The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010?1234
Identifieur interne : 001536 ( Pmc/Curation ); précédent : 001535; suivant : 001537The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010?1234
Auteurs : Arne Astrup ; J Rn Dyerberg ; Peter Elwood ; Kjeld Hermansen ; Frank B. Hu ; Marianne Uhre Jakobsen ; Frans J. Kok ; Ronald M. Krauss ; Jean Michel Lecerf ; Philippe Legrand ; Paul Nestel ; Ulf Risérus ; Tom Sanders ; Andrew Sinclair ; Steen Stender ; Tine Tholstrup ; Walter C. WillettSource :
- The American Journal of Clinical Nutrition [ 0002-9165 ] ; 2011.
Abstract
Current dietary recommendations advise reducing the intake of saturated fatty acids (SFAs) to reduce coronary heart disease (CHD) risk, but recent findings question the role of SFAs. This expert panel reviewed the evidence and reached the following conclusions: the evidence from epidemiologic, clinical, and mechanistic studies is consistent in finding that the risk of CHD is reduced when SFAs are replaced with polyunsaturated fatty acids (PUFAs). In populations who consume a Western diet, the replacement of 1% of energy from SFAs with PUFAs lowers LDL cholesterol and is likely to produce a reduction in CHD incidence of ≥2–3%. No clear benefit of substituting carbohydrates for SFAs has been shown, although there might be a benefit if the carbohydrate is unrefined and has a low glycemic index. Insufficient evidence exists to judge the effect on CHD risk of replacing SFAs with MUFAs. No clear association between SFA intake relative to refined carbohydrates and the risk of insulin resistance and diabetes has been shown. The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. The combination of multiple biomarkers and the use of clinical endpoints could help substantiate the effects on CHD. Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk. Research is needed to clarify the role of SFAs compared with specific forms of carbohydrates in CHD risk and to compare specific foods with appropriate alternatives.
Url:
DOI: 10.3945/ajcn.110.004622
PubMed: 21270379
PubMed Central: 3138219
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<front><div type="abstract" xml:lang="en"><p>Current dietary recommendations advise reducing the intake of saturated fatty acids (SFAs) to reduce coronary heart disease (CHD) risk, but recent findings question the role of SFAs. This expert panel reviewed the evidence and reached the following conclusions: the evidence from epidemiologic, clinical, and mechanistic studies is consistent in finding that the risk of CHD is reduced when SFAs are replaced with polyunsaturated fatty acids (PUFAs). In populations who consume a Western diet, the replacement of 1% of energy from SFAs with PUFAs lowers LDL cholesterol and is likely to produce a reduction in CHD incidence of ≥2–3%. No clear benefit of substituting carbohydrates for SFAs has been shown, although there might be a benefit if the carbohydrate is unrefined and has a low glycemic index. Insufficient evidence exists to judge the effect on CHD risk of replacing SFAs with MUFAs. No clear association between SFA intake relative to refined carbohydrates and the risk of insulin resistance and diabetes has been shown. The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. The combination of multiple biomarkers and the use of clinical endpoints could help substantiate the effects on CHD. Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk. Research is needed to clarify the role of SFAs compared with specific forms of carbohydrates in CHD risk and to compare specific foods with appropriate alternatives.</p>
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<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Am J Clin Nutr</journal-id>
<journal-id journal-id-type="publisher-id">ajcn</journal-id>
<journal-title-group><journal-title>The American Journal of Clinical Nutrition</journal-title>
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<article-id pub-id-type="publisher-id">004622</article-id>
<article-id pub-id-type="doi">10.3945/ajcn.110.004622</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Perspective</subject>
</subj-group>
</article-categories>
<title-group><article-title>The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010?<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="author-notes" rid="fn1"><sup>2</sup>
</xref>
<xref ref-type="author-notes" rid="fn2"><sup>3</sup>
</xref>
<xref ref-type="corresp" rid="cor1"><sup>4</sup>
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<contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Astrup</surname>
<given-names>Arne</given-names>
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<contrib contrib-type="author"><name><surname>Dyerberg</surname>
<given-names>Jørn</given-names>
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<contrib contrib-type="author"><name><surname>Elwood</surname>
<given-names>Peter</given-names>
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<contrib contrib-type="author"><name><surname>Hermansen</surname>
<given-names>Kjeld</given-names>
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</contrib>
<contrib contrib-type="author"><name><surname>Hu</surname>
<given-names>Frank B</given-names>
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<contrib contrib-type="author"><name><surname>Jakobsen</surname>
<given-names>Marianne Uhre</given-names>
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</contrib>
<contrib contrib-type="author"><name><surname>Kok</surname>
<given-names>Frans J</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Krauss</surname>
<given-names>Ronald M</given-names>
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</contrib>
<contrib contrib-type="author"><name><surname>Lecerf</surname>
<given-names>Jean Michel</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>LeGrand</surname>
