Oral Steroid Made My Hair Grow Back Thicker!

ChemHead

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Water going up into the hair shaft and making it thicker is an absolutely bonkers proposition.
You're making too many generalizations, which is exactly why no one gets anywhere in the hair loss industry. Water making the hair shaft thicker is absolutely not bonkers unless you're also willing to say that water doesn't cause plumper skin in women as well as bloating due to water retention. What you're saying is non-sense. You'd essentially be denying that women (or really anyone) don't experience water retention in the skin.. and if water retention can happen in the skin (and it does), then it is certainly capable of happening in the hair. Women experience variations in water retention every month due to their menstrual cycle. In addition, I've literally experienced this phenomenon in my own hair multiple times... like literally during 5 independent experiments I did using finasteride. So, by saying that it's not possible that the hair shaft can change in volume and texture in a very short time span, as I've said it does (and as OP apparently experienced), you're directly contradicting my own experience and essentially calling me a liar.

Besides that, aldosterone shreds hair. It's not good for it, and it's upregulated in bald scalp. Mr antagonists have been shown to promote hair growth. Aldosterone and the MR promote collagen synthesis and fibrosis, and that's probably why spironolactone works so well, because it's an MR antagonist.
Aldosterone does not "shred" hair and you should be more specific and qualify statements when you want to use vague language like that. Aldosterone, on it's own does not have negative effects on hair. It's only aldosterone binding the mineralocorticoid receptor which has negative effects in both the body in general, and hair growth. However, aldosterone has physiological effects which are mineralocorticoid receptor-independent and rely on c-Src induced phosphorylation of the IGF-1 receptor which promotes the PI3 kinase/Akt signaling pathway... which ties in nicely with the long-held notion that IGF-1 plays a role in hair growth. So, the reason that spironolactone likely has positive effects on hair loss is due to the fact that:

1. aldosterone can't bind the mineralocorticoid receptor and cause its negative effects on not only hair, but also vascular, cardiac, and other tissues.
2. the lack of mineralocorticoid receptor activation will cause a reflexive upregulation in aldosterone synthesis, which means increased induction of IGF-1 phosphorylation.

So, in short, aldosterone induced fibrosis of many different types of tissues via mineralcorticoid receptor activation = bad. Aldosterone induced phosphorylation of the IGF-1 receptor can be a good thing. This is why specificity is important. You can't just go around making blanket statements like "aldosterone is bad" or it shreds hair or whatever. It's not aldosterone itself. It's cascade of events that occur as a direct result of aldosterone overactivating the mineralocorticoid receptor either due to overexpression of the receptor, overproduction of aldosterone, or both.

However, fibrosis isn't the cause of hair loss, it's just inhibits regrowth.
I never claimed fibrosis is the cause of hair loss. It's just another piece in the same puzzle. My stance on the true cause of hair loss has been consistent and it's littered all over this thread, this forum, and other forums. Here's a quote from a post I made like an hour ago:

ALL forms of hair loss (with the exception of alopecia universalis), whether male pattern, female pattern, accutane induced, or most other drug-induced forms of loss, are caused by insufficient intrafollicular estrogen synthesis. They're all just slight variations in what causes the lack of intrafollicular estrogenic activity.

In male pattern, the primary cause is the high intrafollicular expression of 5AR which draws away the follicle's entire supply of androgens and leaves insufficient levels behind for aromatization. The male pattern is simply due to the variation in both 5AR and aromatase expression in different areas of the scalp.

In female pattern, the primary cause is low aromatase expression and/or low estrogen receptor expression. The female scalp usually has quite low expression of 5AR, so it generally plays very little role in the "female pattern" you see in their hair loss. Females that experience diffuse "female" pattern hair loss have uniformly (or globally) lower levels of aromatase and/or estrogen receptor expression than normal, which leads to insufficient intrafollicular estrogenic activity. This manifests in an evenly distributed pattern of loss across the entire scalp.

In accutane-induced loss, there is an impairment of the aromatase pathway which leads to a linear increase in hair loss on top of any other condition (like male pattern hair loss), if there is any. Accutane-induced loss on its own (with no underlying male pattern loss) will manifest the same as female pattern loss because accutane affects the aromatase pathway uniformly.. not just in the scalp, but the entire body.


Sorry, but there's no getting around the fact that DHT is the cause.
This is easily false. If it were the case, finasteride or any other 5AR antagonist would be the cure. Case closed. None of us would be on here if DHT were the cause of hair loss because we already have a very effective way of completely wiping out the body's synthesis of DHT.
 

pegasus2

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I'm not calling you a liar, I'm saying you suffer from the placebo effect. Sorry, but your personal observations don't carry any weight when they contradict the observations of independent observations. Maybe if there was no scientific evidence contradicting you then I would give more weight to your perceptions, but there is no shortage of data showing that hair shaft diameter does not change in the manner you suggest. Just look at any finasteride study where it takes 6 months to see hair shafts get thicker.

Aldosterone does not "shred" hair and you should be more specific and qualify statements when you want to use vague language like that. Aldosterone, on it's own does not have negative effects on hair. It's only aldosterone binding the mineralocorticoid receptor which has negative effects in both the body in general, and hair growth.

Come on man, this is a red herring and you know it. You're not trying to have a serious debate, you're just trying to be right. I guess whenever any of the experts says DHT shreds hair they are wrong because it's actually only by binding to the AR that it exerts its androgenic effects and causes hair loss. Oh wait, you think all the experts are smoking crack for believing in DHT theory. Honestly, going against DHT theory is about as retarded as saying the earth is flat. I can't take any argument seriously that begins with "DHT does not cause hair loss". Your post didn't say anything about IGF-1, you were saying that hair growth is mediated by aldosterone binding to the MR and increasing water in the hair shaft. When aldosterone binds to the MR it causes hair loss, period. Your changing your theory now and moving the goalposts. I refuse to play that game.

I've posted the reasons any theory besides DHT is bogus all over this forum. If you care to still chase after a fantasy that's on you.

This is easily false. If it were the case, finasteride or any other 5AR antagonist would be the cure. Case closed. None of us would be on here if DHT were the cause of hair loss because we already have a very effective way of completely wiping out the body's synthesis of DHT.

Excellent reasoning there. If a gas leak causes an explosion and blows up your house, then shutting off the gas leak should rebuild your house. Makes total sense. Here I thought it would just prevent additional explosions. Silly me.
 

ChemHead

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but there is no shortage of data showing that hair shaft diameter does not change in the manner you suggest.
Lol, there's literally no data at all because it's never been proposed nor researched in any form. Can anybody find a study for me that explains the mechanism behind the difference in hair shaft diameters of perfectly healthy individuals that don't experience hair loss? Why does one have a thicker hair shaft diameter than another (without just saying "genetics" because that just means "I don't know")? Cite one example of this abundance of data... I'm interested in seeing it.

Come on man, this is a red herring and you know it. You're not trying to have a serious debate, you're just trying to be right.
I literally don't know what to even say to this. What is your definition of a serious debate? Honestly, I wasn't really trying to have any kind of debate. I stated what I believe, why I believe it, and the underlying mechanisms which have led me to what I believe. The only thing you've done is essentially gaslighting. You're literally telling me that I didn't experience what I, in fact, 100% experienced.. not once, not twice, not thrice, but literally like 5 times I experienced this effect.. and you're telling me that it's all in my head. Dude.. I can perceive the difference in my hair when the hair shaft literally doubles in volume. There's nothing remotely placebo about that. Why tf do you think I dedicated so much time and effort in research and performing experiments to understand the mechanism? No one does that over a placebo effect that they experienced 5 times.

