From the Clinical Memory Research Unit (I.G., K.N., A.-M.G., Erik Stomrud, S.P., O.H.), Department of Clinical Sciences Malmö, Lund University, Sweden; Memory Clinic (I.G., A.-M.G., Erik Stomrud, S.P., O.H.), Skåne University Hospital, Malmö, Sweden; Department of Clinical Sciences in Malmö(Emily Sonestedt, E.G.-P., Y.B.), Nutritional Epidemiology, Lund University, Skåne University Hospital, Malmö, Sweden; Department of Acute Internal Medicine and Geriatrics (K.N.), Linköping University, Sweden; and Department of Clinical Sciences Malmö (O.M., P.M.N.), Lund University, Skåne University Hospital, Malmö, Sweden.
Neurology. 2023 Jan 3;100(1):e28-e37. doi: 10.1212/WNL.0000000000201336. Epub 2022 Oct 12.
Dementia cases are expected to triple during the next 30 years, highlighting the importance of finding modifiable risk factors for dementia. The aim of this study was to investigate whether adherence to conventional dietary recommendations or to a modified Mediterranean diet are associated with a subsequent lower risk of developing all-cause dementia, Alzheimer disease (AD), vascular dementia (VaD), or with future accumulation of AD-related β-amyloid (Aβ) pathology.
Baseline examination in the prospective Swedish population-based Malmö Diet and Cancer Study took place in 1991-1996 with a follow-up for incident dementia until 2014. Nondemented individuals born 1923-1950 and living in Malmö were invited to participate. Thirty thousand four hundred forty-six were recruited (41% of all eligible). Twenty-eight thousand twenty-five had dietary data and were included in this study. Dietary habits were assessed with a 7-day food diary, detailed food frequency questionnaire, and 1-hour interview. Main outcomes were incident all-cause dementia, AD, or VaD determined by memory clinic physicians. Secondary outcome was Aβ-accumulation measured using CSF Aβ42 (n = 738). Cox proportional hazard models were used to examine associations between diet and risk of developing dementia (adjusted for demographics, comorbidities, smoking, physical activity, and alcohol).
Sixty-one percent were women, and the mean (SD) age was 58.1 (7.6) years. One thousand nine hundred forty-three (6.9%) were diagnosed with dementia (median follow-up, 19.8 years). Individuals adhering to conventional dietary recommendations did not have lower risk of developing all-cause dementia (hazard ratio [HR] comparing worst with best adherence, 0.93, 95% CI 0.81-1.08), AD (HR 1.03, 0.85-1.23), or VaD (HR 0.93, 0.69-1.26). Neither did adherence to the modified Mediterranean diet lower the risk of developing all-cause dementia (HR 0.93 0.75-1.15), AD (HR 0.90, 0.68-1.19), or VaD (HR 1.00, 0.65-1.55). The results were similar when excluding participants developing dementia within 5 years or those with diabetes. No significant associations were found between diet and abnormal Aβ accumulation, conventional recommendations (OR 1.28, 0.74-2.24) or modified Mediterranean diet (OR 0.85, 0.39-1.84).
In this 20-year follow-up study, neither adherence to conventional dietary recommendations nor to modified Mediterranean diet were significantly associated with subsequent reduced risk for developing all-cause dementia, AD dementia, VaD, or AD pathology.
在未来 30 年内,痴呆症病例预计将增加两倍,这凸显了寻找可改变的痴呆症风险因素的重要性。本研究旨在调查遵循传统饮食建议或改良的地中海饮食是否与随后发生全因痴呆、阿尔茨海默病(AD)、血管性痴呆(VaD)的风险降低或 AD 相关β-淀粉样蛋白(Aβ)病理的累积有关。
前瞻性的瑞典基于人群的马尔默饮食与癌症研究于 1991-1996 年进行基线检查,随访至 2014 年发生痴呆症。邀请 1923-1950 年出生且居住在马尔默的非痴呆个体参加。共招募了 3446 人(合格人数的 41%)。有 28025 人有饮食数据并纳入本研究。饮食习惯通过 7 天饮食日记、详细的食物频率问卷和 1 小时访谈进行评估。主要结局是由记忆诊所医生确定的全因痴呆、AD 或 VaD 发生情况。次要结局是使用 CSF Aβ42 测量的 Aβ 累积(n=738)。使用 Cox 比例风险模型来检验饮食与发展为痴呆症的风险之间的关联(调整了人口统计学、合并症、吸烟、身体活动和酒精)。
61%为女性,平均(SD)年龄为 58.1(7.6)岁。1943 人(6.9%)被诊断为痴呆症(中位随访时间为 19.8 年)。遵循传统饮食建议的人患全因痴呆症的风险没有降低(最差与最佳依从性相比的风险比[HR],0.93,95%CI 0.81-1.08)、AD(HR 1.03,0.85-1.23)或 VaD(HR 0.93,0.69-1.26)。遵循改良的地中海饮食也没有降低患全因痴呆症(HR 0.93,0.75-1.15)、AD(HR 0.90,0.68-1.19)或 VaD(HR 1.00,0.65-1.55)的风险。排除在 5 年内发生痴呆症或患有糖尿病的参与者后,结果相似。饮食与异常 Aβ 累积之间没有显著关联,常规推荐(OR 1.28,0.74-2.24)或改良地中海饮食(OR 0.85,0.39-1.84)也没有显著关联。
在这项为期 20 年的随访研究中,无论是遵循传统饮食建议还是改良的地中海饮食,与随后发生全因痴呆、AD 痴呆、VaD 或 AD 病理的风险降低均无显著关联。