OBJECTIVES: The authors used nationwide survey data to characterize current public conceptions related to recognition of mental illness and perceived causes, dangerousness, and desired social distance. METHODS: Data were derived from a vignette experiment included in the 1996 General Social Survey. Respondents (n = 1444) were randomly assigned to 1 of 5 vignette conditions. Four vignettes described psychiatric disorders meeting diagnostic criteria, and the fifth depicted a "troubled person" with subclinical problems and worries. RESULTS: Results indicate that the majority of the public identifies schizophrenia (88%) and major depression (69%) as mental illnesses and that most report multicausal explanations combining stressful circumstances with biologic and genetic factors. Results also show, however, that smaller proportions associate alcohol (49%) or drug (44%) abuse with mental illness and that symptoms of mental illness remain strongly connected with public fears about potential violence and with a desire for limited social interaction. CONCLUSIONS: While there is reason for optimism in the public's recognition of mental illness and causal attributions, a strong stereotype of dangerousness and desire for social distance persist. These latter conceptions are likely to negatively affect people with mental illness.

These findings represent the first serologic evidence that prenatal influenza plays a role in schizophrenia. If confirmed, the results may have implications for the prevention of schizophrenia and for unraveling pathogenic mechanisms of the disorder.

Context Prenatal folic acid supplements reduce the risk of neural tube defects in children, but it has not been determined whether they protect against other neurodevelopmental disorders. Objective To examine the association between maternal use of prenatal folic acid supplements and the subsequent risk of autistic disorder in children. Design, Setting, and Patients The study sample of 85,176 was derived from the population-based, prospective Norwegian Mother and Child Cohort Study (MoBa). The children were born in 2002–08. By the end of follow-up on March 31st, 2012, the age range was 3.3–10.2 years and the mean age 6.4 years. The exposure of primary interest was use of folic acid from 4 weeks before to 8 weeks after the start of pregnancy. The start of pregnancy was defined as the first day of the last menstrual period before conception. Relative risks of ASD were estimated by odds ratios (ORs) with 95% confidence intervals (CIs) in a logistic regression analysis. Analyses were adjusted for maternal education level, year of birth, and parity. Main Outcome Measure Specialist-confirmed diagnosis of autistic disorder. Results To date, 114 children in the study sample have been diagnosed with autistic disorder. In children whose mothers took folic acid, 0.10% (64/61,042) had autistic disorder, compared with 0.21% (50/24,134) in those unexposed to folic acid. The adjusted OR for autistic disorder in children of folic acid users was 0.61 (95% CI, 0.41–0.90). Similar analyses for prenatal fish oil supplements showed no such association with autistic disorder, even though fish oil use was associated with the same maternal characteristics as folic acid use. Conclusion Prenatal folic acid supplements around the time of conception were associated with a lower risk of autistic disorder in the MoBa cohort.

Objective To examine the relation between birth weight and measured intelligence at age 7 years in children within the normal range of birth weight and in siblings. Design Cohort study of siblings of the same sex. Setting 12 cities in the United States. Subjects 3484 children of 1683 mothers in a birth cohort study during the years 1959 through 1966. The sample was restricted to children born at >37 weeks gestation and with birth weights of 1500-3999 g. Main outcome measure Full scale IQ at age 7 years. Results Mean IQ increased monotonically with birth weight in both sexes across the range of birth weight in a linear regression analysis of one randomly selected sibling per family (n = 1683) with adjustment for maternal age, race, education, socioeconomic status, and birth order. Within same sex sibling pairs, differences in birth weight were directly associated with differences in IQ in boys (812 pairs, predicted IQ difference per 100 g change in birth weight = 0.50, 95% confidence interval 0.28 to 0.71) but not girls (871 pairs, 0.10, − 0.09 to 0.30). The effect in boys remained after differences in birth order, maternal smoking, and head circumference were adjusted for and in an analysis restricted to children with birth weight > 2500 g. Conclusion The increase in childhood IQ with birth weight continues well into the normal birth weight range. For boys this relation holds within same sex sibships and therefore cannot be explained by confounding from family social environment.

