Personality, Perfectionism, and Attitudes
Toward Eating in Parents of Individuals with
Eating Disorders
D. Blake Woodside,1* Cynthia M. Bulik,2 Katherine A. Halmi,3 Manfred M. Fichter,4
Allan Kaplan,1 Wade H. Berrettini,5 Michael Strober,6 Janet Treasure,7
Lisa Lilenfeld,8 Kelly Klump,9 and Walter H. Kaye9
1
Department of Psychiatry, Toronto General Hospital, Toronto, Canada
Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry,
Virginia Commonwealth University, Richmond, Virginia
3
New York Presbyterian Hospital-Westchester, Weill Medical College of Cornell
University, White Plains, New York
4
Klinik Roseneck, Hospital for Behavioral Medicine, Munich, Germany
5
Center for Neurobiology and Behavior, Department of Psychiatry, University of
Pennsylvania School of Medicine, Philadelphia, Pennsylvania
Neuropsychiatric Institute and Hospital, School of Medicine, University of California at
Los Angeles, Los Angeles, California
7
Institute of Psychiatry, Maudsley and Bethlem Royal Hospital, London, England
8
Department of Psychology, Georgia State University, Atlanta, Georgia
9
Eating Disorders Module, Western Psychiatric Institute and Clinic, University of
Pittsburgh School of Medicine, Pittsburgh, Pennsylvania
2
6
Accepted 27 November 2001
Abstract: Objective: This study compares personality and eating-related traits in parents of
probands with eating disorders, with age-band matched healthy normal controls. Method:
Data were abstracted from an international genetic study of anorexia nervosa. Information
was available for the Multidimensional Perfectionism Scale (MPS), the Eating Disorders
Inventory (EDI), and the Temperament and Character Inventory (TCI). Comparisons were
done by multivariate analysis of variance. Results: Mothers of probands showed elevated
levels of perfectionism on the MPS and more concerns about weight and shape on the EDI
compared with controls. Mothers who had daughters with diagnoses other than the restricting subtype of anorexia nervosa showed elevated levels of perfectionism on the MPS.
Conclusion: These data are compatible with the notion that some personality traits, such as
perfectionism, and weight and shape concerns may cluster in families of probands with
eating disorders. Ó 2002 by Wiley Periodicals, Inc. Int J Eat Disord 31: 290 299, 2002;
DOI 10.1002/eat.10032
Key words: personality traits; eating-related traits; parents; genetic factors
*Correspondence to: D. Blake Woodside, Toronto General Hospital, 200 Elizabeth Street, 8EN-219, Toronto,
Ontario Canada M5G 2C4. E-mail: b.woodside@utoronto.ca
Ó 2002 by Wiley Periodicals, Inc.
Traits in parents
291
INTRODUCTION
A well-recognized problem in the investigation of genetic factors in complex psychiatric disorders is phenotypic definition. Diagnostic categories in the 4th ed. of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV; American Psychiatric
Association, 1994), although clinically reliable, may not map well onto possible genetic
determinants of psychiatric illnesses. This issue becomes especially relevant when investigations have reached the point of attempting to identify specific susceptibility genes,
where the precise definition of ``affected'' status has critical effects on the outcome of
analyses.
There may be little empirical basis to guide the fashion in which an expanded definition of phenotype is to be determined. Studies of associated factors may lead to some
informed guesses. However, family-genetic studies have rarely, if ever, been performed
on anything except phenotypes defined by clinical symptom counts. Studies that examine
the parents of affected probands are one way in which to increase the information
available to make informed choices as to expanded phenotypic definition.
In the eating disorders, some studies have examined Axis I pathology in parents
(Lilenfeld et al., 1998; Strober, Lampert, Morrell, Burroughs, & Jacobs, 1990). There is also
a rich literature comprising studies that focus on how family environment, family interactions, and parenting skills (Humphrey, 1986; Kog & Vandereycken, 1989; Woodside
& Shekter-Wolfson, 1990) might affect the onset of eating disturbance. An extensive
clinical literature describes purported personality types in parents with anorexia nervosa
6 (AN; Bruch, 1973; Minuchin, Rosman, & Baker, 1978; Selvini-Palazzoli, 1974). However,
studies of the personality of parents of individuals with AN are rare. Lilenfeld et al.
