The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease

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Abstract

Dietary guidelines continue to recommend restricting intake of saturated fats. This recommendation follows largely from the observation that saturated fats can raise levels of total serum cholesterol (TC), thereby putatively increasing the risk of atherosclerotic coronary heart disease (CHD). However, TC is only modestly associated with CHD, and more important than the total level of cholesterol in the blood may be the number and size of low-density lipoprotein (LDL) particles that contain it. As for saturated fats, these fats are a diverse class of compounds; different fats may have different effects on LDL and on broader CHD risk based on the specific saturated fatty acids (SFAs) they contain. Importantly, though, people eat foods, not isolated fatty acids. Some food sources of SFAs may pose no risk for CHD or possibly even be protective. Advice to reduce saturated fat in the diet without regard to nuances about LDL, SFAs, or dietary sources could actually increase people's risk of CHD. When saturated fats are replaced with refined carbohydrates, and specifically with added sugars (like sucrose or high fructose corn syrup), the end result is not favorable for heart health. Such replacement leads to changes in LDL, high-density lipoprotein (HDL), and triglycerides that may increase the risk of CHD. Additionally, diets high in sugar may induce many other abnormalities associated with elevated CHD risk, including elevated levels of glucose, insulin, and uric acid, impaired glucose tolerance, insulin and leptin resistance, non-alcoholic fatty liver disease, and altered platelet function. A diet high in added sugars has been found to cause a 3-fold increased risk of death due to cardiovascular disease, but sugars, like saturated fats, are a diverse class of compounds. The monosaccharide, fructose, and fructose-containing sweeteners (e.g., sucrose) produce greater degrees of metabolic abnormalities than does glucose (either isolated as a monomer, or in chains as starch) and may present greater risk of CHD. This paper reviews the evidence linking saturated fats and sugars to CHD, and concludes that the latter is more of a problem than the former. Dietary guidelines should shift focus away from reducing saturated fat, and from replacing saturated fat with carbohydrates, specifically when these carbohydrates are refined. To reduce the burden of CHD, guidelines should focus particularly on reducing intake of concentrated sugars, specifically the fructose-containing sugars like sucrose and high-fructose corn syrup in the form of ultra-processed foods and beverages.

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.

References (145)

  • D.M. Dreon et al.

    Change in dietary saturated fat intake is correlated with change in mass of large low-density-lipoprotein particles in men

    Am J Clin Nutr

    (1998)
  • S. Mora et al.

    LDL particle subclasses, LDL particle size, and carotid atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA)

    Atherosclerosis

    (2007)
  • O. Stein et al.

    Atheroprotective mechanisms of HDL

    Atherosclerosis

    (1999)
  • H.H. Vorster et al.

    Added sugar intake in South Africa: findings from the Adult Prospective Urban and Rural Epidemiology cohort study

    Am J Clin Nutr

    (2014)
  • M.J. Albrink et al.

    Serum lipids, hypertension and coronary artery disease

    Am J Med

    (1961)
  • L.A. Te Morenga et al.

    Dietary sugars and cardiometabolic risk: systematic review and meta-analyses of randomized controlled trials of the effects on blood pressure and lipids

    Am J Clin Nutr

    (2014)
  • J. Yudkin

    Dietary prevention of atherosclerosis

    Lancet

    (1970)
  • A.H. Hite et al.

    In the face of contradictory evidence: report of the Dietary Guidelines for Americans Committee

    Nutrition

    (2010)
  • S. Reiser et al.

    Isocaloric exchange of dietary starch and sucrose in humans. II. Effect on fasting blood insulin, glucose, and glucagon and on insulin and glucose response to a sucrose load

    Am J Clin Nutr

    (1979)
  • R.H. Lustig

    Fructose: metabolic, hedonic, and societal parallels with ethanol

    J Am Diet Assoc

    (2010)
  • S.P. Bhatt et al.

    Chronic obstructive pulmonary disease and cardiovascular disease

    Transl Res

    (2013)
  • S. Reiser et al.

    Effect of isocaloric exchange of dietary starch and sucrose in humans on the gastric inhibitory polypeptide response to a sucrose load

    Am J Clin Nutr

    (1980)
  • J.J. DiNicolantonio et al.

