Oral Steroid Made My Hair Grow Back Thicker!

[Norwoody]

It's also important to understand that a serum hormone profile doesn't really tell you much. It's more of a relic or an artifact of activity going on at a much deeper level. For example, the fact that women have a higher serum estrogen concentration compared to men doesn't mean that estrogenic activity in the liver tissue or joint tissue is higher in women than men.

Yeah I think there's a lot of users on these forums who don't comprehend this. Some are taking anti-androgens and still have normal T levels (I remember reading about one specifically but forget the name), but that doesn't mean that it's binding to local tissues, right?

 

[Johnsmith63747]

Technically, your production of testosterone is actually not higher. This might seem counterintuitive at first, but let me explain.

I will frequently use this analogy because it's the simplest and most accurate way of thinking about what is occurring when you take a 5AR antagonist like finasteride or Avodart. Imagine your production of "steroid"... just generalized term for all steroids that are being synthesized form cholesterol... Imagine your steroid production as a large flowing river where the water represents a particular steroid. Now imagine this river branches off into other (perhaps, smaller) rivers and the junction of each of these branchings represent a sort of gateway that represents a steroid metabolizing enzyme and the water of this particular branch represents a new steroid that has been metabolized from the water flowing from the larger river.

Now let's focus on a large branch that comes from one of the main rivers and this branch represents the flow of testosterone. For the sake of simplicity, let's say the testosterone river splits into two rivers downstream. One of these rivers represents estradiol and the other represents dihydrotestosterone. The junctions where the testosterone river splits into estradiol and dihydrotestosterone are represented by aromatase and 5a-reductase, respectively. Let's also assume in our analogy that we have some kind of sensor to measure the level of the river and a way to regulate that level to keep it at a certain height that is considered safe.

Now, let's say that you build a dam at the junction where the river branches into the "DHT branch". This dam represents a 5AR inhibitor like Avodart, where you are blocking the steroid flow from the testosterone river into the DHT river. When you suddenly and completely block flow to the DHT river, the level of the main river starts to back up and the level spikes in height because you have blocked off a path of flow, but the river is still flowing at the same rate it was before you blocked it off. This goes on for a short while before an engineer that is responsible for keeping that river at a safe level decides to reduce the flow of the main river in order to drop the level of the river to a safer level (an analogy for the brain or hypothalamus acting as a regulatory entity).

So consider what's happened here. The level of the river rose and it had to be brought back down as best as possible in order to make the environment safer. So, now, the level of the testosterone river may be about the same as it was before or, perhaps even a little higher, but the flow rate of the river has been decreased. The measured level (or concentration) may show that your testosterone is higher than it was before. However, there is actually less water flowing through the river now... Your body is now synthesizing less "steroid" than before even though the measured level is higher. Your total steroid throughput has been reduced because you blocked off an avenue of flow and started pooling high concentrations of steroids and your body's regulatory system compensated for that by reducing the overall flow rate.

Here's why this is unhealthy: in response the the increased concentration of certain steroids in serum, your body doesn't just reduce the synthesis of steroids to protect itself. It will also downregulate enzyme expression and receptor expression if too much activation is occurring. So, let's take estradiol as an example because it's one of those steroids your brain tightly regulates because high serum concentrations are dangerous and unhealthy.

If your body reduces aromatase expression and estrogen receptor expression in tissues that require a certain level of local synthesis (consider joints as an example of tissues that require a certain level of estrogenic activity), your body is protecting you from high serum concentrations of estrogens, but it's doing this at the expense of local or tissue specific synthesis of estrogens. So, you now have safer levels of estrogens in serum, but low levels in specialized tissues that require it. In the long run, this protects you from near-term death, but specialized tissues are not functioning optimally and you are going to age faster because of it. So, you don't die from a heart attack induced from hyperestrogenic activity in heart or vascular tissue, but it's at the expense of optimal health and function of other parts of the body. So, your body sacrifices the health of your joints in order to protect against a much bigger problem.

