TRT Clinic Revenue Loop

Testosterone converts to estrogen inside your body, and that is not a malfunction. That is the system working exactly as it should.

Understanding why requires a quick map of the whole chain. Testosterone gets converted into estrogen through a process called aromatization, which is what happens when an enzyme called aromatase transforms testosterone molecules into estradiol. Your body does this automatically, and the estrogen that gets produced is not waste. It has jobs to do, and one of the most important ones happens in your liver.

Your liver takes growth hormone and converts it into something called IGF-1, which stands for insulin-like growth factor 1 and is the molecule your body actually uses to build and repair tissue. Growth hormone is the signal, but IGF-1 is the thing that does the work. And that liver conversion, the step where growth hormone becomes usable IGF-1, depends heavily on estrogen to function properly.

So the chain looks like this. You take testosterone. Some of it aromatizes into estrogen. That estrogen signals your liver to convert growth hormone into IGF-1. Your IGF-1 goes up, your body has more of the raw material it needs for recovery and lean tissue, and the system hums along.

Now here is where the revenue loop starts.

When your estrogen rises on testosterone, some clinics treat that as a problem to be solved, and they prescribe something called an aromatase inhibitor, or AI, which is a drug that blocks the aromatase enzyme and prevents testosterone from converting into estrogen. Estrogen drops. But when estrogen drops, your liver loses the signal it needs to run that growth hormone conversion efficiently, and your IGF-1 production collapses with it.

The 2017 randomized controlled trial by Dias and colleagues measured this directly. They took 37 men over 65 and compared a testosterone group to an AI group, and the difference was stark. The testosterone group saw their IGF-1 rise by 15.3 nanograms per milliliter, because the testosterone was aromatizing into estrogen and that estrogen was driving liver conversion. The AI group saw an increase of 0.3 nanograms per milliliter, which is effectively zero. Same study population, same timeframe, and that single variable, whether estrogen was preserved or suppressed, explained almost the entire difference in outcome.

So now the clinic has a patient whose IGF-1 is low, and they offer IGF-1.

That is the loop. The AI created the deficiency, and the IGF-1 product is the fix the clinic sells for it.

What makes this particularly worth understanding is the regulatory context around IGF-1 itself. The FDA-approved version of IGF-1 is called mecasermin, and it was approved specifically for children with something called growth hormone insensitivity, a rare genetic condition where the body cannot respond to growth hormone and therefore cannot produce IGF-1 on its own. This condition, sometimes called Laron syndrome, affects somewhere between 350 and 500 people worldwide. The drug exists for an orphan disease of extreme rarity, not as a supplement for someone on TRT whose estrogen was pharmacologically suppressed.

The AI use itself is not supported by the major clinical bodies that govern this area. A 2020 survey by Butaney and colleagues of 489 physicians found that 69.4 percent prescribed AIs for symptomatic elevated estrogen in their TRT patients, despite the fact that neither the Endocrine Society nor the American Urological Association recommends routine AI use for estradiol management during testosterone therapy. More than two thirds of practicing physicians doing something the two leading professional organizations in the field do not endorse.

There is a common belief that elevated estrogen on testosterone is inherently a problem that needs to be corrected, and there is something partially correct about that. In cases of genuinely high estrogen causing symptoms like gynecomastia, some management may be warranted in specific clinical contexts. But the routine prophylactic use of AIs to keep estrogen suppressed, without reference to symptoms or clinical thresholds, is a different thing entirely, and it is the version that sets up the IGF-1 deficiency the video describes.

If you are currently on testosterone and an AI, the practical step is to get your IGF-1 levels checked. If those levels are low and your clinic is now suggesting IGF-1 supplementation, you have a clear picture of what happened. The AI suppressed the pathway that was naturally producing it.

The deeper point here is about how iatrogenic problems, meaning problems that are caused by medical treatment itself, can get repackaged as new diagnoses requiring new treatments. The patient experiences a real deficiency. The deficiency is real. The lab number is real. And the product being offered to address it is being sold as if the deficiency arrived from nowhere, when in fact it was the predictable downstream consequence of the previous prescription.

Once you understand how estrogen fits into the IGF-1 production chain, the protocol stops looking like a series of independent clinical decisions and starts looking like what it is.

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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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