AFAIK the adrenal glands don't directly produce T.
View attachment 979942
Essentially they synthesize pregnenolone (P5) from cholesterol. P5 is NOT progestogenic, it is instead a precursor to sex steroids and an endocannabinoid in its own right.
Different enzymes convert P5 into various other steroids within the adrenal glands and these circulate within the body. The androgens are on the right of the image, DHEA and androstenedione (A4). So the adrenal glands are sending out two weak androgens: DHEA, which has biological functions on its own but is also a precursor in other parts of the body for A4, and A4 itself. But not T.
A4 (non-anabolic androgen): C
19H
26O
2
hydrogenates (gains 2 hydrogen atoms) in the presence of certain forms of the 17β-HSD enzyme to become
T (anabolic androgen): C
19H
28O
2
or dehydrogenates (losing 4 hydrogen atoms & 1 carbon atom) in the presence of aromatase to
E1 (estrone: weak estrogen): C
18H
22O
2
T: C
19H
28O
2
hydrogenates (gains 2 hydrogen atoms) in the presence of 5-alpha-reductase (missing from Caster Semenya) to become
DHT (non-anabolic androgen that is responsible for body hair, odour, etc.): C
19H
30O
2
or dehydrogenates (losing 4 hydrogen atoms & 1 carbon atom) in the presence of aromatase to
E2 (estradiol: strong estrogen/titty skittles): C
18H
24O
2
E1 hydrogenates (+2 hydrogen atoms) in the presence of certain forms of 17β-HSD to make E2.
All the 17β-HSD reactions are interconversions, i.e. two-way
17β-HSD type 1 is found in breast tissue and the ovaries and does E1<->E2 (and to a lesser degree A4 <-> T). After menopause the depletion of the ovarian ococytes means that E1 stays high, but E2 falls, except in breast cancer (due to cancerous cells and 17β-HSD type 1 converting E1 to E2 in breast tissue).
17β-HSD type 3 is found in the testes, and it's A4 <-> T, and to a lesser degree E1 <-> E2.
17β-HSD type 5 is found in both sexes and is the main enzyme for T production (from A4) in the ovaries.
You also have different types of 17β-HSD in fatty tissue producing both T and E2, which could explain why bearded women tend to be fat, and also has some connection to women's higher % of body fat.
Rhys could choose to take E2/titty skittles, and that would increase his body fat %, but I guess his lardiness is coming from being a greedy pig, not from exogenous hormones/titty skittles.
In terms of hormone levels it's pretty complicated as the different hormones feed back to each other in various ways such that while if Reeeeees had his balls chopped off they are obviously no longer producing testosterone, he has T elsewhere.
He once published this
View attachment 980051
His free testosterone was at 0.4pg/mL, which is 1.4 pmol/mL. And his total testosterone was <3ng/dL, which is <0.1 nmol/L.
The average female levels are respectively 10 pmol/mL, and 0.6 nmol/L.
So he produces testosterone, but it is 'extremely low'.
He doesn't understand that 'low' is not the same thing as 'none'.
And he's repeating this
View attachment 980063
He's choosing to ignore the accurate point being made which is that Rhys' body is permanently virilized (male) by the 20 years of male T, and that as a purely factual aside, he definitely still has endogenous T even if it is not anabolic at his levels. (And while Reees has sub-female T levels, female T levels aren't anabolic either - that's why women don't look like men. There isn't really a link between endogenous actual female testosterone levels and sporting performance, because women don't produce enough testosterone for it to be performance-enhancing - 0.1 vs 0.5 vs 1.0 doesn't make any difference. What DOES make a difference is when, like Rhys, you produced ~20 nmol/l for 20 years.)
Hormones are a red herring because Reeeees still has a male body.