Loneliness in schizophrenia: Just loneliness

Abstract

Loneliness is reported by the majority of people with schizophrenia (∼80%), yet the cognitive and neural mechanisms underlying loneliness in this population are incompletely understood. Similar to the general population, loneliness in schizophrenia is associated with cognitive biases toward mistrusting others, as well as structural barriers to social activity. In addition, some evidence suggests that predisposing genetic and environmental factors, as well as some of the neural changes and the poor cardiometabolic health linked with the illness, are associated with loneliness in schizophrenia. However, much evidence supports a transdiagnostic model of the causes and consequences of loneliness, with similar factors playing a role in loneliness in schizophrenia and the general population. Currently there are no validated treatments targeting loneliness associated with schizophrenia, although interventions focusing on cognitive bias modification, positive psychology, mindfulness, or interpersonal synchrony have shown promise. Taken together, the current state of the field suggests that future research on schizophrenia should include measurements of social isolation and loneliness. Overall, there is a need for novel intervention approaches that can interrupt the cycle of mutually reinforcing neurocognitive biases and environmental conditions linked with loneliness in schizophrenia and other populations.

Keywords: cardiovascular disease; default network; hippocampus; isolation; loneliness; mistrust; paranoia; psychosis; schizophrenia; social homeostasis.

FIGURE 1

Contributors and correlates of loneliness in schizophrenia. Potential contributors to loneliness (purple box) are listed in white boxes and correlates or consequences in red boxes (pink indicates that the direction of effects is likely bidirectional). See Lim et al., for a related model. HPA, hypothalamic–pituitary–adrenal; SI/L, social isolation/loneliness.

FIGURE 2

A schematic of the social homeostasis model and factors that may contribute to expected and actual (perceived) levels of social connection in people with schizophrenia and other populations. The social homeostasis model proposes that discrepancies between expected versus perceived levels of social connection are detected by the brain, which subsequently generates responses aiming to reduce such discrepancies. The hippocampus, other closely connected regions of the default network, and brain regions known to be involved in prediction error signaling (i.e., in identifying these discrepancies), such as the midbrain, striatum, and prefrontal cortex, may be involved in these comparator processes. Detected discrepancies (expected > actual levels of social connection) are thought to trigger a cascade of behavioral and systemic physiological responses and the subjective feeling of loneliness. Successful and unsuccessful corrections may each lead to additional responses of the brain (e.g., reward signals and persistent stress responses, respectively). Various factors that may influence the brain's calculation (i.e., the perception) of the actual and expected levels of social connection are listed within the orange circles. Actual levels of social connection can reflect the quantitative amount of social contact or activity, as well as the quality of those relationships and the degree of intimacy or attunement with others; cognitive biases that lead to greater mistrust and assumptions about the negative intentions of others can reduce the perceived level of social connection (independent of the amount of social activity or number of social contacts). The expected level of social connection may reflect genetic and related personality or temperament factors (e.g., introversion, behavioral inhibition), as well as positive and negative early and/or current experiences within the social environment, such as experiences of childhood social adversity (e.g., abuse, bullying, exclusion), discrimination, or social fragmentation within one's local environment.