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. 2019 Feb 12;9:2045125318814734. doi: 10.1177/2045125318814734

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© The Author(s), 2019

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 1. — Schematic and simplified depiction of a pathophysiological model of eating disorders based on genetic findings.

SCFAs, short chain fatty acids; LPS, lipopolysaccharides; GABA, gamma-aminobutyric acid; B ClpB, caseinolytic protease; EBF1, early B-cell factor 1; EPHX2, epoxide hydrolase 2; MHC, major histocompatibility complex; 5-HT, serotonin; DA, dopamine; CB, cannabinoid; Op, opioids; α-MSH, melanocyte-stimulating hormone.

For further details see section ‘A pathophysiological model of eating disorders based on genetic findings’.