It is now well-established that there is a genetic vulnerability for developing bipolar disorders. For instance, the rate of bipolar disorders in first degree relatives of bipolar probands (19%) is higher than in the general population (1%); monozygote twins have higher concordance rates for bipolar diseases (67%) than dizygote (19%); finally affective disorders are more frequent in biological parents than in adoptive parents in adopted bipolar patients. However, currently genes predisposing for the disease are not known, in part because bipolar disorders are very heterogeneous. New research strategies should be developed based on more homogeneous groups of patients defined by the presence of "candidate symptoms" or by the evidence of endophenotypes in healthy relatives. However, it is clear now that there is an interaction between the genetic vulnerability and environmental factors in the aetiology and course of the disorder. Environmental factors have been neglected for a long time because bipolar disorder was considered an endogenous disease. Thus, very recently, studies have shown that early trauma could contribute to the occurrence or the severity of the disease. During a lifetime, many environmental components (stressful life events, changes in daily schedules, drug abuse, some medications) could also trigger the onset of the pathology or the occurrence of new episodes. It is very important to recognize these factors in order to develop preventive strategies for limiting their impact.