Dietetic Department, Saint George Hospital University Medical Center, Beirut, Lebanon.
Division of Medicine, Eating Disorders and Clinical Nutrition, University College London, London, UK.
Eat Weight Disord. 2021 Jun;26(5):1323-1344. doi: 10.1007/s40519-020-00978-5. Epub 2020 Aug 11.
The genetic aspect of anorexia nervosa (AN) involving specific genes of the central-nervous-system has not yet been clearly understood. The aim of this systematic review is to assess the impact of three candidate genes of the brain: catechol-O-methyltransferase, brain-derived neurotrophic factor (BDNF) and serotonin transporter protein, on the susceptibility to AN and identify whether a clear connection persists between each of the gene-polymorphisms and AN.
A total of 21 articles were selected for this review conforming to the PRISMA guidelines. Detailed keyword combinations were implemented within specific databases such as MEDLINE, SCIENCEDIRECT and PUBMED.
The catechol-O-methyltransferase gene-polymorphism did not show any change in phenotypic variation between AN and control subjects; but the familial association was rather strong with an over-transmission of the H allele. The latter also correlated with several dimensions of the Temperament and Character Inventory (TCI) scale. A notable relation was indicated between BDNF gene-polymorphism and anorexia-restrictive in terms of phenotypic distribution; the Met66-allele also depicted high association with anorexic behavioral traits. The 5-HTTLPR gene-polymorphism was found to be significantly associated with AN susceptibility with an over-transmission of the S-allele from parents to offspring.
The systematic review distinctively emphasized the genetic contribution of the brain-genes on the development of AN. Despite significant study findings, no clear and standardized genetic route was determined to be the cause of AN development. Future research is needed on these specific genes to closely monitor the genetic polymorphisms and their mechanism on AN susceptibility.
I, systematic review.
涉及中枢神经系统特定基因的厌食症（AN）的遗传方面尚未得到明确理解。本系统评价的目的是评估大脑的三个候选基因：儿茶酚-O-甲基转移酶、脑源性神经营养因子（BDNF）和 5-羟色胺转运蛋白对 AN 易感性的影响，并确定每种基因多态性与 AN 之间是否存在明确的联系。
根据 PRISMA 指南，共选择了 21 篇符合条件的文章进行综述。在 MEDLINE、SCIENCEDIRECT 和 PUBMED 等特定数据库中实施了详细的关键词组合。
儿茶酚-O-甲基转移酶基因多态性在 AN 和对照组之间的表型变异中没有显示任何变化；但家族关联性很强，H 等位基因过度传递。后者还与气质和性格量表（TCI）的几个维度相关。BDNF 基因多态性与厌食症的限制表型分布之间存在显著关系；Met66-等位基因也与厌食症行为特征高度相关。5-HTTLPR 基因多态性与 AN 易感性显著相关，父母向后代传递 S 等位基因的频率过高。
系统评价明确强调了大脑基因对 AN 发展的遗传贡献。尽管有重要的研究发现，但没有确定明确和标准化的遗传途径是 AN 发展的原因。需要对这些特定基因进行进一步研究，以密切监测遗传多态性及其对 AN 易感性的机制。
I，系统评价。
