There are multiple distinct flavors of diabetes/obesity, as evidenced by the fact that some people have: 1) impaired glucose tolerance (but normal fasting glucose); 2) others have impaired fasting glucose (but normal glucose tolerance); and 3) others have both. This means there isn’t a linear relationship between these phenomena*. There are also: 4) obese patients with normal glucose metabolism; and 5) lean patients with type 2 diabetes.
*I think the great Dr. Kraft
There is not 100% overlap among these, suggesting [confirming] distinct diabetes/obesity phenotypes (and probably causes & best treatments).
discussed low carb ketogenic diets and plant-based diets with John Mackey. Although I disagree with the dichotomy (keto vs. plant-based), it’s well-worth a watch:
(~43g, ~245 kcal) daily for four weeks, at different times of the day (with breakfast, midmorning snack, lunch, or afternoon snack).
… especially because it was accompanied with [modest] reductions in body fat (NS). To be clear, they were instructed to eat more (in the form of almonds), but ended up eating less, BECAUSE ALMONDS. This wasn’t a cross-sectional study, so no healthy user bias or other obvious confounders.
!
protect against alcohol-induced liver damage (in rats) (
and one of 
, not 
.
. Anti-aging (mostly worm studies, but still).
and 138 mg 
(that’d be a LOT of 
).
is very ketogenic! (
. PUFAs in general are more ketogenic than saturated fats in humans, too (eg, 
, meaning some of that weight re-gain was muscle:
? …perhaps, but 19% vs 24% (71 vs 85 grams) isn’t a very big difference. Alternatively, since the LC group really just maintained absolute protein intake (86 grams at baseline, 85 at month 12), whereas low-fat (LF) dieters decreased (86 grams at baseline, 71 at 12 months); perhaps this is why LF lost muscle mass..? Still, those changes in protein intake are small, and I think people can be too quick to chalk up the benefits of LC to “high protein.”
have been giving me headaches for years… the low fat diet caused headaches (P<0.05):
