EVERYONE Will Get Finasteride Side-Effects Eventually

hemingway_the_mercenary

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I know this is against the general opinion but hear me out

(This is about sexual side effects)

You were exposed to your natural DHT levels for all your post puberty life. Depending on when you started finasteride you may have had more or less time reaping the benefits of DHT to your sexual organs. For those that are not aware DHT strengthens the smooth muscle in the penis and the muscles surrounding the penis (the Kegel muscles) AND also is very responsible for libido being that it is a much stronger androgen than finasteride.

Initially inhibiting DHT will not have much noticeable effect for most people as the penis tissues are already quite strong and are able to deliver sufficient bloodlfow. However, over time, it could be one or two or even 10 years depending on the person, the tissue that you built with DHT will begin to atrophy and get weaker and T alone will not be enough to sustain it. This is typically a very slow process and hence hard to notice. This is when the sexual sides will be less noticeable

Usually by this time you will have aged 5 or so years, if you started in your late 20s or early 30s, and you might think that this drop in erectile quality is normal. This can carry on for a few more years while you use Cialis or other remedies to "hold you over" but eventually they won't be enough.

Your Penis NEEDS DHT to function at 100%! There is no way around this. Anyone denying this is denying that androgens increase sex drive and sexual function. This is the equivalent of saying that some 60 year old man will not get a boost in erectile quality if they go on TRT w/ Proviron ed.


Here's an analogy to help you understand. You're on the highway and going 160, the speed limit is 100. You have more speed than you need. THEN you lift your foot of the gas by 60% and the car starts slowing down BUT as long as you're over a 100 it's not a problem and you won't really notice the negative effects. Once you go under a 100 that's when you will realize that it's problematic to inhibit over 60% of your bodies strongest androgen.

As for the studies which show that only 5% of people get side effects this is why that's not accurate. This is self reported sides and no man actually wants to believe that they have erectile dysfunction and after a couple of years on the drug with normal erectile function most men will not notice or attribute to finasteride the increased time it takes to achieve and erection or the decreased maximal maintainable erection strength.

If the studies were done by scientifically observing 1) The time it takes to achieve maximal erection with a normal stimuli, 2) The strength of the maximal level of maintainable erection during intercourse, and 3) How long the male is able to hold an erection without physical stimuli THEN they'd have to report that 80-90% of men have side effects especially after 5 years on the drug



Also, the bigger your penis the more likely you will be of experiencing serious ED issues down the line with finasterde as it has a much heavier demand of blodflow and thus an overall healthier penis. Someone who is 5 inches long needs much less blood flow to achieve a maximal erection than someone who is 7 inches long ( the blood flow needed per length of the penis is not a linear line but an exponential curve).

Anyone thinking you can have the same erectile function on finasteride as they did before it is a fool! The gap of 5 or so years makes worse erectile function harder to notice and/or attribute to finasteride but there is just no way around this fact: DHT is our most powerful androgen and it is 100% necessary for optimal penile function
 
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-G-

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But what would you suggest people who are currently on finasteride?

I do think in the next 2-3 years something new can come out. Not a cure by any stretch of the imagination just something new. New could mean something as simple as Triple Hair which "plans" to launch this Q and the other company with the min inhancing shampoo that is supposed to hit the markets in this Q as well.

It is small but positive steps?

I am on the fence and plan to hop off within 3-4 years. One year in so far.
 

hemingway_the_mercenary

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But what would you suggest people who are currently on finasteride?

I do think in the next 2-3 years something new can come out. Not a cure by any stretch of the imagination just something new. New could mean something as simple as Triple Hair which "plans" to launch this Q and the other company with the min inhancing shampoo that is supposed to hit the markets in this Q as well.

It is small but positive steps?

I am on the fence and plan to hop off within 3-4 years. One year in so far.

I don't think people truly understand how difficult a new treatment is. Topical absorption is not high enough to allow for topical AR blockers to be used to block sufficient AR in the scalp to stop miniaturization and targeting hairless downstream has potentially hundreds to thousands of pathways that would need to be manipulated etc.

