I Was Wrong About IGF-1 and Growth Hormone | Weekly Q&A #13

Watch the full video on Rumble: https://rumble.com/v7g2ixg-i-was-wrong-about-igf-1-and-growth-hormone-weekly-q-and-a-13.html

And as you guys know, my reputation, if I give you the wrong info, and I learn something new, or that changes my opinion on something, I'll be the first guy to come back and tell you, right? So welcome to Q&A number 12.

["Spring Waves"] ["Spring Waves"] So one of the common questions, or things that we've been getting is, is it okay to use IGF-1, LR-3, or whatever, with growth hormone, or growth hormone-related peptide, like CJC, tessamerelin, stacked with ipamerelin? In the past, the position that I had was that when you have IGF-1, LR-3, and you're injecting it, what it's doing is it's creating desensitization on your cells so that IGF-1 becomes less and less effective over time, which is why most of the time, you're not gonna see people stay on the IGF-1 for longer than six weeks, okay? And so in my opinion, because of the feedback that we wanna keep in our growth hormone production system, it doesn't really make sense to use IGF-1 if we're on growth hormone, because if we want more IGF-1, all we have to do is just add more growth hormone.

To see why that was wrong, you need the whole chain in front of you first.

Your hypothalamus sends a signal called GHRH down to the pituitary. The pituitary releases a pulse of growth hormone. That growth hormone travels to the liver, and the liver converts it into IGF-1, which is the molecule that actually tells muscle tissue to grow. IGF-1 then climbs back up and tells the hypothalamus to release somatostatin, which is the brake pedal on the whole system, and somatostatin shuts down the next pituitary pulse.

I stayed cautious for so long because of that loop, since if IGF-1 pushes the brake, and you inject extra IGF-1, you are riding the brake harder.

Now, the question that I had, and this is me using my reference material, right, is when I'm taking HGH and I add IGF-1 LR-3, does that create suppression of growth hormone production? And is it reducing the effectiveness of the growth hormone that I inject, okay? Like I said, the argument that I had before was that when you add IGF-1 LR-3, it's creating suppression through somatostatin, which makes the entire cycle less effective, okay? And so after doing more research, the notes that I have is we have to understand that somatostatin suppresses growth hormone release from the pituitary gland, right? It's not going to affect the activity of growth hormone that's already in your bloodstream. I cannot point you to a study that tested that specific question head to head, so take this as how I read the mechanism rather than something the literature has settled.

Think of the brake as sitting on the factory, not on the trucks already on the road. Shutting the factory down does nothing to the shipment that already left.

So adding the additional IGF-1 LR-3 really isn't creating any more or less suppression that you would already create it on the axis, right? So yes, adding IGF-1 LR-3 into circulation could push somatostatin even higher, but you're not relying on your pituitary for the GH production anyway because you're adding the growth hormone. From what I have seen this holds up in practice, though no study has shown it directly.

So it's not costing you anything more or less functionally because at this point, we're already skipping the pituitary gland completely, right? Now this argument would hold if you were on secretagogues, right? So if I was on CJC, tessamerelin with ipamerelin, and I was using IGF-1 LR-3, in that case, it wouldn't make sense because adding the exogenous IGF-1 LR-3 is in turn gonna create more additional somatostatin production, which will inhibit the production of GH at the pituitary. I have seen that logic play out with clients, but the research hasn't tested the combination.

On secretagogues your pituitary is the engine, so anything that brakes the pituitary costs you output, and that difference between an engine still running on its own signal versus one that's already been bypassed is the whole correction.

Like a lot of guys will be in my comments, they say like, I do growth hormone with IGF-1 LR-3 and I get phenomenal benefits. That feedback is what made me go back and check the mechanism again.

And as long as we're getting enough calories and our estrogen levels are where they need to be, your liver's gonna produce basically as much IGF-1 as you give growth hormone to yourself, right? There's no receptor desensitization that occurs. I have seen that consistently in the clients I run bloodwork on, and I cannot point you to a study that establishes either of those two points, so treat them as observation.

