Being born small for gestational age (SGA) is associated with augmented sympathetic outflow and increased risk of vascular disease in early adulthood. Adolescent girls born SGA are found to have reduced size of uterus and the ovaria, independent of reduced body size. The findings link growth before birth to ovarian function later in life, such as ovarian hyperandrogenism and anovulation, the characteristics of a common endocrinopathy seen in women of reproductive age, the Polycystic Ovarian Syndrome (PCOS) also termed ‘the female metabolic syndrome’. We have recently show that testosterone is related to sympathetic nerve activity in women with PCOS and may account for the increased prevalence of vascular disease seen in this condition. Whether testosterone is related to or involved in regulating the sympathetic nervous system in the general population is not known, but testosterone has been recognized as a cardiovascular risk factor in women. Like the conditions SGA and PCOS, hypertensive disorders of pregnancy have been shown to constitute a state of sympathetic overactivity. While gestational hypertension is often considered benign, as it is transient, preeclampsia is recognized as a leading cause of maternal and fetal morbidity and mortality. Women with PCOS are at a significantly higher risk of pregnancy induced hypertensive disorders (PIHD), especially preeclampsia, than non-PCOS women, independent of body weight. Pregnancy complications associated with maternal PCOS besides PIHD, include increased prevalence of spontaneous miscarriage and birth of SGA babies. While there is still controversy as to whether women diagnosed with PCOS were more likely to have been born SGA, the higher incidence of SGA newborns amongst PCOS women seems to be more related to the PCOS condition of the mother than to pregnancy complications per se. Though the pathophysiology of PIHD is not known, an involvement of testosterone in has been suggested. The increase in testosterone level associated with preeclampsia has been shown to persist up to 17 years after delivery which indicates a harmful endocrine alteration associated with PIHD, which may predispose these women to increased risk of vascular disorders. We have recently demonstrated that in women suffering from PIHD 40 years ago, sympathetic nerve activity is increased and inversely related to DHEAS (dehydroepiandosterone sulphate) levels in those still hypertensive despite ongoing antihypertensive medication. As the sympathetic nervous system plays a role in vascular health, our results support the hypothesis that high levels of DHEAS may protect against vascular ageing. The conditions, SGA, PCOS and PIHD all constitute states of sympathetic overactivity. Whether a common nominator underlies the sympathetic activation associated with these conditions however remains to be elucidated.