PPARs And Keratin

[eddiem991]

@Travis
Based on the general interpretation of your much appreciated and extensively supported theory, would you agree with this list of general applications (feel free to add or remove any applications):

-avoid PUFA/ toxins in the diet by focusing primarily on ruminant based meats (beef, lamb, goat), non-allergenic dairy sources, shellfish (shrimp, oyster, mussel, scallop), fruits, honey, maybe a carrot

-avoid excessive stress from pyshcological mediums (toxic relationships, poor employment situation), chronic cardio, lack of sleep, lack of light exposure, lack of meaningful human interaction and other emotional mediums (perhaps practice meditation and letting go to manage the unavoidables)

-optimization of colonic flora, specifically in the context of its immune regulating and t-cell interaction (starch avoidance, synthetic gums avoidance, grain avoidance, no high fiber diet, etc.)

-supplementation of vit D3 to maintain adequate blood levels, K2-Mk4, perhaps some topical magnesium chloride. Obtain calcium from dairy, vit a from liver, zinc from oysters

-regular use of aspirin and perhaps vit e to possibly control the prostaglandin situation if the body is loaded on linolate.

-elimination of any hidden chronic infections.

(For other people reading almost every single one of these points have been discussed by Peat or others on the forum in some degree. Even though these things are being talked about in this context of hairloss I think these are generally applicable to almost all health situations and conditions with each manifestation perhaps being a predisposed variation of the same general etiology.)

Thanks for your time and research @Travis, I have been following ur posts since u posted on the "Cause of baldness thread"; very nice work although some is beyond my current knowledge base. I very much appreciate it. I havent seen work like this anywhere else on the internet. Most researchers seem to be pigeon- holed into one very discrete area of research and the civilian scientist on the forums are looking into different permutations of the same general theories endlessly.

I agree to almost everything on your list (and Peats work in general), but I think one should in addition to your list also keep carbs under 100/g per day (maybe even 50 g for some people), eating good amounts of butter and cocunut oil, once in a while water fast for a couple of days and also meditating or going for long walks daily. :)

As you say this is for health in general.

 

[CLASH]

@eddiem991
Thanks for your comment.
Based on my experience here, I dont think you will find much support for lower carb or water fasts on this forum in general.
The long walks are a nice addition though, atleast in my experience and understanding.

 

[eddiem991]

@eddiem991
Thanks for your comment.
Based on my experience here, I dont think you will find much support for lower carb or water fasts on this forum in general.
The long walks are a nice addition though, atleast in my experience and understanding.

I know, but besides high carb consumption I agree to everything Peat says. But as an advice to you, if you already havn't, try out a high calorie low carb/ketogenic diet just to know how it feels. I'm on it right now and I feel so mentally sharp and calm at the same time. It feels amazing.

Huge amounts of sugar actually do cause insulin resistance and Non alcoholic fatty liver. Having stable blood sugar is important for hair health.

 

[Travis]

@Travis
Based on the general interpretation of your much appreciated and extensively supported theory, would you agree with this list of general applications (feel free to add or remove any applications):

-avoid PUFA/ toxins in the diet by focusing primarily on ruminant based meats (beef, lamb, goat), non-allergenic dairy sources, shellfish (shrimp, oyster, mussel, scallop), fruits, honey, maybe a carrot

-avoid excessive stress from pyshcological mediums (toxic relationships, poor employment situation), chronic cardio, lack of sleep, lack of light exposure, lack of meaningful human interaction and other emotional mediums (perhaps practice meditation and letting go to manage the unavoidables)

-optimization of colonic flora, specifically in the context of its immune regulating and t-cell interaction (starch avoidance, synthetic gums avoidance, grain avoidance, no high fiber diet, etc.)

-supplementation of vit D3 to maintain adequate blood levels, K2-Mk4, perhaps some topical magnesium chloride. Obtain calcium from dairy, vit a from liver, zinc from oysters

-regular use of aspirin and perhaps vit e to possibly control the prostaglandin situation if the body is loaded on linolate.

-elimination of any hidden chronic infections.

(For other people reading almost every single one of these points have been discussed by Peat or others on the forum in some degree. Even though these things are being talked about in this context of hairloss I think these are generally applicable to almost all health situations and conditions with each manifestation perhaps being a predisposed variation of the same general etiology.)