So I don't think anything that works is going to come out for the next 12 years minus CB which has already been shown to be much less effective than finasteride again due to the poor topical absorption.

My best advice would be at least switch to a low dose of topical finasteride, the lowest you find effective for you, and try to minimize systemic absorption so that you can increase the duration of time you will be able to use finasteride without a unmanageable side effect burder.

I'm going to try a derma needling protocol with applying AR blockers immediately after in hopes of reaching sufficient levels at the follies to reverse miniaturization. I'll keep you updated, especially if it works
 

-G-

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I don't think people truly understand how difficult a new treatment is. Topical absorption is not high enough to allow for topical AR blockers to be used to block sufficient AR in the scalp to stop miniaturization and targeting hairless downstream has potentially hundreds to thousands of pathways that would need to be manipulated etc.

So I don't think anything that works is going to come out for the next 12 years minus CB which has already been shown to be much less effective than finasteride again due to the poor topical absorption.

My best advice would be at least switch to a low dose of topical finasteride, the lowest you find effective for you, and try to minimize systemic absorption so that you can increase the duration of time you will be able to use finasteride without a unmanageable side effect burder.

I'm going to try a derma needling protocol with applying AR blockers immediately after in hopes of reaching sufficient levels at the follies to reverse miniaturization. I'll keep you updated, especially if it works


I will look into topical finasteride in a few months and see where I can get it.
 

hemingway_the_mercenary

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The opposite is true. As men age their erectile function declines, and they blame it on finasteride because no man wants to believe he's just getting older and less virile.

The main reason for erectile decline is a decrease in overall androgens in the body and an increase in estrogens... all things that finasteride does to a much larger degree than getting older will. Someone who is fit and 50 years old not on finasteride will have better erectile function than someone who is 35 and been on finasteride for 10 years
 

-G-

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Also, why do we have so much contradicting information? I would think it would be more consistent?
 

NickyA

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The opposite is true. As men age their erectile function declines, and they blame it on finasteride because no man wants to believe he's just getting older and less virile.

Also erectile function tends to decline as you age, ironically following a similar pattern to alopecia:

-20% of men will experience ED a couple of times in their 20s
-30% of men will experience ED a couple of times in their 30s
-40% of men will experience ED a couple of times in their 40s
-50% of men will experience ED a couple of times in their 50s
-60% of men will experience ED a couple of times in their 60s

The actual percentage of men who suffer permanent ED or persistent ED most of the time is much lower for each age percentile. Men should grow up and realise that their libido isn't stable and may vary sometimes, just like women's. Real life isn't a p**rn flick.
 

hemingway_the_mercenary

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Also erectile function tends to decline as you age, ironically following a similar pattern to alopecia:

-20% of men will experience ED a couple of times in their 20s
-30% of men will experience ED a couple of times in their 30s
-40% of men will experience ED a couple of times in their 40s
-50% of men will experience ED a couple of times in their 50s
-60% of men will experience ED a couple of times in their 60s

The actual percentage of men who suffer permanent ED or persistent ED most of the time is much lower for each age percentile. Men should grow up and realise that their libido isn't stable and may vary sometimes, just like women's. Real life isn't a p**rn flick.
This has nothing to do with my post and I’m not sure where you’re pulling these numbers from but it doesn’t really matter

bottom line, erectile function decreases with age due to a decrease in the bodies androgens and typically as men get fatter with age also an increase in amortization. Progression of heart disease has a minor effect as well

Inhibiting over 60% of your bodies main androgen will have side effects for almost all men in the long run
 

Xenophon

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I know this is against the general opinion but hear me out

(This is about sexual side effects)

You were exposed to your natural DHT levels for all your post puberty life. Depending on when you started finasteride you may have had more or less time reaping the benefits of DHT to your sexual organs. For those that are not aware DHT strengthens the smooth muscle in the penis and the muscles surrounding the penis (the Kegel muscles) AND also is very responsible for libido being that it is a much stronger androgen than finasteride.

