Abstract：
Hyperhomocysteinemia and cognitive impairment both predict mortality and partly because of dietary associations. We have hypothesized that for, nutritional reasons, homocysteine and cognition may act jointly to determine elder survival. In a Nutrition and Health Survey in Taiwan (1999-2000), some 1412 representative elderly were followed up for mortality up to 10 years. Cognition was assessed by the Short Portable Mental Status Questionnaire. Food and B vitamin intakes with their biomarkers, and plasma homocysteine, were measured at baseline. The possible effects of cognition on homocysteine-associated mortality were ascertained with Cox proportional-hazards models. Homocysteine was higher in those who were older, male, and single, consumed less fish and tea, and with alcohol and smoking. In models adjusted for these variables, when homocysteine exceeded 14.5 μmol/L, mortality was 1.80-fold more than when <9.3 μmol/L (hazard ratio [HR], 1.80; 95% confidence interval [95% CI], 1.20-2.71). P for trend was 0.002 and interactive with sex (P < .002). However, these homocysteine-mortality associations were dependent on cognition (P = .03); adjustment for food intake or nutrient status made little difference. Homocysteine did not predict cognitive impairment (adjusted OR, 1.40; 95% CI = 0.50-3.93). Vitamins B(1), B(2), and B(6) accounted somewhat for cognitive impairment. Cognition predicted mortality, fully adjusted for available covariates and also for homocysteine (HR, 3.66; 95% CI, 1.64-8.20) but interactively with homocysteine. Thus, the B-group vitamin insufficiency and cognitive impairment associations with premature mortality are confirmed. Yet cognition is inter-related with homocysteine in its association with survival in ways not detectably altered by foods or food-derived vitamins.
摘要：
高同型半胱氨酸血症和认知障碍都可以预测死亡率，部分原因是饮食相关。我们假设，营养原因,同型半胱氨酸和认知可能共同决定老年人的生存。在台湾的营养与健康调查(1999-2000)中，约1412名具有代表性的老年人接受了长达10年的死亡率随访.通过简短的便携式精神状态问卷评估认知。食物和B族维生素摄入量及其生物标志物，和血浆同型半胱氨酸，在基线测量。使用Cox比例风险模型确定认知对高半胱氨酸相关死亡率的可能影响。同型半胱氨酸在年龄较大的人群中更高,男性,单身,少吃鱼和茶，酒精和吸烟。在针对这些变量进行调整的模型中，当同型半胱氨酸超过14.5μmol/L时，死亡率是<9.3μmol/L时的1.80倍(危险比[HR]，1.80；95%置信区间[95%CI]，1.20-2.71)。趋势P为0.002，与性别相互作用（P<.002）。然而,这些同型半胱氨酸与死亡率之间的关联依赖于认知(P=.03);对食物摄入或营养状况的调整几乎没有差异.同型半胱氨酸不能预测认知障碍(调整后的OR，1.40；95%CI=0.50-3.93）。维生素B(1),B(2)、B(6)在一定程度上解释了认知障碍。认知预测死亡率，完全调整了可用的协变量和高半胱氨酸(HR，3.66；95%CI，1.64-8.20），但与高半胱氨酸相互作用。因此，B组维生素不足和认知障碍与过早死亡的相关性得到证实.然而，认知与同型半胱氨酸有关，其与生存的关系无法被食物或食物来源的维生素检测到。
