Genetic Contributions to Loneliness and Their Relevance to the Evolutionary Theory of Loneliness

Abstract

Loneliness is a negative and distressing emotional state that arises from a discrepancy between one’s desired and achieved levels of social connectedness. The evolutionary theory of loneliness (ETL) posits that experiencing loneliness is an inherited adaptation that signals that salutary social relations are endangered or damaged and prompts people to reconnect to significant others. The basic tenets of the ETL has led researchers to examine the genetic underpinnings of loneliness. The current review provides an updated overview of genetic studies on loneliness and discusses the importance of genetic research for the ETL. The most recent studies suggest that the many genes that contribute to a small degree to differences in loneliness partially overlap with genes that contribute to neuroticism, but not with depression. In addition, the genetic studies discussed in this review show that genes are unlikely to have a direct effect on loneliness. Instead, environmental factors determine in a dynamic fashion how genes that contribute to loneliness are expressed. Future research on epigenetic processes, such as DNA methylation, can further elucidate the dynamic interplay between genes and the environment and how this interplay contributes to loneliness.

The Stability and Change of Loneliness Across the Life Span: A Meta-Analysis of Longitudinal Studies

“…According to the results of the present meta-analysis, the mean levels of loneliness appear to decrease in childhood but to be rather stable afterward. This finding is especially important, as it has been recently demonstrated that loneliness and neuroticism share a common genetic basis (Abdellaoui et al, 2019; Aitken Schermer & Martin, 2019; for a review, see Spithoven, Cacioppo, Goossens, & Cacioppo, 2019). These findings might indicate that neuroticism reflects the overall propensity of individuals to experience negative affect, whereas loneliness reflects the tendency to experience negative affect particularly in social situations.…”

“…These differences are also mirrored in moderate meta-analytic phenotypic correlations between loneliness and neuroticism in the magnitude of r=.30 (Buecker et al, 2018). Thus, despite their common core, several mechanisms seem to pull the development of loneliness and neuroticism in different directions in the long run (Spithoven et al, 2019).…”

“…However, there are several more indices of stability and change that might be worthwhile to consider for future research such as individual or profile stability and change (Roberts et al, 2008). Third, both genetic and environmental influences contribute to phenotypic loneliness (Boomsma, Willemsen, Dolan, Hawkley, & Cacioppo, 2005; Bartels et al, 2008; Goossens et al, 2015; Spithoven et al, 2019). In explaining the observed patterns of rank-order and mean-level development, we often had to draw on findings of genetic and environmental contributions reported for other personality characteristics (Bleidorn et al, 2009; Briley & Tucker-Drob, 2014 ; Hopwood et al, 2011; Kandler, 2012).…”

Lonely Me, Lonely You: Loneliness and the Longitudinal Course of Relationship Satisfaction

“…In addition, another study using data from four nationally representative samples has shown that between 50 and 60% of inter-individual differences in loneliness can be attributed to stable, trait-like sources . Finally, from a behavior genetic point of view, approximately 40% of the phenotypic variation in loneliness has been found to be accounted for by genotypic variation (for reviews, see Goossens et al 2015;Spithoven et al 2019). Taken together, this line of research suggests that inter-individual differences in loneliness are largely stable over time.…”

Epigenetic Mechanisms in the Neurodevelopmental Theory of Depression

“…The role of specific classes of long noncoding RNAs in resiliency or susceptibility to develop depression with a reciprocal response to antidepressant treatment is underlined [83]. Epigenetic changes in the signalling pathway of glucocorticosteroids (e.g., NR3C1, FKBP5), with regard to serotonergic neurotransmission (e.g., SLC6A4) and in the area of genes encoding neurotrophic factors (e.g., BDNF), seem to be the most promising therapeutic targets for future research [23,84].…”