Your post didn't say anything about IGF-1, you were saying that hair growth is mediated by aldosterone binding to the MR and increasing water in the hair shaft.
You made vague statements like "aldosterone" shreds hair with nothing to back up that statement. If you would have said overactivation of the mineralocorticoid receptor by aldosterone "shreds hair", I don't think I would have had a problem with that. I explained to you under what context aldosterone can play a role in hair loss, but why it is not directly responsible for those effects and that, rather, it is actually overactivation of the mineralocorticoid receptor which is responsible for those effects. I then clearly explained to you that aldosterone can actually be beneficial (in a multitude of ways, not just for hair) through another pathway that is mineralocorticoid receptor-independent.

you were saying that hair growth is mediated by aldosterone binding to the MR
Nowhere did I state hair growth is mediated by aldosterone. I speak with deliberate specificity and, yet, you won't even quote what I actually say. I precisely stated that I believe the change in thickness of the hair shaft diameter I experienced was due to a shift in water retention of the hair shaft and that this change was due to a "mystery" steroid that causes water retention. Aldosterone fits that description. I then gave my reasoning for why. Hair growth and hair shaft thickness are independent phenomena. Hair growth is the synthesis of new proteins. A change in hair shaft volume can be due to its ability to retain water. If you don't believe this then you're denying the existence of a multibillion dollar industry that develops shampoos and conditioners that are specifically meant to hydrate the hair shaft and attempt to retain that moisture as best as possible.

When aldosterone binds to the MR it causes hair loss, period.
I did not dispute this anywhere in my response. I did the opposite. I completely confirmed it. The only thing I disputed was that aldosterone causes hair loss. Aldosterone on its own doesn't cause hair loss. Binding the mineralocorticoid receptor does. Stating things with specificity is important.

Your changing your theory now and moving the goalposts. I refuse to play that game.
I don't know what you're talking about. I'm not changing any part of my theory. What has changed? I brought IGF-1 into the conversation because it is a direct example of how aldosterone can be positive for hair loss via a mineralocorticoid receptor-independent pathway that involves IGF-1 phosphorylation. The whole reason I brought it up is because you said aldosterone causes hair loss. I simply told you that you were wrong for making the blanket statement that aldosterone causes hair loss and then gave you an example of how aldosterone can help with hair loss through another pathway, independent of the mineralocorticoid receptor.


Oh wait, you think all the experts are smoking crack for believing in DHT theory.
I don't think they're smoking crack. I think they are still clinging to an idea that is demonstrably flawed at its core and they're ignoring the role of other very important and relatively unexplored areas of physiology. Why is there an abundance of clinical research on the androgen receptor and 5AR and DHT, but relatively little research on the role of estrogens and the estrogen receptor in hair growth and loss? The industry has rolled with the notion that DHT is the cause of hair loss spanning many decades now and where has that gotten hair loss sufferers? We have multiple drugs that can permanently denature and disrupt all known isoforms of the 5AR enzyme and lower DHT to nearly undetectable levels and, yet, we still have hair loss. I think that speaks for itself.

Excellent reasoning there. If a gas leak causes an explosion and blows up your house, then shutting off the gas leak should rebuild your house. Makes total sense. Here I thought it would just prevent additional explosions. Silly me.
This is not even close to a logical analogy. It is a FACT that many people (including myself, at one point) use 5AR antagonists and continue to experience hair loss despite reducing their DHT synthesis to almost nothing. This fact ALONE is evidence that DHT is NOT the underlying mechanism of hair loss. That doesn't mean it has no involvement in hair loss or the hair cycle, but it 100% means that it is not the direct cause of hair loss. There's absolutely no logical way around that. We have had the ability to completely wipe out human metabolism of testosterone to DHT for 30 years with finasteride and then with dutasteride and, yet, pretty much everyone with hair loss is still plagued with hair loss. Hell, we can even completely wipe out the androgen receptor and it still won't cause hair to grow back. The only thing that has a consistent track record in growing a full head of hair on a previously bald head is MTF transition and pumping the body full of estrogens, which I'm completely against because it's incredibly unhealthy it solves a problem by a brute force approach rather than through mechanisms the female body is naturally equipped with. Not only that, it only solves the problem if you want to be a woman. And before you say that people who transition MTF also take finasteride... yes, I'm aware, but none of them would be capable of growing back a full head of hair without serious doses of exogenous estrogens. For fs, look at the former Wachowski brothers... they were both bald and then once they transitioned they had a full head of hair after like 8 months.


Look, if there's something you would like for me to qualify more or if there's a specific claim or statement I've made that you would like a citation for, I'd be happy to do that. But don't start throwing broad generalizations at me. I'm not going to sit her for 10 hours and qualify every single word I say with 50 cited publications. If there's a specific claim you disagree with and you want to know what has led me to make that claim, let me know and I'll happily cite a publication containing data I believe supports my claim. If I don't have a citation, then I'll simply just tell you it's my opinion and I don't have any clinical publications to cite.
 

czecha

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The reason I started replying to this thread is that my finasteride experience a decade ago was similar to chemheads. finasteride „regrew“ my crown back to full density incredibly quickly. Just as quick as I experienced horrible estrogenic sides.

chemhead, first of all thank you for all your research and sharing it with us. Here are some questions:

do you believe your dietary approach only stops balding or can even reverse several norwoods? Did you regrow a significant amount of hair yourself or just maintain?

do you feel you have adequate steroid production on just raw veggies, fruit nuts?

how much Calories are you eating a day if you don’t mind me asking?
 

Gunnersup

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@ChemHead I vividly remember that 2 days after I was on accutane my hair felt way thicker. I did not know the possible science behind this. Also, after ending my accutane course my skin rapidly debloated, maybe that's related to my hair miniturization as well. They both occured at the same time frame.
 

ChemHead

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@ChemHead I vividly remember that 2 days after I was on accutane my hair felt way thicker. I did not know the possible science behind this. Also, after ending my accutane course my skin rapidly debloated, maybe that's related to my hair miniturization as well. They both occured at the same time frame.
My guess for why this may possibly occur is that when you take accutane (specifically oral trans-retinoic acid), the first tissues the drug encounters would be the digestive tissues and then other organs blood carries the drug to. And the drug's effect is diminishing as the it diffuses from its origin (the digestive system) to the extremities. So, the effect has a lot to do with dynamically changing reaction kinetics. As the drug diffuses, it's being not only "used" along the way, but its concentration is also becoming weaker compared to what it was at the point of origin. Think about dumping a giant bucket of salt in a giant pool. A person swimming right next to where the bucket was dumped will taste salty water, but a person at the other end of the pool will not taste any salt in the water because it has not yet diffused to that area... and by the time it does reach that area, it will not be as salty as it was for the person tasted it when it was dumped around them.

So, what's happening is that accutane could be causing aromatase inhibition (or, at the very least, decreased estrogenic activation) at the hypothalamus before the skin or hair follicles even begin to experience decreased estrogenic activity. The hypothalamus will then command that both estrogen receptor expression and aromatase expression be upregulated. Right... because that's what the hypothalamus does. It is a biological feedback control loop and when it gets signals that are saying "not enough estrogenic stimulation", it sends commands to the pituitary to do whatever it takes to upregulate estrogenic activity.

