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Article(id=1321169693818340347, tenantId=1146029695717560320, journalId=1319373219989389464, issueId=1321169578152014376, articleNumber=null, orderNo=null, doi=10.11847/zgggws1145208, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1730476800000, receivedDateStr=2024-11-02, revisedDate=1733241600000, revisedDateStr=2024-12-04, acceptedDate=1744128000000, acceptedDateStr=2025-04-09, onlineDate=1792921001152, onlineDateStr=2026-10-25, pubDate=1760025600000, pubDateStr=2025-10-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1792921001152, onlineIssueDateStr=2026-10-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1792921001152, creator=13701087609, updateTime=1792921001152, updator=13701087609, issue=Issue{id=1321169578152014376, tenantId=1146029695717560320, journalId=1319373219989389464, year='2025', volume='41', issue='10', pageStart='1153', pageEnd='1280', issueExtLink='null', onlineDate='null', pubDate='1760025600000', pubDateStr='2025-10-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1792920973575, creator='13701087609', updateTime=1792920973575, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=1269, endPage=1273, ext={EN=ArticleExt(id=1321169694065804284, articleId=1321169693818340347, tenantId=1146029695717560320, journalId=1319373219989389464, language=EN, title=Research progress on the effects of iodine on the nervous system and related mechanisms: a review, columnId=1320427713148597230, journalTitle=Chinese Journal of Public Health, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Iodine is an essential micronutrient for humans, and inadequate iodine status can negatively impact neurological development and function. Currently, iodine nutritional issues in the population remain a concern. Numerous epidemiological studies have confirmed that severe iodine deficiency causes a series of neurological dysfunctions, while the adverse consequences and related mechanisms of mild/moderate iodine deficiency or excess on the nervous system have not been fully elucidated. This article reviews epidemiological studies related to mild/moderate iodine deficiency, iodine excess, and neurological function, as well as their possible mechanisms of action. This review aims to provide a theoretical basis for the prevention and treatment of the neurological effects of inadequate iodine nutrition.

, authors=Xiaoxue SHI1, 2, Mengjie YANG1, 2, Chun XIE2, Hong XIANG1, authorsList=Xiaoxue SHI, Mengjie YANG, Chun XIE, Hong XIANG, authorCompany=null, correspAuthors=Hong XIANG, authorNote=null, correspAuthorsNote=
XIANG Hong, E-mail:
, copyrightStatement=Copyright © 2025 Chinese Journal of Public Health. All rights reserved., copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1321169694434903037, articleId=1321169693818340347, tenantId=1146029695717560320, journalId=1319373219989389464, language=CN, title=碘对神经系统影响及其相关机制研究进展, columnId=1320427713358312432, journalTitle=中国公共卫生, columnName=综　述, runingTitle=null, highlight=null, articleAbstract=

碘作为人体的必需微量营养物质，机体碘状态不佳可对神经发育及功能产生负面影响。目前，人群碘营养问题仍不容忽视。大量流行病学研究证实，严重碘缺乏将造成一系列神经系统功能障碍，而轻/中度碘缺乏或碘过量对神经系统的不良后果及相关机制尚未完全阐明。为此，本文就轻/中度碘缺乏、碘过量与神经系统相关的流行病学研究及其可能的作用机制进行综述，以期为防治碘营养不佳对神经系统的影响提供理论依据。

, authors=石小雪1, 2, 杨梦洁1, 2, 谢春2, 向红1, *, *, authorsList=石小雪, 杨梦洁, 谢春, 向红, authorCompany=null, correspAuthors=向红, authorNote=

石小雪（1999—），硕士在读，研究方向：碘与人群健康

, correspAuthorsNote=
向红，E-mail：
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石小雪（1999—），硕士在读，研究方向：碘与人群健康

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石小雪（1999—），硕士在读，研究方向：碘与人群健康

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碘对神经系统影响及其相关机制研究进展
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石小雪 1, 2 , 杨梦洁 1, 2 , 谢春 2 , 向红 1, *, *
中国公共卫生 | 综　述 2025,41(10): 1269-1273
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中国公共卫生 |综　述 2025 , 41 (10) : 1269 -1273
碘对神经系统影响及其相关机制研究进展
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石小雪1, 2, 杨梦洁1, 2, 谢春2, 向红1, *, *
作者信息
  • 1贵州省疾病预防控制中心，贵阳 550004
  • 2贵州医科大学公共卫生与健康学院 环境污染与疾病监控教育部重点实验室，贵阳，561113
通讯作者:
向红，E-mail：
作者简介:

