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Lowering the Bar on the Low-Fat Diet | JAMA | JAMA Network

Lowering the Bar on the Low-Fat Diet | JAMA | JAMA Network:

David S. Ludwig, MD, PhD1

The recent revelation that the sugar industry attempted to manipulate science in the 1960s1 has once again focused attention on the quality of the scientific evidence in the field of nutrition and how best to prevent diet-related chronic disease.



 Beginning in the 1970s, the US government and major professional nutrition organizations recommended that individuals in the United States eat a low-fat/high-carbohydrate diet, launching arguably the largest public health experiment in history. Throughout the ensuing 40 years, the prevalence of obesity and diabetes increased several-fold, even as the proportion of fat in the US diet decreased by 25%. Recognizing new evidence that consumption of processed carbohydrates—white bread, white rice, chips, crackers, cookies, and sugary drinks—but not total fat has contributed importantly to these epidemics, the 2015 USDA Dietary Guidelines for Americans essentially eliminated the upper limit on dietary fat intake.2 However, a comprehensive examination of this massive public health failure has not been conducted. Consequently, significant harms persist, with the low-fat diet remaining entrenched in public consciousness and food policy. In addition, critical scientific questions have been muddled.



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To facilitate this change, the Healthy People 2000 goals included a call to the food industry to increase from 2500 items “to at least 5000 brand items the availability of processed food products that are reduced in fat.” The food industry followed suit, systematically replacing fat in food products with starch and sugar.

As a result of these efforts, dietary fat decreased to near the recommended limit of 30% total energy. But contrary to prediction, total calorie intake increased substantially, the prevalence of obesity tripled, the incidence of type 2 diabetes increased many-fold, and the decades-long decrease in cardiovascular disease plateaued and may reverse, despite greater use of preventive drugs and surgical procedures. However, other changes in diet (such as meals away from home) and lifestyle (such as physical activity level) may have influenced these trends.

Recent research suggests that the focus on dietary fat reduction has directly contributed to this growing burden of chronic disease.2,6- 9 In contrast to older, cross-sectional designs, high-quality prospective observational studies consistently show that total fat intake does not predict change in body fat, after controlling for confounding and reverse causation. Some foods previously relegated to the top of the pyramid because of high fat content (nuts, full-fat yogurt) are associated with lower rates of weight gain than common high-carbohydrate foods (processed grains, potato products, sugary beverages).9 Moreover, meta-analyses of clinical trials report that low-fat diets are inferior to comparisons controlled for treatment intensity, including low-carbohydrate diets,6 Mediterranean diets, and all higher-fat diets. Of particular importance, the major low-fat diet studies, such as the Women’s Health Initiative clinical trial and Look Ahead, failed to reduce risk for heart disease despite use of lower-intensity control conditions. In contrast, the PREDIMED study was terminated early when cardiovascular disease incidence decreased more rapidly than expected in the higher-fat diet groups compared with the low-fat control. Consistent with these findings, men and women adhering to low-fat/high-carbohydrate diets had higher, not lower, rates of premature death, although the type of dietary fats consumed importantly modified risk.7

One reason for the apparent failure of low-fat diets is that they may elicit biological adaptations—increasing hunger, slowing metabolic rate, and other hallmarks of the starvation response—that antagonize ongoing weight loss. Preliminary studies suggest that the reduced insulin secretion with low-carbohydrate and low-glycemic-index diets may attenuate these adaptations, facilitating long-term weight-loss maintenance and reducing diseases associated with hyperinsulinemia (the carbohydrate-insulin model).8
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