Does HGH Permanently Kill Your Natural Growth Hormone? | Q&A

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Growth hormone shuts down your natural production while you are using it. That part of the concern is correct, and anyone telling you otherwise does not understand the loop.

What most people get wrong is what happens after.

Before we get into suppression, you need the whole pathway in front of you, because the suppression question only makes sense once you see where the signal starts and where it ends up.

Your hypothalamus sends out growth hormone releasing hormone about every four hours on a clock telling you to produce more growth hormone. That hormone hits the pituitary, the pituitary fires off a pulse of growth hormone, and how big that pulse is depends heavily on your hunger level at the time.

The growth hormone then travels to your liver, where it gets converted into IGF-1, and that IGF-1 is what does most of the work you actually want from growth hormone.

There's another hormone called somatostatin that's produced, which basically provides that negative feedback in the system telling your brain to produce more growth hormone, and this is what closes the loop. Rising IGF-1 drives somatostatin release from the hypothalamus, and somatostatin puts the brakes on the next growth hormone pulse (Bermann 1994).

None of this happens on a random schedule, since the pulse pattern itself carries information, and cells respond differently to the same total amount of hormone depending on how it arrives (Goldbeter 2000).

But it's important to keep in mind that IGF-1, growth hormone, they have a relatively low half-life, meaning they're spending not very much time in your blood.

Injected growth hormone clears out of circulation in a matter of hours, not days (Bidlingmaier 2010). The brake gets applied, and then the brake comes off.

But the studies actually show that your pituitary typically kicks back on within 18 hours after introducing the exogenous GH. And if we do it for the long term, you're not creating enough suppression on the pituitary where it's going to create any permanent damage. I cannot point you to a study that tracked recovery timelines in healthy adults on therapeutic doses, so treat both of those as what I see with clients rather than something the literature has settled, and the research hasn't given us a clean controlled answer on what happens to natural production years after children stop long-term therapy either.

The gland keeps working because its design does not depend on one input alone. Pulsatile growth hormone secretion continues even in people with a genetic resistance to growth hormone releasing hormone (Maheshwari 2002).

Sleep is another one of those inputs, and there is a dedicated circuit that couples deep sleep to growth hormone release (Ding 2025).

What separates one dosing approach from another shows up in practice, not in theory. Split-dosing, meaning twice a day, is something I have only seen people do once they push past a certain daily amount, and I have never seen long-term suppression become a problem at two to four IU for men or one to two IU for women, though there is no study I can hand you that tested that comparison directly.

So as far as I'm concerned, as long as you can mitigate the side effects, which is just really as simple as finding the right dose for you, there's no downside to using GH. Now this is a question that I've been getting a lot recently, and I actually had to do quite a bit of studying.

People kept asking me whether clomiphene lowers IGF-1, and the answer is yes, and it holds across the whole class of these drugs.

And clomophene is a CIRM. CIRM stands for Selective Estrogen Receptor Modulator, which means it sits on the estrogen receptors and changes what the tissue does with the estrogen signal.

In the brain, it blocks the estrogen signal, your brain reads that as low estrogen, and it responds by pushing out more LH and FSH. That's basically the function of these CIRMs. And that's the half that you guys already know, and I've taught you guys frequently in the past.

The half nobody talks about is the liver.

Estrogen receptors sit in more places than people assume, and liver tissue is one of them. Estrogen signaling at the liver is part of what sets how much IGF-1 the liver releases when growth hormone arrives.

So if you guys remember last week, the mechanism that I talked about, which is where you're basically tricking your brain into thinking that you have low E2 by occupying those receptors.

That trick does not stay in your brain. The drug travels everywhere, and it occupies receptors everywhere.

And in order for your liver to convert HGH into IGF-1, which I've taught you in the past, your body has to have estrogen present in your blood.

Well, if we're using in clomophene, Novadex, whatever, to trick your body into thinking it doesn't have estrogen, then at the liver, this is basically telling your body that you don't have enough estrogen to convert your HGH into IGF-1.

It is the same choke point you hit when you crush estradiol with an aromatase inhibitor. Different drug, different mechanism at the receptor, identical outcome at the liver.

