Insulin resistance is driven by sugar, not fat. What are these guys talking about?
"saturated fat significantly worsen insulin-resistance, while monounsaturated and polyunsaturated fatty acids improve it through modifications in the composition of cell membranes which reflect at least in part dietary fat composition"[0]
"Fat in the bloodstream can build up inside the muscle cell and create toxic fatty breakdown products and free radicals that can block the insulin signaling process. When that happens, no matter how much insulin we have in our blood, it won’t be able to open the glucose gates." [1]
So it's interesting to me, then, that the crux of what Tim Ferris says is accurate in a different light- the fat seems to clog the insulin response from the cells (including fat cells) which would lead me to believe that's beneficial in some way to stop the addition of sugar to fat cells. IANADr tho.
[0] http://www.ncbi.nlm.nih.gov/pubmed/15297079
[1] http://www.forksoverknives.com/fat-insulin-resistance-blood-...
Edit: Just found this one too... very interesting
"In conclusion, the present study shows that a high-fat KD causes hepatic insulin resistance in mice, which can be attributed to an increase in hepatic DAG content, leading to PKCε activation and subsequent impaired insulin signaling. Moreover, this study found that a KD increases energy expenditure, which results in weight loss. Given the widespread use of KD in the treatment of obesity and the role of NAFLD and hepatic insulin resistance in promoting type 2 diabetes, these results may have important clinical implications, as obese patients on such diets could lose weight but develop NAFLD and hepatic insulin resistance."
IOW, the diet is an artificial construct not resembling any occurrence in nature. Artificially low protein in a KD sounds just dangerous, as adequate dietary protein will produce any needed blood glucose via gluconeogenesis, keeping those pathways active in a more natural sense.
2) note the second paragraph in Discussion where they discuss effects of BAT (Brown Adipose Tissue aka "brown fat"). BAT is present in significantly higher %age in mice vs humans.
3) later that paragraph: "most studies have found that weight loss improves insulin sensitivity in humans (41) and mice (36)." Well, we have kind of an impasse, then -- were those studies' KDs more realistic in terms of macronutrient ratios?
Insulin sensitivity seems to recover once the high-fat diet has been curtailed. That makes it a bit different from the usual course of insulin resistance, no?
Along the same lines, it seems to me that a LCHF (low carb, high fat) diet may solve its own problems. What I mean is that while the body may be slow to respond to blood sugar spikes, that situation should be occurring infrequently, if ever.
On the other hand, it makes me wonder if "part-time keto" may be worse than the alternatives. In a situation where you switch from keto to...whatever, I picture fat-laden cells unable to deal with the sudden onslaught of sugar.