Self-reported symptoms of depressed mood, trait anxiety and aggressive behavior in post-pubertal adolescents: Associations with diurnal cortisol profiles
Introduction
Mood and anxiety disorders are among the most common disorders. Some subtypes of these disorders are associated with changes in the activity of the hypothalamus-pituitary-adrenocortical (HPA)-axis activity. It is suggested that the full maturation of the HPA-axis – including the full diurnal cortisol rhythm, which is reached with the attainment of Tanner stage three – may have implications for the heightened risk of psychopathology noted among post-pubertal adolescents (Forbes et al., 2006, Goodyer et al., 2001, Gunnar and Quevedo, 2007). Different cortisol measures have been studied, e.g., changes in cortisol referring to overall hypersecretion over 12 or 24 h, changes in absolute levels of cortisol secretion at different times during the day such as lowered morning cortisol or elevated evening cortisol, and changes in diurnal or circadian cortisol rhythms. It is clear that post-pubertal adolescents have been understudied with respect to cortisol rhythms, a measure that clearly is gaining in importance (Adam, 2006).
In a recent meta-analysis, Miller et al. (2007: 38) concluded that even when a person does not develop a full-blown psychiatric condition, greater emotional distress is associated with flatter diurnal cortisol profiles. Also, to the extent that people report higher levels of distress, they showed greater daily cortisol output and elevated afternoon/evening cortisol, though morning levels may be somewhat lower. A high, flattened diurnal profile has been shown to be indicative of a chronically stressed, hyperactive HPA-axis (Deuschle et al., 1997, McEwen, 2002, McEwen and Wingfield, 2003, Rosmond et al., 1998) and is associated with depression in adult outpatients (den Hartog et al., 2003, Sachar et al., 1970, Young et al., 2006), or adolescent outpatients (Kaufman and Charney, 2001, Forbes et al., 2006). Other dysregulations imply low cortisol levels at awakening which remain constant throughout the day. Such a low, flattened diurnal profile (i.e., lacking of expected strong diurnal rhythm) reflects reduced cortisol output (hypocortisolism) and is seen in adult patients with posttraumatic stress disorders, atypical depression or chronic fatigue syndrome (Gunnar and Quevedo, 2007, Heim et al., 2000, Heim et al., 2004, Miller et al., 2007, Van Praag et al., 2004) and in neglected children (e.g., orphanage-reared children) (see Gunnar and Vazquez, 2001, Gunnar and Quevedo, 2007, Tarullo and Gunnar, 2006).
Intriguing observations are that disturbed anxiety and/or aggression regulation are frequently seen as components of depression. Nearly half of the patients meeting life time criteria for major depression also have met criteria for co-morbid anxiety disorders (e.g., Murphy et al., 2004, Regier et al., 1998). Aggression can be turned inward, manifesting itself as self-denigration or suicidality, or can be directed outward with symptoms such as irritability, short-temperedness, impatience, outburst of anger after only slight provocations (Van Praag et al., 2004). Sudden spells of anger have been observed in approximately 30–40% of both, patients with major depression and patients with dysthemia. Depressed persons with anger attacks have higher anxiety scores in comparison to both, depressed patients without anger attacks and normal control subjects (Painuly et al., 2007). It has been suggested that anxiety and/or aggression co-morbidity may explain some of the differences in HPA-axis functioning among depressed patients (Van Praag et al., 2004). For instance, high cortisol levels are only seen in the subgroup of depressive patients who were also anxious (Kara et al., 2000, Korte, 2001, Young et al., 2004).
The aim of our study is twofold. First, we examine the influences of self-reported symptoms of depressed mood, anxiety and aggression on diurnal cortisol rhythm with univariate (longitudinal) repeated measurements regression in post-pubertal adolescents. Second, we question whether depressed mood, anxiety and aggression each make independent contributions to diurnal cortisol profiles above their shared variance. By doing so we also try to examine whether anxiety disorder co-morbidity might explain some of the differences in HPA-axis among post-pubertal adolescents with depressed mood.
Section snippets
Participants
The current study involved a sample of 68 14- and 15-year olds, participating in the third wave of a prospective follow-up study, that included 86 pregnant mothers and their newborns in the first wave and 72 mother–infant pairs in the second wave, when the child was 8/9 years old (see Van den Bergh et al., 2006). The 58 participants who had complete data for all cortisol measures are included (29 boys and 29 girls, Mage = 15.06 years, SD = 26 years). Most of them had reached Tanner stage four of
Descriptive statistics, correlational and incomplete case analysis
Descriptives for all relevant variables are presented in Table 1. Using the cut-off scores of the CDI, we can tentatively conclude that 14 % (N = 8; 4 females, 4 males) may suffer from a minor depressive episode (score range 13–18), while 9 % (N = 5; 4 females, 1 male) may suffer from a major depressive period (score > 18). Taking into account the range of scores obtained and the fact that the mean and median CDI scores (Timbremont and Braet, 2002) for girls (9.3 and 7 respectively) and boys (8.6
Discussion
We studied the influence of self-reported symptoms of depressed mood, anxiety, and aggressive behavior on diurnal cortisol profiles in 58 post-pubertal adolescents. Univariate RM regressions revealed that, in our sample, depressed mood and trait anxiety were strongly associated with a flattened diurnal cortisol profile. For aggressive behavior, a similar yet much weaker trend was found. Emotional distress is associated with a flattened diurnal cortisol profile. Multivariate RM regressions,
Acknowledgments
We are extremely grateful to the adolescents, parents and teachers who took part in this study. Funding for this study was provided by Grant n° G.0211.03 of the Fund for Scientific Research — Flanders (Belgium), by IUAP Phase V-22, GOA-AMBioRICS, EU projects BIOPATTERN (FP6-2002-IST 508803) and eTUMOUR (FP6-2002-LIFESCIHEALTH 503094) and by grants IMPH/06/GHW and IDO 05/010 EG-FMRI of the Katholieke Universiteit Leuven (K.U.Leuven). None of these organisations had a further role in the study
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