Finasteride cause DNA damage . new study in vivo

[jamesbooker1975]

For all the finasteride groupies , enjoy it :
Prolonged use of finasteride-induced gonadal sex steroids alterations, DNA damage and menstrual bleeding in women

 

[jamesbooker1975]

It's a study done on women though but none the less even more proof to what every rational person already knew, fina is poison.

Yes, human are another specie, lucky us, male DNA is super DNA and can't be damage, lol

 

[TurboFixer]

they say this is the mechanism of hair loss in men and women

Why doesn't taking exogenous progesterone solve the problem then

 

[TurboFixer]

Yes, human are another specie, lucky us, male DNA is super DNA and can't be damage, lol

Its pretty relevant considering female and male hormones are obviously quite different.

 

[Michael1986]

For what its worth, several mouse studies have shown 5AR inhibitors to have neuroprotective properties. I know they are just mouse studies, but it is still evidence.

For example, the following two studies provide evidence that Dutasteride has neuro-protective properties in Parkinson's disease:

Study 1:
Effect of the 5α-reductase enzyme inhibitor dutasteride in the brain of intact and parkinsonian mice:
http://www.sciencedirect.com/science/article/pii/S0960076017302698
Highlights:
1. Dutasteride prevented the MPTP-induced striatal loss of dopamine contents.
2. Dutasteride prevented striatal MPTP-induced loss of DAT and VMAT2 transporters.
3. Dutasteride increased striatal DAT binding and glycosylation.
4. Dutasteride affected androgen and progesterone metabolism in brain and plasma.
5. Dutasteride prevented MPTP-induced increase of GFAP.

Study 2:
The 5α-reductase inhibitor Dutasteride but not Finasteride protects dopamine neurons in the MPTP mouse model of Parkinson's disease: http://www.sciencedirect.com/science/article/pii/S0028390815001963
Highlights:
• The 5α-reductase inhibitors Dutasteride and Finasteride were studied in MPTP mice.
• Dutasteride prevented the MPTP-induced striatal loss of dopamine concentrations.
• Dutasteride prevented striatal MPTP-induced loss of DAT and VMAT2 transporters.
• Finasteride did not protect striatal dopamine concentrations, DAT or VMAT2 levels.
• Dutasteride and Finasteride prevented MPTP-induced decreases of plasma testosterone.
And the last paragraph reads:
In summary, our results showed that a 5α-reductase inhibitor, Dutasteride has neuroprotective activity preventing in male mice the MPTP-induced loss of several dopaminergic markers.


And this study found evidence that finasteride may improve the course of hepatic encephalopathy:

Finasteride Has Regionally Different Effects on Brain Oxidative Stress and Acetylcholinesterase Activity in Acute Thioacetamide-Induced Hepatic Encephalopathy in Rats:

Finasteride Has Regionally Different Effects on Brain Oxidative Stress and Acetylcholinesterase Activity in Acute Thioacetamide-Induced Hepatic Encephalopathy in Rats

Finasteride (finasteride) inhibits neurosteroid synthesis and potentially improves the course of hepatic encephalopathy (HE). This study aimed to investigate the effects of finasteride on brain oxidative stress and acetylcholinesterase (AchE) activity in acute thioacetamide-induced HE in rats. Male Wistar rats...

journals.plos.org

Abstract:
Finasteride inhibits neurosteroid synthesis and potentially improves the course of hepatic encephalopathy (HE). This study aimed to investigate the effects of finasteride on brain oxidative stress and acetylcholinesterase (AchE) activity in acute thioacetamide-induced HE in rats. Male Wistar rats were divided into groups: 1. control; 2. thioacetamide-treated group (TAA; 900 mg/kg); 3. finasteride-treated group (Finasteride; 150 mg/kg); 4. group treated with finasteride and TAA (finasteride+TAA). Daily doses of finasteride (50 mg/kg) and TAA (300 mg/kg) were administered intraperitoneally during three days and in finasteride+TAA group finasteride was administered 2h before every dose of TAA. Finasteride pretreatment prevented TAA-induced rise in malondialdehyde level in the cortex due to restoration of catalase activity and increased expression of superoxide dismutase 1 (SOD1) and induced an increase in malondialdehyde level in the thalamus due to reduction of glutathione peroxidase (GPx) and glutathione reductase (GR) activity. Although finasteride pretreatment did not affect malondialdehyde level in hippocampus and caudate nucleus, hippocampal SOD1 expression was higher (p<0.05) and GR activity lower in finasteride+TAA vs. TAA group (p<0.05). GPx activity was lower in caudate nucleus in finasteride+TAA vs. TAA group (p<0.01). Finasteride pretreatment prevented TAA-induced rise in AchE activity in the thalamus and caudate nucleus and AchE activity correlates inversely in the thalamus (p<0.05) and positively in caudate nucleus (p<0.01) with malondialdehyde level. Finasteride has regionally selective effects on oxidative stress and AchE activity in the brain in acute TAA-induced HE in rats. The prooxidant role of finasteride in the thalamus may be causally linked with inhibition of AchE.


