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首页> 外文期刊>International journal of geriatric psychiatry >Cerebrovascular burden and depressive symptomatology interrelate over 18?years: support for the vascular depression hypothesis
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Cerebrovascular burden and depressive symptomatology interrelate over 18?years: support for the vascular depression hypothesis

机译:脑血管负担和抑郁症状学相互关联18多年:年份:对血管抑郁假设的支持

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Objective 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. Methods 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. Results 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. Conclusions 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.
机译:目标潜在的不一致研究文献提出了三个关于抑郁症状的发散假设:(1)症状是复发的; (2)后生命抑郁症来自高脑血管负担(CVB); (3)抑郁症状导致血管负担的合并症。过去的血管抑郁研究假定稍后生活抑郁症状均为高CVB而不是先前的复发性抑郁症。本研究审查了这些发散假设。方法数据包括威斯康星州纵向研究(1993年的平均年龄为53岁)的5175年的参与者。使用流行病学研究中心抑郁症测量抑郁症状。 CVB是作为高血压,高血糖,糖尿病和其他心脏问题的。通过交叉滞后的结构方程模型和Logistic回归检查假设。结果模型适合是可接受的(近似的根均方误差(RMSEA)?=?0.047;比较适合指数?=?0.963)。支持假设1和2。 2004年和2011年的抑郁症症术通过早期的抑郁症状和先前的CVB预测了随访。假设3被部分支持; 2004年抑郁症术预测后续CVB。 Logistic回归结果是CVB基于流行病学研究中心预测临床显着的抑郁症状抑郁症临床截止。结论中期脑血管负担在后续生活中预测抑郁症状症状,即使核算抑郁症状学,也支持血管抑郁假设的根本假设。中年抑郁症术还预测了在后续生活中的CVB升级。结果表明,后续抑郁症状发展的过程模型,通过整合初级保健和行为健康专家,在整个寿命中相互关联CVB和抑郁症状,对这一过程中断的临床意义。版权? 2017年John Wiley& SONS,LTD.

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