What wasn't correct was saying that insulin use causes insulin resistance. While there may be some situations that I'm not familiar with, insulin like Lantus is actually used to help manage insulin resistance and prevent type 2 in bodybuilders. I imagine things used in excessive doses of course will have issues, but something like 15-20iu of Lantus from what I know isn't going to cause it. I don't have the sources off hand to cite, but Jewett has a pretty good lecture explaining that and how it doesn't actually lead to insulin resistance in his course on managing blood glucose
With the 90mins, I don't have a source to cite on it, it's just what I've been taught by some of the higher level guys, a few being Jewett, JP and Efferding.
Optimal in terms of my response is optimal for fat loss, which is what I think op was looking for. He isn't usually looking for the most healthy option. I do agree that what is optimal for bodybuilding goals isn't always what's optimal for health.
Who are this guys? This is not at all how insulin resistance (IR) works. Respectfully, you are either misinterpreting what they are saying, or they don't understand what they are talking about.
There is a difference between elevated fasted blood glucose levels, which can be fixed via exogenous insulin, and IR. Insulin resistance happens via chronic insulin (over)stimulation of the glucose transporter - Glut4 - which can lead to a decrease in it's expression and function, ie. it becomes resistant to insulin.
Chronically elevated fasted blood sugar levels when using GH, are due to gluconeogenesis, which is stimulated by GH in the liver. This leads to chronically elevated insulin secretion, which leads to IR.
The other mechanism in which GH can cause IR is actually via it's "fat burning" mechanism. Free fatty acids interfere with insulin signaling, either directly via activating PKC which then phosphorylates insulin receptor substrate-1, or indirectly via FFA metabolites (DAG and ceramide for instance) accumulation in the liver and muscles.
You are not solving IR via exogenous insulin, you are merely resolving it's outcome, ie. elevated blood glucose. You are however making insulin resistance worse, because more insulin = more glut4 desensitization. You wont notice this with fasted blood glucose monitoring, as that will now be "in range", but you will notice it via a poorer post prandial glucose management response, which will result in brain fog, or just brain fog in general, not just after a meal. There are many other really unwelcomed outcomes of IR, like dementia, even parkinsons ...
Nowadays, Alzheimer's disease (AD) is a severe sociological and clinical problem. Since it was first described, there has been a constant increase in its inc...
www.frontiersin.org
Background: Insulin resistance (IR), considered a hallmark of diabetes at the cellular level, is implicated in pre-diabetes, results in type 2 diabetes, and negatively affects mitochondrial function. Diabetes is increasingly associated with enhanced ...
www.ncbi.nlm.nih.gov
There is a lot more to it then "just" dementia and parkinsons. But I'm not getting in to all of that now as I'm brain dead from doxy. Writing this literary feels like a marathon. But the long story short is no, you are not helping IR much with exogenous insulin.
However, it is a bit more complicated then that as chronically high BG levels can lead to inflammation, which is also a big factor in IR. This happens through several mechanisms: activation of inflammatory signaling pathways, formation of advanced glycation end-products (AGEs), and off course, yours truly, oxidative stress, So this is how you're helping to mitigate some damage via insulin use.