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Recent analysis of the Faroe Islands MS outbreak suggests that initiation of MS could occur at any time of life (before menopause), with puberty acting as an inducer for those with early onset of disease. It was further suggested that disease induction relates to hormonoimmunologic factors. This paper critiques current epidemiologic knowledge of MS and suggest where the Faroe Islands analysis leads. The generally accepted unimodality of the age-incidence curve is challenged with several examples of bimodality, and the concept of the hormonoimmunologic nature of MS induction is strengthened by analogies with tuberculosis, postvaccinal rabies encephalitis, and systemic lupus erythematosus (SLE). Major hormonal, lipid, and neurologic changes occur during the puberty period, but their roles in MS induction are undetermined. The concept of bimodality suggests that the search for etiologic risk factor relationships using small age at onset groups is more appropriate than using total MS populations. The question of the representativeness of the Faroe Islands outbreak can only be resolved by studies in other populations.