Over the past several days there have been many more fascinating presentations at this year’s SMFM Meeting. In all the time I have attended this meeting, I have not seen research at this level presented. Unfortunately, much of the information would not be of much interest or use to the lay person who is reading this post. But, I want to mention briefly a few highlights that might give you some idea of where we are now from a research standpoint and what that might mean for the future.
Dr. Ursula Harkness (another former resident of mine while I was at the University of Minnesota) presented the results of studies (conducted during her fellowship in maternal-fetal medicine at the University of Cincinnati) in an animal model that consistently results in ‘intrauterine growth restriction’ of the fetus (rats). She and her colleagues were able to overcome the fetal growth problems by injecting a growth factor gene (IGF-1), contained within a virus (adenovirus vector), into the placentas of these babies, overcoming not only the intrauterine growth delays, but the growth and metabolic problems that these animals have following birth.
Dr. Kjersti Aagaard-Tillery presented very convincing evidence from nonhuman primate (macaque) experiments confirming the hypothesis that offspring from obese mothers are, themselves, programmed in the womb to go down the path of obesity, hypertension, and diabetes, that this ‘programming’ occurs not only in the liver (the site of the metabolic pathways that lead to these problems), but also in the brain, and is indeed the result of aberrations of methylation that alter normal DNA gene expression. She and her colleagues demonstrated quite elegantly that genes that ordinarily produce chemicals (Npas2) that regulate the part of the brain that tells us we are full when eating (the satiety center) can also be ‘reprogrammed’ in a way that reduces their expression (making us feel less hungry when we have actually had enough to eat). (I am so glad I finally have an excuse for craving the triple whopper with cheese in the jumbo-sized combo.)
Dr. Darine El-Chaar and coworkers from the University of Ottawa reported data from a large perinatal database that contained information about birth outcomes in patients who had undergone conception with the help of ‘assisted reproductive technology (ART).’ (We have mentioned in the past that these women are at increased risk for pregnancy complications such as preterm birth, cervical incompetence, hypertension, HELLP syndrome, placenta previa, low birth weight, diabetes, and chromosomal abnormalities, not to mention multiple gestations). The report confirmed that such women also have a prevalence of babies with birth defects that is overall almost twice that of the general population. In the year they reviewed the data, gastrointestinal, cardiovascular, and musculoskeletal defects were significantly higher in ART women than those who had spontaneous conceptions. Risks of birth defects for different methods of ART were 2.72% for intrauterine insemination, 3.35% for in vitro fertilization, and 2.23 for ovulation induction. Reasons for these increased risk rates are yet to be determined.
Lastly, here is something you don’t want to hear, although I have had my suspicion of this for many years now. Dr. William Dobak from Emory University (and colleagues from around the country) evaluated the effects of coital frequency and number of partners during pregnancy and pregnancy outcome. In brief, women who had more frequent sex and 3 or more partners were at greater risk for early delivery, intrauterine growth restriction and low birth weight babies. This effect was NOT the result of age, race, smoking status, history of preterm delivery, or presence of sexually transmitted infections. I always knew we weren’t doing much when we told patients to “get more bed rest” but now it appears we may actually be doing more harm than good. I mean, what else are you going to do if you are lying around in bed all day?