A rise in mental illness is expected to follow the COVID-19 pandemic, which has also been projected to lead to a deep global economic recession, further adding to risk factors.

The aim of this review was to assess the impact of the COVID-19 pandemic and previous pandemics, epidemics and economic crises on mental health.

Searches were conducted in PubMed, Web of Science, PsycINFO and Sociological Abstracts. We included studies of all populations exposed to the COVID-19 pandemic, and other similar pandemics/epidemics and economic crises, compared with non-exposed time periods or regions. The outcome was mental health.

The 174 included studies assessed mental health impacts of the COVID-19 pandemic (87 studies), 2008 economic crisis (84 studies) and severe acute respiratory syndrome (SARS) epidemic (three studies). Outcomes were divided into affective disorders, suicides, mental healthcare utilisation and other mental health. COVID-19 pandemic studies were of lesser quality than those for the economic crisis or SARS epidemic. Most studies for all exposures showed increases in affective disorders and other mental health problems. For economic crisis exposure, increases in mental healthcare utilisation and suicides were also found, but these findings were mixed for COVID-19 pandemic exposure. This is probably because of quarantine measures affecting help-seeking and shorter follow-ups of studies of COVID-19 pandemic exposure.

Our findings highlight the importance of available, accessible and sustainable mental health services. Also, socioeconomically disadvantaged populations should be particular targets of policy interventions during the COVID-19 pandemic.

Experiencing exceptionally threatening or horrifying traumas can lead to posttraumatic stress disorder (PTSD). Increasing political unrest/war/natural disasters worldwide could cause more traumatic events and change the population burden of PTSD. Most PTSD research is based on surveys, prone to selection/recall biases with inconsistent results. The aim was therefore, to use register-based data to identify the occurrence of PTSD and contributing factors in the Swedish general population.

This register-based cohort study used survival analysis. Individuals born between 1960–1995, aged ≥15 years, registered and living in Sweden, not emigrating, anytime between 1990–2015, not receiving specialized care for PTSD before 2006 were included (N = 4,673,764), and followed from their 15th/16th birth date until first PTSD diagnosis between 2006–2016 or study endpoint (31-December-2016). PTSD cases (ICD-10: F43.1) were identified from the national patient register. Mean follow-up time was 18.8 years.

Between 2006–2016, the incidence of specialized healthcare utilization for PTSD nearly doubled, and 0.7% of the study population received such care. The highest risk was observed for refugees [aHR 8.18; 95% CI:7.85–8.51] and for those with depressive disorder [aHR 4.51; 95% CI:3.95–5.14]. Higher PTSD risk was associated with female sex, older age, low education, single parenthood, low household income, urbanicity, and being born to a foreign-born parent.

PTSD is more common among refugee migrants, individuals with psychiatric disorders, and the socioeconomically disadvantaged. It is important that provision of services for PTSD are made available, particularly to these higher risk, and often hard-to-reach groups.

Underutilisation of mental health services among migrant youth has been demonstrated repeatedly, but little is known about potential discrepancies in terms of treatment receipt for those who do reach services. This study examines the type and level of care received among migrant children and descendants of migrants, particularly investigating disparities in treatment receipt given a specific diagnosis.

We used register data of the total population aged 6–17 years in Stockholm, followed from 2006 to 2015, comprising 444 196 individuals, categorised as refugees, non-refugee migrants, descendants of migrants and Swedish-born. To identify recommended treatments for specific diagnoses we used official clinical guidelines. We report logistic regression estimated odds ratios (ORs) and 95% confidence intervals (CIs) of diagnosis receipt, treatment provision and level of care where a diagnosis was first registered.

Migrant children had a lower likelihood of receiving a wide range of psychiatric diagnoses, including mood disorder (OR 0.58; 95% CI 0.52–0.64), anxiety disorder (OR 0.62; 95% CI 0.57–69) and neurodevelopmental disorder (OR 0.59; 95% CI 0.55–0.63). Moreover, when these diagnoses were set, migrant children had a lower likelihood of receiving the recommended treatments for these conditions compared to the majority individuals with the same diagnosis (OR of receiving psychotherapy for anxiety disorder and depression: 0.71; 95% CI 0.62–0.95 and 0.50; 95% CI 0.33–0.75, respectively; OR for receiving ADHD-medication: 0.49; 95% CI 0.43–0.54).

