早期缺铁与大脑发育

缺铁(iron deficiency, ID)和缺铁性贫血(iron deficiency anemia, IDA)是最常见的单一营养缺乏性疾病, 在孕妇与学龄前儿童中发病率最高。在缺铁所致的所有结局中, 最令人关注的是早期缺铁对儿童大脑和发育的影响。大量研究发现, 早期缺铁通过改变脑结构、神经递质功能和神经代谢, 伴随基因和蛋白组分的改变, 影响着感觉运动、认知语言和社会情绪的发育。新的研究进展提示了生命早期的脑发育存在着铁依赖的关键期, 重申了早期预防缺铁的重要性。     

儿童铁缺乏与认知功能的相关性研究进展

虽然儿童营养不良发生率已逐年下降,但缺铁性贫血(iron deficiency anemia,IDA)依旧是严重的世界性公共卫生问题。大量研究表明,铁缺乏(iron deficiency,ID)除了可导致缺铁性贫血外,还可引起一系列中枢神经系统功能的紊乱,包括情绪、运动和认知等多个方面。为了解近年来在ID与认知方面的研究状况,同时为儿童保健工作中预防ID、IDA及由此而引发的神经精神发育问题提供一定的科学依据,现将近年来有关ID与认知方面的研究做一综述。     

婴幼儿缺铁性贫血对认知功能的影响及干预研究

目的 通过总结婴幼儿缺铁性贫血对认知功能产生近期和远期影响以及影响机制和干预措施,发现贫血影响婴幼儿的关键期,为提出更高效的干预措施提供科学依据。方法 使用“anemia”、“infants”、“iron deficiency”、“cognition”和“贫血”、“铁缺乏”以及“认知功能”等为关键词,通过PubMed和中国知网（CNKI）进行文献检索,共收集38篇相关文献,用描述性研究对婴幼儿缺铁性贫血对认知功能的影响及干预措施进行综述。结果 婴幼儿缺铁性贫血对认知功能的影响具有持续性及不可逆性以及对认知功能影响存在关键期,目前对婴幼儿缺铁性贫血的干预措施。结论 孕期补铁、延迟期待结扎以及婴幼儿补铁可以改善缺铁性贫血对认知功能的影响。     

铁缺乏对学龄青少年注意力和学习成绩的影响

铁不仅是人体正常生长发育的必需营养元素,而且对正常的智能、行为发育和认知功能非常重要,而注意是认知功能的重要组成部分,会影响认知、操作效率、活动水平等,并对学生学习成绩产生一定影响。有报道表明,铁缺乏会影响缺铁性贫血(iron deficient anemia,IDA)儿童的注意稳定性,铁剂治疗后IDA儿童的注意持久性显著改善。由于儿童青少     

铁缺乏症婴幼儿认知水平研究

目的 了解非贫血铁缺乏症和缺铁性贫血婴幼儿的认知水平, 为进一步治疗提供科学依据。方法 采用Gesell发育测试法评估非贫血铁缺乏症和缺铁性贫血婴幼儿适应性、大运动、精细动作、语言和个人社交5个能区发育水平。结果 患铁缺乏症的男婴较女婴更多(χ²=13.06, P=0.001), 非贫血铁缺乏症(non-anemia iron deficiency, NAID)组、缺铁性贫血(iron deficiency anemia, IDA)组较铁充足(iron sufficiency, IS)组婴幼儿的5个能区发育水平落后(F_适应性=13.64;F_大运动=6.24;F_精细动作=6.25;F_语言=4.89;F_个人社交=9.14, P值均<0.01), NAID和IDA婴幼儿之间差异无统计学意义;但男性婴幼儿在语言和个人社交发育商分数较女婴更低(F=9.299, P=0.003;F=4.250, P=0.042)。结论 铁缺乏症伴或不伴贫血对婴幼儿的认知水平都有影响, 提示在临床工作中应早期干预铁缺乏。     

