Elsevier

Journal of Clinical Lipidology

Volume 6, Issue 3, May–June 2012, Pages 216-234
Journal of Clinical Lipidology

Original Article
Fatty acids in cardiovascular health and disease: A comprehensive update

https://doi.org/10.1016/j.jacl.2012.04.077Get rights and content

Abstract

Research dating back to the 1950s reported an association between the consumption of saturated fatty acids (SFAs) and risk of coronary heart disease. Recent epidemiological evidence, however, challenges these findings. It is well accepted that the consumption of SFAs increases low-density lipoprotein cholesterol (LDL-C), whereas carbohydrates, monounsaturated fatty acids (MUFAs), and polyunsaturated fatty acids (PUFAs) do not. High-density lipoprotein (HDL)-C increases with SFA intake. Among individuals who are insulin resistant, a low-fat, high-carbohydrate diet typically has an adverse effect on lipid profiles (in addition to decreasing HDL-C, it also increases triglyceride and LDL particle concentrations). Consequently, a moderate fat diet in which unsaturated fatty acids replace SFAs and carbohydrates are not augmented is advised to lower LDL-C; compared with a low-fat diet, a moderate-fat diet will lower triglycerides and increase HDL-C. Now, there is some new evidence that is questioning the health benefits of even MUFAs and PUFAs. In addition, in a few recent studies investigators have also failed to demonstrate expected cardiovascular benefits of marine-derived omega-3 fatty acids. To clarify the clinical pros and cons of dietary fats, the National Lipid Association held a fatty acid symposium at the 2011 National Lipid Association Scientific Sessions. During these sessions, the science regarding the effects of different fatty acid classes on coronary heart disease risk was reviewed.

Section snippets

University of Miami, Miami, FL, USA

Triglycerides (TG), also known as triacylglycerols, are the primary constituents of vegetable oil and animal fats.1 Glycerol, a polyalcohol, is esterified with one, two, or three fatty acids, resulting in monoglycerides, diglycerides, or TG, respectively. During the intestinal absorption of TG, bile acids emulsify fat to very small fat-containing globules.1 The interaction of lipases with TG results in the formation of monoglycerides and free fatty acids (FFAs). These can then be transported

Harvard School of Public Health, Boston, MA, USA

This presentation provides an overview of the available evidence on the topic of SFA and carbohydrates in relation to CVD risk. Fifteen years ago, this debate would have been considered impossible because it was believed that SFA intake was the primary determinant of the high rates of CVD in Western countries. However, in recent years, that question has been reexamined, or, more accurately, seriously examined for the first time. In truth, there was not very good epidemiological evidence for

Tufts University, Medford, MA, USA

The objectives of this presentation are to address issues related to the temporal association between dietary fat and CVD rates, dietary fat type and CVD outcomes, and the translation of scientific findings to messages for patients and the general public. Since approximately 1970, the incidence of CVD has decreased dramatically. It is of interest to parse what contributed to this decline, ie, more sophisticated medical modalities, or improved risk factors contributed to by changes in lifestyle.

Wake Forest University School of Medicine, Winston-Salem, NC, USA

According to the lipid hypothesis for atherogenesis, apolipoprotein (apo) B-containing lipoproteins enter the artery wall, accumulate, are oxidized, and become ligands for scavenger receptors on macrophages. They are taken up by and accumulate within macrophages, converting them into foam cells. In this way, the process of atherogenesis begins. HDLs are the cholesterol efflux promoters. When an imbalance between influx and efflux occurs, more foam cells form and atherosclerosis progresses. Not

Biofortis-Provident Clinical Research, Addison, IL, USA

The National Cholesterol Education Program Third Adult Treatment Panel introduced the Therapeutic Lifestyle Changes (TLC) diet, which was more restrictive regarding SFA and cholesterol than the previous Step I diet.43 However, total fat intake was liberalized from <30% to up to 35% of calories, with an emphasis on unsaturated fats, primarily from MUFA (up to 20% total calories) and secondarily PUFA (up to 10% total calories). There are several sources of MUFA in the diet, including nuts and

University of Tennessee, Knoxville, TN, USA

LA is the parent compound for all n-6 PUFAs. When consumed, LA can be theoretically converted to and enrich tissues with AA via the rate limiting Δ6-desaturase enzyme. AA subsequently can be converted to bioactive eicosanoids, which have been linked to processes involved in the development of cancer, CVD, and inflammation.

Elevated LDL-C and LDL particle concentrations contribute to the atherosclerotic process by injuring the vascular endothelium resulting in lipid deposition and necrosis. It is

NIH, Bethesda, MD, USA

Are all PUFAs created equal? The main objective of this presentation is to evaluate whether n-6 LA is cardioprotective, on the basis of the best-available evidence from clinical trials that selectively increased LA in place of SFA and trans-fatty acids. Key questions addressed are: (1) Are all PUFAs equivalent? Use of the general term PUFA implies that all PUFAs are a single molecular species with shared metabolic and health effects when, in reality, the situation is more complex; and (2) Is

University of Rochester Medical Center, Rochester, NY, USA

This presentation reviews recent marine-derived n-3 fatty acid clinical trials that evaluated potential benefits for reducing CVD. Also considered are evidence-based dietary guidelines for n-3 fatty acids, as well as the potential safety, and multi-organ effects of EPA and DHA.

The Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto (GISSI) Miocardico Prevenzione Trial randomized ∼11,000 subjects (85% men) soon after they had an MI (within 3 months) to 1 g/d fish oil concentrate,

Conclusion

The National Lipid Association 2011 Fatty Acid Summit included presentations that summarized current controversies in fatty acid science relative to CVD risk. Food is extraordinarily complex; thus, it is unlikely that randomized controlled trials assessing dietary interventions will be able to determine definitively the effects of altering intakes of various fatty acids on CVD risk. To make dietary recommendations, we will have to rely on epidemiologic evidence coupled with controlled clinical

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