Genetic risk factors for disordered eating in adolescent males and females.

Baker, Jessica H.; Maes, Hermine H.; Lissner, Lauren; Aggen, Steven H.; Lichtenstein, Paul; Kendler, Kenneth S.

doi:10.1037/a0016314

Cited by 48 publications

(53 citation statements)

References 78 publications

(125 reference statements)

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“…Furthermore, this difference in disordered eating scores emerged during mid-late puberty (147), suggesting that the developmental effect forms a substrate for a later activational effect of gonadal steroids (as described below). These associations, however, were detected in only one (577) of several (31,95,449,571,581) subsequent studies involving patients with eating disorders. Thus, Klump's organizational hypothesis requires further research.…”

Section: Physiological Sex Differences In Disordered Human Eatingmentioning

confidence: 96%

Sex differences in the physiology of eating

Asarian

Geary²

2013

American Journal of Physiology-Regulatory, Integrative and Comp

414

349

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(HPG) axis function fundamentally affects the physiology of eating. We review sex differences in the physiological and pathophysiological controls of amounts eaten in rats, mice, monkeys, and humans. These controls result from interactions among genetic effects, organizational effects of reproductive hormones (i.e., permanent early developmental effects), and activational effects of these hormones (i.e., effects dependent on hormone levels). Male-female sex differences in the physiology of eating involve both organizational and activational effects of androgens and estrogens. An activational effect of estrogens decreases eating 1) during the periovulatory period of the ovarian cycle in rats, mice, monkeys, and women and 2) tonically between puberty and reproductive senescence or ovariectomy in rats and monkeys, sometimes in mice, and possibly in women. Estrogens acting on estrogen receptor-␣ (ER␣) in the caudal medial nucleus of the solitary tract appear to mediate these effects in rats. Androgens, prolactin, and other reproductive hormones also affect eating in rats. Sex differences in eating are mediated by alterations in orosensory capacity and hedonics, gastric mechanoreception, ghrelin, CCK, glucagon-like peptide-1 (GLP-1), glucagon, insulin, amylin, apolipoprotein A-IV, fatty-acid oxidation, and leptin. The control of eating by central neurochemical signaling via serotonin, MSH, neuropeptide Y, Agouti-related peptide (AgRP), melanin-concentrating hormone, and dopamine is modulated by HPG function. Finally, sex differences in the physiology of eating may contribute to human obesity, anorexia nervosa, and binge eating. The variety and physiological importance of what has been learned so far warrant intensifying basic, translational, and clinical research on sex differences in eating.neuroendocrinology; estrogens; testosterone; eating disorders; obesity SEX DIFFERENCES ARE PERVASIVE in physiology and medicine (51,64,73,109,110,466,797,826). The controls of eating and energy homeostasis are no exceptions. It was observed approximately 100 years ago that removal of the ovaries leads to marked accretion of adipose tissue in rats (697), that daily food intake expressed as kilocalories per gram body weight differs between male and female rats (778), and that food intake varies regularly through the ovarian cycle in intact female rats (674, 779). Sex differences in eating have been the subject of physiological research ever since. The clinical relevance of this work is increasingly evident. In the United States, women are approximately threefold more vulnerable than men to psychiatric eating disorders (346,351) and approximately twofold more vulnerable to severe and morbid obesity (BMI Ն 35 and 40 kg/m 2 , respectively, mass/height 2 ) (226). Women also appear to suffer more from these disorders in terms of physical and psychological functioning and quality of life (24,84,273,292,465,531,762). The increased obesity burden suffered by women is reflected in the fact that Ͼ80% of bariatric surgery patients in the U...

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Section: Physiological Sex Differences In Disordered Human Eatingmentioning

confidence: 96%

Sex differences in the physiology of eating

Asarian

Geary²

2013

American Journal of Physiology-Regulatory, Integrative and Comp

414

349

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“…The female to male ratio for EDs is between 4: 1 and 10: 1 [7], and there is a significant increase in EDs in females during puberty. When investigating heritability in males and females separately, heritability appears higher in females (51-61%) than in males (0-40%) for intentional weight loss, body dissatisfaction, drive for thinness [108][109][110], and weight concerns [111]. A moderate overlap is also suggested in the genetic factors influencing ED symptoms including body dissatisfaction, drive for thinness [112], and behaviors such as binge eating [42,113] between genders.…”

Section: Gender Influences On Genetic and Environmental Risk Factors mentioning

confidence: 97%

An Evolutionary Genetic Perspective of Eating Disorders

Mayhew

Pigeyre

Couturier³

et al. 2017

Neuroendocrinology

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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).

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“…The cause of AN is unclear, but is likely multifactorial, including psychological, familial, environmental, societal, genetic, and other biological factors (4). Prevalence of AN is 1-4% and there was a higher concordance rate in monozygotic twins (56%) than in dizygotic twins (7%) (5).…”

Section: Introductionmentioning

confidence: 99%