big questions, Mew ,Awor or any body please clarify it.

I put a study about two young kids born in Pakistan with micro penises due to absence of 5AR enzymes. These siblings were treated with DHT which helped them grow their penises bigger.

Please look at Fig 1 or file attached [WARNING: NOT SAFE FOR WORK PHOTOS OF MALE GENITALIA]: ncbi.nlm.nih.gov/pmc/article … figure/F1/

This is very informative reprot and we can go for high urinary tetrahydrocortisol (THF)/allotetrahydrocortisol (5 alpha-THF) ratio test.

as it says

In the younger sibling the diagnosis of 5 alpha-reductase deficiency was provisionally made at the early age of 3 days on the basis of high urinary tetrahydrocortisol (THF)/allotetrahydrocortisol (5 alpha-THF) ratio and this ratio increased with age confirming the diagnosis.
ncbi.nlm.nih.gov/pmc/articles/PMC1793798/

My question is why the gene responsible for Androgen action was not turned off? why these young boys responded well to DHT application as opposed to us? I am asking for the sake of knowledge only. I don’t mean I win you lose the attitude here. Mew or Awor if you read this pleas respond.

You have done well here. I think our bodies are mistaking testosterone for finasteride and or mistaking dht as a Xenobiotic. The clues are all there in members urine panels, and low testosterone blood results.

I believe our problem is neurologically based, the transmission/synthesis problem, it would explain why adding any of the hormones does very little because our bodies can produced them, but not synthesize them. This is sort of where all research is pointing and makes the most sense based on all the finasteride studies.