石小雪（1999—），硕士在读，研究方向：碘与人群健康

Research progress on the effects of iodine on the nervous system and related mechanisms: a review
Xiaoxue SHI1, 2, Mengjie YANG1, 2, Chun XIE2, Hong XIANG1
Affiliations
  • 1Guizhou Center for Disease Control and Prevention, Guiyang 550004, China
  • 2School of Public Health, Guizhou Medical University, Key Laboratory for Environmental Pollution Monitoring and Disease Control, Ministry of Education, Guiyang 561113, China
    • Corresponding Author:
    XIANG Hong, E-mail:
出版时间: 2025-10-10 doi: 10.11847/zgggws1145208
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摘要
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碘作为人体的必需微量营养物质，机体碘状态不佳可对神经发育及功能产生负面影响。目前，人群碘营养问题仍不容忽视。大量流行病学研究证实，严重碘缺乏将造成一系列神经系统功能障碍，而轻/中度碘缺乏或碘过量对神经系统的不良后果及相关机制尚未完全阐明。为此，本文就轻/中度碘缺乏、碘过量与神经系统相关的流行病学研究及其可能的作用机制进行综述，以期为防治碘营养不佳对神经系统的影响提供理论依据。

碘缺乏  /  碘过量  /  神经系统  /  效应  /  作用机制  /  碘营养

Iodine is an essential micronutrient for humans, and inadequate iodine status can negatively impact neurological development and function. Currently, iodine nutritional issues in the population remain a concern. Numerous epidemiological studies have confirmed that severe iodine deficiency causes a series of neurological dysfunctions, while the adverse consequences and related mechanisms of mild/moderate iodine deficiency or excess on the nervous system have not been fully elucidated. This article reviews epidemiological studies related to mild/moderate iodine deficiency, iodine excess, and neurological function, as well as their possible mechanisms of action. This review aims to provide a theoretical basis for the prevention and treatment of the neurological effects of inadequate iodine nutrition.