Initially inhibiting DHT will not have much noticeable effect for most people as the penis tissues are already quite strong and are able to deliver sufficient bloodlfow. However, over time, it could be one or two or even 10 years depending on the person, the tissue that you built with DHT will begin to atrophy and get weaker and T alone will not be enough to sustain it. This is typically a very slow process and hence hard to notice. This is when the sexual sides will be less noticeable

Usually by this time you will have aged 5 or so years, if you started in your late 20s or early 30s, and you might think that this drop in erectile quality is normal. This can carry on for a few more years while you use Cialis or other remedies to "hold you over" but eventually they won't be enough.

Your Penis NEEDS DHT to function at 100%! There is no way around this. Anyone denying this is denying that androgens increase sex drive and sexual function. This is the equivalent of saying that some 60 year old man will not get a boost in erectile quality if they go on TRT w/ Proviron ed.


Here's an analogy to help you understand. You're on the highway and going 160, the speed limit is 100. You have more speed than you need. THEN you lift your foot of the gas by 60% and the car starts slowing down BUT as long as you're over a 100 it's not a problem and you won't really notice the negative effects. Once you go under a 100 that's when you will realize that it's problematic to inhibit over 60% of your bodies strongest androgen.

As for the studies which show that only 5% of people get side effects this is why that's not accurate. This is self reported sides and no man actually wants to believe that they have erectile dysfunction and after a couple of years on the drug with normal erectile function most men will not notice or attribute to finasteride the increased time it takes to achieve and erection or the decreased maximal maintainable erection strength.

If the studies were done by scientifically observing 1) The time it takes to achieve maximal erection with a normal stimuli, 2) The strength of the maximal level of maintainable erection during intercourse, and 3) How long the male is able to hold an erection without physical stimuli THEN they'd have to report that 80-90% of men have side effects especially after 5 years on the drug



Also, the bigger your penis the more likely you will be of experiencing serious ED issues down the line with finasterde as it has a much heavier demand of blodflow and thus an overall healthier penis. Someone who is 5 inches long needs much less blood flow to achieve a maximal erection than someone who is 7 inches long ( the blood flow needed per length of the penis is not a linear line but an exponential curve).

Anyone thinking you can have the same erectile function on finasteride as they did before it is a fool! The gap of 5 or so years makes worse erectile function harder to notice and/or attribute to finasteride but there is just no way around this fact: DHT is our most powerful androgen and it is 100% necessary for optimal penile function

finasteride is poison, AIDS and cancer rolled into one, plus it's racist (that's bad). The point being, this is probably heinous stuff. Pretty much just take anything the system offers/says/believes, and go the opposite way. This is a heuristic that will never steer you wrong. The system plays the 'infinite skeptical regression' game with this 'no evidence' bit. There's 'no evidence' that finasteride destroys your manhood at the spiritual level, just like there's 'no evidence' that Roundup causes cancer, just like there's 'no evidence' that the election was stolen. Anything that contradicts the mainstream: 'no evidence.' Fine. Then we needn't bother throwing 'peer reviewed papers' at each other.

There is no such thing as science. The only advances have come in engineering and anesthetics. This is why surgery is extremely effective now. But we know absolutely d*** about the body, about hormones, about what hair even is, or what anything is for, teleologically speaking. But we have great surgical techniques. Anyone can scrounge 5-15k for 1 or more surgeries. It's not that hard. After that, there are many ways to go about maintenance.
 

Charger

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Whether or not side effects are inevitable (which I agree with to an extent), I think inhibiting 5AR for hair is an archaic/outdated approach. 5AR is simply responsible for too much beyond hair for any sensible person to feel comfortable inhibiting it's function.

At least for as long as I'm not on exogenous testosterone (which doesn't guarantee no side effects), I'm not interested in using any treatments that affect androgen production, it's strictly PGD2/PGE/WNT angle options for me from now on. I think that is where the potential for more tolerable treatments lie unless someone invents a topical that truly stays local to the scalp somehow.