Thanks for your time and research @Travis, I have been following ur posts since u posted on the "Cause of baldness thread"; very nice work although some is beyond my current knowledge base. I very much appreciate it. I havent seen work like this anywhere else on the internet. Most researchers seem to be pigeon- holed into one very discrete area of research and the civilian scientist on the forums are looking into different permutations of the same general theories endlessly.

That looks like a good approach. I think we need to look for epidemiological evidence at some point to see how well linoleic acid itself correlates with hair loss. I used to think that the word 'multifactorial' was a cop‐out, in a way, but now I think a little differently. It's true that some people use the term 'multifactorial' as an excuse to stop investigating—or to obfuscate—but in this case it's a fitting term. For prostaglandin D₂ production: arachidonic acid is needed, cylcooxygenase is needed, and cytokines greatly contribute by inducing the release of arachidonic acid from the cell membrane—by initiating the transcription of these enzymes or by 'activating' phospholipase A₂ directly. The mineralcorticoid receptor plays a role as a nuclear chaperone for cyclophilins, as well as transcribing TGF‐β₁. Although the mechanisms of cortisol's effect are a bit more indirect, it can't be argued that hydrocortisone on the skin will lead to a bald spot and that cortical adrenalectomy will cause profound hair loss. I think we'd be on much firmer ground if certain drugs were cheap and available, such as: cyclosporine A, FK‐506, spironolactone, enoxolone (topical only), and a powerful prostaglanin D₂ inhibitor.

Mice genetically bred expressing cyclooxygenase on the skin are bald in the same way as mice expressing phospholipase A₂ on the skin, which are in turn bald in nearly the same way as those expressing interferon-γ or interleukin-1β on the skin. All evidence converges on the innate, cellular immune system defined by prostaglandins and controlled by the induction of cytokines.

To give you an idea that prostaglanins were likely used initially as defense, look up plant defensins—similar molecules created by the addition of either O₂ or H₂O₂ on an unsaturated lipid of the cell membrane . . . to create ones with reactive peroxy, cylcoperoxy, and epoxide functional groups. This was likely the original function of prostaglandins, and all eicosanoids: to help destroy bacteria with reactive oxygenated lipids. This is likely why the production of prostaglanins is controlled by cytokines—an evolutionary latecomer which can upregulate prostaglandin production in nearly all cells—or just cells in the immediate vicinity—through increasing the transcription of phosphilipase A₂ or cyclooxygenase in the nucleus.

Arachidonic acid seems to be derived only from linoleic acid. This is what Ray Peat had said, and I'm fairly certain that he's right. The natural one, made in its absence, is the Mead Acid. This cannot form prostaglandins, technically, but can form ones similar in structure but quite different in effect. Prostaglandins E₂ and D₂ are isomers, having the same chemical formula and differing only slightly. Nonetheless, they have radically different effects. Small changes on the cyclopentenone prostaglandin are nearly as specific as the changes on the steroid ring structure.

I have actually looked at the analytical data, and the prostaglandins themselves aren't actually incorporated in the hair Some oils are incorporated in the hair, but none are prostaglandins are. For this reason, I don't think they can interact directly with keratin; I think the only way to account for the disparate effects of prostaglandins E₂, F₂α, I₂, and D₂, is through their disparate effects on the four separate PPAR(α, β, γ, δ) nuclear receptors—transcription factors which have DNA binding domains and transcribe mRNA for proteins such as keratin, and enzymes, in enigmatic and interesting ways.

I can even link a rat study showing even the ingestion of prostaglandins themselves leads to hair loss—through the ingestion of oxygenated lipids.

➫ Wan, Y. "Maternal PPARγ protects nursing neonates by suppressing the production of inflammatory milk." Genes & development (2007)​

Prostaglandins are cellular defense molecules, but can rightly be considered hormones too. They don't get the attention that steroid hormones do, but they appear to be the primary controllers of the hair cycle through transcribing keratin.

I'll let you know if I can find any prostaglandin D₂ inhibitors, something I'll start reading about any time now. I think oleuropein could be one, but I've only seen it described as inhibiting cyclooxygenase. That is, however, not to say that it doesn't; molecules can only be said to inhibit the enzymes and receptors they're actually tested on, and they're tested on the most popular targets—such as PPARγ and cyclooxygenase—more often.

There is surprisingly little data on PPARβ and PPARδ.

