Cerebrovascular burden and depressive symptomatology interrelate over 18 years: support for the vascular depression hypothesis.
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.
University of Central Florida, Orlando, FL, USA.
Rosanna
http://orcid.org/0000-0002-7871-8085
R
Scott
University of Central Florida, Orlando, FL, USA.
Daniel
D
Paulson
D000328:Adult; D002318:Cardiovascular Diseases / Q000150:complications; D002561:Cerebrovascular Disorders / Q000150:complications*; D015897:Comorbidity; D003866:Depressive Disorder / Q000209:etiology*; D005260:Female; D044882:Glucose Metabolism Disorders / Q000150:complications; D006801:Humans; D006973:Hypertension / Q000150:complications; D016015:Logistic Models; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D014922:Wisconsin
comorbid; development; life span; mood; psychopathology