TY - JOUR
T1 - Clinical depression and inflammatory risk markers for coronary heart disease
AU - Miller, Gregory E.
AU - Stetler, Cinnamon A.
AU - Carney, Robert M.
AU - Freedland, Kenneth E.
AU - Banks, William A.
N1 - Funding Information:
This study was supported by a Grant-In-Aid from the American Heart Association, Dallas, Texas and a Veterans Administration Merit Review, St. Louis, Missouri.
PY - 2002/12/15
Y1 - 2002/12/15
N2 - Despite mounting evidence that psychiatric depression heightens risk for cardiac morbidity and mortality, little is known about the mechanisms responsible for this association. The present study examined the relation between depression and the expression of inflammatory risk markers implicated in the pathogenesis of coronary heart disease (CHD). One hundred adults were enrolled (68% women, 48% Caucasian, 48% African-American, mean age 30 ± 2 years). Fifty subjects met the diagnostic criteria for clinical depression; the remaining 50 were demographically 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 regular medication regimen aside from oral contraceptives. The depressed subjects exhibited significantly higher levels of the inflammatory markers C-reactive protein (3.5 ± 0.5 vs 2.5 ± 5 mg/L, p = 0.04) and interleukin-6 (3.0 ± 0.3 vs 1.9 ± 0.2 pg/ml, p = 0.007) compared with control subjects. Mediational analyses aimed at identifying the pathways contributing to this association revealed that neither cigarette smoking nor subclinical infection with cytomegalovirus or Chlamydia pneumoniae had been responsible. However, depressed subjects exhibited greater body mass than control subjects, and analyses were consistent with adiposity accounting for a portion of the relation between clinical depression and increased expression of inflammatory markers. These findings indicate that in otherwise healthy adults, depression is associated with heightened expression of inflammatory markers implicated in the pathogenesis of CHD. Increased body mass appears to be partially, although not completely, responsible for this relation.
AB - Despite mounting evidence that psychiatric depression heightens risk for cardiac morbidity and mortality, little is known about the mechanisms responsible for this association. The present study examined the relation between depression and the expression of inflammatory risk markers implicated in the pathogenesis of coronary heart disease (CHD). One hundred adults were enrolled (68% women, 48% Caucasian, 48% African-American, mean age 30 ± 2 years). Fifty subjects met the diagnostic criteria for clinical depression; the remaining 50 were demographically 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 regular medication regimen aside from oral contraceptives. The depressed subjects exhibited significantly higher levels of the inflammatory markers C-reactive protein (3.5 ± 0.5 vs 2.5 ± 5 mg/L, p = 0.04) and interleukin-6 (3.0 ± 0.3 vs 1.9 ± 0.2 pg/ml, p = 0.007) compared with control subjects. Mediational analyses aimed at identifying the pathways contributing to this association revealed that neither cigarette smoking nor subclinical infection with cytomegalovirus or Chlamydia pneumoniae had been responsible. However, depressed subjects exhibited greater body mass than control subjects, and analyses were consistent with adiposity accounting for a portion of the relation between clinical depression and increased expression of inflammatory markers. These findings indicate that in otherwise healthy adults, depression is associated with heightened expression of inflammatory markers implicated in the pathogenesis of CHD. Increased body mass appears to be partially, although not completely, responsible for this relation.
UR - http://www.scopus.com/inward/record.url?scp=0037114792&partnerID=8YFLogxK
U2 - 10.1016/S0002-9149(02)02863-1
DO - 10.1016/S0002-9149(02)02863-1
M3 - Article
C2 - 12480034
AN - SCOPUS:0037114792
VL - 90
SP - 1279
EP - 1283
JO - American Journal of Cardiology
JF - American Journal of Cardiology
SN - 0002-9149
IS - 12
ER -