小儿缺铁性贫血的诊治——铁的代谢

缺铁性贫血（iron deficiency anemia,IDA）是全球四大营养缺乏病之一,发病率相当高,是儿童常见病,主要发生在6个月～2岁的婴幼儿,对儿童健康危害极大,影响其体格智力发育和免疫代谢等功能,是儿童保健中需要重点防治的常见病之一。缺铁性贫血是由于体内储存铁缺乏而影响血红蛋白合成所引起的贫血,具有小细胞低色素性、血清铁及血清铁蛋白降低、血清总铁结合力升高、铁剂治疗效果良好等特点。本刊特组织相关专家撰写缺铁性贫血的诊治专题笔谈,以期对读者有所帮助。     

婴幼儿缺铁性贫血现状及影响因素

营养性缺铁性贫血是婴幼儿时期常见的营养性疾病,缺铁性贫血（iron—deficiency anemia,IDA）是由于体内铁缺乏导致血红蛋白减少所致,IDA是铁缺乏症的晚期表现。铁缺乏不仅影响造血机能,还影响儿童生长发育、运动和免疫等各种功能。本文对在我院儿保门诊系统管理的婴幼儿贫血状况及影响因素作一分析。     

铁缺乏对啮齿类动物中枢神经系统的影响

铁缺乏(iron deficiency,ID)是最常见的营养素缺乏症和全球性健康问题,6~24月婴幼儿是儿童铁缺乏的高危人群。啮齿类动物铁缺乏的研究也模仿人类,研究胎儿期到断奶期的幼鼠,此时是啮齿类动物神经系统发育的敏感期。在啮齿类动物研究中发现单纯铁缺乏不但可以导致脑内铁、单胺类化合物及其转运体、受体受到不同程度的影响,还影响中枢神经系统髓鞘化形成,导致幼鼠即使经过治疗后仍然表现为行为、学习、记忆等受损。本文就啮齿类动物铁缺乏对中枢神经系统的影响进行综述。     

铁与儿童精神运动发育、认知功能和神经行为关系的研究进展

铁是大脑新陈代谢的基本元素,缺铁可引起神经递质稳态的改变、减少髓鞘的产生、损害突触的形成、并使基底神经节功能下降,因此,缺铁性贫血会对精神运动发育、认知功能和神经行为产生不利影响,危害婴幼儿的健康发育。了解铁缺乏与精神运动发育、认知功能和神经行为的关系,弄清补充铁的疗效并在儿童保健时开展血清铁含量检验,对制定早期预防铁缺乏的公共卫生策略具有十分重要的意义。     

早期儿童喂养行为与缺铁性贫血

缺铁性贫血(iron deficiency anemia,IDA)是因体内铁缺乏致使血红蛋白合成减少而引起的贫血.IDA为小儿贫血中最常见,尤其在婴幼儿中发病率最高.科学合理的喂养方法,有助于预防与饮食有关的营养性疾病.早期正确地儿童喂养行为可以减少或减轻儿童IDA患病率和贫血程度.     

Iron Metabolism Dysregulation and Cognitive Dysfunction in Pediatric Obesity: Is There a Connection?

Obesity and iron deficiency (ID) are two of the most common nutritional disorders in the world. In children both conditions deserve particular attention. Several studies revealed an association between obesity and iron deficiency in children and, in some cases, a reduced response to oral supplementation. The connecting mechanism, however, is not completely known. This review is focused on: (1) iron deficiency in obese children and the role of hepcidin in the connection between body fat and poor iron status; (2) iron status and consequences on health, in particular on cognitive function; (3) cognitive function and obesity; (4) suggestion of a possible link between cognitive dysfunction and ID in pediatric obesity; and implications for therapy and future research.     

