I wanted to post some evidence that DHT level is increased only in the balding scalp and only in the areas with thinning hair. And evidence that inflammation is persistent in Androgenetic Alopecia.
https://www.ncbi.nlm.nih.gov/books/NBK278957/
DHT levels and androgen receptor levels are not the same in balding and non balding scalp. And there is no difference between dht levels in occipital area in both non balding and balding people.
https://core.ac.uk/download/pdf/82562988.pdf
https://www.ncbi.nlm.nih.gov/pubmed/14757277
If under tension, the hair follicles are slowly damaged and DHT arrives in damaged area and it stays there consistently because it can't reduce the inflammation because it is chronic. The temporal areas are the first damaged because the tension is highest there. The way you hair follicles fused in the womb play the major role and how much layer of skin you have under them to protect them from the mechanical tension. Look at the way Androgenetic Alopecia progresses. I begins with very small recession at the temples and then it becomes deeper and deeper. Where the tension is highest it begins, and then it spreads slowly to the areas with low degree of tension. We don't know the exact point when it starts because the chronic daily mechanical tension needs years to damage the tissues. The area at the temples where the recession begins is probably in constant tension everyone since birth and that's why almost everybody loses hair there.
Some people are born with it and in some it happens with age.
If the mechanical tension wasn't the cause of hair loss bald people wouldn't have these stiff, shiny scalps. The skin gets stiff due to lack of blood flow, because as I said is blamed on DHT- induced calcification.