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Introduction The Covid-19 pandemic affects maternal health both directly and indirectly, and direct and indirect effects are intertwined. To provide a comprehensive overview on this broad topic in a rapid format behooving an emergent pandemic we conducted a scoping review. Methods A scoping review was conducted to compile evidence on direct and indirect impacts of the pandemic on maternal health and provide an overview of the most significant outcomes thus far. Working papers and news articles were considered appropriate evidence along with peer-reviewed publications in order to capture rapidly evolving updates. Literature in English published from January 1st to September 11 2020 was included if it pertained to the direct or indirect effects of the COVID-19 pandemic on the physical, mental, economic, or social health and wellbeing of pregnant people. Narrative descriptions were written about subject areas for which the authors found the most evidence. Results The search yielded 396 publications, of which 95 were included. Pregnant individuals were found to be at a heightened risk of more severe symptoms than people who are not pregnant. Intrauterine, vertical, and breastmilk transmission were unlikely. Labor, delivery, and breastfeeding guidelines for COVID-19 positive patients varied. Severe increases in maternal mental health issues, such as clinically relevant anxiety and depression, were reported. Domestic violence appeared to spike. Prenatal care visits decreased, healthcare infrastructure was strained, and potentially harmful policies implemented with little evidence. Women were more likely to lose their income due to the pandemic than men, and working mothers struggled with increased childcare demands. Conclusion Pregnant women and mothers were not found to be at higher risk for COVID-19 infection than people who are not pregnant, however pregnant people with symptomatic COVID-19 may experience more adverse outcomes compared to non-pregnant people and seem to face disproportionate adverse socio-economic consequences. High income and low- and middle-income countries alike faced significant struggles. Further resources should be directed towards quality epidemiological studies. Plain English summary The Covid-19 pandemic impacts reproductive and perinatal health both directly through infection itself but also indirectly as a consequence of changes in health care, social policy, or social and economic circumstances. The direct and indirect consequences of COVID-19 on maternal health are intertwined. To provide a comprehensive overview on this broad topic we conducted a scoping review. Pregnant women who have symptomatic COVID-19 may experience more severe outcomes than people who are not pregnant. Intrauterine and breastmilk transmission, and the passage of the virus from mother to baby during delivery are unlikely. The guidelines for labor, delivery, and breastfeeding for COVID-19 positive patients vary, and this variability could create uncertainty and unnecessary harm. Prenatal care visits decreased, healthcare infrastructure was strained, and potentially harmful policies are implemented with little evidence in high and low/middle income countries. The social and economic impact of COVID-19 on maternal health is marked. A high frequency of maternal mental health problems, such as clinically relevant anxiety and depression, during the epidemic are reported in many countries. This likely reflects an increase in problems, but studies demonstrating a true change are lacking. Domestic violence appeared to spike. Women were more vulnerable to losing their income due to the pandemic than men, and working mothers struggled with increased childcare demands. We make several recommendations: more resources should be directed to epidemiological studies, health and social services for pregnant women and mothers should not be diminished, and more focus on maternal mental health during the epidemic is needed.

