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Letters to the Editor |
The Pennsylvania State University Nutrition Department S-126 Henderson Building University Park, PA 16802 E-mail: pmk3{at}psu.edu
Dear Sir:
Numerous studies, including one we published recently (1), have shown beneficial effects of a weight-maintenance, high– monounsaturated fatty acid (MUFA), blood cholesterol–lowering diet compared with a high-carbohydrate, low-fat diet on important cardiovascular disease (CVD) risk factors, notably triacylglycerol, HDL-cholesterol, and plasma glucose and insulin concentrations (2, 3). It is clear that elevated triacylglycerol and glucose and insulin concentrations increase the risk of CVD, as does a low HDL-cholesterol concentration. Lowering plasma triacylglycerol, glucose, and insulin and increasing HDL cholesterol decrease the risk of CVD. Although not measured in our recent study, a weight-maintenance, high-carbohydrate, low-fat diet has also been shown to increase fibrinogen concentrations, whereas a high-MUFA, blood cholesterol–lowering diet does not (4). An elevated fibrinogen concentration was shown to increase the risk of CVD. Thus, the evidence is convincing that a weight-maintenance, high-MUFA, blood cholesterol–lowering diet beneficially affects CVD risk.
As noted by Marckmann and Astrup, body weight is an important factor that must be considered in contemporary dietary recommendations. The key questions are 1) What is the best diet for weight loss and weight maintenance? and 2) Will a higher-fat diet promote weight gain?
In our recent meta-analysis (5), we observed a linear relation between decreasing percentage of energy from fat and a decrease in body weight. Although this finding suggests that higher-fat diets promote weight gain, 3 important limitations of this study must be noted. First, a higher-fat weight-loss diet was not tested, so one can question whether weight loss might be less, the same, or maybe even greater because of better adherence to the higher-fat (ie, high MUFA), energy-reduced diet. It is generally accepted that "a calorie is a calorie" regardless of whether the energy is derived from fat, carbohydrate, or protein. Thus, weight loss with any energy-reduced diet is due to the reduction in energy intake relative to expenditure. What is not clear is whether macronutrient-manipulated weight-loss diets have any effect on adherence and, hence, on long-term weight loss and weight maintenance. Second, the weight loss was small despite a large reduction in energy intake from fat (ie, 2.6-kg weight loss associated with an 8–percentage point decrease in percentage of energy from fat). A smaller decrease in fat, consistent with current intake recommendations, would be expected to result in less weight loss (only 
1.3 kg for a 4–percentage point decrease in fat intake). Finally, in long-term studies over a period of 2–4 y, only small changes in body weight were shown (0.5-kg weight loss).
Targeting fat reduction as the sole means of affecting the global epidemic of overweight and obesity is not justified. Obesity is a complex problem—its causes are not fully understood. Although it is clear that an energy imbalance is the root cause, there is no compelling evidence that this is due to changes in fat intake. A case in point relates to the ongoing increase in the incidence of overweight and obesity in the United States that is concurrent with little or no change in absolute intake of fat and a decrease in percentage of energy from fat (6). It is clear that an increase in energy intake in conjunction with a more sedentary lifestyle (ie, less physical activity) accounts, in part, for the fattening of Americans. Further evidence comes from Sweden, where a small increase in overweight occurred despite virtually no change in the diet (8, 9). In addition, there is ample evidence from other countries that there is no consistent association between increasing overweight and obesity and fat intake (7, 8).
Energy balance and, if needed, weight loss in individuals who are following any diet is dependent on energy intake irrespective of the macronutrient profile. In the context of a high-MUFA, blood cholesterol–lowering diet, it is clear that this diet has beneficial effects on CVD risk factors in weight-stable individuals. Although it has not been tested as a weight-loss diet compared with a high-carbohydrate, low-fat diet in free-living subjects, such a diet could be planned that would have a low energy density (ie, high in fruit and vegetables) to provide bulk and promote satiety. The key issue for controlling energy intake may not be the macronutrient profile of the diet but rather the energy density, because the fat content and energy density of foods are not always perfectly correlated. As argued by Rolls and Bell (9), energy density is more closely related to factors such as the water and fiber contents of foods. In that study and others, subjects ate less when consuming foods of low energy density compared with foods of high energy density, regardless of fat content. Thus, focusing solely on the fat content of foods when designing weight-loss diets may limit the effectiveness of the diets if the effects of energy density are not considered.
We advocate a reexamination of the effects of the macronutrient content of the diet on risk of CVD. While acknowledging that the ultimate test of higher-fat diets will be in free-living individuals consuming foods ad libitum, we believe that by promoting the addition of fruit, vegetables, whole grains, and legumes to these diets, it may be possible to achieve long-term success in terms of both weight control and CVD risk reduction.
REFERENCES
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