7 (2000) reported elevated rates of perfectionism in the first-degree relatives of bulimic
probands. Otherwise, there has been essentially no examination in parents of affected
individuals of those dimensions of temperament or cognitive/psychological domains
believed to be important in the development of eating disorders.
This paper explores dimensions of personality, temperament, and eating attitudes and
behaviors in parents of individuals with AN compared with controls. Moreover, we
explore whether differences exist between parents of individuals with the restricting
subtype of AN versus parents of individuals with AN accompanied by binging and/or
purging. These findings may offer insight into temperamental traits that may be trans8 mitted through families that have an increased risk for liability to AN.
METHODS
Participants
The sample reported on here is a subset of those participants from the multisite, international Price Foundation genetic study of AN (Kaye et al., 2000). This genetic study
includes 196 relative pairs affected with AN, bulimia nervosa (BN), or eating disorder not
otherwise specified (ED-NOS) recruited from seven sites in North America and Europe
including Pittsburgh, New York, Los Angeles, Toronto, London, Munich, and Philadelphia. Sample ascertainment and recruitment strategies are discussed in detail elsewhere
(Kaye et al., 2000). Parents of probands were also recruited for blood sampling and the
completion of a battery of psychometric tests. Probands and sibs were accepted into the
study even if parents did not agree to participate or were unavailable for some reason.
292
Woodside et al.
Male or female probands meeting modified (i.e., criterion D, amenorrhea, not required)
DSM-IV criteria for AN were identified through treatment facilities and advertisements.
Upon initial screening, probands were questioned about eating disorders (i.e., AN, BN, or
ED-NOS) in their male and female relatives. Permission to contact first, second, and
third-degree relatives with suspicion of an eating disorder was then sought and the
relative(s) were subsequently contacted. If upon initial screening, the proband met
modified DSM-IV criteria for AN and the identified relative(s) met DSM-IV criteria for
AN, BN, or ED-NOS, then the proband and relative(s) were included in the Price genetic
study and administered an assessment battery including the assessments described below. However, if only the proband or relative appeared to meet criteria, then neither
individual was included in the Price study. A total of 185 parents (78 fathers and 107
mothers) were available for the present study. No parents were probands or affected
relatives in the study: that is, we did not accept parent/child affected relative pairs.
However, because parents were not interviewed directly about their own lifetime history
of psychopathology, it is possible that some parents did have an eating disorder. Institutional ethics approval was obtained for the study at each participating site and all
subjects and parents gave written consent to participate in the study.
Control Data
The primary goals of the Price Foundation genetic study of AN were to use familybased association and linkage studies to identify susceptibility genes for the development
of AN. For these types of analyses, community control data are not required. As a result
of this ascertainment strategy, we did not have access to community control women
directly matched to the parents of the probands in the sample. Consequently, for the
current study, we obtained control data from a variety of sources. For the Temperament
and Character Inventory (TCI), data were obtained from the normative TCI database
provided by Cloninger, Przybeck, Svrakic, and Wetzel (1994). Control data on the Multidimensional Perfectionism Scale and the Eating Disorder Inventory (EDI) were obtained
from a previous family study performed in Pittsburgh (Lilenfeld et al., 1998). Control
subjects were matched for gender and age-band matched to the parent groups.
Measures
TCI
Parents completed the 240-item TCI version 9 (Cloninger, Svrakic, & Przybeck, 1993).
The TCI has been normed in a large U.S. national probability sample (Cloninger et al.,
1994) and shows acceptable internal consistency (range = .76 .89; Cloninger et al., 1993).
