PERSISTENT EFFECTS OF EARLY-LIFE IRON DEFICIENCY
Open Access
- Author:
- Wilkinson, Amanda L
- Area of Honors:
- Nutritional Sciences
- Degree:
- Bachelor of Science
- Document Type:
- Thesis
- Thesis Supervisors:
- Erica Unger, Thesis Supervisor
Dr. Erica Unger, Thesis Supervisor
Rebecca L Corwin, Thesis Honors Advisor - Keywords:
- iron deficiency
- Abstract:
- Iron deficiency is the leading nutrient deficiency disease in the world, and deficits in iron during early life can lead to irreversible damage in brain development if left untreated. This global health problem exists despite low dietary requirements of just milligram amounts each day to maintain good health. The World Health Organization (WHO) estimates that nearly 50% of the world’s infants may suffer from iron deficiency; if there are persistent effects of early-life deficiency into adulthood, the impact on productivity and health could be profound. The two current long-term longitudinal studies in the medical literature indicate that these persistent effects can occur into the individual’s second decade of life. The goal of the current rodent project is to determine the appropriate time period for iron repletion and the optimal amount of iron given during this time period to prevent the long-term consequences of early iron deficiency. Rodent models have shown that alterations in brain monoamine metabolism due to dietary iron deficiency in early life appear to be associated with changes in neurobehavioral development. Based on earlier studies, the ideal time for iron repletion in the rat appears to be after day 4 (P4) of postnatal life and sometime before P15. In this study, rats were subjected to one of three treatments: 1) iron sufficient through gestation and lactation; 2) iron deficient beginning on gestational day 5 (G5) and continuing through lactation, 3) iron deficient beginning on G5 followed by iron sufficient at P8. Although regional brain iron levels in iron repleted rats were similar to control by P21, dopamine and other monoamine levels were significantly reduced in prefrontal cortex and ventral midbrain at P21 and P90 and in striatum at P90. Monoamine-related protein levels were also disturbed in the iron supplemented group at both time points. These results suggest that iron repletion at P8 is too late to normalize changes in brain monoamine neurotransmission caused by early life iron deficiency.