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Association of Serotonin and Cortisol Indices With Childhood Abuse in Bulimia Nervosa
Howard Steiger, PhD;
Lise Gauvin, PhD;
Mimi Israël, MD;
Naomi Koerner, BA;
N. M. K. Ng Ying Kin, PhD;
Joel Paris, MD;
Simon N. Young, PhD
Arch Gen Psychiatry. 2001;58:837-843.
ABSTRACT
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Background Bulimia nervosa (BN) is reported to co-occur with childhood abuse and
alterations in central serotonin (5-hydroxytryptamine [5-HT]) and cortisol
mechanisms. However, findings also link childhood abuse to anomalous 5-HT
and cortisol function, and this motivated us to explore relationships between
childhood abuse and neurobiological variations in BN.
Methods Thirty-five bulimic and 25 nonbulimic women were assessed for childhood
physical and sexual abuse, eating symptoms, and comorbid psychopathological
tendencies. These women provided blood samples for measurement of platelet
hydrogen-3–paroxetine binding and serial prolactin and cortisol responses
following oral administration of the partial 5-HT agonist meta-chlorophenylpiperazine (m-CPP).
Results Bulimic women showed markedly lower mean ± SD density (Bmax) of paroxetine-binding sites (631.12 ± 341.58) than did normal
eaters (1213.00 ± 628.74) (t54
= -4.47; P = .001). Paroxetine binding did
not vary with childhood abuse. In contrast, measures of peak change on prolactin
levels after m-CPP administration ( -peak prolactin)
indicated blunted response in abused bulimic women (7.26 ± 7.06), nonabused
bulimic women (5.62 ± 3.95), and abused women who were normal eaters
(5.73 ± 5.19) compared with nonabused women who were normal eaters
(13.57 ± 9.94) (F3,51 = 3.04, P
= .04). Furthermore, individuals reporting childhood abuse showed decreased
plasma cortisol levels relative to nonabused women who were normal eaters.
Conclusion Findings imply that BN and childhood abuse are both generally associated
with reduced 5-HT tone but that childhood abuse may be somewhat more specifically
linked to reduced cortisol levels (ie, hypothalamic-pituitary-adrenal axis)
activity.
INTRODUCTION
FINDINGS LINK traumatic experiences to alterations in central serotonin
(5-hydroxytryptamine [5-HT]) and cortisol systems. For example, data have
linked posttraumatic stress disorder (PTSD) to reduced platelet binding of
the selective 5-HT reuptake inhibitor hydrogen-3–paroxetine ([3H]-paroxetine)1 and childhood abuse
(in women with personality disorders) to "blunting" of prolactin and cortisol
following the partial 5-HT agonist meta-chlorophenylpiperazine
(m-CPP).2 Various
traumas have similarly been associated with decreased resting cortisol and
altered cortisol stress responses, suggesting posttraumatic alterations of
the hypothalamic-pituitary-adrenal (HPA) axis.3, 4
Findings in bulimia nervosa (BN) indicate comparable anomalies. Consistent
with reduced 5-HT activity, studies document decreased 5-HT metabolites in
cerebrospinal fluid,5 reduced platelet binding
of [3H]-paroxetine,6 and blunted
prolactin responses to m-CPP.7
Suggesting altered cortisol function, one study8
links atypical depression (ie, with hyperphagia and hypersomnolence) in BN
to reduced plasma cortisol; another9 links
BN, in general, to decreased nocturnal and postglucose cortisol responses.
Since many bulimic women report childhood sexual and physical abuse,10, 11 one obvious conjecture is that neurobiological
and psychopathological variations in BN may sometimes be attributable to abuse
history. We compared bulimic women reporting childhood abuse, bulimic women
without childhood abuse, normal eaters with a history of abuse, and normal
eaters with no abuse history on symptom, 5-HT, and cortisol indices. We expected
abuse to coincide with increased eating and psychopathological symptoms and
decreased 5-HT and cortisol activity.
