More GH Doesn't Mean More IGF-1 — Here's Why | Weekly Q&A

The most common question I get about growth hormone is some version of "I raised my dose and my IGF-1 barely moved, what's wrong?" And the answer almost never has anything to do with the growth hormone itself.

So I want you to understand the way that growth hormone works and how the conversion to IGF-1 occurs in your body, because it's kind of a paradox actually.

Growth hormone leaves your pituitary and travels through your blood, and while it's circulating, it's doing one set of jobs, then your liver picks it up and turns a portion of it into IGF-1, which is a completely different molecule that does a completely different set of jobs, so you end up with two hormones and two roles from one starting point.

So when HGH is present in your bloodstream, that's basically when it's doing all the work, helping your body burn fat, and that's the lipolysis side of the picture, and in my experience it tracks with how lean clients get on a given protocol, though I cannot point you to a study that cleanly isolates insulin as the on-off switch for that effect in humans on exogenous GH.

Then there's the liver side, and when you eat, especially carbohydrates, your insulin rises, and when that occurs, that's when it basically triggers your growth hormone to be converted into IGF-1 in the liver. I'll say plainly that the research hasn't given me a clean human trial pinning that conversion to insulin in the way I'm describing it, so treat this as the model I run protocols on rather than settled literature.

And that's when you're going to get all of that muscle growth, anabolic related effects that come with growth hormone through IGF-1.

The thing that ends the fat-burning window is the same thing that opens the muscle-building window, so you cannot have both at maximum at the same time, and the whole game becomes sequencing them correctly.

Which is why most practitioners put growth hormone before bed. You inject fasted, insulin is at its floor, and the GH circulates for hours while you sleep. And then when you wake up in the morning, you eat and that basically converts all that growth hormone into IGF-1 so that you can put it toward tissue repair, muscle building, recovery, et cetera. I have seen this sequencing work well enough that it's my default, but no study has shown that pre-bed timing produces more total fat loss than any other timing.

So the ideal protocol for me, two to four IU of growth hormone per day, taken at night before bed, fasted, paired with about 250 milligrams of testosterone per week, taken split into seven daily doses, and that's actually my exact protocol. I've been on some version of this for years and I'll stay on it. In fact, we're going to go back and see if we can pull up a photo of me from when I was in my 20s and compare it to the way I look right now.

People ask whether they should move GH to post-workout to catch the anabolic window. Yes, it would be appropriate to take your HGH after you lift and then consume a meal within 30 to 60 minutes because you introduce the HGH and then when you eat the carbs, they're going to trigger the release of insulin, which will eventually convert that HGH into IGF-1.

But you've now spent your GH on the conversion and given up the overnight circulating window, and you get the same anabolic endpoint from a cleaner route.

If you spent time watching the YouTube video that I dropped last week on IGF-1, you understand the way that it works and why I don't really recommend the use of IGF-1 LR-3 in any protocol. The LR-3 modification gives it a long half life, it floods the system, and it sits there long enough to start shutting down your own production.

And so if you want to use the anabolic benefits of IGF-1, rather than doing LR-3 or growth hormone around your workout, what you would do is you would keep your GH protocol before bed, do your testosterone, et cetera, then introduce IGF-1 DEZ pre-workout directly into the muscle that you look to train.

The IGF-1 DEZ has a very, very, very short half life, which means it's going to clear your system quickly, similar to the way that normal IGF-1 does. It hits the tissue you just trained, does its job, and clears before it can create meaningful negative feedback.

So if you're looking to do the post-workout HGH for more muscle growth, just go to the IGF-1 DEZ route and keep the GH before bed.

OK, so the next question is, is my baseline IGF-1 was 186, then I started taking 2.4 IU of growth hormone, my IGF-1 went up to 265, then I increased to 4 IU and I tested again and it was at 250.

So basically what he's saying is he increases growth hormone dose, but he didn't see any meaningful increase in IGF-1 levels.

You have to understand that the conversion of HGH to IGF-1 that occurs in your liver is reliant upon a few very important signals that require your effort.

And those signals are going to have more of a meaningful impact on the increase in IGF-1 than just simply increasing your HGH dose.

Calories come first here, and IGF-1 is an anabolic signal, so your body will not build tissue it cannot afford, and chronic underfeeding suppresses IGF-1 regardless of how much GH you inject, so if you're in a steep deficit, that number is going to stay where it is.

Estrogen matters just as much, and if you're on gear, that's going to be somewhere between 40 and 60, so crash your estrogen with an aromatase inhibitor while running GH or a secretagogue and you are wasting your time and your money, because estrogen participates in hepatic IGF-1 output and you've removed one of the inputs.

Training is the third piece, but if you're not going to the gym and training with the level of intensity that's forcing your body into a position where it feels like it needs to adapt, like meaning, holy shit, I'm not strong enough to do what I'm being asked to do, then you're not going to signal the adaptation that's necessary for your body to say, hey, we need to turn up the volume on the IGF-1 so we can recover and repair from this damage and build more muscle.

Your body does not make a hormone it does not need. Going from 2.4 to 4 IU while all three of those inputs stay flat gives the liver more raw material and no reason to use it.

There's a second sequencing problem that sits underneath all of this, and it's about which cellular signal you're running at any given moment.

OK, so when I'm doing high intensity cardio aerobic type activity, this is when AMPK turns on and what's occurring is that signal is basically calling for the glut 4 transport, which means we're pulling energy directly into the cell and using that on demand to produce ATP. OK, so what does that mean? Well, it's going to pull whatever substrate is available at the time, meaning if I have sugar in my blood, aka I ate carbohydrates and that sugar is readily available in my bloodstream, my cell is going to pull that sugar in and use it.

OK, there's another signal that's almost opposite of AMPK that we don't really spend as much time talking about, and that's called mTOR or mTORP1, which is the signal your cells produce that calls for muscle protein synthesis and getting stronger.

One shuts the other down, so when you finish a hard lifting session, walk out of the gym and jump on the assault bike for twenty minutes of intervals, you are switching off the exact signal you spent an hour creating.

Keep them separated by at least three hours, and after lifting, stick to zone two only. If you're running something like MOTC to push AMPK, do it fasted before a cardio session and keep weight training on the other side of the day.

A couple more things keep coming up, so I want to close with those.

There is a lot more of this inside the free community, and it is genuinely free, so if you want somewhere to ask the follow-up question the men's group is here: https://www.skool.com/jh-iron-forge-brotherhood/about