And this study found that finasteride exerts neuroprotection against ischemic brain injury in aged male rats:

The 5α-Reductase Inhibitor Finasteride Exerts Neuroprotection Against Ischemic Brain Injury in Aged Male Rats:

The 5α-Reductase Inhibitor Finasteride Exerts Neuroprotection Against Ischemic Brain Injury in Aged Male Rats - PubMed

Progesterone (P4) exerts potent neuroprotection both in young and aged animal models of stroke. The neuroprotection is likely to be mediated by allopregnanolone (ALLO) metabolized from P4 by 5α-reductase, since the neuroprotection is attenuated by the 5α-reductase inhibitor finasteride, which...

pubmed.ncbi.nlm.nih.gov

Abstract:
Progesterone (P4) exerts potent neuroprotection both in young and aged animal models of stroke. The neuroprotection is likely to be mediated by allopregnanolone (ALLO) metabolized from P4 by 5α-reductase, since the neuroprotection is attenuated by the 5α-reductase inhibitor finasteride, which was done only with young animals though. Thus, we do not know the contribution of ALLO to the P4-induced neuroprotection in aged animals. We examined effects of finasteride on the P4-induced neuroprotection in aged (16-18-month-old) male rats subjected to transient focal cerebral ischemia. Transient focal cerebral ischemia was induced by left middle cerebral artery occlusion (MCAO) and occlusion of the bilateral common carotid arteries. MCAO rats were given an 8 mg/kg P4 6 h after MCAO followed by the same treatment once a day for successive 3 days. Finasteride, a 5α-reductase inhibitor, at 20 mg/kg was intraperitoneally injected 30 min prior to the P4-injections. P4 markedly reduced neuronal damage 72 h after MCAO, and the P4-induced neuroprotection was apparently suppressed by finasteride in the aged animals. However, post-ischemic administration of finasteride alone (20 mg/kg) significantly prevented neuronal damage and the impairment of Rotarod performance after MCAO in aged male rats, but not in young ones. The androgen receptor antagonist flutamide markedly suppressed the neuroprotection of finasteride in the cerebral cortex, but not in the striatum, suggesting the androgen receptor-dependent mechanism of the finasteride-induced neuroprotection in the cerebral cortex. Our findings suggested, for the first time, the potential of finasteride as a therapeutic agent in post-ischemic treatment of strokes in aged population.

 

[jamesbooker1975]

Its pretty relevant considering female and male hormones are obviously quite different.

Finasteride-induced secondary infertility associated with sperm DNA damage

 

[jamesbooker1975]

For what its worth, several mouse studies have shown 5AR inhibitors to have neuroprotective properties. I know they are just mouse studies, but it is still evidence.

For example, the following two studies provide evidence that Dutasteride has neuro-protective properties in Parkinson's disease:

Study 1:
Effect of the 5α-reductase enzyme inhibitor dutasteride in the brain of intact and parkinsonian mice:
http://www.sciencedirect.com/science/article/pii/S0960076017302698
Highlights:
1. Dutasteride prevented the MPTP-induced striatal loss of dopamine contents.
2. Dutasteride prevented striatal MPTP-induced loss of DAT and VMAT2 transporters.
3. Dutasteride increased striatal DAT binding and glycosylation.
4. Dutasteride affected androgen and progesterone metabolism in brain and plasma.
5. Dutasteride prevented MPTP-induced increase of GFAP.

