Multiple Sclerosis Research Center; Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran
The relationship between cognitive function and body mass index in multiple sclerosis patients.
Many patients with multiple sclerosis (MS) endure cognitive impairment, which affects their everyday life and lowers their life quality. It has been demonstrated that obesity can result in poor cognitive performance in healthy individuals through various mechanisms. Therefore, we aimed at assessing the association between body mass index (BMI) and cognitive function in MS patients, using minimal assessment of cognitive functions in MS (MACFIMS) battery.
This study included eighty-one patients with relapsing-remitting MS (RRMS). After collecting the demographic data, patients' height and weight were measured in order to calculate BMI. Then, MACFIMS battery was administered in one session, after obtaining information using expanded disability status scale (EDSS).
Paced Auditory Serial Addition Test (PASAT) and Symbol Digit Modalities Test (SDMT) scores were negatively correlated with BMI (P values are equal to 0.005 and 0.037, respectively). PASAT score correlated with BMI after controlling for sex, age, and EDSS, but SDMT score did not correlate. Nevertheless, no significant variation was observed in the BMI level among individuals having MS with or without cognitive deficit.
We have shown that, BMI is associated with poor cognitive performance in some tests which, MACFIMS battery was included. This could suggest that obesity might be an important factor, which have effect on the cognitive performance.
Human Genetics Unit, Department of Pathology, Faculty of Medicine, Kuwait University, Kuwait
The FTO gene polymorphism rs9939609 is associated with obesity and disability in multiple sclerosis patients.
Obesity is a well-known risk factor for multiple diseases including multiple sclerosis (MS). Polymorphisms in the fat-mass obesity (FTO) gene have been consistently found to be associated with obesity, and recently found to increase the risk of developing MS. We therefore assessed the common FTO gene polymorphism (rs9939609) in relation to obesity, risk of developing MS and its disability in a cohort of MS patients. A cohort of 200 MS patients (135 females and 65 males) were genotyped for the FTO rs9939609 polymorphism. Using both logistic and linear regression we assessed the relationship between the variant and the selected phenotypes under both an additive and recessive genetic models. The A-allele was found to be associated with being overweight/obese in MS patients (OR = 2.48 (95% CI 1.17-5.29); p = 0.01). In addition, The A-allele was also found to be associated with increased MS disability (β = 0.48 (95% CI 0.03-0.92); p = 0.03). However, no association was found with risk of developing MS (p > 0.05). Moreover, our association with obesity is consistent with previous reports, whereas the association with disability is novel and warrants further investigation on the role of FTO in disease progression.
From the Preventive Neurology Unit (B.M.J., A.J.N., G.G., R.D.), Wolfson Institute of Preventive Medicine, Barts and Queen Mary University of London; and Royal London Hospital NHS
BMI and low vitamin D are causal factors for multiple sclerosis: A Mendelian Randomization study.
To update the causal estimates for the effects of adult body mass index (BMI), childhood BMI, and vitamin D status on multiple sclerosis (MS) risk.
We used 2-sample Mendelian randomization to determine causal estimates. Summary statistics for SNP associations with traits of interest were obtained from the relevant consortia. Primary analyses consisted of random-effects inverse-variance-weighted meta-analysis, followed by secondary sensitivity analyses.
Genetically determined increased childhood BMI (ORMS 1.24, 95% CI 1.05-1.45, p = 0.011) and adult BMI (ORMS 1.14, 95% CI 1.01-1.30, p = 0.042) were associated with increased MS risk. The effect of genetically determined adult BMI on MS risk lessened after exclusion of 16 variants associated with childhood BMI (ORMS 1.11, 95% CI 0.97-1.28, p = 0.121). Correcting for effects of serum vitamin D in a multivariate analysis did not alter the direction or significance of these estimates. Each genetically determined unit increase in the natural-log-transformed vitamin D level was associated with a 43% decrease in the odds of MS (OR 0.57, 95% CI 0.41-0.81, p = 0.001).
We provide novel evidence that BMI before the age of 10 is an independent causal risk factor for MS and strengthen evidence for the causal role of vitamin D in the pathogenesis of MS.