MPS
The MPS (Frost, Marten, Lahart, & Rosenblate, 1990) is a 35-item, factor analytically
developed self-rating instrument that consists of an overall assessment of perfectionism,
as well as six specific dimensions of perfectionism. These dimensions include concern
over mistakes, high personal standards, high perceived parental expectations, high
perceived parental criticism, doubt about quality of performance, and finally, organization, order, and precision. The coefficients of internal consistency for the factor scales
Traits in parents
293
range from .77 to .93 and the reliability of the overall perfectionism scale is .90 (Frost et al.,
1990). The MPS has been found to discriminate successfully between subjects with and
without eating disorders (Srinivasagam et al., 1995).
EDI-2
The EDI-2 (Garner, 1990) is a 91-item, standardized self-report measure consisting of 11
subscales that assess specific cognitive and behavioral dimensions of eating disorders:
Drive for Thinness, Bulimia, Body Dissatisfaction, Ineffectiveness, Perfectionism, Interpersonal Distrust, Interoceptive Awareness, Maturity Fears, Asceticism, Impulse Regulation, and Social Insecurity. The last three subscales are new to the revised edition of the
EDI. The original EDI showed good internal consistency, as well as good convergent and
discriminant validity (Garner, Olmsted, & Polivy, 1983). Alpha coefficients for the eight
original subscales range from .82 to .90. Internal consistency for the three new subscales is
fair to good, with alpha coefficients between .70 and .80 (Garner, 1990). The EDI has been
used in numerous studies and has been found to discriminate successfully between
subjects with and without eating disorders (Garner et al., 1983).
Data Analytic Approach
All analyses were performed separately for mothers and fathers. The first set of analyses compared all parents of restricting anorexia nervosa (RAN) probands to controls.
Some authors have suggested that individuals with the binging or purging forms of AN
9 differ from those with the restricting form (Garfinkel et al., 1980; Garner, Garner, &
Rosen, 1993). To attempt to achieve greater homogeneity in the parent groups, we conducted a secondary analysis. We divided parents of AN probands into two groups. The
first group, called RAN parents, were parents who had children in the study with only a
diagnosis of RAN and no history of binging or purging. The second group, labeled mixed
parents, included all other possible combinations. For example, these parents could have
one child with RAN and another child with BN or ED-NOS. The breakdown of these
subgroups is shown in Table 1.
All data were tested for normality. Square root transformations were calculated for
nonnormally distributed data. A multivariate analysis of variance (MANOVA) was
performed separately for the MPS, EDI, and TCI. Univariate analyses of variance
(ANOVAs) were then performed for the subscales. Confidence intervals were calculated
for the three groups using Tukey's studentized range test.
A significance level of p < .05 was set for all comparisons. We chose not to correct for
multiple comparisons given that this was an exploratory study on a relatively small but
unique sample.
Table 1.
Mothers
Fathers
Breakdown of parents into subgroups
Total
RAN
Mixed
107
78
20
12
87
66
Note: RAN parents have only RAN children entered into the study as subjects. Mixed parents have at least
one child entered into the study with an eating disorder diagnosis other than RAN. RAN = restricting anorexia
nervosa.
294
Woodside et al.
RESULTS
Means and standard deviations for the MPS, EDI, and TCI are presented in Table 2.
Because of the unique nature of this study, and the relatively small sample sizes, univariate test results are shown for information even when the relevant overall multivariate
test is not significant. An analysis of results by site (Pittsburgh, New York, Toronto,
Los Angeles, Munich, and London) was not performed because of the small number of
subjects from several sites.
In the first set of analyses comparing all mothers and fathers of anorexic probands with
controls (Table 3), mothers of anorexic probands demonstrated elevated scores on the
overall MPS and EDI (MANOVA, F = 3.75, 6 df, p = .002 and F = 2.59, 8 df, p = .01,
respectively). Fathers scored signi®cantly differently on the TCI (F = 2.10, 7 df, p = .04)
than male controls.
Univariate comparisons for mothers on the MPS showed elevated scores on the subscales Concern over Mistakes (F = 6.84, 1 df, p = .01) and Parental Criticism (F = 9.03, 1 df,
p = .003) compared with controls. For the EDI, mothers had elevated scores on Drive for
Thinness (F = 9.38, 1 df, p = .003), Ineffectiveness (F = 4.39, 1 df, p = .04), and Interoceptive
Awareness (F = 4.92, 1 df, p = .03) compared with controls. Fathers of the AN probands
showed increased scores on the Self-Directedness subscale of the TCI (F = 8.04, 1 df, p =
.005) compared with controls.