<given-names>Philippe</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Nestel</surname>
<given-names>Paul</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Risérus</surname>
<given-names>Ulf</given-names>
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<contrib contrib-type="author"><name><surname>Sanders</surname>
<given-names>Tom</given-names>
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<contrib contrib-type="author"><name><surname>Sinclair</surname>
<given-names>Andrew</given-names>
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<contrib contrib-type="author"><name><surname>Stender</surname>
<given-names>Steen</given-names>
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</contrib>
<contrib contrib-type="author"><name><surname>Tholstrup</surname>
<given-names>Tine</given-names>
</name>
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<contrib contrib-type="author"><name><surname>Willett</surname>
<given-names>Walter C</given-names>
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<aff id="aff1"><label>1</label>
From the Department of Human Nutrition, Faculty of Life Sciences, University of Copenhagen, Copenhagen, Denmark (AA, JD, and TT); the Department of Primary Care and Public Health, School of Medicine, Cardiff University, Cardiff, United Kingdom (PE); the Department of Endocrinology and Metabolism, Aarhus University Hospital, Aarhus, Denmark (KH); the Department of Cardiology, Center for Cardiovascular Research, Aalborg Hospital, Aarhus University Hospital, Aalborg, Denmark and the Department of Epidemiology, School of Public Health, Aarhus University, Aarhus, Denmark (MUJ); the Division of Human Nutrition, Wageningen University, Wageningen, Netherlands (FJK); the Children's Hospital, Oakland Research Institute, Oakland, CA (RMK); the Nutrition Department, Institut de Pasteur de Lille, Lille, France (JML); Agrocampus, INRA, Rennes et Anger, France (PL); the Baker IDI Heart & Diabetes Institute, Melbourne, Australia (PN); the Unit for Clinical Nutrition and Metabolism Department of Public Health and Caring Sciences, Faculty of Medicine, Uppsala University, Uppsala, Sweden (UR); the Nutritional Sciences Division, King's College London, London, United Kingdom (TS); the School of Medicine, Deakin University, Victoria, Australia (AS); the Clinical/Biochemical Department, Gentofte Hospital, University of Copenhagen, Copenhagen, Denmark (SS); and the Department of Nutrition, Harvard School of Public Health, Boston, MA (FBH and WCW).</aff>
<author-notes><fn id="fn1" fn-type="financial-disclosure"><label>2</label>
<p>The symposium was held at the Department of Human Nutrition, The Faculty of Life Sciences at The University of Copenhagen, Denmark, 28–29 May 2010, as a closed consensus meeting of invited scientists. The symposium was organized and sponsored by The Nordea Foundation OPUS Research Centre, The Centre for Advanced Food Studies, Denmark; and the program and speakers were selected by the co-chairs: Arne Astrup and Walter Willett. Unrestricted grants were received from The Beef Checkoff (USA), Centre National Interprofessionnel de l'Economie Laitière (CNIEL), The Danish Agriculture & Food Council, Dairy Australia, the Dairy Council for Great Britain, the Dairy Council of California, the Dairy Farmers of Canada, The Global Dairy Platform, Milchindustrie-Verband, the National Dairy Council (USA), and Svensk Mjölk.</p>
</fn>
<fn id="fn2"><label>3</label>
<p>This article reports consensus reached by all of the authors at a 2-d invitation-only symposium organized by AA and WCW and held in Copenhagen, Denmark, in May 2010.</p>
</fn>
<corresp id="cor1"><label>4</label>
Address correspondence to A Astrup, Department of Human Nutrition, Faculty of Life Sciences, University of Copenhagen, Rolighedsvej 30, DK-1958 Frederiksberg, Denmark. E-mail: <email>ast@life.ku.dk</email>
.</corresp>
</author-notes>
<pmc-comment>Fake ppub date generated by PMC from publisher pub-date/@pub-type='epub-ppub' </pmc-comment>
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<volume>93</volume>
<issue>4</issue>
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<lpage>688</lpage>
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<permissions><copyright-statement>© 2011 American Society for Nutrition</copyright-statement>
<copyright-year>2011</copyright-year>
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<abstract><p>Current dietary recommendations advise reducing the intake of saturated fatty acids (SFAs) to reduce coronary heart disease (CHD) risk, but recent findings question the role of SFAs. This expert panel reviewed the evidence and reached the following conclusions: the evidence from epidemiologic, clinical, and mechanistic studies is consistent in finding that the risk of CHD is reduced when SFAs are replaced with polyunsaturated fatty acids (PUFAs). In populations who consume a Western diet, the replacement of 1% of energy from SFAs with PUFAs lowers LDL cholesterol and is likely to produce a reduction in CHD incidence of ≥2–3%. No clear benefit of substituting carbohydrates for SFAs has been shown, although there might be a benefit if the carbohydrate is unrefined and has a low glycemic index. Insufficient evidence exists to judge the effect on CHD risk of replacing SFAs with MUFAs. No clear association between SFA intake relative to refined carbohydrates and the risk of insulin resistance and diabetes has been shown. The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. The combination of multiple biomarkers and the use of clinical endpoints could help substantiate the effects on CHD. Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk. Research is needed to clarify the role of SFAs compared with specific forms of carbohydrates in CHD risk and to compare specific foods with appropriate alternatives.</p>
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