TRT Clinic Revenue Loop

Your liver is constantly converting growth hormone into something called IGF-1, which is insulin-like growth factor 1, and it is the downstream signal that actually tells your tissues to grow, recover, and repair. That conversion process does not happen automatically. It requires estrogen to work properly. Estrogen is not just a female sex hormone sitting passively in a man's body. It is an active co-factor in one of the most important anabolic pathways you have.

That is the system. And once you understand it, a very specific clinical pattern becomes visible.

When a man takes testosterone, some of that testosterone converts into estrogen through a process called aromatization, and that is completely normal and expected. The enzyme responsible is called aromatase, and it exists in fat tissue, the brain, the testes, and the liver. Aromatization is not a side effect of testosterone. It is part of how testosterone works in the male body, because some of what testosterone does, it does after converting to estrogen first.

So testosterone goes up, estrogen goes up with it, and estrogen then helps the liver convert growth hormone into IGF-1. The whole chain rises together.

A 2017 randomized controlled trial by Dias and colleagues tested this directly in 37 men over the age of 65. The group given transdermal testosterone saw their IGF-1 rise by 15.3 nanograms per milliliter. That rise was not from the testosterone itself acting on the liver. It was from the testosterone aromatizing into estrogen, and that estrogen driving the liver's conversion of growth hormone into IGF-1. The hormone you think is the end product is actually a starting point for something further downstream.

Now here is where the clinical problem enters.

When a TRT patient's estrogen rises, many clinics prescribe something called an aromatase inhibitor, or AI, which is a drug that blocks the aromatase enzyme and prevents testosterone from converting into estrogen. The theory is that high estrogen causes symptoms like water retention, mood changes, or sensitivity in breast tissue, and reducing estrogen will relieve those symptoms. That reasoning has some basis in reality for some patients at very high estrogen levels. But the approach has become routine in a way that the major medical bodies do not support.

A 2020 survey by Butaney and colleagues of 489 physicians found that 69.4 percent of them prescribed AIs for symptomatic elevated estrogen in their TRT patients. Neither the Endocrine Society nor the American Urological Association, in their 2018 guidelines, recommends routine AI use for estradiol management during testosterone replacement therapy. The practice is widespread and it is not guideline-supported.

And here is what that practice does to IGF-1.

In the same Dias study, the group given an aromatase inhibitor instead of testosterone saw their IGF-1 rise by only 0.3 nanograms per milliliter. Not 15.3. Point three. That is essentially no change at all, from the same study, using the same measurement, in the same population. The only difference was whether estrogen was present to drive the conversion. When you remove estrogen from the system, the pathway from growth hormone to IGF-1 collapses.

So when a clinic puts a patient on testosterone and then adds an AI to manage the estrogen that naturally follows, they are giving with one hand and taking with the other. The patient gets testosterone but loses the estrogen-dependent IGF-1 production that testosterone would have supported. The net anabolic effect is substantially smaller than it should be.

And then some clinics offer to sell that patient IGF-1 directly.

The FDA-approved form of IGF-1 is a drug called mecasermin, sold under the brand name Increlex. It is approved specifically for children with a genetic condition called severe primary IGF-1 deficiency, sometimes called Laron syndrome, where the body cannot respond to growth hormone at all due to a receptor defect. Laron syndrome affects roughly 350 to 500 people worldwide. The drug exists for a tiny population with a specific genetic inability to produce IGF-1 through normal pathways.

A man on TRT whose estrogen was suppressed by an AI does not have Laron syndrome. He has an iatrogenic deficiency, meaning a deficiency caused by a medical intervention. The pathway still works. The receptor still works. The growth hormone is still there. The only thing missing is the estrogen that the AI removed, which was present before the AI was prescribed.

The clinic created the gap in the pipeline and is selling a workaround for the gap they created.

There are two ways to read that pattern. The first is that the physicians involved do not understand that estrogen is required for hepatic IGF-1 conversion, and so they are prescribing an AI for perceived symptom management without realizing what it costs downstream. Given that the mechanism is well-documented and the Dias data are not obscure, that reading is not flattering. The second is that they understand the mechanism and the economics both, and the protocol reflects that.

Either reading has the same practical implication for the patient.

If you are on testosterone and an aromatase inhibitor, get your IGF-1 levels measured. If your clinic has mentioned IGF-1 as an add-on, the sequence of events matters. The question is not whether IGF-1 is low. The question is why it is low and whether the thing that lowered it was something your clinic prescribed.

The body already knows how to make IGF-1. It needs estrogen to do it. Estrogen is not the problem testosterone creates. In many cases, it is part of the solution testosterone was already providing.

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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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