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Finasteride-induced Inhibition Of 5α-reductase Type 2 Could Lead To Kidney Damage-animal, Experiment
- Thread starter jamesbooker1975
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I read the abstract and it is still just speculation and the fact that they are stating that DHT plays a vitol role in the kidneys seems like they are grasping a bit. If anything, it is the opposite. Lowering DHT should help prevent renal disease because DHT increases aldosterone which has been implicated in kidney disease (as well as hypertension). Don't forget that the pseudohermaphrodites live their entire lives without this enzyme and their kidneys are just fine.
DHT increases Aldosterone
https://www.ncbi.nlm.nih.gov/pubmed/19428991
Aldosterone and progression of renal disease.
https://www.ncbi.nlm.nih.gov/pubmed/18090669
Males experience much more frequent and rapid kidney disease progression than females. The authors of this study conclude that DHT is the cause. Shocking.
https://www.ncbi.nlm.nih.gov/pubmed/28062795
Also, they don't mention how much finasteride was given. Often times in mice studies it can be several mg per kg of body weight. FInasteride metabolites are excreted through urine so if they are giving supraphysiological doses of finasteride, some of these changes they mention like abnormal cell growth, could be from large quantities of the drug passing through the kidneys and not the lack of 5AR2.
If they wanted to look at the other roles that 5AR plays in the kidneys, such as deactivating glucocorticoids, that would be more worthwhile in my opinion but trying to claim that DHT plays a vital role in kidney function, the evidence I see is hinting at the opposite conclusion and this is not surprising as DHT is a carcinogenic hormone and very pro aging and pro cancer.
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AHAHAWHAHAHA GO take finasteride THEN
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It is nothing in comparison to the copes of people who take it, yet convince themselves that it's perfectly safe in spite of ever-increasing evidence to the contrary.
What evidence? (I am not trying to come across as a pro-fina user, just genuinely interested)
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https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1527-3458.2006.00053.x
https://pdfs.semanticscholar.org/cfbb/6e441d2f878a71ba13a2ecaf70c4b7a43394.pdf
https://www.longdom.org/open-access...eview-of-the-literature-2472-1212-1000170.pdf
https://onlinelibrary.wiley.com/doi/10.1111/jsm.12269
https://www.ncbi.nlm.nih.gov/pubmed/24717976
http://www.associazionevittimefinas...oads/2017/05/Melcangi-Research-April-2017.pdf
For the record, I took 1.25 mg of Finasteride for 1 year. Probably one of the worst decisions I made in my life, but alas, you live and learn, sometimes at a high price.
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Try RU or CB then, those who get sides on finastride shouldn’t actually give up and instead look for alternatives.
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Dou you have any study to back that big claim?
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These are actually legitimate concerns, the effects of of 5AR inhibition as a whole, not just DHT inhibition. IMO, DHT creation in the adult male is largely an unintended byproduct of the body increasing 5AR enzymes for OTHER purposes as it ages.
That being said, it's not all black and white. Some of the effects on neurosteroids can be a benefit for people. There are studies showing parkinson's prevention and neuroprotection with dutasteride. Overproduction of neurosteroids can be detrimental if you have overly expressed 5AR.
https://www.ncbi.nlm.nih.gov/pubmed/28982631
https://www.ncbi.nlm.nih.gov/pubmed/26006269
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This article discusses the pro-carcinogenic nature of DHT and its anti-carcinogenic metabolite 3 beta adiol which binds to estrogen receptor beta.
https://www.thefreelibrary.com/The+anticancer+testosterone+metabolite+3[beta]+-+Adiol-a0297056560
DHT activates mTOR, really all androgens do but DHT is by far the most androgenic. This can be good in short term for growth but bad for longevity. If you are unfamiliar with mTOR simply google "mTOR aging". The links below are in regards to the prostate but the effects would extrapolate to any tissue that has high 5AR.
http://cancerres.aacrjournals.org/content/66/8_Supplement/688.1
https://www.ncbi.nlm.nih.gov/pubmed/16885382
https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.114.012066
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