Canadian researchers sought to systematically evaluate the strength of the evidence supporting links between dietary factors and coronary heart disease. Coronary heart disease (CHD) is the number one cause of death in Western societies.
It’s important to understand the two types of studies meta-analyzed by the Canadians.
Prospective cohort studies can be used to identify a dietary factor that may be associated with a disease or outcome. For example, researchers could study the health of 20,000 people over the course of 10 years, giving them questionnaires to find out what foods they typically ate. They might find after 10 years that the people who ate the most saturated fat tended to die earlier and had more heart attacks and strokes compared to the people who ate the least saturated fat. This would establish an association between dietary saturated fat and premature death, heart attacks, and strokes. It does not prove that saturated fats cause those outcomes, it’s just an association.
Randomized trials, often called randomized controlled trials (RCTs), typically take two groups of people and apply an intervention to one group but not the other. The groups are followed over time to see if there is a difference in outcome. For example, take another group of 20,000 people. Randomly assign 10,000 of them to eat more-than-usual saturated fat. The other 10,000 similar people serve as the control group, eating their usual amount of saturated fat. Follow these 20,000 people over 10 years, then compare their health outcomes: death, heart attacks, strokes. If the high-saturated-fat group has worse outcomes, you are much closer to proving that dietary saturated fat causes premature death, heart attacks, and strokes.
The scientists located and analyzed every English-language prospective cohort study (146 studies) or randomized trial (43) investigating food intake and coronary heart disease (CHD), from 1950 through June, 2007. They wrote:
We used the Bradford Hill guidelines to derive a causation score based on four criteria (strength, consistency, temporality, and coherence) for each dietary exposure in cohort studies and examined for consistency with the findings of randomized trials.
The different dietary patterns evaluated in studies were noted. The “Mediterranean” dietary pattern emphasizes a higher intake of vegetables, legumes, fruits, nuts, whole grains, cheese or yogurt, fish, and monounsaturated relative to saturated fatty acids. The “prudent” dietary pattern is characterized by a high intake of vegetables, fruit, legumes whole grains, and fish and other seafood. The “western” pattern is characterized by a high intake of processed meat, red meat, butter, high-fat dairy products, eggs, and refined grains.
Strong evidence (four Bradford Hill criteria satisfied) supported protection against CHD with consumption of:
- monounsaturated fatty acids [prominent in olive oil, for example]
- Mediterranean diet
- prudent diet
Modertately strong evidence (three criteria satisfied) supported protection against CHD with consumption of:
- marine omega-3 fatty acids
- whole grains
- dietary vitamins E and C (as opposed to vitamin supplements)
- beta carotene
Strong evidence supported the following as harmful dietary factors, in terms of CHD:
- trans-fatty acids
- foods with a high-glycemic index or load
- western diet
Researchers found insufficient evidence (two or less criteria) to support an association between CHD and:
- total fat
- saturated and polyunsaturated fatty acids
- vitamin supplements E and C
- alpha-linolenic acid
Selected Comments of the Researchers [my comments in brackets]
Cohort studies provide abundant evidence of an association with total mortality for many dietary exposures. Randomized controlled trials corroborate these associations for the consumption of omega-3 fatty acids and a Mediterraneandiet because most of the other dietyary factors have not been evaluated to date.
Among the dietary exposures with strong evidence of causation from cohort studies, only a Mediterranean dietary pattern is related to CHD in randomized trials. [The association is inverse: Higher adherence to the Mediterranean diet leads to lower rates of CHD.]
A wealth of epidemiologic studies have evaluated associations between dietary exposures and CHD. The general consensus from the evidence currently available is that a reduced consumption of saturated and trans-fatty acids and a higher intake of fruits and vegetables, polyunsaturated fatty acids including omega-3 fatty acids, and whole grains are likely beneficial. This is reflected in the revised Dietary Guidelines for Americans 2005 from the US Departments of Health and Human Services and Agriculture. However, little direct evidence from RCTs supports these recommendations. [Emphasis added.] In some cases, RCTs have not been conducted, and RCTs that have been conducted have generally not been adequately powered or have evaluated surrogate end points rather than clinical outcomes.
Single-nutrient RCTs have yet to evaluate whether reducing saturated fatty acid intake lowers the risk of CHD events.
More recently, the lack of benefit of diets of reduced total fat has been established [in women only? (reference below)], and the evidence supporting the adverse effect of trans-fatty acids on cholesterol levels and CHD has increased, which is reflected in our findings. [This is the only mention of cholesterol in the report.]
I wonder about vegetarian/vegan diets. Have they been tested for efficacy against CHD? What about Dr. Dean Ornish’s program?
Although not mentioned in the text of the article, Table 3 on page 664 shows that the positive association between CHD and high-glycemic index/load is much stonger in women than in men. Relative risk for women on a high-glycemic index/load diet was 1.5 (95% confidence interval = 1.29-1.71), and for men the relative risk was 1.06 (95% confidence interval = 0.91-1.20). I question whether the association for men is statistically significant.
Why wasn’t there discussion of dietary cholesterol? The public and physicians have been told for years that dietary cholesterol causes or aggravates coronary heart disease. Is there no evidence?
Note that the researchers found no clear association between CHD and saturated and total fat intake. In traditional medical circles, these findings are considered sacrilegious!
Medical schools and cardiologists have been teaching for thirty or more years that they are related positively. “Positively” means the more saturated and total fat in your diet, the more likely you are to develop atherosclerosis, which in the heart is coronary heart disease. Dietary cholesterol is often thrown into the equation. The is the dogmatic Diet-Heart Hypothesis. It doesn’t hold much water these days, if any.
Mente, Andrew, et al. A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease. Archives of Internal Medicine, 169 (2009): 659-669.
van Dam, R.M., et al. Dietary glycemic index in relation to metabolic risk factors and incidence of coronary heart disease: the Zutphen Elderly Study. European Journal of Clinical Nutrition, 54 (2000): 726-731.
Howard, B.V., et al. Low-fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. Journal of the American Medical Association, 295 (2006): 655-666.