Although mental health and healthy lifestyle interventions are associated with functional outcomes in adolescence, the extent to which particular lifestyle factors explain relationships between mental health and outcome are unclear. Here we examined mediating effects of lifestyle factors on relationships between mental health and two functional outcomes measured 2–3 years later, as well as moderating effects of environmental risk factors on mediation strength in early adolescence.

We analyzed data from three waves of the Adolescent Brain Cognitive Development Study (ages 10–11, 11–12, and 12–13 years). Mediating effects of sleep quality, screen time, physical activity, and Mediterranean diet on the relationships between depression, anxiety, psychotic-like experience (PLE) distress, and total problems with two subsequent functional outcomes (academic functioning and social problems) were examined. Secondary analyses included environmental factors as moderators.

Sleep quality mediated 18.5%, 36.3%, and 8.3% of the relationships between depression, anxiety, and PLE distress with academic functioning, respectively (total problems mediation was nonsignificant). Screen time was the second strongest mediator. For social problems, only sleep quality showed >3% mediation (19.6–23.3%). Mediating effects of sleep and screen time on academic functioning decreased as financial adversity increased. Conversely, mediating effects of sleep quality on social problems increased with worsening family conflict, financial adversity, and school environment.

These results suggest that healthy lifestyle factors (particularly sleep quality) may partially explain associations between mental health and functioning in adolescents and suggest that these effects are modulated by environmental factors. These results may have implications for future intervention studies.

Cognitive complaints are common in multiple sclerosis, but their relationship to non-cognitive symptoms such as fatigue, sleep dysfunction and psychopathology has not been systematically examined in patients referred for specialist cognitive evaluation. These potentially modifiable symptoms may warrant attention in a clinical context.

This study aimed to characterise common patterns of cognitive and non-cognitive symptoms in a referred patient cohort and determine whether cognitive complaints are associated with clinically significant fatigue, sleep dysfunction and psychopathology.

Cognitive complaints were captured using (a) a binary classification derived from clinical impression and (b) a severity rating from a self-report instrument. Objective cognitive performance was measured across five cognitive domains. Patients also completed self-report measures of fatigue, sleep dysfunction and psychopathology.

Fifty-one patients were included. Although 98% had cognitive complaints, only 29% had objective cognitive impairment. Most (90%) had significant non-cognitive symptoms, primarily fatigue (86%), sleep dysfunction (28%) and depression (26%). Pattern analysis revealed that the most common symptom phenotype was cognitive complaints with significant non-cognitive symptoms, occurring in the absence of objective cognitive impairment. More severe cognitive complaints were associated with greater psychopathology (r = 0.57, BF10 = 2188.48), fatigue (r = 0.53, BF10 = 366.44) and sleep dysfunction (r = 0.47, BF10 = 69.27).

Cognitive complaints in multiple sclerosis may reflect broader non-cognitive symptom burden rather than objective cognitive impairment, even among patients referred for specialist evaluation. Their presence should prompt consideration of fatigue, sleep disturbance and psychopathology as potential targets for intervention.

Existing evidence highlights sleep’s critical role in regulating cortisol stress recovery; the underlying neural pathways remain unclear. To address this gap, the current study aims to elucidate the neurobiological pathway linking objective sleep efficiency to cortisol stress recovery using functional magnetic resonance imaging (fMRI), with a focus on the functional connectivity (FC) between prefrontal cortex (PFC) and hippocampus.

Seventy-seven participants completed an acute stress task during a task-dependent and resting-state fMRI scanning. Salivary samples were collected and analyzed as an indicator of cortisol stress recovery. Objective sleep efficiency was measured the night before the fMRI scanning. Using Seed-based gPPI and resting-state FC analysis, we examined the mediating role of PFC-hippocampus FC in the association between objective sleep efficiency and cortisol stress recovery, both during the stress task and in the post-stress resting-state.

Objective sleep efficiency was significantly related to cortisol stress recovery but not with cortisol reactivity. Neurologically, higher sleep efficiency was linked to enhanced prefrontal activity and increased the left dlPFC-hippocampus FC during the acute stress task. Importantly, objective sleep efficiency promoted cortisol stress recovery by the weakened resting-state left dlPFC-hippocampus FC.

This study highlights the pivotal role of left dlPFC-hippocampus regulation underlying sleep’s effect on HPA axis recovery to acute stress. These results suggest a model whereby high objective sleep efficiency promotes adaptive stress recovery through dynamic reallocation of neural resources across acute stress process, characterized by task-dependent coupling and post-stress decoupling of frontal-hippocampal circuitry.

