The Relation between Eating Habits and Abdominal Fat, Anthropometry, PON1 and IL-6 Levels in Patients with Multiple Sclerosis

Abstract

Background: Multiple sclerosis (MS) is a chronic neurodegenerative disease of an inflammatory, demyelinating and autoimmune nature. Diets with a high caloric density could be especially relevant in terms of the pathogenesis related to an increase in adipose tissue that is metabolically active and releases mediators, which can induce systemic inflammation and an increased oxidation state. The aim of this study was to analyse the eating habits related to calorie intake and their impact on abdominal obesity associated with anthropometric variables, the activity of the oxidation marker paraoxonase 1 (PON1), and interleukin 6 (IL-6) levelsin MS patients. Methods: An analytical and quantitative observational study was conducted with a population of 57 MS patients. The dietary-nutritional anamnesis was gained through the Food Frequency Questionnaire and a food diary. Diet and eating habits have been analysed through the Easy Diet–Programa de gestión de la consulta® software. Anthropometric measurements were taken in order to determine the presence of abdominal obesity. In addition, PON1 was quantified in serum by means of automated spectrophotometric assays and IL-6 was quantified using the ELISA technique. Results: A normal calorie intake was determined for women, yet a slightly lower intake was observed in men. Carbohydrate consumption was below what was established, and protein and lipids were over, in both cases. Furthermore, most patients had abdominal obesity, with significantly higher body mass index (BMI), waist-to-hip ratio (WHR), waist-to-height ratio (WHtR), fat percentage and IL-6 levels. IL-6 is greatly correlated with waist circumference and WHtR. Conclusion: MS patients’ nutrient intake shows an imbalance between macronutrients. This seems to favour the abdominal obesity associated with high values of proinflammatory IL-6 that is not correlated with a lower activity of PON1.