Study 2:
The 5α-reductase inhibitor Dutasteride but not Finasteride protects dopamine neurons in the MPTP mouse model of Parkinson's disease: http://www.sciencedirect.com/science/article/pii/S0028390815001963
Highlights:
• The 5α-reductase inhibitors Dutasteride and Finasteride were studied in MPTP mice.
• Dutasteride prevented the MPTP-induced striatal loss of dopamine concentrations.
• Dutasteride prevented striatal MPTP-induced loss of DAT and VMAT2 transporters.
• Finasteride did not protect striatal dopamine concentrations, DAT or VMAT2 levels.
• Dutasteride and Finasteride prevented MPTP-induced decreases of plasma testosterone.
And the last paragraph reads:
In summary, our results showed that a 5α-reductase inhibitor, Dutasteride has neuroprotective activity preventing in male mice the MPTP-induced loss of several dopaminergic markers.


And this study found evidence that finasteride may improve the course of hepatic encephalopathy:

Finasteride Has Regionally Different Effects on Brain Oxidative Stress and Acetylcholinesterase Activity in Acute Thioacetamide-Induced Hepatic Encephalopathy in Rats:

Finasteride Has Regionally Different Effects on Brain Oxidative Stress and Acetylcholinesterase Activity in Acute Thioacetamide-Induced Hepatic Encephalopathy in Rats

Finasteride (finasteride) inhibits neurosteroid synthesis and potentially improves the course of hepatic encephalopathy (HE). This study aimed to investigate the effects of finasteride on brain oxidative stress and acetylcholinesterase (AchE) activity in acute thioacetamide-induced HE in rats. Male Wistar rats...

journals.plos.org

Abstract:
Finasteride inhibits neurosteroid synthesis and potentially improves the course of hepatic encephalopathy (HE). This study aimed to investigate the effects of finasteride on brain oxidative stress and acetylcholinesterase (AchE) activity in acute thioacetamide-induced HE in rats. Male Wistar rats were divided into groups: 1. control; 2. thioacetamide-treated group (TAA; 900 mg/kg); 3. finasteride-treated group (Finasteride; 150 mg/kg); 4. group treated with finasteride and TAA (finasteride+TAA). Daily doses of finasteride (50 mg/kg) and TAA (300 mg/kg) were administered intraperitoneally during three days and in finasteride+TAA group finasteride was administered 2h before every dose of TAA. Finasteride pretreatment prevented TAA-induced rise in malondialdehyde level in the cortex due to restoration of catalase activity and increased expression of superoxide dismutase 1 (SOD1) and induced an increase in malondialdehyde level in the thalamus due to reduction of glutathione peroxidase (GPx) and glutathione reductase (GR) activity. Although finasteride pretreatment did not affect malondialdehyde level in hippocampus and caudate nucleus, hippocampal SOD1 expression was higher (p<0.05) and GR activity lower in finasteride+TAA vs. TAA group (p<0.05). GPx activity was lower in caudate nucleus in finasteride+TAA vs. TAA group (p<0.01). Finasteride pretreatment prevented TAA-induced rise in AchE activity in the thalamus and caudate nucleus and AchE activity correlates inversely in the thalamus (p<0.05) and positively in caudate nucleus (p<0.01) with malondialdehyde level. Finasteride has regionally selective effects on oxidative stress and AchE activity in the brain in acute TAA-induced HE in rats. The prooxidant role of finasteride in the thalamus may be causally linked with inhibition of AchE.


And this study found that finasteride exerts neuroprotection against ischemic brain injury in aged male rats:

The 5α-Reductase Inhibitor Finasteride Exerts Neuroprotection Against Ischemic Brain Injury in Aged Male Rats:

The 5α-Reductase Inhibitor Finasteride Exerts Neuroprotection Against Ischemic Brain Injury in Aged Male Rats - PubMed

Progesterone (P4) exerts potent neuroprotection both in young and aged animal models of stroke. The neuroprotection is likely to be mediated by allopregnanolone (ALLO) metabolized from P4 by 5α-reductase, since the neuroprotection is attenuated by the 5α-reductase inhibitor finasteride, which...

