Copper and iron are both essential micronutrients. Because they can both accept and donate electrons, they are central to many energy dependent chemical reactions. For example, copper is a critical part of ferroxidase enzymes ceruloplasmin, hephaestin and zyklopen, as well as enzymes such as dopamine-ß-monoxygenase, while iron is part of the catalytic site of many cytochromes and enzymes involved in fatty acid desaturation. Unsurprisingly, therefore, copper and iron deficiency, especially during pregnancy, when cell proliferation and differentiation are very active, sub-optimal nutrient status can lead to serious consequences. These problems can persist into adulthood, with an increased risk of mental problems such as schizophrenia and, in animal models at least, hypertension and obesity. In this review, we consider what these problems are and how they may arise. We examine the role of copper and iron deficiencies separately during fetal development, in terms of birth outcome and then how problems with status in utero can have long term sequelae for the offspring. We examine several possible mechanisms of action, both direct and indirect. Direct causes include, for example, reduced enzyme activity, while indirect ones may result from changes in cytokine activity, reductions in cell number or increased apoptosis, to name but a few. We examine a very important area of nutrition-interactions between the micronutrients and conclude that, while we have made significant advances in understanding the relationship between micronutrient status and pregnancy outcome, there is still much to be learned.