Preadolescents’ Somatic and Cognitive-Affective Depressive Symptoms Are Differentially Related to Cardiac Autonomic Function and Cortisol: The TRAILS Study NIENKE M. BOSCH, MSC,HARRIËTTE RIESE,PHD, ANDREA DIETRICH,PHD, JOHAN ORMEL,PHD, FRANK C. VERHULST, MD, PHD, AND ALBERTINE J. OLDEHINKEL,PHD Objective: To examine in a nonclinical sample of preadolescents the possibility that somatic and cognitive-affective depressive symptoms are differentially related with the autonomic nervous system (ANS) and the hypothalamic-pituitary-adrenal (HPA) axis. Depression is a well-known risk factor for cardiovascular disease and mortality. Dysregulation of the ANS and the HPA axis have been proposed as underlying mechanisms. Several studies suggest that only a subset of the depression symptoms account for associations with cardiovascular prognosis. Methods: Self-reported somatic and cognitive-affective depressive symptoms were examined in relationship to heart rate variability (HRV), spontaneous baroreflex sensitivity (BRS), and the cortisol awakening response (CAR) in 2049 preadolescents (mean age = 11.1 years; 50.7% = girls) from the Tracking Adolescents’ Individual Lives Survey (TRAILS). Results: Physiological measurements were not associated with the overall measure of depressive symptoms. Somatic depressive symptoms were negatively related to HRV and BRS, and positively to the CAR; cognitive-affective depressive symptoms were positively related to HRV and BRS, and negatively to the CAR. Associations with the CAR pertained to boys only. Conclusions: Somatic and cognitive-affective depressive symptoms differ in their association with both cardiac autonomic and HPA axis function in preadolescents. Particularly, somatic depression symptoms may mark cardiac risk. Key words: depressive symptoms, autonomic function, heart rate, baroreflex, cortisol, children. ANS = autonomic nervous system; BP = blood pressure; BRS = baroreflex sensitivity; CAR = cortisol awakening response; CVD = cardiovascular disease; HPA = hypothalamic-pituitary-adrenal; HR = heart rate; HRV = heart rate variability; HRV-LF = heart rate variability in the low-frequency band; HRV-HF = heart rate variability in the high-frequency band; MI = myocardial infarction; SD = standard deviation; YSR = Youth Self-Report. INTRODUCTION D epression has been shown to be associated with worse prognosis and mortality in patients with various cardio- vascular diseases (CVDs) (1–3). Also, without the presence or a prior history of heart disease, depressed individuals are at increased risk of CVD and cardiac death (4). Even subclinical levels of depressive symptoms have been found to be propor- tionally associated with cardiovascular mortality and morbid- ity in both patients with CVD and healthy individuals (4). Alterations of the cardiac autonomic nervous system (ANS) and the hypothalamic-pituitary-adrenal (HPA) axis have been proposed as possible physiological links between depression and cardiovascular prognosis (5,6). Low heart rate variability (HRV) and reduced baroreflex sensitivity (BRS) are not only well-established risk factors for cardiac mortality in patients with CVD (7), but have also been related to depression in individuals with (8,9) and without CVD (10,11). Likewise, elevated cortisol levels have been associated with CVD and increased mortality risk in patients with chronic heart failure (12,13) as well as with depression in individuals with (14) and without (15) CVD, although decreased levels of cortisol have also been reported (13,16). Depression is a heterogeneous disorder, involving a range of cognitive, somatic, and affective symptoms. Several studies suggest that only a subset of the depression symptoms account for the associations with cardiovascular prognosis (17–19). De Jonge et al. (18) showed that, in patients with myocardial infarction (MI), somatic/affective depressive symptoms were associated with a poor cardiovascular prognosis 2.5 years later, whereas cognitive/affective depressive symptoms were not. These findings were recently replicated in a study by Linke et al. (19) in women with suspected myocardial isch- emia. Furthermore, Watkins et al. (20) reported that somatic depressive symptoms in depressed patients with MI were more strongly related to medical comorbidity than nonsomatic (cognitive) depressive symptoms. Barefoot et al. (17), on the other hand, found that only affective and not somatic depres- sive symptoms predicted long-term mortality in a sample of patients hospitalized for coronary angiography. This seeming contradiction might partly be explained by different instru- ments used or item overlap. Barefoot’s affective dimension overlapped considerably with De Jonge’s somatic/affective dimension; that is, both contained sadness, crying, and irrita- bility. In sum, despite differences in design, sample, and From the Interdisciplinary Center for Psychiatric Epidemiology and Grad- uate Schools for Behavioral and Cognitive Neurosciences and for Health Research (N.M.B., H.R., J.O., A.J.O.), University Medical Center Groningen, University of Groningen, Groningen, Netherlands; Unit of Genetic Epidemi- ology and Bioinformatics (H.R.), Department of Epidemiology, University Medical Center Groningen, Groningen, Netherlands; Department of Child- and Adolescent Psychiatry (A.D.), University Medical Center Groningen, Groningen, Netherlands; and Department of Child and Adolescent Psychiatry (F.V., A.J.O.), Erasmus University Medical Center - Sophia Children’s Hos- pital Rotterdam, Rotterdam, Netherlands. Address correspondence and reprint requests to Albertine J. Oldehinkel, Interdisciplinary Center for Psychiatric Epidemiology, University Medical Center Groningen, CC72, P.O. Box 30001, 9700 RB Groningen, Netherlands. E-mail: a.j.oldehinkel@med.umcg.nl Received for publication May 18, 2009; revision received July 21, 2009. This work was supported, in part, by various grants from the Netherlands Organization for Scientific Research NWO (Medical Research Council Pro- gram Grant GB-MW 940-38-011; ZonMW Brainpower Grant 100-001-004; ZonMw Risk Behavior and Dependence Grants 60-60600-98-018 and 60- 60600-97-118; ZonMw Culture and Health Grant 261-98-710; Social Sci- ences Council medium-sized investment Grants GB-MaGW 480-01-006 and GB-MaGW 480-07-001; Social Sciences Council Project Grants GB-MaGW 457-03-018, GB-MaGW 452-04-314, and GB-MaGW 452-06-004; NWO large-sized investment Grant 175.010.2003.005); the Sophia Foundation for Medical Research (Projects 301 and 393); the Dutch Ministry of Justice (WODC); the European Science Foundation (EuroSTRESS Project FP-006); and the participating universities. DOI: 10.1097/PSY.0b013e3181bc756b 944 Psychosomatic Medicine 71:944 –950 (2009) 0033-3174/09/7109-0944 Copyright © 2009 by the American Psychosomatic Society