pubmed.ncbi.nlm.nih.gov

Abstract:
Progesterone (P4) exerts potent neuroprotection both in young and aged animal models of stroke. The neuroprotection is likely to be mediated by allopregnanolone (ALLO) metabolized from P4 by 5α-reductase, since the neuroprotection is attenuated by the 5α-reductase inhibitor finasteride, which was done only with young animals though. Thus, we do not know the contribution of ALLO to the P4-induced neuroprotection in aged animals. We examined effects of finasteride on the P4-induced neuroprotection in aged (16-18-month-old) male rats subjected to transient focal cerebral ischemia. Transient focal cerebral ischemia was induced by left middle cerebral artery occlusion (MCAO) and occlusion of the bilateral common carotid arteries. MCAO rats were given an 8 mg/kg P4 6 h after MCAO followed by the same treatment once a day for successive 3 days. Finasteride, a 5α-reductase inhibitor, at 20 mg/kg was intraperitoneally injected 30 min prior to the P4-injections. P4 markedly reduced neuronal damage 72 h after MCAO, and the P4-induced neuroprotection was apparently suppressed by finasteride in the aged animals. However, post-ischemic administration of finasteride alone (20 mg/kg) significantly prevented neuronal damage and the impairment of Rotarod performance after MCAO in aged male rats, but not in young ones. The androgen receptor antagonist flutamide markedly suppressed the neuroprotection of finasteride in the cerebral cortex, but not in the striatum, suggesting the androgen receptor-dependent mechanism of the finasteride-induced neuroprotection in the cerebral cortex. Our findings suggested, for the first time, the potential of finasteride as a therapeutic agent in post-ischemic treatment of strokes in aged population.

Yes, all done in MICE ! is show exactly the opposite in humans. Is is easy, you inhibit DHT, by inhibiting and enzyme that is in charge of many other reaction, like the convertion of pregnolone to allopregnolone, a potent " chill out " neurohormone. That is why all the 5-alpha reductase increase anxiety, depression , etc . Finasteride, dutasteride, isotretinoin all have this side effect.

 

[jamesbooker1975]

The prove that Merck ( if you want to know how Merck work, or worked but the era of Propecia, read the Vioxx scandal ) is that in their 10 years follow up case ( phase 4 ) they didn't show a single blood work result, not estrogen, not testosterone, not progesterone, etc, etc, etc.
IF is so safe, why they didn't gave us that value and compare it to normal range at that age ? Why ? Why Glaxo never release it for male pattern baldness even after show us that phase 2 were a complete success ?

 

[jamesbooker1975]

they say this is the mechanism of hair loss in men and women
View attachment 151488
Why doesn't taking exogenous progesterone solve the problem then

1) IF you progesterone are low, that could be . Yes, progesterone could solve the problem. Specially if your DHT and your Estradiol are high . Anyway, Progesterone is much safer option than oral finasteride. But, not any big pharma will make money with it. Plus most of the docts not even know what actually progesterone is or what effect have in males.
2) You can also take pregnenolone.

 

[Michael1986]

There certainly is a lot of information to go through in this thread. As I see it, there are pluses and minuses to 5AR inhibitors. Yes, they may pose some degree of risk to our bodies and our brains, but at the same time, they might also have some beneficial effects, and likely not just in terms of hair growth. It is a complicated picture that is not black and white. And yes, the studies I quoted which showed neuroprotective effects of 5AR inhibitors were indeed done on mice, but that doesn't make these studies irrelevant. Mouse studies are still useful. I suppose each hair loss sufferer should just carry out their own research from varied sources so that they can make an informed decision on whether using finasteride is worth it in terms of risk versus reward. I'm a long-term user of dutasteride, and I'm aware that the drug has an element of risk associated with it, but what I also know is that if I had never treated my hair loss and had let myself go bald, I would be deeply unhappy right now. In my case, treating my hair loss was worth it.

 

[jamesbooker1975]

There certainly is a lot of information to go through in this thread. As I see it, there are pluses and minuses to 5AR inhibitors. Yes, they may pose some degree of risk to our bodies and our brains, but at the same time, they might also have some beneficial effects, and likely not just in terms of hair growth. It is a complicated picture that is not black and white. And yes, the studies I quoted which showed neuroprotective effects of 5AR inhibitors were indeed done on mice, but that doesn't make these studies irrelevant. Mouse studies are still useful. I suppose each hair loss sufferer should just carry out their own research from varied sources so that they can make an informed decision on whether using finasteride is worth it in terms of risk versus reward. I'm a long-term user of dutasteride, and I'm aware that the drug has an element of risk associated with it, but what I also know is that if I had never treated my hair loss and had let myself go bald, I would be deeply unhappy right now. In my case, treating my hair loss was worth it.

Reach the 40s , and you will see it was not worth it . At least, did you do blood work ? you liver enzymes must be high , etc

 

[Catagen]

Yeah no, blocking DHT and other cascading hormones due to duta/fina has MUCH more serious health impacts......

