ABSTRACT

This nationally representative study queried effects of community dwelling older adults’ depression and inflammation at baseline on over-time changes in surrogate markers of their cardiometabolic risk. Data were from the 2005–2006 and 2010–2011 waves of the U.S. National Social Life, Health, and Aging Project. Inflammation was indicated by C-reactive protein and depression by the CES-D scale. Cardiometabolic markers included hemoglobin A1c and systolic BP. Lagged dependent variable models were used to examine effects. In none of the models did Wave 1 depression predict residual change in cardiometabolic states (i.e., Wave 2 values net of Wave 1). In contrast, men’s baseline C-reactive protein predicted their Wave 2 hemoglobin A1c (Coeff. = 0.02, p < .05) as well as their systolic BP (Coeff. = 3.22, p < .05). No such effects were found among women. Contrary to a growing clinical literature, depression may not increase cardiometabolic risk among older adults on average. Moderators that may interact with depression to yield such effects in delimited samples remain to be identified. Inflammation, in contrast, does seem linked to increase in physiological risk—but only among men, not women. Clinical research is needed to identify biological factors responsible for this sex difference.

抽象的

这项全国代表性的研究询问了社区居民在基线时的抑郁和炎症对他们心血管代谢风险替代指标随时间变化的影响。数据来自美国国家社会生活，健康与老龄化项目的2005–2006年和2010–2011年浪潮。C反应蛋白指示炎症，CES-D评分指示抑郁。心脏代谢指标包括血红蛋白A1c和收缩压。滞后因变量模型用于检查效果。在这些模型中，没有一个波1抑郁预测心脏代谢状态的残留变化（即，波2值减去波1值）。相比之下，男性的基线C反应蛋白预测其Wave 2血红蛋白A1c（Coeff。= 0.02，p  <.05）和收缩压（Coeff。= 3.22，p  <.05）。在女性中未发现此类影响。与越来越多的临床文献相反，抑郁症可能平均不会增加老年人的心脏代谢风险。可能与抑郁相互作用的主持人在有限的样本中产生这种影响仍有待确定。相比之下，炎症似乎确实与生理风险增加有关，但仅在男性中，而不在女性中。需要进行临床研究来确定造成这种性别差异的生物学因素。