Introduction

Major concerns regarding dietary stem from their role in the promotion of atherosclerotic cardiovascular disease; other issues of concern relate to their possible roles in the genesis of obesity, and possibly malignancy. Despite decades of research, however, the relationship between fat intake and these clinical outcomes still remains controversial. While recommendations from several authoritative United States organizations over the past two decades have emphasized decreasing the total amount of fat in the diet, most research indicates that the type of fat is more important than total fat content. Guidelines from the National Cholesterol Education Program (NCEP) Expert Panel and Adult Treatment Panel III (ATP III) have begun to recognize this distinction. Instead of the previous recommendation that calories from fat should not exceed 30% of total energy intake, the panel now recommends a range of 25%-35 %. Similarly, the 2005 Dietary Guidelines for Americans recommended that between 20% and 35% of energy come from fat.

Total fat intake

There are several reasons to be cautious about any strong recommendations to reduce total fat intake to below 30% of energy. First, the evidence that a high total fat intake may be harmful is weak. Furthermore, the recommendation to limit fat intake was based primarily on research of its effects on total blood cholesterol. As a result, emphasis on fat intake has obscured the true purpose behind dietary recommendations, the concept of a disease-protecting diet, which may possibly limit the progression of atherosclerosis, as well as other age-related degenerative disease processes. For instance, other pathways have been elucidated by which dietary constituents can affect not only the atherosclerotic process, but also thrombosis, as well as other chronic diseases of adulthood which continue to plague industrialized societies. Such factors include antioxidants, folate and its cofactors, and other vitamins and minerals.

The relationship between fat intake and the development of cancer is even less well documented than that of coronary heart disease. Some cross-cultural studies have suggested a potential role for high total fat intake in the genesis of breast, colon, and prostate cancers, but these studies, like those of heart disease, may well be confounded by other factors.

Other issues with regard to the recommendation for a low-fat diet remain unclear. These include the following:

1) The role of dietary fat in the etiology of obesity and the metabolic syndrome.

2) The inability to accurately explain to patients how to achieve a target level of fat intake. The message to reduce dietary fat has been translated by food manufacturers and consumers into a potentially harmful set of food choices.

3) The evidence that a high intake of fat, in and of itself, is harmful in terms of heart disease, cancer, or obesity.

Dietary Fat and Heart Disease

Populations whose diets consist of a higher total fat intake do not always develop more atherosclerotic cardiovascular disease. In the Seven Countries Study, for example, the locations with the lowest incidence of coronary heart disease were Crete and Japan. However, the diets of the two populations could not be more dissimilar; the Japanese had a very low fat intake, while the population in Crete typically had a high total fat intake, which however, was chiefly composed of monounsaturated fats from vegetable sources (olive oil in the Mediterranean diet).

Epidemiologic studies, however, have not provided corroborating evidence. In addition, the few well-conducted, randomized trials of dietary fat reduction to treat obesity have resulted in effects that are modest at best. A meta-analysis of longer term weight loss trials found no significant difference in net weight loss between patients who consumed a low-fat diet versus other weight reducing diets, suggesting that low-fat diets may not be any more effective than calorie restricted diets in achieving long-term weight loss. The key factor concerning obesity is that excess intake of calories from any source, relative to the amount of physical activity undertaken, is what actually results in weight gain.

A major difficulty with low-fat diets is that it is easier for patients to understand advice given in terms of food types (e.g., "eat more fresh fruit") rather than nutrient type (e.g., "reduce your intake of fat to less than 30% of your total energy intake"). Patients often look to their clinicians as a credible source of dietary advice. Many physicians however, know the frustration of trying to educate their patients in terms of an appropriate nutritious diet. They often lack the time and/or expertise to deliver detailed nutritional counseling to their patients. Reasonable messages that are relatively easy to discuss with adult patients who do not require special diets for existing diseases (e.g., renal failure, Sprue, eating disorders) include the following:

It may be counterproductive to make restriction of total fat a primary recommendation. Physicians should focus instead on recommending natural alternatives to foods high in animal and hydrogenated fats, such as fruits, vegetables, legumes, and whole grain products. Recommend reducing saturated fat intake by substituting skim or 1% milk for whole milk, and by replacing animal products with those of vegetable origin as much as possible. Recommend reducing the intake of trans fatty acids by avoiding stick margarine and reducing the consumption of commercially baked goods and deep-fried fast foods.

When fats are needed for cooking, spreads, and other uses, recommend oils with high amounts of monounsaturated and/or polyunsaturated fatty acids, especially n-3 polyunsaturated fats such as canola and olive oils and, to a lesser extent, soybean oil. Patients may also consume nuts and seeds in moderate amounts.