I'd rather be bald and firing on all cylinders mentally, physically, and sexually than keep my hair and be a depressed eunuch with no drive.
 

whatintheworld

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Funny how the people who always say I'd rather be bald, well, aren't bald at all.

Easy to say you would rather be bald when all you have is a whispy horshoe around your head.

I'll keep taking my chances with finasteride, I don't know if side effects are guaranteed eventually, but I know the side effects of baldness which would be 100% guaranteed: depression, self loathing, anxiety. No thanks.
 

Charger

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Funny how the people who always say I'd rather be bald, well, aren't bald at all.

Easy to say you would rather be bald when all you have is a whispy horshoe around your head.

I'll keep taking my chances with finasteride, I don't know if side effects are guaranteed eventually, but I know the side effects of baldness which would be 100% guaranteed: depression, self loathing, anxiety. No thanks.
It's a catch-22. Most of us are here because we would prefer to have hair. However, if side effects are interfering with your ability to function in your job and make a living, for example, are you really going to prioritize your hair over making a living? I can understand being anxious and depressed over hair loss while you're in your teens or early 20s, if you're over 30 and self-destructing over hair loss, you need to grow up and get your priorities straight.
 

whatintheworld

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It's a catch-22. Most of us are here because we would prefer to have hair. However, if side effects are interfering with your ability to function in your job and make a living, for example, are you really going to prioritize your hair over making a living? I can understand being anxious and depressed over hair loss while you're in your teens or early 20s, if you're over 30 and self-destructing over hair loss, you need to grow up and get your priorities straight.

Being Norwood 7 would interfere with my ability to function and make a living. I would likely progress to Norwood 7 if it wasn't for finasteride, so for me it is a godsend.

If I was Norwood 3 or 4 I probably wouldn't give a sh*t, some hair loss is normal in men.
 

Pigeon

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Completely agree OP.

It's only a matter of time before you get and notice side effects. DHT is imperative and crucial for many functions in the body, I know balding guys here want to ignore that simple biological fact and try to cope any way they can by lying to themselves that blocking a hormone for years will only have "minor" side effects.

Most will have to learn the hard way sadly.
 

hemingway_the_mercenary

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Completely agree OP.

It's only a matter of time before you get and notice side effects. DHT is imperative and crucial for many functions in the body, I know balding guys here want to ignore that simple biological fact and try to cope any way they can by lying to themselves that blocking a hormone for years will only have "minor" side effects.

Most will have to learn the hard way sadly.
Too many idiots like Kevin on YouTube have spread the myth that DHT is only needed before puberty and is a shitty useless hormone after it. Unfortunately, that’s far from true
 

Charger

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Too many idiots like Kevin on YouTube have spread the myth that DHT is only needed before puberty and is a shitty useless hormone after it. Unfortunately, that’s far from true

Every YouTube 'Guru' that pushes finasteride is sketchy in some way/has some variable at play that doesn't apply to normies & natties.

Derek is on exogenous hormones.
Kevin is clearly on some sort of dopaminergic or drug... no one acts like that. Plus there's evidence he had sides from the drug in the past yet claims PFS is bullshit. Also, I love his denial of side effects while at the same time suggesting a lower dose for when these non-existent side effects do occur.. which is it?
Leo and Longevity, the newcomer on the block, has said he had finasteride sides when he first used it, and basically uses SSRIs to offset the mental effects of the drug.
 

Pigeon

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The thing is that you have no evidence for this claim, since the long term finasteride trials do not show this
Lol'd at "no evidence", on the contrary, more and more studies are showing how dangerous fina is and less and less doctors want to prescribe it. Also, there are no long term finasteride trials, that's the problem. Show me a legit fina trial with young men who take it for 5 years. We also know the official studies by Merck are bullshit. "The judge sealed evidence – uncovered by Reuters – suggesting the maker downplayed the side effects." https://www.reuters.com/investigates/special-report/usa-courts-secrecy-propecia/ Btw, it's also not the first time Merck tampers with their trials: "Merck Manipulated the Science about the Drug Vioxx" https://www.newscientist.com/article/dn13685-drug-giant-merck-accused-of-deaths-cover-up/ , "Merck Agrees to Settle Vioxx Suits for $4.85 Billion"

The truth on DHT: what the research shows​


DHT is an essential male hormone, not just for libido, or feeling manly, but for general health as well.


