Hypothyroidism (Cortisol, Prolactin And Adrenal Hyperactivity) Causes Balding

[Broken man]

I think niacinamide should certainly increase metabolism, both by becoming NADH and by removing methyl groups. I was surprised to see how fast radio-labeled niacin became NADH in the cell, it was incorporated in the brain as such within two hours after injection. This certainly seems to be an energy molecule (probably why it's always, always in energy drinks) but it can raise both serotonin and homocysteine. These are things to keep in mind, and homocysteine are in part determined by methionine intake (and serotonin determined by tryptophan.)

I think it can make people too wigged-out, but also make some people more alert and better-off in general. It would seem as though the methylation and serotonin status of the user is just as important as anything.
I just did some reading just now on the downstream mechanisms—the ones after cortisol and aldosterone activation. A main player appears to be TGF-β₁, which shut's off the anagen phase of the hair cylcle. The genetic mice which over-express this, or it's receptor, have the same bald skin as mineralcorticoid hyperexpressed mice: It is shiny and has no pores. Aldosterone has been shown to upregulate TGF-β₁ about threefold, and skin is the other natural target for mineralcorticoid activity; sodium excretion needs to be regulated in the skin as well—through the sweat.

It almost looks like an evolutionary mechanism to prevent mineral loss through the skin, and aquatic animals in saline water would certainly need such a device. Why cortisol activates the mineralcorticoid receptor could be somewhat accidental, but it has much to do with 11β-HSD₁ expression (which DHT actually upregulates slightly, so there's a link there.) At the moment, the cell signal downstream of even TGF-β₁ appears to be prostaglandin E₂—linking oleuropein and inflammation in with mineralcorticoid pathway.

And I found what appears to be the best natural mineralcorticoid inhibitor. It is called wedelolactone and it's found in Eclipta species. It has been shown to both lower blood pressure and grow hair in nude mice, just what you'd expect from an anti-mineralcorticoid. This is safe internally.

The ones safe only topically are spironolactone (mineralcorticoid receptor inhibitor) and enoxolone (11β-HSD₁ inhibitor). Cyclosporine A is impossible to find and I'm really starting to question the standard mechanism for how this works. It's a really big molecule, a cyclic protein, and I'm getting the feeling that it actually inhibits TGF-β₁ directly—perhaps by binding to its cell membrane receptors.

I think oleuropein might end-up on the list by inhibiting the intracellular signalling cascade downstream of 11β-HSD₁. This would be convenient, if true, because it would tie everything together neatly.

Taurine is 11β-HSD₁ inhibitor too ye?

 

[ivy]

I think niacinamide should certainly increase metabolism, both by becoming NADH and by removing methyl groups. I was surprised to see how fast radio-labeled niacin became NADH in the cell, it was incorporated in the brain as such within two hours after injection. This certainly seems to be an energy molecule (probably why it's always, always in energy drinks) but it can raise both serotonin and homocysteine. These are things to keep in mind, and homocysteine are in part determined by methionine intake (and serotonin determined by tryptophan.)

I think it can make people too wigged-out, but also make some people more alert and better-off in general. It would seem as though the methylation and serotonin status of the user is just as important as anything.
I just did some reading just now on the downstream mechanisms—the ones after cortisol and aldosterone activation. A main player appears to be TGF-β₁, which shut's off the anagen phase of the hair cylcle. The genetic mice which over-express this, or it's receptor, have the same bald skin as mineralcorticoid hyperexpressed mice: It is shiny and has no pores. Aldosterone has been shown to upregulate TGF-β₁ about threefold, and skin is the other natural target for mineralcorticoid activity; sodium excretion needs to be regulated in the skin as well—through the sweat.

It almost looks like an evolutionary mechanism to prevent mineral loss through the skin, and aquatic animals in saline water would certainly need such a device. Why cortisol activates the mineralcorticoid receptor could be somewhat accidental, but it has much to do with 11β-HSD₁ expression (which DHT actually upregulates slightly, so there's a link there.) At the moment, the cell signal downstream of even TGF-β₁ appears to be prostaglandin E₂—linking oleuropein and inflammation in with mineralcorticoid pathway.

And I found what appears to be the best natural mineralcorticoid inhibitor. It is called wedelolactone and it's found in Eclipta species. It has been shown to both lower blood pressure and grow hair in nude mice, just what you'd expect from an anti-mineralcorticoid. This is safe internally.