Subgroup Analyses
The second set of analyses compared RAN, mixed, and control parents. Again, the
overall MANOVA for mothers was significantly different for the MPS (F = 2.43, 12 df, p =
.005, with mixed mothers having the highest overall scores. Univariate comparisons
across the three groups showed the mixed mother group to have elevated scores compared with controls on Concern over Mistakes (F = 5.60, 2 df, p = .005) and Parental
Criticism (F = 6.28, 2 df, p = .003). Although the subscale Personal Standards showed a
signi®cant difference across the three groups of mothers (F = 3.56, 2 df, p = .03), none of
the groups differed signi®cantly from one another.
Fathers did not show any significant differences across the three groups. For fathers,
the overall MPS MANOVA showed a trend toward differences (F = 1.762, 12 df, p = .06),
with RAN fathers having lowered scores on Parental Expectations (F = 3.53, 2 df, p = .03)
relative to controls and lowered scores on Doubts about Actions (F = 3.62, 2 df, p = .03)
relative to mixed AN fathers.
DISCUSSION
We examined dimensions of temperament, personality, psychological functioning,
and eating-related pathology in parents of individuals affected with AN. The most
salient differences between mothers of individuals with AN and female controls were
greater perfectionism and higher levels of some aspects of eating disordered-type attitudes and behaviors. Fathers of individuals with AN differed minimally from males,
with the exception of elevated perfectionism in fathers of offspring with RAN. Our
limited sample size for fathers may have precluded the detection of other significant
differences.
Comparisons of personality and eating attitudes between mothers of anorexic probands and controls
Controls
(n ˆ 248)
M
a
All AN Mothers
(n ˆ 107)
SD
M
SD
RAN Type
(n ˆ 20)
M
SD
Mixed Type
(n ˆ 87)
M
SD
All AN Vs.
Controls
F(df)
RAN Vs. Mixed
Vs. Controls
p
d
F(df)
p
MPS
Overall
CM
PS
PE
PC
DA
O
58.52
14.81
18.19
11.29
6.39
7.84
23.55
15.25
4.94
5.33
4.68
2.68
2.95
4.25
68.95
19.34
20.40
11.48
9.06
8.78
22.79
24.46
9.07
6.49
5.13
4.57
4.06
4.79
59.75
16.17
18.06
9.89
7.53
7.76
21.17
22.63
7.15
7.07
4.28
4.33
3.56
5.94
70.94
20.02
20.91
11.82
9.39
8.99
23.14
24.51
9.33
6.28
5.26
4.58
4.15
4.47
3.75(6)
6.84(1)
3.73(1)
0.06(1)
9.03(1)
1.13(1)
0.28(1)
.002
.01
.06
.80
.003
.29
.60
2.43(12)
5.60(2)
3.56(2)
0.84(2)
6.28(2)
1.35(2)
1.48(2)
.005
.005e
.03
.43
.003e
.26
.23
EDIb
Overall
DT
B
BD
I
P
IED
IEA
MF
0.90
0.58
10.61
1.00
3.10
1.65
0.45
1.16
1.27
0.85
7.68
1.71
2.76
1.62
1.18
1.19
3.85
1.15
9.02
2.97
4.06
2.06
2.02
1.78
5.36
2.99
8.22
5.13
3.97
3.22
3.90
3.21
2.21
0.21
7.64
2.00
3.03
1.14
0.86
0.79
3.07
0.58
7.82
4.08
2.65
1.17
1.70
1.05
4.16
1.33
9.28
3.16
4.25
2.23
2.24
1.96
5.65
3.23
8.32
5.32
4.16
3.46
4.16
3.45
2.59(8)
9.38(1)
1.14(1)
0.78(1)
4.39(1)
1.49(1)
0.52(1)
4.92(1)
1.09(1)
.01
.003
.29
.38
.04
.22
.47
.03
.30
1.49(16)
5.84(2)
1.69(2)
