Person:

Lee, Eunjung Alice

Background: A limited amount of research, primarily conducted in Western countries, has suggested that higher socioeconomic status (SES) is associated with higher risk of eating disorders (EDs). However, little is known about this association in Asian countries. We examined the association of SES with disturbed eating behavior (DEB) and related factors in Korean adolescents. Subjects A nationwide online panel survey was conducted in a sample of adolescents (n = 6,943, 49.9% girls). DEB was measured with the 26-item Eating Attitudes Test (EAT-26). Participants who scored ≥20 on the EAT-26 were considered to have DEB. Participants’ SES was determined based on self-reported household economic status. Results: The prevalence of DEB was 12.7%: 10.5% among boys and 14.8% among girls. Both boys and girls with DEB were more likely to perceive themselves as obese, experience higher levels of stress, and have lower academic achievement. The risk for DEB was significantly higher in boys of higher SES than in those of middle SES (OR = 1.45, 95%CI = 1.05–1.99 for high SES; OR = 5.16, 95%CI: 3.50–7.61 for highest SES). Among girls, higher risk of DEB was associated with the highest and lowest SES (OR = 1.52, 95%CI: 1.13–2.06 for lowest SES; OR = 2.22, 95%CI: 1.34–3.68 for highest SES). Conclusions: Despite the lower prevalence of obesity in Korea compared with Western countries, the prevalence of DEB in Korean adolescents was high, especially among girls. Moreover, the association between SES and DEB followed a U-shaped curve for girls and a J-shaped curve for boys.

Various types of somatic mutations occur in cells of the human body and cause human diseases including cancer and some neurological disorders1. Recently, Lee et al.2 (hereafter “the Lee study”) reported somatic copy number gains of the APP gene, a known risk locus of Alzheimer’s disease (AD), in 69% and 25% of neurons of AD patients and controls. The authors argue that the mechanism of these copy number gains was somatic integration of APP mRNA into the genome, creating what they called genomic cDNA (gencDNA). Our reanalysis of the data from the Lee study and two additional whole exome sequencing (WES) datasets by the authors of the Lee study3 and Park et al.4 revealed evidence that APP gencDNA originates mainly from exogenous contamination by APP recombinant vectors, nested PCR products, and human and mouse mRNA, respectively, rather than from true somatic integration of endogenous APP. We further present our own single-cell whole genome sequencing (scWGS) data that show no evidence for somatic APP retrotransposition in AD neurons or in neurons from normal individuals of various ages.