This can cause a temporary increase in estrogenic activity in bodily extremities (such as the hair follicles) that experience the effects of accutane last (after other areas of the body) and with much less magnitude because the concentration is already low by the time it reaches those extremities. Then, after you've taken accutane for a few days or longer at a consistent dosage, the concentration of accutane begins to stabilize or reach equilibrium and the hair follicles eventually experience the same level of aromatase inhibition that the rest of the body experiences.
 

ChemHead

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Also, keep in mind that the rationalization above also explains why you may often see clinical research contradict what actually happens in practice when people are given drugs and then give anecdotal feedback. Why would something that should cause "x" temporarily cause the opposite of "x"? This is why.

It's why I think anecdotal reports are just as important and valuable as clinical data. It's unwise to look at clinical data and assume that the conclusions drawn from them are always correct or always complete and not lacking. We're not gods. We don't know everything and there's almost always more to the story than the conclusions of a clinical publication. So, there's that.
 

ChemHead

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do you believe your dietary approach only stops balding or can even reverse several norwoods? Did you regrow a significant amount of hair yourself or just maintain?
It's difficult to answer this question because I never had enough time to allow further improvement before screwing up my entire ecosystem again with finasteride. Let me give you a little information about what my hair loss was like before I ever began using finasteride and I'll explain why this is important later.

I started very aggressively losing hair between the age of 16-17. My skin has generally always been irritated and red even though it improved a little as I went into my 20s. My scalp and forehead was also very irritated and itchy... almost kind of a burning sensation at times. Now, let's fast forward to me recovering from finasteride. So, what's actually happening during this recovery is that my body is gradually regaining its ability to properly express the genes that encode for the 5AR enzymes. And as this improves, these newly synthesized 5AR enzymes begin drawing from the pool of steroids your body has to offer. This means that you temporarily end up with lower than ideal concentrations of testosterone and estrogens (among other steroids, obviously). Keep in mind, at this stage, your body is still generally synthesizing lower than ideal levels of steroids and your expression of aromatase and estrogen receptors is also lowered as well.. and this is due to the effects that finasteride has caused.

So, anyway, 5AR starts drawing away 5a-reducible steroids (like testosterone, androstenedione, etc.) and there is now less available to be aromatized. This will start to bring back symptoms of itchy and irritated skin as the hypothalamus begins to command an increase in steroid synthesis. As steroid synthesis grows these symptoms become a little worse. However, these symptoms should improve to a certain extent because the hypothalamus also begins to upregulate aromatase and estrogen receptor expression.. and this is due to the increased activation of the androgen receptor that is occurring due to its high affinity for DHT (of which tissues are now making much higher levels).

So, this, in essence, is exactly what I experienced. I started feeling incredible, cognitively and physically... I started growing new facial hair in areas that were somewhat barren, my voice became much deeper, and my skin became more like it was before I began using finasteride. I was more sensitive, it was more itchy, kind of pinkish and irritated most of the time and I started experiencing accelerated shedding of hair. This is exactly what I was expecting to happen... that everything would kind of just go back to the way it was before finasteride and that I would just have to live with it. And I was actually ok with this because of how amazing I had felt.

What I did not expect was for things to actually continue improving. Around 3 weeks later, my skin started producing a very thick oil, but it didn't look nasty and greasy... it actually looked very matte and waxy and it looked incredible. I also had a more youthful skin tone (maybe reddish-orange glow from better blood flow?) and the itchiness and irritation in my skin and scalp went away and ALL shedding ceased. I couldn't even get hair to come out from pulling on it. What did not change was the thickness of the hair shaft. The hair shaft became slightly finer... closer to what is has always been for me naturally. But the hair wasn't falling out at all and that's something you can work with. If the hair isn't falling out, that means when new growth cycles start, the density of hair at any given moment will begin to increase.

Now, the problem was: I didn't just want my hair to grow back. I wanted my hair shaft to be thicker and I wanted to continue experimenting with 5AR inhibitors to see if I could come up with a way to localize the effects to the scalp and maybe get the best of both worlds. I foolishly assumed that if things didn't work out, that I would likely suffer some sides for a few months, but I would be able to recover more quickly because I was using much smaller doses.. microdoses. Finasteride is incredibly potent, though, and it didn't matter if I used 0.01mg or 1mg. It wrecked me just as hard.

So, back to your original question.. it's kind of difficult to answer that question because I barely gave myself a month after all of these amazing changes before I started messing around with finasteride again.

do you believe your dietary approach only stops balding or can even reverse several norwoods? Did you regrow a significant amount of hair yourself or just maintain?
I believe it can and when I'm fully recovered from finasteride again, I'll keep you up to date on improvements. However, I will tell you why I think this is possible and I'll answer the other questions you asked along with that explanation.

do you feel you have adequate steroid production on just raw veggies, fruit nuts?
At the moment, my steroid production is already insufficient due to finasteride, but it's still much better than it would be with a diet heavy in meats, dairy, and grains. And I have another interesting story about what happened when I recovered from finasteride related to this, but, in short, when I fully recovered my 5AR functionality, I had far more than adequate steroid production.. it was well beyond abundant. After reaching recovery, I remember a day waking up and looking in the mirror and seeing that I had increased muscularity, vascularity, and muscular volume/hydration without having done anything at all. I hadn't been doing any weight training or any type of exercise because it's kind of an act in futility to workout when your steroid synthesis is impaired due to finasteride. I also developed an intense need to be physically active after that. Many people struggle with being motivated to exercise (and while screwed up on finasteride, myself included), but I didn't actually need any motivation... it was really more of a necessity.. I would actually feel a certain level of anxiety without it and it made it more difficult for me to focus on thing that required me to sit still.. like staring a computer. But, I wasn't bothered by this because I felt incredible.

So, this question actually converges upon what I believe is actually the heart of what causes hair loss and I'll use myself as an example for what I'm going to explain:

What I think is actually happening.. and I believe this is for most men that suffer male pattern baldness, but it obviously occurs in varying degree (some experience early and aggressive, other more mild and later in life).. is that when you're younger you're obviously producing higher levels of steroids. If you are like me, you naturally have very low levels of aromatase and estrogen receptor expression. Now, due to a variety of environmental, dietary, and lifestyle habits, your steroid synthesis begins to lower as the body protects itself from steroids that may be produced in excess due to these habits. Your enzymatic profile also begins adjusting to help facilitate the protection of your body, upregulating certain enzymes maybe to create more of a certain steroids and endogenous chemicals to deal with stress and inflammation, as well as downregulating certain enzymes for which their products are maybe starting to be overproduced and threaten the overall well-being of your organism. Right?... this is what epigenetics is about.. you encounter harsh environments or you have poor dietary habits and your body alters its epigenome to handle these changes as best as it can to help you survive as long as possible with what it's been dealt. So, for someone like me (that already has naturally low levels of aromatase expression and likely, estrogen receptor expression), the little amount of estrogenic activity I was getting as a teenager before hair loss started was barely enough to keep my hair from aggressively falling out. And when my body began to lower its steroid synthesis and/or increase its 5alpha-reduction of aromatizable steroids (perhaps, as a reaction to handle chronic inflammation), it was no longer capable of producing enough intrafollicular estrogens to sustain the hair growth cycle properly. An interesting side note I'll add is that before my hair actually started falling out during my teenage years, the quality of my hair began to decline well in advance.. it got dry, wispy, and kind of curly.. just not healthy looking. When it finally reached a certain threshold of lowered estrogenic activation, that's when it began to shed.