This is why I'm against use of steroid metabolizing enzyme inhibitors for really any problem. They cause more problems than they fix. If drug companies can develop enzyme antagonists that can target enzymes in specific tissues and nowhere else in the body, they would have some value. However, at this point, developing a drug like that seems like the wrong approach and an overcomplication. Targeting the genes that encode enzyme expression in specific tissues is a more reasonable approach and permanently solves the problem. And.. with CRISPR and quantum computing already being used today, the prospect for something like this is right at the doorstep.

edit: btw, your sudden increase in testosterone is likely due to a difference in dosage between the generic and name brand. If you're splitting larger pills, you're probably just getting a higher dosage. It's also possible (though less likely) that the generic is actually purer and, thus, more potent that the Avodart.

makemyhairgrowfast.com/supplements/soy-isoflavones-for-hair-loss/

Think there’s any merit to the information here? You mentioned finasteride etc not causing selective targeted effects in the desired tissues. Is it possible soy consumption can do this?

 

[czecha]

There's definitely something genetically inferior about those people that makes them more susceptible to arthritic pain than other people, but many of them can get rid of their pain so that it's pretty much unnoticeable if they're saints about what they eat.

did you consider that finasteride usage caused these autoimmune diseases in you in the first place? that its not genetic in your case?

I think finasteride is known to do that


btw what supplements do you take if you dont mind me asking?

 

[ChemHead]

did you consider that finasteride usage caused these autoimmune diseases in you in the first place? that its not genetic in your case?

I think finasteride is known to do that


btw what supplements do you take if you dont mind me asking?

I think in that context, I was specifically just speaking about the fact that most people have some form of genetic malfunction that manifests in one form or another. For some people, it maybe be hair loss. For some, maybe skin problems. For some, maybe rheumatoid arthritis... etc. I wouldn't doubt that finasteride could induce some form of rheumatic condition, though. I know a young female that has rheumatoid arthritis and has no hair loss whatsoever. She does, however have some mild ketatosis pilaris, which I believe is directly related to the rheumatic condition.

Before I took finasteride, though, I had pretty bad skin... Lots of redness and irritation in general. Finasteride caused some changes.. Positive ones actually, but there was always still underlying inflammation and the decrease in steroid synthesis that finasteride caused didn't help the skin. The diet, without question has changed a lot of aspects of my health in a really positive way.

For supplements, I take B12, biotin, D3, Lugol's 5% iodine, and selenomethionine. I also take around 10-15 grams of vitamin c powder daily. That's pretty much it.

 

[TheHawk]

This thread resonates with me because I had instant regrowth and extreme sides on the 5 mg version of finasteride as a 17 year old.

Like Hispanic girl hairline from mature male hairline.

It was a matter of a few months.

Gynecometasia, watery eyes, mildly watery sperm, and lowered libido by like half.

A year into it at 18 or so, I had blurred vision, and even couldn’t see my minds eye clearly after a while. My memory was also terrible.

But I was growing my hair. That’s when I quit finasteride for a long time.

Saw studies showing higher doses are much more likely to give sides. I got on 1 mg Propecia 3 years later.

Hair regrowth started again with no sides, but stopped after a few months, and I have been constantly receding ever since non-stop.

finasteride does nothing to me now. No side effects, definitely no visible benefits on my scalp.

ChemHead’s story’s about high finasteride doses reminded me of that.

My hypothalamus has figured finasteride out, yeah? Whatever it does in response, pretty much kills it’s power in my body. Because before I got insane sides all over the place.

 

[Norwoody]

This thread resonates with me because I had instant regrowth and extreme sides on the 5 mg version of finasteride as a 17 year old.

Like Hispanic girl hairline from mature male hairline.

It was a matter of a few months.

Gynecometasia, watery eyes, mildly watery sperm, and lowered libido by like half.

A year into it at 18 or so, I had blurred vision, and even couldn’t see my minds eye clearly after a while. My memory was also terrible.

But I was growing my hair. That’s when I quit finasteride for a long time.

Saw studies showing higher doses are much more likely to give sides. I got on 1 mg Propecia 3 years later.

Hair regrowth started again with no sides, but stopped after a few months, and I have been constantly receding ever since non-stop.

finasteride does nothing to me now. No side effects, definitely no visible benefits on my scalp.

ChemHead’s story’s about high finasteride doses reminded me of that.

My hypothalamus has figured finasteride out, yeah? Whatever it does in response, pretty much kills it’s power in my body. Because before I got insane sides all over the place.

This is exactly why I think the doctors on the hair loss show are right about 0.25-0.5mg 3 days a week being enough. Especially when you're young, you have a chance of really messing yourself up on those high doses. Sure, there are some people who can tolerate dutasteride at like 16 but it's certainly rare.

 

[ChemHead]

Hair regrowth started again with no sides, but stopped after a few months, and I have been constantly receding ever since non-stop.

finasteride does nothing to me now. No side effects, definitely no visible benefits on my scalp.