The message to reduce fat in the United States has been misunderstood and therefore translated, by food manufacturers and consumers, into a potentially harmful set of food choices. Instead of replacing high-fat foods with naturally low-fat foods which have other nutritional benefits benefits, such as fruits, vegetables, legumes, and whole grain foods, consumers have often increased their consumption of low-fat or "fat-free" varieties of naturally high-fat foods, such as fat-free snack foods. The result is an increase in processed carbohydrates, lower HDL-cholesterol concentrations, a possible increase in the incidence of type 2 diabetes mellitus and obesity, and failure to gain any of the benefits of more healthful alternatives.

The evidence to date suggests that saturated fat and trans fat contribute to the genesis of heart disease, while monounsaturated and polyunsaturated fats are protective. Based on data from the Nurses' Health Study, the risk of coronary heart disease would be reduced by 42% if 5% of energy from saturated fat were replaced by energy from unsaturated fats, and by 53% if 2% of energy from trans fat was replaced by energy from unhydrogenated, unsaturated fat.

With these opposing effects of different types of fat, the amount of total fat in the diet is obviously a less significant factor than is the type of fat. Fewer data are available regarding the role of intake of fats in the incidence of stroke, cancer, and other outcomes, although most of the evidence suggests results that are consistent with those concerning heart disease, the leading cause of death in the United States.

Obviously, cross-population comparisons can be confounded by other factors, such as genomics. However, even studies of individuals within a population have not produced compelling evidence that total fat intake is related to the incidence of coronary heart disease. In an analysis from the Nurses' Health Study involving 14-year follow-up of 80,000 women, the multivariate adjusted relative risk of coronary heart disease for the highest quintile of dietary fat compared with the lowest was 1.04 (95 % confidence interval 0.83 to 1.28. This statistically insignificant result is consistent with other cohort studies.

Randomized trials of diets no more than 30 % of calories from fat" rule have shown relatively little effect upon the total serum cholesterol concentration. In an overview of 16 published trials, such diets resulted in a change in serum cholesterol ranging from a fall of 2.1 % to a rise of 1.0 % over 4 to 10 years.Only a small number of randomized trials have examined the effect of changing diet on cardiovascular end points, and even fewer trials have achieved substantial differences in total fat intake between the intervention and control diets:

The Women's Health Initiative randomly assigned 48,835 women (97% with no history of CVD) to an intensive behavior modification group, with the goal of reducing total fat intake to 20% of calories and to increase daily intake of vegetables and grains, versus a control group who received dietary education materials only; mean follow-up was 8.1 years. After 6 years, women in the intervention group had decreased total fat intake compared with the control group (28.8% versus 37.0% of calories from fat respectively), but still no significant impact on CHD (hazard ratio [HR] 0.94, 95% CI 0.86-1.02) or stroke (HR 1.02, CI 0.90-1.17) was demonstrated. Apparently, although the intervention group reduced fats considered harmful, such as saturated fat and trans fat, the intervention group seemed to also reduce potentially beneficial fat intake (monounsaturated and polyunsaturated fat).

Similar to the primary prevention trials, randomized studies of the prevention of recurrent coronary events (secondary prevention trials) have not demonstrated a beneficial effect of lowering total fat.

A systematic review of randomized, controlled trials (performed prior to the Women's Health Initiative trial discussed above) addressed the effect of reduction or modification of fat intake on cardiovascular endpoints. The authors found that in these trials, total mortality was unchanged (odds ratio 0.98, 95 % confidence interval 0.86 to 1.12). There were trends toward reduced cardiovascular events (0.86 [0.72 to 1.03]) and mortality (0.91 [0.77 to 1.07]) and stronger effects in trials of at least 2 years duration. In some of the trials included in the review, however, total fat reduction was confounded by fat being replaced by carbohydrate, whereas in other trials, patients modified the type of fat, replacing saturated fat with unsaturated fat. Thus the implications for dietary recommendations are still unclear.

Case-control studies of diet and breast cancer have suggested a modest role for total fat intake. In one summary of results from 12 case-control studies, the relative risk of breast cancer was estimated to be 1.35 for each 100 gm increment in daily intake of fat. In contrast, cohort studies, which do not have the inherent recall bias of case-control studies, have generally not found this association. In a meta-analysis of seven cohort studies, for example, each 25 gm increment of fat intake, adjusted for energy intake, was associated with a relative risk of breast cancer of only 1.05 (95 % confidence interval 0.94 to 1.11). Furthermore, in an analysis of the Nurses' Health Study, a prospective cohort study of 88,795 women, there was no evidence that either lower total fat intake or lower intake of specific types of fat decreased the risk of breast cancer. Associations between fat intake and colon cancer are also confounded by red meat consumption.

The bulk of epidemiologic evidence suggests a role for dietary fat in the pathogenesis of prostate cancer, although the data are still not definitively conclusive. The association may be stronger with animal fat than with vegetable fat. Perhaps most importantly, the Women's Health Initiative trial described above found that, at a mean follow-up of 8.1 years, the intervention to reduce total fat intake had no meaningful effect on risk of colorectal cancer (hazard ratio [HR] 1.08, 95% CI 0.90-1.29) or breast cancer (HR 0.91, CI 0.83-1.01).