Now, this is not the same for everyone, but it is some variation of this same problem. In my case, my naturally low expression of aromatase/estrogen receptors means that my body needs to deliver its peak level of steroid synthesis in order to be able to provide a sufficient level of estrogenic activation to satisfy the requirements of maintaining a healthy hair cycle. Compare this to someone that doesn't experience hair loss despite eating absolute trash. They likely have much higher expressions of aromatase and estrogen receptors and their lowered steroid synthesis has relatively little effect on their abundantly sufficient supply of estrogenic activity in the scalp. On the flip side, they are more like to gain weight very easily due to their ability to produce higher estrogenic stimulation. They may also be more susceptible to conditions like gynecomastia. In my case, I couldn't become obese if I tried, nor am I able to induce gynecomastia.

So, doing anything that removes inflammatory burden from your body and causes it to operate at its highest level is going to:
1. increase total steroid synthesis
2. decrease unnecessary metabolism of steroids which was previously necessary to deal with an increased inflammatory burden brought about by poor environment/diet/lifestyle
3. increase metabolism of steroids that was reduced previously as a reaction to increased inflammatory burden....


how much Calories are you eating a day if you don’t mind me asking?
Currently, if I had to guess... probably well under 2000 calories. But this only until my body is healed again. When I first started eating this way, my brain had to get used to it. I felt hungry a lot and I just pushed through it. I started fasting as well and the desire to shove loads of food down my throat went away. It's literally addiction. I eat far fewer calories now, but much higher in nutrition and I don't get hungry at all. In fact, I can easily go a week without eating anything at all.. and I mean literally nothing.. no snacks, no small bite of this or taste of that.. just water.

Once I've recovered, though, my appetite will naturally increase quite a lot and I'll have to increase my dietary intake. For now, though, I eat enough to be fully satisfied. Ideally, I would like to weigh more and be physically bigger, but it's simply not worth bothering to do until I'm recovered and my body is producing ideal levels of steroids. Doing weight training and eating more at this point is like swimming against the current in a river. It's completely futile. Also, keeping my dietary intake as nutritionally dense and calorically low as possible will help in accelerating recovery. If it were possible to fast and then fast again a week later, that would be even better, but that's not actually possible.

So, I'll be increasing dietary intake when my body actually calls for it (and it will... it did before). One amazing thing I've learned, though, is how little your body actually needs to not just survive, but actually thrive when you remove nutritionally void foods from your diet and replace them with nutritionally dense, low calorie foods. Your body obviously needs a certain amount of calories to operate, but it's much less than most people think. Also, what most people lack is certainly not caloric intake, it's nutritional intake.
 

Gunnersup

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It's difficult to answer this question because I never had enough time to allow further improvement before screwing up my entire ecosystem again with finasteride. Let me give you a little information about what my hair loss was like before I ever began using finasteride and I'll explain why this is important later.

I started very aggressively losing hair between the age of 16-17. My skin has generally always been irritated and red even though it improved a little as I went into my 20s. My scalp and forehead was also very irritated and itchy... almost kind of a burning sensation at times. Now, let's fast forward to me recovering from finasteride. So, what's actually happening during this recovery is that my body is gradually regaining its ability to properly express the genes that encode for the 5AR enzymes. And as this improves, these newly synthesized 5AR enzymes begin drawing from the pool of steroids your body has to offer. This means that you temporarily end up with lower than ideal concentrations of testosterone and estrogens (among other steroids, obviously). Keep in mind, at this stage, your body is still generally synthesizing lower than ideal levels of steroids and your expression of aromatase and estrogen receptors is also lowered as well.. and this is due to the effects that finasteride has caused.

So, anyway, 5AR starts drawing away 5a-reducible steroids (like testosterone, androstenedione, etc.) and there is now less available to be aromatized. This will start to bring back symptoms of itchy and irritated skin as the hypothalamus begins to command an increase in steroid synthesis. As steroid synthesis grows these symptoms become a little worse. However, these symptoms should improve to a certain extent because the hypothalamus also begins to upregulate aromatase and estrogen receptor expression.. and this is due to the increased activation of the androgen receptor that is occurring due to its high affinity for DHT (of which tissues are now making much higher levels).

So, this, in essence, is exactly what I experienced. I started feeling incredible, cognitively and physically... I started growing new facial hair in areas that were somewhat barren, my voice became much deeper, and my skin became more like it was before I began using finasteride. I was more sensitive, it was more itchy, kind of pinkish and irritated most of the time and I started experiencing accelerated shedding of hair. This is exactly what I was expecting to happen... that everything would kind of just go back to the way it was before finasteride and that I would just have to live with it. And I was actually ok with this because of how amazing I had felt.

What I did not expect was for things to actually continue improving. Around 3 weeks later, my skin started producing a very thick oil, but it didn't look nasty and greasy... it actually looked very matte and waxy and it looked incredible. I also had a more youthful skin tone (maybe reddish-orange glow from better blood flow?) and the itchiness and irritation in my skin and scalp went away and ALL shedding ceased. I couldn't even get hair to come out from pulling on it. What did not change was the thickness of the hair shaft. The hair shaft became slightly finer... closer to what is has always been for me naturally. But the hair wasn't falling out at all and that's something you can work with. If the hair isn't falling out, that means when new growth cycles start, the density of hair at any given moment will begin to increase.

Now, the problem was: I didn't just want my hair to grow back. I wanted my hair shaft to be thicker and I wanted to continue experimenting with 5AR inhibitors to see if I could come up with a way to localize the effects to the scalp and maybe get the best of both worlds. I foolishly assumed that if things didn't work out, that I would likely suffer some sides for a few months, but I would be able to recover more quickly because I was using much smaller doses.. microdoses. Finasteride is incredibly potent, though, and it didn't matter if I used 0.01mg or 1mg. It wrecked me just as hard.

So, back to your original question.. it's kind of difficult to answer that question because I barely gave myself a month after all of these amazing changes before I started messing around with finasteride again.


I believe it can and when I'm fully recovered from finasteride again, I'll keep you up to date on improvements. However, I will tell you why I think this is possible and I'll answer the other questions you asked along with that explanation.


At the moment, my steroid production is already insufficient due to finasteride, but it's still much better than it would be with a diet heavy in meats, dairy, and grains. And I have another interesting story about what happened when I recovered from finasteride related to this, but, in short, when I fully recovered my 5AR functionality, I had far more than adequate steroid production.. it was well beyond abundant. After reaching recovery, I remember a day waking up and looking in the mirror and seeing that I had increased muscularity, vascularity, and muscular volume/hydration without having done anything at all. I hadn't been doing any weight training or any type of exercise because it's kind of an act in futility to workout when your steroid synthesis is impaired due to finasteride. I also developed an intense need to be physically active after that. Many people struggle with being motivated to exercise (and while screwed up on finasteride, myself included), but I didn't actually need any motivation... it was really more of a necessity.. I would actually feel a certain level of anxiety without it and it made it more difficult for me to focus on thing that required me to sit still.. like staring a computer. But, I wasn't bothered by this because I felt incredible.

