Beruflich Dokumente
Kultur Dokumente
a r t i c l e
i n f o
Article history:
Received 7 January 2009
Received in revised form 12 March 2009
Accepted 17 March 2009
Keywords:
Eating disorders
Latent classes
Serotonin
Genetics
5HTTLPR
a b s t r a c t
Context: Efforts to classify eating-disordered individuals based on concurrent personality traits have
consistently converged on a typology encompassing over-regulated, dysregulated, and low
psychopathology subgroups. In various populations, evidence has associated personality variations of
an over-regulated/dysregulated type with differences on serotonin-system indices, and specically,
with different loadings of serotonin transporter promoter regulatory region polymorphism (5HTTLPR)
genotypes and alleles. We explored the extent to which an empirical, trait-dened typology of eatingdisordered individuals coincided systematically with variations in 5HTTLPR, assayed using biallelic and
triallelic models.
Method: We tested 185 women with a DSM-IV eating disorder (108 with Bulimia Nervosa, 17 Anorexia
Nervosa, and 60 an Eating Disorder Not Otherwise Specied) and 93 with no eating disorder on measures
reecting psychopathological traits and 5HTTLPR (biallelic and triallelic) genotypes and alleles.
Results: The highest-function, triallelic (LA/LA) genotype occurred signicantly more frequently among
eating-disordered individuals than among controls. However, a more ne-grained analysis suggested that
this association was attributable to the fact that, among eating-disordered participants, those displaying
an Inhibited/Compulsive prole (derived using latent class analysis) were more likely than those of a
Dissocial/Impulsive or a Low Psychopathology group to carry the triallelic 5HTTLPR gain-of-function
LA allele and to be LA/LA homozygotes.
Discussion: This studys empirically derived classes coincide with interpretable differences on genetic
indicesassociating an Inhibited/Compulsive group with 5HTTLPR gain-of-function genotypes (and
alleles) that have elsewhere been linked to trait compulsivity. The ndings, furthermore, suggest that
5HTTLPR, by inuencing personality-trait manifestations may, in turn, inuence eating-disorder risk
and symptom expression.
2009 Elsevier Ltd. All rights reserved.
1. Introduction
Evidence implies that concurrent psychopathological traits
demarcate clinically relevant sub-phenotypes within the eatingdisordered population. For example, factor- or cluster-analytic
studies in the area yield consistent support for the occurrence of
compulsive (over-regulated), impulsive (dysregulated), and
psychologically intact eating-disorder (ED) subgroups (e.g., Westen and Harnden-Fischer, 2001; Steiger and Bruce, 2007; Wonderlich et al., 2005). Anorexic ED variants (especially those of the
restricter variety) tend to occur preferentially within the overregulated subgroup, whereas bulimic variants, although heterogeneously distributed, tend to occur preferentially in the dysregu* Corresponding author. Tel.: +1 514 761 6131x2895; fax: +1 514 888 4085.
E-mail address: stehow@douglas.mcgill.ca (H. Steiger).
0022-3956/$ - see front matter 2009 Elsevier Ltd. All rights reserved.
doi:10.1016/j.jpsychires.2009.03.009
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2. Methods
2.1. Participants
All participants in this institutional ethics-board approved
study differed from those assessed by Wonderlich et al. (2005).