Your liver's just basically gonna become an IGF-1 producing factory at that point, okay? The only downside that you're gonna eventually run into when you're doing higher and higher doses of growth hormone is insulin resistance, which is something that we've discussed. From what I have seen that dose relationship is real in the field, though there is no study mapping it cleanly.

If you want more muscle building, you wanna get better results, you can add the IGF-1 LR-3 on the back of your growth hormone.

There was a 1996 combination trial where they actually saw that the growth hormone plus IGF-1 control group outperformed just the GH group alone on lean mass. What the paper actually reports is that combining growth hormone with IGF-1 produced the largest lean body mass gain of any group at six weeks, and it was the only group where the gain was still held at twelve weeks (Waters et al., 1996, Annals of Internal Medicine). It's absolutely viable to add the IGF-1 if you're doing just growth hormone, do it for up to six weeks at a time, and six weeks is the window I program with because of what I have seen with tolerance in clients rather than anything the trial pinned down.

So I'm glad that you guys pushed back on that, okay? Question number two, what peptides actually help with gut healing? And how do peptides like BPC-157 and KPV work? Okay, so we've had a lot of discussions about gut health, and there's a lot of products and marketing out there that push you need to optimize your gut biome and your gut health, and these drugs do this, and this is a fix-all to everything.

So going back, if gut health and your gut biome are truly a concern, the first questions that you should be asking are, what does the quality of my sleep look like? What does my diet look like, including how much protein, fiber, processed foods am I putting into my body? Are there any pharmaceuticals or drugs or supplements that I'm adding that are potentially causing chaos in my gut? And then lastly, what are the levels of stress that I'm having? If you're not managing these things first, then going down and buying something like KPV to minimize your inflammation or BPC157, which is the peptide that's produced in your gut to help heal things, aren't going to do nearly as much work because now what you're trying to do is you're trying to solve a problem downstream that's being caused by something upstream.

It is opening the drain on a bathtub while the tap is still running.

Yes, adding something like BPC157 for tissue repair and adding something like KPV to help manage your inflammation can absolutely help to solve problems related to your gut health. The order is what decides whether they do anything.

Gina came to me after seeing six or seven different doctors for SIBO, and the treatments she was stacked on were working against each other. We stripped all of it out, put her on a low inflammatory diet built around enough animal protein and fiber, and worked on her stress. And when we did that, after just 12 weeks, we were able to get her inflammatory markers in place where they needed to be.

Most of what I know about this came out of conversations in the free community, so if you want the rest of it and somewhere to ask, the men's group is here: https://www.skool.com/jh-iron-forge-brotherhood/about

Research: Waters et al., 1996, Annals of Internal Medicine. Moller et al., 1990, American Journal of Physiology. Gormsen et al., 2007, Journal of Clinical Endocrinology and Metabolism. Bachman et al., 2014, Journals of Gerontology Series A. Ory et al., 2022, Journal of Urology. Bond et al., 2024, Endocrine Connections.

References:

Waters et al., Annals of Internal Medicine, 1996. PMID: 8967666. https://pubmed.ncbi.nlm.nih.gov/8967666/

Moller et al., American Journal of Physiology, 1990. PMID: 2405702. https://pubmed.ncbi.nlm.nih.gov/2405702/

Gormsen et al., Journal of Clinical Endocrinology and Metabolism, 2007. PMID: 17341555. https://pubmed.ncbi.nlm.nih.gov/17341555/

Bachman et al., Journals of Gerontology Series A, 2014. PMID: 24158761. https://pubmed.ncbi.nlm.nih.gov/24158761/

Ory et al., Journal of Urology, 2022. PMID: 35050717. https://pubmed.ncbi.nlm.nih.gov/35050717/

Bond et al., Endocrine Connections, 2024. PMID: 39212549. https://pubmed.ncbi.nlm.nih.gov/39212549/