So, this question actually converges upon what I believe is actually the heart of what causes hair loss and I'll use myself as an example for what I'm going to explain:

What I think is actually happening.. and I believe this is for most men that suffer male pattern baldness, but it obviously occurs in varying degree (some experience early and aggressive, other more mild and later in life).. is that when you're younger you're obviously producing higher levels of steroids. If you are like me, you naturally have very low levels of aromatase and estrogen receptor expression. Now, due to a variety of environmental, dietary, and lifestyle habits, your steroid synthesis begins to lower as the body protects itself from steroids that may be produced in excess due to these habits. Your enzymatic profile also begins adjusting to help facilitate the protection of your body, upregulating certain enzymes maybe to create more of a certain steroids and endogenous chemicals to deal with stress and inflammation, as well as downregulating certain enzymes for which their products are maybe starting to be overproduced and threaten the overall well-being of your organism. Right?... this is what epigenetics is about.. you encounter harsh environments or you have poor dietary habits and your body alters its epigenome to handle these changes as best as it can to help you survive as long as possible with what it's been dealt. So, for someone like me (that already has naturally low levels of aromatase expression and likely, estrogen receptor expression), the little amount of estrogenic activity I was getting as a teenager before hair loss started was barely enough to keep my hair from aggressively falling out. And when my body began to lower its steroid synthesis and/or increase its 5alpha-reduction of aromatizable steroids (perhaps, as a reaction to handle chronic inflammation), it was no longer capable of producing enough intrafollicular estrogens to sustain the hair growth cycle properly. An interesting side note I'll add is that before my hair actually started falling out during my teenage years, the quality of my hair began to decline well in advance.. it got dry, wispy, and kind of curly.. just not healthy looking. When it finally reached a certain threshold of lowered estrogenic activation, that's when it began to shed.

Now, this is not the same for everyone, but it is some variation of this same problem. In my case, my naturally low expression of aromatase/estrogen receptors means that my body needs to deliver its peak level of steroid synthesis in order to be able to provide a sufficient level of estrogenic activation to satisfy the requirements of maintaining a healthy hair cycle. Compare this to someone that doesn't experience hair loss despite eating absolute trash. They likely have much higher expressions of aromatase and estrogen receptors and their lowered steroid synthesis has relatively little effect on their abundantly sufficient supply of estrogenic activity in the scalp. On the flip side, they are more like to gain weight very easily due to their ability to produce higher estrogenic stimulation. They may also be more susceptible to conditions like gynecomastia. In my case, I couldn't become obese if I tried, nor am I able to induce gynecomastia.

So, doing anything that removes inflammatory burden from your body and causes it to operate at its highest level is going to:
1. increase total steroid synthesis
2. decrease unnecessary metabolism of steroids which was previously necessary to deal with an increased inflammatory burden brought about by poor environment/diet/lifestyle
3. increase metabolism of steroids that was reduced previously as a reaction to increased inflammatory burden....



Currently, if I had to guess... probably well under 2000 calories. But this only until my body is healed again. When I first started eating this way, my brain had to get used to it. I felt hungry a lot and I just pushed through it. I started fasting as well and the desire to shove loads of food down my throat went away. It's literally addiction. I eat far fewer calories now, but much higher in nutrition and I don't get hungry at all. In fact, I can easily go a week without eating anything at all.. and I mean literally nothing.. no snacks, no small bite of this or taste of that.. just water.

Once I've recovered, though, my appetite will naturally increase quite a lot and I'll have to increase my dietary intake. For now, though, I eat enough to be fully satisfied. Ideally, I would like to weigh more and be physically bigger, but it's simply not worth bothering to do until I'm recovered and my body is producing ideal levels of steroids. Doing weight training and eating more at this point is like swimming against the current in a river. It's completely futile. Also, keeping my dietary intake as nutritionally dense and calorically low as possible will help in accelerating recovery. If it were possible to fast and then fast again a week later, that would be even better, but that's not actually possible.

So, I'll be increasing dietary intake when my body actually calls for it (and it will... it did before). One amazing thing I've learned, though, is how little your body actually needs to not just survive, but actually thrive when you remove nutritionally void foods from your diet and replace them with nutritionally dense, low calorie foods. Your body obviously needs a certain amount of calories to operate, but it's much less than most people think. Also, what most people lack is certainly not caloric intake, it's nutritional intake.
very, very, very interesting. I also can not gain weight at all even if I tried. Same goes for gyno, I have no sign of it.
 

czecha

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very, very, very interesting. I also can not gain weight at all even if I tried. Same goes for gyno, I have no sign of it.
I'm the same. And I always observed the same thing about people with gyno, wide hips etc.
thanks a ton @ChemHead
as a heads up, I'm on your diet for 5 days now (although its just 90% clean as of now) and I am feeling GREAT. Kinda sucks that I will have to get super skinny again, but it is what it is.
 

czecha

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It's difficult to answer this question because I never had enough time to allow further improvement before screwing up my entire ecosystem again with finasteride. Let me give you a little information about what my hair loss was like before I ever began using finasteride and I'll explain why this is important later.

I started very aggressively losing hair between the age of 16-17. My skin has generally always been irritated and red even though it improved a little as I went into my 20s. My scalp and forehead was also very irritated and itchy... almost kind of a burning sensation at times. Now, let's fast forward to me recovering from finasteride. So, what's actually happening during this recovery is that my body is gradually regaining its ability to properly express the genes that encode for the 5AR enzymes. And as this improves, these newly synthesized 5AR enzymes begin drawing from the pool of steroids your body has to offer. This means that you temporarily end up with lower than ideal concentrations of testosterone and estrogens (among other steroids, obviously). Keep in mind, at this stage, your body is still generally synthesizing lower than ideal levels of steroids and your expression of aromatase and estrogen receptors is also lowered as well.. and this is due to the effects that finasteride has caused.

So, anyway, 5AR starts drawing away 5a-reducible steroids (like testosterone, androstenedione, etc.) and there is now less available to be aromatized. This will start to bring back symptoms of itchy and irritated skin as the hypothalamus begins to command an increase in steroid synthesis. As steroid synthesis grows these symptoms become a little worse. However, these symptoms should improve to a certain extent because the hypothalamus also begins to upregulate aromatase and estrogen receptor expression.. and this is due to the increased activation of the androgen receptor that is occurring due to its high affinity for DHT (of which tissues are now making much higher levels).

So, this, in essence, is exactly what I experienced. I started feeling incredible, cognitively and physically... I started growing new facial hair in areas that were somewhat barren, my voice became much deeper, and my skin became more like it was before I began using finasteride. I was more sensitive, it was more itchy, kind of pinkish and irritated most of the time and I started experiencing accelerated shedding of hair. This is exactly what I was expecting to happen... that everything would kind of just go back to the way it was before finasteride and that I would just have to live with it. And I was actually ok with this because of how amazing I had felt.

What I did not expect was for things to actually continue improving. Around 3 weeks later, my skin started producing a very thick oil, but it didn't look nasty and greasy... it actually looked very matte and waxy and it looked incredible. I also had a more youthful skin tone (maybe reddish-orange glow from better blood flow?) and the itchiness and irritation in my skin and scalp went away and ALL shedding ceased. I couldn't even get hair to come out from pulling on it. What did not change was the thickness of the hair shaft. The hair shaft became slightly finer... closer to what is has always been for me naturally. But the hair wasn't falling out at all and that's something you can work with. If the hair isn't falling out, that means when new growth cycles start, the density of hair at any given moment will begin to increase.

Now, the problem was: I didn't just want my hair to grow back. I wanted my hair shaft to be thicker and I wanted to continue experimenting with 5AR inhibitors to see if I could come up with a way to localize the effects to the scalp and maybe get the best of both worlds. I foolishly assumed that if things didn't work out, that I would likely suffer some sides for a few months, but I would be able to recover more quickly because I was using much smaller doses.. microdoses. Finasteride is incredibly potent, though, and it didn't matter if I used 0.01mg or 1mg. It wrecked me just as hard.

