While allowing discontinuation of medications most likely to cause serious hypoglycemia

Topics were drawn from two prior behavioral intervention models for diet and health behavior change, including components aimed at increasing positive affect and decreasing depressive symptoms and teaching mindful eating techniques. Specific topics included: setting attainable goals; scheduling, noticing, and savoring positive events; developing self-compassion; practicing positive reappraisal, gratitude, and acts of kindness; being aware of one’s personal strengths; and being mindful of hunger, fullness, cravings, taste satisfaction, triggers for overeating, thoughts and emotions. To develop mindful eating skills, participants were asked to practice a guided meditation 10 minutes per day at least three times a week using audio CDs recorded for the intervention, and to use several mindful eating practices during meal times, such as focusing awareness on the taste and texture of foods while eating. The psychological skills training hour was led by a psychologist with experience teaching mindfulness and health behavior change. An important function of insulin is to inhibit lipolysis and reduce levels of plasma non-esterified fatty acids, switching the main fuel source away from fatty acids and toward carbohydrates. Nutritional ketosis thus serves as a marker indicating that insulin levels are reduced to a level that lipolysis is not inhibited. As the level of carbohydrate intake that is needed to release inhibition of lipolysis varies between individuals, monitoring nutritional ketosis potentially provides an individualized marker for titrating carbohydrate restriction. Nutritional ketosis may serve as a particularly relevant marker of carbohydrate restriction in the context of diabetes because it indicates a shift away from reliance on glucose as a primary energy source to fatty acids and ketones. As carbohydrates lead to elevated glucose levels in diabetes, fatty acids provide an alternative energy source that can provide adequate fuel without elevating glucose levels in the same way as carbohydrate. This level of ”nutritional ketosis” is safe and physiologically different from ketoacidosis. A key finding of this randomized, controlled trial was that a low carbohydrate diet was more effective than a standard, moderate carbohydrate diet at reducing HbA1c at three months, our primary outcome point. These results are consistent with those of several prior studies, which have found substantial improvements in glycemic control with low carbohydrate diets in the setting of a metabolic ward, or in LY2109761 uncontrolled studies. These results provide important support for the Evofosfamide benefit of low carbohydrate diets in type 2 diabetes for glycemic control, as well as the feasibility of adhering to the diet for at least three months in a community setting. In addition, the improvement in glycemic control was observed despite greater decreases in diabetes medications, particularly sulfonylureas, in the LCK group. This combination of findings suggests another possible benefit of a low carbohydrate diet intervention that may warrant further investigation. Of note, we observed no episodes of clinically evident hypoglycemia in our study, though any reassurance this might provide is substantially limited by the small numbers and short duration of study. However, our findings suggest a low carbohydrate diet may hold promise as a strategy to simultaneously improve glycemic control.

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