Professor Philip Gorwood, MD, PhD

About the author

When do we acquire the vulnerability to anorexia nervosa: from genes & pregnancy to early childhood and adulthood?

Anorexia nervosa is a complex entity (Gorwood et al., 2016) with severe outcome, as 1% of patients die every year, half of them by suicide, half of them for medical reasons. Furthermore, no psychotropic drug is available to treat such severe condition, with a specific indication.

It is therefore particularly important to scrutinize the definition criteria and the potential mechanisms of action, in order to invent new techniques and potentially new treatments.

One well known vulnerability factor is the familial aggregation of the disorder, as having one first‐degree relative affected with anorexia nervosa, multiply the risk of the same disorder by 11 for the rest of the siblings. In this view, a child who has a mother with anorexia nervosa also has a significantly increased risk for this disorder. The mechanism by which such mother/child transmission occurs is therefore interesting, as genetic as well as cultural factors have been proposed.

Significant progress has been made in the detection of the involved genes (Huckins et al., 2018) and how a stable vulnerability can be acquired by the environment (through epigenetic modifications). Even more interesting is the interaction between these two sets of vulnerability factors, explaining how the acquired epigenetic vulnerability can be genetically driven.

We will give some examples of how reconceptualizing (Clarke et al., 2017) anorexia nervosa (for example as a reward disorder) could help to better understand both the disorder and its mechanisms of action.

Clarke J, Ramoz N, Fladung AK, Gorwood P (2016) Higher reward value of starvation imagery in anorexia nervosa and association with the Val66Met BDNF polymorphism. Transl Psychiatry 7;6(6):e829.

Gorwood P et al (2016) New Insights in Anorexia Nervosa. Front Neurosci (2016) Jun 29;10:256.

Huckins et al. (2018) Investigation of common, low‐frequency and rare genome‐wide variation in anorexia nervosa. Mol Psychiatry. May; 23(5):1169–1180.

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