 

[CLASH]

So essentially what we're looking at in concise terms is a stimulus producing an inflammatory response carried out through the prostaglandin cascade with the precursor of linolate/ arachidonate and subsequent counter action of HPA axis leading to an influence on the genetic level (most likely involving a predisposition) involving PPARs and thus kerarin formation ratios ultimately effecting the cells differentiated state thus leading to symptomatology (hairloss)?

If this is the case, then wouldnt we want to adress the inflammatory stimulus at its route i.e. Allergen, toxin, infection, gut dysbiosis etc. and avoid the utilization of the aformentioned pharmaceuticals? I think its helpful to see their effects in research to elucidate the discrete mechanism that you have described but say you utilize the pharma to inhibit the symptomatology of for example, hairloss, yet the inflammatory stimulus is still present wouldnt the other metabolic pathways be hindered even though the symptoms are absent?

Also, not to derail the thread but couldnt this generalized pathway:

Stimulus-> inflammation + genetic predisposition-> disease

Basically describe almost every disease process? Im sure the discrete cellular mechanisms may adjust but the basic premise is the same. If this is so, I think even without all the discrete mechanisms (not to say theyre not important) we could pretty much eradicate/ prevent all disease with some very basic lifestyle adjustments over the next few generations. This pathway would basically narrow all disease down to infection, toxic exposure, malnutrition, nutrient deficiencies and psychological stress (obviously the terms would have to be defined to some extent, specifically in toxic exposure).

 

[eddiem991]

@Travis According to your theory, what substance do you think is the most important/potent for:

1. Stopping hairloss
2. Regrowing hair?

Topic/Oral?

Your posts are highly appreciated.

 

[Travis]

So essentially what we're looking at in concise terms is a stimulus producing an inflammatory response carried out through the prostaglandin cascade with the precursor of linolate/ arachidonate and subsequent counter action of HPA axis leading to an influence on the genetic level (most likely involving a predisposition) involving PPARs and thus kerarin formation ratios ultimately effecting the cells differentiated state thus leading to symptomatology (hairloss)?

That does seem like a fairly accurate summary.

If this is the case, then wouldnt we want to adress the inflammatory stimulus at its route i.e. Allergen, toxin, infection, gut dysbiosis etc. and avoid the utilization of the aformentioned pharmaceuticals?

I wouldn't consider most phytochemicals harmful. The only synthetic molecule I even talk about, really, is spironolactone. Enoxolone is an all‐natural phytochemical, and cyclosporine A is simply a cyclic peptide made by a microorganism. As long as you understand how a drug works than it becomes harmless—because you'll always know exactly how much to take, if any. I think understanding how the phytochemicals work goes a long way in understanding the process itself. Many experiments use drugs as a research tool, and much can be learned through the application of various antagonists.

I'll let you know what I learn about Mead Acids. Would it not be something if prostaglandin D₂ could only be made from achachadonic acid? and that arachidonic acid could only be made from linoleic acid? . . . with Mead Acid capable of forming no analogue?

That would be interesting. since all of the investigative research points to just that one prostaglandin. It almost makes you wonder if linoleic acid is creating noise within the natural signalling system?

I'll take a look at the Ian Prior studies and let you know what I find out. I think it's good to avoid linoleic acid, of course—a fatty acid which could perhaps be a requisite for hair loss.

 

[Travis]

@Travis According to your theory, what substance do you think is the most important/potent for:

1. Stopping hairloss
2. Regrowing hair?

Topic/Oral?

Your posts are highly appreciated.

Cyclosporine A and FK‐506 work the best simply because they severely disrupt the T cell's ability to synthesize γ‐interferon—showing how inhibiting the killer cytokines is more effective than anything. This is very likely because these cytokines amplify the production of prostaglandin D₂ more than anything, by upregulating transcription of phospholipase A₂. But of course, other ways of inhibiting γ‐interferon would be helpful. This could mean avoiding allergenic foods, which have been shown to increase γ‐interferon. Many people have a subclinical food allergy or two without even knowing it. The immune system does respond to foreign proteins.

I would imagine that regrowing hair would necessitate the reduction of prostaglandin D₂ synthesis, which would in turn require limiting the release of killer cytokines—interleukin‐1, TNFα, and γ‐interferon—as well as limiting linoleic acid in general. The influence of the mineralcorticoid receptor seems undeniable, so reductions in cortisol may be desired. Perhaps the best would be with enoxolone: this strongly inhibits the enzyme 11β-HSD₁ on the skin, preventing the cortisone→cortisol conversion. As it's well-known, spironolactone is used to regrow hair clinically and was designed as a mineralcorticoid receptor antagonist (although its hair-regrowth function is generally falsely-attributed to its relatively minor ability to antagonize the androgen receptor.)

