scholarly journals A review on association and correlation of genetic variants with eating disorders and obesity

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Sayed Koushik Ahamed ◽  
Md Abdul Barek ◽  
Uthpall Kumar Roy ◽  
Md Kouser ◽  
Md Sharif Reza ◽  
...  

Abstract Background Now, eating disorders and obesity and their correlations are danger signal in worldwide which is caused by multifactor and associated with significant mortality and morbidity. Main body Every aspect of a patient’s life is influenced by eating disorders and obesity and their correlations. Due to frequent seeing of obese patients, eating disorders have been included in the review as they can sometimes be associated with obesity. However, it should be noted that most patients having eating disorder are at risk to be obese or overweight. This research explores the risk factors for the two disorders, as well as the assessment of medical complications and treatment recommendations for the disorders. In these two disorders, there is also a correlation. The essential consideration is that eating disorders are impulse-control disorders which are similar to addictive behaviors in some aspects. So it is a crying need to treat a patient with obesity and eating disorders simultaneously to ensure success. Genome-wide association studies (GWASs) have increased our knowledge of the pathophysiology of eating disorders (EDs) and obesity and their correlation. Conclusion This review enlightens on the summary of eating disorder, obesity, genotypic traits, molecular relations, interaction, correlation, and effect of eating disorder and obesity which outline potential future directions and clinical implications for patients with EDs and obesity.

2020 ◽  
Author(s):  
Christopher Hübel ◽  
Mohamed Abdulkadir ◽  
Moritz Herle ◽  
Ruth J.F. Loos ◽  
Gerome Breen ◽  
...  

AbstractObjectiveGenome-wide association studies have identified multiple genomic regions associated with anorexia nervosa. Relatively few or no genome-wide studies of other eating disorders, such as bulimia nervosa and binge-eating disorder, have been performed, despite their substantial heritability. Exploratively, we aimed to identify traits that are genetically associated with binge-type eating disorders.MethodWe calculated genome-wide polygenic scores for 269 trait and disease outcomes using PRSice v2.2 and their association with anorexia nervosa, bulimia nervosa, and binge-eating disorder in up to 640 cases and 17,050 controls from the UK Biobank. Significant associations were tested for replication in the Avon Longitudinal Study of Parents and Children (up to 217 cases and 3018 controls).ResultsIndividuals with binge-type eating disorders had higher polygenic scores than controls for other psychiatric disorders, including depression, schizophrenia, and attention deficit hyperactivity disorder, and higher polygenic scores for body mass index.DiscussionOur findings replicate some of the known comorbidities of eating disorders on a genomic level and motivate a deeper investigation of shared and unique genomic factors across the three primary eating disorders.


2021 ◽  
pp. 1-11
Author(s):  
Hunna J. Watson ◽  
Alish B. Palmos ◽  
Avina Hunjan ◽  
Jessica H. Baker ◽  
Zeynep Yilmaz ◽  
...  

Abstract Enabled by advances in high throughput genomic sequencing and an unprecedented level of global data sharing, molecular genetic research is beginning to unlock the biological basis of eating disorders. This invited review provides an overview of genetic discoveries in eating disorders in the genome-wide era. To date, five genome-wide association studies on eating disorders have been conducted – all on anorexia nervosa (AN). For AN, several risk loci have been detected, and ~11–17% of the heritability has been accounted for by common genetic variants. There is extensive genetic overlap between AN and psychological traits, especially obsessive-compulsive disorder, and intriguingly, with metabolic phenotypes even after adjusting for body mass index (BMI) risk variants. Furthermore, genetic risk variants predisposing to lower BMI may be causal risk factors for AN. Causal genes and biological pathways of eating disorders have yet to be elucidated and will require greater sample sizes and statistical power, and functional follow-up studies. Several studies are underway to recruit individuals with bulimia nervosa and binge-eating disorder to enable further genome-wide studies. Data collections and research labs focused on the genetics of eating disorders have joined together in a global effort with the Psychiatric Genomics Consortium. Molecular genetics research in the genome-wide era is improving knowledge about the biology behind the established heritability of eating disorders. This has the potential to offer new hope for understanding eating disorder etiology and for overcoming the therapeutic challenges that confront the eating disorder field.


