Contributions
Abstract: P455
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Environmental risk factors
Objective: Obesity in childhood and during adolescence has repeatedly been associated with increased risk of developing multiple sclerosis (MS). We aimed to investigate whether the most critical period occurs during childhood or later, during adolescence.
Methods: Using a population-based case-control study (1586 cases and 2800 controls), subjects with different body sizes at age 10 and different body mass indices at age 20 were compared regarding MS risk, by calculating odds ratios with 95% confidence intervals. Potential interactions between HLA-DRB1*15 and absence of HLA-A*02, respectively, and both childhood and adolescent obesity were evaluated by calculating the attributable proportion due to interaction.
Results: Regardless of body size at age 10, subjects with adolescent obesity had a 90% increased risk of MS. Among subjects who were not obese at age 20, no association was observed between body size at age 10 and subsequent MS risk. An interaction was observed between the HLA MS risk genes and adolescent, but not childhood, obesity.
Conclusions: Our results suggest that BMI during adolescence, rather than childhood, is critical in determining MS risk.
Disclosure:
Dr. Hedström reports no disclosures.
Dr. Olsson received compensation for scientific advisory boards or lectures for Biogen and Genzyme, unrestricted MS resarch grants from Biogen, Bovartis, Genzyme, Allmiral and AstraZeneca, the Swedish Research Council (07488), EU fp7 Neurinox, Knut and Alice Wallenberg Foundation, Margareta af Ugglas Stiftelse, the Afa Foundation and the Swedish Brain Foundation.
Dr. Alfredsson receives research support from the Swedish Medical Research Council (K2013-69X-14973-10-4) and Swedish Council for Working life and Social Research (Dnr 2012-0325).
Source of funding: The study was supported by grants from the Swedish Medical Research Council; from the Swedish Research Council for Health, Working Life and Welfare, Knut and Alice Wallenberg Foundation, the AFA foundation, the Swedish Brain Foundation and the Swedish Association for Persons with Neurological Disabilities.
Abstract: P455
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Environmental risk factors
Objective: Obesity in childhood and during adolescence has repeatedly been associated with increased risk of developing multiple sclerosis (MS). We aimed to investigate whether the most critical period occurs during childhood or later, during adolescence.
Methods: Using a population-based case-control study (1586 cases and 2800 controls), subjects with different body sizes at age 10 and different body mass indices at age 20 were compared regarding MS risk, by calculating odds ratios with 95% confidence intervals. Potential interactions between HLA-DRB1*15 and absence of HLA-A*02, respectively, and both childhood and adolescent obesity were evaluated by calculating the attributable proportion due to interaction.
Results: Regardless of body size at age 10, subjects with adolescent obesity had a 90% increased risk of MS. Among subjects who were not obese at age 20, no association was observed between body size at age 10 and subsequent MS risk. An interaction was observed between the HLA MS risk genes and adolescent, but not childhood, obesity.
Conclusions: Our results suggest that BMI during adolescence, rather than childhood, is critical in determining MS risk.
Disclosure:
Dr. Hedström reports no disclosures.
Dr. Olsson received compensation for scientific advisory boards or lectures for Biogen and Genzyme, unrestricted MS resarch grants from Biogen, Bovartis, Genzyme, Allmiral and AstraZeneca, the Swedish Research Council (07488), EU fp7 Neurinox, Knut and Alice Wallenberg Foundation, Margareta af Ugglas Stiftelse, the Afa Foundation and the Swedish Brain Foundation.
Dr. Alfredsson receives research support from the Swedish Medical Research Council (K2013-69X-14973-10-4) and Swedish Council for Working life and Social Research (Dnr 2012-0325).
Source of funding: The study was supported by grants from the Swedish Medical Research Council; from the Swedish Research Council for Health, Working Life and Welfare, Knut and Alice Wallenberg Foundation, the AFA foundation, the Swedish Brain Foundation and the Swedish Association for Persons with Neurological Disabilities.