Oral Steroid Made My Hair Grow Back Thicker!

[EndlessPossibilities]

if finasteride isnt working for you, what do you plan on doing to keep your hair or get regrowth

Finasteride is working amazingly well. It’s this urge to urinate side effect that is the problem. Right now I am backing off then getting back on low dose. I honestly don’t know what to do cause I have tried every alternate testament except minoxidil

 

[I'mme]

Just applied my first application of topical dexa to one specific area on my Fading temple POINTs. I will do this for 2 weeks then stop.

I took hire photos to document of any progress. I expect to see it get worse then blooom after the 2 weeks if it were to work.

Wish me luck

Hey @EndlessPossibilities, how is dexa working out for you? I'm about to order some topical steroid, as I've read my persons saying it completely halt their hair loss as well as they regrew hair.

 

[fuggles]

which one ?

List of conversions
The following reactions are known to be catalyzed by 5α-reductase:[9]

• Cholestenone → 5α-Cholestanone
• Progesterone → 5α-Dihydroprogesterone
• 3α-Dihydroprogesterone → Allopregnanolone
• 3β-Dihydroprogesterone → Isopregnanolone
• Deoxycorticosterone → 5α-Dihydrodeoxycorticosterone
• Corticosterone → 5α-Dihydrocorticosterone
• Cortisol → 5α-Dihydrocortisol
• Aldosterone → 5α-Dihydroaldosterone
• Androstenedione → 5α-Androstanedione
• Testosterone → 5α-Dihydrotestosterone
• Nandrolone → 5α-Dihydronandrolone

 

[fuggles]

Aldosterone is 5alpha reduced?

Can you share where you found this info?

I find it hard to believe that aldosterone is reduced by 5ar. Because in that one article I pointed it out that DHT increased aldosterone.

You would thinking aldosterone would go down if it is 5alpha reduced right?

List of conversions
The following reactions are known to be catalyzed by 5α-reductase:[9]

• Aldosterone → 5α-Dihydroaldosterone

 

[czecha]

It is insanity. And because of my experiences with finasteride, I don't believe DHT really has a very strong role in hair loss. The scalp doesn't have the right environment to grow hair properly because there is a deficiency in "something" that is temporarily increased due to the inhibition of 5 alpha reductase. That could be an estrogen, a mineralocorticoid, a glucocorticoid... These are all options. I know for certain that if DHT were the problem, then my hair would be amazingly thick and stay that way with finasteride. It doesn't, though. It reaches a peak after about 3 weeks and then becomes thin and sheds again after whatever increased is downregulated. Many hair loss sufferers could possibly be suffering from a low grade, undiagnosed form of adrenal hyperplasia due to an enzyme malfunction or deficiency.

NLRP3 Inflammasome Cause Of Male Pattern Baldness

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...

raypeatforum.com

Do you want to chime in on this?

 

[ChemHead]

NLRP3 Inflammasome Cause Of Male Pattern Baldness

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...

raypeatforum.com

Do you want to chime in on this?

I think there's definitely something that could be going on there. I strongly believe there's a correlation between hair loss and the mineralocorticoid and glucocorticoid receptors, and aldosterone. I think the fibrosis in scalp tissue may very well be related to overexpression of mineralocorticoid receptor.

In your link, someone mentions that casp1 damages or denatures the glucocorticoid receptor. If that's actually true, I would say (if I had to guess) that, in response to decreased expression of normally functioning glucocorticoid receptors, the body upregulates its expression of the mineralocorticoid receptor to compensate and the pathology is excessive activation of the mineralocorticoid receptor in the skin by aldosterone, resulting in a higher ratio of collagen with respect to elastin and causing the tissue to become fibrotic. There is a mineralocorticoid receptor-independent induction of elastin gene expression stimulated by aldosterone in the skin.

This may explain the reason why spironolactone can work to reverse hair loss. Spironolactone is a mineralocorticoid receptor (MR) antagonist. We know that binding of the MR by aldosterone stimulates collagen type I expression. So, in a person that is already overproducing collagen (causing fibrotic, inelastic skin), using a MR antagonist like spironolactone prohibits MR activation and, thus, collagen production. Also, since aldosterone is not binding the MR, it is free to amplify production of elastic fibers via IGF-1 receptor-mediated signaling (I'm sure many people have heard that IGF-1 seems to play a role in hair growth, right?). So, aldosterone stimulates both elastic fiber production and type I collagen by two independent pathways, but, if you cut out the MR-mediated pathway, you get a decrease in collagen expression and an amplification of elastin expression. This can also be very useful for proper wound healing and prevention of scar tissue formation. This also gives more credibility to microneedling and scalp massages to break up fibrotic tissue and restore elasticity in the scalp.

