Autoimmune thyroid disease (AITD) is suppressed during pregnancy and is exacerbated in the postpartum period. Studies indicate that new-onset AITD occurs in up to 10% of all women in the postpartum period and that up to 60% of Graves' patients in the reproductive years give a history of postpartum onset. Despite this extraordinary epidemiological evidence, the causes of these exacerbations are uncertain and have yet to be adequately investigated. Explaining these postpartum changes, therefore, remains hypothetical. Mechanisms invoked include the passage of fetal cells to the mother during pregnancy establishing maternal microchimerism, pregnancy-induced changes in the thyroid gland itself, and the role of prolactin as a consequence of breast-feeding. Once the disease onset or exacerbation, is established, then there have been considerable advances in our understanding of the immunopathology. Thyroid cell destruction (via apoptosis) or activation (via thyrotropin [TSH] receptor autoantibody induction) appear to be similar to nonpostpartum-related disease. The reasons for the transience in postpartum disease, particularly thyroiditis, is likely to be related to the induction of clonal suicide and the mechanisms for this phenomenon are beginning to be explored. While we have a number of clinical indicators that allow us to predict postpartum thyroid disease (such as autoantibody titers), at present, we have no treatment to prevent the disease. Furthermore, our predictions are not helpful in a high enough proportion of the population to warrant screening of all women before delivery. At this time, the best clinical approach is watchful waiting and postpartum thyroid function testing where suspected.