Low carb cannot put T2 diabetes into remission by repairing damaged beta cells. Only weight loss can do this. All it can do is lower blood sugar. Off course if the low carb diet chosen is one that simultaneously causes weight loss then it can play a part in repairing beta cells. Eg Some, but not all, low carb diets involve just reducing calories from carbs without replacing them with equivalent calories from other macronutrients such as fat. And there are some versions in between that replace only some of the missing carb calories with fat calories. These can also bring about a degree of weight loss. Repairing Beta cell function is the only way of putting T2 diabetes, as opposed to it's symptom, high blood sugar, into reverse.
"Insulin resistance in muscle and liver and β-cell failure represent the core pathophysiologic defects in type 2 diabetes. It now is recognized that the β-cell failure occurs much earlier and is more severe than previously thought. Subjects in the upper tertile of impaired glucose tolerance (IGT) are maximally/near-maximally insulin resistant and have lost over 80% of their β-cell function) Treatment should be based upon reversal of known pathogenic abnormalities and not simply on reducing the A1C, and therapy must be started early to prevent/slow the progressive β-cell failure that already is well established in IGT subjects. A treatment paradigm shift is recommended in which combination therapy is initiated with diet/exercise, metformin (which improves insulin sensitivity and has antiatherogenic effects), a thiazolidinedione (TZD) (which improves insulin sensitivity, preserves β-cell function, and exerts antiatherogenic effects), and exenatide (which preserves β-cell function and promotes weight loss)."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/
"Insulin resistance in muscle and liver and β-cell failure represent the core pathophysiologic defects in type 2 diabetes. It now is recognized that the β-cell failure occurs much earlier and is more severe than previously thought. Subjects in the upper tertile of impaired glucose tolerance (IGT) are maximally/near-maximally insulin resistant and have lost over 80% of their β-cell function) Treatment should be based upon reversal of known pathogenic abnormalities and not simply on reducing the A1C, and therapy must be started early to prevent/slow the progressive β-cell failure that already is well established in IGT subjects. A treatment paradigm shift is recommended in which combination therapy is initiated with diet/exercise, metformin (which improves insulin sensitivity and has antiatherogenic effects), a thiazolidinedione (TZD) (which improves insulin sensitivity, preserves β-cell function, and exerts antiatherogenic effects), and exenatide (which preserves β-cell function and promotes weight loss)."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661582/
Last edited by a moderator: