Beard John L
Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA 16802, USA.
J Nutr. 2008 Dec;138(12):2534-6. doi: 10.1093/jn/138.12.2534.
Infants who experience iron deficiency during the first 6-12 mo of life are likely to experience persistent effects of the deficiency that alter functioning in adulthood. A lack of sufficient iron intake may significantly delay the development of the central nervous system as a result of alterations in morphology, neurochemistry, and bioenergetics. Depending on the stage of development at the time of iron deficiency, there may be an opportunity to reverse adverse effects, but the success of repletion efforts appear to be time dependent. Publications in the past several years describe the emerging picture of the consequences of iron deficiency in both human and animal studies. The mechanisms for iron accumulation in the brain and perhaps redistribution are being understood. The data in human infants are consistent with altered myelination of white matter, changes in monoamine metabolism in striatum, and functioning of the hippocampus. Rodent studies also show effects of iron deficiency during gestation and lactation that persist into adulthood despite restoration of iron status at weaning. These studies indicate that gestation and early lactation are likely critical periods when iron deficiency will result in long-lasting damage.
在生命的最初6至12个月经历缺铁的婴儿,可能会出现缺铁的持续影响,这些影响会改变成年后的功能。由于形态学、神经化学和生物能量学的改变,铁摄入不足可能会显著延迟中枢神经系统的发育。根据缺铁时的发育阶段,可能有机会逆转不良影响,但补充铁的成功似乎取决于时间。过去几年的出版物描述了人类和动物研究中缺铁后果的新情况。大脑中铁积累甚至重新分布的机制正在被了解。人类婴儿的数据与白质髓鞘形成改变、纹状体单胺代谢变化以及海马体功能有关。啮齿动物研究还表明,妊娠和哺乳期缺铁的影响会持续到成年,尽管断奶时铁状态已恢复。这些研究表明,妊娠和早期哺乳期可能是缺铁会导致长期损害的关键时期。