Saturated fat is the bad boy once again according to a paper recently published online in the Journal of the American College of Cardiology (1).
The authors of the paper, led by Li Yanping from the Department of Nutrition at the Harvard School of Public Health, conclude that unsaturated fatty acids, especially polyunsaturated fatty acids (PUFAs) and/or high-quality carbohydrates can be used to replace saturated fatty acids (SFAs) to reduce the risk of coronary heart disease (CHD).
Although in line with current dietary recommendations, these results contradict a systematic review and meta-analysis published last year by Chowdhury and coworkers which found no significant association between the intake of SFAs and the risk of coronary heart disease (2).
Furthermore, last February, The Scientific Report of the 2015 Dietary Guidelines Advisory Committee (DGAC) in the USA concluded that “while the body of research linking saturated fat intake to the modulation of LDL and other circulating lipoprotein concentrations is significant, this evidence is essentially irrelevant to the question of the relationship between diet and risk for cardiovascular disease (3).”
However, things tend to change rapidly (except the guidelines) in the world of nutrition science. Now, after what appeared to be a successful rehabilitation, saturated fat is back in the gutter.
But a closer look at the Yanping paper raises questions about some more obvious conclusions not addressed by the authors.
The Yanping Study
Yanping and coworkers studied combined data from the large, observational Nurses’ Health (NHS) and Health Professionals Follow-up Studies (HPFS). Approximately 127 thousand individuals free of diabetes, cardiovascular disease, and cancer were followed for 30 years. Diet was assessed by a semiquantitative food frequency questionnaire every four years.
At baseline, those who consumed the highest amount of SFAs were slightly younger, had a higher body mass index, a lower prevalence of physical activity, were more likely to be smokers, and consumed more cholesterol. They also tended to have a higher energy intake from monounsaturated fatty acids (MUFAs) and trans fats and lower energy intake from carbohydrates.
A multivariable adjusted model was used to adjust for known risk factors for coronary heart disease, including body mass index, family history of diabetes and myocardial infarction, menopausal status and hormone therapy, regular use of aspirin, smoking status, physical activity, presence of hypertension and hypercholesterolemia, and percentage of energy from protein and cholesterol.
Higher intakes of PUFAs and carbohydrates from whole grains were significantly associated with a lower risk of CHD. In contrast, carbohydrates from refined starches and added sugars were associated with higher risk of CHD. Intake of SFAs and MUFAs was not significantly associated with the risk of CHD in the multivariate model.
Replacing 5% of energy intake from SFAs with equivalent energy intake from PUFAs, MUFAs or carbohydrates from whole grains was associated with a 25%, 15% and 9% lower risk of CHD respectively. Replacing SFAs with trans fat or carbohydrates from refined starches and added sugars did not significantly affect the risk of CHD.
Interestingly, participants generally replaced calories from SFAs with calories from low-quality carbohydrates rather than calories from PUFAs or high-quality carbohydrates.
The authors conclude that their findings “provide epidemiological evidence of the current dietary guidelines, which recommend both replacing saturated fatty acids with monounsaturated and polyunsaturated fatty acids and replacing refined grains with whole grains.
They claim that consuming less SFAs will lower the risk of coronary heart disease as long as they are replaced with PUFAs or high-quality carbohydrates such as whole grains but not if they are replaced with trans fats or low-quality carbohydrates such as white bread, white rice, or potatoes.
A Closer Look at the Data
The study participants were divided into quintile categories (five groups of equal size), based on their nutritional intakes. So, for each macronutrient, there were five groups. If we take SFAs for example, the lowest quartile is the group (20% of the study population) with the lowest intake of SFAs, and the highest quartile is the group (20% of the study population) with the highest intake of SFAs.
I’ve created the table below to show the number of CHD cases (sum of NHS and HPFS data) for each of the macronutrients in the groups with the highest and lowest intakes respectively. The numbers were extracted from data presented in Table 2 in the Yanping paper.
There were 16% more cases of CHD in the group with the lowest fat intake (ca. 26% of calories) compared with the group with the highest intake (ca. 41% of calories).
Similarly, there were 12% more cases of CHD in the group with the lowest intake (ca. 9% of calories) of SFAs compared to the group with the highest intake (ca. 15% of calories).
Remember that, although slightly younger, the group who consumed most SFAs had a higher body mass index, a lower prevalence of physical activity, were more likely to be smokers, and consumed more cholesterol.
The group with the highest (ca. 56% of calories) carbohydrate consumption had 25% more cases of CHD than the group with the lowest (ca 37% of calories) carbohydrate consumption.
These numbers are not dealt with by the authors of the paper.
Saturated Fat – The Bigger Picture
Surely the study by Yanping and coworkers will encourage authors of dietary guidelines to stick with their previous recommendations highlighting restriction of SFAs and that they should be replaced with PUFAs and high-quality carbohydrates.
However, it is important to understand that, due to the study’s observational nature, it cannot prove causality. Despite the use of complex statistical methods, it is difficult to rule out confounding factors that may affect the results.
Furthermore, there are many types of SFAs with different metabolic effects and their association with CHD varies. For example, while palmitic acid appears to be associated with adverse metabolic effects, other SFAs may be associated with metabolic benefits (4).
Dietary SFAs are derived from many different foods, and these have many other ingredients and characteristics that modify their health effects. Therefore judging the health effects of foods entirely from the amount of SFAs may be dreadfully misleading.
When looking more closely at the data it appears that individuals with the highest intake of dietary fats have a lower risk of CHD than those with the lowest fat consumption.
Furthermore, those with the highest carbohydrate intake appear to have a higher risk of CHD than those with the lowest carbohydrate consumption.
Despite my deep respect for the use of statistical methods to adjust for confounding factors, I find it hard to see how statistical acrobatics might reverse this picture.
So, the numbers appear to suggest that; less fats-more heart disease, more fats-less heart disease and more carbs-more heart disease, less carbs-less heart disease. Yes, I know; correlation does not prove causation but…
I suspect the Yanping study may convince many of us that choosing PUFAs rather than SFAs and choosing whole grains rather than starches and added sugar is preferable. But what’s most important about this paper are the questions raised but regrettably left unanswered by the authors.
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