Functional disorders (FDs) are associated with internalizing disorders (IDs). Studies investigating the nature of these associations over time are limited. We tested the direction of causation between measures of IDs (major depressive disorder [MDD], generalized anxiety disorder [GAD]) and FDs (fibromyalgia [FM] and myalgic encephalomyelitis/chronic fatigue syndrome [ME/CFS]) measured across two waves of longitudinal data (N = 108,034 and N = 73,590).

The Lifelines Cohort Study is a large prospective population-based cohort study in the northeast of the Netherlands. We tested competing causal models for the longitudinal association between IDs and FDs and, to follow-up results from the model with all IDs and FDs, tested the direction of causation between MDD and FM.

FDs were more stable over time than IDs. Initial model comparisons support a bidirectional relationship between most IDs and FDs. Follow-up analyses support a unidirectional model where FM predicts MDD over time (β = 0.14, 95% confidence interval = [0.11, 0.18]), but not vice versa.

The cross-time associations between ME/CFS, MDD, and GAD appear bidirectional (causal in both directions). Our results are consistent with, but not demonstrative of, a causal relationship from FM to MDD. The consequences of specific FDs vary, underscoring the value of studying these conditions as distinct constructs.

Limited longitudinal research examining developmental changes in visuospatial working memory (WM) among children and adolescents with autism spectrum disorder (ASD) has prompted our investigation.

We assessed 123 autistic children and adolescents and 145 typically developing controls (TDC) using the Cambridge Neuropsychological Test Automated Battery at baseline (Time 1 [mean age ± SD]: ASD: 13.04 ± 2.86; TDC: 11.53 ± 2.81) and 2–9 years later (Time 2: ASD: 18.08 ± 3.17; TDC: 16.41 ± 3.09) to measure changes of visuospatial (working) memory over time. The linear mixed model was used to compare the differences between ASD and TDC and estimate the effect of changes over time, age, ASD diagnosis, and interactions of Time×Age×ASD. The overall Age×ASD effect was calculated in the spline regression.

Autistic children and adolescents exhibited significantly poorer performance on all spatial tasks and some visual tasks than their TDC counterparts at Time 1 and Time 2, after adjusting for sex, age, attention deficit/hyperactivity disorder (ADHD), and full-scale intelligence quotient. There was an overall improvement from Time 1 to Time 2 across all tasks with significant Age×Time interactions. Significant Age×ASD interactions were observed in the delayed matching to sample, pattern recognition memory (PRM), spatial span (SSP), and spatial working memory (SWM) tasks with no significant Time×ASD interactions. In the quadratic nonlinear model, Age×ASD interactions were significant in PRM and SSP.

Despite significant improvements during the follow-up period, autistic children and adolescents continue to experience persistent deficits in SWM, with a weaker age-related improvement in visuospatial WM than TDC.

Postpartum depression is prevalent among Black women and associated with intersecting systemic factors and interpersonal discrimination. However, gaps remain in understanding pregnancy-related changes in discrimination experiences that influence postpartum mental health and could inform preventive interventions. We hypothesized that young Black women would experience increasing levels of discrimination across the transition to parenthood, heightening depression risk relative to non-pregnant peers.

Participants comprised 335 Black primiparous women (ages 17-30 at delivery) and 335 age- and discriminationmatched non-pregnant controls from the Pittsburgh Girls Study. Self-reported discrimination experiences were collected at four timepoints: two years pre-pregnancy, one year pre-pregnancy, pregnancy, and one year postpartum for the childbearing sample, with corresponding data from the non-pregnant sample across the same interval (matched pairwise).

Linear increases in discrimination were observed for the nonpregnant participants (BS = .480, SE = .090, p <.001), while childbearing participants showed no overall changes, though younger age predicted greater increases over time. For childbearing participants, both baseline discrimination (BI = .626, SE = .077, p < .001) and increasing discrimination (BS = 2.55, SE = .939, p < .01) predicted postpartum depressive symptoms, controlling for pre-pregnancy depression. Among non-pregnant participants, only baseline discrimination predicted later depression (BI = .912, SE = .081, p < .001).

Experiencing increasing levels of interpersonal discrimination across the transition to parenthood may heighten postpartum depression risk among young Black women, indicating a need for interventions supporting well-being and promoting resilience before, during and after pregnancy.

Psychotic-like experiences (PLEs) are associated with cognitive impairment and premature mortality, which may be indicative of accelerated biological ageing. Epigenetic clocks provide a measure of biological age based on DNA methylation, yet the long-term relationship between epigenetic ageing and PLEs remains largely unclear. We tested the relationship between epigenetic ageing and PLEs using a 17-year longitudinal approach.

