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Abstract

Social isolation and social loss are amongst the most stressful experiences in life. Although the individuals affected can cope with the situation and adapt after a certain amount of time, there is nevertheless ample evidence of long-term psychological and physical consequences in certain subgroups. For example, about 10% of mourners develop complicated grief (CG) symptoms after loss, such as intense yearning, preoccupation with thoughts of the deceased, identity disruption, marked sense of disbelief about the death or intense emotional pain. To better understand which subgroups are affected and to take preventive measures, it is important to explore factors and underlying mechanisms that might elevate the chronification risk of psychological and physical health issues following social isolation and social loss. The aim of the present dissertation is to contribute to ongoing research on moderators and mechanisms of long-term adaptation to isolation and loss by using a multifactorial approach. More precisely, 1) I analyse and compare reactions to social isolation and social loss both on a neuroendocrine and a psychological level, and 2) I examine psychological and contextual factors that are promoting vs. hindering adaptive reactions to social isolation and social loss. Paper I aims to test associations between widowhood and temporary separation in romantic relationships on state and trait loneliness as well as cortisol levels and the role of relationship status as moderator during social isolation (COVID-19 lockdown). Paper II systematically reviews neuroendocrine correlates of grief and bereavement and identifies factors that moderate those responses. Finally, Paper III analyses whether various aspects of continuing bonds (CB) to the deceased loved one differentially affect CG and post-traumatic growth. In addition, it examines whether insecure attachment style and features of the loss event are linked to CB. All in all, results reveal divorce and widowhood (permanent separation) as risk factors for trait loneliness during extreme social isolation. More interestingly, loneliness was equally high in those who were not living with their partner (temporary separation) and those who were single. Furthermore, neuroendocrine stress responses were higher in singles compared to individuals who were in a relationship during social isolation. Higher relationship quality additionally predicted lower levels of loneliness in the latter (Paper I). Neuroendocrine stress responses were also found in social loss, e.g., flattened diurnal cortisol slopes and elevated mean cortisol levels, which are indicators of neuroendocrine dysregulation (Paper II). Neuroendocrine responses after social loss were moderated by closeness to the deceased, psychiatric symptoms, time since death, emotional reactions, suddenness of the loss, grief severity, age, and sex. Regarding the role of CB in adaptation to social loss (Paper III), externalized CB, which has been assumed to be higher in unresolved grief, was elevated in individuals who suffered a violent loss, who felt responsible for the death and who had a closer relationship to the deceased. Contrary to our expectations, both internalized and externalized CB were associated with CG and post-traumatic growth. Lastly, insecure attachment style predicted higher levels of CG symptoms. To sum up, results indicate that it is the subjective reaction to social isolation and social loss, as well as features of the person, the relationship, and the loss event itself, that determine the adaptivity of the trajectories. Although social isolation and social loss do not represent the same situation, they both are associated with loneliness and neuroendocrine disruptions. This dissertation contributes particularly to research on psychological and neuroendocrine correlates of social isolation and social loss, while also revealing important future research questions.