Which means if you are running CJC, tesamorelin, ipamorelin, sermorelin, any secretagogue, you are still getting the pulse. The signal arrives at the liver and the liver just does not respond to it the way it should.

You get the LH and FSH recovery you wanted from the SERM. But when it comes to all the muscle building benefits that come with the IGF-1 conversion, that's basically where you're gonna be missing out if you are on a CERN. So this is actually really important information that I think you guys need to know and apply.

Your whole stacking logic has to shift once you see this, because running a growth hormone protocol on top of a SERM means you are paying for one of them and getting a fraction of it.

Retatrutide produces a similar confusion, where people assume the drug itself is doing something hormonal. There is no evidence Retatrutide lowers testosterone, and if you are overweight with insulin resistance, losing that fat mass is probably going to help your testosterone long term.

What lowers testosterone is starvation, and these drugs make starvation easy to do by accident.

We've talked about this ad nauseum, right? Like if you have shitty habits, you have shitty lifestyle, there's no peptide that's gonna come in and save the day for you and solve that problem except maybe Rettitrutide, right? Rettit is gonna do a phenomenal job of helping your body get back into a metabolically functional state.

But when you starve yourself, your body starts to shut down. Women lose their cycles, men get impotence, hair falls out.

So you floor the fat and protein and let carbs move. Half a gram per pound of goal body weight in healthy fat, because that is what keeps hormone production running, and one gram per pound of goal body weight in protein at minimum, because that is what keeps your muscle on you.

Carbohydrates are the one variable you adjust by feel. More carbs means better training performance, fewer carbs means more hunger but faster fat loss.

People forget about water more than anything else on the list. The GLP-1 agonist in all these drugs is going to make it even more necessary for your body to get enough water because everything is already being slowed down as it is.

Gastric emptying slows, transit time through your gut stretches out, and food sits there longer than it used to. Then if you take the water out, you're making it that much more difficult for your body to process all this food that's already being held up inside of your digestive tract.

That is where the constipation comes from, and it is entirely avoidable.

So protein, fat, water, use the carbs sparingly to impact performance, and that's the best way to make sure that you're getting all the benefits from the RETTA without experiencing the, we'll say, hormonal shutdown.

Every one of these questions has the same shape underneath it. Somebody takes a number, or a drug, or a lab value, and treats it as the thing itself instead of one input into a loop with several other inputs.

The pituitary is not a switch you break. It is a gland responding to sleep, hunger, IGF-1 feedback, and a clock that keeps ticking whether you inject or not.

Converting a hormone into something usable is not a mechanical step the liver performs on autopilot either. It needs an estrogen signal to do the job, so blocking that signal upstream costs you downstream even when the upstream block was exactly what you wanted.

Understand which loop you are in, and the dose almost picks itself.

Research: Bermann 1994; Goldbeter 2000; Bidlingmaier 2010; Maheshwari 2002; Ding 2025

References:

. Pasireotide. . 2012. https://pubmed.ncbi.nlm.nih.gov/31644171/

Bidlingmaier M, Strasburger CJ. Growth hormone. Handb Exp Pharmacol. 2010. https://pubmed.ncbi.nlm.nih.gov/20020365/

Goldbeter A, Dupont G, Halloy J. The frequency encoding of pulsatility. Novartis Found Symp. 2000. https://pubmed.ncbi.nlm.nih.gov/10752063/

Maheshwari HG, Pezzoli SS, Rahim A et al.. Pulsatile growth hormone secretion persists in genetic growth hormone-releasing hormone resistance. Am J Physiol Endocrinol Metab. 2002. https://pubmed.ncbi.nlm.nih.gov/11882517/

Ding X, Hwang FJ, Silverman D et al.. Neuroendocrine circuit for sleep-dependent growth hormone release. Cell. 2025. https://pubmed.ncbi.nlm.nih.gov/40562026/

Bermann M, Jaffe CA, Tsai W et al.. Negative feedback regulation of pulsatile growth hormone secretion by insulin-like growth factor I. Involvement of hypothalamic somatostatin. J Clin Invest. 1994. https://pubmed.ncbi.nlm.nih.gov/7913710/