MRI of functional connectivity, cortical thickness, surface area, and gray matter volume was carried out in 28 female-to-male transsexuals (FtM-TR) and 68 cis-sexual controls (34 male). FtM-TR displayed thicker mid-frontal, precuneal-parietal, and lingual cortex than both male and female controls, whereas, in regions with reported anatomical sex differences among the controls, FtM-TR followed patterns of the gender assigned at their birth. FtM-TR also displayed weaker functional connections from the pregenual anterior cingulate to the insular cortex, and the temporo parietal junction compared with both control groups. Distinct structural and functional pattern in the own-body image network may represent biological markers for the dysphoric own-body perception in transgender individuals.

BackgroundChildren of parents with mental disorder face multiple challenges.AimsTo summarise evidence about parental mental disorder and child physical health.MethodWe 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).ResultsSearches 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.ConclusionsChildren 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.Declaration of interestNone.

Summary Background Little information exists about the prevalence of children exposed to maternal mental illness. We aimed to estimate the prevalence of children and adolescents exposed to maternal mental illness in the UK between 2005 and 2017 using primary care data. Methods In this national retrospective cohort study, we included children aged 0–16 years born between Jan 1, 1991, and Dec 31, 2015, who were linked to their mothers and registered on the primary care Clinical Practice Research Datalink (CPRD) between 2005 and 2017. We extracted data on diagnosis, symptoms, and therapy from the CRPD to define the following maternal mental illnesses: depression, anxiety, non-affective psychosis, affective psychosis, eating disorders, personality disorders, alcohol misuse disorder, and substance misuse disorder. We also extracted data on socioeconomic status from the Index of Multiple Deprivation 2010 and data on ethnicity from the Hospital Episode Statistics dataset. The main outcome was prevalence of maternal mental illness. Prevalence was calculated for each 2-year period of childhood (from age 0–<2 to 14–<16 years) using marginal predictions from a logistic regression model. We used survival analysis to estimate the incidence and cumulative risk of children experiencing maternal mental illness by age 16 years. Findings We identified 783 710 children registered in the UK CPRD mother-baby link database, and included 547 747 children (381 685 mothers) in our analysis. Overall prevalence of maternal mental illness was 23·2% (95% CI 23·1–23·4), which increased during childhood (21·9%, 21·7–22·1 among the 0–<2 year age group vs 27·3%, 26·8–27·8 among the 14–<16 year age group). Depression and anxiety were the most prevalent maternal mental illnesses. The proportion of children exposed to maternal mental illness increased from 22·2% (21·9–22·4) between 2005 and 2007 to 25·1% (24·8–25·5) between 2015 and 2017. Geographically, the highest prevalence of maternal mental illness was observed in Northern Ireland (29·8%, 29·0–30·5). In England, prevalence of maternal mental illness was highest among children in the most deprived areas (28·3%, 27·8–28·8). The incidence of maternal mental illness was highest between 0–3 months (26·7 per 100 person years, 26·4–27·1). By age 16 years, the cumulative risk of maternal mental illness was 53·1% (52·8–53·3). Interpretation One in four children aged 0–16 years are exposed to maternal mental illness and the prevalence of diagnosed and treated maternal mental illness is increasing. Policy makers and commissioners should consider this information and channel resources to target individuals in greatest need. Funding The European Research Council and the National Institute for Health Research.

Although many studies indicate the interplay of genetic and environmental factors in the etiology of autism spectrum disorder (ASD), our limited understanding of the underlying mechanisms hampers the development of effective ways of detecting and preventing the disorder. Recent studies support the hypothesis that prenatal androgen exposure contributes to the development of ASD. This would suggest that maternal polycystic ovary syndrome (PCOS), a condition associated with excess androgens, would increase the risk of ASD in the offspring. We conducted a matched case–control study nested within the total population of Sweden (children aged 4–17 who were born in Sweden from 1984 to 2007). The sample consisted of 23 748 ASD cases and 208 796 controls, matched by birth month and year, sex and region of birth. PCOS and ASD were defined from ICD codes through linkage to health-care registers. Maternal PCOS increased the odds of ASD in the offspring by 59%, after adjustment for confounders (odds ratio (OR) 1.59, 95% confidence interval (CI) 1.34–1.88). The odds of offspring ASD were further increased among mothers with both PCOS and obesity, a condition common to PCOS that is related to more severe hyperandrogenemia (OR 2.13, 95% CI 1.46–3.10). Risk estimates did not differ between sexes. In conclusion, children of women with PCOS appear to have a higher risk of developing ASD. This finding awaits confirmation, and exploration of potentially underlying mechanisms, including the role of sex steroids in the etiology of ASD.