Dataset Information

Tracing the origins of midlife despair: association of psychopathology during adolescence with a syndrome of despair-related maladies at midlife.

ABSTRACT:

Background

Midlife adults are experiencing a crisis of deaths of despair (i.e. deaths from suicide, drug overdose, and alcohol-related liver disease). We tested the hypothesis that a syndrome of despair-related maladies at midlife is preceded by psychopathology during adolescence.

Methods

Participants are members of a representative cohort of 1037 individuals born in Dunedin, New Zealand in 1972-73 and followed to age 45 years, with 94% retention. Adolescent mental disorders were assessed in three diagnostic assessments at ages 11, 13, and 15 years. Indicators of despair-related maladies across four domains - suicidality, substance misuse, sleep problems, and pain - were assessed at age 45 using multi-modal measures including self-report, informant-report, and national register data.

Results

We identified and validated a syndrome of despair-related maladies at midlife involving suicidality, substance misuse, sleep problems, and pain. Adults who exhibited a more severe syndrome of despair-related maladies at midlife tended to have had early-onset emotional and behavioral disorders [β = 0.23, 95% CI (0.16-0.30), p < 0.001], even after adjusting for sex, childhood SES, and childhood IQ. A more pronounced midlife despair syndrome was observed among adults who, as adolescents, were diagnosed with a greater number of mental disorders [β = 0.26, 95% CI (0.19-0.33), p < 0.001]. Tests of diagnostic specificity revealed that associations generalized across different adolescent mental disorders.

Conclusions

Midlife adults who exhibited a more severe syndrome of despair-related maladies tended to have had psychopathology as adolescents. Prevention and treatment of adolescent psychopathology may mitigate despair-related maladies at midlife and ultimately reduce deaths of despair.

SUBMITTER: Brennan GM

PROVIDER: S-EPMC10636241 | biostudies-literature | 2023 Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Tracing the origins of midlife despair: association of psychopathology during adolescence with a syndrome of despair-related maladies at midlife.

Brennan Grace M GM Moffitt Terrie E TE Ambler Antony A Harrington HonaLee H Hogan Sean S Houts Renate M RM Mani Ramakrishnan R Poulton Richie R Ramrakha Sandhya S Caspi Avshalom A

Psychological medicine 20230510 16

<h4>Background</h4>Midlife adults are experiencing a crisis of deaths of despair (i.e. deaths from suicide, drug overdose, and alcohol-related liver disease). We tested the hypothesis that a syndrome of despair-related maladies at midlife is preceded by psychopathology during adolescence.<h4>Methods</h4>Participants are members of a representative cohort of 1037 individuals born in Dunedin, New Zealand in 1972-73 and followed to age 45 years, with 94% retention. Adolescent mental disorders were ...[more]

PMID: 37161676

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Project description:ImportanceIndividuals with mental disorders are at an elevated risk of developing chronic age-related physical diseases. However, it is not clear whether psychopathology is also associated with processes of accelerated aging that precede the onset of age-related disease.ObjectiveTo test the hypothesis that a history of psychopathology is associated with indicators of accelerated aging at midlife.Design, setting, and participantsThis prospective cohort study was based on the Dunedin Multidisciplinary Health and Development Study, a population-representative birth cohort of 1037 individuals born between April 1, 1972, and March 31, 1973, in Dunedin, New Zealand. Members were followed up to age 45 years (until April 2019). Data were analyzed from January 6 to December 7, 2020.ExposuresMental disorders were assessed in 6 diagnostic assessments from ages 18 to 45 years and transformed through confirmatory factor analysis into continuous measures of general psychopathology (p-factor) and dimensions of internalizing, externalizing, and thought disorders (all standardized to a mean [SD] of 100 [15]).Main outcomes and measuresSigns of aging (biological pace of aging; declines in sensory, motor, and cognitive functioning; and facial age) were assessed up to age 45 years using previously validated measures including biomarkers, clinical tests, and self-reports.ResultsOf the original 1037 cohort participants, 997 were still alive at age 45 years, of whom 938 (94%) were assessed (474 men [50.5%]). Participants who had experienced more psychopathology exhibited a faster pace of biological aging (β, 0.27; 95% CI, 0.21-0.33; P < .01); experienced more difficulties with hearing (β, 0.18; 95% CI, 0.12-0.24; P < .01), vision (β, 0.08; 95% CI, 0.01-0.14; P < .05), balance (β, 0.20; 95% CI, 0.14-0.26; P < .01), and motor functioning (β, 0.19; 95% CI, 0.12-0.25; P < .01); experienced more cognitive difficulties (β, 0.24; 95% CI, 0.18-0.31; P < .01); and were rated as looking older (β, 0.20; 95% CI, 0.14-0.26; P < .01). Associations persisted after controlling for sex, childhood health indicators, maltreatment, and socioeconomic status and after taking into account being overweight, smoking, use of antipsychotic medication, and the presence of physical disease. Tests of diagnostic specificity revealed that associations were generalizable across externalizing, internalizing, and thought disorders.Conclusions and relevanceIn this cohort study, a history of psychopathology was associated with accelerated aging at midlife, years before the typical onset of age-related diseases. This link is not specific to any particular disorder family but generalizes across disorders. Prevention of psychopathology and monitoring of individuals with mental disorders for signs of accelerated aging may have the potential to reduce health inequalities and extend healthy lives.