孕期缺铁对婴幼儿运动发育的研究进展

铁缺乏(ID)和缺铁性贫血(IDA)是全球最常见的单一营养缺乏性疾病。孕妇和婴幼儿是ID的高危人群,孕母ID到一定程度会影响胎儿/新生儿的铁营养状况。早期ID主要通过影响髓鞘化、纹状体和多巴胺神经递质影响个体的运动发育。生后早期给予足量的铁剂治疗能纠正婴幼儿循环及组织内的ID,但无法完全逆转孕期ID所致的行为改变。深入研究孕期ID对婴幼儿运动发育的影响及其可逆性,明确铁剂治疗的关键时间窗,对提高儿童生存质量,改善远期预后具有十分重要的意义。     

早期铁缺乏与婴幼儿情绪发展

缺铁是世界范围内最常见的单一营养缺乏性疾病,在孕妇与学龄前儿童中发病率最高.缺铁不仅能够引起贫血,而且早期铁缺乏通过影响大脑发育过程可影响感觉、运动、认知、社会情感功能等方面的发育.目前对精神运动功能发育方面的研究已经比较深入,但对社会情感或情绪方面的研究还相对较少,缺铁导致的多巴胺及其受体的变化被认为与情绪行为改变密切相关.该文就早期铁缺乏与婴幼儿情绪发展的关系作以综述.     

An overview of evidence for a causal relation between iron deficiency during development and deficits in cognitive or behavioral function

This review, intended for a broad scientific readership, summarizes evidence relevant to whether a causal relation exists between dietary iron deficiency with (ID+A) or without (ID-A) anemia during development and deficits in subsequent cognitive or behavioral performance. An overview of expert opinion and major evidence in humans and animals is provided. Cognitive and behavioral effects observed in humans with ID-A and in animals with ID+/-A are provided in tables. The degree to which 5 conditions of causality are satisfied and whether deleterious effects of ID-A might be expected to occur are discussed. On the basis of the existing literature, our major conclusions are as follows. Although most of the 5 conditions of causality (association, plausible biological mechanisms, dose response, ability to manipulate the effect, and specificity of cause and effect) are partially satisfied in humans, animals, or both, a causal connection has not been clearly established. In animals, deficits in motor activity are consistently associated with severe ID+A, but adverse effects on performance in tests that target cognitive function have not been clearly shown. Resistance to iron treatment was observed in most trials of children <2 y of age with ID+A, but not in older children. Similar observations were made in rodents when ID+A occurred before rather than after weaning. In children >2 y of age and in adolescents with ID-A, evidence suggests cognitive or behavioral deficits; however, the surprisingly small number of studies conducted in either humans or animals prevents a thorough assessment.     

铁碘缺乏致甲状腺功能减退大鼠血中微量元素的变化

目的观察微量元素变化与铁、碘缺乏大鼠甲状腺功能变化之间的关系。方法健康SPF/VAF级初断乳SD大鼠32只,雌雄各半,按体重随机分为碘铁联合缺乏组(IFD)、碘缺乏组(ID)、铁缺乏组(FD)和对照组(N),每组各8只。通过饲料控制4周使各组大鼠铁、碘营养水平达到实验预期。测定尿碘浓度、甲状腺重量、血红蛋白、血清甲状腺激素和促甲状腺激素水平,测量血清中镁(Mg)、钙(Ca)、铬(Cr)、锰(Mn)、铜(Cu)、锌(Zn)和硒(Se)的含量。结果大鼠碘营养和铁营养各项指标均符合试验设计要求。与对照组相比,铁缺乏组、碘缺乏组、碘铁联合缺乏组均出现甲状腺功能减退(甲减)或甲减趋势;碘铁联合缺乏组大鼠血清Ca、Mn、Zn浓度增加(P0.05,P0.01),其他元素变化无统计学意义;碘缺乏组大鼠血清Cu、Zn、Se浓度增加(均P0.05),其他元素变化无统计学意义;铁缺乏组大鼠血清Ca、Zn浓度增加(P0.05,P0.01),其他元素变化无统计学意义。结论多种微量元素的变化可能协同铁、碘对甲状腺的功能产生影响。     

Iron-Enriched Nutritional Supplements for the 2030 Pharmacy Shelves

Iron deficiency (ID) affects people of all ages in many countries. Due to intestinal blood loss and reduced iron absorption, ID is a threat to IBD patients, women, and children the most. Current therapies can efficiently recover normal serum transferrin saturation and hemoglobin concentration but may cause several side effects, including intestinal inflammation. ID patients may benefit from innovative nutritional supplements that may satisfy iron needs without side effects. There is a growing interest in new iron-rich superfoods, like algae and mushrooms, which combine antioxidant and anti-inflammatory properties with iron richness.     