Enoxolone is not for oral consumption, as it inhibits a similar enzyme in the kidneys (11β-HSD₂). Enoxolone is all-natural and comes from a plant.

I think the less linoleic acid one eats—and the less allergenic foods they consume—the less drugs they will need to inhibit prostaglandin D₂ synthesis, what seems to be the primary cause of hair loss. I've shown that the only thing downstream of prostaglandin D₂ is keratin itself—which it most likely inhibits the formation of through the activation of either PPARβ or PPARδ, both of which antagonize PPARs α and γ. The transcription factors (and nuclear receptors) PPARs α and γ have been shown to transcribe keratin DNA, and all hair keratins but one have PPAR response elements.

 

[eddiem991]

Cyclosporine A and FK‐506 work the best simply because they severely disrupt the T cell's ability to synthesize γ‐interferon—showing how inhibiting the killer cytokines is more effective than anything. This is very likely because these cytokines amplify the production of prostaglandin D₂ more than anything, by upregulating transcription of phospholipase A₂. But of course, other ways of inhibiting γ‐interferon would be helpful. This could mean avoiding allergenic foods, which have been shown to increase γ‐interferon. Many people have a subclinical food allergy or two without even knowing it. The immune system does respond to foreign proteins.

I would imagine that regrowing hair would necessitate the reduction of prostaglandin D₂ synthesis, which would in turn require limiting the release of killer cytokines—interleukin‐1, TNFα, and γ‐interferon—as well as limiting linoleic acid in general. The influence of the mineralcorticoid receptor seems undeniable, so reductions in cortisol may be desired. Perhaps the best would be with enoxolone: this strongly inhibits the enzyme 11β-HSD₁ on the skin, preventing the cortisone→cortisol conversion. As it's well-known, spironolactone is used to regrow hair clinically and was designed as a mineralcorticoid receptor antagonist (although its hair-regrowth function is generally falsely-attributed to its relatively minor ability to antagonize the androgen receptor.)

Enoxolone is not for oral consumption, as it inhibits a similar enzyme in the kidneys (11β-HSD₂). Enoxolone is all-natural and comes from a plant.

I think the less linoleic acid one eats—and the less allergenic foods they consume—the less drugs they will need to inhibit prostaglandin D₂ synthesis, what seems to be the primary cause of hair loss. I've shown that the only thing downstream of prostaglandin D₂ is keratin itself—which it most likely inhibits the formation of through the activation of either PPARβ or PPARδ, both of which antagonize PPARs α and γ. The transcription factors (and nuclear receptors) PPARs α and γ have been shown to transcribe keratin DNA, and all hair keratins but one have PPAR response elements.

Okay, I won't start experimenting with strong immunosuppresive drugs, that could probably f*ck you up bad if you're not at a hospital. I thought of applying cycloporine A topically but it's very very expensive. I will start applying enoxolone and sprio in the near future though.

Would blocking prostaglandin D2 systemically cause any negative side effects?

About womens protection from hairloss: Estrogen lowers the number of cytokines in the body.

 

[Such_Saturation]

Can polysorbate80 remove the linoleic acid from the scalp?

 

[Koveras]

I'll let you know if I can find any prostaglandin D₂ inhibitors, something I'll start reading about any time now. I think oleuropein could be one, but I've only seen it described as inhibiting cyclooxygenase. That is, however, not to say that it doesn't; molecules can only be said to inhibit the enzymes and receptors they're actually tested on, and they're tested on the most popular targets—such as PPARγ and cyclooxygenase—more often..

Maybe oleuropein is why argan oil has a reputation for increasing hair growth

 

[Travis]

Maybe oleuropein is why argan oil has a reputation for increasing hair growth

I think oleuropein works primarily by inhibiting cyclooxygenase‐2 directly. In fact, a very similar molecule—also a product of the olive tree—was headlined in 2005 as being capable of just that, in journal nature:

➫ Beauchamp, Gary K. "Phytochemistry: ibuprofen-like activity in extra-virgin olive oil." Nature (2005)​

More powerful than ibuprofen per gram.

It could also work by binding to PPARγ, but since there's been no direct demonstration of this—and the fact that so many things can activate PPARγ due to its cavernous binding domain—it means little.

