New research suggests that having obesity in childhood is linked to more than double the risk of later developing multiple sclerosis.

Emerging evidence suggests a link between high BMI in adolescence and an increased risk of MS. Most studies evaluating this association are cross-sectional, have retrospective design with self-reported data, used solely genetic correlations, or pediatric weight data before the obesity epidemic. Therefore, researchers at the Karolinska Institutet, Stockholm, Sweden, aimed to prospectively evaluate the risk of developing MS in a large cohort of patients with pediatric obesity compared with the general population.

They included patients with obesity aged two to 19 years enrolled in the Swedish Childhood Obesity Treatment Register between 1995 – 2020, and a matched comparison group from the general population. Matching criteria included biologically assigned sex, year of birth, and residential area. MS was identified through Sweden’s National Patient Register. Individuals were followed from obesity treatment initiation, or from 15 years of age if treatment was initiated earlier, until MS diagnosis, death, emigration, or August 2023, whichever came first. The researchers’ used computer and statistical modelling to calculate any potential association. Because of previous reported genetic links to MS, the authors also assessed levels of parental MS that was present in 99 percent in the obesity cohort and 68 percent in the general population comparators.

The data included 21,661 patients (54 percent boys) from the pediatric obesity cohort. The median age of obesity treatment initiation (behavior and lifestyle modification) was 11.4 years. The median follow-up time was 5.6 years, corresponding to median age of 20.8 years in the follow-up population (and 50 percent of the population were aged between 18 and 25 at the point analysis, with the highest age in the cohort 45 years).

During follow-up, 13 percent developed MS in the obesity cohort, whereas the corresponding number in the general population was 6 percent. The mean age of MS diagnosis was comparable between the groups; 23.4 years in the obesity cohort versus 22.8 years in the general population comparators. The small numbers who developed MS so far means that the study was not sufficiently statistically powered to state the increased risk to females developing MS – however the results follow the general increased risk to females (the estimated ratio of female:male affected by MS in the general population is 4:1).

The crude incidence rate of MS per 100,000 person years was 19.3 in the obesity cohort and 8.3 in the general population cohort. Analyses adjusted for presence of parental MS (heredity) (which was more prevalent in the obesity cohort) revealed that the risk of developing MS was more 2.3 times higher than in the pediatric obesity cohort.

The researchers said that despite the limited follow-up time, their findings highlight obesity in childhood is linked to an increased susceptibility of early-onset MS more than two-fold. Given that pediatric obesity is prevalent, it is likely to serve as a critical contributor to the escalating prevalence of MS. Pediatric obesity is linked to several autoimmune diseases and the leading hypothesis is that the persistent low-grade inflammatory state, typically observed in obesity, is mediating the association. Understanding these pathways is crucial for developing targeted prevention and intervention strategies to normalize the risk for MS in children and adolescents with obesity.

The findings will be presented at this year’s European Congress on Obesity in Venice, Italy.