFA or other cause for concern for the immune system. But why does the body immune system overreact in such a dramatic fashion? Let me remind you guys about the specific L-Reuteri ATCC PTA 6475 and its effect on hair. What this non-pathogenic microbe and other so called 'non-pathogenic' or 'friendly' gut bacteria do is to regulate the immune response and increase Tregs (whatevever the hell Tregs are?). Read this:

What are T Regulatory Cells (Tregs)?​

Tregs comprise ∼5% – 10% of T helper cells and can be identified by the DNA reading protein ‘Foxp3’ or a lot of CD25 proteins on its membrane/surface.

There are two types of Tregs: ‘natural’ (nTregs) or ‘induced’ (iTregs). Both types are anti-inflammatory. Natural means that they are part of the cells naturally found in our thymus gland. Induced means that they are created outside the thymus. (There are 2 kinds of induced Tregs: Tr1 and Th3) [1, 2].

Tregs produce TGF-B and interleukin IL-10, both of which mostly inhibit the immune system [3].

Tregs suppress the harmful/activated (effector) Th1, Th2, Th17 cells and their cytokines, eosinophils, mast cells, basophils, IgE’s (switches to IgG4), and the migration of inflammatory cells to tissues [4].

In addition, they suppress CD8+ T cells, dendritic cells (DCs), monocytes/macrophages, B cells, natural killer cells and natural killer T cells [5].

Tregs need to be ‘activated’ in order to have their suppressor functions [6].

Tregs inhibit immune activation by a direct cell to cell contact. This means that it doesn’t only work through cytokine intermediaries such as TGF-B and IL-10. These cells are directly anti-inflammatory [7]. For some reason, this information excites me.

The Good​

Treg cells help to restrain the immune system and prevent an excessive T Cell response [8].

Even in healthy people, immune cells can attack our own tissue. Tregs stop our immune cells from attacking our own tissue [9].

In particular, TGFb and IL-10 seem to be crucial for sustained tolerance induction by Treg [10]. On the other hand, TNF, IL-1, and IL-6 block the ability of Tregs to induce tolerance [10].

Tregs can also reverse food intolerances and allergies.

Probably the single most important reason we develop IgE-related allergies is that we aren’t creating Treg cells in the gut, but instead Th2 or Th17 cells [11].

This happens in 3 ways: by changing the type of dendritic cells that reside in our gut, by blocking Th2/mast cells/other immune cells, and by actually changing the tissue structure of our gut [11].

Our gut has dendritic cells that capture proteins from food and bring them to the lymph nodes. To produce Tregs, we need sufficient vitamin A, TGF-B, and the enzyme IDO [11].

If we produce Tregs, then they will tell the dendritic cells that the protein they carry is cool and there’s no need to ring the alarm bells [11].

For oral tolerance, immune cells (DCs) are told not to react to a protein in the gut tissue, and these cells circulate to other tissues, which trains the immune system [12].

Technical: Tregs produce inhibitory cytokines (eg, IL-10, TGFb, and IL-35), absorb inflammatory cytokines, kill target cells directly (secretion of granzymes, perforin), block important cellular functions (through CD25, 39, 73 and adenosine), increase cAMP (and therefore energy), decrease costimulatory molecules (CD80/CD86) and turn the dendritic cells off by activating surface proteins that inhibit immune function (CTLA-4, PD-1, or Histamine Receptor 2) [11, 12].

I’ve tried all different ways to induce tolerance, but I haven’t found this to be effective for lectin sensitivity at all. This works for probably most other food allergies.

Treg cells, surprisingly, can be important for clearing some infections. They are crucial for the establishment of a functional Th17 response after the infection in the gut (with the help of IL-2) [13].

Tregs can improve wound healing [14] and are neuroprotective in stroke models [15].

The Bottom Line: If you’ve got autoimmune or inflammatory problems, there’s a good chance that you’re deficient in Tregs or that they’re dysfunctional. Tregs can then be considered ‘good’.