You don't have side effects because finasteride has already taken its toll on hypothalamic regulation of your body's steroid synthesis, as well as enzymatic steroid metabolism. In other words you don't notice the side effects because they've become permanent and you've become accustomed to them. Trust when I say this. When I first fully recovered from finasteride use, I felt like a completely different human being. I actually almost felt superhuman. I wondered if everyone felt the way I was feeling and maybe I was just overexuberant about feeling the way most people are already used to. I'm still not entirely sure of the answer to that question, but I'd say it's probably a little bit of both. I probably did feel better than most because of my diet and lifestyle habits, but I also certainly regained functionality that is simply normal for most people.

Especially when you're young, you have a chance of really messing yourself up on those high doses.

Very small doses can also affect you just as powerfully as larger doses. In terms of length of time which side effects will persist, the frequency with which your body is exposed to a 5AR antagonist is more important than the dosage. If one person takes 50mg of finasteride once and another takes 0.5mg 100 days in a row, the person that took the 50mg dose once has a much higher chance of recovering quickly because their body will still have unadulterated genetic instructions for synthesis of the 5AR enzyme. The person that took 0.5mg daily will be less likely to recover quickly due to consistent repeated exposure... once finasteride has bound a 5AR enzyme, that protein is permanently denatured.. gone. If you give finasteride more time in the body by repeated exposure over days to months, it will eventually encounter nearly all of your 5AR enzymes. With little to no usable 5AR proteins, your body loses its ability to synthesis the enzyme. I can't say I'm exactly sure why this is, but it seems that the enzyme itself might be involved in its own regulatory production feedback loop.

 

[Norwoody]

5mg a day is a lot for a teen.

And yes, 0.25mg 3 times a week may be intolerable too, sure. My point is, that it is likely to be effective though for most people in terms of its efficacy. Even 1mg a day is probably an overprescription for a lot of people.



IMO


And I got hyperandrogenicity reflex from it. But I'm not one of those people who says it's totally detrimental. It may be, it may not be. Everything is a risk - even the most studied of chemicals.

 

[ChemHead]

And I got hyperandrogenicity reflex from it. But I'm not one of those people who says it's totally detrimental. It may be, it may not be. Everything is a risk - even the most studied of chemicals.

Reflex hyperandrogenicity is definitely a possible side effect and much of that depends on enzymatic expression... where and to what extent you express 5AR, aromatase, and other steroid metabolizing enzymes in the body. For example, it's possible that finasteride works only in certain areas of your body and others not so much. So, you could end up with less 5AR activity in one area of the body and the same 5AR activity in another part of the body, but higher testosterone will then increase DHT in that other area that wasn't affected by finasteride. Couple that with an increase in androgen receptor expression and you could end up with hyperandrogenicity. It all really depends on individual genetic differences. This is why some people seem to tolerate these drugs better than others, while some are totally wrecked by them.

 

[TheHawk]

You don't have side effects because finasteride has already taken its toll on hypothalamic regulation of your body's steroid synthesis, as well as enzymatic steroid metabolism. In other words you don't notice the side effects because they've become permanent and you've become accustomed to them. Trust when I say this. When I first fully recovered from finasteride use, I felt like a completely different human being. I actually almost felt superhuman. I wondered if everyone felt the way I was feeling and maybe I was just overexuberant about feeling the way most people are already used to. I'm still not entirely sure of the answer to that question, but I'd say it's probably a little bit of both. I probably did feel better than most because of my diet and lifestyle habits, but I also certainly regained functionality that is simply normal for most people.


Very small doses can also affect you just as powerfully as larger doses. In terms of length of time which side effects will persist, the frequency with which your body is exposed to a 5AR antagonist is more important than the dosage. If one person takes 50mg of finasteride once and another takes 0.5mg 100 days in a row, the person that took the 50mg dose once has a much higher chance of recovering quickly because their body will still have unadulterated genetic instructions for synthesis of the 5AR enzyme. The person that took 0.5mg daily will be less likely to recover quickly due to consistent repeated exposure... once finasteride has bound a 5AR enzyme, that protein is permanently denatured.. gone. If you give finasteride more time in the body by repeated exposure over days to months, it will eventually encounter nearly all of your 5AR enzymes. With little to no usable 5AR proteins, your body loses its ability to synthesis the enzyme. I can't say I'm exactly sure why this is, but it seems that the enzyme itself might be involved in its own regulatory production feedback loop.