I've recently exonerated PPARδ of any suspicion of wrongdoing. The receptor PPARδ appears to be anabolic, and the target for illicit performance enhancers and likely even vitamin D. How prostaglandin D₂ causes hair loss should no longer be suspected to be related to PPARδ. If you read the following study you'd be forced to agree:

➫ Kim, D. H. "15-Deoxy-Δ¹²⁻¹⁴-prostaglandin J₂ stabilizes, but functionally inactivates p53 by binding to the cysteine 277 residue." Oncogene (2010)​

In which! it had been proven that 15-deoxy-Δ¹²⁻¹⁴-prostaglandin J₂ binds covalently to p53, while the near analogue 9,10-dihydro-15-deoxy-Δ¹²⁻¹⁴-prostaglandin J₂ had absolutely no effect. The difference is two hydrogens: The difference is a double-bond:

The transcription factor p53 (yellow) is usually found in the nucleus nestled within a larger protein called MDM2:

click to embiggen

The release of p53 causes apoptosis, and it also causes hair loss.

It has been shown, indisputably, that 15-deoxy-Δ¹²⁻¹⁴-prostaglandin J₂ binds to cysteine²²⁷ of p53 causing its release from MDM2. This release has been confirmed by Western blot and by antibody staining. The physical binding itself was confirmed through thiol reduction techniques, gel-shift assays, and radio-labeled 15-deoxy-Δ¹²⁻¹⁴-prostaglandin J₂ followed by autoradiography. Directed mutation of cysteine²²⁷ to alanine abrogated this effect completely.

Below is a brief depiction of the event: a Michael Addition between p53 and 15-deoxy-Δ¹²⁻¹⁴-prostaglandin J₂:

The carbonyl group on 15-deoxy-Δ¹²⁻¹⁴-prostaglandin J₂ is electronegative, and withdraws electron density away from carbon⁹ of the prostaglandin J₂. This creates a partial postive charge on carbon⁹. This ∂-positive charge allows C⁹ to be attracted to, and bound by, the negatively-charged thiol of Cys²²⁷ of the transcription factor p53. Strong reducing agents can break this sulfur–carbon bond, regenerating p53 and prostaglandin J₂.

This event has the effect of releasing p53 from its binding protein. The p53 protein then goes on to do what p53 does best: Cause apoptosis by unpregulating caspase enzymes.

And, of course, prostaglandin J₂ is formed exclusively through the spontaneous dehydration of prostaglandin D₂.

prostaglandin D₂ ⟶ 15-deoxy-Δ¹²⁻¹⁴-prostaglandin J₂ + H₂O​

The only issue I take with the study in question is somewhat semantic: the use of the term 'inactive,' by the authors, seems quite inaccurate. They claim that this binding event 'inactivates' p53.

However! Look at the Northern and Western blots as a function of time:

click to embiggen

It's plainly evident that p53 is not 'inactive' here, as it transcribes some mRNA for MDM2. This is p53's binding protein, and it is known to do this. When p53 is released, it creates more binding protein ostensibly as a way to prevent overshoot—a negative feedback mechanism.

If p53 was really 'inactive' it wouldn't do anything at all. Yet! . . it does.

It could have been considered 'inactive' in its native state—bound to MDM2, and before the prostaglandin was added. The authors seem to think that 15-deoxy-Δ¹²⁻¹⁴-prostaglandin J₂ binds to the DNA binding domain of p53: This is incorrect. Prostaglandin J₂ binds to a thiol-rich region, while the DNA-binding site of p53 is protected by MDM2. The transcription factor p53 is like a doomsday switch—the Red Button—likely released upon severe oxidative stress sensed by way of its redox-sensitive thiol domain, thereby exposing its DNA-binding to upregulate apoptosis DNA.

I'll admit that p53 may be released with slightly-less activity when done so by 15-deoxy-Δ¹²⁻¹⁴-prostaglandin J₂, but it obviously retains enough activity to transcribe MDM2. Therefore, the authors use of the word 'inactive' is not accurate at all. This borderline-negligent term seems to originate either from duplicity or an innocent misinterpretation; but since this article appears to have been translated from Korean, I will give them the benefit of a doubt—probably just an inexperienced translator…

How can this liberated p53—which had been proven to transcribe mRNA for MDM2—rightly be considered 'inactive'?

