This will most likely be my last post
Much of the biological role of DHT has been elucidated in studies of individuals with
congenital 5α-reductase type II deficiency, an
intersex condition caused by a
loss-of-functionmutation in the
gene encoding
5α-reductase type II, the major enzyme responsible for the production of DHT in the body.
[13][19][2] It is characterized by a defective and non-functional 5α-reductase type II enzyme and a partial but majority loss of DHT production in the body.
[13][19] In the condition, circulating testosterone levels are within or slightly above the normal male range, but DHT levels are low (around 30% of normal),
[20][
better source needed] and the ratio of circulating testosterone to DHT is greatly elevated (at about 3.5 to 5 times higher than normal).
[13]
Genetic males (46,XY) with 5α-reductase type II deficiency are born with
undervirilization including
pseudohermaphroditism (ambiguous genitalia),
pseudovaginal perineoscrotal hypospadias, and usually
undescended testes. Their external genitalia are female-like, with
micropenis (a small,
clitoris-like
phallus), a partially unfused,
labia-like
scrotum, and a blind-ending, shallow
vaginal pouch.
[13] Due to their lack of conspicuous
male genitalia, genetic males with the condition are typically raised as girls.
[19] At the time of
pubertyhowever, they develop striking phenotypically masculine
secondary sexual characteristics including partial virilization of the genitals (enlargement of the phallus into a near-functional penis and
descent of the testes),
voice deepening, typical male
musculoskeletal development,
[12] and no
menstruation,
breast development, or other signs of
feminization that occur during female puberty.
[13][19][2] In addition, normal
libido and
spontaneous erections develop,
[21] they usually show a
sexual preference for females, and almost all develop a male
gender identity.
[13][22]
Nonetheless, males with 5α-reductase type II deficiency exhibit signs of continued undervirilization in a number of domains.
Facial hair was absent or sparse in a relatively large group of
Dominican males with the condition, known as the
Güevedoces. However, more facial hair has been observed in patients with the disorder from other parts of the world, although facial hair was still reduced relative to that of other men in the same communities. The divergent findings may reflect racial differences in androgen-dependent hair growth. A female pattern of
androgenic hair growth, with
terminal hair largely restricted to the
axillae and lower
pubic triangle, is observed in males with the condition. No temporal recession of the hairline or
androgenic alopecia (pattern hair loss or baldness) has been observed in any of the cases of 5α-reductase type II deficiency that have been reported, whereas this is normally seen to some degree in almost all Caucasian males.
[13] Individuals with 5α-reductase type II deficiency were initially reported to have no incidence of
acne,
[8][2] but subsequent research indicated normal
sebum secretion and acne incidence.
[12]
In genetic males with 5α-reductase type II deficiency, the
prostate gland is rudimentary or absent, and if present, remains small, underdeveloped, and unpalpable throughout life.
[8][4]In addition, neither BPH nor prostate cancer have been reported in these individuals.
[14] Genetic males with the condition generally show
oligozoospermia due to undescended testes, but
spermatogenesis is reported to be normal in those with testes that have descended, and there are case instances of men with the condition successfully fathering children.
[21][23]
Unlike males, genetic females with 5α-reductase type II deficiency are phenotypically normal. However, similarly to genetic males with the condition, they show reduced body hair growth, including an absence of hair on the arms and legs, slightly decreased axillary hair, and moderately decreased pubic hair.
[24][21] On the other hand,
sebum production is normal.
[24][25] This is in accordance with the fact that sebum secretion appears to be entirely under the control of 5α-reductase type I.
[25] (Source:
https://en.wikipedia.org/wiki/Dihydrotestosterone)
... His hair looked good on propercia anyways, but that improvement after adding Min is incredible. There is no need for a hair transplant at all. A lot of people improve on the Big 3, but still need to get temples fixed or the frontal 3rd, just like I do.
