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Pionier · 23 november 2020, 13:02

https://men-elite.com/2020/09/29/the...esearch-shows/

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
5?-androstane-3?, 17-?-diol (dihydroandrosterone/3?-diol) via the intracrine reverse synthesis pathway (3?-hydroxysteroid dehydrogenase (3?-HSD))

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

DHT has a 4 time higher affinity to AR (androgen receptor) than testosterone.
Binding of DHT to the AR transforms the AR to its DNA-binding state.
DHT upregulates AR synthesis and reduces AR turnover.
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 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).

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-? 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).

23 november 2020, 13:02	#127
Pionier HaarWeb lid Geregistreerd: 12 augustus 2016 Berichten: 289 Geslacht:	https://men-elite.com/2020/09/29/the...esearch-shows/ 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 5?-androstane-3?, 17-?-diol (dihydroandrosterone/3?-diol) via the intracrine reverse synthesis pathway (3?-hydroxysteroid dehydrogenase (3?-HSD)) DHT is 2.5-10 times more potent than testosterone and here’s why: DHT has a 4 time higher affinity to AR (androgen receptor) than testosterone. Binding of DHT to the AR transforms the AR to its DNA-binding state. DHT upregulates AR synthesis and reduces AR turnover. 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 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). 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-? 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).