2019 ◽  
Vol 28 (7) ◽  
pp. 1095-1102 ◽  
Author(s):  
Tracy A. O'Mara ◽  
Dylan M. Glubb ◽  
Pik Fang Kho ◽  
Deborah J. Thompson ◽  
Amanda B. Spurdle

2020 ◽  
Vol 127 (1) ◽  
pp. 21-33 ◽  
Author(s):  
Carolina Roselli ◽  
Michiel Rienstra ◽  
Patrick T. Ellinor

Atrial fibrillation is a common heart rhythm disorder that leads to an increased risk for stroke and heart failure. Atrial fibrillation is a complex disease with both environmental and genetic risk factors that contribute to the arrhythmia. Over the last decade, rapid progress has been made in identifying the genetic basis for this common condition. In this review, we provide an overview of the primary types of genetic analyses performed for atrial fibrillation, including linkage studies, genome-wide association studies, and studies of rare coding variation. With these results in mind, we aim to highlighting the existing knowledge gaps and future directions for atrial fibrillation genetics research.


2021 ◽  
Vol 128 (12) ◽  
pp. 1988-2002
Author(s):  
Richard A. Baylis ◽  
Nicholas L. Smith ◽  
Derek Klarin ◽  
Eri Fukaya

Venous disease is a term that broadly covers both venous thromboembolic disease and chronic venous disease. The basic pathophysiology of venous thromboembolism and chronic venous disease differ as venous thromboembolism results from an imbalance of hemostasis and thrombosis while chronic venous disease occurs in the setting of tissue damage because of prolonged venous hypertension. Both diseases are common and account for significant mortality and morbidity, respectively, and collectively make up a large health care burden. Despite both diseases having well-characterized environmental components, it has been known for decades that family history is an important risk factor, implicating a genetic element to a patient’s risk. Our understanding of the pathogenesis of these diseases has greatly benefited from an expansion of population genetic studies from pioneering familial studies to large genome-wide association studies; we now have multiple risk loci for each venous disease. In this review, we will highlight the current state of knowledge on the epidemiology and genetics of venous thromboembolism and chronic venous disease and directions for future research.


2020 ◽  
Vol 26 (1) ◽  
Author(s):  
Melissa A. Munn‐Chernoff ◽  
Emma C. Johnson ◽  
Yi‐Ling Chou ◽  
Jonathan R.I. Coleman ◽  
Laura M. Thornton ◽  
...  

Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1735 ◽  
Author(s):  
Robino ◽  
Concas ◽  
Catamo ◽  
Gasparini

Genetic variation plays a crucial role in individual differences in food preferences which ultimately influence food selection and health. Our current understanding of this pathway has been informed through twin studies (to assess the heritability of food preferences), candidate gene studies, and genome-wide association studies (GWAS). However, most of this literature is mainly focused on genes previously identified as having taste or smell functions. New data suggests that genes not associated with taste or smell perception may be involved in food preferences and contribute to health outcomes. This review highlights these emerging findings and suggests a polygenic risk assessment approach to explore new relationships between food preferences and health risks.


2021 ◽  
Vol 22 (8) ◽  
pp. 4182
Author(s):  
Michal Vrablik ◽  
Dana Dlouha ◽  
Veronika Todorovova ◽  
Denes Stefler ◽  
Jaroslav A. Hubacek

Despite the rapid progress in diagnosis and treatment of cardiovascular disease (CVD), this disease remains a major cause of mortality and morbidity. Recent progress over the last two decades in the field of molecular genetics, especially with new tools such as genome-wide association studies, has helped to identify new genes and their variants, which can be used for calculations of risk, prediction of treatment efficacy, or detection of subjects prone to drug side effects. Although the use of genetic risk scores further improves CVD prediction, the significance is not unambiguous, and some subjects at risk remain undetected. Further research directions should focus on the “second level” of genetic information, namely, regulatory molecules (miRNAs) and epigenetic changes, predominantly DNA methylation and gene-environment interactions.


CNS Spectrums ◽  
2015 ◽  
Vol 20 (6) ◽  
pp. 522-529 ◽  
Author(s):  
Caroline Davis

This narrative review provides an overview of the epidemiology of binge eating disorder (BED), highlighting the medical history of this disorder and its entry as an independent condition in the Feeding and Eating Disorders section of the recently publishedDiagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Estimates of prevalence are provided, as well as recognition that the female to male ratio is lower in BED than in other eating disorders. Evidence is also provided of the most common comorbidities of BED, including mood and anxiety disorders and a range of addiction disorders. In addition, discussion of the viewpoint that BED itself may be an addiction — at least in severe cases — is presented. Although the genetic study of BED is still in its infancy, current research is reviewed with a focus on certain neurotransmitter genes that regulate brain reward mechanisms. To date, a focal point of this research has been on the dopamine and the μ-opioid receptor genes. Preliminary evidence suggests that a predisposing risk factor for BED may be a heightened sensitivity to reward, which could manifest as a strong dopamine signal in the brain’s striatal region. Caution is encouraged, however, in the interpretation of current findings, since samples are relatively small in much of the research. To date, no genome-wide association studies have focused exclusively on BED.


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