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The developmental course of loneliness in adolescence: Implications for mental health, educational attainment, and psychosocial functioning

Published online by Cambridge University Press:  03 February 2022

Timothy Matthews
Affiliation:
Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK
Pamela Qualter
Affiliation:
Manchester Institute of Education, University of Manchester, Manchester, UK
Bridget T. Bryan
Affiliation:
Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK
Avshalom Caspi
Affiliation:
Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK Departments of Psychology and Neuroscience, Psychiatry and Behavioral Sciences, and Institute for Genome Sciences and Policy, Duke University, Durham, NC, USA
Andrea Danese
Affiliation:
Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK National and Specialist CAMHS Trauma and Anxiety Clinic, South London and Maudsley NHS Foundation Trust, London, UK
Terrie E. Moffitt
Affiliation:
Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK Departments of Psychology and Neuroscience, Psychiatry and Behavioral Sciences, and Institute for Genome Sciences and Policy, Duke University, Durham, NC, USA
Candice L. Odgers
Affiliation:
Sanford School of Public Policy, Duke University and Department of Psychology and Social Behavior, University of California, Irvine, CA, USA
Lily Strange
Affiliation:
Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK
Louise Arseneault*
Affiliation:
Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK
*
Corresponding author: Louise Arseneault, email: Louise.Arseneault@kcl.ac.uk
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Abstract

The present study examined patterns of stability and change in loneliness across adolescence. Data were drawn from the Environmental Risk (E-Risk) Longitudinal Twin Study, a UK population-representative cohort of 2,232 individuals born in 1994 and 1995. Loneliness was assessed when participants were aged 12 and 18. Loneliness showed modest stability across these ages (r = .25). Behavioral genetic modeling indicated that stability in loneliness was explained largely by genetic influences (66%), while change was explained by nonshared environmental effects (58%). Individuals who reported loneliness at both ages were broadly similar to individuals who only reported it at age 18, with both groups at elevated risk of mental health problems, physical health risk behaviors, and education and employment difficulties. Individuals who were lonely only at age 12 generally fared better; however, they were still more likely to finish school with lower qualifications. Positive family influences in childhood predicted reduced risk of loneliness at age 12, while negative peer experiences increased the risk. Together, the findings show that while early adolescent loneliness does not appear to exert a cumulative burden when it persists, it is nonetheless a risk for a range of concomitant impairments, some of which can endure.

Information

Type
Regular Article
Creative Commons
Creative Common License - CCCreative Common License - BY
This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright
© The Author(s), 2022. Published by Cambridge University Press
Figure 0

Figure 1. Bivariate Cholesky decomposition. Due to the temporal ordering of the variables, genetic and environmental effects on age 12 loneliness are also allowed to explain variance in age 18 loneliness, but not vice versa. Paths a11, c11, and e11 reflect the genetic and environmental effects specific to loneliness at age 12. Paths a21, c21, and e21 reflect genetic effects on age 12 loneliness that are also shared by age 18 loneliness. Paths a22, c22, and e22 reflect genetic and environmental effects unique to age 18 loneliness.

Figure 1

Figure 2. Bivariate AE model of loneliness at age 12 and age 18. Path estimates reflect the proportion of variance explained by the A and E factors. The contribution of A to stability in loneliness is calculated as the product of paths a11 and a21, divided by the phenotypic correlation: (√.25 * √.11) / .25 = 66%. Similarly, for E: (√.75 * √.01) / .25 = 34%. The contribution of genetic factors to change in loneliness is calculated as path a22 divided by the sum of paths a22 and e22: √.30 / (√.30 + √.58) = 42%. Similarly, for E: √.58 / (√.30 + √.58) = 58%.

Figure 2

Table 1. Associations between loneliness group membership and age-18 outcomes

Figure 3

Table 2. Pairwise comparisons between loneliness groups for age-18 outcomes

Figure 4

Table 3. Childhood predictors of loneliness group membership in adolescence

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