Migrant children risk underdiagnosis of various mental health conditions, and, when reaching mental health services, risk not receiving the optimal care available.

We aimed to examine the temporal relationships between traumatic events (TE), post-traumatic stress disorder (PTSD) and non-affective psychotic disorders (NAPD).

A prospective cohort study of 1 965 214 individuals born in Sweden between 1971 and 1990 examining the independent effects of interpersonal and non-interpersonal TE on incidence of PTSD and NAPD using data from linked register data (Psychiatry-Sweden). Mediation analyses tested the hypothesis that PTSD lies on a causal pathway between interpersonal trauma and NAPD.

Increasing doses of interpersonal and non-interpersonal TE were independently associated with increased risk of NAPD [linear-trend incidence rate ratios (IRR)adjusted = 2.17 [95% confidence interval (CI) 2.02–2.33] and IRRadjusted = 1.27 (95% CI 1.23–1.31), respectively]. These attenuated to a relatively small degree in 5-year time-lagged models. A similar pattern of results was observed for PTSD [linear-trend IRRadjusted = 3.43 (95% CI 3.21–3.66) and IRRadjusted = 1.45 (95% CI 1.39–1.50)]. PTSD was associated with increased risk of NAPD [IRRadjusted = 8.06 (95% CI 7.23–8.99)], which was substantially attenuated in 5-year time-lagged analyses [IRRadjusted = 4.62 (95% CI 3.65–5.87)]. There was little evidence that PTSD diagnosis mediated the relationship between interpersonal TE and NAPD [IRRadjusted = 0.92 (percentile CI 0.80–1.07)].

Despite the limitations to causal inference inherent in observational designs, the large effect-sizes observed between trauma, PTSD and NAPD in this study, consistent across sensitivity analyses, suggest that trauma may be a component cause of psychotic disorders. However, PTSD diagnosis might not be a good proxy for the likely complex psychological mechanisms mediating this association.

Characteristics of the neighbourhood environment, including population density, social fragmentation, and trust, have been linked to mental health outcomes. Using a longitudinal population-based cohort, we explored the relationship between objective and subjective neighbourhood characteristics and the odds of suicidal thoughts and attempts.

We conducted a longitudinal study of 20764 participants living in Stockholm County who participated in the Stockholm Public Health Survey. We used multilevel modelling to examine if suicidal thoughts and attempts were associated with neighbourhood characteristics, independent of individual associations. We included objective and subjective measures to explore if there was a different relationship between these measures of the neighbourhood environment and suicidality.

Associations between neighbourhood factors and suicidality were predominantly explained by individual characteristics, with the exception of neighbourhood-level deprivation and average residential trust. Each unit increase of deprivation was linked to increased odds of suicidal thoughts [Odds ratio (OR) 1.04, 95% confidence interval (CI) 1.00–1.07] and attempts (OR 1.11, 95% CI 1.06–1.17). Decreasing residential trust was associated with increased odds of suicide attempts (OR 1.09, 95% CI 1.02–1.17). There was no evidence that neighbourhood-level fragmentation or average trust in public and political institutions had an independent effect on suicidality once individual and sociodemographic factors were accounted for.

This study showed that much of the neighbourhood-level variation in suicidal thoughts and attempts could be explained by compositional factors, including sociodemographic clustering within neighbourhoods. The independent effect of neighbourhood-level deprivation and average residential trust provide evidence that the neighbourhood context may exert an independent effect on suicidality beyond the impact of individual characteristics.

Children of parents with mental disorder face multiple challenges.

To summarise evidence about parental mental disorder and child physical health.

We searched seven databases for cohort or case–control studies quantifying associations between parental mental disorders (substance use, psychotic, mood, anxiety, obsessive–compulsive, post-traumatic stress and eating) and offspring physical health. Studies were excluded if: they reported perinatal outcomes only (<28 days) or outcomes after age 18; they measured outcome prior to exposure; or the sample was drawn from diseased children. A meta-analysis was conducted. The protocol was registered on the PROSPERO database (CRD42017072620).

