scholarly journals An Evolutionary Genetic Perspective of Eating Disorders

2017 ◽  
Vol 106 (3) ◽  
pp. 292-306 ◽  
Author(s):  
Alexandra J. Mayhew ◽  
Marie Pigeyre ◽  
Jennifer Couturier ◽  
David Meyre

Eating disorders (ED) including anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED) affect up to 5% of the population in Western countries. Risk factors for developing an ED include personality traits, family environment, gender, age, ethnicity, and culture. Despite being moderately to highly heritable with estimates ranging from 28 to 83%, no genetic risk factors have been conclusively identified. Our objective was to explore evolutionary theories of EDs to provide a new perspective on research into novel biological mechanisms and genetic causes of EDs. We developed a framework that explains the possible interactions between genetic risk and cultural influences in the development of ED. The framework includes three genetic predisposition categories (people with mainly AN restrictive gene variants, people with mainly BED variants, and people with gene variants predisposing to both diseases) and a binary variable of either the presence or absence of pressure to be thin. We propose novel theories to explain the overlapping characteristics of the subtypes of AN (binge/purge and restrictive), BN, and BED. For instance, mutations/structural gene variants in the same gene causing opposite effects or mutations in nearby genes resulting in partial disequilibrium for the genes causing AN (restrictive) and BED may explain the overlap of phenotypes seen in AN (binge/purge).

Author(s):  
Jessica H. Baker ◽  
Lauren Janson ◽  
Sara E. Trace ◽  
Cynthia M. Bulik

2004 ◽  
Vol 4 (4) ◽  
pp. 209-223 ◽  
Author(s):  
Anke Hinney ◽  
Susann Friedel ◽  
Helmut Remschmidt ◽  
Johannes Hebebrand

2014 ◽  
Vol 33 (1) ◽  
pp. 22-27 ◽  
Author(s):  
Valentina Đorđević

Summary Thrombophilia is a multifactorial disorder, involving both genetic and acquired risk factors that affect the balance between procoagulant and anticoagulant factors and lead to increased thrombotic tendency. The severe forms of thrombophilia are caused by a deficiency of natural anticoagulants: antithrombin, protein C and protein S. The advances in DNA technology played an important role in the identification of the exact nature of these deficiencies and opened up new possibilities in genetic research and molecular diagnostics of thrombophilia. The major breakthrough came with the discovery of activated protein C resistance and the Factor V Leiden gene mutation. Shortly afterwards, a variant in the 3’ untranslated region of the Factor II gene (FII G20210A) associated with an increased concentration of Factor II in plasma was described. These two gene variants represent the most common thrombophilic genetic risk factors. Recently, a novel prothrombin mutation (c.1787G>T) was identified in a Japanese family with juvenile thrombosis. This mutation leads to impaired inhibition of mutant thrombin by antithrombin, proposing a new mechanism of thrombophilia named resistance to antithrombin. In the last decade, several prothrombotic genetic risk factors have been described, including gene variants associated with defects of natural coagulation inhibitors, increased levels of coagulation factors or their impaired inhibition and defects of the fibrinolytic system. However, most of them are not of diagnostic value, due to their minor or unknown impact on the thrombotic risk. Large-scale DNA analysis systems are now becoming available, opening a new era in the genetic studies of the molecular basis of thrombophilia.


Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1655-P
Author(s):  
SOO HEON KWAK ◽  
JOSEP M. MERCADER ◽  
AARON LEONG ◽  
BIANCA PORNEALA ◽  
PEITAO WU ◽  
...  

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 107-OR
Author(s):  
SUNA ONENGUT-GUMUSCU ◽  
UMA DEVI PAILA ◽  
WEI-MIN CHEN ◽  
AAKROSH RATAN ◽  
ZHENNAN ZHU ◽  
...  

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