Did you do anything special to recover from the drug?

You don't have side effects because finasteride has already taken its toll on hypothalamic regulation of your body's steroid synthesis, as well as enzymatic steroid metabolism. In other words you don't notice the side effects because they've become permanent and you've become accustomed to them. Trust when I say this. When I first fully recovered from finasteride use, I felt like a completely different human being. I actually almost felt superhuman. I wondered if everyone felt the way I was feeling and maybe I was just overexuberant about feeling the way most people are already used to. I'm still not entirely sure of the answer to that question, but I'd say it's probably a little bit of both. I probably did feel better than most because of my diet and lifestyle habits, but I also certainly regained functionality that is simply normal for most people.


Very small doses can also affect you just as powerfully as larger doses. In terms of length of time which side effects will persist, the frequency with which your body is exposed to a 5AR antagonist is more important than the dosage. If one person takes 50mg of finasteride once and another takes 0.5mg 100 days in a row, the person that took the 50mg dose once has a much higher chance of recovering quickly because their body will still have unadulterated genetic instructions for synthesis of the 5AR enzyme. The person that took 0.5mg daily will be less likely to recover quickly due to consistent repeated exposure... once finasteride has bound a 5AR enzyme, that protein is permanently denatured.. gone. If you give finasteride more time in the body by repeated exposure over days to months, it will eventually encounter nearly all of your 5AR enzymes. With little to no usable 5AR proteins, your body loses its ability to synthesis the enzyme. I can't say I'm exactly sure why this is, but it seems that the enzyme itself might be involved in its own regulatory production feedback loop.

Guys have had results recovering from years of finasteride use from prohormones, fasting, other hormone drugs, diet changes

I don’t doubt for one second I’ve been damaged from it all this time

The way you described it, recovering from PFS should help your hair loss

 

[ChemHead]

Did you do anything special to recover from the drug?

Guys have had results recovering from years of finasteride use from prohormones, fasting, other hormone drugs, diet changes

I don’t doubt for one second I’ve been damaged from it all this time

The way you described it, recovering from PFS should help your hair loss

I'll describe the exact process of recovering from finasteride. I've been through this process once to completion and I'm currently going through the same process again after using finasteride a little over 2 years ago.

When healing from this, there are constant peaks and valleys. In fact, the healing process is a decaying oscillation of highs and lows. It's like a dropping a bouncy ball and watching it bounce until the bounces become so small that it's difficult to discern whether the ball is on the way up or down. So, you go through periods of low steroid synthesis to VERY low steroid synthesis and then the process is repeated until biochemical factors in your body have adjusted which allow this process to decay or become less severe.

What's happening is that your body is attempting to synthesize higher levels of steroids because you are in a chronically deprived state. Your testosterone level may appear "normal", but these numbers are just blood concentrations... they say nothing about the throughput or the flow of steroids from synthesis to elimination. By cutting off the 5AR pathway, you've created a stagnation in the flow of steroid synthesis from "prohormones" to---> testosterone to---> DHT. To understand this, go back through this thread and look for the post I created discussing the "river" analogy... where steroid synthesis and its flow through the body is like a large river that splits into many other smaller rivers downstream.

Anyway, you're in this chronic state of steroid deprivation and as your body is repairing itself, your brain will send the command signals to synthesize more steroids. The problem is that I don't think it has a very tight regulation on how much it commands your body to make... I'm not sure it has the best ability to say: "make only a tiny bit... this much and no more". It's almost more binary, like an on/off switch. Your body will make a change, overshoot it's mark, pullback, and the repeat the same process until its error in missing its mark has diminished.. it's like a feedback control loop (for any of you that know about control theory and PID controllers), but it's not very good knowing what's going to happen ahead of time so that it can make adjustments without volatile changes in physiology. So, you'll temporarily feel better than usual... you won't feel as tired, you'll feel much better socially, you'll notice some interesting physiological changes like: the texture of your skin will change, your skin might produce a little more oil, your eyes may look less dark and a little more "alive", etc.

This doesn't last very long, though, and the reason for this is that, under normal circumstances, those newly synthesized steroids have pathways they go through and one of those pathways is still damaged (the 5AR pathway). So, with all that new "steroid" that was synthhesized, much of it needs to go through this 5AR pathway for normal physiological function, but it can't because it's damaged. So, it goes through every other available metabolic pathway.. and this causes an increase, obviously, in all other steroid metabolites, but, particularly, the one that is heavily involved in the brain's regulation of steroid synthesis... which is estradiol. Now, when estradiol is increased in concentration (especially without a corresponding increase in DHT), your steroid synthesis gets shut down again.

