Autoimmune hyperthyroidism has a complex aetiology including both environmental and inherited components. Amongst the environmental factors that are well documented to be important are smoking and stressful life events. The prevalence of all forms of autoimmune hyperthyroidism is known to be higher in women, but the effects of oestrogen are complex: the combined oral contraceptive pill protecting against Graves disease, whereas pregnancy predisposes. Autoimmune hyperthyroidism also occurs in rare individuals during recovery from an immunosuppressed state due to HIV infection or following alemtuzumab treatment. Genomic factors that are well documented include predisposing alleles at the MHC, CTLA4 and PTPN22 loci. Other candidate genes that have a role include TSHR. Recent genome-wide linkage studies have also shown several other loci with weak effects that appear to contribute, including PTPN2 and CD226.