One important line of epidemiologic inquiry implicating social context in the etiology of psychosis is the examination of spatial variation in the distribution of psychotic illness. The authors conducted a systematic review of evidence from urbanicity and neighborhood studies regarding spatial variation in the incidence of psychosis in developed countries since 1950. A total of 44 studies (20 of urbanicity and 24 of neighborhood) were culled from three databases with similar time frames: Medline (1950-2007), PsychInfo (1950-2007), and Sociological Abstracts (1952-2007). With a special emphasis on social factors potentially relevant to etiology, the authors elucidated contributions, limitations, and issues related to study design, measurement, and theory. Evidence from both arenas supports a possible etiologic role for social context. Studies of urbanicity indicate that early-life exposure may be important; dose-response relations, spatial patterning of schizophrenia, and interactions with other factors may exist. Neighborhood studies indicate heterogeneity in rates, hint at spatial patterning of schizophrenia, and offer intriguing evidence implying more proximal social (as opposed to physical) exposures. The authors encourage the exploration of social pathways engaging theory, methodological advances, and the life-course perspective. They also propose a conceptual shift from studies of spatial variation in outcomes to research addressing the etiologic effect of exposures shaped by place as a reservoir of risk or resilience.

Advancing paternal and maternal age have both been associated with risk for autism spectrum disorders (ASD). However, the shape of the association remains unclear, and results on the joint associations is lacking. This study tests if advancing paternal and maternal ages are independently associated with ASD risk and estimates the functional form of the associations. In a population-based cohort study from five countries (Denmark, Israel, Norway, Sweden and Western Australia) comprising 5 766 794 children born 1985–2004 and followed up to the end of 2004–2009, the relative risk (RR) of ASD was estimated by using logistic regression and splines. Our analyses included 30 902 cases of ASD. Advancing paternal and maternal age were each associated with increased RR of ASD after adjusting for confounding and the other parent's age (mothers 40–49 years vs 20–29 years, RR=1.15 (95% confidence interval (CI): 1.06–1.24), P-value<0.001; fathers⩾50 years vs 20–29 years, RR=1.66 (95% CI: 1.49–1.85), P-value<0.001). Younger maternal age was also associated with increased risk for ASD (mothers <20 years vs 20–29 years, RR=1.18 (95% CI: 1.08–1.29), P-value<0.001). There was a joint effect of maternal and paternal age with increasing risk of ASD for couples with increasing differences in parental ages. We did not find any support for a modifying effect by the sex of the offspring. In conclusion, as shown in multiple geographic regions, increases in ASD was not only limited to advancing paternal or maternal age alone but also to differences parental age including younger or older similarly aged parents as well as disparately aged parents.

The data indicate substantially elevated rates of schizophrenia among African Americans in comparison with whites in this birth cohort. The association may have been partly but not wholly mediated by an effect of race on family SES.

Standard gross placental measures capture dimensions relevant to specific placental functions. Our objective was to determine their accountability independent of placental weight for variance in birthweight, an important proxy for intrauterine 'adequacy' in fetal origins studies. The sample consisted of 24 152 singleton liveborn children of the Collaborative Perinatal Project delivered from 34 to 42 completed weeks gestation, with complete data for six placental measures (placental disc shape, umbilical cord length, distance from cord insertion to nearest margin, large diameter, small diameter, placental thickness) and placental weight. Associations between birthweight and placental measures were examined using multiple linear regression. Placental weight alone accounted for 36.6% of birthweight variation; the six other placental measures accounted for 28.1%. Combined, all placental measures accounted for 39.1% of birthweight variation. Seven maternal characteristics (age, height, weight, parity, socio-economic status, cigarette use, and race) were investigated to determine whether their known associations with birthweight were mediated by placental markers. Analysis suggested that the impact of all maternal characteristics except smoking was consistent with mediation by placental characteristics.