The Fidgety Fetus Hypothesis

Abstract

Postprandial hyperglycemia appears to increase the risk of macrosomia, but it is not clear why a majority of fetuses are unaffected. One possibility, the “fidgety fetus hypothesis,” posits that fetal activity is an intrinsic trait that influences birth weight. This study was an attempt to learn whether some infants whose mothers have gestational diabetes mellitus (GDM) may be more active in utero and able to compensate for hyperglycemia, thereby minimizing their risk of macrosomia. Initially, 10 women with diabetes counted kicks twice a day for 30 minutes, and also monitored their blood glucose before and 1 hour after each meal. In a second phase, 13 women with GDM used a home fetal monitoring device (the Card Guard-900P), making it possible to monitor fetal heart rate (FHR) accelerations telemetrically. Finally, fetal monitoring strips from 46 women with GDM were analyzed retrospectively. An active fetus was taken to be one having 4 or more FHR accelerations in a 20-minute period. In no phase of the study were there significant differences between the active and inactive groups in the time that GDM was diagnosed, the time insulin treatment began, or glycosylated hemoglobin levels. In the first phase of the study, there was little variation in fetal movements during an average follow up of 8.5 weeks. Maternal postprandial glucose levels correlated positively with increased birth weight. In the second phase, active fetuses were always active and inactive fetuses always were inactive. Average birth weight percentile, corrected for gestational age, was 37% in the active group and 63% in the inactive group (P = .05). In the final phase, the fetal monitoring strips demonstrated an inverse correlation between the number of FHR accelerations and birth weight corrected for gestational age. Average birth weight percentiles in the active and inactive groups were 37% and 62%, respectively. Macrosomic fetuses were found only in the inactive group. These findings support the “fidgety fetus” hypothesis that increased fetal activity may minimize the effect of hyperglycemia on subsequent birth weight. Inactive fetuses are at increased risk of glucose-mediated macrosomia, making it especially important to treat hyperglycemia and maintain close surveillance in these cases.