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1 From Hattner/Coulston Nutrition Associates, LLC, 1386 Cuernavaca Circulo, Mountain View, CA.
2 Address reprint requests to A Coulston, Hattner/Coulston Nutrition Associates, LLC, 1386 Cuernavaca Circulo, Mountain View, CA 94040. E-mail: ann.coulston{at}attglobal.net.
See corresponding article on page 999.
Cardiovascular disease (CVD) represents a leading cause of death in the Western world, and, according to World Health Organization data, in the general population, the risk of heart disease in women is only half that in men (1). On the other hand, type 2 diabetes is associated with a 2- to 4-fold greater risk of CVD, and, unlike in the general population, women with diabetes are at a higher risk of CVD than are men with diabetes (2).
What accounts for the high CVD risk in persons with diabetes? All of the answers are not in, but plasma lipid abnormalities and insulin resistance are 2 major factors. The most common plasma lipid abnormalities in patients with type 2 diabetes are high triacylglycerol and low HDL-cholesterol concentrations (3). The mean LDL-cholesterol concentrations in these persons are not significantly different from those in persons without diabetes, but persons with diabetes tend to have a greater proportion of smaller and denser LDL particles, which are associated with increased CVD risk (4). Diabetes is designated an independent CVD risk factor in the National Cholesterol Education Panel Adult Treatment Panel III report, and those investigators set a goal of an LDL-cholesterol concentration < 100 mg/dL for persons with diabetes (5). In that report, the clinical approach to primary prevention of CVD recommended lifestyle changes of reduced intakes of saturated fat and cholesterol, increased physical activity, and weight control (5). Additional considerations with respect to persons with clinical signs of insulin resistance and primary dyslipidemia were discussed. High plasma triacylglycerol concentrations and low HDL-cholesterol concentrations—the dyslipidemia of type 2 diabetes—respond to weight loss and increased physical activity but also may be aggravated by high carbohydrate intakes.
Insulin resistance is a key factor in the pathogenesis of type 2 diabetes, and it predates the development of frank hyperglycemia by many years. Characteristic features of the insulin resistance syndrome include dyslipidemia, glucose intolerance, central obesity, hypertension, and specific abnormalities of endothelial and vascular function. The interplay between these signs of insulin resistance and their vascular, metabolic, and clinical consequences points to increased risks of CVD and type 2 diabetes (6). The metabolic abnormalities associated with insulin resistance and type 2 diabetes can be improved by reducing the body weight of overweight and obese persons.
Because lowering LDL cholesterol is the primary means of reducing CVD risk in the general population, dietary guidelines have focused on decreasing saturated and total fat intakes by substituting calories from an increased carbohydrate intake. However, intervention studies found that, in persons with insulin resistance and type 2 diabetes, low-fat, high-carbohydrate diets accentuated dyslipidemia and resulted in increased triacylglycerol and decreased HDL-cholesterol concentrations, and no improvement in plasma lipid CVD risk factors occurred (7). In contrast, when calories from saturated fatty acids were replaced with calories from monounsaturated and polyunsaturated fatty acids, no adverse changes in plasma lipid concentrations were observed (8). Data from several small intervention studies in persons with type 2 diabetes led to nutritional guidelines of more modest dietary fat and moderate carbohydrate intakes for persons with diabetes (9).
How do these guidelines square with the findings of observational studies? A report by Tanasescu et al (10) from the Nurses’ Health Study cohort in this issue of the Journal describes the dietary patterns of 5674 women with diabetes, including 619 who had a fatal cardiac event, nonfatal myocardial infarction, or stroke between 1980 and 1998. CVD risk was associated with dietary intakes of animal fat, saturated fatty acids, and cholesterol but not with total fat intake. Data on plasma lipid concentrations or other signs of insulin resistance were not reported. However, when the authors examined fat and carbohydrate intakes as continuous variables, the replacement of 5% of energy from saturated fat with equivalent energy from carbohydrates was associated with a 22% lower risk of CVD. The same replacement with monounsaturated fat was associated with a 37% lower risk. The reduction in CVD risk that resulted from changes in the type of dietary fat, as compared with a decrease in total fat, supports the notion that many of these women probably had insulin resistance syndrome.
Although there is some controversy about the optimal diet for adults with type 2 diabetes, there is a consensus for decreasing the consumption of saturated fats and increasing the consumption of fruit and vegetables (9). These goals are apparently not being met in the American diet. When dietary intakes were assessed for persons (both men and women) with diabetes who participated in the third National Health and Nutrition Examination Survey (NHANES III), 61% reported that >10% of calories were obtained from saturated fat, and 26% reported that their total fat intake was >40% of calories (11).
The role of specific dietary fatty acids in persons with diabetes mellitus needs additional investigation. We are beginning to obtain good data in animals and in humans that allow us to associate types of dietary fatty acids with insulin sensitivity (12, 13). However, the amount of dietary fat that is optimal for nutrition management to meet plasma lipid goals in persons with diabetes remains uncertain. One size clearly does not fit all, and individual history, dietary practices, and associated health conditions must be taken into consideration when dietary prescriptions are developed (9). When we can lower the risk of CVD through dietary intervention in all persons with diabetes, we will have made great strides.
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