0.67(2)
2.58(2)
1.37(2)
1.14(2)
3.50(2)
1.59(2)
.11
.004e
.19
.52
.08
.26
.32
.03e
.21
TCIc
Overall
NS
HA
RD
P
SD
C
ST
18.04
15.12
17.61
5.54
32.68
36.88
16.99
5.64
7.00
3.81
1.90
7.30
4.65
6.13
18.27
15.61
17.90
5.16
34.19
36.51
16.66
5.47
7.43
3.83
2.00
7.92
5.09
6.30
16.09
14.67
17.83
5.39
33.12
36.64
15.37
5.52
7.29
3.51
1.92
6.42
4.03
6.10
18.75
15.82
17.92
5.11
34.42
36.49
16.94
5.37
7.49
3.92
2.02
8.23
5.31
6.34
1.72(7)
0.17(1)
0.27(1)
0.36(1)
2.70(1)
1.93(1)
0.71(1)
0.12(1)
.10
.68
.61
.55
.10
.17
.40
.73
1.49(14)
1.86(2)
0.31(2)
0.18(2)
1.51(2)
1.10(2)
0.39(2)
0.59(2)
.11
.16
.74
.83
.22
.34
.68
.55
295
Note: RAN = restricting anorexia nervosa; AN = anorexia nervosa. F and p values that are bold are signi®cant at p £ 0.05.
a
MPS scales: CM = Concern over mistakes; PS = Personal Standards; PE = Parental Expectations; PC = Parental Criticism; DA = Doubts about Actions;
O = Organization.
b
EDI subscales: DT = Drive for Thinness; B = Bulimia; BD = Body Dissatisfaction; I = Ineffectiveness; P = Perfectionism; ID = Interpersonal Distrust;
IA = Interoceptive Awareness; MF = Maturity Fears. Overall Fs and ps are for overall multivariate analysis of variance (MANOVA) signi®cance.
c
TCI subscales: NS = Novelty Seeking; HA = Harm Avoidance; RD = Reward Dependence; P = Persistence; SD = Self-Directedness; C = Cooperativeness; ST = SelfTranscendence. Overall Fs and ps are for overall MANOVA signi®cance.
d
Overall Fs and ps refer to overall MANOVA result. Frost MPS means and SDs are presented only for information and were not tested separately.
e
Mixed AN > controls.
Traits in parents
15 Table 2.
Comparisons of personality and eating attitudes between fathers of anorexic probands and controls
296
15 Table 3.
Fathers
All AN Fathers
(n = 78)
Controls
(n = 24)
M
a
SD
M
SD
RAN Type
(n = 12)
M
SD
Mixed Type
(n = 66)
All AN Vs.
Controls
M
F(df)
SD
f
RAN Vs.
Mixed Vs. Controls
p
F(df)
p
.07
.42
.58
.03
.24
.61
.06
1.76(12)
0.72(2)
0.21(2)
3.53(2)
1.94(2)
3.62(2)
1.84(2)
.06
.49
.81
.03d
.15
.03e
.16
MPS
Overall
CM
PS
PE
PC
DA
O
73.83
19.83
22.96
13.58
8.42
9.04
23.67
16.11
6.23
5.12
3.57
2.76
2.56
4.99
68.43
18.50
22.16
11.46
7.58
8.78
21.57
18.72
7.18
5.47
4.61
3.62
3.65
4.61
61.67
17.25
21.75
9.92
6.17
6.58
21.25
17.43
7.21
6.28
4.32
1.80
2.43
4.39
69.78
18.85
22.24
11.78
7.86
9.22
21.63
18.81
7.20
5.34
4.64
3.83
3.71
4.69
2.02(6)
0.65(1)
0.31(1)
4.78(1)
1.40(1)
0.27(1)
3.69(1)
EDIb
Overall
DT
B
BD
I
P
ID
IA
MF
1.38
0.63
4.08
0.54
3.63
2.75
0.29
2.08
1.95
1.28
3.34
0.93
2.55
1.54
0.62
2.06
1.33
0.53
4.01
1.14
4.16
2.79
0.71
1.73
1.95
1.48
4.75
2.40
3.69
3.13
1.37
2.76
0.80
0.00
3.80
0.10
3.80
3.10
0.32
1.40
1.93
0.00
6.09
0.32
2.97
2.28
0.74
2.07
1.43
0.63
4.04
1.33
4.22
2.73
0.78
1.79
2.74
1.59
4.52
2.56
3.83
3.28
1.45
2.88
0.74(8)
0.01(1)
0.08(1)
0.01(1)
1.40(1)
0.42(1)
0.00(1)
2.04(1)
0.33(1)
.66
.94
.78
.94
.24
.52
.95
.16
.57
0.76(16)
0.27(2)
0.86(2)
0.02(2)
2.19(2)
0.27(2)