Iron deficiency: Differential effects on monoamine transporters

Abstract

In this study, we extend previous work on iron deficiency and dopamine (DA) transporters to include an examination of central serotonin (5-HT) and noradrenergic (NE) transporters. Rats were fed either iron deficient (ID) or iron adequate (CN) diets from weaning until adulthood. In males, an additional group of iron deficient animals (IR) were given iron supplementation. DA, 5-HT, and NE transporter binding was done in situ on thin sections. ID males, but not females, decreased DA transporter binding in the nucleus accumbens, caudate putamen and substantia nigra by 20–40%. ID males also had a 20–30% reduction in 5-HT transporter binding in several areas (nucleus accumbens, olfactory tubercle, colliculus) while in ID females there was 15–25% increased serotonin transporter binding in the olfactory tubercle, zona incerta, anteroventral thalamic nucleus and vestibular nucleus. Iron deficiency reduced 3 H-nisoxetine binding to the NE transporter in locus ceruleus and anteroventral thalamic nucleus in males but not females. Only some of the changes observed in DA, serotonin and NE transporter binding were reversible by iron supplementation. These findings show that iron deficiency affects monoamine systems related to homeostasis and in most cases males appear to be more vulnerable than females.     

The Long Term Impact of Micronutrient Supplementation during Infancy on Cognition and Executive Function Performance in Pre-School Children

Brain growth and development are critically dependent on several micronutrients. During early development cellular activity may be sensitive to micronutrient deficiencies, however the evidence from human studies is equivocal. The objective of this study was to examine the long-term cognitive and social-emotional effects of multiple micronutrient supplementation compared with iron supplementation alone, administered during infancy. This study was a follow-up to an initial randomized, double-blind controlled trial (RCT) in 2010 in which 902 infants, aged 6–17 months, from Lima, Peru, were given daily supplements of either iron (Fe) or multiple micronutrients (MMN) including zinc (451 in each group). The supplementation period for both groups was six months. In 2012, a subsample of 184 children from the original cohort (now aged 36–48 months) was randomly selected to participate in a follow-up trial and was assessed for intelligence, working memory, inhibition, and executive function. The tests showed no significant differences between the supplementation groups though there were some gender differences, with girls displaying higher scores than boys across both groups on the Wechsler Preschool and Primary Scale of Intelligence (WPPSI) Verbal IQ sentences subtest, the Day-Night cognitive test and on the Brief Infant-Toddler Social Emotional Assessment (BITSEA) social competency, and boys scoring higher than girls in problem behaviour. The results indicate that MMN supplementation had no long term additional effects on cognitive function compared with iron supplementation alone. The timing of supplement administration for maximum impact on a child’s cognitive development requires further investigation.     

Early-Life Iron Deficiency Anemia Programs the Hippocampal Epigenomic Landscape

Iron deficiency (ID) anemia is the foremost micronutrient deficiency worldwide, affecting around 40% of pregnant women and young children. ID during the prenatal and early postnatal periods has a pronounced effect on neurodevelopment, resulting in long-term effects such as cognitive impairment and increased risk for neuropsychiatric disorders. Treatment of ID has been complicated as it does not always resolve the long-lasting neurodevelopmental deficits. In animal models, developmental ID results in abnormal hippocampal structure and function associated with dysregulation of genes involved in neurotransmission and synaptic plasticity. Dysregulation of these genes is a likely proximate cause of the life-long deficits that follow developmental ID. However, a direct functional link between iron and gene dysregulation has yet to be elucidated. Iron-dependent epigenetic modifications are one mechanism by which ID could alter gene expression across the lifespan. The jumonji and AT-rich interaction domain-containing (JARID) protein and the Ten-Eleven Translocation (TET) proteins are two families of iron-dependent epigenetic modifiers that play critical roles during neural development by establishing proper gene regulation during critical periods of brain development. Therefore, JARIDs and TETs can contribute to the iron-mediated epigenetic mechanisms by which early-life ID directly causes stable changes in gene regulation across the life span.