Rapid weight gain commonly occurs following the onset of first-episode psychosis (FEP), leading to cardiometabolic disease. Most weight gain in FEP occurs in the first 3 months of treatment, offering a critical window for prevention. Despite this, most studies aiming to prevent antipsychotic-induced weight gain include people with chronic illness or people who have had lengthy exposure to antipsychotic medication. We aimed to synthesize and analyze the literature on interventions aimed at preventing antipsychotic-induced weight gain.

We conducted a systematic review in PsycInfo, MEDLINE, CINAHL, and EMBASE of studies that examined the effectiveness of interventions in preventing antipsychotic-induced weight gain in FEP. We examined their effect on weight gain and a range of cardiometabolic markers.

We screened 2,092 articles, 13 of which were eligible. Behavioral interventions, all three of which consisted of a multidisciplinary team approach, resulted in a mean of 3.05 kg less weight gain than treatment-as-usual (95% CI 1.36 kg to 4.73 kg). Pharmacological interventions displayed marked clinical and statistical heterogeneity, with each of the seven trials in adults using a different pharmacological intervention. Few studies collected comprehensive data on metabolic health. Only two pharmacological studies, and five studies in total, have been published since 2010.

Despite the importance of preventing weight gain in FEP, there have been few recent studies investigating this topic. Our results indicate that multidisciplinary team interventions are effective in preventing weight gain in FEP and should be offered to all patients.

Social anxiety disorder (SAD) is one of the most common anxiety disorders and is associated with significant impairment and societal costs. The association between SAD and mortality remains poorly understood, partly because in epidemiological research it is rarely studied independently from other anxiety disorders. In this population-based matched cohort and sibling control study, we estimated the risk of all-cause and cause-specific mortality in individuals with SAD.

From a population of individuals born from 1932 and living in Sweden between 1997 and 2020, we identified all cases of SAD (Swedish ICD-10 code F40.1) in the National Patient Register. Each of these individuals was matched on sex, birth year and county of residence with 10 individuals who had never received a diagnosis. Mortality data were extracted from the Cause of Death Register. Risks were estimated using Cox proportional hazards regression models. Models adjusted for sociodemographic covariates and other lifetime psychiatric disorders. We also identified all clusters of full siblings and conducted within-sibling comparisons to account for unmeasured familial confounding.

The matched cohort included 57,360 individuals with SAD and 573,600 unexposed individuals. During the follow-up, 2355 deaths were registered within the exposed cohort vs. 7800 deaths in the matched cohort (crude mortality rates, 5.25 and 1.73 per 1000 person-years, respectively). The full cohort was followed up for a mean of 7.87 years (standard deviation 5.23). In models adjusting for sociodemographic variables, individuals with SAD had a 2.24-fold increased hazard of all-cause mortality (95% confidence interval [CI], 2.13–2.35). The increased risk was observed for both natural (adjusted hazard ratio [HR], 1.62; 95% CI 1.52–1.72) and unnatural causes of death (HR, 4.18; 95% CI 3.82–4.58). The results were robust to additional adjustment for psychiatric comorbidities, but the magnitude of the associations was attenuated, particularly when adjusting for substance use disorders. In the sibling cohort, 39,993 individuals with SAD were compared with their 64,640 unaffected siblings. While the estimates were also attenuated, they remained statistically significant (HR for all-cause mortality, 1.40; 95% CI 1.36–1.45).

Individuals with SAD face an increased risk of mortality, attributable primarily to unnatural causes of death, such as suicide, but also to natural causes, even after adjusting for socioeconomic variables. Psychiatric comorbidities, particularly substance use disorders, and shared familial factors may also contribute to this excess death. Further study of underlying mechanisms may inform prevention and early intervention strategies to reduce mortality in this vulnerable population.

Adolescent mental health has worsened, and prevention efforts have become increasingly important. The purpose of this study was to examine longitudinal symptom trajectories of depression and anxiety throughout adolescence, in a contemporary sample. The stress–diathesis model was used to inform potential vulnerability factors and stressors associated with these trajectories.

