Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016 Jun 29:10:256.
doi: 10.3389/fnins.2016.00256. eCollection 2016.

New Insights in Anorexia Nervosa

Philip Gorwood  1 , Corinne Blanchet-Collet  2 , Nicolas Chartrel  3 , Jeanne Duclos  4 , Pierre Dechelotte  5 , Mouna Hanachi  6 , Serguei Fetissov  7 , Nathalie Godart  8 , Jean-Claude Melchior  6 , Nicolas Ramoz  9 , Carole Rovere-Jovene  10 , Virginie Tolle  9 , Odile Viltart  11 , Jacques Epelbaum  9
Affiliations
Review

New Insights in Anorexia Nervosa

Philip Gorwood et al. Front Neurosci. .

Abstract

Anorexia nervosa (AN) is classically defined as a condition in which an abnormally low body weight is associated with an intense fear of gaining weight and distorted cognitions regarding weight, shape, and drive for thinness. This article reviews recent evidences from physiology, genetics, epigenetics, and brain imaging which allow to consider AN as an abnormality of reward pathways or an attempt to preserve mental homeostasis. Special emphasis is put on ghrelino-resistance and the importance of orexigenic peptides of the lateral hypothalamus, the gut microbiota and a dysimmune disorder of neuropeptide signaling. Physiological processes, secondary to underlying, and premorbid vulnerability factors-the "pondero-nutritional-feeding basements"- are also discussed.

Keywords: autoantibodies; eating disorders; mental homeostasis; microbiota; reward system adaptations; susceptibility factors.

PubMed Disclaimer

Figures

Figure 1
Figure 1
How genetic and epigenetic factors could influence the risk and/or the maintenance of anorexic behaviors (driving for further thinness while underweight).
Figure 2
Figure 2
Main physiological effects of the orexigenic hormone ghrelin. In anorexia nervosa, some of the symptoms classically described might be due to a resistance or insensitivity to ghrelin effect (in red squares). AG, acyl ghreline; BBB, blood brain barrier; DA, dopamine; OAG, deacyl ghrelin; GH, growth hormone; GHS-R, ghrelin receptor; GOAT, ghrelin O -acyltransferase; IGF-1, insulin growth factor 1; VTA, ventral tegmental area.
Figure 3
Figure 3
Schematic representation of the hypothetical chronic stimulation of orexigenic neuropeptides on the reward circuitry in anorexia nervosa. Briefly, decrease of food ingestion induces a stimulation of the neuronal activity of the lateral hypothalamic area (LHA) that will release the orexigenic neuropeptides orexins (ORX), melanin-concentrating hormone (MCH), and 26RFain the ventral tegmental area (VTA). This results in an increase of dopamine (DA) release in the accumbens nucleus (NAc). In anorectic patients, this stimulation of the reward system results in food aversion associated with enhanced anxiety that will, in turn, reinforce the decrease in food intake.
Figure 4
Figure 4
Gut microbiota as an important contributing factor in Anorexia Nervosa.
Figure 5
Figure 5
Implication of microbial protein and specific Immunoglobulins in the dysfunction of neuropeptide signaling during anorexia nervosa.
Figure 6
Figure 6
Pubertal process and pondero-nutritional-eating basements: the mismatching team.
Figure 7
Figure 7
A model of anorexia nervosa as an attempt to preserve mental homeostasis.
Figure 8
Figure 8
A global model of anorexia nervosa.
See this image and copyright information in PMC

Comment in

  • Commentary: New Insights in Anorexia Nervosa.
    Södersten P, Bergh C, Leon M. Södersten P, et al. Front Neurosci. 2016 Oct 25;10:483. doi: 10.3389/fnins.2016.00483. eCollection 2016. Front Neurosci. 2016. PMID: 27826227 Free PMC article. No abstract available.

References

    1. Abizaid A., Liu Z. W., Andrews Z. B., Shanabrough M., Borok E., Elsworth J. D., et al. (2006). Ghrelin modulates the activity and synaptic input organization of midbrain dopamine neurons while promoting appetite. J. Clin. Invest. 116, 3229–3239. 10.1172/JCI29867 - DOI - PMC - PubMed
    1. Agnati L. F., Barlow P. W., Baluška F., Tonin P., Guescini M., Leo G., et al. (2011). A new theoretical approach to the functional meaning of sleep and dreaming in humans based on the maintenance of ‘predictive psychic homeostasis. Commun. Integr. Biol. 4, 640–654. 10.4161/cib.17602 - DOI - PMC - PubMed
    1. American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders, 5th Edn., (DSM-5). Washington, DC: American Psychiatric Publishing.
    1. Armougom F., Henry M., Vialettes B., Raccah D., Raoult D. (2009). Monitoring bacterial community of human gut microbiota reveals an increase in Lactobacillus in obese patients and Methanogens in anorexic patients. PLoS ONE 4:e7125. 10.1371/journal.pone.0007125 - DOI - PMC - PubMed
    1. Asakawa A., Inui A., Fujimiya M., Sakamaki R., Shinfuku N., Ueta Y., et al. (2005). Stomach regulates energy balance via acylated ghrelin and desacyl ghrelin. Gut 54, 18–24. 10.1136/gut.2004.038737 - DOI - PMC - PubMed

LinkOut - more resources