Association of body mass index with longitudinal rates of retinal atrophy in multiple sclerosis
Angeliki Filippatou, Jeffrey Lambe, Elias S. Sotirchos, Kathryn C. Fitzgerald, S. Andrew Aston, Olwen C. Murphy, Nicole Pellegrini, Nicholas Fioravante, Hunter Risher, Esther Ogbuokiri, Ohemaa Kwakyi, Brandon Toliver, Simidele Davis, Nicholas J. Luciano, Ciprian M. Crainiceanu, Jerry L. Prince, Ellen M. Mowry, Peter A. Calabresi, Shiv Saidha
Abstract
Background: Studies evaluating associations between body mass index (BMI) and optical coherence tomography (OCT) measures in multiple sclerosis (MS) are lacking. Objective: To assess whether elevated BMI is associated with accelerated retinal atrophy. Methods: In this observational study, 513 MS patients were followed with serial spectral-domain OCT for a median of 4.4 years. Participants were categorized as normal weight (BMI: 18.5–24.9 kg/m 2 ), overweight (BMI: 25–29.9 kg/m 2 ), and obese (BMI: ⩾30 kg/m 2 ). Participants with diabetes mellitus or uncontrolled hypertension and eyes with optic neuritis (ON) ⩽6 months prior to baseline OCT or during follow-up were excluded. Statistical analyses were performed with mixed-effects linear regression. Results: Obese patients ( n = 146) exhibited accelerated rates of ganglion cell + inner plexiform layer (GCIPL) atrophy relative to normal weight patients ( n = 214; –0.57%/year (95% confidence interval (CI): –0.65% to –0.48%) versus –0.42%/year (95% CI: –0.49% to –0.35%); p = 0.012). GCIPL atrophy rate did not differ between overweight ( n = 153) and normal weight patients (–0.47%/year vs –0.42%/year; p = 0.41). Each 1 kg/m 2 higher BMI was associated with accelerated GCIPL (–0.011%/year; 95% CI: –0.019% to –0.004%; p = 0.003) atrophy. Multivariable analyses accounting for age, sex, race, MS subtype, and ON history did not alter the above findings. Conclusions: Elevated BMI, in the absence of overt metabolic comorbidities, may be associated with accelerated GCIPL atrophy. Obesity, a modifiable risk factor, may be associated with accelerated neurodegeneration in MS.