All gave informed consent. Eating-disordered participants were recruited through a specialized Eating Disorders (ED) program in
Montreal, Quebec, Canada. Given that diagnostic heterogeneity
suited our interest in the spectrum of traits found in a broad, eating-disordered population, we included individuals with the DSMIV ED diagnoses Anorexia Nervosa (AN), Bulimia Nervosa (BN) and
Eating-Disorder Not Otherwise Specied (EDNOS). Our eating-disordered sample consisted of 185 women, 99 (53.5%) meeting DSMIV criteria for BN-Purging (BN-P) subtype, 9 (4.9%) for BN-Nonpurging (BN-NP) subtype, 9 (4.9%) for AN Restricting (AN-R) subtype, 8
(4.3%) for AN binge-eating/purging (AN-BP) subtype, 47 (25.4%) for
a bulimia-spectrum EDNOS (EDNOS-BN), and 13 (7.0%) for an anorexia-spectrum EDNOS (EDNOS-AN/R or EDNOS-AN/BP). EDNOS
disorders were dened as follows: subjects (n = 47) with BMI of
18 or more who binged or purged, but at less than the requisite
twice weekly (on average over the past 3 months), were regarded
as having a BN-spectrum EDNOS (EDNOS-BN); individuals (n = 7)
who had lower body weight, and engaged in regular bingeing
and/or purging, but either failed to meet AN criteria due to weight
above BMI of 17.5 or presence of menses were classied as having
an AN Binge/Purge spectrum EDNOS (EDNOS-AN/BP); individuals
(n = 6) who engaged in restriction and/or excessive exercise without binging or purging, but who failed to meet AN criteria due to
weight above BMI of 17.5 or presence of menses were classied
as having an AN Restricting spectrum EDNOS (EDNOS-AN/R).
When interested in comparing anorexic versus bulimic disorders,
we compared AN/R, AN/BP, EDNOS-AN/R and EDNOS-AN/BP
groups to BN and EDNOS/BN groups. When interested in comparing restricters to bingers/purgers, we compared AN/R and EDNOS-AN/R to BN, EDNOS/BN, AN/BP and EDNOS-AN/BP groups. A
major part of the sampling for this study was conducted through
a project concerned with bulimia-spectrum disorders (to which
consecutive, consenting patients with such eating syndromes were
recruited), with patients with Anorexia Nervosa added in an ad hoc
way. Therefore, proportions of cases with different diagnoses
achieve a desired degree of heterogeneity as to ED diagnoses, but
do not reect actual patterns of referral to our program.
We also recruited 93 normal-eater control women, drawn from
an age group comparable to that of our ED sample, and with
recruitment through public media and school-based announcements, so as to produce a group that included comparable propor-
1088
into four higher-order personality dimensions, based upon previously established factor analyses conducted on data from large
general, personality-disordered and twin samples (Livesley et al.,
1992; Bagge and Trull, 2003). The studies in question support the
validity of the higher-order dimensions Emotional Dysregulation
(onto which load DAPP-BQ subscales measuring Anxiousness,
Identity Problems, Social Avoidance, Affective Lability, Cognitive
Distortion, Oppositionality, Submissiveness, Insecure Attachment,
Suspiciousness and Narcissism), Dissocial Behavior (encompassing
Stimulus Seeking, Conduct Problems, Rejection, and Callousness),
Inhibition (including Intimacy Problems and Restricted Expression)
and Compulsivity (including the Compulsivity subscale alone). To
complement our assessment, we added the Barrat Impulsivity
Scale (BIS, version 11: Patton et al., 1995) and the Centre for Epidemiological Studies Depression (CES-D: Weissman et al., 1977), both
widely-known and validated for the measurement of the intended
constructs.
Screening for comorbid (past 12 months) DSM-IV Axis-I disorders in control subjects was accomplished using the Structured
Clinical Interview for DSM-IV Axis-I disorders (SCID-I: First et al.,
1996), a computer-guided, interview-based version of the Diagnostic Interview Schedule, Version IV (DIS4: Bucholz et al., 1991), and/
or the Clinician-Administered Post-Traumatic Stress Disorder Scale
(CAPS: Blake et al., 1995) all industry standard measures,
exhibiting excellent reliability, and convergent and discriminant
validity. (Variations in interviews applied reected shifts in study
protocols occurring during the patient recruitment reported here).
Elsewhere, we have evaluated agreement between DIS4 and SCID-I
diagnoses, and obtained excellent Kappas (and percent agreements) for past 12-month presence of Axis-I disorders (Steiger
et al., 2006).
2.3. Genotyping
DNA samples, obtained from whole blood, were amplied by
polymerase chain reaction (PCR) in a total volume of 20 ll, which
contained 100 ng of genomic DNA, 200 lM of dNTPs, 10 pmol each
of the forward and reverse primer, 1 U of Taq DNA Polymerase
(Qiagen, Alameda, CA), 1 PCR buffer, and 1 Q solution (Qiagen).
