Liu Yuxi, Gu Xiao, Li Yanping, Rimm Eric B, Willett Walter C, Stampfer Meir J, Hu Frank B, Wang Dong D
Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, United States; Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, United States.
Department of Nutrition, Harvard T. H. Chan School of Public Health, Boston, MA, United States.
Am J Clin Nutr. 2025 Jan;121(1):141-150. doi: 10.1016/j.ajcnut.2024.11.012. Epub 2024 Nov 16.
The associations between changes in fatty acid intake over time and subsequent mortality are unclear.
The objective of this study was to prospectively examine associations between changes in fatty acid intake (as percentage of total energy) and mortality.
Among 65,179 adults from the Nurses' Health Study and Health Professionals Follow-up Study, free from cardiovascular disease, cancer, and diabetes at baseline in 1994, we documented 20,571 deaths through 2020 (1,334,603 person-years). Diets were assessed every 4 years using validated questionnaires. Hazard ratios (HRs) and 95% confidence intervals (CIs) for mortality risk were estimated from Cox proportional hazards models.
A 5% energy increment in total fat intake was associated with 5% lower all-cause mortality (HR: 0.95; 95% CI: 0.93, 0.96; isocaloric comparison was total carbohydrate). The HRs of all-cause mortality (95% CI) were 0.83 (0.78, 0.89) and 0.91 (0.87, 0.94) for a 5% increment in energy intake from polyunsaturated fatty acid (PUFA) and monounsaturated fatty acid (MUFA), respectively, and was 1.10 (1.04, 1.17) for a 1% increase in energy intake from trans fatty acid (TFA; all P ≤ 0.001). Changes in saturated fatty acid (SFA) were not associated with all-cause mortality. Increases in intakes of linoleic acid, marine n-3 PUFA, and MUFA from plant sources were each significantly associated with lower all-cause mortality. In substitution analyses, replacing 5% energy from SFA with PUFA was associated with 19% lower all-cause mortality (HR: 0.81; 95% CI: 0.75, 0.87), whereas replacing 0.3% of energy from SFA with marine n-3 PUFA was associated with 11% lower all-cause mortality (HR: 0.89; 95% CI: 0.84, 0.93). Isocaloric substitution of SFA by PUFA, particularly marine n-3 PUFA, was associated with lower mortality due to cardiovascular, neurodegenerative, and respiratory diseases.
These findings support replacing SFA with unsaturated fatty acids (especially from plant sources) and eliminating dietary TFA to reduce premature death.
脂肪酸摄入量随时间的变化与随后的死亡率之间的关联尚不清楚。
本研究的目的是前瞻性地研究脂肪酸摄入量（占总能量的百分比）变化与死亡率之间的关联。
在护士健康研究和卫生专业人员随访研究的65179名成年人中，这些人在1994年基线时无心血管疾病、癌症和糖尿病，我们记录了截至2020年的20571例死亡（1334603人年）。每4年使用经过验证的问卷评估饮食情况。根据Cox比例风险模型估计死亡率风险的风险比（HRs）和95%置信区间（CIs）。
总脂肪摄入量增加5%能量与全因死亡率降低5%相关（HR：0.95；95%CI：0.93，0.96；等热量比较为总碳水化合物）。多不饱和脂肪酸（PUFA）和单不饱和脂肪酸（MUFA）能量摄入量增加5%时，全因死亡率的HRs（95%CI）分别为0.83（0.78，0.89）和0.91（0.87，0.94），反式脂肪酸（TFA）能量摄入量增加1%时，HRs为1.10（1.04，1.17）（所有P≤0.001）。饱和脂肪酸（SFA）的变化与全因死亡率无关。亚油酸、海洋n-3多不饱和脂肪酸和植物来源的单不饱和脂肪酸摄入量的增加均与较低的全因死亡率显著相关。在替代分析中，用多不饱和脂肪酸替代5%能量的饱和脂肪酸与全因死亡率降低19%相关（HR：0.81；95%CI：0.75，0.87），而用海洋n-3多不饱和脂肪酸替代0.3%能量的饱和脂肪酸与全因死亡率降低11%相关（HR：0.89；95%CI：0.84，0.93）。用多不饱和脂肪酸，特别是海洋n-3多不饱和脂肪酸等量替代饱和脂肪酸与心血管、神经退行性和呼吸系统疾病导致的较低死亡率相关。
这些发现支持用不饱和脂肪酸（特别是植物来源的）替代饱和脂肪酸并消除膳食反式脂肪酸以减少过早死亡。