This "yo-yo" like process of oscillation between highs and lows just continues repeating until the 5AR pathway has been completely restored. As the pathway begins to edge closer to being repaired, you start to notice more significant physiological changes, but there's a certain point at which this healing process reaches kind of a tipping point... and at this point improvement begins to accelerate pretty rapidly. You could be going through this up and down process for years with slow, steady changes (like I am, and once did before) and the, suddenly, things begin to change rapidly.

I'm currently at one of the late stages I recognize from the first time. This may sound odd and possibly bad to someone that may not understand the mechanism behind what I'm about to explain. So, in the past few weeks, my balls and scrotum have literally shrunk and I've been extremely tired... far more than I have been in quite awhile. This very same thing happened to me maybe less than a couple months before I had healed the first time. Now, if you know anything about endocrinological function, you might guess that the reason for this happening would be reduced steroid synthesis, right?.. steroid synthesis drops and then you get this sort of testicular atrophy. However, I don't believe this is what is actually happening (and I have to stress, again, that I've already been through this and I know what comes next after this stage). What I think has happened is that the 5AR pathway is nearly recovered and steroids are now beginning to be metabolized (or 5a-reduced). Back to the river analogy... picture a river that has been dammed. When you remove the dam, water flows into an area that it previously had been restricted from flowing (the 5AR pathway) and the water level of the dammed area (the pool of other non-5a-reduced steroids) suddenly drops as it flows into the previously restricted area.

So, I'm getting an increase in 5a-reduced steroids and a decrease in other steroids that are precursors to 5a-reduced steroids (like testosterone). And, this reduction in steroids like testosterone will also reduce its other metabolites (like estradiol). So, I've experienced an increase in DHT, but a decrease in both testosterone and estradiol (among other steroids). Contrary to what most people probably think, I don't believe that DHT causes an increase in testicular growth. I think it causes a masculinization or virilization of sorts, but a combination of androgens along with estradiol is what causes growth. Estradiol is the growth hormone. So, now, I have testicular aching (exactly as I had before) and the next stage is for my brain to upregulate the body's steroid synthesis to make up for the now lowered levels of testosterone and estradiol (again, among other steroids that have been lowered by the repair of the 5AR pathway). What happens next, from a physiological standpoint, is that I begin to experience an increase in testicular volume... literal growth. More aching comes along with this, as well as discomfort due the scrotum being kind of too small for the rapid increase in testicular volume (this eventually gets better). As the body restores previous levels of 5a-reduced steroids, my personality begins to change and I start to feel... almost kind of invincible (and I really say this for lack of better wording). I get this electric feeling when looking at a female, I need much less sleep, I'm incredibly quick-witted (whereas before, I would have been cognitively slow.. late to the party, in a sense), I have quicker physical reflexes. I literally feel like a completely different person. In addition, my skin becomes incredible and my under-eye area looks juvenile.. no hollowness or darkness, completely filled in. During this period, my scalp actually began to itch like previous to finasteride use, but a few weeks later, the itching went away completely and my hair completely stopped falling out.. like 100%. The reason this happened is likely because as 5AR functionality was improving, it was drawing away more testosterone to be 5a-reduced and leaving not enough testosterone leftover to be aromatized (which is, IMO, the actual cause of hair loss in most men). However, as my body started synthesizing more steroids, more testosterone was leftover which could be aromatized and the itching and hair loss immediately ceased.

Now here's the part where I say that I don't believe that some of these improvements occur simply from the recovery from finasteride. The recovery definitely allows me to actually experience some of these benefits simply because my body is able to function normally and produce a much higher level of steroids, but I believe the reason I don't return to the hair loss and average looking skin like I would have had before taking finasteride is due to the consistent dietary and lifestyle changes that I've made and maintained for the past 4-5 years.

Other than the positive hair and skin changes, here's an example of something I've NEVER had, even previous to finasteride use... never even had as a teenager: when I fully recovered the first time from finasteride, I would get nocturnal erections that were so hard, I would literally wake up every single night in the middle of sleep almost in pain because it felt like my dick was going to explode. And during the day, I would walk around with a full hard-on just naturally. I never experienced this prior to using finasteride (and definitely not during) and I can only attribute this to the dietary changes that I've consistently kept.

