Contact:
Dr. Eugene Albrecht, University of Maryland Medical School, 
(410) 706-3391 orealbrech@umaryland.edu.
Dr. Pepe can be reached at (757) 446-5616 or PepeGJ@evmsmail.evms.edu.
Professor Baker can be reached at david.barker@mrc.soton.ac.uk;
Dr. Seckl at j.seckl@ed.ac.uk;
Dr. Nathanielsz at pwn1@cornell.edu.
 

FETAL NUTRITION, HORMONE LEVELS, STRESS MAY CAUSE ADULT PROBLEMS

Recent physiological, clinical and epidemiological studies have suggested that what happens during fetal development - nutrition and hormonal levels, for example -- may be as important as genetic makeup in determining the health of the infant and also the likelihood of developing specific diseases, including hypertension, heart disease, and diabetes.  Dr. Eugene Albrecht, University of Maryland, chairs a symposium at Experimental Biology 2001 with scientists responsible for some of the leading work in this field.

Dr. Albrecht and Dr. Gerald Pepe, Eastern Virginia Medical School will present collaborative work showing that the level of estrogen to which a fetus is exposed plays a central role in the development of the baby's adrenal gland and, consequently, may have significant impact on endocrine function when that baby becomes an adult.  In addition, Dr. Pepe and Dr. Albrecht will show that estrogen in utero regulates ovarian development and the number of follicles (eggs). Thus ovarian dysfunction in adulthood has its origin in utero.

Professor David Barker, MRC Environmental Epidemiology Unit, Southampton General Hospital, London, will present data showing that people who had small body size at birth and during infancy have persisting changes in their physiology and metabolism and increased rates of coronary heart disease.  The weight and height of the mother are among the influences known to induce these changes.  Dr. Barker says that the 'fetal origins hypothesis' states that these associations reflect the persistence of fetal and infant responses to undernutrition.

Dr. Jonathan Seckl, Edinburgh West General Hospital, Scotland, has been addressing the role of glucocorticoid (stress) hormones in mediating this link discovered by Dr. Barker between low birth weigh and an increased risk of cardiovascular and metabolic disorders in adulthood. These hormones have for many years been known to reduce birth weight and to alter the maturation of fetal tissues, and in fact are used for this in obstetric practice.  Studies in rodents have shown that fetal exposure to excess glucocorticoids indeed lowers birth weight and produces permanent hypertension, higher blood glucose and insulin levels and behavioral changes throughout adult life. A key process appears to be the permanent programming of higher stress hormone levels themselves. This is also observed in low birth weight human populations and appears to be an early feature of this process.

The work of Dr. Peter Nathanielsz, Cornell University, addresses the life time consequences of an altered trajectory of development of the fetal stress axis. Dr. Nathanielsz says there are marked similarities in programming effects between antenatal stress, nutritional deficit and the glucocorticoid therapies used to advance the maturation of the fetal lung. While it is clear that several factors act as mediators of fetal programming, maternal and fetal glucocorticoids play a central role in altering the development of the peripheral vessels in a way that can lead to high blood pressure in later life.