The forward primer (50 -ATG CCA GCA CCT AAC CCC TAA TGT-30 )
and reverse primer (50 -GG ACC GCA AGG TGG GCG GGA-30 ) were
used to amplify a region encompassing 5HTTLPR; long and short
alleles were then resolved on a 2% agarose gel. The PCR protocol involved preheating the samples at 94 C for 5 min, followed by 35
cycles of denaturation at 94 C (30 s), annealing at 64 C (30 s),
and extension at 72 C (45 s), as well as a nal hold of 5 min at
72 C. The LG and LA alleles were subsequently studied by enzymatic digestion of 7 ll of the above mentioned PCR product using
5 U of MspI and incubating at 37 C for a minimum of 3 h. The LG
and LA alleles were then resolved on a 2% agarose gel.
2.4. Statistical analysis
2.2. Measures
ED diagnoses and symptoms were assessed using the widely
used Eating Disorders Examination (EDE: Fairburn and Cooper,
1993) interview. We also computed Body Mass Index (BMI: Kg/m2).
To achieve a comprehensive, dimensional assessment of personality pathology, while limiting the number of variables implicated, we applied established, higher-order factors obtained from
the Dimensional Assessment of Personality Pathology-Basic Questionnaire (DAPP-BQ: Livesley et al., 1992). The DAPP-BQ is an
empirically derived, self-report measure that systematically describes personality traits using 290 items, organized into 18 trait
subscales. In the present study, DAPP subscales were aggregated
3. Results
3.1. Latent class analysis
Criteria indicated a 3 latent-class model to provide best t to
our data (BIC values: 1 class: 4406.33; 2 classes: 4320.04; 3 classes: 4308.96; 4 classes: 4328.17; 5 classes: 4352.35; 6 classes:
4391.41). Analysis of classication errors also supported a 3-class
model. To rule out potentially confounding effects of ED diagnosis
on model estimation, we re-ran the LCA twice, once with a covariate differentiating individuals with AN-spectrum disorders (AN-R,
AN-BP, EDNOS-AN/R or EDNOS-AN/BP) from those with BN-spectrum disorders (BN-P, BN-NP, or EDNOS-B), and a second time with
a covariate differentiating individuals who binged and/or purged
(i.e., with AN-BP, EDNOS-AN/BP, BN-P, BN-NP, or EDNOS-B diagnoses) from those who did not (i.e., AN-R or EDNOS-AN/R diagnoses).
Although the covariate always emerged as a signicant predictor of
classication, both analyses yielded best-tting 3-class solutions
that differed in no substantive way from the original (no-covariate)
analysis. (For brevitys sake, we report results from the original
analysis here.)
Table 1 shows means on the six scale scores entered into the
LCA. Three classes were indicated which, in decreasing order of
group size, encompassed individuals who showed elevated (a) Dissocial Behavior, Impulsivity, Emotional Dysregulation and Depression (n = 80, or 43.2% of the sample), (b) None of the pathological
indices (n = 73, or 39.5%), or (c) Inhibition, Compulsivity, Emotional
Dysregulation and Depression (n = 32, or 17.3%). As both psychopathological groups (a and c) showed heightened affectivity, a
pattern similar to that noted by Wonderlich et al. (2005), we assumed emotional reactivity to be a non-specic characteristic,
and opted to assign labels according to the more-unique characteristics. Correspondingly, we named the three LCA derived groups
Dissocial/Impulsive, Low Psychopathology, and Inhibited/
Compulsive, respectively.
Table 1 also provides mean values for members of the control
group on the six trait/symptom scores, along with results obtained
in univariate ANOVAs that tested for group differences on each variable. Results indicate mean scores of eating-disordered individuals
to have generally been higher (in a pathological direction) than
those of normal-eater controls (signicantly so on Emotional Dysregulation, Inhibition, and Depression.) Dissocial-Impulsive group
members had higher scores than did all other groups on Emotional
Dysregulation, Dissocial Behavior, and Impulsivity, reecting these
individuals uniquely dysregulatory propensities. In contrast,
indicating a unique connection with over-regulation, Inhibited/Compulsive group members scores exceeded those of all
other groups on Inhibition and Compulsivity.