0.07(2)
1.61(2)
0.26(1)
.73
.76
.43
.98
.12
.76
.93
.21
.77
TCIc
Overall
NS
HA
RD
P
SD
C
ST
17.89
13.20
14.71
5.39
31.86
34.28
15.53
6.37
7.30
4.43
2.12
8.22
6.83
6.53
16.78
12.99
15.11
5.09
34.97
35.22
14.03
6.02
7.36
3.74
2.08
7.19
5.85
5.79
15.33
11.92
13.80
5.50
34.69
33.73
13.00
6.26
5.88
3.93
1.88
7.14
6.85
4.95
17.07
13.21
15.38
5.00
35.03
35.52
14.24
5.98
7.65
3.67
2.12
7.26
5.65
5.96
2.10(7)
1.32(1)
0.11(1)
0.51(1)
0.78(1)
8.04(1)
1.00(1)
2.67(1)
.04
.25
.74
.48
.38
.005
.32
.10
1.31(14)
1.08(2)
0.17(2)
1.00(2)
0.63(2)
4.02(2)
0.88(2)
1.52(2)
.20
.34
.84
.38
.54
.02
.42
.22
Woodside et al.
Note: RAN = restricting anorexia nervosa; AN = anorexia nervosa. F and p values that are bold are signi®cant at p £ 0.05.
a
MPS scales: CM = Concern over mistakes; PS = Personal Standards; PE = Parental Expectations; PC = Parental Criticism; DA = Doubts about Actions; O =
Organization.
b
EDI subscales: DT = Drive for Thinness; B = Bulimia; BD = Body Dissatisfaction; I = Ineffectiveness; P = Perfectionism; ID = Interpersonal Distrust; IA =
Interoceptive Awareness; MF = Maturity Fears. Overall Fs and ps are for overall multivariate analysis of variance (MANOVA) signi®cance.
c
TCI subscales: NS = Novelty Seeking; HA = Harm Avoidance; RD = Reward Dependence; P = Persistence; SD = Self-Directedness; C = Cooperativeness; ST = SelfTranscendence. Overall Fs and ps are for overall MANOVA signi®cance.
d
RAN < Controls.
e
Mixed AN > RAN.
f
Overall Fs and ps refer to overall MANOVA result. Frost MPS means and SDs are presented only for information and were not tested separately.
Traits in parents
297
Perfectionism has been noted frequently as a key clinical feature of individuals with AN
10 (Janet, 1903; King, 1963; Palmer & Jones, 1939) and the trait appears to persist even after
weight restoration and recovery (Bastiani, Rao, Weltzin, & Kaye, 1995; Srinivasagam
et al., 1995). Although true prospective studies have not been conducted, retrospective
clinical reports of premorbid personality in individuals with AN have noted perfectionistic tendencies (Bruch, 1978).
Our observation of elevated perfectionism in mothers (and to a lesser extent fathers)
of individuals with AN has several possible interpretations. First, it is conceivable that
perfectionism is an environmentally transmitted trait and that parental perfectionism
``flows down'' to the offspring generation via an environmental pathway such as
modeling. Second, as we have no data on perfectionism in the parents prior to the
development of AN in their offspring, it is also possible that pervasive perfectionism
in the offspring could increase perfectionistic tendencies in parents, given that environmental transmission can be bidirectional (Kendler, 1998). Third, and perhaps
most likely, perfectionism could be a genetically mediated personality trait that is
transmitted through families and increases liability to the development of AN.