So, this is why I believe that you can trigger some pretty powerful epigenetic changes by changing diet and lifestyle and this is also why I will never touch finasteride, or any other 5AR antagonist, again. It's been difficult to live with the mistake I made a couple years ago because I should have known not to toy around with finasteride again after making a full recovery.. especially because I probably had even further improvement to experience, but I was already messing with finasteride again (attempting to use it topically) not even a month after I had fully recovered. I guess I figured that if thing went wrong, I could recover quicker knowing what I know, but it has taken over two years to get back to the point where I'm close to a full recovery again.

So, I'm really looking forward to putting all this behind me and giving my body the chance to improve even further beyond where I had allowed it the first time. I'm 100% confident that if I hadn't touched finasteride again, I would easily have a full head of hair right now with no pharmaceutical intervention. And the reason I know this is because if your hair isn't falling out AT ALL (even by forcibly pulling on it), you're going to have more hair on your head at any given moment as new growth cycles occur. The only reason I wanted to use finasteride is because I wanted the best of both worlds... I wanted not only for my hair to grow and not fall out, but I wanted a thicker texture to my hair.. which is what finasteride can do. But, again, I don't even know how much further everything could have improved because I didn't even give it a month, after being in a place that I felt like was basically "recovered", before messing around with finasteride again.

Hard lessons to learn... and anyone reading this should learn from my mistakes before making them yourselves.

 

[pegasus2]

After 7 weeks your hair grew back, and then one day after stopping it fell out again.

 

[ChemHead]

After 7 weeks your hair grew back, and then one day after stopping it fell out again.

Not sure what you mean or what your are referring to.. can you elaborate a bit on what you're talking about? I'm not sure what you mean by 7 weeks or really any of that. Is there something I said specifically that you're referring to?

 

[pegasus2]

Not sure what you mean or what your are referring to.. can you elaborate a bit on what you're talking about? I'm not sure what you mean by 7 weeks or really any of that. Is there something I said specifically that you're referring to?

Not you, the OP.

 

[ChemHead]

@pegasus2 I think I may know what you're referring to now... if you're talking about the positive effect that finasteride had on me... YES. In a very short period of time (not sure about the 7 week figure), finasteride was able to block off the 5AR pathway AND (this is important) while the body is still producing its normal levels of steroids (before finasteride has had it's negative effect on hypothalamic regulatory feedback), a sudden spike in both serum estrogen concentration, as well as (more importantly) intrafollicular estrogen synthesis via aromatization occurs. So you get this very short term spike in intrafollicular estrogen synthesis which is responsible for a drastic change in the texture/hair shaft volume, as well as the follicle's ability to maintain growth phase. And yes, this can change literally overnight 9or over the course of a few days) and this DOES happen. Once your hypothalamic regulation intervenes and lowers your steroid synthesis as well as enzymatic and receptor expression (aromatase and estrogen receptor expression), the hair follicle's ability to produce its own estrogens is severely impacted. When this happens, you can go from full thick hair that doesn't fall out to thin, weak, dry hair that rapidly sheds... in literally a matter of days. So, yes, what I'm telling you is exactly what happens and I've proven it multiple times through experimentation with finasteride.

 

[ChemHead]

Not you, the OP.

Ah, ok.. well, I guess you can disregard my last post. I'll leave it, though, just in case someone stumbling on this thread hasn't already ready my other posts. But, actually, my last post probably still applies to OP's situation. It's the same mechanism IMO.

 

[pegasus2]

@pegasus2 I think I may know what you're referring to now... if you're talking about the positive effect that finasteride had on me... YES. In a very short period of time (not sure about the 7 week figure), finasteride was able to block off the 5AR pathway AND (this is important) while the body is still producing its normal levels of steroids (before finasteride has had it's negative effect on hypothalamic regulatory feedback), a sudden spike in both serum estrogen concentration, as well as (more importantly) intrafollicular estrogen synthesis via aromatization occurs. So you get this very short term spike in intrafollicular estrogen synthesis which is responsible for a drastic change in the texture/hair shaft volume, as well as the follicle's ability to maintain growth phase. And yes, this can change literally overnight 9or over the course of a few days) and this DOES happen. Once your hypothalamic regulation intervenes and lowers your steroid synthesis as well as enzymatic and receptor expression (aromatase and estrogen receptor expression), the hair follicle's ability to produce its own estrogens is severely impacted. When this happens, you can go from full thick hair that doesn't fall out to thin, weak, dry hair that rapidly sheds... in literally a matter of days. So, yes, what I'm telling you is exactly what happens and I've proven it multiple times through experimentation with finasteride.

