Praagman Jaike, de Jonge Ester A L, Kiefte-de Jong Jessica C, Beulens Joline W J, Sluijs Ivonne, Schoufour Josje D, Hofman Albert, van der Schouw Yvonne T, Franco Oscar H
From the Department of Epidemiology, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands (J.P., J.W.J.B., I.S., Y.T.v.d.S.); Department of Epidemiology (E.A.L.d.J., J.C.K.-d.J., J.D.S., A.H., O.H.F.) and Department of Internal Medicine (E.A.L.d.J.), Erasmus Medical Center, Rotterdam, The Netherlands; Department of Global Public Health, Leiden University College, The Hague, The Netherlands (J.C.K.-d.J.); Department of Epidemiology and Biostatistics, EMGO Institute for Health and Care Research, VU University Medical Center, Amsterdam, The Netherlands (J.W.J.B.); and Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA (A.H.).
Arterioscler Thromb Vasc Biol. 2016 Sep;36(9):2011-8. doi: 10.1161/ATVBAHA.116.307578. Epub 2016 Jul 14.
We assessed whether the association between dietary saturated fatty acids (SFA) and incident coronary heart disease (CHD) depends on the food source, the carbon chain length of SFA, and the substituting macronutrient.
From the Rotterdam Study, 4722 men and women (≥55 years) were included. Baseline (1990-1993) SFA intake was assessed using a validated food frequency questionnaire. CHD (nonfatal myocardial infarction and fatal CHD) was ascertained by medical records. Using multivariable Cox regression analysis, we calculated CHD risks for higher intakes of total SFA, SFA from specific food sources, SFA differing in carbon chain length, and substituting other macronutrients instead of SFA. During a median follow-up of 16.3 years, 659 CHD events occurred. Total SFA intake was not associated with CHD risk (hazard ratio [HR] per 5 en%, 1.13; 95% confidence interval, 0.94-1.22), and neither was SFA from specific food sources. A higher CHD risk was observed for palmitic acid (16:0) intake (HRSD, 1.26; 95% confidence interval, 1.05-1.15) but not for SFA with other chain lengths. Except for a higher CHD risk for substitution of SFA with animal protein (HR5en%, 1.24; 95% confidence interval, 1.01-1.51), substitution with other macronutrients was not associated with CHD.
In this Dutch population, we observed that a higher intake of palmitic acid, which accounts for ≈50% of the total SFA intake, was associated with a higher CHD risk, as was substitution of total SFA with animal protein. Nevertheless, we found no association between total SFA intake and CHD risk, which did not differ by food source.
我们评估了膳食饱和脂肪酸（SFA）与冠心病（CHD）发病之间的关联是否取决于食物来源、SFA的碳链长度以及替代的常量营养素。
纳入了鹿特丹研究中的4722名男性和女性（≥55岁）。使用经过验证的食物频率问卷评估基线（1990 - 1993年）SFA摄入量。通过医疗记录确定冠心病（非致死性心肌梗死和致死性CHD）。使用多变量Cox回归分析，我们计算了总SFA摄入量增加、特定食物来源的SFA、碳链长度不同的SFA以及用其他常量营养素替代SFA时的冠心病风险。在中位随访16.3年期间，发生了659例冠心病事件。总SFA摄入量与冠心病风险无关（每5个能量百分比的风险比[HR]为1.13；95%置信区间为0.94 - 1.22），特定食物来源的SFA也是如此。棕榈酸（16:0）摄入量与较高的冠心病风险相关（HRSD为1.26；95%置信区间为1.05 - 1.15），但其他碳链长度的SFA则不然。除了用动物蛋白替代SFA会增加冠心病风险（每5个能量百分比的HR为1.24；95%置信区间为1.01 - 1.51）外，用其他常量营养素替代与冠心病无关。
在这个荷兰人群中，我们观察到，占总SFA摄入量约50%的棕榈酸摄入量增加与较高的冠心病风险相关，用动物蛋白替代总SFA也是如此。然而，我们发现总SFA摄入量与冠心病风险之间没有关联，且冠心病风险在不同食物来源之间并无差异。