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1090
Table 1
Mean scores (and standard deviations) for each latent-class derived cluster of eating-disordered patients and for normal-eater controls on Emotional Dysregulation, Dissocial
Behavior, Inhibition, Compulsivity, Impulsivity and Depression scales. Contribution of scale scores to cluster classications is reected by Wald test values (betas are equal among
classes). One-way ANOVAs reect differences between actual group means (including controls). Values with different letters in their superscripts differ at the p < .05 level or
better on Tukeys HSD tests. Variations in ns and dfs reect isolated missing values.
Dissocial/Impulsive
M (SD)
n = 80
Low psycho-pathology
M (SD)
n = 73
Inhibited/Compulsive
M (SD)
n = 32
Normal-eater
M (SD)
n = 93
F value,
p value
df = 3, 274
199.20
p < .001
40.17 p < .001
56.94 p < .001
27.78 p < .001
112.08
p < .001
df = 3, 272
72.10 p < .001
Emotional
Dysregulation
Dissocial Behavior
Inhibition
Compulsivity
CES-D depression
3.57a (0.39)
2.56c (0.44)
3.34b (0.34)
2.07d (0.48)
2.66a (0.52)
2.93b (0.71)
3.41b (0.81)
34.84a (9.96)
2.07b (0.38)
2.34c (0.57)
3.18b,c (0.53)
21.56b (9.95)
1.95b (0.42)
3.43a (0.59)
4.23a (0.50)
34.47a (13.45)
60.69
64.68
66.34
57.04
2.07b (0.36)
2.03d (0.58)
2.97c (0.75)
9.79c (7.63)
Barrat impulsivity
n = 80
78.47a (8.19)
n = 73
67.42b (8.35)
n = 32
58.35c (4.12)
p < .001
p < .001
p < .001
p < .001
n = 91
61.89c (9.55)
Wald test values pertain only to eating-disordered participants, who were included in the latent class analysis.
Table 2
Frequencies of diagnoses (AN-spectrum and Restricter), diagnostic history (history of AN) and medication use, as well as means for Age, BMI and Binge Days per Month, and for
Monthly Binge, Vomit and Purge Frequencies (including episodes of vomiting, and laxative or diuretic misuse) by LCA-based groups. Chi-Square and F values reecting intergroup difference are also reported. Values with different letters in their superscripts differ at the p < .05 level or better on Turkeys HSD tests.
AN-spectrum
Restricter
History of AN
Psychiatric medication
Age
BMI
Binge days/month
Binge episodes/month
Vomit episodes/month
Purge episodes/month
Dissocial/Impulsive (n = 80)
Inhibited/Compulsive (n = 32)
Frequency (%)
Frequency (%)
Frequency (%)
Chi-Squared df = 2
8 (10.0)
2 (2.5)
35 (44.3)
39 (48.8)
Mean (SD)
24.70 (5.36)
21.30 (3.03)
13.69a (9.74)
23.52a (23.48)
34.21 (43.50)
42.03 (46.38)
10 (13.7)
6 (8.2)
25 (35.7)
22 (30.1)
Mean (SD)
26.77 (7.48)
22.06 (4.35)
11.50a,b (9.40)
18.82a,b (23.58)
27.51 (42.87)
31.29 (43.09)
12 (37.5)
7 (21.9)
19 (59.4)
16 (50.0)
Mean (SD)
27.06 (9.21)
20.11 (4.43)
7.41b (9.57)
11.31b (17.41)
18.72 (28.46)
23.48 (28.42)
13.29 p = .001
11.52 p = .003
5.02 p = .081
6.56 p = .038
F value df = 2, 182
2.17 p = .117
2.91 p = .057
4.96 p = .008
3.39 p = .036
1.69 p = .187
2.54 p = .082
Statistical test
Normal-eater control
group (n = 93)
Chi-Square
(p value)
Frequency (%)
17 (18.3)
54 (58.1)
22 (23.7)
4.01
(p = .135)
df = 2
(b) Allele
S
L
168 (45.4)
202 (54.6)
88 (47.3)
98 (52.7)
Eating disorder
(n = 185)
Control (n = 92)
0.18
(p = .670)
df = 1
17 (18.5)
43 (46.7)
10 (10.9)
0 (0.0)
10 (10.9)
12 (13.0)
9.26
(p = .099)
df = 5
(d) Allele
S
LG
LA
168 (45.4)
28 (7.6)
174 (47.0)
87 (47.3)
20 (10.9)
77 (41.8)
2.37
(p = .306)
df = 2
58 (31.4)
80 (43.2)
47 (25.4)
27 (29.3)
53 (57.6)
12 (13.0)
7.13
(p = .028)
df = 2
(f) Allele
S, LG
LA
196 (53.0)
174 (47.0)
107 (58.2)
77 (41.8)
1.33
(p = .249)
df = 1
[v2 = 8.07; df = 1; p = .005; p = .005 on a Fishers exact test; odds ratio of 2.17 (95% CI: 1.213.88) and 2.34 (95% CI: 1.294.24), respectively] (see Table 4f for values in question).