This study investigated the association between pre-pregnancy body mass index (BMI) and adverse pregnancy outcomes among women participated in the National Free Preconception Health Examination Project in Guangdong Province, China, and explored these associations according to maternal age. Pre-pregnancy BMI was classified into underweight (BMI < 18.5 kg/m 2 ), healthy weight (18.5–23.9 kg/m 2 ), overweight (24.0–27.9 kg/m 2 ), and obesity (≥ 28.0 kg/m 2 ) according to Chinese criteria. Outcomes were preterm birth (PTB, delivery before 37 weeks of gestation), large for gestational age (LGA, birthweight above the 90th percentile for gestational age by infants’ sex), small for gestational age (SGA, birthweight below the 10th percentile for gestational age by infants’ sex), primary caesarean delivery, shoulder dystocia or birth injury, and stillbirth. Adjusted incidence risk ratios (aIRR) were calculated for underweight, overweight and obesity, respectively. Compared with healthy weight, underweight was associated with increased risk of PTB (aIRR 1.06, 95%CI 1.04–1.09) and SGA (1.23, 1.22–1.26) but inversely associated with LGA (0.83, 0.82–0.85), primary caesarean delivery (0.88, 0.87–0.90) and stillbirth (0.73, 0.53–0.99). Overweight was associated with increased risk of LGA (1.17, 1.14–1.19), primary caesarean delivery (1.18, 1.16–1.20) and stillbirth (1.44, 1.03–2.06), but inversely associated with SGA (0.92, 0.90–0.95) and shoulder dystocia or birth injury (0.86, 0.79–0.93). Obesity was associated with increased risk of PTB (1.12, 1.05–1.20), LGA (1.32, 1.27–1.37), primary caesarean delivery (1.45, 1.40–1.50), but inversely associated with SGA (0.92, 0.87–0.97). The aIRRs for underweight, overweight and obesity in relation to these adverse pregnancy outcomes ranged from 0.65 to 1.52 according to maternal age. In Chinese population, maternal pre-pregnancy BMI was significantly associated with the risk of adverse pregnancy outcomes and the risk differs according to maternal age. Further investigation is warranted to determine whether and how counselling and interventions for women with low or increased BMI before pregnancy can reduce the risk of adverse pregnancy outcomes.

Loneliness is a major risk factor for both psychological disturbance and poor health outcomes in adults. This study aimed to assess whether loneliness is associated with a long-term disruption in mental health that extends into adulthood. This study is based on the longitudinal, community-representative Great Smoky Mountains Study of 1420 participants. Participants were assessed with the structured Child and Adolescent Psychiatric Assessment interview up to eight times in childhood (ages 9-16; 6674 observations; 1993-2000) for childhood loneliness, associated psychiatric comorbidities and childhood adversities. Participants were followed up four times in adulthood (ages 19, 21, 25, and 30; 4556 observations of 1334 participants; 1999-2015) with the structured Young Adult Psychiatric Assessment Interview for psychiatric anxiety, depression, and substance use outcomes. Both self and parent-reported childhood loneliness were associated with adult self-reported anxiety and depressive outcomes. The associations remained significant when childhood adversities and psychiatric comorbidities were accounted for. There was no evidence for an association of childhood loneliness with adult substance use disorders. More associations were found between childhood loneliness and adult psychiatric symptoms than with adult diagnostic status. Childhood loneliness is associated with anxiety and depressive disorders in young adults, suggesting that loneliness - even in childhood - might have long-term costs in terms of mental health. This study underscores the importance of intervening early to prevent loneliness and its sequelae over time.

Background Sexual minority status is associated with face-to-face bullying and cyberbullying victimization. However, limited studies have investigated whether such a relationship differs by sex or grade in a nationally representative sample. Methods We concatenated the national high school data from the Youth Risk Behavior Surveillance System (YRBSS) chronologically from 2015 to 2019, resulting in a sample of 32,542 high school students. We constructed models with the interaction term between sexual minority status and biological sex assigned at birth to test the effect modification by sex on both the multiplicative and additive scales. A similar method was used to test the effect modification by grade. Results Among heterosexual students, females had a higher odds of being bullied than males, while among sexual minority students, males had a higher odds of being bullied. The effect modification by sex was significant on both the multiplicative and additive scales. We also found a decreasing trend of bullying victimization as the grade increased among both heterosexual and sexual minority students. The effect modification by the grade was significant on both the multiplicative and the additive scale. Conclusions Teachers and public health workers should consider the difference in sex and grade when designing prevention programs to help sexual minority students.

