TRT Clinic Revenue Loop
Your liver makes IGF-1, but it cannot do that job without estrogen, and that single fact is the foundation of a protocol that gets sold to men on testosterone every day without them knowing what is actually happening.
Start with the basic chain. When you take exogenous testosterone, your body does not treat it as a fixed molecule. Some of it converts into estrogen through a process called aromatization, which is a normal enzymatic conversion that happens in fat tissue, the liver, and other sites. This is not a malfunction. Your body has always used testosterone as a precursor to estrogen, because estrogen is not just a female hormone. It regulates bone density, cardiovascular function, cognitive performance, and as we will get to in a moment, it is the key that turns on IGF-1 production in the liver. Both men and women need it, just in different amounts.
When a clinic sees your estrogen rise after starting TRT, a common response is to prescribe something called an aromatase inhibitor, or AI, which is a drug that blocks the aromatase enzyme so the conversion from testosterone to estrogen is suppressed. The idea is that elevated estrogen causes side effects, and while that is true at genuinely high levels, the threshold for when to intervene is heavily contested and neither the Endocrine Society nor the American Urological Association recommends routine AI use during TRT. A 2020 survey by Butaney and colleagues found that 69.4 percent of 489 surveyed physicians were prescribing AIs for symptomatic elevated estrogen anyway.
So you have a drug being prescribed by the majority of practitioners in the space, without endorsement from the major governing bodies, to suppress a hormone that your body actually needs for a downstream process your liver is running right now.
That downstream process is IGF-1 production. IGF-1, which stands for insulin-like growth factor 1, is a hormone your liver produces in response to growth hormone, and it is the molecule that actually carries out most of what we attribute to growth hormone. Muscle protein synthesis, tissue repair, cellular growth, those outcomes come from IGF-1 acting on your cells, not growth hormone acting directly. Growth hormone is the signal. IGF-1 is the execution.
The part that matters here is that the liver's conversion of growth hormone into IGF-1 is not just driven by growth hormone alone. Estrogen is required for that conversion pathway to function efficiently. When you block estrogen with an AI, you are not just lowering one number on a lab panel. You are removing the signal the liver needs to respond to growth hormone in the first place.
A 2017 randomized controlled trial by Dias and colleagues tested this directly in 37 men over the age of 65. One group received testosterone gel, which raises testosterone and allows normal aromatization into estrogen. The other 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, which is effectively no change. Same population, same study, the only meaningful variable was whether estrogen was allowed to rise or was suppressed, and the IGF-1 outcome was nearly fifty times larger in the group that kept their estrogen.
Now you can see the shape of what happens when a clinic runs this protocol in sequence.
They start you on testosterone. Your estrogen goes up, which is expected and partly beneficial. They prescribe an AI, which suppresses that estrogen. Your liver loses the co-signal it needs to convert growth hormone into IGF-1. Your IGF-1 drops. Then your clinic checks your labs, sees the low IGF-1, and offers you IGF-1.
That is the loop.
The FDA-approved form of IGF-1 is called mecasermin, sold under the name Increlex, and it is an orphan drug approved specifically for children with a rare genetic condition called growth hormone insensitivity, or Laron syndrome, which affects somewhere between 350 and 500 people worldwide. In that condition, the body cannot respond to growth hormone at all, so the liver never produces IGF-1, and exogenous IGF-1 is the only path to normal growth. That is what the approval exists for. It was not developed for a man whose clinic suppressed the estrogen his liver needed to do the job itself.
The question is not whether low IGF-1 is a real problem, it clearly is, and the Dias data shows exactly how much it can drop when estrogen is blocked. The question is what caused it, and whether the solution is to address the cause or to sell the patient a replacement for what was taken from them.
If you are on testosterone and an aromatase inhibitor and your clinic has suggested IGF-1, the most direct place to start is simply getting your IGF-1 levels tested now so you know where you actually stand, and then asking what would happen to those levels if the AI dose were reduced or removed. That conversation forces the mechanism into the room. Either your provider understands it and can explain why your estrogen needs to be suppressed below the threshold that supports IGF-1 production, or they cannot explain it, and that answer matters too.
Most people assume that if a clinic prescribes two things, those two things are solving two separate problems. The possibility they are not prepared for is that one of those things is creating the condition the other one treats, because that is not a mistake that announces itself. It just looks like comprehensive care.
References
- **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.
- **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.
- **FDA Label (NDA 021839):** Increlex (mecasermin) approved for growth failure in children with severe primary IGF-1 deficiency. Orphan drug. Pediatric only.
- **Orphanet:** Laron syndrome affects approximately 350-500 individuals worldwide. Prevalence: 1-9 per 1,000,000.
- **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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