You can read more about aldosterone, MR antagonists, and collagen/elastin here if you're interested: https://www.sciencedirect.com/science/article/pii/S0022202X15345863

 

[EndlessPossibilities]

Chemhead nice analysis. But how would this explain the fact that the fibrosis is perifollicular instead of all the scalp tissue?

i mean aldosterone causing mitochondiral dysfunction in the follicle ? So the body attacks it?

 

[ChemHead]

Chemhead nice analysis. But how would this explain the fact that the fibrosis is perifollicular instead of all the scalp tissue?

i mean aldosterone causing mitochondiral dysfunction in the follicle ? So the body attacks it?

Wherever there are mineralocorticoid receptors is where fibrosis could be. This also happens in vascular tissue, which is why you might generally find an association with chronically high aldosterone and atherosclerosis. However, if you were to take spironolactone, I would imagine you would see an improvement in elasticity of vascular tissue since it would inhibit mineralocorticoid receptor mediated collagen expression and increase elastin expression. So, if these receptors are overexpressed in the perifoliculum due to the lack of functional glucocorticoid receptors, I wouldn't be surprised if it is causing fibrosis.

Not sure what you mean with regard to aldosterone. Aldosterone appears to be critical in synthesis of collagen and elastin, so I don't see it causing any issues on its own. It's the overexpression of the mineralocorticoid receptor which causes excess collagen synthesis that seems to be a problem. This is how I believe spironolactone works. It blocks the mineralocorticoid receptor and inhibits aldosterone's binding and subsequent expression of collagen, but it does this without affecting aldosterone's receptor-independent action on increasing elastin expression.

 

[EndlessPossibilities]

8 months ago i focused on GaBa and that Gaba A recptor activation was the best solution and now it seems like that may be it. Gaba A activation not only can lead to less aldosterone but also is very helpful with bph and can explain the phenotype sever balders exhibit of being very tense and stressed like. ‍

 

[Johnsmith63747]

Hi @ChemHead , could I could ask you a question over the DMs, I can’t seem to message first being a new member

 

[ChemHead]

8 months ago i focused on GaBa and that Gaba A recptor activation was the best solution and now it seems like that may be it. Gaba A activation not only can lead to less aldosterone but also is very helpful with bph and can explain the phenotype sever balders exhibit of being very tense and stressed like. ‍

I actually don't necessarily believe that aldosterone is a problem. Like most things in the body, the answer is never just one thing that is pinpointed as the problem because the body is a very complex whole system and its processes are all very closely interrelated.

If one were to take oral spironolactone, you should see a subsequent increase in aldosterone. Yet, we see improvement in hair loss in many people that use spironolactone despite the increase in aldosterone that would've been caused.

So, we have to be very precise when we call out a particular chemical or process in the body that we believe is causing an issue. More appropriately, it seems like an overexpression of the mineralocorticoid receptor that aldosterone binds to is closer to the root of a possible problem. Aldosterone is involved in the body's ability to create both collagen and elastin in tissues. High aldosterone and low mineralocorticoid receptor expression leads to a higher elastin to collagen ratio. If the mineralocorticoid receptor expression were high, that ratio may be reversed. Induction of collagen synthesis is related to the binding of aldosterone to the mineralocorticoid receptor, but aldosterone also induces elastin gene expression in a non-mineralocorticoid-receptor-dependent manner. Aldosterone is the key to gene expression of both elastin and collagen, but by completely different mechanisms.. Collagen by the mineralocorticoid receptor, and elastin by the IGF-I receptor.

So, for someone with atherosclerosis, having higher aldosterone may be causal, but taking spironolactone (or any mineralocorticoid receptor antagonist) could help improve the elasticity of their vascular tissue because the high aldosterone present in their blood can no longer bind the mineralocorticoid receptor (thus, inducing overexpression of collagen), but it does induce elastin expression via phosphorylation of IGF-I receptor through c-Src activation.

So, overall, I think aldosterone is necessary and even a good thing in a properly functioning body for supple and elastic tissues that don't develop fibrosis, but there are other mechanisms involved and mineralocorticoid receptor overexpression may be a component that causes premature tissue fibrosis.

 

[ChemHead]

Also, I believe that fasting should increase aldosterone due to the need to retain salt over a long period of time consuming only water with very little to no salt intake. I believe long term fasting has a very positive effect on hair and skin, as well as just the entire body in general. Aldosterone and mineralocorticoid receptor expression may be a single component in a myriad of other pathways activated (or not activated) by long term fasting.

 

[EndlessPossibilities]

Chem do you have dandruff. Take ur phone put a bright white screen on and run your hand thru ur scalp over and over. Do u see small flakes fall?

