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Eating disorders (EDs) are damaging mental and metabolic illnesses that predominantly affect women. While the early origins of these disorders remain largely unknown, recent evidence suggests that epigenetic mechanisms may be involved in initiating and maintaining EDs. While epigenetic mechanisms are known to modulate behavior and health at various stages during the life cycle, it is in the womb where these processes begin to shape the exposed offspring, with a potentially adverse impact on later physical health, emotional adjustment, and stress reactivity. This maladaptation is particularly frequent in response to intrauterine stress, with the general consensus that early life stress can dramatically increase the probability of developing an ED later in life.

Schroeder et al. explored the effects of chronic variable stress during the whole period of gestation on basal metabolism, response to food restriction, and susceptibility to develop activity based-anorexia, binge eating, and metabolic syndrome in male and female offspring. They report that chronic prenatal stress induces sexually dimorphic effects on placental function, affecting fetal hypothalamic programming and subsequent basal metabolism as well as the response to a variety of different metabolic challenges.

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The 60 Second Metabolist
In this section authors briefly report on their work recently published in Molecular Metabolism.

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Florian Merkle
University of Cambridge, UK
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