Project description:ImportanceBiological aging is a distinct construct from health; however, people who age quickly are more likely to experience poor health. Identifying pediatric health conditions associated with accelerated aging could help develop treatment approaches to slow midlife aging and prevent poor health in later life.ObjectiveTo examine the association between 4 treatable health conditions in adolescence and accelerated aging at midlife.Design, setting, and participantsThis cohort study analyzed data from participants in the Dunedin Study, a longitudinal investigation of health and behavior among a birth cohort born between April 1, 1972, and March 31, 1973, in Dunedin, New Zealand, and followed up until age 45 years. Participants underwent an assessment at age 45 years and had data for at least 1 adolescent health condition (asthma, smoking, obesity, and psychological disorders) and outcome measure (pace of aging, gait speed, brain age, and facial age). Data analysis was performed from February 11 to September 27, 2021.ExposuresAsthma, cigarette smoking, obesity, and psychological disorders were assessed at age 11, 13, and 15 years.Main outcomes and measuresThe outcome was a midlife aging factor composite score comprising 4 measures of biological aging: pace of aging, gait speed, brain age (specifically, BrainAGE score), and facial age.ResultsA total of 910 participants (459 men [50.4%]) met the inclusion criteria, including an assessment at age 45 years. Participants who had smoked daily (0.61 [95% CI, 0.43-0.79] SD units), had obesity (0.82 [95% CI, 0.59-1.06] SD units), or had a psychological disorder diagnosis (0.43 [95% CI, 0.29-0.56] SD units) during adolescence were biologically older at midlife compared with participants without these conditions. Participants with asthma were not biologically older at midlife (0.02 [95% CI, -0.14 to 0.19] SD units) compared with those without asthma. These results remained unchanged after adjusting for childhood risk factors such as poor health, socioeconomic disadvantage, and adverse experiences.Conclusions and relevanceThis study found that adolescent smoking, obesity, and psychological disorder diagnoses were associated with older biological age at midlife. These health conditions could be treated during adolescence to reduce the risk of accelerated biological aging later in life.