 

[jamesbooker1975]

which one ?

List of conversions
The following reactions are known to be catalyzed by 5α-reductase:[9]

• Cholestenone → 5α-Cholestanone
• Progesterone → 5α-Dihydroprogesterone
• 3α-Dihydroprogesterone → Allopregnanolone
• 3β-Dihydroprogesterone → Isopregnanolone
• Deoxycorticosterone → 5α-Dihydrodeoxycorticosterone
• Corticosterone → 5α-Dihydrocorticosterone
• Cortisol → 5α-Dihydrocortisol
• Aldosterone → 5α-Dihydroaldosterone
• Androstenedione → 5α-Androstanedione
• Testosterone → 5α-Dihydrotestosterone
• Nandrolone → 5α-Dihydronandrolone

Incredible, think that when someone is taking finasteride or dutasteride, they are blocking all that ! most people still believe they are only blocking DHT.

 

[Selb]

Incredible, think that when someone is taking finasteride or dutasteride, they are blocking all that ! most people still believe they are only blocking DHT.

Did you have a bad experience with finasteride or something?

 

[ChemHead]

Chem do you have dandruff. Take ur phone put a bright white screen on and run your hand thru ur scalp over and over. Do u see small flakes fall?

I have not generally had dandruff historically, but it's difficult to give you a definitive answer on that because I have had various things cause dandruff over the past couple years. The least significant is that caused by scalp massage because that's obviously due to mechanical disruption.

The more significant case is that which was caused by a dietary change/healing from finasteride. I had large chunks of skin shedding and, after some couple months, it stopped and skin underneath was much softer and more supple. Hair also completely stopped falling out. Unfortunately, I didn't give it even a month to see how things would continue to progress before I screwed that all up trying to use finasteride topically. And now, here I am (exactly two years later) nearly, but not quite, recovered from finasteride and going through the exact same stages that I noticed the first time I healed from it.

 

[ChemHead]

Incredible, think that when someone is taking finasteride or dutasteride, they are blocking all that ! most people still believe they are only blocking DHT.

This is part of the reason why some people experience serious side effects from 5a-reductase inhibitors. I believe they cause damage at a genetic level. They cause a loss of genetic information or genetic senescence that takes years for the body to recover from. I believe that the damage is indefinitely unless you're encouraging your body to heal by forcing it into a state of autophagy (fasting).

 

[jamesbooker1975]

Did you have a bad experience with finasteride or something?

from 1998 to 2002 Finasteride, from 2002 ( December ) to 2018 Dutasteride, none stop . So, I guess, yes .
Weak orgasm , depression, extremely anxiety, over reaction to little things , and what all my body, joints, etc hurts , that one I am not 100 % if to blame them, but, we have no idea what really are the effects of all this hormones on bones, I bet there is a conection .
Also, high estrogen , low T , etc . What it really surprise me was my progesterone level were so low that they inform me simple as the lower limit, they can't even detect it .

But, for exampe, for progesterone. Progesterone is the one that is the natural inhibition of 5-alpha-reductase and aromatase . Cause estrogen and DHT go hand to hand, if one goes up, the other goes up, How ? the body produce less progesterone. So, what will be the answer to the new state of almost 0 DHT and normal estrogen, how the body will react to that ? Incredible , there is not a single study that answer that. Progesterone is a KEY hormone, and , somehow, it is forgotten .

And Dutasteride , thing that I didn't know it was possible back that days, f*** my liver enzyme, my cholesterol and my triglycerides ! That was a surprise that I got it after I stoped. 6 month after I stoped, everything all this ones back to normal ( except for T, progesterone and estrogen )

 

[Jakejr]

I think originally if it was this thread or a similar one someone posted they used Anavar (Oxandrolone) for 7 weeks, which resulted in significant overall hair growth.
The thread has digressed into a discussion of obscure biological interactions of equally obscure cellular interactions which just obfuscates the original claim. The question to me is: Has anyone else experienced significant hair growth using Anavar (Oxandrolone)? I understand there is even a cream. Thanks!

 

[jazz1]

I think originally if it was this thread or a similar one someone posted they used Anavar (Oxandrolone) for 7 weeks, which resulted in significant overall hair growth.
The thread has digressed into a discussion of obscure biological interactions of equally obscure cellular interactions which just obfuscates the original claim. The question to me is: Has anyone else experienced significant hair growth using Anavar (Oxandrolone)? I understand there is even a cream. Thanks!

I believe this is a mild steroid in the bodybuilding industry, hence this does not effect DHT. You think this could be linked to more oestrogen when taking the drug......