Bereavement is among life’s most stressful events, and a minority of mourners develop prolonged and disabling grief. Biological markers have been proposed as signals of this risk, but no systematic review has examined them across bereaved family members or asked how well bereaved parents (parents who have lost a child) are represented. We systematically reviewed observational studies linking a cortisol/HPA-axis, inflammatory/immune, or cardiovascular/autonomic biomarker to a validated measure of coping or grief in bereaved family members of any age or relationship to the deceased (PROSPERO CRD420261446539). Five databases were searched, with citation searching of a related review. Eighteen studies met inclusion criteria across the three domains. More severe grief was linked to blunted or flatter diurnal cortisol in three of five cortisol studies. Bereavement and greater grief were linked to raised inflammatory markers (IL-6, IL-1RA, and related cytokines), although five of seven inflammatory studies appear to come from one research programme, and one study found divergent Type I interferon gene transcription in complicated relative to uncomplicated grief. Cardiovascular and autonomic findings were mixed and depended on moderators such as coping style and childhood adversity. Some cortisol associations weakened with time since loss, so they may not be stable markers of grief severity. Only one participant across all 18 studies was an identifiable bereaved parent. Biological markers show domain-specific associations with grief, but the evidence is exploratory, and bereaved parents are largely absent from it. They should be a priority for future prospective work.
Background Borderline personality disorder (BPD) is a complex disorder associated with severe interpersonal instability and common relationship problems. Oxytocin has emerged as a candidate neuropeptide, with cross-sectional studies showing reduced levels in individuals with BPD. Longitudinal data – particularly in adolescents – remain scarce, leaving unresolved whether changes in oxytocin reflect treatment effects, developmental processes, or reciprocal influences with symptom trajectories. The present study examines the longitudinal associations of oxytocin and the number of fulfilled criteria for BPD diagnosis in adolescents. Methods We examined plasma oxytocin in adolescents who attended a specialized early intervention clinic for BPD. Individuals were assessed at baseline (n = 239) and at one-year follow-up (n = 84). We tested for cross-lagged associations of plasma oxytocin and the number of fulfilled criteria for BPD diagnosis using structural equation modelling (SEM). Age, sex, estradiol levels, and scores of the Symptom Checklist were included as covariates. Results SEM showed a significant negative cross-lagged effect of oxytocin levels at baseline on BPD criteria at one-year follow-up, but no significant effect of BPD criteria on subsequent oxytocin levels. Conclusions The exploratory findings suggest that oxytocin may represent a potential biological correlate of future BPD symptom trajectories. A better understanding of the neurobiological processes underlying BPD may inform future treatment development. However, given the exploratory nature and methodological limitations of the present study, any clinical implication including the potential exploration of oxytocin-based lifestyle interventions remain preliminary and require replication before they can be translated into practice.