So is it possible, that the single biggest factor (because lets face it there is more than one at play here) is that due to basic dysbiosis causing an autoimmune response and couldn't this explain why bald men are more likely to suffer other autoimmune conditions such as RA?

I'm not the first one to think this, many on here have raised this theory - I'm sure John Wester was one of them.

A single strain modulating specific aspects of a snippet of the vast amplitude of immune responses is neither the cause nor the cure to hairloss

What’s true is that the composition of the gut microbiome and every other mictobiome that is by some way „in contact“ with hair follicle and sourrounding tissue will influence if, when, how and how severe MPB becomes.

Cells and tissues don’t discriminate between so called autoimmunity and responses to other effectors. All is long included into the intricate signaling and response mechanism. There is no auto-immunity, only immunity. And homeostasis. You are not „healthy“ if no autoimmunity goes on and it’s not „curious“ that „healthy“ people have auto immune action going on.


What causes a hair follicle to eventually go catagen, remain telogen, dormant or get destructed to disfunctionality by immune responses is not a linear causal chain

It’s a huge web of chain-elements working against another and reinforcing one another. But within this myriad of proceedings something due to necessity will lead to another chain element within the next web. And on and on.

If, how, and to what strength of effect the composition of the micobiome leads to hairloss or prevents it - or speeds it up or retards it - depends on the countless other factors in the chain-webs-chain.

And even if let’s say 3 strains eliminated in the gut and 3 substituted for it would balance things out to a less catagen situation this will leads to unpredictable homeostatic events.

Only and least unpredictable intervention is to come as far as possible in any chain on the most powerful element or link. And then modulate that in the specific tissue.

It can hardly ever be done.

In hairloss, it seems there is actual progress. Autophagy seems a good point high and low enough on the chain, and powerful enough to be a key factor modulated. It already subsummizes many immunological / microbiome Signals prior.

It certainly always seems useful to alleviate inflammation and immunity ssystemically when it clearly causes disfunction, pain, distress and so on. I doubt that the gut microbiome offers a strong enough lever to reverse hairloss.

 

[GorillaHead]

Imo the reason covid causes hairloss in a MPB fashion based on some documented anecdotes with photos. I saw a women who got covid and she started receding on the temples. Its because it activates the RAS system this results in aldosterone secretion. Franky that study that showed mpb had higher aldosterone levels shouldnt be ignored especially because the levels were basically 100% more!

 

[LeeLemonoil]

Cortisol sets Nlrp3 signaling in motion. Chronic nlrp3 then apparently induces casp-1 to „cut off“ GC-Receptors, as Panbecker determined. Why is that? To protect the cells from destruction? And altered Androgen-signaling substitutes for physiological GC action in a way I assume.

If similar mechanisms as portrayed here are valid in hairloss too, this is another hint for upstream inflammation and „stress“ of various sorts.
I’d be cautious with applying local estrogen given its properties of modulating cortisol. As Chemhead said, it’s neither about DHT nor estrogens. It’s more about enzymatic distortions revolving around 5-ar and aromatase.
Both cortisol action before and after chronic nlrp3 will affect that massively.

In keeping with these premises, exogenous corticosterone (CORT) administration in rodents has been proposed as a pharmacological stress model of depression that mimics the behavioral and neurochemical alterations associated with HPA dysfunction in the depressive state (Pazini et al., 2016; Rosa et al., 2014; Zhao et al., 2008). Despite the numerous studies reporting that chronic stress underlies the genesis of MDD, the mechanisms by which glucocorticoids contribute to the depressive symptoms have not been entirely established. Compelling evidence indicates that glucocorticoids may induce a peripheral and central pro-inflammatory state that involves the stimulation of the nod-like receptor pyrin domain containing 3 (NLRP3), an intracellular multiprotein complex responsible for the inflammatory response (Busillo et al., 2011; Kaufmann et al., 2017). Importantly, NLRP3-driven pro-inflammatory response culminates in neuronal damage and death remarkably in brain regions involved with mood modulation, and these events are thought to underlie depressive symptoms (Miller et al., 2009)."

