Psychopharmacology
DOI 10.1007/s00213-007-1048-9
LETTER TO THE EDITORS
Serotonin transporter binding after recovery from eating
disorders
Walter Kaye & Ursula Bailer & Guido Frank &
Shannan Henry & Julie Price & Carolyn Meltzer &
Carl Becker & Scott Ziolko & Chester Mathis &
Angela Wagner & Nicole Barbarich-Marsteller &
Karen Putnam
Received: 29 November 2007 / Accepted: 4 December 2007
# Springer-Verlag 2007
Dear Dr. Cowen:
When malnourished and emaciated, individuals with anorexia nervosa (AN) have alterations of the brain (Bailer
et al. 2007) and peripheral organ function that are arguably
more severe than in any other psychiatric disorder. It has
long been debated whether symptoms in individuals with
AN are the cause or consequence of malnutrition and
weight loss. We cannot fully exclude the possibility that
chronic disturbances of nutrition, such as chronic malnutrition and emaciation, during the ill state of an eating
disorder may contribute to a persistent “scar” in recovered
individuals, and by this, lead to persistent alterations in
monoamine activity after recovery.
W. Kaye (*)
Department of Psychiatry,
University of Pittsburgh Medical School,
Pittsburgh, USA
e-mail: kayewh@upmc.edu
W. Kaye
University of California,
San Diego, USA
U. Bailer
Department of Psychiatry and Psychotherapy,
Division of Biological Psychiatry, Medical University of Vienna,
Waehringer Guertel 18-20,
A-1090 Vienna, Austria
G. Frank
Child and Adolescent Psychiatry,
University of Colorado at Denver and Health Sciences Center,
Denver, USA
S. Henry : A. Wagner
Department of Psychiatry, University of Pittsburgh,
Pittsburgh, USA
However, in the past decade, considerable evidence has
shown that individuals with AN display, in childhood,
certain temperament and personality traits, such as negative
emotionality, harm avoidance, perfectionism, inhibition,
drive for thinness, altered interoceptive awareness, and
obsessive–compulsive personalities (Anderluh et al. 2003;
Fairburn et al. 1999; Lilenfeld et al. 2006). In brief,
malnutrition tends to exaggerate these premorbid behavioral traits (Pollice et al. 1997) and adds considerably other
symptoms that maintain or accelerate the disease process,
including exaggerated emotional dysregulation and obsessionality (Godart et al. 2007; Kaye et al. 2004). Importantly,
these traits persist after recovery from an AN (Casper 1990;
J. Price : C. Meltzer : C. Becker : S. Ziolko : C. Mathis
Department of Radiology, University of Pittsburgh,
Pittsburgh, USA
C. Meltzer
Radiology and Neurology, Emory School of Medicine,
Atlanta, USA
N. Barbarich-Marsteller
Psychiatry, New York State Psychiatric Institute,
New York, USA
K. Putnam
Environmental Health,
Division of Epidemiology and Biostatistics,
University of Cincinnati,
Cincinnati, USA
Psychopharmacology
Srinivasagam et al. 1995; Strober 1980; Wagner et al.
2006). It is well known that 5-HT function contributes to
altered affect, behavioral inhibition and obsessionality.
Thus, altered 5-HT function could play a role in the
development of these behavioral traits in childhood and
persistence of these symptoms after recovery. In support of
this argument, considerable studies (Bulik et al. 2007;
Holliday et al. 2005; Steiger et al. 2006) suggest these traits
as well as serotonergic disturbances are heritable, often
occur in unaffected family members and are independent of
body weight. In summary, the weight of evidence is that
these traits confer liability to the development of AN and
are not an “epiphenomenon to the symptoms and unrelated
to the eating disorder.”
Unfortunately, for many individuals, AN is a chronic
illness, because these behavioral symptoms persist even if
weight is gained or normalized. To confirm that someone is
truly recovered, or a treatment is truly effective, requires
long-term outcome studies following individuals over
months or years of time after discharge from treatment.
Finally, there were no negative values for estradiol. The
reason for the large standard deviation is that some values
for estradiol were high.
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