Bipolar disorder is a recurrent and disabling condition, with a critical clinical need to prevent transitions from euthymia or depression (normal or low activation states) to mania (a high activation state). This study investigates how disruptions in sleep–wake and circadian rhythms may trigger these high activation states, to inform more effective relapse prevention strategies.

We developed a computational agent-based model integrating empirical evidence, clinical expertise, and lived experience to simulate how 24-hour sleep–wake behaviors (SWBs) influence manic episodes. Individual characteristics were drawn from the Brain and Mind Youth Cohort (N = 2,330), and multiple scenarios were simulated to assess how SWB dynamics affect the emergence and course of mania.

In the absence of all irregularities, no individuals experienced a manic episode. Removing behavioral feedback loops resulted in a substantial reduction in manic episodes and delayed onset. In contrast, eliminating light–dark entrainment slightly increased the frequency of manic episodes, suggesting that seasonal adaptation plays a stabilizing role. When examining components of SWB separately, removing sleep irregularities alone had only a modest effect on mania rates, whereas reducing activity irregularities led to the largest benefit: a significant drop in mean manic episodes, a delay in onset, and preventing mania in 65% of the simulated agent population.

Our findings highlight the value of computational modeling for uncovering causal dynamics in mental health. These specific findings demonstrate how daily irregularities in sleep–wake behavior may be a necessary condition for mania. Targeting behavioral regularity may offer a powerful pathway for prevention and early intervention.

Although most couples share a bed, current interventions rarely consider dyadic sleep patterns.

We investigated whether bedtime alignment between partners affects longitudinal sleep outcomes in older couples, with particular attention to gender differences.

Based on the temporal relationship between partners’ bedtimes and the earlier sleeper’s sleep onset latency, 859 couples (1718 individuals) aged ≥60 years were classified into 5 mutually exclusive bedtime alignment groups. Pittsburgh Sleep Quality Index (PSQI) scores, sleep onset latency and sleep efficiency were compared using analysis of variance and multivariate analysis of covariance. Both cross-sectional and 8-year longitudinal trajectory analyses were conducted.

Bedtime alignment significantly affected sleep outcomes (P < 0.001, Pillai’s Trace = 0.37, F24, 3352 = 14.04, P < 0.001, η2P = 0.09). Couples with synchronised bedtimes demonstrated excellent sleep quality, whereas those with bedtime differences less than the earlier sleeper’s sleep onset latency exhibited the worst. The earlier sleepers in such couples experienced longer sleep onset latencies (53.4 ± 46.8 min) and greater sleep quality impairment (PSQI = 7.9 ± 4.1). The 8-year trajectory analysis revealed gender-specific vulnerability: only women in misaligned groups experienced progressive sleep deterioration over time (5.84 ± 8.42 min/year increase in sleep onset latency, P < 0.001; 1.27 ± 1.93%/year decrease in sleep efficiency, P < 0.001), whereas men maintained stable sleep parameters regardless of alignment.

Bedtime alignment represents a modifiable determinant of sleep health in older couples, with synchronised bedtimes providing optimal outcomes and partial sleep onset overlap creating disruption. This particularly benefits women, who show progressive deterioration with misalignment. These findings support the development of gender-informed, couple-based interventions for sleep disorders.

Existing research demonstrates that insomnia is common, with significant negative impacts on health and quality of life. Cognitive–behavioural therapy for insomnia (CBT-I), the first-line treatment, is highly cost-effective. However, healthcare records have not been used in the UK to establish real-world insomnia prevalence, inequalities or unmet need.

This study’s aim was to establish the above in North Central London.

Data were extracted from primary care records across three London boroughs for 765 035 patients. Prevalence was determined by identifying those with a recent code for insomnia, insomnia treatment or sleeping tablet prescription.

Insomnia prevalence was 4.3%. Prevalence increased steadily with age, and was highest for women (4.9%), those of Bangladeshi ethnicity (7.3%) and those in the most deprived quintile (5.2%). Prevalence was significantly higher in patients with comorbidities (including chronic obstructive pulmonary disease (17.5%), severe mental illness (16.6%) and depression (14.1%)). Only 1.7% of people with insomnia had been referred for CBT-I.

Findings suggested that insomnia is at least as common as illnesses receiving high levels of focus and resourcing in the UK, and that prevalence estimates were probably underestimates. Variation in prevalence by demographic factors and deprivation may represent health inequalities. Insomnia was particularly common among patients with certain comorbidities and of advancing age, indicating that those groups should be actively screened. Concerningly, referral rates for CBT-I were extremely low. This has important implications regarding population health management, commissioning and training. Prevalence and unmet need are likely to be high in many other areas and should be investigated locally.