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:

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.

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

And also:

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).

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:

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:

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.

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 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).

"DHT IS A TRASH HORMONE"

 

[JohnSmith21]

Patients treated for male pattern hair with finasteride show, after discontinuation of the drug, altered levels of neuroactive steroids in cerebrospinal fluid and plasma.

Abstract

Observations performed in a subset of patients treated for male pattern hair loss indicate that persistent sexual side effects as well as anxious/depressive symptomatology have been reported even after discontinuation of finasteride treatment. Due to the capability of finasteride to block the metabolism of progesterone (PROG) and/or testosterone (T) we have evaluated, by liquid chromatography-tandem mass spectrometry, the levels of several neuroactive steroids in paired plasma and cerebrospinal fluid (CSF) samples obtained from post-finasteride patients and in healthy controls. At the examination, post-finasteride patients reported muscular stiffness, cramps, tremors and chronic fatigue in the absence of clinical evidence of any muscular disorder or strength reduction. Although severity of the anxious/depressive symptoms was quite variable in their frequency, overall all the subjects had a fairly complex and constant neuropsychiatric pattern. Assessment of neuroactive steroid levels in CSF showed a decrease of PROG and its metabolites, dihydroprogesterone (DHP) and tetrahydroprogesterone (THP), associated with an increase of its precursor pregnenolone (PREG). Altered levels were also observed for T and its metabolites. Thus, a significant decrease of dihydrotestosterone (DHT) associated with an increase of T as well as of 3?-diol was detected. Changes in neuroactive steroid levels also occurred in plasma. An increase of PREG, T, 3?-diol, 3?-diol and 17?-estradiol was associated with decreased levels of DHP and THP. The present observations show that altered levels of neuroactive steroids, associated with depression symptoms, are present in androgenic alopecia patients even after discontinuation of the finasteride treatment. This article is part of a Special Issue entitled 'Sex steroids and brain disorders'.


https://www.ncbi.nlm.nih.gov/pubmed/24717976

Pigeon, just wondering what state your hair is in? Do you have pics? Bc your very anti finasteride and I’m wondering if it’s cuz you have good hair and don’t find it necessary to go on, or you think it’s too late. Most docs don’t even recognize Pfs as a real thing. My thought process is if you try it and don’t get sides, great, and if you try it and get sides just stop taking it? Worse case is your in the same position if you stop. Also, in all the studies I’ve seen on finasteride BMI was no different. I also don’t see any studies linking dht and fat burning. You are super anti finasteride , and say cope a lot but you seem like the one coping lol. I take finasteride, I don’t have sides, If I get sides, I’ll stop taking it and just do transplants..... where is the cope there? Lol. My guess is that you have terrible hair, and coping with your situation by praising dht lol. Not many people get sides, and they go away when you stop dude.... not that serious. I bet you have more “sides” in your life with your current hair situation. You always wanna disuade people from using finasteride? Why? It’s the same advice for everything - If you get sides stop? You say cope and it’s so funny bc your coping so hard with balding that you want to shout f*** finasteride lmao. I barely think about my hair on finasteride and I have no sides, but again, if I do get sides I’ll lower the dose or stop lol

 

[Will Be an Egg in 5 years]

Yes, human are another specie, lucky us, male DNA is super DNA and can't be damage, lol

Are you really that dumb?

 

[JohnSmith21]

Pigeon, just wondering what state your hair is in? Do you have pics? Bc your very anti finasteride and I’m wondering if it’s cuz you have good hair and don’t find it necessary to go on, or you think it’s too late. Most docs don’t even recognize Pfs as a real thing. My thought process is if you try it and don’t get sides, great, and if you try it and get sides just stop taking it? Worse case is your in the same position if you stop. Also, in all the studies I’ve seen on finasteride BMI was no different. I also don’t see any studies linking dht and fat burning. You are super anti finasteride , and say cope a lot but you seem like the one coping lol. I take finasteride, I don’t have sides, If I get sides, I’ll stop taking it and just do transplants..... where is the cope there? Lol. My guess is that you have terrible hair, and coping with your situation by praising dht lol. Not many people get sides, and they go away when you stop dude.... not that serious. I bet you have more “sides” in your life with your current hair situation. You always wanna disuade people from using finasteride? Why? It’s the same advice for everything - If you get sides stop? You say cope and it’s so funny bc your coping so hard with balding that you want to shout f*** finasteride lmao. I barely think about my hair on finasteride and I have no sides, but again, if I do get sides I’ll lower the dose or stop lol