Epigenetic ageing was calculated using four epigenetic clocks (DunedinPACE, Cortical EpiAge, Horvath, and PCGrimAge) in a sample from the Avon Longitudinal Study of Parents and Children (ALSPAC), a large population-based birth cohort (n = 1840, 56.8% females). We modeled epigenetic ageing from up to three repeated measures collected between ages 7 and 24 using a linear mixed-effects model to calculate (1) average epigenetic age [mean-centered intercept] and (2) rate of epigenetic ageing over this 17-year period [slope]. We then compared these two measures between individuals who developed PLEs in early adulthood (n = 95) against those who did not (n = 1745).

Results showed that a faster rate (slope) of longitudinal PCGrimAge was predictive of PLEs (OR = 1.79, 95% CI [1.13–2.85], p = .014), although this association was no longer significant after adjusting for smoking. There was a non-significant effect in the same direction for other clocks. Average epigenetic age (mean-centered intercept) was not associated with PLEs.

Our findings suggest that the observed association between accelerated rate of epigenetic ageing, measured with PCGrimAge, from childhood to early adulthood, and the development of PLEs in early adulthood may be explained by smoking.

This study aims to explore the everyday experiences of people living with Lewy body dementia and their families, to deepen understanding of their care needs. Lewy body dementia is a neurodegenerative condition associated with shorter life-expectancy and poorer quality of life than other forms of dementia. Cognitive fluctuations, visual hallucinations, falls, and motor features of Parkinsonism gives rise to complex and debilitating symptoms. Other prominent features include behavioral and emotional problems, rapid eye movement sleep disorder, and autonomic dysfunction. Improving palliative care for people with dementia continues to be an international priority; however, little is known as to how a palliative care approach could support people living with Lewy body dementia and their families.

Drawing on narrative theory of self and personhood, a qualitative, longitudinal narrative approach provided unique insights into 5 couples’ experiences of living with Lewy body dementia. Analysis was conducted using Murray’s levels of narrative analysis in health psychology to explore stories at the personal, interpersonal, positional, and societal level.

Participants with Lewy body dementia described losses associated with communication, continence, and energy leading to a progressive loss of independence. For their family caregivers a loss of companionship was particularly salient. These losses, compounded by a perceived lack of clinical support, resulted in suffering both for the person with Lewy body dementia, and for those close to them.

There has been a societal and political shift to move beyond loss in dementia, to a focus on abilities and living well. However, acknowledging loss, while supporting symptom management is an important aspect of Lewy body dementia care. Providing person-centered, palliative supportive care throughout the disease trajectory could reduce suffering and enhance well-being.

Posttraumatic stress disorder (PTSD) is often chronic and impairing. Mechanisms that maintain symptoms remain poorly understood because of heterogenous presentation. We parsed this heterogeneity by examining how individual differences in stress-symptom dynamics relate to the long-term maintenance of PTSD.

We studied 7,308 trauma-exposed World Trade Center responders who self-reported PTSD symptoms and stressful life events at annual monitoring visits for up to 20 years (average = 8.8 visits; [range = 4–16]). We used multilevel structural equation models to separate the stable and time-varying components of symptoms and stressors. At the within-person level, we modeled stress reactivity by cross-lagged associations between stress and future symptoms, stress generation by cross-lagged associations between symptoms and future stress, and autoregressive effects represented symptom persistence and stress persistence. The clinical utility of the stress-symptom dynamics was evaluated by associations with PTSD chronicity and mental health care use.

Stress reactivity, stress generation, and symptom persistence were significant on average (bs = 0.03–0.16). There were significant individual differences in the strength of each dynamic (interquartile ranges = 0.06–0.12). Correlations among within-person processes showed some dynamics are intertwined (e.g. more reactive people also generate stress in a vicious cycle) and others represent distinct phenotypes (e.g. people are reactive or have persistent symptoms). Initial trauma severity amplified some dynamics. People in the top deciles of most dynamics had clinically significant symptom levels across the monitoring period and their health care cost 6–17× more per year than people at median levels.

Individual differences in stress-symptom dynamics contribute to the chronicity and clinical burden of PTSD.

Posttraumatic stress disorder (PTSD) has been associated with advanced epigenetic age cross-sectionally, but the association between these variables over time is unclear. This study conducted meta-analyses to test whether new-onset PTSD diagnosis and changes in PTSD symptom severity over time were associated with changes in two metrics of epigenetic aging over two time points.

We conducted meta-analyses of the association between change in PTSD diagnosis and symptom severity and change in epigenetic age acceleration/deceleration (age-adjusted DNA methylation age residuals as per the Horvath and GrimAge metrics) using data from 7 military and civilian cohorts participating in the Psychiatric Genomics Consortium PTSD Epigenetics Workgroup (total N = 1,367).

Meta-analysis revealed that the interaction between Time 1 (T1) Horvath age residuals and new-onset PTSD over time was significantly associated with Horvath age residuals at T2 (meta β = 0.16, meta p = 0.02, p-adj = 0.03). The interaction between T1 Horvath age residuals and changes in PTSD symptom severity over time was significantly related to Horvath age residuals at T2 (meta β = 0.24, meta p = 0.05). No associations were observed for GrimAge residuals.

