Beard John L, Connor James R
Department of Nutritional Sciences The Pennsylvania State University, University Park, Pennsylvania 16802, USA.
Annu Rev Nutr. 2003;23:41-58. doi: 10.1146/annurev.nutr.23.020102.075739. Epub 2003 Apr 10.
Iron deficiency in early life is associated with delayed development as assessed by a number of clinical trials using similar global scales of development; this poor development during infancy persists in most cases after iron therapy has corrected iron status. If iron deficiency occurs in preschool and older children, the consequences appear reversible with treatment. The biologic understanding of this relationship between development, brain iron status, and functioning is sparse though animal studies repeatedly demonstrate alterations in dopamine metabolism and in the myelination process. Dietary iron deficiency can rapidly deplete brain iron concentrations and repletion is able to normalize them. Residual alterations in striatal dopamine metabolism and myelin production persist if neonatal animals are used. Future studies with more specific measures of neurodevelopment in iron-deficient human infants, and animal models, will allow investigators to more clearly define causal roles of brain iron in neural development and functioning.
多项使用类似整体发育量表的临床试验评估发现,生命早期缺铁与发育迟缓有关;在大多数情况下,婴儿期这种发育不良在铁疗法纠正铁状态后仍会持续。如果缺铁发生在学龄前及大龄儿童中,治疗后后果似乎是可逆的。尽管动物研究反复证明多巴胺代谢和髓鞘形成过程会发生改变,但对于发育、脑铁状态和功能之间这种关系的生物学理解仍很匮乏。膳食缺铁会迅速耗尽脑铁浓度,补充铁能够使其恢复正常。如果使用新生动物,纹状体多巴胺代谢和髓鞘生成的残留改变会持续存在。未来对缺铁人类婴儿进行更具体神经发育测量的研究以及动物模型研究,将使研究人员能够更清楚地界定脑铁在神经发育和功能中的因果作用。