The Real Reason I Got Banned From YouTube: Weekly Q&A 11

Q&A number 10? 11? Fuck, I don't know. What I do know is that this one got recorded after my channel went dark, so the first part of it is about why that happened, and the rest is the usual stuff about hormones, GLP-1s, and injection timing.

Eli Lilly is pursuing several lawsuits against compounding pharmacies and peptide distributors over retatrutide, which is a synthetic peptide that hits three receptors at once, GLP-1, GIP, and glucagon. They put millions into clinical trials and it is just now reaching the point of FDA approval, so the molecule should hit the regular market sometime next year.

What they sued for matters more than the fact that they sued, since they skipped patent infringement entirely and instead filed for selling illegal unapproved or compounded knockoffs, and the punishment for doing this is far less than the punishment for actually selling a patented product, which tells you the goal was speed, not damages.

Along with the six people named in the suits, they passed over hundreds of names of people teaching how to use, prescribe, sell, or distribute these drugs. And then we're going to take this list of 200 names, which we're not going to make public, and we're going to give it to the court.

I was banned from YouTube inside the same window that JD, Trevor, and several other health, fitness, and peptide creators all got nuked. I cannot point you to a study or a document proving those two events are connected, so treat that as my read on the timing and nothing more.

That's where I draw the line, right? There should not be a relationship behind closed doors that exists between these big corporations, big pharma, big tech, and the Justice Department or the executive branch of the government. Either way, when this is happening, to meet the best interest of these people, that's where, in my opinion, the problem lies.

These are the things that you need to consider, right? Like how it works, the science, the development, the nerd shit, that's OK. But once you cross the line of reconstitution, dosing, anecdotal experiences, what you could expect, titration, stacks, protocols, anything in between? Now you're implying human use and you're promoting an illegal or a, we'll say, regulated drug.

So if you want to follow me on Rumble, you can, but the reality is in order for my business to continue growing at the rate that it's been growing, I have to rely on YouTube, and in order for me to keep using YouTube, I have to learn to play by YouTube's rules, which means that I need to make sure that I'm putting the community guidelines at the forefront of the process of us creating content for the future.

Am I upset? Yeah, but I'm also grateful because YouTube has been a tool that I've been able to employ for the last year to grow our audience, and it helped me scale my business from, you know, half a million a year to 15 million a year.

Here are the actual questions.

Someone wrote in overweight with low testosterone asking whether to start TRT. Before answering that, you need the whole loop in front of you, because the answer lives inside the loop.

Your hypothalamus releases GnRH, which tells the pituitary to put out luteinizing hormone and follicle-stimulating hormone. LH travels down and tells the testes to make testosterone, FSH tells them to make sperm, and then some of that testosterone gets converted into estradiol, which travels back up and tells the hypothalamus to ease off, and that last loop back up is what functions as the thermostat for the whole system.

You have a high aromatization problem, which is creating your low T. Okay? So, if we have a lot of body fat, what that means is most of the testosterone that I'm producing is getting converted into estradiol by the excess aromatase in our body fat, which creates an excess of feedback to the hypothalamus telling it to stop producing more testosterone.

The enzyme that does the converting, aromatase, lives in fat tissue. More fat means more aromatase, more aromatase means more of your testosterone becomes estradiol, and more estradiol means a louder shut-down signal going back to the brain. Being fat and having low T is actually kind of an indication that your HPG axis works the way it's supposed to be working.

The more body fat you lose, the less aromatase conversion that, you know, the less E2 conversion you have, which means that frees up a lot of that testosterone to bind to the androgen receptors and then you start feeling good.

Now, I've said in the past, I say, hey, look, like, if you want to go on to TRT, you have low testosterone, your numbers are within range, and you're obese, you know, we'll say above 25-30% body fat, you absolutely can. But you are very likely going to need an aromatase inhibitor alongside it, because you are pouring more testosterone into a system that is already converting too much of it, and testosterone replacement is typically a lifetime decision.

The other path is enclomiphene to block that estrogen feedback at the brain so your own production climbs, paired with a GLP-1 for the actual fat loss. Enclomiphene has no washout period, you can come off whenever you want, and the side effect profile is low.

The trade is hidden in the numbers, though, because enclomiphene is known for increasing your SHBG, so you can go from a testosterone level of 400 with normal SHBG to a testosterone level of 900 three months later with triple the SHBG, and your free testosterone is basically the same number it was. People who tell you that enclomiphene is just as good as tests are fucking liars.

So the question is, okay, well, what is the threshold? I don't think there's like a magic threshold of like, once you're below this percent body fat, then you can go on to TRT. I think that you should be looking at your labs from an objective standpoint, right? Typically when you look at somebody who's excessively overweight, they're going to have normal LH, they're going to have low testosterone, but their E2 will be slightly elevated is typically what's going to happen with somebody like that.

That normal LH reading is the tell, because it means your pituitary is still firing and the signal is getting through fine, so the problem is downstream in the conversion, which is a problem weight loss fixes and exogenous testosterone does not.

But to answer your question, if I was to give a range, I would say around 20% would be a good place to start. And then you can go forth and add like the Ironforge baseline stack, which is partially available on Anvil now, the multivitamin, zinc, D3K2, magnesium.

Question number two, can type 1 diabetics use peptides like growth hormone, tessamerelin, or retitrutide? So understand that when you're a type 1 diabetic, it's a lot different than somebody who's type 2 diabetic.

Type 2 diabetes is typically something that's driven by insulin resistance. Where type 1 diabetes is significantly different because your body just doesn't produce the insulin, which is why we have to supplement with insulin itself.

So rather than talking about the growth hormone stuff because I don't really think that's a major concern for people who have diabetes, just because the only time insulin resistance becomes a problem for people using growth hormone is when they're using an excess of it. But the real question is, can you use it with the GLP-1 type drugs? There's good news here.

It's called the ADJUST-T1D trial, and it was published in NEGM, where they took 72 type 1 adults with a BMI over 30 and gave half of them semiglutide for 1 mg weekly alongside their insulin pumps.

And after 26 weeks, 36% of the semiglutide group hit the composite target of good glucose control plus meaningful weight loss compared to 0% on placebo. There were zero cases of diabetic ketoacidosis and the rate of severe hypoglycemia was identical between the two arms.

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: Son JW, le Roux CW, Blüher M et al. Novel GLP-1-based Medications for Type 2 Diabetes and Obesity, published in Endocrine Reviews, 2026. Roskoski R Jr., The role of GLP-1 and GIP receptor agonists in the treatment of diabetes and obesity, published in Pharmacological Research, 2026.

References

Son JW, le Roux CW, Blüher M et al.. Novel GLP-1-based Medications for Type 2 Diabetes and Obesity. Endocr Rev. 2026. https://pubmed.ncbi.nlm.nih.gov/41054801/

Roskoski R Jr. The role of GLP-1 and GIP receptor agonists in the treatment of diabetes and obesity. Pharmacol Res. 2026. https://pubmed.ncbi.nlm.nih.gov/42556625/