I’m sure your gonna post some stupid long response like you normally do, so just simply post your hair and I will have all the answers

 

[JohnSmith21]

like I have a low chance of sides on finasteride. And they will go away when I stop lmao. Why not try it??? If I told you if you were to gamble, you’d have a 2% chance of losing money, and If you did lose, that you can stop gambling and Be in the same position as when you walked in, you’d obviously do it lol. The drug has been out since the 90s. It’s well studied and tolerated. Millions of men take it, there’s nothing here. People like pigeon are just so bald that they can’t do anything about it, and then wanna cope like “dht is the most important hormone!”, while they rub their scalp, use topicals, and search hair forums 24-7 while seeing no progress

 

[corkmeister]

like I have a low chance of sides on finasteride. And they will go away when I stop lmao. Why not try it??? If I told you if you were to gamble, you’d have a 2% chance of losing money, and If you did lose, that you can stop gambling and Be in the same position as when you walked in, you’d obviously do it lol. The drug has been out since the 90s. It’s well studied and tolerated. Millions of men take it, there’s nothing here. People like pigeon are just so bald that they can’t do anything about it, and then wanna cope like “dht is the most important hormone!”, while they rub their scalp, use topicals, and search hair forums 24-7 while seeing no progress

He tried it like you said and the drug fucked him over permanently, so what do you expect? Let's cut the guy some slack. The drug is not the literal poison he's making it out to be but pretending like it's totally safe without any chance of permanent damage is just cope at this point. Have you taken a good look around this forum?

 

[JohnSmith21]

He tried it like you said and the drug fucked him over permanently, so what do you expect? Let's cut the guy some slack. The drug is not the literal poison he's making it out to be but pretending like it's totally safe without any chance of permanent damage is just cope at this point. Have you taken a good look around this forum?

But there is absolutely zero evidence of permanent damage. The doctor who wrote me my script (Bernstein in nyc) told me that he doesn’t write it for people with diagnosed ocd bc there’s a strong correlation between ocd and pfs. I was also informed that there is no documented cases of pfs until the internet became more mainstream. For the first 10 years the drug was out there was zero risk of permanent sides, and now all of a sudden when all the hypochondriacs are conversing online, there is something called pfs. There is absolutely zero evidence of permanent sides. Zero. Are there sides of the drug that a minority of people get? Yes for sure. But that’s it. To constantly scream from the hills that finasteride is poison and that everyone who takes it is coping is literally the definition of coping (ironically). I have zero sides. I’m 10% body fat 186 lbs. I have a good sex drive. I have a full beard. And thanks to the drug I’m Maintaining my hair! If I lost a significant amount more hair I’d honestly probably have anxiety and depression. And if I DO get sides, the worst case scenario is I stop, and be where I otherwise would be without the drug.... and honestly if finasteride doesn’t work and you don’t use minoxidil your out of options. Only hair transplant. People don’t realize that. All this other bs won’t do anything. If you have hair loss it’s truly is either you take finasteride, get a transplant, or Both.

 

[inmyhead]

Most of these anti-finasteride studies are ridiculous. Usually it's people's own estimation what side efffects they are feeling. There is 0 science in that. Another usual bullshit is that people with some abnormalities appear which may have even existed before they started finasteride or appeared due to some other reasons. That is not science.

 

[inmyhead]

If those studies are ridiculous then Merck's study must be hilarious because we know they downplayed and lied about the side effects.

But let's be serious here, do you guys really expect that blocking 70% of DHT (and disturbing other hormones and your endocrine system) for years and years will only affect your hair? Do you really believe that?

I know balding fcks you up mentally and makes one hopeless but put your emotions aside for once and think about it rationally and look into what fina actually does to your body.

Bodybuilders are injecting more serious stuff for even longer and they are fine. You're saying 'I know that these studies are invalid, but finasteride must still be horrible!'. Doesn't that sound emotional? If I remember correctly, asians had their own studies for finasteride, dutasteride.
I'm not saying that it's completely safe to take finasteride, but there isnt' any proof that it's very risky either except from these PFS forums guys and few guys here. People claim all kind of sh*t on the internet - for example gyno from minoxidil, PFS from minoxidil, PFS from keto shampoo and some other stuff...