The current study aimed to assess the secular trends in overweight and obesity status and high blood pressure (HBP) in Chinese children and adolescents for 2 decades. Data on 943 128 participants aged 7 to 17 years were obtained from the Chinese National Survey on Students' Constitution and Health from 1995 to 2014. The population attributable risk of overweight status for HBP was calculated. The prevalence of overweight increased from 4.3% in 1995 to 18.4% in 2014, whereas HBP prevalence fluctuated in the range of 4.4% to 6.4% during the same time period, the lowest in 2005. Within each survey year, blood pressure levels and HBP prevalence increased with higher body mass index. Notably, the population attributable risk of HBP because of being overweight steadily increased from 6.3% in 1995 to 19.2% in 2014. The same trends of linear growth for obesity, fluctuating blood pressure, and its sustained increasing population attributable risk for overweight also occurred among the domestic 29 provinces. Despite dramatic increases in overweight prevalence among Chinese children from 1995 to 2014, the HBP prevalence remained relatively stable, suggesting that other independent factors are affecting HBP trends to a greater extent. Yet, over time, the magnitude of the impact of being overweight or obese on HBP increased sharply, predicting looming heavy burden of HBP. Reductions in overweight status may aid in preventing HBP so as to prevent coronary risk in adulthood.

Multiple sclerosis (MS) is a complex disease of the CNS thought to require an environmental trigger. Gut dysbiosis is common in MS, but specific causative species are unknown. To address this knowledge gap, we used sensitive and quantitative PCR detection to show that people with MS were more likely to harbor and show a greater abundance of epsilon toxin-producing (ETX-producing) strains of C. perfringens within their gut microbiomes compared with individuals who are healthy controls (HCs). Isolates derived from patients with MS produced functional ETX and had a genetic architecture typical of highly conjugative plasmids. In the active immunization model of experimental autoimmune encephalomyelitis (EAE), where pertussis toxin (PTX) is used to overcome CNS immune privilege, ETX can substitute for PTX. In contrast to PTX-induced EAE, where inflammatory demyelination is largely restricted to the spinal cord, ETX-induced EAE caused demyelination in the corpus callosum, thalamus, cerebellum, brainstem, and spinal cord, more akin to the neuroanatomical lesion distribution seen in MS. CNS endothelial cell transcriptional profiles revealed ETX-induced genes that are known to play a role in overcoming CNS immune privilege. Together, these findings suggest that ETX-producing C. perfringens strains are biologically plausible pathogens in MS that trigger inflammatory demyelination in the context of circulating myelin autoreactive lymphocytes.