Results indicated that individuals who developed new-onset PTSD or showed increased PTSD symptom severity over time evidenced greater epigenetic age acceleration at follow-up than would be expected based on baseline age acceleration. This suggests that PTSD may accelerate biological aging over time and highlights the need for intervention studies to determine if PTSD treatment has a beneficial effect on the aging methylome.

Pubertal development variations have consequences for adolescent internalizing problems, which likely continue into adulthood. Key questions concern the extent of these links between pubertal timing and adult symptoms, as well as the underlying mechanisms.

Longitudinal data were available for 475 female and 404 male participants. Pubertal timing was indicated by age at mid-puberty for both groups and age at menarche for female participants (both assessed continuously). Adult self-reported outcomes of recent and lifetime depression and anxiety were predicted from pubertal timing, also controlling for adolescent (then childhood) internalizing problems. Emerging adulthood self-esteem, body dissatisfaction, education level, and age at sexual initiation were examined as mediators of the pubertal timing-adult internalizing link. Multilevel models tested hypotheses.

Pubertal timing had persisting and sex-dependent psychological associations. Specifically, in female, but not male, adults, early puberty was associated with all adult internalizing outcomes, and for past year and lifetime depression symptoms, even after controlling for adolescent internalizing problems. Pubertal timing links with past-year depression symptoms were mediated by age at sexual initiation, while all other persisting pubertal timing links with adult symptoms were mediated by body dissatisfaction. Most findings concerning depression held when childhood internalizing problems were also a covariate.

Leveraging data spanning four developmental periods, findings highlight the associations between pubertal variations and adult internalizing symptoms by revealing underlying sex-dependent behavioral pathways. Only for female participants did pubertal timing affect depression and anxiety in established adulthood, with body dissatisfaction and age at sexual initiation as unique developmental mechanisms.

Social anhedonia, indicating reduced pleasure from social interaction, is heightened in autistic youth and associated with increased internalizing symptoms transdiagnostically. The stability of social anhedonia over time and its longitudinal impact on internalizing symptoms in autism have never been examined.

Participants were 276 autistic children (Mage = 8.60, SDage = 1.65; 211 male) with IQ ≥ 60 (MIQ = 96.74, SDIQ = 18.19). Autism severity was measured using the Autism Diagnostic Observation Schedule, Second Edition. Caregivers completed the Child and Adolescent Symptom Inventory, Fifth Edition (CASI-5) at baseline, 6 weeks, and 6 months. The CASI-5 includes a social anhedonia subscale derived from relevant items across domains. ICC (Intraclass Correlation Coefficient) analysis assessed stability, while cross-lagged panel models examined associations among social anhedonia, depression, and social anxiety across time.

At baseline, social anhedonia correlated with autism severity, as well as parent-reported social anxiety and depression. Social anhedonia showed relative stability (ICC = 0.763) over 6 months, with a significant decline between baseline and 6 weeks (β = −0.52, p < .001). Cross-lagged models revealed a bidirectional relationship between social anhedonia and depression over time, while social anxiety displayed concurrent, but not predictive, associations across time.

Social anhedonia demonstrated stability over 6 months, suggesting that it may be a relatively stable characteristic in autistic children. Concurrent relationships were observed between social anhedonia and depression, as well as social anxiety and attention-deficit/hyperactivity disorder. Only depression demonstrated a bidirectional longitudinal association with social anhedonia. This bidirectional relationship aligns with developmental models linking early negative social experiences to subsequent internalizing symptoms in autistic children, underscoring the clinical significance of social anhedonia assessment in this population.

The cumulative effects of long-term exposure to pandemic-related stressors and the severity of social restrictions may have been important determinants of mental distress in the time of COVID-19.

This study aimed to investigate mental health among a cohort of Chinese university students over a 28-month period, focusing on the effects of lockdown type.

Depression, anxiety, stress and fear of COVID-19 infection were measured ten times among 188 Chinese students (females 77.7%, meanage = 19.8, s.d.age = 0.97), every 3 months: from prior to the emergence of COVID-19 in November 2019 (T1) to March 2022 (T10).

Initially depression, anxiety and stress dipped from T1 to T2, followed by a sudden increase at T3 and a slow upward rise over the remainder of the study period (T3 to T10). When locked down at university, participants showed greater mental distress compared with both home lockdown (d = 0.35–0.48) and a no-lockdown comparison period (d = 0.28–0.40). Conversely, home lockdown was associated with less anxiety and stress (d = 0.19 and 0.21, respectively), but not with depression (d = 0.13) compared with a no-lockdown period.

This study highlights the cumulative effects of exposure to COVID-19 stressors over time. It also suggests that the way in which a lockdown is carried out can impact the well-being of those involved. Some forms of lockdown appear to pose a greater threat to mental health than others.