Are insulin resistant people less likely to gain weight?

(Bob M) #1

Hat tip to Mark’s Daily Apple for this.

Here’s a blog post by Peter D. He appears to be arguing that insulin resistant people are less likely to gain weight:

The Pima Indian study is here and you can download it:

They use a “Hyperinsulinemic-euglycemic clamp technique” to measure insulin resistance. This is described here:

They really do get these curves (these are the modified ones from Peter’s blog), where the most insulin resistant gain the least weight and the most insulin sensitive gain the most weight.


Much like MIMO (mass in, mass out), I can’t wrap my head around this and don’t know what to do with it.

(KM) #2

That is peculiar. I’m hoping people with more biochem weigh in here! One study I would have an easy explanation for, the formerly obese women being more insulin sensitive than the control. They’re possibly looking at ketovores or carnivores v. TOFI’s. I.e. the diet that reduced the obese women’s weight is also the diet giving them more insulin sensitivity.

(Bacon is a many-splendoured thing) #3

I would have thought, insulin being the major signal to store fat, that insulin-resistant people would be more likely to be obese. But then, I suppose it depends on which organs are involved. The liver and pancreas accumulate fat when insulin-resistant, and I suppose other organs must, as well.

Given the existence of TOFI’s and MHO’s, I guess insulin-resistance isn’t the only factor causing obesity, and given that there are actually a few million more TOFI’s than metabolically ill obese people, that obesity isn’t a necessary result of insulin-resistance.

Huh! I never thought about it in precisely these terms before.


That’s interesting. Back on my HCLF WOE I always pondered why I didn’t gain weight. That I could eat buns, sandwiches and pizzas and not put on an ounce. My carbohydrate intake must’ve been up in the 600-800s worth of grams. I had systemic inflammation, but I believe it was due to both gluten sensitivity and overexposure to antibiotics. I also ate a lot of fruits, nuts and dried fruits, and vegetables, to balance out my weekend treats, everything in moderation was how I lived back then. I was slim, I thought at the time my metabolism was high. I am still lean now, on keto, but since embarking on a ketogenic WOE I haven’t been experiencing my blood sugar crashing and feeling hangry, and dizzy and lightheaded. Perhaps I was, and am insulin resistant. I wouldn’t have a clue. I’ve certainly never thought of myself as TOFI, and my blood count test result from 12 Oct. 2022 showed everything to be within normal range. I don’t see carbs as not essential, and plants as toxic. I’ve discovered by reinstating a few carbs while still keeping it below 20 grams has been beneficial, in several ways. The skin on my hands on carnivore got to be so dry I didn’t know what to do. I kept moisturising them like crazy. And I was looking more tired. Feeling more my age. When I reinstated vegetables, nuts, some fruit and berries, my hands (without the aid of moisturiser) turned smooth again, I began looking more youthful again (I’ve always looked young for my years) and I have more energy, I cannot ignore such signs, no matter how much the statement carbs are not essential is repeated.


I’ve seen that argument made before, makes sense in different contexts. I’ve never signed on to the insulin being the enemy thing, it’s clearly part of the equation, but I’ve never though it was causal either. Way too many super fit high performing athletes slamming carbs all day long and they’re not fat and very much Insulin senstive.

Then look at T1D’s that usually can’t put on weight if they tried. Then even in myself, since going to TKD/CKD, although I’m not eating a lot of carbs by “normal” standards, I am eating 10x what I was eating when I was doing standard keto, my bodyfat is lower than it’s been in years, including the 4yrs of strict keto, my A1C is fine, my LP-IR is good, simply can’t make Inuslin a super villian.

Then look at all the fat loss with Semaglutide becoming insanely popular the last couple years, it makes you secrete MORE Insulin, and people are losing fat and lowering their A1C’s with it. Some of it’s the calorie restriction because it puts a dent in your appetite, but still can’t ignore the Insulin role with it.

(Michael) #6

“Why fat people cannot get fat enough, and why thin people are too fat”. If you are not insulin resistant, you can pack more energy into your cells, and thereby you can get fatter. If you are insulin resistant, your cells do not want to take in more energy (glucose or fat) and it is harder to add fat mass. Neither of these statements rely on the initial weight upon measurement, simply the amount of insulin resistance.

(Bacon is a many-splendoured thing) #7

In fact, they starve to death from lack of endogenous insulin, unless treated.

(Bob M) #9

I guess I don’t understand what “insulin resistant” or “insulin sensitive” is in this context. That test fixes a high level of insulin, then adjusts glucose until the glucose intake = glucose uptake (and they know this how? Because glucose stops moving?).

So, the insulin is telling anything that will listen to it to take up glucose. And then something (muscles? fat? both? organs?) is taking in the glucose.

I assume “insulin sensitive” in this context means that more glucose can be infused and “insulin resistant” means less glucose can be infused.

What is the pancreas doing in this time period? Nothing? What about the liver? Also nothing?

This seems to say that organs are involved, at least by using radioactively-labeled glucose:

But when I think of “insulin resistance”, I think of a person whose insulin-producing mechanism (mainly the pancreas) has to produce more insulin to get the same result, or perhaps has higher blood sugar due to cells not being responsive to insulin, or both.

I can’t decipher if what I think of as “insulin resistance” is the same as that determined by using a Hyperinsulinemic-euglycemic clamp technique. For instance, could you be “insulin sensitive” according to this clamp technique, but actually be “insulin resistant” according to my definition? For instance, they seem to be infusing a fixed amount of insulin; could the pancreas produce even more insulin, thereby causing more glucose to be taken in? Or do they account for that by adjusting the amount of insulin necessary to hold that 100 μU/ml of insulin?


Note: there are multiple refs/links in this pertaining specifically to insulin resistance.


It is possible I had insulin resistance in the past though I was thin, with no abdominal adiposity. As my body would react oddly to foods, I didn’t gain weight, but felt poorly all the time, and weak. I have been feeling so much better since embarking on a ketogenic WOE so there must have been some healing and possibly normalising going on, I’ve been paying attention to this thread as I find it interesting. The idea a ketogenic WOE could cure or prevent insulin resistance, and normalise one’s metabolic system, and therefore prevent associated diseases. I definitely have been experiencing health benefits on keto/ketowore, and am absolutely pro a well formulated ketogenic WOE.