Insomnia is the second most prevalent mental disorder, with no sufficient treatment available. Despite substantial heritability, insight into the associated genes and neurobiological pathways remains limited. Here, we use a large genetic association sample ( n  = 1,331,010) to detect novel loci and gain insight into the pathways, tissue and cell types involved in insomnia complaints. We identify 202 loci implicating 956 genes through positional, expression quantitative trait loci, and chromatin mapping. The meta-analysis explained 2.6% of the variance. We show gene set enrichments for the axonal part of neurons, cortical and subcortical tissues, and specific cell types, including striatal, hypothalamic, and claustrum neurons. We found considerable genetic correlations with psychiatric traits and sleep duration, and modest correlations with other sleep-related traits. Mendelian randomization identified the causal effects of insomnia on depression, diabetes, and cardiovascular disease, and the protective effects of educational attainment and intracranial volume. Our findings highlight key brain areas and cell types implicated in insomnia, and provide new treatment targets. Genome-wide analyses in >1 million individuals identify new loci and pathways associated with insomnia. The findings implicate key brain areas and cell types in the neurobiology of insomnia and highlight potential targets for developing new treatments.

Being a morning person is a behavioural indicator of a person’s underlying circadian rhythm. Using genome-wide data from 697,828 UK Biobank and 23andMe participants we increase the number of genetic loci associated with being a morning person from 24 to 351. Using data from 85,760 individuals with activity-monitor derived measures of sleep timing we find that the chronotype loci associate with sleep timing: the mean sleep timing of the 5% of individuals carrying the most morningness alleles is 25 min earlier than the 5% carrying the fewest. The loci are enriched for genes involved in circadian regulation, cAMP, glutamate and insulin signalling pathways, and those expressed in the retina, hindbrain, hypothalamus, and pituitary. Using Mendelian Randomisation, we show that being a morning person is causally associated with better mental health but does not affect BMI or risk of Type 2 diabetes. This study offers insights into circadian biology and its links to disease in humans. GWAS have previously found 24 genomic loci associated with chronotype, an individual’s preference for early or late sleep timing. Here, the authors identify 327 additional loci in a sample of 697,828 individuals and further explore the relationships of chronotype with metabolic and psychiatric diseases.

Sleep is an essential state of decreased activity and alertness but molecular factors regulating sleep duration remain unknown. Through genome-wide association analysis in 446,118 adults of European ancestry from the UK Biobank, we identify 78 loci for self-reported habitual sleep duration ( p  < 5 × 10 −8 ; 43 loci at p  < 6 × 10 −9 ). Replication is observed for PAX8 , VRK2 , and FBXL12/UBL5/PIN1 loci in the CHARGE study ( n  = 47,180; p  < 6.3 × 10 −4 ), and 55 signals show sign-concordant effects. The 78 loci further associate with accelerometer-derived sleep duration, daytime inactivity, sleep efficiency and number of sleep bouts in secondary analysis ( n  = 85,499). Loci are enriched for pathways including striatum and subpallium development, mechanosensory response, dopamine binding, synaptic neurotransmission and plasticity, among others. Genetic correlation indicates shared links with anthropometric, cognitive, metabolic, and psychiatric traits and two-sample Mendelian randomization highlights a bidirectional causal link with schizophrenia. This work provides insights into the genetic basis for inter-individual variation in sleep duration implicating multiple biological pathways. Sleep is essential for homeostasis and insufficient or excessive sleep are associated with adverse outcomes. Here, the authors perform GWAS for self-reported habitual sleep duration in adults, supported by accelerometer-derived measures, and identify genetic correlation with psychiatric and metabolic traits

