Medical Review of finasteride

MEDICAL REVIEW OF FINASTERIDE

The type II and type III 5'-reductase enzymes are inhibited by finasteride.

Finasteride limits the conversion of testosterone to dihydrotestosterone by inhibiting 5-reductase (DHT). Serum DHT levels are reduced by roughly 65-70% by Type II and III isoenzymes, and in the prostate, where Type II isoenzyme is predominant, DHT levels are reduced by up to 85-90%. Finasteride's inability to significantly inhibit the 5a-reductase type I isoenzyme prevents it from having the same inhibitory impact as triple inhibitors of all three 5a-reductase isoenzymes, such as dutasteride, which can significantly lower whole-body DHT levels (by more than 99%).

Finasteride decreases androgen activity in the scalp by preventing DHT synthesis. Inhibition of 5a-reductase improves and lowers the risk of prostate cancer by reducing prostate volume and prostatic hyperplasia in the prostate.The weight of the epididymis is similarly decreased by 5-reductase inhibition, along with the spermatozoa's normal motility and shape. It is currently officially licenced for the treatment of both hair loss and benign prostatic hyperplasia (enlarged prostate). Think carefully about the drug's range of effects prostatic hyperplasia. For the treatment of prostate enlargement, doctors utilise finasteride. Finasteride may alleviate symptoms like discomfort and reduced urine flow.

Compared to alpha-1 blockers like tamsulosin, it offers superior symptomatic relief; nevertheless, symptom reduction occurs more gradually (treatment with finasteride may take six months or more to determine the therapeutic outcome).Finasteride, but not alpha-1 inhibitors, were found to lower the likelihood of acute urinary retention (-57% at 4 years) and the requirement for surgery (-54% at 4 years) in long-term investigations. Within 6 to 8 months after stopping the medication, the prostate's alterations return.

Only men are treated with finasteride for androgenetic alopecia. After six months of treatment, the treatment slows down further hair loss and reduces hair loss by roughly 30%, but it is only effective for as long as the medication is taken.Women's hair loss has also been investigated with finasteride, but the outcomes were no better than a placebo.

Hirsutism can be effectively treated with finasteride (excessive growth of hair on the face or body). After two years of treatment, finasteride reduced body and facial hirsutism by 73% and 93%, respectively, in 89 women with hyperandrogenemia brought on by prolonged puberty syndrome.Finasteride has been demonstrated to be successful in other hirsutism treatment studies, including those including men.

Doping history

Because it may be used to cover up steroid usage, finasteride was prohibited by the World Anti-Doping Agency from 2005 to 2009. It was taken off the list in 2009 when advancements in testing techniques rendered the prohibition unnecessary. The enzyme 5'-reductase is blocked by finasteride in order to prevent harmful effects from its interaction with steroid hormones like testosterone. When using steroids, it's crucial to be able to prevent excessive androgenic side effects with high dosages of testosterone or another substance, especially when a suitably aesthetic  appearance is required, as in the case of actors, models, and other professions. Finasteride is frequently used by women who are concerned about becoming virilized yet view testosterone as doping in sports to lessen androgenic side effects, but read the caution below.

ATTENTION

Due to the potential for birth abnormalities in the baby, finasteride is not recommended for use in women during or before to pregnancy. The FDA has categorised it as pregnancy category X. But when testosterone interacts with 5-reductase, other substances also change. In our previous post, we discussed the effects of nandrolone and one of its metabolites, 5-Dihydronandrolone, on the brain. It is a primary metabolite of nandrolone and is produced by the enzyme 5-reductase in a manner similar to how dihydrotestosterone (DHT) is produced from testosterone. Contrary to testosterone and DHT, 5-DHN is a significantly weaker androgen receptor (AR) agonist than nandrolone itself, but it inhibits the androgenic receptor for a longer period of time, which results in a greater number of adverse side effects. In contrast to testosterone and other AAS, the ability of nandrolone to cause androgenic side effects is significantly increased when used with a 5-reductase inhibitor like finasteride, which prevents the conversion of nandrolone into 5-DHN.

Therefore, a knowledgeable athlete can benefit from a medicine as obscure as finasteride!