TRT Clinic Revenue Loop

Testosterone converts into estrogen inside your body, and that conversion is not a bug in the system. It is how the system is supposed to work. Understanding why that matters requires walking the whole pathway first, because the individual steps only make sense once you can see where they lead.

Here is the chain. You take testosterone. An enzyme called aromatase, which is a protein your body produces specifically to convert androgens into estrogens, takes a percentage of that testosterone and converts it into estradiol. Your estradiol rises. That rising estradiol signals your liver to ramp up its conversion of growth hormone into something called IGF-1, which is insulin-like growth factor 1, the downstream molecule that actually does most of what people attribute to growth hormone itself. Higher testosterone therefore means higher estrogen, which means higher IGF-1. That is the intended sequence.

Now here is where the revenue loop enters.

A clinic sees your estrogen rise during TRT and prescribes something called an aromatase inhibitor, or AI, which is a drug that blocks the aromatase enzyme so testosterone cannot convert into estradiol. Your estrogen drops. And when your estrogen drops, the liver signal that drives IGF-1 production disappears with it.

This is not theoretical. A randomized controlled trial published in 2017 by Dias and colleagues tested this directly in 37 men aged 65 and older. The men given transdermal testosterone saw their IGF-1 increase by 15.3 nanograms per milliliter over the course of the study. The men given an aromatase inhibitor instead saw an increase of 0.3 nanograms per milliliter. Same population, same study design, same goal of raising testosterone. The difference between 15.3 and 0.3 is estrogen.

The AI group got the testosterone effect without the estrogen, and as a result, they got essentially none of the IGF-1 benefit.

So once the clinic has prescribed the AI and your IGF-1 has collapsed, you now have low IGF-1. And low IGF-1 has real symptoms: fatigue, poor recovery, reduced muscle protein synthesis, cognitive fog. The clinic runs a panel, sees the number is low, and offers you IGF-1 replacement. The logic of the offer sounds reasonable because the deficiency is real. What is missing from the conversation is that the clinic created it.

The FDA-approved version of injectable IGF-1 is called mecasermin, sold under the brand name Increlex, and it is approved for a condition called severe primary IGF-1 deficiency, specifically a genetic disorder called growth hormone insensitivity or Laron syndrome. Laron syndrome affects approximately 350 to 500 people worldwide. The drug exists for a pediatric orphan population that cannot produce IGF-1 at all because their growth hormone receptors do not function. It does not exist for a middle-aged man on TRT whose clinic suppressed his estrogen.

What makes this pattern more widespread than it should be is a disconnect between what the evidence recommends and what is actually being prescribed. A 2020 survey by Butaney and colleagues of 489 physicians found that 69.4 percent prescribed aromatase inhibitors to manage estrogen during TRT. 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 clinical practice is running ahead of the guideline consensus in the direction of more prescriptions, not fewer.

There are cases where estrogen genuinely needs to be managed. If someone aromatizes heavily and develops symptomatic gynecomastia that is confirmed and progressing, a short and targeted intervention may be warranted. That is the edge case. The routine use of AIs to keep estradiol within a narrow range on a standard TRT protocol is a different thing, and it is the routine use that opens the door to the IGF-1 deficiency downstream.

The reason this matters practically is that the deficiency feels real because it is real. A patient who is fatigued and recovering poorly after their clinic put them on an AI is not imagining the symptoms. The IGF-1 suppression is measurable and the symptoms are consistent with it. That is what makes the second offer so easy to accept. The clinic is not selling you something you do not need in the moment. They are selling you something you only need because of the moment they created.

If you are on testosterone and your clinic also has you on an aromatase inhibitor, the first thing worth doing is getting your IGF-1 level tested before accepting any new prescription. If the number is low and you are already on an AI, the question is not how to replace the IGF-1. The question is why the estrogen is being suppressed in the first place, and whether removing that suppression would let the liver do the job it was already designed to do.

Estrogen is not the enemy of testosterone therapy. In men, it is part of how testosterone therapy produces its benefits. The Dias data makes that visible in a single number: 15.3 versus 0.3. That gap is what estrogen was doing the whole time.

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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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