So, back to your original question.. it's kind of difficult to answer that question because I barely gave myself a month after all of these amazing changes before I started messing around with finasteride again.


I believe it can and when I'm fully recovered from finasteride again, I'll keep you up to date on improvements. However, I will tell you why I think this is possible and I'll answer the other questions you asked along with that explanation.


At the moment, my steroid production is already insufficient due to finasteride, but it's still much better than it would be with a diet heavy in meats, dairy, and grains. And I have another interesting story about what happened when I recovered from finasteride related to this, but, in short, when I fully recovered my 5AR functionality, I had far more than adequate steroid production.. it was well beyond abundant. After reaching recovery, I remember a day waking up and looking in the mirror and seeing that I had increased muscularity, vascularity, and muscular volume/hydration without having done anything at all. I hadn't been doing any weight training or any type of exercise because it's kind of an act in futility to workout when your steroid synthesis is impaired due to finasteride. I also developed an intense need to be physically active after that. Many people struggle with being motivated to exercise (and while screwed up on finasteride, myself included), but I didn't actually need any motivation... it was really more of a necessity.. I would actually feel a certain level of anxiety without it and it made it more difficult for me to focus on thing that required me to sit still.. like staring a computer. But, I wasn't bothered by this because I felt incredible.

So, this question actually converges upon what I believe is actually the heart of what causes hair loss and I'll use myself as an example for what I'm going to explain:

What I think is actually happening.. and I believe this is for most men that suffer male pattern baldness, but it obviously occurs in varying degree (some experience early and aggressive, other more mild and later in life).. is that when you're younger you're obviously producing higher levels of steroids. If you are like me, you naturally have very low levels of aromatase and estrogen receptor expression. Now, due to a variety of environmental, dietary, and lifestyle habits, your steroid synthesis begins to lower as the body protects itself from steroids that may be produced in excess due to these habits. Your enzymatic profile also begins adjusting to help facilitate the protection of your body, upregulating certain enzymes maybe to create more of a certain steroids and endogenous chemicals to deal with stress and inflammation, as well as downregulating certain enzymes for which their products are maybe starting to be overproduced and threaten the overall well-being of your organism. Right?... this is what epigenetics is about.. you encounter harsh environments or you have poor dietary habits and your body alters its epigenome to handle these changes as best as it can to help you survive as long as possible with what it's been dealt. So, for someone like me (that already has naturally low levels of aromatase expression and likely, estrogen receptor expression), the little amount of estrogenic activity I was getting as a teenager before hair loss started was barely enough to keep my hair from aggressively falling out. And when my body began to lower its steroid synthesis and/or increase its 5alpha-reduction of aromatizable steroids (perhaps, as a reaction to handle chronic inflammation), it was no longer capable of producing enough intrafollicular estrogens to sustain the hair growth cycle properly. An interesting side note I'll add is that before my hair actually started falling out during my teenage years, the quality of my hair began to decline well in advance.. it got dry, wispy, and kind of curly.. just not healthy looking. When it finally reached a certain threshold of lowered estrogenic activation, that's when it began to shed.

Now, this is not the same for everyone, but it is some variation of this same problem. In my case, my naturally low expression of aromatase/estrogen receptors means that my body needs to deliver its peak level of steroid synthesis in order to be able to provide a sufficient level of estrogenic activation to satisfy the requirements of maintaining a healthy hair cycle. Compare this to someone that doesn't experience hair loss despite eating absolute trash. They likely have much higher expressions of aromatase and estrogen receptors and their lowered steroid synthesis has relatively little effect on their abundantly sufficient supply of estrogenic activity in the scalp. On the flip side, they are more like to gain weight very easily due to their ability to produce higher estrogenic stimulation. They may also be more susceptible to conditions like gynecomastia. In my case, I couldn't become obese if I tried, nor am I able to induce gynecomastia.

So, doing anything that removes inflammatory burden from your body and causes it to operate at its highest level is going to:
1. increase total steroid synthesis
2. decrease unnecessary metabolism of steroids which was previously necessary to deal with an increased inflammatory burden brought about by poor environment/diet/lifestyle
3. increase metabolism of steroids that was reduced previously as a reaction to increased inflammatory burden....



Currently, if I had to guess... probably well under 2000 calories. But this only until my body is healed again. When I first started eating this way, my brain had to get used to it. I felt hungry a lot and I just pushed through it. I started fasting as well and the desire to shove loads of food down my throat went away. It's literally addiction. I eat far fewer calories now, but much higher in nutrition and I don't get hungry at all. In fact, I can easily go a week without eating anything at all.. and I mean literally nothing.. no snacks, no small bite of this or taste of that.. just water.

Once I've recovered, though, my appetite will naturally increase quite a lot and I'll have to increase my dietary intake. For now, though, I eat enough to be fully satisfied. Ideally, I would like to weigh more and be physically bigger, but it's simply not worth bothering to do until I'm recovered and my body is producing ideal levels of steroids. Doing weight training and eating more at this point is like swimming against the current in a river. It's completely futile. Also, keeping my dietary intake as nutritionally dense and calorically low as possible will help in accelerating recovery. If it were possible to fast and then fast again a week later, that would be even better, but that's not actually possible.

So, I'll be increasing dietary intake when my body actually calls for it (and it will... it did before). One amazing thing I've learned, though, is how little your body actually needs to not just survive, but actually thrive when you remove nutritionally void foods from your diet and replace them with nutritionally dense, low calorie foods. Your body obviously needs a certain amount of calories to operate, but it's much less than most people think. Also, what most people lack is certainly not caloric intake, it's nutritional intake.
follow up questions: how long do you expect it to take to fully heal, and then regrow hair, in your case?


and:
when we have recovered, would standalone dermarolling start being effective? perhaps coupled with fasting/autophagy?
 

ChemHead

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how long do you expect it to take to fully heal, and then regrow hair, in your case?
I've been consistently wrong about my timeframe on this for over a year. Back in September, I was thinking that I would probably be recovered by December. I certainly continued to improve, but I was clearly still wrong. Right now, I have a hard time believing that I won't be recovered by the end of March, but I'm more skeptical of my predictions about when this will be resolved.

However, the more important markers of improvement are all of the "milestones" I reached in the 2-3 months leading up to my first recovery.. and I'm experiencing many of those now. Something that has happened in just the past week is that new beard hair has started sprouting. In addition to new terminal beard hairs, there are also easily visible vellus beard hairs that are growing. So, it's still occurring.

Other milestones I'm looking out for:

-the beginning of itchiness in skin, as well as increased oil output of the skin (this has already begun, but it's not quite to the expected output yet)

-change in voice. My voice has changed multiple times in the past few months... I'd wake up one day and my voice was discernably much deeper than the day before. However, these changes have not persisted... they're still oscillating back and forth due to the way the body recovers. When the change in voice persists, I'll be within a few weeks of "full recovery".