4. Discussion
Based on comorbid psychopathological traits, this study classied treatment-seeking eating-disordered patients, and then examined the association of resulting empirical classications with
variations in the serotonin transporter promoter polymorphism
(5HTTLPR). Our results indicated a trio of latent classes, accommodating progressively smaller proportions of our eating-disordered
sample, to which we could t the descriptors Dissocial/ Impulsive, Low Psychopathology and Inhibited/ Compulsive. The
classes derived closely resemble those obtained in comparable
classication effortsone study in an eating-disordered sample
characterizing groups obtained as emotionally dysregulated/
undercontrolled, high-functioning/perfectionistic and constricted/ overcontrolled (Westen and Harnden-Fischer, 2001)
and another, groups described as impulsive, low comorbidity,
and affective/ perfectionistic (Wonderlich et al., 2005). Evident
correspondences across these studies suggest that the tendency
for eating-disordered individuals to cluster into impulsive, relatively intact, and compulsive sub-groups is quite a replicable one.
Making such correspondences all-the-more striking, the studies
in question apply disparate psychopathological indices and statistical techniques.
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The main goal of the present study was to explore the association of 5HTTLPR variations with presence of an eating disorder, and
with trait proles that characterize eating-disorder sufferers.
Although we found the highest-function 5HTTLPR genotype
(LA/LA) to be more common in eating-disorder sufferers than in
controls, ner-grained analyses examining associations of genetic
variations with variations in psychopathological traits suggested
that the association observed was not so much characteristic of
our eating-disordered sample (in a wholesale fashion), or of particular diagnostic subgroups (e.g., those with Anorexia-spectrum syndromes), as it was of those members of the sample who were
markedly Inhibited/Compulsive. In other words, our results associate genetic variations more specically with trait variations (such
as the Inhibited/Compulsive versus Dissocial/Impulsive distinction
we derived) than with presence or absence of an ED syndrome per
se. In this respect, our results corroborate other ndings (obtained
in eating- and non-eating-disordered populations) suggesting that
heightened inhibition/compulsivity coincides with the gain-offunction (LA) allele (triallelic model) of 5HTTLPR (Hu et al., 2006),
and heightened impulsivity and affective instability with the
low-function 5HTTLPR alleles (Anguelova et al., 2003; Lesch
et al., 1996; Sander et al., 1998; Steiger et al., 2005b, 2007). Our
study may, furthermore, take a step beyond the simple corroboration of the association noted, in suggesting a correspondence between the polymorphism of interest and phenotypic variations
(or latent classes) that are validated empiricallyour hope being
that this effort may improve the stability (and hence replicability)
of the ndings. Members of an empirically derived Inhibited/
Compulsive subgroup (when compared to those of Dissocial/
Impulsive or Low Psychopathology ED subgroups, or members of
a normal-eater control group) were signicantly more likely to carry at least one copy of the triallelic 5HTTLPR gain-of-function LA allele, and to be high-function homozygotes (i.e., LA/LA genotype
carriers) which for 5HTTLPR represents the highest-expressing
genotype.