Searches revealed 15 945 non-duplicated studies. Forty-one studies met our inclusion criteria: ten investigated accidents/injuries; eight asthma; three other atopic diseases; ten overweight/obesity; ten studied other illnesses (eight from low-and middle-income countries (LMICs)). Half of the studies investigated maternal perinatal mental health, 17% investigated paternal mental disorder and 87% examined maternal depression. Meta-analysis revealed significantly higher rates of injuries (OR = 1.15, 95% CI 1.04–1.26), asthma (OR = 1.26, 95% CI 1.12–1.41) and outcomes recorded in LMICs (malnutrition: OR = 2.55, 95% CI 1.74–3.73; diarrhoea: OR = 2.16, 95% CI 1.65–2.84). Evidence was inconclusive for obesity and other atopic disorders.

Children of parents with mental disorder have health disadvantages; however, the evidence base is limited to risks for offspring following postnatal depression in mothers and there is little focus on fathers in the literature. Understanding the physical health risks of these vulnerable children is vital to improving lives. Future work should focus on discovering mechanisms linking physical and mental health across generations.

None.

It has been hypothesised that refugees have an increased risk of suicide.

To investigate whether risk of suicide is higher among refugees compared with non-refugee migrants from the same areas of origin and with the Swedish-born population, and to examine whether suicide rates among migrants converge to the Swedish-born population over time.

A population-based cohort design using linked national registers to follow 1 457 898 people born between 1 January 1970 and 31 December 1984, classified by migrant status as refugees, non-refugee migrants or Swedish-born. Participants were followed from their 16th birthday or date of arrival in Sweden until death, emigration or 31 December 2015, whichever came first. Cox regression models estimated adjusted hazard ratios for suicide by migrant status, controlling for age, gender, region of origin and income.

There were no significant differences in suicide risk between refugee and non-refugee migrants (hazard ratio 1.28, 95% CI 0.93–1.76) and both groups had a lower risk of suicide than Swedish born. During their first 5 years in Sweden no migrants died by suicide; however, after 21–31 years their suicide risk was equivalent to the Swedish-born population (hazard ratio 0.94, 95% CI 0.79–1.22). After adjustment for income this risk was significantly lower for migrants than the Swedish-born population.

Being a refugee was not an additional risk factor for suicide. Our findings regarding temporal changes in suicide risk suggest that acculturation and socioeconomic deprivation may account for a convergence of suicide risk between migrants and the host population over time.

None.

Prenatal infections have been proposed as a putative risk factor for a number of psychiatric outcomes across a continuum of severity. Evidence on eating disorders is scarce. We investigated whether exposure to prenatal maternal infections is associated with an increased risk of disordered eating and weight and shape concerns in adolescence in a large UK birth cohort.

We used data from the Avon Longitudinal Study of Parents and Children. The primary exposure was maternal experience of infections at any time in pregnancy. Study outcomes were presence of any, monthly or weekly disordered eating at 14 and 16 years of age, and weight and shape concerns at 14 years. We defined the causal effect of the exposure on these outcomes using a counterfactual framework adjusting our analyses for a number of hypothesised confounders, and imputing missing confounder data using multiple imputation.

In total, 4884 children had complete exposure and outcome data at age 14 years, and 4124 at 16 years. Exposed children had a greater risk of reporting weekly disordered eating at both age 14 [risk difference (RD) 0.9%, 95% confidence interval (CI) −0.01 to 1.9, p = 0.08] and 16 (RD 2.3%, 95% CI 0.6–3.9, p < 0.01), though evidence of an association was weak at age 14 years. Exposed children also had greater weight and shape concerns at age 14 years (mean difference 0.15, 95% CI 0.05–0.26, p < 0.01).

Exposure to prenatal maternal infection is associated with greater risk of disordered eating in adolescence. This association could be explained by in utero processes leading to impaired neurodevelopment or altered immunological profiles. Residual confounding cannot be excluded.

We assessed whether the risk of various psychotic disorders and non-psychotic bipolar disorder (including mania) varied by migrant status, a region of origin, or age-at-migration, hypothesizing that risk would only be elevated for psychotic disorders.

