@chris_practical's TRT libido claims need more context

What did @chris_practical actually say?

The core claim here is that HCG improves libido on TRT not primarily because it raises testosterone, but because it upregulates 5-alpha reductase and 3-beta HSD activity in the scrotum, which increases local DHT production. He also argued that DHEA supplements help libido partly because they "convert to DHT" and act as a neurosteroid. His bottom line: "HCG increases DHT" is the mechanism that matters.

To his credit, he's not overselling a simple fix. He acknowledges that pregnenolone and DHEA "play some role" without being the whole story. The framing is more nuanced than most TRT influencer content. But nuanced framing doesn't mean the biochemistry is accurate, and some of it here deserves real scrutiny.

Does the science back this up?

Partially, yes, but the DHT story is more complicated than he makes it sound. The claim that HCG upregulates intratesticular 5-alpha reductase activity has biological plausibility, and there is some supporting evidence. But calling DHT the primary driver of libido on TRT is a significant overclaim given what the literature actually shows.

LH receptor stimulation by HCG does influence intratesticular steroidogenesis beyond just testosterone production. Traish et al. (2007, Journal of Andrology) documented that DHT plays a role in male sexual function, but the relationship between circulating or local DHT and subjective libido is not cleanly dose-dependent. A 2021 review by Kovac and Lipshultz in Translational Andrology and Urology noted that libido is regulated by a network of androgens, neurosteroids, dopaminergic signaling, and psychosocial factors. Pointing at DHT as the primary lever is too clean.

On DHEA: it does convert peripherally to androgens including androstenedione and, to a lesser extent, testosterone and DHT. The neurosteroid claim is also real. Baulieu et al. (1998, PNAS) identified DHEA and DHEAS as neuroactive steroids with CNS effects. But the magnitude of DHT conversion from oral DHEA supplementation in adult men is modest and variable.

What did they get wrong (or right)?

He got the general direction right: HCG does more than just replace LH signaling, and intratesticular steroidogenesis produces compounds beyond testosterone that matter. That's a legitimate and often-ignored point in TRT discussions. Credit where it's due.

What's weaker is the confident mechanistic precision. The claim that HCG works "because of" DHT via 5-alpha reductase upregulation in the scrotum is stated as established fact. It isn't. The 3-beta HSD claim is also slightly misapplied here: 3-beta HSD is involved in converting pregnenolone to progesterone and DHEA to androstenedione, not directly in DHT synthesis. That step belongs to 5-alpha reductase acting on testosterone. Conflating these enzymatic steps suggests the explanation is being retrofitted onto a clinical observation rather than derived from solid mechanistic data.

The DHEA-to-DHT conversion pathway he describes is real but overstated. In practice, oral DHEA raises DHEAS and androstenedione more reliably than it raises DHT, particularly in eugonadal or TRT-supplemented men where feedback is already altered.

What should you actually know?

If your libido is still suboptimal on standard TRT, the honest answer is that no one fully knows why, and it's rarely one molecule. Morgentaler and Traish (2009, European Urology) noted that androgen effects on libido involve both peripheral and central mechanisms that don't map cleanly onto any single hormone level.

HCG does preserve intratesticular steroidogenesis and maintains production of hormones that exogenous testosterone suppresses, including pregnenolone, progesterone, and yes, some additional DHT. Whether that DHT increase is the reason libido improves for some men, versus the neurosteroid effects of restored pregnenolone or simply the psychological effect of feeling more hormonally complete, has not been cleanly separated in clinical trials.

DHEA supplementation shows inconsistent results in men. Some studies show modest libido improvement (Reiter et al., 1999, Journal of Clinical Endocrinology and Metabolism), others show no significant effect. The neurosteroid angle is biologically real but clinically unproven as a reliable libido driver in men on TRT.

The takeaway: the DHT hypothesis for HCG and libido is plausible and worth your doctor's attention, but it's a hypothesis, not settled science. Be skeptical of anyone, including well-meaning creators, who turns a plausible mechanism into a confident clinical explanation.