-testicular discomfort. As 5AR functionality returns, there are phases of steroidal insufficiency and as the hypothalamus calls for higher steroid synthesis, the testicles (I believe) kind of get overworked and I experience somewhat sharp, random testicular pains... it's difficult to describe. I'm experiencing it now, but, based on my previous experience, it's not as intense as it will soon get. As testicular volume grows, this also becomes uncomfortable in its own way because... it doesn't really fit all that well in the scrotum. The skin of the scrotum actually changes and gets thicker and tighter.. more taut.. and the increase in testicular volume doesn't have much accommodation in terms of space. This does get better eventually, but it's uncomfortable and kind of annoying while trying to sleep. Right now, I've experienced the change in the scrotum just these past 2-3 weeks. The skin is taut, but the testicular volume is currently pretty low... my junk looks like the size of a walnut right now. I attribute this to the increase in 5AR activity drawing away androgens and leaving that area deficient in both androgens and estrogens. This will be temporary, though. As soon as the hypothalamus begins commanding higher steroid synthesis, this will get better and testicular volume will increase.

-continued improvements in sleep.. the need for less sleep. I'll start to experience the deeper sleep phase much earlier and will require less sleep. I also begin to experience incredibly vivid dreams and my ability to recall dreams also improves. This actually occurred a few months ago and lasted for a few weeks. It didn't stick, though, which means that I wasn't fully recovered and my body rebounded (or oscillated) back toward the other end of the spectrum. This happened the first time I recovered as well. When it happened, though, it only happened once and the next time the change occurred, the change persisted. There was not more than 2-3 months between these occurrences of improved sleep/dreaming the last time I recovered, so I expect something similar this time around.

-sexual improvements.. I started experiencing very frequent wet dreams. Nocturnal erections increased for a phase, then went away, and then returned much stronger and for good. A few months back, I was getting nocturnal erections and they've gone away. The next time they return, I expect them to stay for good just like the first recovery. When I was fully recovered, I pretty much walked around with a 24/7 erection.. no joke. And I've never been capable of this even as a teenager, so I attribute this to the dietary change. Keep in mind, I made this dietary change and was perfectly consistent with it for close to two years before I recovered the first time. So, it wasn't like I changed my diet and then a couple months later I was magically a hard-dick charger.

-this is one of my favorites: I started laughing a lot more. I found myself happier and then I would wonder why. There was nothing that was particularly making me happier, I just was. I would be sitting around reading something on Reddit or whatever and I would just start randomly laughing almost uncontrollably at things that I was probably too braindead to recognize were hilarious. And the whole time I'm doing this, I'm sure people around me thought I was probably nuts because it's not something that was typical for me.

-I became, cognitively, much sharper. I would respond to something... maybe a question asked or response to a joke or whatever, with such quickness and wit that I had to stop and ask myself "did I just do that?.. was that me?". For quite a long time, I had believed that for some reason, other people were better at interacting socially or being quick to respond to certain things because I was somehow built differently. I soon came to understand that I wasn't built differently, I was broken... handicapped by the lasting effects of finasteride.

So, you can kind of see that as I recovered, I began to feel almost kind of superhuman. And then I started wondering I maybe I just felt that way because I had been deprived of all these qualities for so long and that they were just normal to everyone else.

when we have recovered, would standalone dermarolling start being effective? perhaps coupled with fasting/autophagy?
I believe so. In fact, I believe that any natural treatment that has the ability to accelerate hair growth will be effective. Right now, it can't be effective for me because I don't yet have the basic prerequisites for growing hair. My biochemical machinery needs to be working properly, otherwise anything I do to stimulate growth will kind of just be in vain. I do have all that stuff ready to go for when I've recovered, though. I have a derminator and I plan to use other various growth stimulants like rosemary oil and ricinoleic acid extracted from castor oil. Also plan to do daily intense massage, which I've begun doing again, but, admittedly, not very consistently.

One thing that I will continue to do, though, is look out for natural substances that are able to increase aromatase expression locally without causing systemic effects. As I age, my steroid synthesis will naturally decline and the quality of hair growth will decline with it. If I can find other substances, in addition to ricinoleic acid, that can upregulate aromatase more powerfully, I should be able to increase the quality of hair growth and maintain it for a much longer portion of my lifespan. But just giving your body the ability to synthesize as much steroids as it's capable of and also giving it the ability to have as high expression of aromatase as naturally possible by good dietary habits will be the biggest factor.
 
Last edited:

czecha

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I've been consistently wrong about my timeframe on this for over a year. Back in September, I was thinking that I would probably be recovered by December. I certainly continued to improve, but I was clearly still wrong. Right now, I have a hard time believing that I won't be recovered by the end of March, but I'm more skeptical of my predictions about when this will be resolved.

However, the more important markers of improvement are all of the "milestones" I reached in the 2-3 months leading up to my first recovery.. and I'm experiencing many of those now. Something that has happened in just the past week is that new beard hair has started sprouting. In addition to new terminal beard hairs, there are also easily visible vellus beard hairs that are growing. So, it's still occurring.

Other milestones I'm looking out for:

-the beginning of itchiness in skin, as well as increased oil output of the skin (this has already begun, but it's not quite to the expected output yet)

-change in voice. My voice has changed multiple times in the past few months... I'd wake up one day and my voice was discernably much deeper than the day before. However, these changes have not persisted... they're still oscillating back and forth due to the way the body recovers. When the change in voice persists, I'll be within a few weeks of "full recovery".

-testicular discomfort. As 5AR functionality returns, there are phases of steroidal insufficiency and as the hypothalamus calls for higher steroid synthesis, the testicles (I believe) kind of get overworked and I experience somewhat sharp, random testicular pains... it's difficult to describe. I'm experiencing it now, but, based on my previous experience, it's not as intense as it will soon get. As testicular volume grows, this also becomes uncomfortable in its own way because... it doesn't really fit all that well in the scrotum. The skin of the scrotum actually changes and gets thicker and tighter.. more taut.. and the increase in testicular volume doesn't have much accommodation in terms of space. This does get better eventually, but it's uncomfortable and kind of annoying while trying to sleep. Right now, I've experienced the change in the scrotum just these past 2-3 weeks. The skin is taut, but the testicular volume is currently pretty low... my junk looks like the size of a walnut right now. I attribute this to the increase in 5AR activity drawing away androgens and leaving that area deficient in both androgens and estrogens. This will be temporary, though. As soon as the hypothalamus begins commanding higher steroid synthesis, this will get better and testicular volume will increase.

-continued improvements in sleep.. the need for less sleep. I'll start to experience the deeper sleep phase much earlier and will require less sleep. I also begin to experience incredibly vivid dreams and my ability to recall dreams also improves. This actually occurred a few months ago and lasted for a few weeks. It didn't stick, though, which means that I wasn't fully recovered and my body rebounded (or oscillated) back toward the other end of the spectrum. This happened the first time I recovered as well. When it happened, though, it only happened once and the next time the change occurred, the change persisted. There was not more than 2-3 months between these occurrences of improved sleep/dreaming the last time I recovered, so I expect something similar this time around.

-sexual improvements.. I started experiencing very frequent wet dreams. Nocturnal erections increased for a phase, then went away, and then returned much stronger and for good. A few months back, I was getting nocturnal erections and they've gone away. The next time they return, I expect them to stay for good just like the first recovery. When I was fully recovered, I pretty much walked around with a 24/7 erection.. no joke. And I've never been capable of this even as a teenager, so I attribute this to the dietary change. Keep in mind, I made this dietary change and was perfectly consistent with it for close to two years before I recovered the first time. So, it wasn't like I changed my diet and then a couple months later I was magically a hard-dick charger.