iodine deficiency  /  iodine excess  /  nervous system  /  effect  /  mechanism of action  /  iodine nutrition
石小雪, 杨梦洁, 谢春, 向红. 碘对神经系统影响及其相关机制研究进展. 中国公共卫生, 2025 , 41 (10) : 1269 -1273 . DOI: 10.11847/zgggws1145208
Xiaoxue SHI, Mengjie YANG, Chun XIE, Hong XIANG. Research progress on the effects of iodine on the nervous system and related mechanisms: a review[J]. Chinese Journal of Public Health, 2025 , 41 (10) : 1269 -1273 . DOI: 10.11847/zgggws1145208
正文
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碘是支持机体健康不可替代的必需微量营养物质[1]。碘在不同地域环境分布差异较大。因此，环境缺碘是碘缺乏病的最重要致病原因[2]。挪威最近的一项调查研究报道，<55岁的成年人的碘摄入量还略有不足（尿碘中位数为92 µg/L[95%CI=85～99]）[3]；中国浙江省的孕妇也仍存在轻度碘营养不足的风险[4]。另有研究报道，部分国家如喀麦隆、韩国、尼泊尔、哥伦比亚等均存在碘营养过量[5]。碘缺乏或碘过量均会导致机体一系列不同程度的健康损害[6]。不同人群每日所需碘量因生命的不同阶段而异，碘对机体发育的影响也因发育阶段而有所不同[7]。这种影响在神经发育最关键的生命早期阶段更加凸显，母亲受孕前或受孕期间需要摄入足够的碘才能保证胎儿宫内最佳生长和神经发育[8]。既往研究关于碘对大脑发育影响的验证，大量的证据是基于碘缺乏、碘过量以及与补碘有关的干预措施对人或动物认知能力的研究。因此，本文就轻/中度碘缺乏和碘过量对神经系统的影响及其作用机制综述如下。
1　碘对神经系统的影响
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1.1　人群流行病学研究
目前，在食盐加碘策略下，严重的碘缺乏现象基本不存在，轻、中度碘缺乏或过量造成的健康影响引起人们的关注，特别是在神经发育和认知功能受损问题方面[6]。
1.1.1　轻/中度碘缺乏
孕妇及儿童等特殊人群对碘营养不良均很敏感，对于碘的需求量也相对增加。鉴于碘在甲状腺激素生成和胎儿大脑发育中的重要作用，母亲在胎儿关键发育阶段的碘营养不良可能会增加后代发生神经发育障碍的风险[9]。既往研究表明，妊娠期和出生后碘缺乏引起的甲状腺功能障碍会导致学习和记忆障碍、智力迟缓、听力和言语缺陷以及运动能力的改变[10]。日本一项全国性的出生队列研究[11]也显示，母亲妊娠期间最低分位碘摄入量组（≤40 μg/d）和第2分位碘摄入量组（41～123 μg/d）的儿童在1岁时精细运动方面发育迟缓的风险和3岁时在交流、精细运动、解决问题和个人社交方面发育迟缓的风险均增加。妊娠期碘水平与儿童智商得分有关，特别是妊娠早中期，儿童语言智商在此阶段的初始发育过程容易受到机体碘含量不佳的影响[12]。值得注意的是，即使是轻度或边缘性的妊娠期碘缺乏问题也可能对后代神经系统发育造成不可逆的损害[13–16]。中度碘缺乏对学龄儿童的心理发育和认知功能产生影响，主要表现为对智商和语言智商的损害明显，以及对教育表现的负面影响[17]。母亲妊娠期间轻度至中度的碘缺乏（尿碘浓度<100 µg/L）与婴儿期及学步时期的语言能力较低也有关[18]。
Abel M H等[19]采用食物频率问卷法，基于挪威母子队列研究数据共纳入48 297对母子进行随访研究发现，母亲在受孕期间膳食碘摄入低（<160 μg/d）与儿童3岁时神经认知发育（语言迟缓、行为问题和精细运动发育）的风险增加有关。但并未发现孕期补充碘的有益作用，而且该研究的一些结果提示，碘补充剂的使用可能对膳食碘摄入量低（<160 μg/d）的母亲的行为结果造成负面影响。补碘方式因人而异。因此，对于母亲补碘的科学性和具体实施还需要进一步的研究讨论[8,20]。Abel M H研究团队[21]在后续随访中报道，母亲膳食碘摄入量低（<150 μg/d）与儿童8岁时的语言、阅读和写作能力较差以及接受特殊教育服务的可能性增加也有关。也有研究观察到，在儿童时期足够的碘摄入可能并不能完全改善妊娠期碘缺乏造成的所有缺陷，比如拼写方面的持续差异、工作记忆和听觉处理速度等表现；其中，妊娠期轻度碘缺乏所导致后代在9岁时与认知相关的（识字能力）教育表现下降的情况可持续存在到青春期[16]。以上研究提示，妊娠期轻度至中度碘缺乏造成的胎儿期、婴幼儿期的碘缺乏及其所致的不可逆的神经系统相关损伤和影响，难以通过后期延迟的补碘来改善。
1.1.2　碘过量
在低碘风险的同时，碘过量的影响也不容忽视。环境的碘缺乏对儿童脑发育的损害已为人们所公认，而关于碘过量影响的结论一直存有争议。钱明等[22]未发现碘过量对儿童智力的明显影响。而Carvalho I P等 [23]认为高碘与智商平均水平降低相关，即使在调整潜在混杂因素后两者仍然显著关联。还有研究探讨了孕妇在妊娠期间血清碘过量对婴儿的碘状态、神经发育和身体发育的影响。结果显示，在母亲甲状腺功能正常的情况下，母亲在妊娠早期（0～13周）碘摄入过量对婴儿的智力、运动和身体发育也有一定的负面影响[24]。