"...In the present study, we showed that a low dose of cholecalciferol abrogates the depressive- and anhedonic-like behavior induced by chronic corticosterone administration, confirming a previous study from our group (Camargo et al., 2018). We extend these findings providing evidence that these behavioral effects were accompanied by the reestablishment of GR immunocontent impaired by corticosterone. Additionally, the ability of cholecalciferol in reducing NLRP3 inflammasome-related proteins ASC, TXNIP, and caspase-1 in the hippocampus of mice was also demonstrated."

 

[LeeLemonoil]

Do these adrenal Androgens factor into onset and progression of MPB? I think they do, why would they not. And if they factor in, we have to factor them in.
Both in their roles at onset and what they would to when you take 5-AR-inhibitors. It's dumbfounding.

Has Peat ever spoken about these 11-oxyandrogens? No knowledge of our precious androgens and steroid metabolism can be considered complete without factoring these in.
Especially the occurence of 11-Ketotest in so called castration resistant PC is interesting.

11-Ketotestosterone and 11-Ketodihydrotestosterone in Castration Resistant Prostate Cancer: Potent Androgens Which Can No Longer Be Ignored - PubMed

Dihydrotestosterone (DHT) is regarded as the most potent natural androgen and is implicated in the development and progression of castration resistant prostate cancer (CRPC). Under castrate conditions, DHT is produced from the metabolism of the adrenal androgen precursors, DHEA and...

pubmed.ncbi.nlm.nih.gov

11-Ketotestosterone is the Predominant Androgen in Castration Resistant Prostate Cancer | ECE2020 | 22nd European Congress of Endocrinology | Endocrine Abstracts

www.endocrine-abstracts.org

11-Oxygenated androgens in health and disease - Nature Reviews Endocrinology

The adrenal glands are a source of androgens that all share an oxygen atom on carbon 11 (termed 11-oxyandrogens). This Review focuses on the rapidly expanding knowledge regarding the implications of 11-oxyandrogens in human physiology and disease.

www.nature.com

The Rise, Fall, and Resurrection of 11-Oxygenated Androgens in Human Physiology and Disease

Abstract. The 11-oxyandrogens, particularly 11-ketotestosterone, have been recognized as a biologically important gonadal androgen in teleost (bony) fishes for decades, and their presence in human beings has been known but poorly understood. Today, we recognize that 11-oxyandrogens derive from...

www.karger.com

Dihydrotestosterone (DHT) is regarded as the most potent natural androgen and is implicated in the development and progression of castration resistant prostate cancer (CRPC). Under castrate conditions, DHT is produced from the metabolism of the adrenal androgen precursors, DHEA and androstenedione. Recent studies have shown that the adrenal steroid 11β-hydroxyandrostenedione (11OHA4) serves as the precursor to the androgens 11-ketotestosterone (11KT) and 11-ketodihydrotestosterone (11KDHT). In this study we comprehensively assess the androgenic activity of 11KT and 11KDHT. This is the first study, to our knowledge, to show that 11KT and 11KDHT, like T and DHT, are potent and efficacious agonists of the human androgen receptor (AR) and induced both the expression of representative AR-regulated genes as well as cellular proliferation in the androgen dependent prostate cancer cell lines, LNCaP and VCaP. Proteomic analysis revealed that 11KDHT regulated the expression of more AR-regulated proteins than DHT in VCaP cells, while in vitro conversion assays showed that 11KT and 11KDHT are metabolized at a significantly lower rate in both LNCaP and VCaP cells when compared to T and DHT, respectively. Our findings show that 11KT and 11KDHT are bona fide androgens capable of inducing androgen-dependant gene expression and cell growth, and that these steroids have the potential to remain active longer than T and DHT due to the decreased rate at which they are metabolised. Collectively, our data demonstrates that 11KT and 11KDHT likely play a vital, but overlooked, role in the development and progression of CRPC.

