Interest in dietary fat and its effects on cardiovascular disease date to the 1930s, when animal experiments indicated that dietary cholesterol contributed to an elevated serum cholesterol level, which resulted in the development of atherosclerosis.
Interest in dietary fat and its effects on cardiovascular disease (CVD) date to the 1930s, when animal experiments indicated that dietary cholesterol contributed to an elevated serum cholesterol level, which resulted in the development of atherosclerosis.1
Study results from the 1940s and 1950s suggest that the type and amount of fat play a major role in serum cholesterol levels.1 And in 1961, the American Heart Association (AHA) recommended replacing saturated fatty acids (SFAs) with unsaturated fatty acids (UFAs) to prevent CVD.1 The 1980s and 1990s saw a low-fat campaign emerge: Reduce all fats and replace them with carbohydrates.1 This resulted in an increase in carbohydrates, namely added sugar and refined starch, in diets. The decrease in CVD plateaued, the incidence of type 2 diabetes doubled, and the prevalence of obesity soared.1 The 2015-2020 Dietary Guidelines from HHS eliminate the upper limit of total fat consumption but still recommend that less than 10% of daily calories come from SFAs and to replace SFAs with UFAs.2
Saturated Fatty Acids
Saturated fats are fat molecules that have no double bonds between carbon molecules. This happens when hydrogen reacts with the double bonds and saturates the complex, resulting in all single bonds.3
Saturated fats occur naturally in many foods, the majority of which come from animal products. Some examples include beef fat, butter, cheese, cream, fatty beef, lamb, lard, pork, poultry with skin, and reduced fat or whole milk.3 Although there are some exceptions, saturated fats are usually solid at room temperature.3 The typical American diet contains too much saturated fat, mostly from pizza and cheese, with dairy and milk close behind.
Unsaturated Fatty Acids
UFAs are more loosely packed chains and are typically liquid at room temperature. They include monounsaturated fatty acids (MUFAs), which have 1 double bond, and polyunsaturated fatty acids (PUFAs), which have 2 or more double bonds. UFAs come from plants. Some examples include nuts, olives, seeds, and vegetable oils.
MUFAs can improve cholesterol levels, thereby lowering the risk of CVD.4 This type of fat may also help control blood glucose and insulin levels.4 PUFAs are necessary for the body to function. The body does not make this type of fat, so it must be consumed in the diet. PUFAs are further broken down into 2 subtypes: omega-3 fatty acids and omega-6 fatty acids.
Omega-3 fatty acids can be found in canola, safflower, and sunflower oils; fatty fish; chia, hemp, and sunflower seeds; and walnuts. Omega-3 may be beneficial to the heart.4
Omega-6 fatty acids are found in corn, safflower, soybean, sunflower, and walnut, oils. These fatty acids may also protect the heart but may cause inflammatory issues.4
Medical literature is full of articles arguing the benefits and risks of fat consumption to cardiovascular health. For instance, in 2017, the AHA Presidential Advisory said that, “lowering intake of saturated fat and replacing it with unsaturated fats, especially polyunsaturated fats, will lower the incidence of CVD.”
Just 3 months later, the 18-country observational Prospective Rural Urban Epidemiology Study reported the opposite, saying that “total fat and types of fat were not associated with cardiovascular disease, myocardial infarction, or cardiovascular disease mortality.”5
Why are there conflicting results? Take, for example, a study published in the New England Journal of Medicine in 2013, which has since been retracted. PREDIMED was a large, primary prevention, randomized, controlled trial whose participants were at high risk for CVD. The study proclaimed that a Mediterranean diet supplemented with olive oil or nuts significantly reduced the risk of CVD compared with a low-fat dietary group.6
Some reasons exist for controversy related to these findings. First, the intake of UFAs increased in both the olive oil and nut groups but not the low-fat group, which may have influenced clinical outcomes. Second, the intake of saturated fat was not decreased in the olive oil and nut groups, nor was a substitute for saturated fat supplied compared with the low-fat dietary group.5
In the scientific world, hypotheses are looked upon with skepticism until they undergo arduous and repeated experiments. The gold standard in the hierarchy of evidence in the medical field is the randomized, controlled trial, because randomization minimizes confounding variables.5 Ideally, dietary hypotheses are proved by replicated randomized trials. This, however, is often not the case. Clinical trials that evaluate these hypotheses require thousands to tens of thousands of participants randomized to different interventions and followed for years or even decades.
The controversy surrounding the effects of replacing SFAs with PUFAs as a nutritional approach to prevent CVD depends on assumptions about the nature of normal biological functions in human diets.5 It implies that SFAs cause disease and that consumption of PUFAs is healthy and without long-term risks.5 Another topic of controversy is whether these assumptions can be made without long-term clinical trials. Resolving this controversy would require long-term clinical trials, but would the cost, ethical, and methodology challenges be worth it?
Kathleen Kenny, PharmD, RPh, earned her PharmD from the University of Colorado Health Sciences Center in Aurora. She has more than 25 years of experience as a community pharmacist and is a freelance clinical medical writer based in Colorado Springs, Colorado.