In a similar vein, Inhibited/Compulsive group members were
more likely than other LCA-based groups to exhibit Anorexia
Nervosa (versus a bulimic ED variant). Important clues as to
the interpretation of this nding would seem to lie in the observation that the LA allele is, elsewhere, associated with heightened
risk of obsessivecompulsive disorder (Hu et al., 2006), and that
obsessivecompulsive characteristics predominate in anorexic
(and particularly restrictive-anorexic) ED variants (Westen and
Harnden-Fischer, 2001; Steiger and Bruce, 2007). Together, these
observations suggest that the 5HTTLPR LA allele, while not a specic factor in eating-disorder risk, may exercise a pathoplastic
effectheightening the likelihood of expression of obsessive
compulsiveness and pronounced dietary restraint in eatingdisordered individuals. In other words, we may be observing a
shaping impact of a genetic factor (in this case, of the 5HTTLPR
high-function alleles) upon expression of traits (in the Inhibited/Compulsive versus Dissocial/Impulsive spectrum) which, in
eating-disorder sufferers shapes eating-symptom expression
(i.e., anorexic versus bulimic forms). In addition, our results support the notion that Anorexia Nervosa may not only resemble
obsessivecompulsive disorder in a phenomenological sense
(bodily obsessions motivating dieting compulsions), but that
these disorders may also have at least one common, moleculargenetic determinant (i.e., the 5HTTLPR LA allele).
On the opposite side of the same coin, we note that members
of our Dissocial/Impulsive subgroup were signicantly more likely
than members of the Inhibited/Compulsive group to carry lowfunction genotypes and alleles. The preceding corroborates parallel
ndings obtained in eating-disordered (Steiger et al., 2005b,
2007) and non-eating-disordered populations (Lesch et al., 1996;
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Table 4
Frequencies (and percentages) of 5HTTLPR genotypes and alleles (biallelic and triallelic) across LCA-dened eating-disordered groups and normal-eater controls.
Dissocial/Impulsive
eating disorder (n = 80)
Frequency (%)
Low comorbidity
eating disorder (n = 73)
Frequency (%)
Inhibited/Compulsive
eating disorder (n = 32)
Frequency (%)
Normal-eater control
group (n = 93)
Frequency (%)
21 (26.3)
37 (46.3)
22 (27.5)
18 (24.7)
31 (42.5)
24 (32.9)
3 (9.4)
16 (50.0)
13 (40.6)
17 (18.3)
54 (58.1)
22 (23.7)
8.96 p = .176 df = 6
(b) Allele
S
L
79 (49.4)
81 (50.6)
67 (45.9)
79 (54.1)
22 (34.4)
42 (65.6)
88 (47.3)
98 (52.7)
Chi-Square (p value)
Dissocial/Impulsive (n = 80)
Inhibited/Compulsive (n = 32)
Controls (n = 92)
21 (26.3)
27 (33.8)
10 (12.5)
1 (1.3)
5 (6.3)
16 (20.0)
18 (24.7)
28 (38.4)
3 (4.1)
0 (0.0)
5 (6.8)
19 (26.0)
3 (9.4)
14 (43.8)
2 (6.3)
0 (0.0)
1 (3.1)
12 (37.5)
17 (18.5)
43 (46.7)
10 (10.9)
0 (0.0)
10 (10.9)
12 (13.0)
21.95 p = .109 df = 15
(d) Allele
S
LG
LA
79 (49.4)
17 (10.6)
64 (40.0)
67 (45.9)
8 (5.5)
71 (48.6)
22 (34.4)
3 (4.7)
39 (60.9)
87 (47.3)
20 (10.9)
77 (41.8)
12.25 p = .057 df = 6
32 (40.0)
32 (40.0)
16 (20.0)
21 (28.8)
33 (45.2)
19 (26.0)
5 (15.6)
15 (46.9)
12 (37.5)
27 (29.3)
53 (57.6)
12 (13.0)
15.45 p = .017 df = 6
(f) Allele
SLG
LA
96 (60.0)
64 (40.0)
75 (51.4)
71 (48.6)
25 (39.1)
39 (60.9)
107 (58.2)
77 (41.8)
9.67 p = .022 df = 3
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