SUBJECTS AND METHODS
SUBJECTS
Forty-five potential bulimic women were recruited through a specialized
eating disorders (ED) clinic, using the following criteria: female, aged 18
to 40 years, actively bingeing, and not pregnant, anorexic, obese (body mass
index [BMI], a measure of weight in kilograms divided by the square of height
in meters, of  28), or taking psychoactive medications. The ED symptoms
were confirmed using the Eating Disorders Examination.12
We excluded 5 individuals because of electrocardiographic (ECG) abnormalities
or conditions affecting neuroendocrine function and 1 more case with an enzyme-multiplied
immunoassay technique urine screen that revealed amphetamine abuse. In 4 more
cases, a vein could not be obtained for blood draws. We thus completed full
assays in 35 women, 28 (80%) of whom met DSM-IV13 criteria for BN purging subtype, 5 (14%) for BN nonpurging
subtype, and 2 (6%) for a "subclinical" BN purging type (bingeing once vs
twice weekly). Subthreshold cases were fully "BN spectrum" and deemed not
to render the sample heterogeneous. Mean ± SD age and BMI were 23.95
± 4.25 years and 21.73 ± 2.89, respectively.
Healthy women, recruited through university classes or newspaper advertisements
(to approximate student and nonstudent proportions among bulimic women), were
aged 18 to 40 years, had relatively normal BMIs of 19 to 27, and had normal
results on physical examination, blood work, and ECG. They denied (past or
present) ED; intense weight concerns; periods of marked intentional weight
loss, binge eating, or purging; medical problems; mental health problems (eg,
depression, anxiety, substance abuse); pregnancy; or use of psychoactive medications.
Eleven potential candidates showed abnormal eating or weight, 1 reported regular
substance abuse, and 6 reported depression or panic attacks. Two showed ECG
abnormalities, and in 5 more, a vein could not be obtained for blood draws.
After exclusions, we completed assessments in 25 women, who had a mean ±
SD age and BMI of 24.60 ± 7.28 years and 22.02 ± 1.97, respectively. t Tests showed no bulimic and nonbulimic differences on
age or BMI.
ASSESSMENTS
To assess ED symptoms, we used the Eating Disorders Examination12 interview, which quantifies severity of criterion
ED symptoms, and the Eating Attitudes Test,14
which measures global ED attitudes and behaviors. We also computed BMI from
self-reported height and weight. To assess psychiatric comorbidity, we used
a self-administered, computerized Diagnostic Interview Schedule, Version IV
(DIS4),15, 16 a DSM-IV version of the National Institute of Mental Health Diagnostic
Interview Schedule,17 and the well-validated18 Structured Clinical Interview for DSM-IV Axis II.19 We present findings
for current and past major depression and PTSD and for borderline personality
disorder (BPD), all entities associated with antecedent trauma. Interrater
checks on 12 pseudorandomly selected interview pairs yielded a  of
0.80 (and 91.7% agreement) for a BPD and non-BPD distinction. A self-injuriousness
score was created by adding Structured Clinical Interview for DSM-IV Axis II ratings (on a 0-3 scale) for self-mutilation and suicidality.
These components yielded respective values of 0.73 and 0.59.
Additional psychopathological constructs were measured using the Center
for Epidemiological Studies Depression (CES-D) scale,20
the affective instability subscale from the Dimensional Assessment of Personality
Pathology,21 the Barratt Impulsiveness Scale,22 and the Dissociative Experiences Scale (DES).23 In bulimic and nonbulimic women,  values for
CES-D, affective instability, Barratt Impulsiveness Scale, and DES scales
were .91 and .91, .85 and .89, .78 and .80, and .92 and .93, respectively.
We assessed childhood abuse with the Childhood Trauma Interview,24 a structured interview quantifying the nature, frequency,
and duration of childhood physical and sexual abuse, establishing perpetrators'
and subjects' ages when events occurred, and estimating severity of events
(using well-anchored ratings). Subjects were classified as having experienced
childhood abuse when they received a score of 2 or greater on severity of
sexual abuse occurring at or before the age of 14 years (implying serious
"noncontact" experiences, such as being made to observe an adult masturbate,
or lesser "contact" experiences, such as being held in a sexualized way) or
3 or greater on severity of physical abuse at or before the age of 14 years
(implying serious physical maltreatment, such as being hit and bruised with
an object or pushed so hard as to be knocked down). We thought that lower
ratings (reflecting concepts such as "being looked at in a sexualized way"
or "pushed, but not pushed down") indicated abuse too ambiguously.
Given a bilingual sample, we used official French versions of scales
(DIS4,16 DES, and CES-D) or otherwise developed
translations using forward-and-back translation techniques. Comparisons of
global scores and values support psychometric adequacy of translations.