We established a prospective cohort of 1 796 257 Swedish residents born between 1982 and 1996, followed from their 15th birthday, or immigration to Sweden after age 15, until diagnosis, emigration, death, or end of 2011. Cox proportional hazards models were used to model hazard ratios by migration-related factors, adjusted for covariates.

All psychotic disorders were elevated among migrants and their children compared with Swedish-born individuals, including schizophrenia and schizoaffective disorder (adjusted hazard ratio [aHR]migrants: 2.20, 95% CI 1.96–2.47; aHRchildren : 2.00, 95% CI 1.79–2.25), affective psychotic disorders (aHRmigrant1.42, 95% CI 1.25–1.63; aHRchildren: 1.22 95% CI 1.07–1.40), and other non-affective psychotic disorders (aHRmigrant: 1.97, 95% CI 1.81–2.14; aHRchildren: 1.68, 95% CI 1.54–1.83). For all psychotic disorders, risks were generally highest in migrants from Africa (i.e. aHRschizophrenia: 5.24, 95% CI 4.26–6.45) and elevated at most ages-of-migration. By contrast, risk of non-psychotic bipolar disorders was lower for migrants (aHR: 0.58, 95% CI 0.52–0.64) overall, and across all ages-of-migration except infancy (aHR: 1.20; 95% CI 1.01–1.42), while risk for their children was similar to the Swedish-born population (aHR: 1.00, 95% CI 0.93–1.08).

Increased risk of psychiatric disorders associated with migration and minority status may be specific to psychotic disorders, with exact risk dependent on the region of origin.

Schizophrenia is associated with impaired neurodevelopment as indexed by lower premorbid IQ. We examined associations between erythrocyte sedimentation rate (ESR), a marker of low-grade systemic inflammation, IQ, and subsequent schizophrenia and other non-affective psychoses (ONAP) to elucidate the role of neurodevelopment and inflammation in the pathogenesis of psychosis.

Population-based data on ESR and IQ from 638 213 Swedish men assessed during military conscription between 1969 and 1983 were linked to National Hospital Discharge Register for hospitalisation with schizophrenia and ONAP. The associations of ESR with IQ (cross-sectional) and psychoses (longitudinal) were investigated using linear and Cox-regression. The co-relative analysis was used to examine effects of shared familial confounding. We examined mediation and moderation of effect between ESR and IQ on psychosis risk.

Baseline IQ was associated with subsequent risk of schizophrenia (adjusted HR per 1-point increase in IQ = 0.961; 95% confidence interval (CI) 0.960–0.963) and ONAP (adjusted HR = 0.973; 95% CI 0.971–0.975). Higher ESR was associated with lower IQ in a dose-response fashion. High ESR was associated with increased risk for schizophrenia (adjusted HR = 1.14; 95% CI 1.01–1.28) and decreased risk for ONAP (adjusted HR = 0.85; 95% CI 0.74–0.96), although these effects were specific to one ESR band (7–10 mm/hr). Familial confounding explained ESR-IQ but not ESR-psychoses associations. IQ partly mediated the ESR-psychosis relationships.

Lower IQ is associated with low-grade systemic inflammation and with an increased risk of schizophrenia and ONAP in adulthood. Low-grade inflammation may influence schizophrenia risk by affecting neurodevelopment. Future studies should explore the differential effects of inflammation on different types of psychosis.

Maternal vitamin D deficiency may increase risk of autism spectrum disorder (ASD), but direct evidence is lacking.

To clarify the relationship between maternal vitamin D deficiency and offspring risk of ASD with and without intellectual disability.

Using a register-based total population study (N=509 639), we calculated adjusted odds ratios (aORs) and 95% confidence intervals (CIS) of ASD with and without intellectual disability in relation to lifetime diagnoses of maternal vitamin D deficiency. Although rare, such deficiency was associated with offspring risk of ASD with, but not without, intellectual disability (aORs 2.51, 95% CI 1.22–5.16 and 1.28, 0.68–2.42). Relationships were stronger in non-immigrant children.

If reflecting associations for prenatal hypovitaminosis, these findings imply gestational vitamin D substitution as a means of ASD prevention.

Migration has been implicated as a risk factor for autism, but evidence is limited and inconsistent.

To investigate the relationship between parental migration status and risk of autism spectrum disorder, taking into consideration the importance of region of origin, timing of migration and possible discrepancies in associations between autism subtypes.

