Adiposity, Inflammation, and Working Memory: Evidence for a Vicious Cycle.
Adiposity, Inflammation, and Working Memory: Evidence for a Vicious Cycle.
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肥胖、炎症和工作记忆：恶性循环的证据。
DOI：
10.1016/j.bbih.2021.100202
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Hostinar,CameliaE
中科院分区：
文献类型：
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作者：
Shields,GrantS;Deer,LillyBelleK;Hastings,PaulD;Hostinar,CameliaE
超重和肥胖是全世界可预防死亡的第五大原因。超重导致健康状况不佳的一个途径是通过炎症活动和认知过程的变化。先前的理论提出了一个恶性循环，即肥胖增强炎症活动，这改变了认知过程，如工作记忆，这反过来又导致自我调节能力下降，从而管理体重。然而，迄今为止，没有纵向研究已经审查了这一潜在的动态。在目前的研究中，我们解决了这一差距，通过评估脂肪量，C-反应蛋白（CRP）和工作记忆之间的关系，随着时间的推移，在一个大样本的8536名儿童随后通过青春期在雅芳纵向研究的父母和儿童在英国。在9岁和15.5岁时，通过双发射X射线吸收法（DEXA）对肥胖进行定量，并通过在相同年龄时用高灵敏度测定法评估的循环血清C反应蛋白（CRP）水平对炎症活动进行指数化。在这两个时间点之间，在10岁时，工作记忆进行了评估，允许检查工作记忆，肥胖和炎症活动之间的时间关系。正如假设的那样，我们发现脂肪量预测了以后的工作记忆力差，这种关联在统计学上是由CRP介导的。此外，我们发现，工作记忆差预示着随后的脂肪量和CRP更大，工作记忆和随后的CRP之间的联系部分由脂肪量介导。因此，这些结果可以被认为是一个恶性循环的存在，随着时间的推移，相互放大肥胖，炎症活动和工作记忆力差。
Overweight and obesity constitute the fifth leading cause of preventable deaths worldwide. One pathway through which excess weight contributes to poor health outcomes is via inflammatory activity and changes in cognitive processes. Prior theory has proposed a vicious cycle whereby obesity potentiates inflammatory activity, which alters cognitive processes such as working memory, which in turn leads to a reduced ability to self-regulate and therefore manage weight. However, to date no longitudinal studies have examined this potential dynamic. In the current study, we addressed this gap by assessing the relations among fat mass, C-reactive protein (CRP), and working memory across time in a large sample of 8536 children followed through adolescence in the Avon Longitudinal Study of Parents and Children in the United Kingdom. Adiposity was quantified via dual emission x-ray absorptiometry (DEXA) at ages 9 and 15.5 years old, and inflammatory activity was indexed via circulating serum C-reactive protein (CRP) levels assessed with a high-sensitivity assay at those same ages. Working memory was assessed between these two time points, at age 10, permitting examination of the temporal relations between working memory, adiposity, and inflammatory activity. As hypothesized, we found that fat mass predicted later poor working memory, and this association was statistically mediated by CRP. Further, we found that poor working memory predicted greater subsequent fat mass and CRP, and the link between working memory and subsequent CRP was partially mediated by fat mass. These results thus could be taken to suggest the existence of a vicious cycle of mutually amplifying adiposity, inflammatory activity, and poor working memory over time.