“Saturated fat causes heart disease.” We’ve all heard it – your parents have said so, sitcoms have said so, and your doctor has probably even said so. But, despite it’s often convincing nature, repeatedly saying something does not make it true. Of course now you’re thinking “yes, but we repeat such claims for good reasons: government recommendations, presumably backed by science”. Unfortunately, for a while, most the available evidence was epidemiological, meaning that it involved looking at large scale populations and comparing saturated fat (SFA) intake with cardiovascular disease (CVD) risk. Don’t get me wrong, there is nothing wrong with epidemiological studies per se. They can be valuable tools for looking at trends and patterns. However, epidemiological studies generally do not allow us to differentiate between association and cause. They lack the rigor found in randomized control trials (RCTs) that allows us to infer causality. Given the complexity of nutrition science, there still seems to be a shortage of RCTs looking at the effect of SFA on CVD. The problem with studying nutrition is that when you decide to reduce the intake of a nutrient or food, you have to replace the subsequent shortage with some other nutrient or food. In other words, it would not be unreasonable to want to run a different RCT for each kind of replacement of SFA (e.g. sugar, starch, and all the different kinds of fats.) We’ll further address this issue of replacement in a bit. But first, we’ll look at two recent meta-analyses looking at the relationship between either SFA and CVD or total fat intake and blood lipid levels. Meta-analyses are studies that combine several studies addressing the same scientific question together to identify and overarching trend. Conveniently, one of the two meta-analyses looked at prospective cohort studies (a kind of epidemiological study), while the other looked at RCTs.

The meta-analysis of the epidemiological studies, looking at over 300 000 subjects in total, found that SFA intake was not associated with CVD. The authors concluded that there was no significant evidence for claiming that SFA was associated with CVD.

The meta-analysis of the RCTs focused on overweight and obese subjects. Importantly, it looked at total fat intake, not SFA intake. The authors found that low fat intake decreased LDL cholesterol, the supposed bad cholesterol, and that high fat intake increased HDL cholesterol, the supposed good cholesterol. These findings left the authors with a sort of Catch-22: both the low and high fat diets conferred some kind of benefit to blood lipid levels. Ultimately, the authors concluded that, based on their results, no recommendation could be made for either low or high fat diets for the prevention of CVD.

These two meta-analyses suggest that there is no association between SFA intake and CVD, and, further, that there is no association between total fat intake and blood lipid levels predictive of CVD. Although, as mentioned above, it is important to look at the effect of SFA on CVD in the context of the nutrients that might replace SFA. There seems to be support for the notion that replacement of SFA with polyunsaturated fat is beneficial for CVD. However, replacement of SFA with carbohydrate, specifically refined carbohydrates, may influence blood lipids, insulin function, etc. in such a way as to increase the risk of CVD.

After summarizing two recent meta-analyses, it seems clear that the evidence supporting reductions in SFA intake for cardiovascular health is ambiguous at best. Furthermore, even if there was still reason to recommend SFA intake reductions, it’s substitue nutrient would have to be discussed. Replacing SFA with refined carbohydrates, for instance, is likely to do more harm than good. Of course, taking a leap of faith and consuming as many SFA as humanly possible is not a good idea either. Simply, there does not seem to be a basis for consciously andrestricting SFA.


Schwingshackl, L., & Hoffmann, G. (2013). Comparison of effects of long-term low-fat vs high-fat diets on blood lipid levels in overweight or obese patients: a systematic review and meta-analysis. Journal of the Academy of Nutrition and Dietetics, 113(12), 1640–61. doi:10.1016/j.jand.2013.07.010

Siri-tarino, P. W., Sun, Q., Hu, F. B., & Krauss, R. M. (2010a). Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease 1 – 5. American Journal of Clinical Nutrition, 91, 535–546. doi:10.3945/ajcn.2009.27725.1

Siri-tarino, P. W., Sun, Q., Hu, F. B., & Krauss, R. M. (2010b). Saturated fat , carbohydrate , and cardiovascular disease. American Journal of Clinincal Nutrition, (5), 502–509. doi:10.3945/ajcn.2008.26285.