Data_Sheet_1_Associations Between Nutritional Deficits and Physical Performance in Community-Dwelling Older Adults.docx

Background: Whether multiple nutritional deficiencies have a synergic effect on mobility loss remains unknown. This study aims to evaluate associations between multi-nutritional deficits and physical performance evolution among community-dwelling older adults.Methods: We included 386 participants from the Multidomain Alzheimer Preventive Trial (MAPT) (75.6 ± 4.5 years) not receiving omega-3 polyunsaturated fatty acid (PUFA) supplementation and who had available data on nutritional deficits. Baseline nutritional deficits were defined as plasma 25 hydroxyvitamin D 14 μmol/L, or erythrocyte omega-3 PUFA index ≤ 4.87% (lower quartile). The Short Physical Performance Battery (SPPB), gait speed, and chair rise time were used to assess physical performance at baseline and after 6, 12, 24, 36, 48, and 60 months. We explored if nutrition-physical performance associations varied according to the presence of low-grade inflammation (LGI) and brain imaging indicators.Results: Within-group comparisons showed that physical function (decreased SPPB and gait speed, increased chair rise time) worsened over time, particularly in participants with ≥2 nutritional deficits; however, no between-group differences were observed when individuals without deficit and those with either 1 or ≥2 deficits were compared. Our exploratory analysis on nutritional deficit-LGI interactions showed that, among people with ≥2 deficits, chair rise time was increased over time in participants with LGI (adjusted mean difference: 3.47; 95% CI: 1.03, 5.91; p = 0.017), compared with individuals with no LGI.Conclusions: Accumulated deficits on vitamin D, homocysteine, and omega-3 PUFA were not associated with physical performance evolution in older adults, but they determined declined chair rise performance in subjects with low-grade inflammation.Clinical Trial Registration: [https://clinicaltrials.gov/ct2/show/NCT00672685], identifier [NCT00672685].

背景：多项营养缺乏是否对运动能力丧失产生协同效应尚不明确。本研究旨在评估多营养缺乏与居住在社区的老年成年人身体机能演变之间的关联。方法：我们纳入了来自多领域阿尔茨海默病预防试验（MAPT）的386名参与者（平均年龄75.6 ± 4.5岁），他们未接受ω-3多不饱和脂肪酸（PUFA）补充，且拥有关于营养缺乏的数据。基线营养缺乏被定义为血浆25-羟基维生素D浓度14 μmol/L，或红细胞ω-3 PUFA指数≤4.87%（下四分位数）。使用短期身体机能电池（SPPB）、步态速度和起坐时间来评估基线以及6、12、24、36、48和60个月的身体机能。我们探讨了营养与身体机能的关联是否因低度炎症（LGI）和脑部影像指标的存在而有所不同。结果：组内比较显示，身体功能（SPPB和步态速度下降，起坐时间增加）随时间恶化，尤其是在具有≥2项营养缺乏的参与者中；然而，当将无缺乏症的个体与具有1项或≥2项缺乏症的个体进行比较时，并未观察到组间差异。我们对营养缺乏与LGI相互作用进行的探索性分析显示，在具有≥2项缺乏症的参与者中，有LGI的个体随时间起坐时间增加（调整后的平均差异：3.47；95%置信区间：1.03，5.91；p = 0.017），与无LGI的个体相比。结论：维生素D、同型半胱氨酸和ω-3 PUFA的累积缺乏与老年成年人的身体机能演变无关联，但它们决定了低度炎症患者的起坐性能下降。临床试验注册：[https://clinicaltrials.gov/ct2/show/NCT00672685]，标识符[NCT00672685]。