Maternal stress and fetal responses: evolutionary perspectives on preterm delivery.
New epidemiological and neurohormonal evidence provides insights into the persistent public health issue of preterm delivery and its long-term health consequences for the newborn. Mechanisms linked to preterm delivery may originate early in gestation as a result of maternal cues signaling a stressful intrauterine environment. When these signals are present, the fetus responds with a series of facultative responses, including accelerated organ maturation. If these responses are unsuccessful and the environment remains insufficient, a series of feed-forward mechanisms initiate the hormonal cascade that leads to parturition, and thus, early expulsion from a stressful environment. The internal environmental cues are delivered via glucocorticoids (stress hormones) in the circulatory system, but fetal responses and the initiation of the final terminal pathway to parturition are regulated by placentally derived corticotropin-releasing hormone (CRH). The potential costs of early expulsion from a stressful intrauterine environment are high and include an increased likelihood of perinatal and infant mortality. Permanent alterations in organ and metabolic functioning may occur, suggesting considerable fitness trade-offs. There is some evidence that preterm parturition is a maternal adaptation to limit the energetic costs of individual pregnancies in the face of poor condition at the time of conception. Moreover, nutritional stress is not the only indicator that signals a stressful environment: maternal psychosocial stress, and thus her response to an assessment of the social environment, also signal an insufficient internal environment to the fetus. The epidemiological and neurohormonal evidence for these relationships and mechanisms responsible for regulating such delicate negotiations are explored. In turn, the implications of such findings are examined from life history and public health perspectives.
Pike
Ivy L
IL
Department of Anthropology, The University of Arizona, Tucson, Arizona 85721-0030, USA. ilpike@email.arizona.edu
D000305:Adrenal Cortex Hormones / Q000378:metabolism; D005075:Biological Evolution; D004734:Energy Metabolism / Q000502:physiology*; D005260:Female; D047109:Fetal Development / Q000502:physiology*; D006801:Humans; D007231:Infant, Newborn; D008431:Maternal-Fetal Exchange / Q000502:physiology*; D009490:Neurosecretory Systems / Q000378:metabolism*; D007752:Obstetric Labor, Premature / Q000378:metabolism*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000209:etiology / Q000378:metabolism*; D011256:Pregnancy Outcome; D011287:Prejudice; D011297:Prenatal Exposure Delayed Effects; D039401:Prenatal Nutritional Physiological Phenomena / Q000502:physiology; D012306:Risk; D012307:Risk Factors; D012959:Socioeconomic Factors; D013315:Stress, Psychological / Q000150:complications / Q000378:metabolism*
D000305:Adrenal Cortex Hormones