Interesting theory, but there's nothing indicating this in the literature. The literature shows it takes months to get any regrowth from finasteride, longer than minoxidil. Also, hair only grows .4mm per day, and the follicle is 5mm beneath the surface. If it started working immediately it would take 12.5 days for the enlarged hair shaft to reach the surface of the skin, and another two months before it would make any noticeable difference. Then the OP's claim that his hair texture changed the day after he stopped taking the steroid lol. The hair shaft is not alive, it can't be changed. Changes take place at the follicle, and they take months to grow out. Unless you're examining your scalp with a microscope you won't notice anything for 3 months.

 

[ChemHead]

Interesting theory, but there's nothing indicating this in the literature. The literature shows it takes months to get any regrowth from finasteride, longer than minoxidil.

You won't find it in the literature because everyone that conducts clinical research in the field is on some non-sensical wild goose chase with DHT and they still believe that it's the cause of hair loss.

Also, hair only grows .4mm per day, and the follicle is 5mm beneath the surface. If it started working immediately it would take 12.5 days for the enlarged hair shaft to reach the surface of the skin, and another two months before it would make any noticeable difference. Then the OP's claim that his hair texture changed the day after he stopped taking the steroid lol. The hair shaft is not alive, it can't be changed. Changes take place at the follicle, and they take months to grow out.

You're definitely thinking the right way, but it doesn't end there. Believe me, when I was discovering the mechanism of finasteride's miraculous effects on my own hair, I struggled with this exact line of reasoning... trying to reconcile what seemed to be a massive change in texture within a day(s) with the fact that: 1. the hair shaft is not alive, and 2. effects on growth would require much longer than a day or two to actually manifest.

That is, however, until you realize that the change in thickness and texture of the hair shaft is not actually due to stimulated "growth". The increase in intrafollicular estrogens will keep hair in the growth phase and prevent it from falling out. However, in addition to finasteride increasing intrafollicular estrogen synthesis, there is also an increase in concentration of some other hormone. I'm not sure if I mentioned it in this thread, but in other threads and other forums, I've referred to it as this "mystery" steroid. However, I believe I know what this steroid likely is.

It's a mineralocorticoid.. and it's likely aldosterone. So, here's the reason why the texture/thickness of the hair shaft can change in a day:

The change in the hair shaft is not occurring because growth is being stimulated and new proteins are being synthesized. It's an osmotic phenomenon.. the volume of the hair is simply being increased because it's being inflated with water.. it's being puffed up in a sense. Something is causing a higher volume of water to flow into the hair shaft, which is a direct result of a concentration gradient... perhaps a higher concentration of sodium or some other mineral is causing a higher volume of water to flow into the hair shaft. Well, this is exactly what mineralocorticoids like aldosterone do. They cause in increase in water retension.

So, this change in hair shaft texture/thickness is not a "living" growth phenomenon. It's simply the hair shaft being inflated with a greater volume of water. This is exactly why OP's claim (and my own claims through experimentation with finasteride) are completely valid and possible. I've pieced this all together from over a decade of research and experimentation (I would not have come to this understanding without the experiments I've performed) and I would easily stake my life on this claim. A sudden increase in concentration of a steroid that causes water retention can cause a proportionally sudden increase in actual physical water retention manifest through plumper skin (which also happened to me) and thicker hair shaft diameter.

 

[ChemHead]

I also believe, for other reasons, that the mineralocorticoid receptor and aldosterone both together and independently play a role in the expression of collagen and elastin genes, regulating the elasticity of skin.. which can account for the scalp tissue fibrosis and tightness/lack of elasticity.

Keep in mind, I don't just say these things. Almost everything I say is backed by clinical research. It just doesn't all come from one source because no one else has put the pieces together in one single clinical publication. If I had the money and resources to do it (or at least great contacts in the industry), I would do it or at least be involved in helping someone else do it.

 

[pegasus2]

Water going up into the hair shaft and making it thicker is an absolutely bonkers proposition. 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. However, fibrosis isn't the cause of hair loss, it's just inhibits regrowth. Sorry, but there's no getting around the fact that DHT is the cause.