1.2　动物实验研究
碘通过参与甲状腺激素的产生，促进甲状腺的稳态以及机体生长代谢[25]。甲状腺激素直接或间接参与胎儿大多数的神经系统发育过程[9]。以往研究通过对不同物种动物模型的观察得出结论，母体甲状腺功能的细微变化也可能对子代的脑发育产生持久的影响。母体在妊娠期和哺乳期的碘营养状况会影响胎盘和哺乳期乳腺中的碘储存，进而影响后代甲状腺功能及其神经发育和认知水平[26]。
早期研究者利用绵羊实验模型探究碘缺乏对绵羊胎儿脑发育的影响。发现在绵羊妊娠70 d时绵羊胎儿大脑重量和大脑DNA含量均减少，且与母体和胎儿甲状腺激素水平的总体降低有关[27]。另一项狨猴动物低碘膳食实验结果表明，亲代和子代的血浆甲状腺素水平均明显降低，促甲状腺激素水平均升高，子代表现为小脑重量显著减少，甲状腺组织学显示滤泡增生、肥大和滤泡内胶体物质缺失[28]。
至今，大多研究以鼠作为研究对象。有研究显示，当摄碘不足时，母体中的碘会通过增加钠碘转运体（sodium iodide symporter, NIS）和Pendrin转运蛋白的表达而更多地富集在胎盘中，从而缓解碘缺乏对胎儿的损害[29]。当碘过量时，胎盘通过降低NIS和Pendrin的表达来减少胎盘中碘的蓄积，从而起到屏障作用。同样，甲状腺也可以根据体内不同的碘浓度调节NIS和Pendrin的表达，从而调节甲状腺的碘储存以维持正常的甲状腺功能。Zhang L等[30]基于大鼠海马体代谢组学的研究发现，不同碘摄入量主要影响子代大鼠体内氨基酸代谢、能量代谢和嘌呤代谢等过程。表明这些相关代谢物或代谢途径可有助于阐明不同碘摄入量引起的子代大鼠大脑发育相关的病理生理机制。
2　碘致神经损伤的可能机制
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2.1　碘缺乏的相关机制
严重碘缺乏已被大量研究明确报道会导致胎儿大脑发育迟缓。早期绵羊动物实验发现，缺碘胎儿的大脑半球的运动皮层和视觉皮层以及海马的CA1和CA4区域的神经元密度明显增加[27]。事实上，许多大脑结构和功能都受到碘缺乏的影响，包括小脑、海马体、大脑皮层等不同的大脑区域微结构和神经递质[31]。
2.1.1　小脑
小脑是研究影响中枢神经系统形态形成相关机制的良好模型，它与认知、情感、记忆、语言处理和运动及运动协调等神经系统活动有关[32]。其中，浦肯野细胞是小脑皮层的唯一输出神经元，是小脑信息处理中不可缺少的。有研究观察到，轻度碘缺乏通过损伤小脑浦肯野细胞的生长而导致大鼠的运动协调能力损伤[13]。对参与小脑神经元结构、功能和发育的小窝蛋白1（caveolin 1, Cav-1）和突触结合蛋白1（synaptotagmin-1, Syt-1）的机制研究[33]发现，碘缺乏会造成大鼠小脑的形态学损伤，导致小脑浦肯野细胞减少，Cav-1上调，Syt-1下调。通过测量小脑浦肯野细胞（purkinje cells, PCs）的总树突状长度，观察到在小脑PCs中由边缘性碘缺乏引起轻微的树突状生长受限，这可能是由于核因子kappa B（nuclear factor kappa B, NF-κB）信号通路的干扰和微管相关蛋白1B（microtubule-associated protein 1B, MAP1B）的下调所致[34]。此外，Yu Y等[15]的研究还观察到母体边缘性碘缺乏导致小脑伯格曼神经胶质细胞（bergmann glial cells, BGs）发育受限，而BGs有助于浦肯野细胞树突的神经支配与神经元之间突触连接的稳定。该研究结果显示，BGs形态的损伤可能是由于（与细胞形态和发育密切相关的） Notch 信号通路下调所致。
2.1.2　海马体
海马体是与神经元突触可塑性、学习和记忆等认知过程密切相关的大脑重要区域[31]。神经元核中的c-Fos和c-Jun蛋白参与神经可塑性机制和神经元分化，并在记忆形成和巩固中至关重要[35]。有研究发现，与正常对照组相比，7日龄的边缘性碘缺乏组子代大鼠海马中脑源性神经营养因子（brain-derived neurotrophic factor, BDNF）、早期生长反应因子1（early growth response factor, EGR1）的表达水平显著降低，海马CA1区c-Fos和c-Jun的表达水平也明显降低，导致神经功能缺陷；到40日龄时，边缘性碘缺乏组子代大鼠的空间学习和记忆能力较对照组呈下降趋势。结果提示，上述相关蛋白可能参与边缘性碘缺乏对后代神经系统和认知能力的作用机制[14]。Wei W等[36]研究发现，母鼠轻度碘缺乏暴露后所诱导的子代大鼠低甲状腺素血症，可引起其海马体中少突胶质细胞转录因子2（oligodendrocyte lineage transcription factor 2, Olig2）和髓鞘相关蛋白的表达水平显著降低，最终损害发育中的海马髓鞘生长。提示这可能是导致子代大鼠神经系统发育缺陷的原因。
2.1.3　内嗅皮层