Project description:ImportanceNational longitudinal studies that examine the linkages between early family experiences and sex-specific development of depression across the life course are lacking despite the urgent need for interventions in family settings to prevent adult depression.ObjectiveTo examine whether positive adolescent family relationships are associated with reduced depressive symptoms among women and men as they enter midlife.Design, setting, and participantsThis study analyzed data from the National Longitudinal Study of Adolescent to Adult Health, which used a multistage, stratified school-based design to select a prospective cohort of 20 745 adolescents in grades 7 to 12 from January 3, 1994, to December 26, 1995 (wave 1). Respondents were followed up during 4 additional waves from April 14 to September 9, 1996 (wave 2); April 2, 2001, to May 9, 2002 (wave 3); April 3, 2007, to February 1, 2009 (wave 4); and March 3, 2016, to May 8, 2017 (sample 1, wave 5), when the cohort was aged 32 to 42 years. The study sample of 8952 male adolescents and 9233 female adolescents that were analyzed was a US national representation of all population subgroups by sex, race/ethnicity, socioeconomic status, and geography.ExposuresAdolescent family cohesion and low parent-child conflict.Main outcomes and measuresLevels of depressive symptoms (Center for Epidemiologic Studies-Depression Scale [CES-D]) from ages 12 to 42 years were used to estimate propensity score-weighted growth curve models to assess sex differences in trajectories of depression by levels of positive adolescent family relationships.ResultsA total of 18 185 individuals (mean [SD] age at wave 1, 15.42 [0.12] years; 9233 [50.8%] female) participated in the study. Females and males who experienced positive adolescent family relationships had significantly lower levels of depressive symptoms from early adolescence to midlife than did those who experienced less positive adolescent family relationships. For example, depressive symptoms were lower among those with high levels of family cohesion compared with those with low cohesion between 12 (1.26 lower CES-D score; 95% CI, 1.10-1.42) and 40 (0.78 lower CES-D score; 95% CI, 0.50-1.06) years of age among females and between 12 (0.72 lower CES-D score; 95% CI, 0.57-0.86) and 37 (0.21 lower CES-D score; 95% CI, 0.00-0.41) years of age among males. The reduction in depressive symptoms associated with positive adolescent family relationships was greater for females than males during the adolescent and early adulthood years (ie, early 20s) (eg, low-high cohesion difference in mean CES-D score, -1.26 [95% CI, -1.42 to -1.10] for females and -0.72 [95% CI, -0.86 to -0.57] for males at 12 years of age; low-high cohesion difference in mean CES-D score, -0.61 [95% CI, -0.69 to -0.53] for females and -0.40 [95% CI, -0.48 to -0.31] for males at 20 years of age), after which females and males benefited equally from positive adolescent relationships throughout young adulthood to midlife.Conclusions and relevanceThe findings suggest that positive adolescent family relationships are associated with better mental health among females and males from early adolescence to midlife. Interventions in early family life to foster healthy mental development throughout the life course appear to be important.

Project description:ImportanceAir pollution exposure damages the brain, but its associations with the development of psychopathology are not fully characterized.ObjectiveTo assess whether air pollution exposure in childhood and adolescence is associated with greater psychopathology at 18 years of age.Design, setting, and participantsThe Environmental-Risk Longitudinal Twin Study is a population-based cohort study of 2232 children born from January 1, 1994, to December 4, 1995, across England and Wales and followed up to 18 years of age. Pollution data generation was completed on April 22, 2020; data were analyzed from April 27 to July 31, 2020.ExposuresHigh-resolution annualized estimates of outdoor nitrogen oxides (NOx) and particulate matter with aerodynamic diameter less than 2.5 μm (PM2.5) linked to home addresses at the ages of 10 and 18 years and then averaged.Main outcomes and measuresMental health disorder symptoms assessed through structured interview at 18 years of age and transformed through confirmatory factor analysis into continuous measures of general psychopathology (primary outcome) and internalizing, externalizing, and thought disorder symptoms (secondary outcomes) standardized to a mean (SD) of 100 (15). Hypotheses were formulated after data collection, and analyses were preregistered.ResultsA total of 2039 participants (1070 [52.5%] female) had full data available. After adjustment for family and individual factors, each interquartile range increment increase in NOx exposure was associated with a 1.40-point increase (95% CI, 0.41-2.38; P = .005) in general psychopathology. There was no association between continuously measured PM2.5 and general psychopathology (b = 0.45; 95% CI, -0.26 to 1.11; P = .22); however, those in the highest quartile of PM2.5 exposure scored 2.04 points higher (95% CI, 0.36-3.72; P = .02) than those in the bottom 3 quartiles. Copollutant models, including both NOx and PM2.5, implicated NOx alone in these significant findings. NOx exposure was associated with all secondary outcomes, although associations were weakest for internalizing (adjusted b = 1.07; 95% CI, 0.10-2.04; P = .03), medium for externalizing (adjusted b = 1.42; 95% CI, 0.53-2.31; P = .002), and strongest for thought disorder symptoms (adjusted b = 1.54; 95% CI, 0.50-2.57; P = .004). Despite NOx concentrations being highest in neighborhoods with worse physical, social, and economic conditions, adjusting estimates for neighborhood characteristics did not change the results.Conclusions and relevanceYouths exposed to higher levels of outdoor NOx experienced greater psychopathology at the transition to adulthood. Air pollution may be a nonspecific risk factor for the development of psychopathology.

Dataset Information

Tracing the origins of midlife despair: association of psychopathology during adolescence with a syndrome of despair-related maladies at midlife.

Background

Methods

Results

Conclusions

Publications

Tracing the origins of midlife despair: association of psychopathology during adolescence with a syndrome of despair-related maladies at midlife.

Similar Datasets

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