It is a medical truism that fetal health depends on maternal health. Several conditions such as adult diabetes and cardiovascular disease have been linked to fetal exposure to poor maternal health and maternal stress. These insights have sparked investigation into the fetal origins of adult disease (FOAD). When the maternal conditions that are recognized to confer fetal consequences are amenable to medical intervention, then consideration should be given to identifying and correcting these conditions prior to conception. This is especially important when conception requires medical assistance, fetal consequences are significant, when screening strategies exist that are readily available and reliable, or when the condition is infectious and preventable by vaccine. The task of ensuring fetal health is more difficult when the maternal conditions are occult. The mechanisms by which fetal development is altered by maternal conditions are many and include epigenetic mechanisms that alter DNA methylation patterns and therefore have the potential to be multigenerational. A short list of occult maternal conditions for which screening might be of benefit includes maternal thrombophilias, impaired maternal glucose tolerance, stress, hypothyroidism, and nutritional deficiencies, especially those that cause folate deficiency. For instance, celiac disease may cause malabsorption, hyper- or hypothyroidism, and infertility due to oligo-ovulation. Newer diagnostic techniques allow us to screen for celiac disease noninvasively and it is important to consider Abstract of the 8th Royan International Twin Congress, Tehran, Iran, 5-7 September 2007 Yakhteh Medical Journal, Vol 9, Sup 1, Summer 2007 45 screening for celiac disease in women with infertility. Another common but often occult maternal cause of compromised fetal development is hypothyroidism. Worldwide, goiter due to iodine deficiency is a common cause of hypothyroidism and cretinism. Other common causes of maternal hypothyroidism include autoimmune etiologies, including celiac disease, and stress. The mother is the sole source of thyroxine in early gestation and the predominant source during the entire gestation. Women with a known cause of thyroid deficiency due to organic conditions such as Grave’s disease or Hashimoto’s thyroiditis require an increase in thyroxine dose very early in gestation. Alexander EK et al showed that the mean thyroxine requirement increased about 50% by week 8 of gestation (New Engl J Med 2004; 351:241). Thyroxine requirements appear to be greater in women undergoing assisted reproduction and ovulation induction and in those with a multiple gestation. The primary consequence of inadequate fetal exposure to thyroxine is compromised neurodevelopment. There are many important genes that are regulated by thyroxine and this appears to be the mechanism by which inadequate thyroxine exposure compromises fetal neurodevelopment. Since psychosocial stress and inadequate nutrition compromise hypothalamic TRH drive and lead to subtle forms of functional hypothalamic hypothyroidism, it may be more important than previously recognized to mitigate poor maternal psychosocial and nutritional compromise. In summary, recent data on the importance of thyroxine for fetal neurodevelopment support the notion that there should be a high index of suspicion and a low threshold for screening for thyroid disease. Optimally, screening should occur before conception and should include TSH, free thyroxine, and possibly anti-thyroid antibodies such as TSI (thyroid stimulating immunoglobulin) and TPO (thyroid peroxidase). It is more difficult to screen for functional forms of hypothyroidism that accompany psychosocial and metabolic stress and thus amelioration of psychosocial and nutritional stress should receive high priority.