DHT is synthesized from:


  • Testosterone through the enzyme 5 alpha reductase (5AR)
  • 17-hydroxypregnenolone and 17-hydroxyprogesterone in what is termed the “backdoor” pathway
  • 5α-androstane-3α, 17-β-diol (dihydroandrosterone/3α-diol) via the intracrine reverse synthesis pathway (3α-hydroxysteroid dehydrogenase (3α-HSD))

DHT is 2.5-10 times more potent than testosterone and here’s why:


  1. DHT has a 4 time higher affinity to AR (androgen receptor) than testosterone.
  2. Binding of DHT to the AR transforms the AR to its DNA-binding state.
  3. DHT upregulates AR synthesis and reduces AR turnover.
  4. The dissociation rate of testosterone from receptors is 3-5 fold faster than DHT (meaning DHT exerts a much more powerful effect on AR than testosterone)

However, circulating DHT is usually only about 10% or less that of testosterone and high concentrations of intracellular T can shift androgen receptor binding away from DHT by mass action (R).


Furthermore, in the blood, SHBG binds with 5 times higher affinity and for more than 3 times longer to DHT compared to testosterone.


To maximize the androgenic benefits of DHT, we want to maximize 5-AR and inhibit the binding of DHT to SHBG. You can download my guide/PDF on how to do that below.


This article is to show you what happens when men have high DHT or when they are dosed with supra-physiological amounts.


DHT is essential for libido and sexual function​


It’s probably well known that DHT is very important when it comes to libido and sexual function.


According to this study, serum DHT concentration was the only independent hormonal predictor of the frequency of orgasms. An increase in concentration of 1.36 nmol/l corresponded to an average increase of one orgasm a week (R). This shows that DHT directly opposes the anti-libido effects of prolactin.


Inhibiting DHT synthesis impairs corpus cavernosum growth and trabecular smooth muscle relaxation, endothelial function and increases connective tissue deposition. This all contributes to erectile dysfunction, even in the presence of physiological levels of total testosterone (R).


DHT is also critical for activating gene expression of neuronal and endothelial nitric oxide synthases, which are critical physiological mediators of penile erection (R).


Furthermore, DHT is essential for spermatogenesis and thus fertility (R).


Estrogen is thought to be essential for sexual function in men, however, administrating high doses of DHT lowers estrogen dramatically and doesn’t reduce sexual function.


There were no spontaneous complaints, or discontinuations for, adverse effects on sexual function during the study. DHT administration had no effects on any of 33 measures of sexual function and mood, apart from a mild, but significant decrease in overall sexual desire, which was reversible after cessation of treatment… DHT treatment increased serum DHT with complete suppression of serum T, luteinizing hormone, follicle stimulating hormone, and estradiol throughout the 24-month study resulting in reduced spinal bone density.
Reference

DHT isn’t just neutral towards sexual function as shown above, but is essential for it.


As to the clinical effects, the only statistically significant effect was an improvement in early morning erections and ability to maintain erections.
Reference

And also:


Administration of dihydrotestosterone to eugonadal men led to a transient increase of nocturnal sexual dreams and erections and irritability, waning after 3–4 weeks of dihydrotestosterone administration.
Reference

The effects waned after 3-4 weeks, so taking 1-2 weeks off every 4 weeks from DHT (if you’re using it) might enable you to maintain those benefits.


DHT doesn’t cause prostate cancer​


There was a period of time (a few decades) where DHT was thought to promote prostate cancer, however, that thinking is luckily starting to change. It’s about time, since there has been research for over 2 decades showing that DHT doesn’t promote prostate cancer.


There isn’t a correlation between circulating DHT and intraprostatic DHT. The prostate regulates it’s own DHT levels, which is about 10 times higher than circulation.


