[Lotus]

Thanks Lotus.

From what I have read, the side effects of dutasteride are possible reduced libido, breast growth and impotence. It sounds like these side effects are pretty much the same as might apply to GTE.

I have read that another side effect sometimes postulated for dutasteride is that, while reducing the risk of most prostate cancers, it may correlate to a more aggressive form of prostate cancer later on. This correlation has been disputed by some researchers.

Are there other side effects I am not aware of? I would love to know if there are.

Hi spanky, happyme and crew.

Reduced sperm (quite possibly permanently). Dustasteride inhibits two types of 5 alpha reductase (type I & II), it'll tank total and free T. It looks like it has a surge (of T) in the first 30-45 days, most likely from negative feedback of lutenizing hormone. This surge (or flare as they say) also happens to a lesser extent when starting PM, and from my experience BO did the same thing at first. Lowered T can have a strong impact on libido, lowered free T will impact penis size.

Type I is predominate in the liver
Type II is predominant in the prostate, seminal vesicles, epididymes, hair follicles, and liver.

Two new adrenal 5 ar's have been discovered, though negligible. SRS would make then more apparent though.

Long term?, imo it's a top tier anti-androgen. I wouldn't use it just for NBE unless, you seek the kinda of results as in hrt. My experience with dutasteride was approximately 12 months.

Dutasteride: A Review of Current Data on a Novel Dual Inhibitor of 5 Reductase
http://www.ncbi.nlm.nih.gov/pmc/articles...4_0203.pdf

Dutasteride: How Does It Work?
DHT synthesis is catalyzed intracellularly by 5 reductase types 1 and 2 enzymes. Dutasteride is the first dual inhibitor of both 5 reductase isoenzymes. This leads to near-complete suppression of serum DHT—more than 90%, compared with the 70% seen with finasteride. Type 2 5 reductase is the predominant isoform in normal prostate and in BPH tissues. Type 1 5 reductase is present in BPH tissue in lower quantities, but it predominates in prostate cancer cell lines and seems to be over-expressed in some prostate cancers. Theoretically, the greater suppression of DHT arising from the dual 5 -reductase inhibition could result in greater efficacy than is observed in selective type 2 inhibition, and this dual inhibition could prevent type 1–mediated synthesis of DHT.