TY - JOUR
T1 - Pathways linking depression, adiposity, and inflammatory markers in healthy young adults
AU - Miller, Gregory E.
AU - Freedland, Kenneth E.
AU - Carney, Robert M.
AU - Stetler, Cinnamon A.
AU - Banks, William A.
N1 - Funding Information:
This research was supported by a Grant-in-Aid from the American Heart Association, a Young Investigator Award from the National Alliance for Research on Schizophrenia and Depression, a Veterans Administration Merit Review, and the Washington University General Clinical Research Center (MO1 RR00036). We thank Elizabeth Glass and Kathy Wolf for their assistance with this project.
PY - 2003/8
Y1 - 2003/8
N2 - Despite mounting evidence that depression increases risk for cardiovascular morbidity and mortality, little is known about the mechanisms responsible for this association. The current study examined the inter-relationships between depression, adiposity, and inflammatory molecules implicated in the pathogenesis of coronary heart disease. One hundred adults were enrolled. Half were clinically depressed; the others were matched controls with no history of psychiatric illness. All subjects were in excellent health, defined as having no acute infectious disease, chronic medical illness, or prescribed medication regimen. Structural equation modeling yielded support for a model in which depressive symptoms promote weight accumulation, which in turn activates an inflammatory response through two distinct pathways: expanded adipose tissue release of interleukin-6 and leptin-induced upregulation of interleukin-6 release by white blood cells (CFI = .99; NNFI = .99; RMSEA = .05). It did not support a sickness behavior model in which the inflammatory molecules arising from expanded adipose tissue promote depressive symptoms.
AB - Despite mounting evidence that depression increases risk for cardiovascular morbidity and mortality, little is known about the mechanisms responsible for this association. The current study examined the inter-relationships between depression, adiposity, and inflammatory molecules implicated in the pathogenesis of coronary heart disease. One hundred adults were enrolled. Half were clinically depressed; the others were matched controls with no history of psychiatric illness. All subjects were in excellent health, defined as having no acute infectious disease, chronic medical illness, or prescribed medication regimen. Structural equation modeling yielded support for a model in which depressive symptoms promote weight accumulation, which in turn activates an inflammatory response through two distinct pathways: expanded adipose tissue release of interleukin-6 and leptin-induced upregulation of interleukin-6 release by white blood cells (CFI = .99; NNFI = .99; RMSEA = .05). It did not support a sickness behavior model in which the inflammatory molecules arising from expanded adipose tissue promote depressive symptoms.
KW - Coronary disease
KW - Cytokines
KW - Depression
KW - Inflammation
KW - Leptin
KW - Obesity
KW - Psychoneuroimmunology
KW - Sickness behavior
UR - http://www.scopus.com/inward/record.url?scp=0038047054&partnerID=8YFLogxK
U2 - 10.1016/S0889-1591(03)00057-6
DO - 10.1016/S0889-1591(03)00057-6
M3 - Article
C2 - 12831830
AN - SCOPUS:0038047054
SN - 0889-1591
VL - 17
SP - 276
EP - 285
JO - Brain, Behavior, and Immunity
JF - Brain, Behavior, and Immunity
IS - 4
ER -