The ones safe only topically are spironolactone (mineralcorticoid receptor inhibitor) and enoxolone (11β-HSD₁ inhibitor). Cyclosporine A is impossible to find and I'm really starting to question the standard mechanism for how this works. It's a really big molecule, a cyclic protein, and I'm getting the feeling that it actually inhibits TGF-β₁ directly—perhaps by binding to the receptors for this cytokine.

I think oleuropein might end-up on the list by inhibiting the intracellular signalling cascade downstream of 11β-HSD₁.

This is an excellent update, especially regarding oleuropein. Maybe you can update the thread posted by CLASH.

Still, I don't think wedelolactone would be ideal internally if it lowers blood pressure.

 

[Travis]

This is an excellent update, especially regarding oleuropein. Maybe you can update the thread posted by CLASH. [...] Still, I don't think wedelolactone would be ideal internally if it lowers blood pressure.

Not for everybody, but it's safe enough. I read a 60 day trial of it on 30 people, and it's safer than spironolactone because it doesn't have that slight anti-androgenic action. Mineralcorticoids and androgens are similar in structure, and spironolactone can inhibit the androgen receptor.

 

[ivy]

Not for everybody, but it's safe enough. I read a 60 day trial of it on 30 people, and it's safer than spironolactone because it doesn't have that slight anti-androgenic action. Mineralcorticoids and androgens are similar in structure, and spironolactone can inhibit the androgen receptor.

Can you add a reference for that trial? I would like to know what the impact on blood pressure actually was.

 

[Travis]

• Rangineni, Vasavi, D. Sharada, and Saileshnath Saxena. "Diuretic, hypotensive, and hypocholesterolemic effects of Eclipta alba in mild hypertensive subjects: a pilot study." Journal of medicinal food 10.1 (2007): 143-148.

You should see the effect it had on sodium excretion too.

 

[johnwester130]

would a thiamin/baking soda topical actually be best ?

 

[David PS]

In light of those basic factors, what do you think are practical steps for someone to attempt this reversal?

He said,

I think a lot of experimenting is needed, for example with topical use of carbonic anhydrase inhibitors.

Has anyone tried experimenting with topical use of pomegranate juice? Carbonic anhydrase inhibitor - Wikipedia

 

[Scenes]

@Travis

Spiro has been used for a long time (I’m sure you’re aware) with very little success across the board.

Can you comment as to why?

If it’s so effective at what you’re proposing, people would have regrown hair even if they believed it was due to anti-androgen effect.

 

[Travis]

@Travis

Spiro has been used for a long time (I’m sure you’re aware) with very little success across the board.

Can you comment as to why?

If it’s so effective at what you’re proposing, people would have regrown hair even if they believed it was due to anti-androgen effect.

It depends on the concentrations used, and it's slight androgenic effects would prohibit high doses. Oral mineralcorticoid doses are further restricted by blood pressure effects—you can only go so low, even if you start-out hypertensive.

Many commercial topical products are quite weak.

Take cyclosporine A for instance: This is the most effective molecule ever found for regrowing hair, yet many have written it off based on what a few people had said about Optimmune™; where it exists in a fraction of one percent—and with pharmaceutical grade wax.

Certainly people are going to write it off based on a products with .01% that they used twice a week. I'm just going by what steroid hormones, cytokines, and eicosanoids have shown to have the most effect—and the drugs which modify and/or interrupt these pathways.

 

[Scenes]

It depends on the concentrations used, and it's slight androgenic effects would prohibit high doses. Oral mineralcorticoid doses are further restricted by blood pressure effects—you can only go so low, even if you start-out hypertensive.

Many commercial topical products are quite weak.

Take cyclosporine A for instance: This is the most effective molecule ever found for regrowing hair, yet many have written it off based on what a few people had said about Optimmune™; where it exists in a fraction of one percent—and with pharmaceutical grade wax.

Certainly people are going to write it off based on a products with .01% that they used twice a week. I'm just going by what steroid hormones, cytokines, and eicosanoids have shown to have the most effect—and the drugs which modify and/or interrupt these pathways.

Thanks. Ok so is there anything available that we can put to trial topically or orally?

I saw you mention licorice root topical in a different thread...what would the effective dose approximately be?

 

[Travis]

Thanks. Ok so is there anything available that we can put to trial topically or orally?

I saw you mention licorice root topical in a different thread...what would the effective dose approximately be?

I mentioned that only before I had realized that enoxolone, the active 11β-HSD₁ inhibitor, was available commercially—and cheap. You would expect this drug to lower cortisol, and it should be no surprise that it's been shown to stimulate hairgrowth.