Neuroticism is an important risk factor for psychiatric traits, including depression 1 , anxiety 2 , 3 , and schizophrenia 4 – 6 . At the time of analysis, previous genome-wide association studies 7 – 12 (GWAS) reported 16 genomic loci associated to neuroticism 10 – 12 . Here we conducted a large GWAS meta-analysis ( n  = 449,484) of neuroticism and identified 136 independent genome-wide significant loci (124 new at the time of analysis), which implicate 599 genes. Functional follow-up analyses showed enrichment in several brain regions and involvement of specific cell types, including dopaminergic neuroblasts ( P  = 3.49 × 10 −8 ), medium spiny neurons ( P  = 4.23 × 10 −8 ), and serotonergic neurons ( P  = 1.37 × 10 −7 ). Gene set analyses implicated three specific pathways: neurogenesis ( P  = 4.43 × 10 −9 ), behavioral response to cocaine processes ( P  = 1.84 × 10 −7 ), and axon part ( P  = 5.26 × 10 −8 ). We show that neuroticism’s genetic signal partly originates in two genetically distinguishable subclusters 13 (‘depressed affect’ and ‘worry’), suggesting distinct causal mechanisms for subtypes of individuals. Mendelian randomization analysis showed unidirectional and bidirectional effects between neuroticism and multiple psychiatric traits. These results enhance neurobiological understanding of neuroticism and provide specific leads for functional follow-up experiments. A meta-analysis of genome-wide association studies for neuroticism identifies novel loci, pathways and potential drug targets. Further analysis implicates specific brain regions and evaluates genetic overlap with other neuropsychiatric traits.

Attention-deficit and hyperactivity disorder (ADHD) is a common childhood disorder with a substantial genetic component. However, the extent to which epigenetic mechanisms play a role in the etiology of the disorder is unknown. We performed epigenome-wide association studies (EWAS) within the Pregnancy And Childhood Epigenetics (PACE) Consortium to identify DNA methylation sites associated with ADHD symptoms at two methylation assessment periods: birth and school age. We examined associations of both DNA methylation in cord blood with repeatedly assessed ADHD symptoms (age 4–15 years) in 2477 children from 5 cohorts and of DNA methylation at school age with concurrent ADHD symptoms (age 7–11 years) in 2374 children from 9 cohorts, with 3 cohorts participating at both timepoints. CpGs identified with nominal significance ( p  < 0.05) in either of the EWAS were correlated between timepoints ( ρ  = 0.30), suggesting overlap in associations; however, top signals were very different. At birth, we identified nine CpGs that predicted later ADHD symptoms ( p  < 1 × 10 –7 ), including ERC2 and CREB5 . Peripheral blood DNA methylation at one of these CpGs (cg01271805 in the promoter region of ERC2 , which regulates neurotransmitter release) was previously associated with brain methylation. Another (cg25520701) lies within the gene body of CREB5 , which previously was associated with neurite outgrowth and an ADHD diagnosis. In contrast, at school age, no CpGs were associated with ADHD with p  < 1 × 10 −7 . In conclusion, we found evidence in this study that DNA methylation at birth is associated with ADHD. Future studies are needed to confirm the utility of methylation variation as biomarker and its involvement in causal pathways.

Although a genetic basis of depression has been well established in twin studies, identification of genome-wide significant loci has been difficult. We hypothesized that bivariate analyses of findings from a meta-analysis of genome-wide association studies (meta-GWASs) of the broad depression phenotype with those from meta-GWASs of self-reported and recurrent major depressive disorder (MDD), bipolar disorder and schizophrenia would enhance statistical power to identify novel genetic loci for depression. LD score regression analyses were first used to estimate the genetic correlations of broad depression with self-reported MDD, recurrent MDD, bipolar disorder and schizophrenia. Then, we performed four bivariate GWAS analyses. The genetic correlations (rg ± SE) of broad depression with self-reported MDD, recurrent MDD, bipolar disorder and schizophrenia were 0.79 ± 0.07, 0.24 ± 0.08, 0.53 ± 0.09 and 0.57 ± 0.05, respectively. From a total of 20 independent genome-wide significant loci, 13 loci replicated of which 8 were novel for depression. These were MUC21 for the broad depression phenotype with self-reported MDD and ZNF804A, MIR3143, PSORS1C2, STK19, SPATA31D1, RTN1 and TCF4 for the broad depression phenotype with schizophrenia. Post-GWAS functional analyses of these loci revealed their potential biological involvement in psychiatric disorders. Our results emphasize the genetic similarities among different psychiatric disorders and indicate that cross-disorder analyses may be the best way forward to accelerate gene finding for depression, or psychiatric disorders in general.