-this is one of my favorites: I started laughing a lot more. I found myself happier and then I would wonder why. There was nothing that was particularly making me happier, I just was. I would be sitting around reading something on Reddit or whatever and I would just start randomly laughing almost uncontrollably at things that I was probably too braindead to recognize were hilarious. And the whole time I'm doing this, I'm sure people around me thought I was probably nuts because it's not something that was typical for me.

-I became, cognitively, much sharper. I would respond to something... maybe a question asked or response to a joke or whatever, with such quickness and wit that I had to stop and ask myself "did I just do that?.. was that me?". For quite a long time, I had believed that for some reason, other people were better at interacting socially or being quick to respond to certain things because I was somehow built differently. I soon came to understand that I wasn't built differently, I was broken... handicapped by the lasting effects of finasteride.

So, you can kind of see that as I recovered, I began to feel almost kind of superhuman. And then I started wondering I maybe I just felt that way because I had been deprived of all these qualities for so long and that they were just normal to everyone else.


I believe so. In fact, I believe that any natural treatment that has the ability to accelerate hair growth will be effective. Right now, it can't be effective for me because I don't yet have the basic prerequisites for growing hair. My biochemical machinery needs to be working properly, otherwise anything I do to stimulate growth will kind of just be in vain. I do have all that stuff ready to go for when I've recovered, though. I have a derminator and I plan to use other various growth stimulants like rosemary oil and ricinoleic acid extracted from castor oil. Also plan to do daily intense massage, which I've begun doing again, but, admittedly, not very consistently.

One thing that I will continue to do, though, is look out for natural substances that are able to increase aromatase expression locally without causing systemic effects. As I age, my steroid synthesis will naturally decline and the quality of hair growth will decline with it. If I can find other substances, in addition to ricinoleic acid, that can upregulate aromatase more powerfully, I should be able to increase the quality of hair growth and maintain it for a much longer portion of my lifespan. But just giving your body the ability to synthesize as much steroids as it's capable of and also giving it the ability to have as high expression of aromatase as naturally possible by good dietary habits will be the biggest factor.
Great!

I am getting a bit confused what bits of that is recovery from PFS and what is recovery from the state that was leading to male pattern baldness in the first place? A bit of both?

Either way, I'll stick to your diet since mental improvements are already evident and report back to the forum in the coming weeks and months :)
 

ChemHead

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Great!

I am getting a bit confused what bits of that is recovery from PFS and what is recovery from the state that was leading to male pattern baldness in the first place? A bit of both?

Either way, I'll stick to your diet since mental improvements are already evident and report back to the forum in the coming weeks and months :)
Most of the improvements were due to the recovery from finasteride. However, the dietary habits accelerated that recovery and then made improvements well past where my previous "normal" was before I ever took finasteride.
 

whatevr

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To be entirely technical, DHT does not cause hair loss. Lack of epi-testosterone (natural anti-androgen) in balding follicles is what causes hair loss.

Testosterone is balanced in a 1:1 ratio with epitestosterone in serum, around 10:1 in healthy hair follicles, and T prevails up to 40:1 in balding follicles. This is essentially a localized hormonal imbalance that we're dealing with.

For this reason, studies which expose a hair follicle to DHT in a petri dish prove nothing, other than being able to kill a hair follicle by inducing serious hormonal imbalance (in vivo, a healthy, non-balding person's follicle does not bathe in DHT, at least not without other hormones which balance it out). You could formulate that type of study to prove numerous other hormones are bad for hair.

Since that doesn't resemble the in vivo environment that a hair follicle grows in, it's irrelevant. It's been shown that non-balding, occipital follicles from balding people have a similar hormonal balance as vertex hairs from non-balding people. There is no need to invoke the mythical 'increased genetic sensitivity to androgens', when such a vast difference in hormone levels is far more likely to blame.
 

Harleyj888

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To be entirely technical, DHT does not cause hair loss. Lack of epi-testosterone (natural anti-androgen) in balding follicles is what causes hair loss.

Testosterone is balanced in a 1:1 ratio with epitestosterone in serum, around 10:1 in healthy hair follicles, and T prevails up to 40:1 in balding follicles. This is essentially a localized hormonal imbalance that we're dealing with.

For this reason, studies which expose a hair follicle to DHT in a petri dish prove nothing, other than being able to kill a hair follicle by inducing serious hormonal imbalance (in vivo, a healthy, non-balding person's follicle does not bathe in DHT, at least not without other hormones which balance it out). You could formulate that type of study to prove numerous other hormones are bad for hair.

Since that doesn't resemble the in vivo environment that a hair follicle grows in, it's irrelevant. It's been shown that non-balding, occipital follicles from balding people have a similar hormonal balance as vertex hairs from non-balding people. There is no need to invoke the mythical 'increased genetic sensitivity to androgens', when such a vast difference in hormone levels is far more likely to blame.
How do you explain why finasteride works for 80% of people
 

whatevr

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How do you explain why finasteride works for 80% of people

There is nothing to explain. Obviously reducing DHT reduces the ratio of androgens:antiandrogens in the hair follicle which results in a healthier environment for hair to grow in.

That doesn't make it the right way of dealing with things however. Research should be directed at why there is a lack of epitestosterone in balding follicles and how to restore the hormonal balance to normal so that the hair follicle can be protected from androgens once again.
 

Norwoody

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There is nothing to explain. Obviously reducing DHT reduces the ratio of androgens:antiandrogens in the hair follicle which results in a healthier environment for hair to grow in.

That doesn't make it the right way of dealing with things however. Research should be directed at why there is a lack of epitestosterone in balding follicles and how to restore the hormonal balance to normal so that the hair follicle can be protected from androgens once again.
What do you think the best available treatments are currently?
 

czecha

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I’m pretty sure its all about estrogen and that chemhead is correct, just based of anecdotal observations on forums and irl.

Estrogen regrows hair.

women have more hair. When their E drops their hair tends to fall out.

Fatter men, especially with gyno/wide hips seem to be getting away with more

Fatter men, if they go bald, usually hang on their hairline pretty well and go bald in more of a diffuse/female pattern while low E men have more hairline recession. I believe this comes down to E receptor density like ch explained and that there are papers, I would have to look into them though. On estrogen and hairline/ receptors and temples. Maybe someone can chine in on this. I might be wrong. I extremely rarely see balding fat/estrogenic men with hairline recession that matches their density

finasteride increases E, has E sides, and leaves E unopposed by dht.

minoxidil idk tbh, I suspect it could change osmotic pressure to force more E in follicle or slmething?

young females with hairline recession tend to be effortlessly athletic, close to young lean men. I have seen this in @Georgie here I believe, and 2 girls I know irl. This pattern seems to be very common in balding individuals of both genders: prone to being lean, athletic (low e receptor density) —> hairline problems. Prone to gyno (high density)—>getting away with more inflammation —>no/little hairline problems—>diffuse thinning
 

whatevr

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In line with what I wrote above, I believe estrogen is unnecessary when your hair follicles synthesize normal amounts of epi-testosterone to protect them from androgens.

That is why "non-male pattern baldness" dudes can run hard steroid cycles, PCT with antiestrogens like arimidex and tamoxifen, and not have more than a couple of hairs knocked off their head. Estrogen is not that critical for male hair. It is only critical in those prone to male pattern baldness because it marginally helps compensate for lack of epi-T by counteracting T and knocking down 5-AR. As a monotherapy for male pattern baldness, E2 works poorly. You have to use gobs of estrogen to make a dent unless you also use androgen inhibitors with it. I think that says everything.
 
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