Insomnia and the inability to sleep affect people’s health and well-being. However, its systematic estimates of prevalence and distribution in the general population in China are still lacking. A population-based cluster sampling survey was conducted in the rural and urban areas of Hunan, China. Subjects (n = 26,851) were sampled from the general population, with a follow-up using the Pittsburgh Sleep Quality Index (PSQI) for interview to assess quality of sleep and Insomnia (PSQI score >5). While the overall prevalence of insomnia was 26.6%, and little difference was found between males (26.3%) and females (27.0%); the mean PSQI score was 4.26 (±2.67), and significant higher in females (4.32 ± 2.70) than males (4.21 ± 2.64, p = 0.003). Individuals in the rural areas tended to report a higher PSQI score (4.45 ± 2.81) than urban residents did (4.18 ± 2.60) (p < 0.001) and the estimates of prevalence of insomnia was 29.4% in the rural areas, significant higher than 25.5% in the urban areas (p < 0.001). Multiple logistic regression analysis showed that female gender, older age, higher level of education, being unmarried, living in the rural area, cigarette smoking and alcohol drinking were associated with insomnia. Our study may provide important information for general and mental health research.

Autism is a highly heritable neurodevelopmental disorder, and known genetic variants, mostly rare, account only for a small proportion of cases. Here we report a genome-wide association study on autism using two Chinese cohorts as gene discovery (n=2150) and three data sets of European ancestry populations for replication analysis of top association signals. Meta-analysis identified three single-nucleotide polymorphisms, rs936938 (P=4.49 × 10⁻⁸), non-synonymous rs6537835 (P=3.26 × 10⁻⁸) and rs1877455 (P=8.70 × 10⁻⁸), and related haplotypes, AMPD1-NRAS-CSDE1, TRIM33 and TRIM33-BCAS2, associated with autism; all were mapped to a previously reported linkage region (1p13.2) with autism. These genetic associations were further supported by a cis-acting regulatory effect on the gene expressions of CSDE1, NRAS and TRIM33 and by differential expression of CSDE1 and TRIM33 in the human prefrontal cortex of post-mortem brains between subjects with and those without autism. Our study suggests TRIM33 and NRAS-CSDE1 as candidate genes for autism, and may provide a novel insight into the etiology of autism.