Giving testosterone might cause issues, since it can convert to estrogen, but giving DHT directly can actually help to shrink the prostate as it can lower estrogen. It’s actually estrogen and prolactin that drives prostate cancer.


Quite a few studies found that high (supraphysiological) serum DHT levels, DHT gel treatment did not significantly increase total, central, or peripheral prostate volumes, as measured by ultrasonography, nor was serum prostate-specific antigen (PSA) elevated. Additionally, International Prostate Symptom Scores (IPSS) remained unchanged in men treated with DHT gel for 6-24 months (R, R, R).


This 1.8 years survey of 37 men aged 55-70 years treated with daily percutaneous DHT treatment suggested that high plasma levels of DHT (> 8.5 nmol/l) effectively inducing clinical benefits while slightly but significantly reducing prostate size (R).


There is an association in some studies between short telomere length and prostate cancer, but the effects of DHT on leukocyte telomere length may not reflect what occurs in prostate tissue. However, in prostate biopsies from men in the Prostate Cancer Prevention Trial, shorter telomere length was associated with higher odds of prostate cancer (225). Because the concentration of DHT is very high in the prostate, one may hypothesize that if DHT stimulates telomere lengthening in prostate, it may paradoxically play a protective role in some cells.

Reference

DHT isn’t the bad guy when it comes to hair loss​


Hair loss, together prostate cancer, are two of the main reasons why people want to lower DHT.


We all know that DHT is needed for beard growth (R), but it’s thought that DHT promote scalp hair loss.


…the effectiveness of SRD5A therapy likely resides at the level of the hair follicle (i.e., lowered follicular concentrations of DHT) and not a reduction of circulating DHT because this has not been shown to correlate with MAA.
Reference

The above claim is supported by the fact that men who are exposed to exceptionally high levels of DHT in response to the daily application of DHT for a long period of time didn’t experience acne, male androgenic alopecia or other androgen-associated skin pathology (R).


Furthermore, the differences in mean values of DHT were not significant according to the types of alopecia and the control group. And increased serum concentrations of DHT is not correlated with the advance of alopecia (R). This study speculates that hair loss severity is affected by other factors other than DHT, such as the duration of alopecia or the sensitivity of hair follicle cells to androgens (R).


Some people with hair loss have high DHT and others don’t, and some with high DHT have normal hair whereas others don’t (R).


So what’s going on with hairloss, if it’s not DHT?


You also might be wondering: “If DHT is not involved, why does 5-AR inhibitors work?


This study found that although 5α-reductase inhibitors are effective in treating male androgenic alopecia, DHT does not appear to play a primary role in the pathogenesis of male androgenic alopecia or acne (R).


A few reasons for hair loss include:


  1. Androgen receptor polymorphisms and differences in androgen receptor concentrations and steroid-converting enzymes as the principal contributors to male androgenic alopecia (R).
  2. Derangement of the internal cellular environment is primarily caused by the accumulation of free radicals, the reactive oxygen species (ROS) along with poor repair and restoration of the damaged cells due to essential nutrient deficiencies.
  3. “An initial experimental study by Eun[40] discovered that DHT does not directly cause inhibition of hair growth but it induces the release of transforming growth factor beta 1 (TGFß1) which results in the miniaturization and hair loss. Shin et al.[41] followed this research further with cultured androgen sensitive dermal papilla cells and the addition of DHT to this androgen sensitive cell caused an accumulation of free radicles ROS within the cultured cells, which in turn induced the release of TGFß1.” So a better approach than lowering DHT is to:
    • Positively modulate the skin microbiome (think sunlight, micronutrients, clean environment, etc.)
    • Inhibit excess ROS production
    • Prevent excess activation of TGFß1
    • Reduce stress

There are many more reasons for hair loss, but I won’t be diving into that in this article.


DHT for metabolic syndrome​


Metabolic syndrome is a cluster of conditions that increase the risk of heart disease, stroke and diabetes. Metabolic syndrome includes high blood pressure, high blood sugar, excess body fat around the waist and abnormal cholesterol levels. The syndrome increases a person’s risk of heart attack and stroke.


