The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease
Section snippets
Background and history
Atherosclerotic coronary heart disease (CHD) is responsible for one in every six deaths in the United States (US).1 Almost 1 million myocardial infarctions (MIs) occur each year,1 and approximately 15% of patients die as a result of their event.1 CHD is also a leading cause of morbidity throughout the developed world, and a substantial driver of health-care related costs.2
In trying to limit the global burden of CHD, prevention is a key strategy. Historically, dietary approaches to CHD
Saturated fat and CHD risk factors
Although the magnitude of the effect likely varies by specific dietary intake and individual susceptibility,11., 12. it is well-accepted that saturated fats can raise blood levels of total cholesterol (TC).13., 14., 15. Since the majority of blood cholesterol is packaged in low-density lipoproteins (LDL), elevations in TC reflect elevations in LDL.16 LDL is thought to raise the risk of CHD, and LDL is often referred to as “bad cholesterol.”
However, LDL is actually a heterogeneous group of
Sugar and CHD risk factors
Reducing saturated fat or any other component from one's diet almost inevitably means replacement with something else. When carbohydrates (particularly refined carbohydrates like sugar) replace saturated fats, the result can be unfavorable effects on lipid profiles: TC tends to increase,41., 42. HDL tends to fall,13., 43., 44. and triglycerides (TGs)—also associated with CHD45—tend to rise.13., 46., 47.
Consuming moderate amounts of sugar has been shown to increase TC and TGs.48., 49. A diet
Saturated fat and CHD events and mortality
Although some saturated fats may affect some lipid fractions in ways that could theoretically increase the risk of CHD, a large Swedish-population study found no association between fat intake (of any type) and CHD.94 A review of cohort and case–control studies likewise did not demonstrate a clear role of saturated fats in CHD.95 Moreover, meta-analyses show that there is limited and inconclusive evidence for modification of total or saturated fat on CHD,96 or CV morbidity or mortality.97
In
Sugar and CHD events and mortality
A diet high in added sugars promotes insulin resistance56., 65., 75., 112., 113. and diabetes,114., 115., 116., 117. and patients with diabetes have more coronary atherosclerosis than patients without diabetes,118., 119., 120. particularly severe narrowing of the left main coronary artery.121 Diabetes increases the risk of death from MI122., 123. and from CV disease more generally,124 even after controlling for lipids, blood pressure, and other covariates.125
Regardless of diabetes status,
Historical perspective and discussion
It is worth noting that saturated fat and sugar share many common dietary sources today, in an era of ultra-processed foods, but their co-occurrence in the diet is a relatively recent phenomenon over the course of human history.
For most of the roughly 200,000 years that our species has roamed the planet, humans had been hunters and gatherers. Animal-derived foods would have likely contributed at least some calories to the diets of most people through the ages, and some of the fats in those foods
Conclusion
Many lines of evidence implicate added sugars more than saturated fat as etiologic in CHD. We urge dietary guidelines to shift focus away from recommendations to reduce saturated fat and toward recommendations to avoid added sugars. Specifically, recommendations should support the eating of whole foods (e.g. foods from living botanical plants) and the avoidance of ultra-processed foods (i.e., foods from industrial processing plants).
Salient Points
• Dietary guidelines continue to recommend restricting intake of saturated fats. This recommendation is based largely on the observation that saturated fats can raise levels of TC, thereby putatively increasing the risk of CHD. • TC matters less for CHD than how cholesterol is packaged into transport particles. LDL is one class of transport particles, with different implications for CHD depending on particle size and density. Small-dense LDL is more susceptible to oxidation and is pro-atherogenic,
Statement of Conflict of Interest
None of the authors have any conflicts of interests with regard to this publication.
Research by Dr. Lucan reported in this publication was supported by the Eunice Kennedy Shriver National Institute Of Child Health & Human Development of the National Institutes of Health under Award Number K23HD079606. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
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Statement of Conflict of Interest: see page 468.
Authors' contributions: JJD conducted the primary literature review, conceived the paper, and drafted the initial text. SCL and JOK contributed citations, revised arguments, and substantively revised the text. All authors contributed to the writing of the final manuscript.