Symptoms of depression and generalized anxiety were assessed in a school-based population sample of N = 6102 adolescents (aged 13–14 at baseline). Growth mixture models across four time points were used to model longitudinal trajectories of symptoms. Multinomial regression was used to examine factors associated with each trajectory class.

Of the full sample, 49.5% were female, 45.9% were male, and 4.6% were gender diverse. Four discrete classes for both depression and anxiety trajectories were identified, which comprised consistently low symptoms (‘low’; 72.5% depression; 66.9% anxiety), consistently high symptoms (‘high’; 11.5% depression; 18.4% anxiety), elevated symptoms that reduced over time (‘decreasing’; 8.3% depression; 6.9% anxiety), and low-moderate symptoms that increased over time (‘increasing’; 7.7% depression; 7.8% anxiety). Factors associated with poorer trajectories were being female or gender diverse, lower socioeconomic status, higher levels of neuroticism and lower levels of conscientiousness, greater adverse childhood experiences, higher levels of peer problems, bullying victimization, and negative family interactions.

A range of background vulnerabilities and specific stressors were associated with poorer depression and anxiety trajectories over a 3-year period. Prevention approaches may require policy and practice changes that promote more supportive family, school, and societal environments from childhood to adolescence.

The mental healthcare workforce supporting people with dementia and comorbid mental disorders requires specific skills and knowledge.

We co-designed and conducted a survey to understand key issues facing community mental healthcare services accessed by older adults.

We invited all English National Health Service (NHS) older people’s community mental health teams (OPCMHTs) in England to complete the survey. We compared service structures, resourcing and waiting times between regions, and considered how responses might inform current policy priorities.

A total of 182 out of 242 (75.2%) English NHS OPCMHTs participated. We estimated there were 120 233 referrals to OPCMHT services per year, with 77.5% of services reporting increasing referral rates. In a quarter of services (n = 46, 25.3%), clients waited over a month from referral to initial assessment. Most services (107/181, 59.1%) experienced difficulties accessing in-patient beds for people with dementia, with rural regions more likely to report these difficulties. Half of the services (n = 100, 55.2%) reported providing higher-quality care for people with dementia than 5 years ago, despite increasing caseload complexity. Resource limitations challenged opportunities for prevention, care quality and collaborative working, and respondents rated team relationships with social services (n = 86, 47.8%), general hospital in-patient (n = 74, 41.4%) and out-patient (n = 54, 30.2%) services, and primary care (n = 54, 30.2%) as poor or requiring improvement.

OPCMHT service leads are committed to integrated working, but services are insufficiently resourced to realise their potential. Addressing challenges related to workforce retention, training and ways of working could optimise OPCMHT contributions to integrated care for people with dementia.

Although the short-term preventive effects of mHealth consultation intervention on postpartum depressive symptoms have been demonstrated, the long-term effects and role of alleviating loneliness on depressive symptoms remain unclear.

This follow-up study extended our previous trial, which ended at three months postpartum, by continuing observation to 12 months. Participants in the original trial were randomized to the mHealth group (n = 365) or the usual care group (n = 369). Women in the mHealth group had access to free, unlimited mHealth consultation services with healthcare professionals from enrollment through four months postpartum. The primary outcome of this study was the risk of elevated postpartum depressive symptoms at 12 months post-delivery (Edinburgh Postnatal Depression Scale score of ≥9). The mediation effect of alleviating loneliness on the primary outcome was also evaluated, using the UCLA loneliness scale at three months postpartum.

A total of 515 women completed the follow-up questionnaires (mHealth group, 253/365; usual care group, 262/369; 70.2% of the original participants). Compared to the usual care group, the mHealth group had a lower risk of elevated postpartum depressive symptoms at 12 months post-delivery (36/253 [14.2%] vs. 55/262 [21.0%], risk ratio: 0.68 [95% confidence interval: 0.46–0.99]). Mediation analysis showed that reducing loneliness at three months post-delivery mediated approximately 20% of the total effect of the intervention on depressive symptoms 12 months post-delivery.

mHealth consultation services provided during the early perinatal period may help alleviate depressive symptoms at 12 months postpartum.