内嗅皮层—海马神经回路被认为是哺乳动物大脑的记忆中心。刺激内嗅皮层有助于改善学习和记忆相关的过程，内嗅皮层也是神经元网络中负责学习和记忆的信息传递的一个重要功能结构[37]。除了海马体外，内嗅皮层还投射到纹状体、内侧前额叶皮层以及其他参与学习和记忆的皮层下和皮层区域[38]。有研究对大鼠进行妊娠和出生后哺乳期间碘缺乏和丙硫氧嘧啶干预，发现子代大鼠的内嗅皮层中潜在的记忆分子钙/钙调蛋白依赖性蛋白激酶Ⅱ（calcium/calmodulin-dependent protein kinase Ⅱ, CaMKII）及其磷酸化蛋白的表达水平降低，而其中钙调神经磷酸酶的增加，以及神经颗粒素和钙调蛋白的减少，可能是碘缺乏和甲状腺功能减退导致CaMKII磷酸化减少的原因[38]。这些信号分子水平的变化都可能导致认知功能的损害，如注意力、学习和记忆能力等。
2.2　碘过量的可能机制
尽管一些人群研究表明，智商降低与高碘摄入量之间存在显著关联，但在碘过量地区存在智力下降的具体机制尚未被阐明。陆续地，越来越多的研究者为寻找碘过量与大脑发育之间关系的确切证据而展开相应实验研究。Zhang L等[35]]研究发现，在母鼠孕前（12周）至母乳喂养期间（幼鼠出生后21 d）的轻度高碘摄入量的幼鼠中，存在BDNF和神经内分泌特异性蛋白（neuroendocrine-specific protein-A, NSP-A）表达的变化和神经系统发育障碍。BNDF和NSP-A作为大脑发育过程中参与甲状腺激素作用的重要介质，Fu M等[26]也发现，母体高碘摄入会影响后代甲状腺功能及BNDF和NSP-A的表达。
近年来的实验研究以碘过量与凋亡、自噬等现象的关系展开探讨。有研究认为，细胞凋亡是过量碘引起靶器官损伤的主要机制之一。研究者利用体外实验已证实高浓度的碘化物对SH-SY5Y神经细胞有毒性作用，并可诱导细胞凋亡和自噬[39]。Cui Y等[40]通过建立高碘暴露的大鼠模型研究表明，过量碘诱导的学习记忆损伤可能是通过线粒体凋亡途径介导的，还可能与过量碘引起的单胺神经递质紊乱有关。该研究发现，长期过量碘暴露会导致子代大鼠海马结构改变，并损害其学习和记忆能力；此外，子代大鼠海马中裂解的半胱天冬氨酸特异性蛋白酶–3（cysteinyl aspartate-specific proteinase-3, Caspase-3）和多聚ADP核糖聚合酶（poly ADP-ribose polymerase, PARP）蛋白、P53及细胞色素（cytochrome C, Cty C）等线粒体凋亡相关蛋白表达增加，说明过量的碘可以激活线粒体凋亡通路。此外，过量碘导致的大鼠学习记忆能力的下降可能与去甲肾上腺素和5–羟色胺等单胺神经递质紊乱有关。Zhao L等 [41]的研究表明，自噬作为细胞死亡途径参与了碘过量引起的认知功能损伤，而自噬抑制剂3-甲基腺嘌呤可显著减轻上述损伤。这为研究碘过量引起的神经毒性作用机制提供了新的线索。并提出增强自噬抑制可作为预防碘过量引起的认知功能障碍的假设。
3　展　望
收起
人群流行病学研究和动物实验研究证据表明，碘是个体发育过程中神经系统分化的重要元素，也是能量代谢的关键调节因子[42]，其生物学效应作用于不同的大脑区域微结构和神经递质等。目前，大多数关于人类和动物碘代谢的研究都聚焦于碘在甲状腺功能中的作用。实际上，相当多的证据表明，碘本身参与了摄取碘的各种器官组织的病理生理过程[42]。因此，以碘在甲状腺外组织潜在的生理学功能及应用作为不同的角度，来阐明相关机制的思路值得深入研究与探索。事实上，无论是碘缺乏还是碘过量对于神经系统产生不良影响的具体作用机制尚未十分清晰，需要应用多组学与生物信息技术相结合来阐明机体碘状态与神经系统之间的关系性质，更为精准探索碘不足或过量所致神经损伤，为碘营养不当的预防提供科学依据。

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2025年第41卷第10期
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doi: 10.11847/zgggws1145208
  • 接收时间：2024-11-02
  • 首发时间：2026-10-25
  • 出版时间：2025-10-10
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  • 收稿日期：2024-11-02
  • 修回日期：2024-12-04
  • 录用日期：2025-04-09
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    1贵州省疾病预防控制中心，贵阳 550004
    2贵州医科大学公共卫生与健康学院 环境污染与疾病监控教育部重点实验室，贵阳，561113

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genus		 种数
Number of
species		 占总种数比例
Percentage of
total species (%)		 属
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Number of
species		 占总种数比例
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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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