 

[GorillaHead]

Guys omg. Look at this! This goes back to insulin issues and igf

Did yall know that dht serum levels in men are inversely related to insulin resistance. Which means in some ways dht protects against insulin resistance in some way. It probably modulates things.

you guys also know that men are more likely to get diabetes than women BUT men do not suffer from complication as much as women do.

 

[DhtAssassin]

Guys omg. Look at this! This goes back to insulin issues and igf

Did yall know that dht serum levels in men are inversely related to insulin resistance. Which means in some ways dht protects against insulin resistance in some way. It probably modulates things.

you guys also know that men are more likely to get diabetes than women BUT men do not suffer from complication as much as women do.

People destroy DHT with dutasteride and get most regroth. In no way your theory that DHT protects from insuling resistance makes sense.

 

[LeeLemonoil]

People destroy DHT with dutasteride and get most regroth. In no way your theory that DHT protects from insuling resistance makes sense.

It’s not a theory but proven in muscle cells.

It never ceases to amaze how one of the most complex and poorly understood things on earth, physiology, gets dumbed down to reductionist, linear mechanistic thinking and then authoritatively barked out conclusions -that are breathtakingly wrong.

There are three isoforms of 5-AR. Expressed to varying degrees in different tissues. With different evolved effects in different tissue. Dependent in their functionality on poorly understood interconnected factors that are themselves poorly understood. Time and quantity dependent. Energy dependent. Prone to errors.

But because observation x is reduced to linear equation y then the same must apply to every other things loosely related to y and y surely?

Welcome in the world of endless dumbness

 

[GorillaHead]

People destroy DHT with dutasteride and get most regroth. In no way your theory that DHT protects from insuling resistance makes sense.

its not just a theory based off nothing. Not only does the research i mentioned about dht and insulin resistance being inversely related but theres also some science to show that dutasteride increase ur chance of diabetes.

Prostate Drugs Increase Diabetes Risk -- Dutasteride and Finasteride

Prostate drugs increase diabetes risk, say results from a new study led by the University of Edinburgh and UCL of the drugs dutasteride and finasteride.

www.diabetesincontrol.com

Your username checks out. You probably think dht is all bad. Just like people here think estrogen is all bad. Thats not how the body works at all. Its all about homeostasis.

 

[keytothecity]

Fixing insuline resistance is probably involved in the few success stories here as hardcore peating does in fact fix it. If your hair loss is a sign of severe metabolic derangement congrats, you might have just found the right forum here.
Again that’s of no use to guys that are already healthy, lean and with great energy levels and sugar metabolisms though...

 

[GorillaHead]

Fixing insuline resistance is probably involved in the few success stories here as hardcore peating does in fact fix it. If your hair loss is a sign of severe metabolic derangement congrats, you might have just found the right forum here.
Again that’s of no use to guys that are already healthy, lean and with great energy levels and sugar metabolisms though...

well i still think even for those people who think they are healthy because they are lean and have great energy doesnt mean you truly are 100% healthy.

 

[BrianF]

well i still think even for those people who think they are healthy because they are lean and have great energy doesnt mean you truly are 100% healthy.

Been lean most of my life, still think Ive had trouble with insulin sensitivity and pre-diabetes.

 

[keytothecity]

well i still think even for those people who think they are healthy because they are lean and have great energy doesnt mean you truly are 100% healthy.

sure, just as being nw0 doesnt mean you are 100% healthy.
the problem with all of this info gathering is that literally anything will cause mpb in people suspectible to it, and literally (almost) nothing will cause mpb in people not suspectible to it
if you are not obviously diseased (much more so than peers) it seems difficult to regrow hair by "fixing lifestyle" because it's already pretty good, and getting it a bit better will only make a small difference, but probably not keep your hair either