 

[Jackson Chung]

Travis, very good research you are brilliant! If I may ask, what is your academic background in? I'm a Chemical Engineer and I've had a biochemistry class before, but I'm just wondering any idea how to learn the basics very quickly so I can do brilliant research like yourself?

Also a few points:

1. When I was in India, I noticed everyone had very thick luscious hair (2x as thick as mine and 3x as thick as the average person in Michigan). It was very rare to find someone that was bald unlike my college where it seemed 10% were bald and 30% were balding. The interesting thing here is there they use a lot of PUFA when cooking (for the base they start off with vegetable oil, add spices and then add the vegetables, potatoes, etc...). Everyone there also puts oil in their hair. Dabur Amla oil is very popular there which I believe has hydrogenated castor oil and Amla extract
2. What do you think of castor oil? I understand it mimics PGE2 but also has PUFA in it. Would topically applied PUFA get converted into PGD2?
3. I remember Peat saying Naringinen (spelling?) in oranges inhibits prostaglandin formation, what are your thoughts on this?
4. There was someone called "Swiss Temples" swissTemples | A loss recovered. Who I believe did research similar to yours and had pretty good results. What's your opinion about him?
5. You say cyclosporin A is the most effective molecule in stimulating hair growth. I am probably a NW1.5 (not bad, but not perfect), my temples have receded a little bit but they've held steady for 10 years now. I'd like to get back to being a NW1, I wont hold you responsible for anything. But what's your opinion on this molecule growing back my hair that's been lost for 10 years?
6. What do you think of topical niacinamide? I understand it should be combined with caffeine and aspirin, but i'm not there yet. I mix it (.75 TBSPS) with Aloe Vera Gel (12 TBSPS), Glycerin (1 TBSPS). It seems to be a very potent inflammatory inhibitor, before my scalp would itch and flake all the time, now it never does so.
7. Any opinion of derma rolling or wounding to regrow hair cells?

Thanks for all your help! If I could I'd really like to help you with your research, but first I'd like to learn (or relearn) the basics of Biology.

 

[eddiem991]

1. When I was in India, I noticed everyone had very thick luscious hair (2x as thick as mine and 3x as thick as the average person in Michigan). It was very rare to find someone that was bald unlike my college where it seemed 10% were bald and 30% were balding. The interesting thing here is there they use a lot of PUFA when cooking (for the base they start off with vegetable oil, add spices and then add the vegetables, potatoes, etc...). Everyone there also puts oil in their hair. Dabur Amla oil is very popular there which I believe has hydrogenated castor oil and Amla extract

Where in India were you?

 

[Bodhi]

Travis if one is suffering from KP : clogging of hair follicles with too much Keratin , how would this condition fit in your picture? ( overproduction of Keratin)

 

[Jackson Chung]

Where in India were you?

Various parts, mainly the north west. I remember being at the airport and seeing the people who worked there and the flight attendants on Air India all whom had very thick luscious hair. On my mothers side, all my cousins in India have good hair. In the USA we are 4 with 1 having perfect hair, me having decent hair, my two other cousins with semi-thin but not bad hair and one baldie.

 

[LeeLemonoil]

What a fascinating thread. But did Travis fail to realize here that Retinoic acid is a strong agonist of PPARdelta and has numerous downstream effects like mitogenesis from retinoid activation?

There is this substance called Stenabolic which very potently binds PPAR delta, maybe put that on the scalp.

 

[olive]

What a fascinating thread. But did Travis fail to realize here that Retinoic acid is a strong agonist of PPARdelta and has numerous downstream effects like mitogenesis from retinoid activation?

There is this substance called Stenabolic which very potently binds PPAR delta, maybe put that on the scalp.

As far as I can tell stenabolic (SR-9009) does not bind to PPAR delta. Did you mean GW501516?

 

[LeeLemonoil]

Yes! Thanks @olive - it’s the substance you mention. Cardarine, not Stenabol

 

[olive]

Yes! Thanks @olive - it’s the substance you mention. Cardarine, not Stenabol

Do you believe that mead acid is unable to create PGD2? Do you believe PGE2 and PGF2 are necessary for hair health? I think Travis compiled and put together some really good research however I’m not sure the approach would actually work. If the end goal is to have zero 2 series prostaglandins then wouldn’t COX inhibitors give us a pretty solid look at what that would look like? Obviously avoiding Lineolic Acid is a lot safer then constant consumption of aspirin or similar however I don’t believe chronic aspirin usage has ever been shown to help hair substantially.