Low SHBG on TRT: what it actually signals about your health

What did @pa_courtney actually say?

The claim is straightforward: if a patient comes in with sex hormone binding globulin (SHBG) below 10 nmol/L, that's a signal worth asking about. Specifically, "sub 10 sex hormone binding globulin" is something @pa_courtney flags as a potential indicator of past anabolic steroid use, because androgens suppress SHBG production in the liver. She also connects long-term anabolic use to high estrogen symptoms and describes helping clients transition to "bioidentical testosterone and testosterone cypionate."

The framing here is clinical and experience-based, not sensationalized. She's a PA speaking to a patient question, not selling a supplement stack. That context matters when evaluating the claims.

Does the science back this up?

Yes, largely. Androgens suppress SHBG synthesis in the liver, and this effect is well-documented. Whether a very low SHBG reading can function as a historical marker for steroid use is more nuanced, but the underlying mechanism is real.

SHBG is produced by hepatocytes, and androgen receptor activation in the liver downregulates SHBG gene transcription. This has been demonstrated in vitro and confirmed in clinical populations. Longcope et al. (1990, Journal of Clinical Endocrinology and Metabolism) showed that exogenous androgens significantly reduce SHBG concentrations. More recently, Goldman et al. (2017, Journal of Clinical Endocrinology and Metabolism) documented persistently low SHBG in men with a history of anabolic-androgenic steroid (AAS) use, even after cessation. The persistence piece is what gives her clinical heuristic some traction. SHBG suppression does not always fully reverse after stopping AAS, particularly after prolonged use.

So the science supports the mechanism. Whether "sub 10" is the right threshold is less settled, and that's worth examining.

What did they get wrong (or right)?

Credit where it's due: the core mechanism is correct, and using SHBG as a conversation-starter about steroid history is a reasonable clinical practice. The problem is in the framing as a reliable indicator rather than a suggestive one.

Low SHBG has multiple causes that have nothing to do with steroids. Obesity, type 2 diabetes, hypothyroidism, and non-alcoholic fatty liver disease all suppress SHBG. Kalish et al. (2010, Metabolism) found strong inverse associations between insulin resistance and SHBG independent of testosterone. A patient with metabolic syndrome could show up with SHBG in the single digits and have never touched an anabolic steroid in their life.

She also says "testosterone sepenate" which appears to be a transcript garble of testosterone cypionate, already mentioned. Minor, but worth noting for clarity.

The claim that "more will make me feel better" loops are common with AAS users is accurate and clinically relevant. That behavioral pattern, sometimes described as AAS dependence, is documented in the literature. Kanayama et al. (2009, Drug and Alcohol Dependence) identified dependence-like patterns in a subset of long-term AAS users. She gets credit for naming this without dramatizing it.

What should you actually know?

Low SHBG is a clue, not a confession. If your SHBG is below 10 nmol/L, that warrants a full workup, not an assumption. Your provider should be asking about steroid history, yes, but also about metabolic health, liver function, thyroid status, and current medications including insulin sensitizers and glucocorticoids.

The transition from anabolic steroids to prescribed testosterone replacement is a real clinical pathway for men who have suppressed their own hormonal axis through prolonged AAS use. This is a legitimate concern because supraphysiologic androgen use can cause persistent hypothalamic-pituitary-gonadal axis suppression. Rahnema et al. (2014, Fertility and Sterility) documented this in detail, including cases where recovery of endogenous testosterone production took years or did not occur fully.

If you are currently using anabolic steroids and are concerned about your health, a provider who understands the full picture of AAS-related endocrine disruption, not just standard TRT protocols, is what you need. SHBG is one data point in a much larger picture.

Bottom line

@pa_courtney is making a clinically grounded point that most general practitioners would not think to make. The mechanism she describes is real. The threshold she uses is reasonable as a red flag, though not diagnostic. Where the video falls slightly short is in not acknowledging that very low SHBG has other explanations, and patients should not walk away thinking their SHBG level alone tells their whole story. Overall, this is more accurate than most TikTok content in this space.