    Added fructose: a principal driver of type 2 diabetes mellitus and its consequences

    Mayo Clin Proc

    (2015)
  • H. Beck-Nielsen et al.

    Impaired cellular insulin binding and insulin sensitivity induced by high-fructose feeding in normal subjects

    Am J Clin Nutr

    (1980)
  • R.A. Gutman et al.

    Long-term hypertriglyceridemia and glucose intolerance in rats fed chronically an isocaloric sucrose-rich diet

    Metabolism

    (1987)
  • N. Hutter et al.

    Liquid fructose supplementation in LDL-R −/− mice fed a western-type diet enhances lipid burden and atherosclerosis despite identical calorie consumption

    IJC Metab Endocr

    (2015)
  • S. Delbosc et al.

    Involvement of oxidative stress and NADPH oxidase activation in the development of cardiovascular complications in a model of insulin resistance, the fructose-fed rat

    Atherosclerosis

    (2005)
  • J.R. Vasselli et al.

    Dietary components in the development of leptin resistance

    Adv Nutr

    (2013)
  • R. Chhabra et al.

    Association of coronary artery calcification with hepatic steatosis in asymptomatic individuals

    Mayo Clin Proc

    (2013)
  • U. Ravnskov

    The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease

    J Clin Epidemiol

    (1998)
  • P.W. Siri-Tarino et al.

    Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease

    Am J Clin Nutr

    (2010)
  • V.L. Roger et al.

    Heart disease and stroke statistics—2012 update: a report from the American Heart Association

    Circulation

    (2012)
  • W.E. Stehbens

    Anitschkow and the cholesterol over-fed rabbit

    Cardiovasc Pathol

    (1999)
  • C.H. Bailey

    Atheroma and other lesions produced in rabbits by cholesterol feeding

    J Exp Med

    (1916)
  • Scientific Report of the 2015 Dietary Guidelines Advisory Committee. Office of Disease Prevention and Health Promotion

  • Dietary fat and its relation to heart attacks and strokes. Report by the Central Committee for Medical and Community Program of the American Heart Association

    JAMA

    (1961)
  • U. Ravnskov

    Is saturated fat bad?

  • F. Robinson et al.

    Changing from a mixed to self-selected vegetarian diet—influence on blood lipids

    J Hum Nutr Diet

    (2002)
  • R. Clarke et al.

    Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies

    BMJ

    (1997)
  • I.D. Frantz et al.

    Test of effect of lipid lowering by diet on cardiovascular risk. The Minnesota Coronary Survey

    Arteriosclerosis

    (1989)
  • A. Chait et al.

    Rationale of the diet-heart statement of the American Heart Association. Report of the Nutrition Committee

    Circulation

    (1993)
  • K.M. Anderson et al.

    Cholesterol and mortality. 30 years of follow-up from the Framingham study

    JAMA

    (1987)
  • E. Verhoye et al.

    Circulating oxidized low-density lipoprotein: a biomarker of atherosclerosis and cardiovascular risk?

    Clin Chem Lab Med

    (2009)
  • T. Henriksen et al.

    Enhanced macrophage degradation of biologically modified low density lipoprotein

    Arteriosclerosis

    (1983)
  • A. Weidtmann et al.

    Mildly oxidized LDL induces platelet aggregation through activation of phospholipase A2

    Arterioscler Thromb Vasc Biol

    (1995)
  • S.J. Korporaal et al.

    Platelet activation by oxidized low density lipoprotein is mediated by CD36 and scavenger receptor-A

    Arterioscler Thromb Vasc Biol

    (2007)
  • G. Ferretti et al.

    Glycated low density lipoproteins modify platelet properties: a compositional and functional study

    J Clin Endocrinol Metab

    (2002)
  • K. Daub et al.

    Oxidized LDL-activated platelets induce vascular inflammation

    Semin Thromb Hemost

    (2010)
  • M.L. Fernandez

    Rethinking dietary cholesterol

    Curr Opin Clin Nutr Metab Care

    (2012)
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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.

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