TRT Clinic Revenue Loop

Your liver makes IGF-1, but it cannot do it alone. It needs growth hormone as the raw signal, and it needs estrogen as the co-factor that makes the conversion happen. Pull the estrogen out of that equation and the liver's ability to respond to growth hormone collapses, which means your IGF-1 collapses with it.

That is the mechanism at the center of a protocol pattern that has become common inside TRT clinics, and once you see how it works, you cannot unsee it.

Start with the full chain so you have a map.

Testosterone does not just act as testosterone in your body. A percentage of it converts into estrogen through a process called aromatization, which is the enzymatic conversion of androgens into estrogens inside fat tissue, the liver, and other sites. This is completely normal and expected. In men on testosterone therapy, that conversion is actually doing useful work, because estrogen in men is not a villain. It supports bone density, cardiovascular function, mood, and, as we will get to, IGF-1 production.

Now add a clinic to that picture. When a patient's estrogen rises after starting testosterone, some clinics prescribe something called an aromatase inhibitor, or AI, which is a drug that blocks the aromatase enzyme and suppresses estrogen production. The stated rationale is managing symptoms like water retention or breast tissue sensitivity, and there are narrow situations where that makes sense. But the practice is far more widespread than the evidence supports. A 2020 survey by Butaney and colleagues found that 69.4 percent of 489 surveyed physicians prescribed AIs for symptomatic elevated estrogen in men on testosterone therapy, despite the fact that neither the Endocrine Society nor the American Urological Association recommends routine AI use in their TRT guidelines. Most of those prescriptions are going to men who do not have a clinical reason to need one.

That is the setup. Here is where it gets costly.

When you suppress estrogen with an AI, you do not just lower one hormone. You disrupt the signaling environment the liver depends on to produce IGF-1, which stands for insulin-like growth factor 1 and is the primary mediator of the effects of growth hormone in the body. Growth hormone travels from the pituitary to the liver, and the liver converts it into IGF-1, which then drives tissue repair, lean mass, and recovery. Estrogen is what sensitizes the liver to that growth hormone signal. Without enough estrogen, the liver does not respond as strongly, and IGF-1 output drops.

This is not theoretical. A 2017 randomized controlled trial by Dias and colleagues tested exactly this in 37 men over the age of 65. One group received transdermal testosterone. Another group received an aromatase inhibitor. The testosterone group saw their IGF-1 increase by 15.3 nanograms per milliliter. The AI group saw an increase of 0.3 nanograms per milliliter. Same study population, same design, the only difference was whether estrogen was being preserved or suppressed. The gap between 15.3 and 0.3 is the size of what estrogen contributes to that conversion pathway.

So now the patient is on testosterone, their estrogen has been suppressed, and their IGF-1 has dropped. Their clinic runs bloodwork and flags the low IGF-1. Then the clinic offers IGF-1 as a separate add-on to the protocol.

The FDA-approved version of IGF-1 therapy is called mecasermin, sold under the brand name Increlex, and it was approved specifically for children with severe primary IGF-1 deficiency caused by a genetic condition called growth hormone insensitivity, sometimes called Laron syndrome. That condition affects somewhere between 350 and 500 people worldwide. The drug was designed as an orphan treatment for a rare pediatric disorder, not as a recovery tool for adults whose IGF-1 dropped because their estrogen was suppressed by a drug they probably did not need.

The pattern looks like this from inside the clinic: they prescribe something that creates a downstream deficiency, and then they sell the correction for that deficiency. The AI is the gas pedal on the problem. The IGF-1 product is the sale. The patient pays twice, once to create the problem and once to treat it, and they do not know the second payment was triggered by the first.

This is not necessarily deliberate in every case. A significant portion of physicians prescribing AIs may simply not have traced the downstream effect on IGF-1 production. Hormone protocols involve multiple interacting systems, and if your training or clinical habit is to treat each lab value as an isolated number rather than a node in a connected pathway, you will miss this. But the survey data showing nearly 70 percent AI prescribing against a background of zero guideline support suggests the practice is not being driven by evidence.

If you are currently on testosterone and an AI, the relevant question is whether your IGF-1 has been measured, and if it came back low, whether the clinic traced it to the aromatase inhibitor before offering you something to replace it.

The broader point here is about what it costs to not understand the system you are in. Every hormone protocol creates downstream effects. Some of those effects are the intended therapeutic outcome. Some of them are collateral, meaning they are not the goal but they happen anyway because the body is a connected system. And some of those collateral effects can be monetized by a clinic that is either not tracking the mechanism or is tracking it and not telling you.

Estrogen in men is not something to be aggressively eliminated. It is doing real metabolic work. The idea that lower estrogen is always better for a man on TRT is the belief that makes this whole pattern possible, and that belief has no guideline support behind it.

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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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