TY - JOUR
T1 - Neurobiology of anorexia nervosa
T2 - Serotonin dysfunctions link self-starvation with body image disturbances through an impaired body memory
AU - Riva, Giuseppe
AU - Mehta, Mitul
AU - Pazzaglia, Mariella
AU - Walsh, Eamonn
PY - 2016/11/24
Y1 - 2016/11/24
N2 - The etiology of anorexia nervosa (AN) is still unclear, despite that it is a critical and potentially mortal illness. A recent neurobiological model considers AN as the outcome of dysfunctions in the neuronal processes related to appetite and emotionality (Kaye et al., 2009, 2013). However, this model still is not able to answer a critical question: What is behind body image disturbances (BIDs) in AN? The article starts its analysis from reviewing some of the studies exploring the effects of the serotonin systems in memory (episodic, working, and spatial) and its dysfunctions. The review suggests that serotonin disturbances may: (a) facilitate the encoding of third person (allocentric) episodic memories; (b) facilitate the consolidation of emotional episodic memories (e.g., teasing), if preceded by repeated stress; (c) reduce voluntary inhibition of mnestic contents; (d) impair allocentric spatial memory. If we discuss these results within the interpretative frame suggested by the "Allocentric Lock Hypothesis" (Riva, 2012, 2014), we can hypothesize that altered serotoninergic activity in AN patients: (i) improves their ability to store and consolidate negative autobiographical memories, including those of their body, in allocentric perspective; (ii) impairs their ability to trigger voluntary inhibition of the previously stored negative memory of the body; (iii) impairs their capacity to retrieve/update allocentric information. Taken together, these points suggest a possible link between serotonin dysfunctions, memory impairments and BIDs: the impossibility of updating a disturbed body memory using real time experiential data-I’m locked to a wrong body stored in long term memory-pushes AN patients to control body weight and shape even when underweight.
AB - The etiology of anorexia nervosa (AN) is still unclear, despite that it is a critical and potentially mortal illness. A recent neurobiological model considers AN as the outcome of dysfunctions in the neuronal processes related to appetite and emotionality (Kaye et al., 2009, 2013). However, this model still is not able to answer a critical question: What is behind body image disturbances (BIDs) in AN? The article starts its analysis from reviewing some of the studies exploring the effects of the serotonin systems in memory (episodic, working, and spatial) and its dysfunctions. The review suggests that serotonin disturbances may: (a) facilitate the encoding of third person (allocentric) episodic memories; (b) facilitate the consolidation of emotional episodic memories (e.g., teasing), if preceded by repeated stress; (c) reduce voluntary inhibition of mnestic contents; (d) impair allocentric spatial memory. If we discuss these results within the interpretative frame suggested by the "Allocentric Lock Hypothesis" (Riva, 2012, 2014), we can hypothesize that altered serotoninergic activity in AN patients: (i) improves their ability to store and consolidate negative autobiographical memories, including those of their body, in allocentric perspective; (ii) impairs their ability to trigger voluntary inhibition of the previously stored negative memory of the body; (iii) impairs their capacity to retrieve/update allocentric information. Taken together, these points suggest a possible link between serotonin dysfunctions, memory impairments and BIDs: the impossibility of updating a disturbed body memory using real time experiential data-I’m locked to a wrong body stored in long term memory-pushes AN patients to control body weight and shape even when underweight.
KW - 5-HTTLPR
KW - Allocentric lock
KW - Anorexia nervosa (AN)
KW - Body image disturbances
KW - Memory consolidation
KW - Memory reconsolidation
KW - Serotonin
KW - Serotonin transporter gene
UR - http://www.scopus.com/inward/record.url?scp=84998816180&partnerID=8YFLogxK
U2 - 10.3389/fnhum.2016.00600
DO - 10.3389/fnhum.2016.00600
M3 - Article
AN - SCOPUS:84998816180
SN - 1662-5161
VL - 10
JO - Frontiers In Human Neuroscience
JF - Frontiers In Human Neuroscience
IS - NOV2016
M1 - 600
ER -