The research team, led by Tong Gong and Yi Lu of Karolinska Institutet, drew on the Child and Adolescent Twin Study in Sweden, a national cohort that has tracked participants at ages 9, 15, 18 and 24. Because the cohort was linked to national patient registers and prescription drug records, the researchers could examine not only self-reported symptoms of depression and anxiety but also clinically diagnosed disorders and antidepressant dispensing over follow-up periods extending more than a decade. This combination of symptom scales and hard clinical endpoints is rare in screen time research, which has often relied on small samples and coarse self-reports.

The headline results were striking at the population level. At ages 15 and 18, screen time showed a clear dose-response pattern with internalizing symptoms: the more hours per day young people spent on screens, the higher their depression and anxiety scores. Comparing heavy users, defined as those spending more than six hours per day, with restrictive users at two hours or less, the standardized differences in symptom scores ranged from 0.20 to 0.38 in the full sample. The associations were markedly stronger in girls than in boys for interactive activities such as gaming, chatting and browsing, with heavy use corresponding to symptom elevations of 0.37 to 0.51 standard deviations in girls, compared with 0.19 to 0.22 in boys.

The clinical picture was even more dramatic. Heavy interactive screen use at age 15 was associated with a roughly two- to threefold increased risk of being diagnosed with a depressive or anxiety disorder by age 28, with weekday heavy use showing an adjusted hazard ratio of 3.37. Even daily gaming at age 9, reported by parents, was linked to a 38 percent higher risk of clinical outcomes through age 22. Passive activities such as watching television, videos and DVDs showed far weaker and mostly non-significant associations, suggesting that what young people do on screens may matter as much as how long they spend there.

But the study’s most consequential findings emerged when the researchers turned to the twin structure of their data. Monozygotic twins share essentially all of their inherited genes, while dizygotic twins share on average half, and both types share their rearing environment. By comparing one twin who used screens heavily with their co-twin who did not, the co-twin control design effectively removes confounding from shared genetics and family background, factors that ordinary observational studies cannot measure. If the screen-mental health link were purely causal, it should persist within identical twin pairs.

It did not, at least not robustly. Within discordant dizygotic pairs, effect estimates attenuated modestly. Within discordant monozygotic pairs, the attenuation was far more pronounced: at age 15, estimates shrank by 32 to 95 percent relative to the full sample and were no longer statistically significant after correction for multiple testing. At age 18, the corresponding estimates were attenuated by 16 to 45 percent. In the longitudinal analyses, the strong cross-age associations between heavy interactive use at 15 and symptoms at 18, and between use at 18 and symptoms at 24, were reduced by roughly 30 to 60 percent within twin pairs and fell below the significance threshold. The pattern of progressive but incomplete attenuation is consistent with a mixture of genetic confounding, shared environmental confounding and possibly a small residual direct effect.

The clinical outcomes told a similar story. The threefold risk elevation associated with heavy weekday interactive use at age 15 dropped by 57 to 59 percent within discordant twin pairs, leaving a point estimate of a 65 percent increased risk that no longer reached significance after multiple-testing correction. Daily gaming at age 9, which showed a significant hazard ratio of 1.38 in the full sample, showed no comparable association within discordant pairs. The authors interpret this cautiously: the analyses had limited statistical power because informative discordant pairs are few, so small direct effects cannot be ruled out entirely, but the evidence for a clear causal effect of screen time on internalizing problems is weak.

The study also probed directionality, a persistent puzzle in this field. Screen use at age 9 did not predict symptoms at 15, but heavy interactive use at 15 and 18 predicted symptoms at 18 and 24 respectively. Intriguingly, the reverse pathway also appeared: adolescents with higher depressive and anxiety symptoms at 15 showed a small but measurable increase in interactive screen use at 18, with an odds ratio of 1.04 per standard deviation of symptoms. Although modest, this reverse association suggests that vulnerable young people may gravitate toward heavier digital engagement, potentially encountering more negative social comparison and mood impacts, a dynamic documented in recent studies of adolescents with mental health conditions.

The findings carry important implications for policy. Public health agencies in several countries have issued guidelines limiting recreational screen time for children and adolescents, but these rest largely on non-causal observational evidence. The new results align with earlier genetically informed work showing that screen behaviors themselves are moderately heritable, with twin-based estimates of 20 to 49 percent, and that genetic confounding accounts for a substantial share of the apparent association between media use and mental health. They also echo the influential analyses by Orben and Przybylski, who found that per-hour effects of screen use on adolescent well-being are small; the co-twin estimates here correspond to roughly 0.03 to 0.05 standard deviations of additional symptoms per extra hour of interactive use at age 18.