Expanding this line of thought, it has been demonstrated that AN is familial (Lilenfeld
et al., 1998; Strober, Freeman, Lampert, & Diamond, 2000). Moreover, twin studies have provided preliminary evidence for the heritability of AN (Holland, Hall,
Murray, Russell, & Crisp, 1984; Holland, Sicotte, & Treasure, 1988; Klump, Miller,
Keel, McGue, & Iacono, 2000). What we do not yet know is precisely what is inherited. Is AN itself the ``unit'' that is transmitted? Conversely, might a personality
trait, such as perfectionism, as suggested by this study, be transmitted through families and represent a vulnerability factor for the development of AN? One family study
has shown an association between a personality construct, obsessive-compulsive personality disorder and AN, pointing to a possible shared etiology (Lilenfeld et al.,
1998).
Our examination of differences between mothers of restrictor anorexic offspring only
and mothers of mixed anorexic offspring suggested that mothers of mixed offspring have
higher levels of perfectionism as reflected in the total MPS score as well as across a
variety of subscales. Although the stereotype of the individual with RAN is of extreme
perfectionism, at least one other study that compared subtypes of individuals with AN
has found that perfectionism (as well as other indicators of severity) is often higher in
individuals with nonrestricting AN (Garner et al., 1993). This study suggests that nonrestricting AN may actually represent a more severe form of the illness. If this is the case,
then one might expect the level of pathology observed in parentsÐespecially traits that
may be of etiological significance to ANÐto be greater in the parents of the more severely
ill group.
The fact that mothers of individuals with AN had elevated scores on the EDI Drive for
Thinness, Ineffectiveness, and Interoceptive Awareness subscales could index either their
own eating-related pathology or could reflect the heightened awareness of weight and
shape issues as well as the emergence of a sense of ineffectiveness that is a not infrequent
outcome of having more than one child with AN. Another possibility is that the results
could be the consequence of the aggregation of subthreshold pathology in parents, as has
been suggested by Strober et al. (2000). Finally, Fairburn, Cooper, Doll, and Welch (1999)
noted an excess of childhood perfectionism and negative self-evaluation in individuals
with AN. These experiences could certainly be affected by the personality of the parents
of the child with AN. The current design does not allow for a differentiation between
these alternative explanations.
298
Woodside et al.
It is of interest that there were few differences detected on the TCI on any of the
analyses performed. Fathers showed a trend toward a difference on the comparison to
controls, but only one difference was detected on univariate tests of specific scales, that is,
higher levels of self-directedness, a construct measuring the extent to which an individual
12 is autonomous and integrated. Another report by our group (Klump et al., 2000) noted
higher levels of self-directedness in individuals with RAN, compared with subjects with
the purging or bulimic form of AN.
The current study has several limitations. First, the absence of a control group that was
ascertained in a fashion similar to the study group may have introduced some bias into
the results. Second, the subgroup analysis suffers from rather small sample sizes that
make it difficult to interpret the results. The sample was ascertained using a sib-pair
design, which may have produced a group of individuals who are not typical for the
population of anorexia individuals as a whole, thus reducing the generalizability of these
data. Finally, eating disorders were not ascertained in parents, especially mothers. It may
be that the elevated scores demonstrated by mothers on a number of measures might be
caused by undiagnosed eating disorders in mothers. The study also has several strengths.
First, although still limited in sample size, we were able to collect personality and eatingrelated information on a substantial number of parents of individuals with eating disorders. Second, we used stringent diagnostic criteria for identifying and diagnosing
probands and affected relatives. Despite our aggressive recruitment, given the rarity of
AN, our sample size for parents (especially for the subgroup of parents with restrictor
offspring only) remains quite small. Nonetheless, this study suggests that perfectionism
may be a worthwhile candidate for a transmissible trait that may be of etiological relevance to AN and one that may assist in refining our phenotypic definition of AN for
future genetic studies.
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