University of Central Florida, Orlando, FL, USA.
Int J Geriatr Psychiatry. 2018 Jan;33(1):66-74. doi: 10.1002/gps.4674. Epub 2017 Feb 9.
Potentially incongruent research literatures suggest three divergent hypotheses about depressive symptomatology: (1) symptoms are recurrent; (2) later-life depression results from high cerebrovascular burden (CVB); and (3) depressive symptoms contribute to comorbidities causing vascular burden. Past vascular depression research assumes that later-life depressive symptoms relate uniquely to high CVB and not to prior, recurrent depression. This study examines these divergent hypotheses.
Data include 5175 participants across 18 years from the Wisconsin Longitudinal Study (mean age at 1993 baseline was 53 years; follow-ups in 2004 and 2011). Depressive symptomatology was measured using the Center for Epidemiological Studies Depression. CVB was operationalized as hypertension, high blood sugar, diabetes, and other heart problems. Hypotheses were examined via a cross-lagged structural equation model and logistic regression.
Model fit was acceptable (root mean square error of approximation (RMSEA) = 0.047; comparative fit index = 0.963). Hypotheses 1 and 2 were supported. Depressive symptomatology at 2004 and 2011 follow-ups was predicted by earlier depressive symptomatology and prior CVB. Hypothesis 3 was partially supported; depressive symptomatology in 2004 predicted subsequent CVB. Logistic regression results were that CVB predicted clinically significant depressive symptoms based on the Center for Epidemiological Studies Depression clinical cutoff.
Cerebrovascular burden in midlife predicts depressive symptomatology in later-life, even after accounting for prior depressive symptomatology, supporting a fundamental assumption of the vascular depression hypothesis. Midlife depressive symptomatology also predicted escalation of CVB in later-life. Results suggest a process model of later-life depressive symptom development that interrelates CVB and depressive symptoms throughout the life span and have clinical implications for the interruption of this process through the integration of primary care and behavioral health specialists. Copyright © 2017 John Wiley & Sons, Ltd.
相互矛盾的研究文献提出了关于抑郁症状的三种不同假说：（1）症状是复发性的；（2）晚年抑郁症是由高脑血管负担（CVB）引起的；（3）抑郁症状导致导致血管负担的合并症。过去的血管性抑郁研究假设，晚年的抑郁症状与高 CVB 有关，而与先前的复发性抑郁无关。本研究检验了这些不同的假说。
数据包括来自威斯康星纵向研究的 18 年 5175 名参与者（1993 年基线时的平均年龄为 53 岁；2004 年和 2011 年进行了随访）。使用流行病学研究抑郁量表测量抑郁症状。CVB 被定义为高血压、高血糖、糖尿病和其他心脏问题。通过交叉滞后结构方程模型和逻辑回归检验假说。
模型拟合良好（近似均方根误差（RMSEA）=0.047；比较拟合指数（CFI）=0.963）。假设 1 和 2 得到支持。2004 年和 2011 年随访时的抑郁症状由早期的抑郁症状和先前的 CVB 预测。假设 3 部分得到支持；2004 年的抑郁症状预测了随后的 CVB。逻辑回归结果表明，根据流行病学研究抑郁量表的临床临界值，CVB 预测了临床上显著的抑郁症状。
中年时期的脑血管负担预测了晚年时期的抑郁症状，即使在考虑到先前的抑郁症状之后，这支持了血管性抑郁假说的一个基本假设。中年时期的抑郁症状也预测了晚年时期 CVB 的升级。结果表明，一种与整个生命周期中 CVB 和抑郁症状相互关联的晚年抑郁症状发展的过程模型，并对通过整合初级保健和行为健康专家来中断这一过程具有临床意义。版权所有©2017 年约翰威立父子公司。
