Postprandial metabolic responses to dietary glycemic index in hypercholesterolemic postmenopausal women.

Cardiovascular disease (CVD) remains the leading cause of mortality in women in the developed world and is a prime target for prevention.1 Postmenopausal loss of estrogen in women unveils a constellation of closely associated adverse changes in metabolic risk factors.2 The key contributors to this increased risk include a proatherogenic lipid profile, higher prevalence of visceral obesity, insulin resistance, and hypertension.3 Nonesterified (or free) fatty acid (FFA) levels have been implicated as a mechanistic underpinning for the development of the metabolic syndrome and ensuing risk for cardiovascular mortality, and elevated serum triglycerides have been shown to be an independent risk factor for CVD.4 Further, recent studies suggest that nonfasting triglyceride levels, especially those measured 2 to 4 hours postprandially, are strongly associated with cardiovascular events.5 Epidemiologic studies support postprandial lipemia as an independent risk factor for CVD.6,7 Patients with CVD exhibit an increased magnitude and duration of lipemia during the postprandial period,4 with an adverse effect on lipid subfractions associated with oxidative damage and induction of an inflammatory response.8 The close relationship between inflammation and CVD suggests that proinflammatory conditions, as promoted by FFAs, serum triglycerides, and insulin resistance, manifested by a high homeostasis model assessment-insulin resistance (HOMA-IR), may be a possible risk factor for coronary heart disease (CHD) or CHD-related disease, ie, diabetes mellitus (DM), in postmenopausal women.9 Many organizations recommend a diet containing at least 55% total energy from carbohydrates to maintain health and prevent CVD.10,11 However, it is clear that the type of carbohydrate is important. Recommendations emphasize the inclusion of complex carbohydrate and fiber, while reducing intake of simple sugars and carbohydrates associated with high glycemic response.12 In the Nurses Health Study, persons in the highest quintile of glycemic index (GI) (and glycemic load) had nearly double the relative risk of coronary artery disease, compared with those in the lowest quintile after adjustment for known risk factors.13,14 In postmenopausal women, high-GI diets were associated with higher fasting C-reactive protein (CRP) levels, high fasting serum triglycerides, and low serum high-density lipoprotein (HDL) cholesterol;15 yet, their effects on postprandial FFA and lipid levels remain unclear.16 While it is known that menopause represents a cardiovascular risk factor for women,2 it is not known whether the risk might be more pronounced among women with higher levels of postprandial lipemia. Most postprandial studies in women to date have tested plasma glycemic and lipemic response to conditions involving a metabolic stress, such as a very high–fat load or postprandial response to exercise. In contrast, our objective was to study postprandial effects of a high-glycemic vs a low-GI meal, representing a realistic test meal within the recommended food spectrum. We sought to test the hypothesis that a high-compared with a low-GI meal results in an adverse postprandial metabolic response.