Yet the authors caution against dismissing the issue entirely. Within age-18 identical twin pairs, weekend heavy interactive use was still associated with 0.26 standard deviations of additional symptoms compared with restrictive use, an effect size comparable to established risk factors such as bullying victimization and childhood maltreatment, which typically fall in the 0.2 to 0.3 range. The study also has limitations: data collection began in 2004, before smartphones and social media became ubiquitous; the crude categories of interactive and passive use do not capture the complexity of modern digital life; and self-reported screen time is known to be underreported. Sensitivity analyses adjusting for physical activity and bullying victimization left the main findings essentially unchanged. The researchers conclude that heavy recreational screen use remains a legitimate public health concern, particularly during adolescence, but that shared genetic and familial factors partly explain the link to depression and anxiety, and that future research should focus on why and how different types of digital engagement affect vulnerable young people, rather than on screen time alone.

Subject of Research: Longitudinal twin study of recreational screen use and internalizing problems from preadolescence to young adulthood

Article Title: Recreational screen use and internalizing problems from preadolescence to young adulthood in a longitudinal twin cohort with co-twin comparison

Article References: Gong, T., Frans, E., Ohlis, A., Yao, S., Zhang, R., Nilsson, A., Molero, Y., Mosing, M. A., Brikell, I., Larsson, H., Lichtenstein, P., Thorell, L. B., Magnusson, P. K., Kuja-Halkola, R., & Lu, Y. (2026). Recreational screen use and internalizing problems from preadolescence to young adulthood in a longitudinal twin cohort with co-twin comparison. Nature Human Behaviour. https://doi.org/10.1038/s41562-026-02607-0

Image Credits: AI Generated

DOI: 10.1038/s41562-026-02607-0

Keywords: screen time, mental health, depression, anxiety, twin study, co-twin control design, adolescence, genetic confounding, internalizing problems, gaming, Nature Human Behaviour, epidemiology

The research, published in SSM – Population Health, drew on Sweden’s extraordinary national registries to follow 2,978,645 individuals born between 1975 and 2005. The researchers, led by Gloria Yuxuan Gu and colleagues including Antti Latvala, Henrik Larsson, and Paul Lichtenstein, linked records spanning births, hospitalizations, criminal convictions, and deaths. Roughly 6.4 percent of children under 15 had experienced a parent being hospitalized for a severe mental illness such as schizophrenia or bipolar disorder, an affective disorder such as depression or anxiety, or a substance use disorder. About one in ten children in Sweden experiences parental psychiatric illness during childhood, a figure comparable to other high-income countries.

At first glance, the raw numbers are stark. Among young people whose parents had never been psychiatrically hospitalized, roughly 2 percent experienced one of the violence-related outcomes by early adulthood. Among those exposed to parental hospitalization for severe mental illness, the figure rose to nearly 4 percent for violent victimization. For children whose parents were hospitalized for substance use disorders, 9.17 percent went on to be convicted of a violent crime. In absolute terms, the researchers calculated an excess of roughly 17 to 66 additional cases per 1,000 exposed offspring, with the heaviest burden attached to violent offending after parental substance-related hospitalization.

Statistical models confirmed the pattern. In conventional population-level analyses that adjusted for birth year, sex, county of residence, and parental education and age, children of psychiatrically hospitalized parents showed hazard ratios ranging from 1.56 to 2.76, meaning a 56 to 176 percent increase in the hazard of a violent outcome. Hospitalization for accidents, by contrast, carried lower risks, between 1.39 and 1.51. These are the kinds of estimates that have populated the literature for years, and they have fueled calls for screening and preventive outreach aimed at children of mentally ill parents.

But the Swedish team went a crucial step further. Using a cousin-comparison design, they compared children whose parents had been hospitalized with their own cousins whose parents had not, holding constant the extended family environment and, critically, a substantial share of shared genetics. Cousins share grandparents and inherit, on average, about 12.5 percent of their genes in common, so differences between cousins cannot easily be explained by the familial liabilities that pervade whole families. When the analysis moved from between-family to within-family comparisons, the hazard ratios dropped substantially, falling to a range of 1.27 to 1.65. On average, the associations shrank by 22.4 percent for severe mental illness, 25.4 percent for affective disorders, and 34.5 percent for substance use disorders.

