The Neuroendocrinology of Social Isolation
By John T. Cacioppo, Stephanie Cacioppo, John Capitanio, Steve W. Cole. Annual Review of Psychology, 2014
824 citations recorded by the source corpus.
Social isolation has been recognized as a major risk factor for morbidity and mortality in humans for more than a quarter of a century. Although the focus of research has been on objective social roles and health behavior, the brain is the key organ for forming, monitoring, maintaining, repairing, and replacing salutary connections with others. Accordingly, population-based longitudinal research indicates that perceived social isolation (loneliness) is a risk factor for morbidity and mortality independent of objective social isolation and health behavior. Human and animal investigations of neuroendocrine stress mechanisms that may be involved suggest that (a) chronic social isolation increases the activation of the hypothalamic pituitary adrenocortical axis, and (b) these effects are more dependent on the disruption of a social bond between a significant pair than objective isolation per se. The relational factors and neuroendocrine, neurobiological, and genetic mechanisms that may contribute to the association between perceived isolation and mortality are reviewed.
Subfields: Applied Psychology, Behavioral Neuroscience, Social Psychology
View Paper: https://www.semanticscholar.org/paper/bd66a0b2b456b711956cb0cef5d982cd02ac9247
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Applied Psychology
- Ruth Feldman
- Stephanie Cacioppo
- Luc Goossens
- J. Holt‐Lunstad
- Timothy B. Smith
- John T. Cacioppo
- W. Mendes
- Louise C. Hawkley
In Behavioral Neuroscience
- Ruth Feldman
- Stephanie Cacioppo
- J. Holt‐Lunstad
- John T. Cacioppo
- W. Mendes
- George M. Slavich
- E. Epel
- Michael W. Kraus
In Social Psychology
- Stephanie Cacioppo
- Ruth Feldman
- Luc Goossens
- J. Holt‐Lunstad
- Timothy B. Smith
- John T. Cacioppo
- W. Mendes
- B. Etheridge
Citations in the corpus
- Loneliness and Social Isolation as Risk Factors for Mortality (2015, background): “…behavioral, and biological pathways by which social isolation and loneliness lead to poorer health and decreased longevity (for reviews, see Cacioppo, Cacioppo, Capitanio, & Cole, 2015, this issue; Shankar et al., 2011; Thoits, 2011; see also Cacioppo et al., 2015; Hawkley & Cacioppo, 2003, 2010).”
- More than a feeling: A unified view of stress measurement for population science (2018, background): “For example, loneliness predicts earlier mortality (Holt-Lunstad et al., 2015), and is associated with less salutary profiles of cortisol and inflammatory responses to acute stress (Cacioppo et al., 2015; Eisenberger et al., 2017; Hawkley and Cacioppo, 2010).”
- Loneliness: Clinical Import and Interventions (2015, background): “animal (e.g., prairie voles, titi monkeys) is chronically housed either with a preferred partner or alone has shown that isolation has deleterious neurological (see review by S. Cacioppo, Capitanio, & Cacioppo, 2014) and neuroendocrinological effects (see review by J. T. Cacioppo et al., 2015).”
- The gender gap in mental well-being during the Covid-19 outbreak: evidence from the UK (2020, background): “We therefore examine the role of social relationships and loneliness, which have been associated with subjective well-being in a predominantly psychological literature (for a review see e.g. Cacioppo et al. 2015).”
- The Neurobiology of Human Attachments. (2017, positive): “Human attachments promote homeostasis, health, and well-being throughout life: Social attachments enhance health and happiness while social isolation increases stress, impaired health, and death [176].”
- COVID-19 and the cardiovascular system: implications for risk assessment, diagnosis, and treatment options (2020, background): “153 The mechanisms of detrimental effects of social isolation are multiple and are related to the activation of the hypothalamic-pituitary-adrenocortical (HPA) axis, [154] [155] [156] [157] changes in the sympathetic vascular tone, 148, 158, 159 elevated levels of cortisol, 156, 160, 161 and a reduc”