학술논문
The impact of COMT, BDNF and 5-HTT brain-genes on the development of anorexia nervosa: a systematic review.
Document Type
Academic Journal
Author
Abou Al Hassan S; Dietetic Department, Saint George Hospital University Medical Center, Beirut, Lebanon.; Division of Medicine, Eating Disorders and Clinical Nutrition, University College London, London, UK.; Cutinha D; Division of Medicine, Eating Disorders and Clinical Nutrition, University College London, London, UK.; Mattar L; Nutrition Division, Department of Natural Sciences, School of Arts and Sciences, Lebanese American University, Beirut, Lebanon. Lama.mattar@lau.edu.lb.
Source
Publisher: Springer Country of Publication: Germany NLM ID: 9707113 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1590-1262 (Electronic) Linking ISSN: 11244909 NLM ISO Abbreviation: Eat Weight Disord Subsets: MEDLINE
Subject
Language
English
Abstract
Purpose: 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.
Methods: 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.
Results: 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.
Conclusion: 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.
Level of Evidence: I, systematic review.
Methods: 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.
Results: 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.
Conclusion: 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.
Level of Evidence: I, systematic review.