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.
CONCLUSION: 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.