TRT Clinic Revenue Loop

Testosterone converts into estrogen inside your body, and that is not a malfunction. It is how the system is supposed to work. But a growing number of TRT clinics treat rising estrogen like a problem to be fixed, and the way they fix it sets off a chain reaction that ends with you buying something you would never have needed if they had left the estrogen alone.

To understand why, you need the full chain first.

When you take testosterone, an enzyme called aromatase, which converts androgens into estrogens, transforms a portion of that testosterone into estradiol. Your liver then uses estradiol as part of the signaling pathway that converts growth hormone into something called IGF-1, which is insulin-like growth factor 1, the downstream messenger that actually carries out most of what people associate with growth hormone. More estrogen, more efficient conversion, more IGF-1. The two are connected at the liver.

Now introduce an aromatase inhibitor, or AI, which is a drug that blocks the aromatase enzyme and suppresses estrogen production. Estrogen drops. The liver loses the signal it needs to drive IGF-1 synthesis. IGF-1 drops with it. The clinic then checks your IGF-1, sees it is low, and offers you a solution.

That is the loop.

A 2017 randomized controlled trial by Dias and colleagues put numbers on exactly this mechanism. They studied 37 men over age 65 and split them into groups: one receiving transdermal testosterone gel, one receiving an aromatase inhibitor. The testosterone group saw their IGF-1 rise by 15.3 nanograms per milliliter. The aromatase inhibitor group saw a rise of 0.3 nanograms per milliliter. Same study, same population, same baseline. The only variable that separated a 15-point increase from a near-zero result was whether estrogen was allowed to do its job.

That number is worth sitting with. A 15-point increase happened naturally, through the body's own conversion pathway, in older men who were already past peak hormonal function. The AI did not just slow that process down. It essentially stopped it.

The reason goes back to how growth hormone works in the liver. Growth hormone circulates in pulses and binds to receptors on liver cells, triggering IGF-1 synthesis. Estrogen up-regulates those liver receptors, meaning more estrogen means more binding sites, which means more IGF-1 produced per pulse of growth hormone. When you suppress estrogen with an AI, you are not just lowering one hormone in isolation. You are reducing the liver's capacity to respond to growth hormone at all. The factory is still shipping raw materials, but you have cut the number of workers who can process them.

This is why the idea that AI use is routine or standard practice does not hold up against the evidence. A 2020 survey by Butaney and colleagues of 489 physicians who were members of the International Society for Sexual Medicine found that 69.4 percent of them prescribed AIs to manage estrogen during TRT. And yet neither the Endocrine Society nor the American Urological Association, in their respective 2018 clinical guidelines, recommends routine AI use for estradiol management during testosterone therapy. The majority practice conflicts directly with the major guideline bodies.

Some of those physicians may be responding to patient symptoms they genuinely associate with elevated estrogen. That part is worth acknowledging. Elevated estrogen in men can produce real symptoms, and the belief that it needs to be suppressed is widespread enough that it persists even among trained clinicians. But the relevant question is not whether estrogen can go too high. It is whether reflexive AI prescription to bring it down is a well-supported protocol, and by the standards of the major endocrinology and urology bodies, it is not.

The downstream product in this loop, injectable or supplemental IGF-1, has a very specific approved context. The FDA-approved form is called mecasermin, sold under the name Increlex, and it carries an orphan drug designation because the condition it treats is that rare. It is approved for growth failure in children with severe primary IGF-1 deficiency caused by growth hormone insensitivity, a genetic condition affecting somewhere between 350 and 500 people worldwide. That approval exists for a population whose bodies are physically incapable of responding to growth hormone at all. It does not exist for a man on TRT whose IGF-1 dropped because his clinic suppressed the estrogen his liver needed.

If you are currently taking testosterone and an aromatase inhibitor, the most direct thing you can do is get your IGF-1 measured. If it is low, and your clinic offers a solution that costs money, ask whether the AI itself might be what caused the deficiency. That question alone tells you a great deal about how the clinic will respond.

The reason this loop functions is that most people experience the symptoms before they understand the mechanism. IGF-1 drops, they feel it, and by the time a solution is being offered, they are not thinking about what happened two steps earlier in the chain. Understanding the mechanism in advance removes the leverage entirely, because you can see the problem before someone else frames it as an opportunity.

Estrogen, in this context, is not the enemy. It is infrastructure.

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References

1. **Dias JP et al.** "Effects of transdermal testosterone gel or an aromatase inhibitor on serum concentration and pulsatility of growth hormone in older men." *Metabolism*, 2017; 69:143-147. PMID: 28285644. RCT, 37 men aged 65+. Testosterone group: +15.3 ng/mL IGF-1. AI group: +0.3 ng/mL.
2. **Butaney M et al.** "Treatment of estrogen levels in the management of hypogonadism: An anonymous survey of ISSM members." *Urology*, 2020; 141:68-74. PMID: 32045591. 69.4% of 489 surveyed physicians prescribed AIs for symptomatic elevated estrogen.
3. **FDA Label (NDA 021839):** Increlex (mecasermin) approved for growth failure in children with severe primary IGF-1 deficiency. Orphan drug. Pediatric only.
4. **Orphanet:** Laron syndrome affects approximately 350-500 individuals worldwide. Prevalence: 1-9 per 1,000,000.
5. **AUA 2018 Guideline** (Mulhall JP et al., PMID: 29601923) and **Endocrine Society 2018** (Bhasin S et al., PMID: 29562364): Neither endorses routine AI use for estradiol management during TRT.

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