Perhaps not complete in itself, since it does nothing to prevent aldosterone from binding to the mineralcorticoid receptor, it is cheap and safe when used topically. It is stable, and should have about the same solubility characteristics as spironolactone—which was developed in the 70s with the express intention of inhibiting the mineralcorticoid receptor.

Wedelolactone appears to function nearly exactly like spironolactone, without any androgenic crosstalk. I think it can be seen as a natural antimineralcortoid.

This is it, unless you're determined enough to find cyclosporine A.

I plan on reading about emodin as another 11β-HSD₁ inhibitor in the future, and perhaps oleuropein as a prostaglandin inhibitor. There is no way anything could be as powerful as enoxolone, but there could perhaps be a molecule out there which inhibits 11β-HSD₁ without inhbiting 11β-HSD₂. They are slightly different enzymes with slightly different catalytic (binding) domains. Such a molecule would be perfect for hypercortisolism without raising blood pressure.

 

[johnwester130]

I mentioned that only before I had realized that enoxolone, the active 11β-HSD₁ inhibitor, was available commercially—and cheap. You would expect this drug to lower cortisol, and it should be no surprise that it's been shown to stimulate hairgrowth.

Perhaps not complete in itself, since it does nothing to prevent aldosterone from binding to the mineralcorticoid receptor, it is cheap and safe when used topically. It is stable, and should have about the same solubility characteristics as spironolactone—which was developed in the 70s with the express intention of inhibiting the mineralcorticoid receptor.

Wedelolactone appears to function nearly exactly like spironolactone, without any androgenic crosstalk. I think it can be seen as a natural antimineralcortoid.

This is it, unless you're determined enough to find cyclosporine A.

I plan on reading about emodin as another 11β-HSD₁ inhibitor in the future, and perhaps oleuropein as a prostaglandin inhibitor. There is no way anything could be as powerful as enoxolone, but there could perhaps be a molecule out there which inhibits 11β-HSD₁ without inhbiting 11β-HSD₂. They are slightly different enzymes with slightly different catalytic (binding) domains. Such a molecule would be perfect for hypercortisolism without raising blood pressure.

what about these ?

Antimineralocorticoid - Wikipedia

and for god's sake can we stop reccomending Spironolactone for hair

 

[Scenes]

There’s a powder called Eclipta alba available that is said to be useful for hair. It has wedelolactone.

https://www.amazon.com/Bhringaraj-E...=2025&creative=165953&creativeASIN=B00KRMZ4O8

Concentration high enough?

 

[tfcjesse]

There’s a powder called Eclipta alba available that is said to be useful for hair. It has wedelolactone.

https://www.amazon.com/Bhringaraj-E...=2025&creative=165953&creativeASIN=B00KRMZ4O8

Concentration high enough?

Interesting.. here's some info.
Eclipta alba - Scientific Review on Usage, Dosage, Side Effects
Check out this part too: "Combination therapy with a 3:2:1 ratio of Cuscuta Reflexa, Eclipta Alba, and Citrullus Colocynthis (totalling 5% solution, all petroleum ether extracts) appears to be significantly better than Minoxidil according to one study"

This is for topical application though.

 

[Scenes]

Also found a powder of >98% wedelolactone but I can’t buy it for personal use.

Is the Eclipta alba herb enough? Seems very unlikely given it’s been around for a while and used for hair in trials before.

@Travis what say you?

 

[Frankdee20]

Another thing would be (and I'm making assumptions here) homeless people don't wash off the vitamin d from their skin. Peat has spoken a few times about how water washes off vitamin d from the skin.

They don’t wash off staphylococcus either

 

[johnwester130]

.............so why do cortisol injections regrow hair and give people energy ?

 

[DuggaDugga]

No speculation required. There have been thousands of studies published on this—all you have to do is read them.
[?]That's because you didn't figure it out. Some people do have this all figured-out.

What are you talking about?

 

[Scenes]

https://www.researchgate.net/public...t_Endometrial_and_Ovarian_Cancer_Cells_Growth

 

[Travis]

What are you talking about?

You cannot just give-up so easily considering that so many things have been shown to cause hair growth, and so many things shown to cause hair catagen.

Much work has gone into understanding the cell cycle and I don't think comment #162 is constructive, especially considering the politics in medicine and pharmaceuticals. You can't expect the most effective drugs to be sold, or even widely-known about. You only have to take a look at the history of methylglyoxal, lapachol, and cardiovascular disease (in general) to convince yourself of this. A drug can be too effective to be profitable; the most profitable are often barely effective.

Very effective drugs are commonly sold at low concentrations, causing people to write them off. This could be done intentionally.