Cortisol Response to Social Stress in Parentally Bereaved Youth

Abstract

Background Parental bereavement is associated with increased risk for psychiatric illness and functional impairment in youth. Dysregulated hypothalamic-pituitary-adrenal (HPA) axis functioning may be one pathway through which bereaved children experience increased risk for poor outcomes. However, few studies have prospectively examined the association between parental bereavement and cortisol response while accounting for psychiatric disorders in both youth and their caregivers. Methods One-hundred and eighty-one bereaved and nonbereaved offspring and their caregivers were assessed at multiple time points over a 5-year period after parental death. Offspring participated in an adaptation of the Trier Social Stress Task (TSST), and salivary cortisol samples were collected before and after exposure to social stressors. Mixed models for repeated measures were used to analyze the effects of bereavement status, psychiatric disorder in both offspring and caregiver, and demographic indices on trajectories of cortisol response. Results After controlling for demographic variables and offspring depression, bereaved offspring demonstrated significantly different trajectories of cortisol response compared with nonbereaved offspring, characterized by higher total cortisol output and an absence of cortisol reactivity to acute social stress. Within the bereaved group, offspring of parents who died by sudden natural death demonstrated significant cortisol reactivity to social stress compared with offspring whose parents died by suicide, who demonstrated more blunted trajectory of cortisol response. Conclusions Parentally bereaved youth demonstrate higher cortisol output than nonbereaved youth but are less able to mount an acute response in the face of social stressors.

Blunted HPA axis activity prior to suicide attempt and increased inflammation in attempters

“…Similar results were obtained in first-time attempters and all attempters including those with multiple attempts; and when excluding subjects less than 18 years of age. Previous studies have reported both HPA axis hypo- and hyper- activity in attempters and relatives of people who died by suicide (Dietz et al, 2013; Jokinen et al, 2010; Mann and Currier, 2007; McGirr et al, 2010; McGirr et al, 2011). These mixed findings could be due to methodological variations and difficulties inherent in the assessment of peripheral cortisol, which varies as a function of circadian rhythm and environmental factors.…”

“…Indeed, dysregulation in the hypothalamic-pituitary-adrenal (HPA) axis, which regulates reactions to stress, is associated with 4.5-fold increased risk for suicide (Mann and Currier, 2007). Both HPA axis hypo- and hyper- activity are described in attempters and relatives of people who died by suicide (Dietz et al, 2013; Jokinen et al, 2010; Mann and Currier, 2007; McGirr et al, 2010; McGirr et al, 2011). We previously reported lower cortisol levels in response to an experimental stressor in attempters compared to high-risk suicidal non-attempters and non-suicidal subjects and compared to healthy controls; and low baseline cortisol prior to the stressor in attempters (Keilp et al, 2016; Melhem et al, 2016).…”

Future Directions in the Study of Social Relationships as Regulators of the HPA Axis Across Development

“…As described above, chronic stress can lead to blunted reactivity to acute stressors due to downregulation effects. For instance, parentally bereaved youth do not show the expected increase in cortisol to a laboratory stressor conducted 5 years after the loss of their parent, but they instead present with high and flat levels of cortisol across the session (Dietz et al, 2013). One could be baffled by the fact that diminished reactivity is also what would be expected in a normative context when youth are buffered by a supportive figure; however, this becomes easier to interpret when considering the functional significance of acute cortisol peaks, which help mobilize energy to cope with perceived threats or stressors.…”

Stress, Psychological Resources, and HPA and Inflammatory Reactivity During Late Adolescence

“…However, youth encounter a variety of stressors in their lives. Furthermore, more mundane and less severe stressors occurring in everyday life (e.g., conflict, work deadlines), in addition to other various chronic stressors (e.g., childhood maltreatment, major life events), have been linked to poor health outcomes and to compromised biological functioning (Chiang, Eisenberger, Seeman, & Taylor, 2012; DeLongis, Folkman, & Lazarus, 1988; Dietz et al, 2013; Luecken & Appelhans, 2006; Miller et al, 2011; Repetti et al, 2011; Stawski, Cichy, Piazza, & Almeida, 2013; Stone et al, 1994). Whether psychological resources protect against the health-related effects of these other stressors is not entirely clear.…”