Insulin sensitivity


This randomized, controlled, double-blind trial provides evidence that DHT specifically (and to a much lesser extent, testosterone), improves insulin sensitivity and decreases plasma leptin level without notable side effects (R). Testosterone treatment caused prostatic nodular hyperplasia, benign at biopsy, whereas DHT didn’t.


Androgens, especially DHT, upregulate insulin receptor expression and activity and increase glycogen synthesis and cholesterol uptake in the liver (R).


Low DHT or lowering DHT with a 5-AR inhibitor, such as finasteride or dutasteride, is associated with an increase in blood glucose and glycosylated hemoglobin A as well as the risk of type 2 diabetes (R, R, R).


5-AR is necessary to inactivate cortisol, so blocking 5-AR increases cortisol, which promotes insulin resistance and liver disorders, such as NAFLD, steatosis, etc. (R, R).


Heart, liver and kidney function


DHT therapy in men with coronary artery disease (CAD) decreased myocardial ischemia and improved left ventricular diastolic function (R).


This in vitro study found:


In summary these in vitro data show that the T and DHT (via their anti-inflammatory effects) preserve endothelial cell function and prevent synthesis of cell adhesion molecules and release of proinflammatory cytokines.
Reference

The findings above could explain some of the previously described clinical observations of the relationship between low T and DHT and peripheral vascular disease and the anti-ischemic effects of acute infusion of testosterone in men with CAD and similar effects by DHT gel treatment (R).


A few more facts:


  • 5-AR inhibition may result in the development of kidney dysfunction (R).
  • Dutasteride, a 5-AR inhibitor, treatment increased activities of liver alanine aminotransferase and aspartate aminotransferase, suggesting dysregulation of liver metabolism (R).
  • DHT is a biomarker for reduced risk of stroke, which means that DHT is inversely correlated with stroke (R).
  • Higher DHT was associated with lower ischemic heart disease mortality in older men (R).

 

Pigeon

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Vascular function


High blood pressure


DHT increases the synthesis of nitric oxide through eNOS phosphorylation thus improving circulation and vascularity (R).


The following in vitro study shows that DHT has anti-inflammatory and protective effects in the vascular system:


DHT inhibited the tumor necrosis factor-α and lipopolysaccharide-induced expression of vascular cell adhesion molecules (VCAMs) and intercellular adhesion molecules (ICAMs). In addition, DHT inhibited messenger RNA (mRNA) expression of IL-6, PAI-1, and Cox-2 and the release of cytokines and chemokines such as growth-regulated oncogene proteins (GRO), granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor in endothelial cell culture.
Reference

Cholesterol


DHT:


  • Reduces lipid accumulation and cholesterol synthesis via increasing expression of carnitine palmitotyltransferase1 (CPT-1) and phosphorylation of 3-hydroxy-3-methyl-glutaryl-CoA reductase (R).
  • Inhibits ox-LDL–induced foam cell formation and atherosclerosis (R).

DHT administration for up to 2 years in normal men, didn’t cause any thrombotic events or detrimental shifts in total cholesterol, HDL and LDL cholesterol, or triglycerides. Nor were exceptionally high levels of DHT associated with a change in right carotid intima-media thickening (R, R).


Inhibiting 5-AR with dutasteride resulted in increased total cholesterol, and low-density lipoprotein cholesterol levels (R). Georgi (Haidut) posted a while ago that “inhibition of DHT synthesis causes severe hypothyroidism, despite the elevated levels of testosterone (T)“. Although the study was in rats, it could still be applicable to humans. I’ve seen quite a few test results from men a few weeks after quitting finasteride who experienced thyroid storm, which is most likely the rebound happening due to the suppression from finasteride.


