I think thrifty gene should probably be replaced by thrifty genetics. There was a study in mice looking at aggression, breeding aggressive mice to aggressive mice and then looking for "aggression" genes. They were hoping for a few major differences, what they got were hundreds of tiny variations.
The insulin resistance leading to obesity thing is sort of contested, alternately maybe once adipose is reaching a certain capacity, there's spillover into the liver and visceral fat depots, and this, increases insulin resistance. I think it's likely a mix, increased insulin is a vote for greater obesity, but the insulin is pushing against a lot of resistance.
In rodent models fructose is more of a model of insulin resistance, but there have been a few studies where feeding animals a high fructose diet for a while, which does make them insulin resistant, and then switching them to a "high fat" but importantly non-atkins diet makes them fat, in this case the previous insulin resistance might set them up to get fatter, though the researchers point to leptin (which doesn't exactly put insulin in the clear, anyways). But these animals didn't develop insulin resistance while getting fat, but before getting fat. Insulin drives fat storage, but trees don't grow to the sky, fat tissue past a certain size is resistant. Sometimes insulin being higher after somebody is fat instead of before is used as evidence that insulin is not fattening. Doesn't work that way, insulin is most fattening when our adipose is most sensitive to it.
So--if you manage to become insulin/leptin resistant without actually getting fat, maybe since your fat cells aren't overloaded, there's some other diet out there that you shouldn't be looking for that would allow you to add obesity to your other problems. If you get fat and insulin resistant at the same time, this is less likely, your fat tissue is nearer its maximal capacity.
https://www.ncbi.nlm.nih.gov/pubmed/18703413
Quote:
Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding.
Shapiro A1, Mu W, Roncal C, Cheng KY, Johnson RJ, Scarpace PJ.
Author information
Abstract
It has been suggested that increased fructose intake is associated with obesity. We hypothesized that chronic fructose consumption causes leptin resistance, which subsequently may promote the development of obesity in response to a high-fat diet. Sprague-Dawley rats were fed a fructose-free control or 60% fructose diet for 6 mo and then tested for leptin resistance. Half of the rats in each group were then switched to high-fat diet for 2 wk, while the other half continued on their respective diets. Chronic fructose consumption caused leptin resistance, while serum leptin levels, weight, and adiposity were the same as in control rats that were leptin responsive. Intraperitoneal leptin injections reduced 24-h food intake in the fructose-free group (73.7 +/- 6.3 vs. 58.1 +/- 8 kcal, P = 0.02) but had no effect in fructose-fed rats (71.2 +/- 6.6 vs. 72.4 +/- 6.4 kcal, P = 0.9). Absence of anorexic response to intraperitoneal leptin injection was associated with 25.7% decrease in hypothalamic signal transducer and activator of transcription 3 phosphorylation in the high-fructose-fed rats compared with controls (P = 0.015). Subsequent exposure of the fructose-mediated, leptin-resistant rats to a high-fat diet led to exacerbated weight gain (50.2 +/- 2 g) compared with correspondingly fed leptin-responsive animals that were pretreated with the fructose-free diet (30.4 +/- 5.8 g, P = 0.012). Our data indicate that chronic fructose consumption induces leptin resistance prior to body weight, adiposity, serum leptin, insulin, or glucose increases, and this fructose-induced leptin resistance accelerates high-fat induced obesity.
Comment in
Fructose-induced leptin resistance: discovery of an unsuspected form of the phenomenon and its significance. Focus on "Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding," by Shapiro et al. [Am J Physiol Regul Integr Comp Physiol. 2008]
PMID: 18703413 PMCID: PMC2584858 DOI: 10.1152/ajpregu.00195.2008
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https://www.ncbi.nlm.nih.gov/pubmed/18703413
I think Seth Robert's Shangri-la diet deserves a mention as well. The basic idea is that exposure to food increases our body fat set point. Taking in flavourless calories, like sugar water or flavourless oils, or eating wearing noseplugs, or eating unfamiliar foods is supposed to lower the set point. This is not quite "palatability." It's more like the body have certain conditioned responses to food, more pleasant/stronger flavours send a stronger signal.
I'm not supporting this idea in its entirety, but the idea that my body acts as if it has an entirely different set point depending on my diet, Pizza and cheerios>Atkins>stricter ketogenic has panned out pretty well for me. But of course you notice these line up from most to least insulin.
Shangri-la dieters talk about appetite suppression, and of course if it really does work for them, a suppressed appetite equals a decrease in insulin. Sometimes Taubes and others argue that a low calorie diet is a low carbohydrate diet, so maybe that's why it works for those it does work for, but you don't really have to mention carbs there, even if you just dropped calories by dropping fat, that would drop insulin. The question is whether or not your body is going to throw a hissy fit when you do that.