It is not well known whether the association between common mental disorders and low socioeconomic status vary with symptom severity, type of socioeconomic indicator or gender.

To study the association between socioeconomic status and risk for different severity levels of psychological distress as well as depression.

A population-based survey was conducted among a random sample of Stockholm County residents aged 18–84 years in 2002, and respondents were reassessed via a follow-up questionnaire in 2007. Participants in both surveys (n = 23 794) were categorized according to socioeconomic status at baseline and followed up for onset of psychological distress (according to the twelve-item general health questionnaire) and depression (according to health data registers).

Occupational class had little impact on risk for distress regardless of severity or gender, but was strongly associated with onset of depression - albeit only in men (ORs being 3.0 [95% CI 1.5–5.9] in men and 1.1 [95% CI (0.7–1.7]) in women, comparing unskilled manual workers with higher non-manual workers). Income was associated with risk for onset of all outcomes and the association grew stronger with symptom severity. High household income was particularly protective of depression in women. Education was unrelated to either outcome in men and women overall.

While psychological distress appears to occur at a similar rate regardless of socioeconomic position, risks for severe distress and especially clinically overt depression are markedly linked with occupational class in men and with family income in women. The socioeconomic gradient in common mental disorders increases with symptom severity.

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.

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.