The accident comparator sharpened the picture further. Accidental hospitalizations share many of the disruptive features of psychiatric admissions, including a parent’s temporary absence, financial strain, and upheaval in daily routines, but they are not systematically tied to the familial psychiatric liability that cousin comparisons are designed to control. Notably, the attenuation from population-level to within-family estimates was smaller for accident hospitalizations, around 15.5 percent on average, than for psychiatric hospitalizations. This asymmetry suggests that the excess risk following psychiatric admissions is driven primarily by disorder-specific familial transmission, including shared genetic liability, related behavioral traits such as impulsivity and emotional dysregulation, and the chronic family environments that travel with these conditions, rather than by the acute disruption of a parent’s absence alone.

The study also probed whether timing matters. Developmental science has long proposed that early childhood represents a sensitive period for attachment and emotional regulation, and that adolescence is critical for social and behavioral development. Yet when the researchers stratified exposure by the child’s age, dividing childhood into windows of 0 to 5, 6 to 10, and 11 to 14 years, the associations were largely stable across periods. An apparent stronger effect of early exposure to parental substance-related hospitalization vanished entirely once familial confounding was accounted for. The authors argue that what looks like a biologically privileged early window in population data may simply reflect the fact that earlier and longer exposure accumulates more socioeconomic disadvantage. Their practical implication is pointed: preventive services should be maintained continuously across childhood rather than concentrated at any single developmental stage.

Dose-response analyses told a similar story. At the population level, each additional cumulative month of parental hospitalization was associated with higher offspring risk, and accidental hospitalizations showed a particularly clean 6 percent increase in risk per month, a pattern that survived within-family comparison. For psychiatric exposures, however, the cumulative-duration signal largely dissolved after adjusting for familial confounding, with the exception of substance use disorders, whose associations remained significant but substantially attenuated. Together with the accident findings, this hints at an intriguing possibility: the disruption of caregiving itself, as captured by accident-related admissions, may have a more direct causal role than previously appreciated, and deserves investigation in its own right.

Perhaps the most actionable results concern what happens next in young people’s lives. When the researchers additionally adjusted for offspring educational attainment, employment status, and civil status one year before the outcome, the hazard ratios fell further, to between 1.20 and 1.48 for psychiatric exposures. This indicates that life-course transitions in emerging adulthood, finishing school, finding work, forming stable relationships, partially channel the residual risk. These are precisely the domains that social policy can reach. The authors suggest that existing programs in education and labor market integration could be evaluated with intergenerational risk transmission as a secondary outcome, turning an etiological insight into a set of modifiable levers.

The findings come with caveats. Cousin comparisons control only part of shared genetic liability, so the within-family estimates are best read as upper bounds of any true environmental effect. Mediation analyses assume, but cannot prove, causal pathways. And Sweden’s generous welfare state buffers many of the socioeconomic consequences of parental illness, meaning the environmental component could be larger in countries with weaker safety nets. Still, the central message is hard to escape: the alarming hazard ratios reported in earlier registry studies should not be interpreted as the causal impact of a parent’s hospitalization, and family-focused prevention calibrated to those raw estimates is likely to yield smaller returns than hoped. The better strategy, the authors conclude, is twofold, sustained support for families carrying high underlying vulnerability, and deliberate protection of the educational, occupational, and relational transitions through which whatever residual environmental risk remains is ultimately expressed.

Subject of Research: Intergenerational transmission of risk for suicidal behavior, violent offending, and violent victimization following parental psychiatric hospitalization

Article Title: Childhood Parental Psychiatric Hospitalization and Offspring Suicidal Behavior, Violent Crime, and Violent Victimization: A Swedish Population-Based Cousin Comparison Study

Article References: Gu, G. Y., Latvala, A., Kuja-Halkola, R., Zhou, M., Larsson, H., D’Onofrio, B. M., Chang, Z., & Lichtenstein, P. (2026). Childhood Parental Psychiatric Hospitalization and Offspring Suicidal Behavior, Violent Crime, and Violent Victimization: A Swedish Population-Based Cousin Comparison Study. SSM – Population Health, Article 101978. https://doi.org/10.1016/j.ssmph.2026.101978

Image Credits: AI Generated

DOI: 10.1016/j.ssmph.2026.101978

Keywords: parental psychiatric hospitalization, suicidal behavior, violent crime, violent victimization, cousin comparison, genetic confounding, Swedish registries, substance use disorders, severe mental illness, life-course transitions, causal inference, public health