Mitochondrial function and energy production


Androgens, especially DHT:


  • Stimulate lipolysis and down-regulates lipoprotein lipase activity and increases the expression of fatty acid-binding protein leading to an increase in fatty acid oxidation and in oxidative phosphorylation.
  • Increase the expression of pyruvate dehydrogenase, which increases the production of oxaloacetate and acetyl-CoA leading to a stimulation of the tricarboxylic acid (TCA) cycle.
  • Increase the expression of succinate dehydrogenase and aconitase, also upregulating TCA and increasing oxidative phosphorylation.
  • Increase the expression of cytochrome c oxidase, which leads to an increase in oxidative phosphorylation. The increase in oxidative phosphorylation leads to a decrease in reactive oxygen species and an increase in insulin sensitivity (R).

Fat loss​


DHT:


  • Inhibits preadipocyte proliferation and adipocyte differentiation, which prevents the excess formation of fat cells (R).
  • Stimulates lipolysis (R).
  • Stimulates lipid disposal (R).
  • Downregulates lipogenesis, which reduces the conversion of carbs to fat (R).
  • Prevents the downregulation of the leptin receptor (R).

Extras​


Gynecomastia


Gyno is known to be due to high estrogen and prolactin and low DHT and DHT treatment can reverse it.


Intramuscular injection of 200 to 400 mg DHT-hp every 2 to 4 weeks for 16 weeks was associated with a 67% to 78% decrease in breast size in adolescent boys with gynecomastia; no regrowth was observed for up 15 months post treatment… There was no change in testicular volume… There was no change in liver or renal function.
Reference

Brain & cognition


DHT promotes stress resiliency. Blocking 5-AR enhances cortisol release during stress, whereas DHT blunts it, most likely through CRH suppression (R, R).


DHT promote spatial memory (R).


DHT protects against neurodegeneration, by antagonizing TGFbeta (R). In this case study, someone with a demyelinating disease, Charcot-Marie-Toot 1, was able to induce neuroregeneration with 20mg/day of Anavar (oxandrolone) (R).


Lastly:


DHT treatment (in mice) promoted expression of synaptic plasticity markers [namely, cAMP-response element binding protein (CREB), postsynaptic density protein 95 (PSD95), synaptophysin (SYN), and developmentally regulated brain protein (Drebrin)], positively modified synaptic structure, and significantly delayed cognitive impairment.
Reference

DHT is needed for blood flow


Lower T or DHT levels, but not E2, is associated with symptoms of intermittent claudication in older men (R).


Bone


High doses of DHT can completely shut down LH and testosterone production and cause a major drop in estrogen. This might be a concern for some people because it’s mainly estrogen that’s been thought to be beneficial for bone, however, there is evidence that estrogen isn’t needed for bone strength/growth (R).


Furthermore, Finasteride increases the risk of fractures, which indicates that it weakens muscle strength and bone quality (R).


Eyes


DHT is needed to keep the eyes moist and prevent dry eyes. 5-AR inhibition may result in the development of dry eye disease (R). Androgen deficiency produces pathophysiological changes manifested in the reduction of tear production and evaporative dry eye conditions.


Suppression


DHT doesn’t have a suppressive effect on testicular steroidogenesis, similar to estrogen. DHT actually suppresses testicular aromatase. DHT inhibits steroidogenesis on a hypothalamic level, and doesn’t affect LH secretion at a pituitary level (R).


Anabolism/catabolism


DHT isn’t very anabolic, however, DHT derivatives, such as Anavar or Masteron are much more anabolic than DHT, and this is partly due to much slower clearance through the liver.


Apart from it not being very anabolic, DHT is anti-catabolic. This study found that people who experience muscle wasting from AIDS, retained more muscle mass if their DHT was normal, compared to those with low DHT (R). Anavar, a DHT derivative, is used to preserve muscle mass in people with wasting disease and to help them add more muscle for recovery (R). Even 5mg was enough to stop catabolism, whereas higher doses such as 15mg daily were needed for muscle growth in these patients.


Furthmore, DHT up-regulates androgen receptors (R).


Serotonin excess and cancer


DHT downregulates tryptophan hydroxylase 1 (TPH1; the rate-limited enzyme in serotonin synthesis in the body), thus protecting against the formation of tumors. Serotonin is also potent inflammatory and causes vasoconstriction, so DHT protects against that as well (R).
 
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