Ciesielski Timothy H, Tosto Giuseppe, Durodoye Razaq O, Rajabli Farid, Akinyemi Rufus O, Byrd Goldie S, Bush William S, Kunkle Brian W, Reitz Christiane, Vance Jeffery M, Pericak-Vance Margaret A, Haines Jonathan L, Williams Scott M
Department of Population and Quantitative Health Sciences, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Taub Institute for Research on Alzheimer Disease and the Aging Brain, Department of Neurology, Columbia University College of Physicians and Surgeons, New York, NY, USA.
Commun Med (Lond). 2025 Jul 31;5(1):326. doi: 10.1038/s43856-025-01059-3.
Clinical and genetic studies have implicated lipid dysfunction in Alzheimer Disease (AD) pathogenesis. While the etiologic impact of lipid intake on individuals is receiving attention, the role of food systems in shaping community-level incidence remains uncharacterized.
Mean country-level lipid intakes were compared to Age-Standardized Alzheimer-and-other-Dementia Incidence Rates (ASAIR) in 183 countries across all inhabited continents. Free-knot penalized spline regression and multivariable-adjusted linear regression, including a lag between intake and incidence, were used to assess the relationships between five lipid intakes and ASAIR. Validation was conducted using longitudinal within-country changes between 1990 and 2019.
Here we show that omega-6 Polyunsaturated-Fatty-Acid (omega-6) intake exhibits a positive linear relationship with ASAIR (multivariable-adjusted model: β = 2.44; 95%CI: 1.70, 3.19; p = 1.38 × 10). ASAIR also increases with saturated-fat, trans-fat, and dietary-cholesterol up to a threshold. The association between omega6-PUFA and ASAIR is confirmed using longitudinal intake changes. The scale of predicted benefits varies by country but, our results predict a 2 standard deviation decrease (-3.8% as a percent of daily energy intake) in omega-6 intake would reduce ASAIR by 8% in the US. This level of consumption has already been achieved in 20 countries. If our other findings are validated in future work, decreasing all four lipids could potentially yield large ASAIR reductions (in the US: a 35% decrease).
Higher levels of omega-6 consumption associate with increased ASAIR. Thus, decreasing omega-6 consumption on the country-level may have substantial benefits in reducing the burden of dementia.
临床和遗传学研究表明脂质功能障碍与阿尔茨海默病（AD）的发病机制有关。虽然脂质摄入对个体的病因学影响已受到关注，但食物系统在塑造社区层面发病率方面的作用仍未得到明确。
将所有有人居住大陆的183个国家的国家层面平均脂质摄入量与年龄标准化的阿尔茨海默病及其他痴呆症发病率（ASAIR）进行比较。使用自由节点惩罚样条回归和多变量调整线性回归（包括摄入量和发病率之间的滞后）来评估五种脂质摄入量与ASAIR之间的关系。利用1990年至2019年期间国家内部的纵向变化进行验证。
我们在此表明，ω-6多不饱和脂肪酸（ω-6）摄入量与ASAIR呈正线性关系（多变量调整模型：β = 2.44；95%置信区间：1.70，3.19；p = 1.38×10）。ASAIR也随着饱和脂肪、反式脂肪和膳食胆固醇的增加而增加，直至达到一个阈值。使用纵向摄入量变化证实了ω-6多不饱和脂肪酸与ASAIR之间的关联。预测益处的规模因国家而异，但我们的结果预测，在美国，ω-6摄入量降低2个标准差（占每日能量摄入量的-3.8%）将使ASAIR降低8%。20个国家已经达到了这个消费水平。如果我们的其他研究结果在未来的工作中得到验证，降低所有四种脂质可能会大幅降低ASAIR（在美国：降低35%）。
较高水平的ω-6消费与较高的ASAIR相关。因此，在国家层面降低ω-6消费可能对减轻痴呆负担有很大益处。
