Cigarette smoking, coffee consumption and multiple sclerosis risk: a case-control study

A lot of studies support hypothesis that Multiple Sclerosis (MS) rises from interaction between genetic predisposition and environmental factors, not yet identified. As regards environmental factors, we investigated association between disease and exposure to smoking and coffee, wether in incidence or in progression of disease. We led a study by a case-control scheme 1:1, where comparison was between a MS patient and an healthy subject. MS patients (cases) were recognized among people attended in MS Ambulatory at the Neurosciences Department Of University Hospital of Palermo. Healthy subjects (controls) were recognized by an epidemiological survey leaded on territory. Cases and controls were given a structured questionnaire to get up informations about cigarette smoking and coffee consumption. We included in our study 100 cases and 100 controls, matched to cases by sex. Our analyses show that MS patients were more exposed to smoking and to high coffee consumption before disease onset than general population, with a dose-dependent relationship (coffee: OR = 1.91, IC al 95% = 1,08-3,34; smoking: OR = 3,27, IC al 95% = 1,82 - 5,89). That is true wether we consider separately these risk factors or we analyse them like associated events (OR = 3,65, IC al 95% = 1,87 7, 11). Instead of we did not found relationships between smoking, coffee and different clinical onset of disease. Using MSSS (Multiple Sclerosis Severity Score), we evaluated MS progression regarding smoking and/or coffee exposure during disease course and we did not notice a significant correlation between a possible worse disease progression and these two environmental factors (coffee: OR = 0,63, CI = 0,27 - 1,47; smoking: OR = 1,17, CI = 0,54 - 2,57). These results support hypothesis that cigarette smoking and high coffee consumption can be associated to an increased MS risk, slightly more if they are at the same time. On the contrary, these two environmental factors are not able to modify neither clinical onset type or disease progression in unfavourable way.