Fetal iron deficiency and genotype influence emotionality in infant rhesus monkeys.
BACKGROUND
Anemia during the third trimester of fetal development affects one-third of the pregnancies in the United States and has been associated with postnatal behavioral outcomes. This study examines how fetal iron deficiency (ID) interacts with the fetal monoamine oxidase A (MAOA) genotype. MAOA metabolizes monoamine neurotransmitters. MAOA polymorphisms in humans affect temperament and modify the influence of early adverse environments on later behavior.


OBJECTIVE
The aim of the study was to advance translation of developmental ID research in animal models by taking into account genetic factors that influence outcomes in human populations.


METHODS
Male infant rhesus monkeys 3-4 mo old born to mothers fed an ID (10 ppm iron) diet were compared with controls (100 ppm iron). Infant monkeys with high- or low-transcription rate MAOA polymorphisms were equally distributed between diet groups. Behavioral responses to a series of structured experiences were recorded during a 25-h separation of the infants from their mothers.


RESULTS
Infant monkeys with low-transcription MAOA polymorphisms more clearly demonstrated the following ID effects suggested in earlier studies: a 4% smaller head circumference, a 39% lower cortisol response to social separation, a 129% longer engagement with novel visual stimuli, and 33% lesser withdrawal in response to a human intruder. The high MAOA genotype ID monkeys demonstrated other ID effects: less withdrawal and emotionality after social separation and lower "fearful" ratings.


CONCLUSIONS
MAOA × ID interactions support the role of monoamine neurotransmitters in prenatal ID effects in rhesus monkeys and the potential involvement of common human polymorphisms in determining the pattern of neurobehavioral effects produced by inadequate prenatal nutrition.
Department of Environmental Toxicology and msgolub@ucdavis.edu.
Mari S
MS
Golub
California National Primate Research Center, University of California, Davis, Davis, CA.
Casey E
CE
Hogrefe
D018798:Anemia, Iron-Deficiency / Q000201:enzymology / Q000235:genetics*; D000818:Animals; D000831:Animals, Newborn; D004195:Disease Models, Animal; D004644:Emotions / Q000502:physiology*; D005260:Female; D047109:Fetal Development; D048070:Fetal Nutrition Disorders / Q000201:enzymology / Q000235:genetics*; D005333:Fetus / Q000201:enzymology*; D005838:Genotype; D006854:Hydrocortisone / Q000378:metabolism; D008253:Macaca mulatta; D008297:Male; D008995:Monoamine Oxidase / Q000235:genetics / Q000378:metabolism
D008995:Monoamine Oxidase; D006854:Hydrocortisone
MAOA polymorphism; anemia; infant; rhesus; social behavior