Low carbohydrate diet and postprandial hyperglycemia

Postprandial hyperglycemia is a risk factor for CVD, particularly in diabetic patients [49-51]. Many studies including the Nurses Health Study [36] have suggested a link between dietary carbohydrates (measured in terms of glycemic load) and CVD risk. Furthermore, control of postprandial hyperglycemia has been shown to provide cardiovascular benefits, and to contribute to the overall decrease of hemoglobin A1c, something that has been clearly shown to reduce microvascular disease in both type 1 and type 2 diabetes [52,53]. Dietary carbohydrates are the major determinants of postprandial glucose levels [17,47,54] and LoCHO diets have been reported to lower postprandial glucose levels directly and indirectly by way of weight loss and may have beneficial effects on CVD risk factors [4,14]. Significant reductions in postprandial plasma glucose and plasma insulin levels with LoCHO diet have been demonstrated in many studies [4,9,42,55]. Furthermore, control of postprandial hyperglycemia with acarbose, an α-glucosidase inhibitor, has been demonstrated to significantly decrease the risk of diabetes in patients with impaired glucose tolerance [56,57].

Low Carbohydrate diet and Dyslipidemia

Type 2 diabetes and metabolic syndrome are commonly associated with atherogenic dyslipidemia, characterized by elevated triglycerides (TG) levels and low HDL levels [17,58]. Additionally, qualitative changes in LDL cholesterol may be present in the form of small, dense LDL particles which are more atherogenic and may be associated with higher risk of CVD [58-60]. Evidence from various studies has confirmed that LDL, HDL and triglycerides are independent predictors of CVD [17,61-63]. Since nearly 75 % of diabetics die of heart disease, control of diabetic dyslipidemia is an important strategy in the primary prevention of CVD and a low fat high carbohydrate diet has been the standard recommendation from various health organizations to achieve this target [33-35]. A mounting body of evidence however, has demonstrated that the traditional low fat high carbohydrate diet is associated with elevated triglyceride and low HDL cholesterol levels and may worsen the dyslipidemia of type 2 diabetes and metabolic syndrome [3,10,25,27,28]. Reduction in dietary intake of fat is frequently associated with increased intake of carbohydrates and leads to carbohydrate induced hypertriglyceridemia (HPTG) [64-69]. This phenomenon has been observed in subjects consuming high carbohydrate low fat diets for as few as 5 days, with replacement of as little as 10% fat with carbohydrate and with dietary fat intake of as much as 30% of energy [64,65]. Decreasing fat without increasing carbohydrate does not appear to elevate triglycerides, thereby suggesting that addition of carbohydrates and not reduction in fat is responsible for this HPTG seen with high carbohydrate low fat diets. Though the exact mechanism for carbohydrate induced HPTG has not been clearly elucidated, both increase in TG synthesis and decrease in fractional TG clearance have been demonstrated [64-66] with a possible contribution from increased hepatic de novo fatty acid synthesis [64,67]. A number of factors influence the occurrence of carbohydrate induced HPTG and these include high BMI (>28 kg/m2), insulin resistance, post menopausal state, and genetic factors [64,65]. Diabetic, insulin resistant and obese subjects are thus at even higher risk. In addition, type and form of carbohydrates, particularly high sugar/starch ratio also contribute to carbohydrate induced HPTG [64]. Conversely, LoCHO diets have been consistently demonstrated to lower triglycerides and increase HDL [8-11,26-28]. Even the studies which failed to show significant differences in weight loss between LoCHO diet and low fat diets after one year [8,27] demonstrated significant reduction in TG and an increase in HDL with the LoCHO diet despite inability of subjects to achieve target carbohydrate intake. This result suggests that the improvement in TG is not only independent of weight loss but, again, even modest reduction in carbohydrate intake may have significant benefits on lipids. Significant clinical implications comes from the VA-HIT study [61], where a modest reduction in TG and elevation of HDL cholesterol were associated with notable improvement in CVD mortality.

Though weight loss per se, in combination with increased physical activity, is usually associated with an increase in HDL cholesterol and decreases in triglyceride and LDL cholesterol concentration, the beneficial effects on lipids of the caloric reduction in LoCHO diets appear to be secondary or additive to carbohydrate restriction and are seen even after adjusting for amount of weight loss[27].

A low fat diet, in the presence of weight loss is effective in lowering serum LDL cholesterol. On the other hand, such a regimen decreases HDL cholesterol without a significant increase in LDL size to less atherogenic form [70]. Emerging evidence suggests that LoCHO diets may actually have beneficial effects on LDL cholesterol by decreasing LDL particle concentration and increasing LDL size to less atherogenic form [25,28,70-73].

In summary, a low carbohydrate diet may be more effective than a low fat diet at improving the characteristic dyslipidemia associated with diabetes, namely high TG, low HDL and increased small dense LDL particles [70].