Record-linkage study within the total child population of Stockholm County between 2001 and 2007. Individuals with high- and low-functioning autism were defined as having autism spectrum disorder with and without comorbid intellectual disability, and ascertained via health and habilitation service registers.

In total, 4952 individuals with autism spectrum disorder were identified, comprising 2855 children with high-functioning autism and 2097 children with low-functioning autism. Children of migrant parents were at increased risk of low-functioning autism (odds ratio (OR) = 1.5, 95% CI 1.3–1.7); this risk was highest when parents migrated from regions with a low human development index, and peaked when migration occurred around pregnancy (OR = 2.3, 95% CI 1.7–3.0). A decreased risk of high-functioning autism was observed in children of migrant parents, regardless of area of origin or timing of migration. Parental age, income or obstetric complications did not fully explain any of these associations.

Environmental factors associated with migration may contribute to the development of autism presenting with comorbid intellectual disability, especially when acting in utero. High- and low-functioning autism may have partly different aetiologies, and should be studied separately.

For complex multifactorial diseases it seems likely that co-exposure to two risk factors will show a greater than additive relationship on disease risk.

To test whether greater than additive relationships occur between risk factors for psychosis.

A cohort study of 50 053 Swedish conscripts. Data on IQ, cannabis use, psychiatric diagnoses, disturbed behaviour and social relations assessed at age 18 were linked to admissions with any non-affective psychoses over a 27-year follow-up period. Statistical interactions between risk factors were examined under both additive and multiplicative models.

There was some evidence of interaction for eight of the ten combinations of risk factors under additive models, but for only one combination under multiplicative models.

Multiplicative models describe the joint effect of risk factors more adequately than additive ones do. However, the implications of finding interactions as observed here, or for most interactions reported to date, remain very limited.

Previously reported associations between advancing paternal age and schizophrenia could be due to an increase in paternal germ cell mutations or be confounded by heritable personality traits associated with schizophrenia that result in delayed parenthood.

To investigate this association while adjusting for personality traits related to poor social integration in the subjects.

A cohort of 50 087 adolescent males was followed up by record linkage to determine hospital admissions for schizophrenia between 1970 and 1996.

Advancing paternal age was associated with an increased risk of developing schizophrenia in a ‘dose-dependent’ manner. The adjusted odds ratio for each 10-year increase in paternal age was 1.3 (95% Cl 1.0–1.5; P=0.015).

Advancing paternal age is an independent risk factor for schizophrenia. Adjusting for social integration in subjects made little difference to this association, consistent with the hypothesis that advancing paternal age may increase liability to schizophrenia owing to accumulating germ cell mutations.

Previous research has found an association between obstetric complications and schizophrenia, but in many studies the sample size was limited, and no assessment of specific exposures was possible.

To assess the role of different complications, and in particular to distinguish between disordered foetal development and hypoxia at birth.

From the Stockholm County In-Patient Register and community registers, we identified 524 cases of schizophrenia and 1043 controls, matched for age, gender, hospital and parish of birth. Data on obstetric complications were obtained from birth records.

There was a strong association between signs of asphyxia at birth and schizophrenia (OR 4.4; 95% C11.9–10.3) after adjustment for other obstetric complications, maternal history of psychotic illness and social class.

Signs of asphyxia at birth are associated with an increased risk of schizophrenia in adults.

Obstetric complications have been studied frequently as possible risk factors for schizophrenia.

To test the hypotheses that individual obstetric complications are most strongly associated with an increased risk of schizophrenia in males, in patients with an early age at first diagnosis and in subjects with a maternal history of psychosis.

Cases of schizophrenia diagnosed between January 1971 and June 1994 were identified in the Stockholm County In-Patient Register. Controls were matched on age, gender, hospital of birth and parish of birth. Obstetric data were recorded blind to case–control status for 524 cases and 1043 controls.

This study did not find any large or consistent effect of gender, age at diagnosis or maternal history of psychosis on the risk of schizophrenia associated with individual complications.

Future studies should examine these effects using a much larger sample that includes patients with schizophrenia and control subjects whose genetic risk of schizophrenia has been assessed accurately.