PROCEDURES
Since 5-HT promotes prolactin secretion from the pituitary and (indirectly)
of cortisol via the HPA axis, it is conventional to draw inferences about
central 5-HT functioning from 5-HT–induced alterations in plasma prolactin
and cortisol levels.25 We measured prolactin
and cortisol levels before and after oral administration of the partial 5-HT
agonist m-CPP, which (since it binds with highest
affinity to 5-HT2c receptors) is thought to be a fairly specific
5-HT probe.25 Cortisol was assumed to also
reflect HPA axis function. In addition, we measured binding in blood platelets
of the selective 5-HT reuptake inhibitor [3H]-paroxetine. Platelets
possess high-affinity sites for 5-HT, comparable to 5-HT reuptake sites in
brain, and platelet binding is selectively associated with binding in brain
tissue. Platelet paroxetine binding, usually measured in terms of density
of binding sites (Bmax) and binding affinity (Kd), is believed to model aspects of central (presynaptic)
5-HT transporter function.26
Subjects, tested as outpatients, were required to have been free of
psychoactive medications for at least 6 weeks and were tested in follicular
phase of menses (ie, 5 to 14 days following start of last menses). Before
testing, participants were asked to refrain from alcohol, exercise, or street
drugs for 48 hours and from binge eating for 24 hours. On the test morning,
participants underwent a urine screen for drug use (enzyme-multiplied immunoassay
technique kit). Samples were drawn after an overnight fast. Detailed procedures
for biochemical assays are described elsewhere.6, 27
Baseline measures on hormones constitute the mean of 2 values obtained from
samples drawn at 8:30 and 9 AM before m-CPP administration.
Prolactin and cortisol levels were determined by radioimmunoassay, using the
corresponding, validated Amersham radioimmunoassay kits from Johnson and Johnson,
Markham, Ontario. Our laboratory could not obtain paroxetine-binding indices
on 1 bulimic woman and cortisol measurements on 1 woman who was a normal eater.
STATISTICAL ANALYSES
Using ED diagnosis (BN/non-BN) and abuse criteria (described earlier),
we organized participants into 4 subgroups: BN with childhood abuse (BN/CA:
n = 26), BN without abuse (BN: n = 8), normal eater with CA (NE/CA: n = 12),
and normal eater without abuse (NE: n = 11). (One bulimic and 2 nonbulimic
women who indicated abuse after the age of 14 years only were excluded.) Analyses
of variance (ANOVAs) showed no mean ± SD group differences in age (24.42
± 4.32, 22.00 ± 3.74, 24.42 ± 6.78, and 23.45 ±
5.52 years, respectively) or BMI (21.75 ± 2.86, 21.75 ± 3.37,
21.92 ± 1.93, and 22.05 ± 2.26, respectively).
Groups were compared on eating and psychopathological symptoms using
ANOVAs, with Newman-Keuls tests (to control family-wise error). Where measures
(eg, binge frequencies) yielded zero values in normal eaters, we applied t tests to examine pairwise differences across abused and
nonabused bulimic women only. Depending on frequencies obtained, childhood
abuse and psychiatric comorbidity indices were analyzed using  2 or Fisher exact tests. We used 1-way ANOVA to explore group effects
on indices of paroxetine binding (Bmax and Kd) and repeated-measures ANOVAs (RANOVAs; 4 x 9) to
test for group effects on serial prolactin and cortisol indices. RANOVAs treated
group (NE, NE/CA, BN, BN/CA) and time (baseline and 30-, 60-, 90-, 120-, 150-,
180-, 210-, and 240-minute) factors. Where the Mauchly test of sphericity
indicated heterogeneity of covariance, we verified repeated-measures results
with Greenhouse-Geisser corrections. We introduced covariates to control known
seasonal variations on prolactin responses after m-CPP
administration,28 Bmax in paroxetine
binding29 and basal cortisol levels,30 and effects of oral contraceptive use on cortisol
(and possibly prolactin) levels.31 Because
our sample size was not sufficiently large to allow for stable estimation
of seasonal effects (once "diagnosis" was crossed with "abuse" and then "contraceptive
use"), we turned to published findings for guidance: prolactin response after m-CPP administration is reportedly larger in winter than
in summer and at intermediate levels in spring and fall.28
In contrast, Bmax for paroxetine binding is reportedly elevated
in summer, low in winter, and at intermediate levels in spring and fall.29 For cortisol, data indicate consistent differences
between winter and summer samplings (but inconsistencies as to direction of
effects, possibly attributable to geographic, meteorologic, or other differences).30 Our own data showed trends or effects consistent
with high peak prolactin levels in winter, high Bmax and cortisol
levels in summer, and intermediate values on these indices in spring and fall.
To control for this range of effects, we entered 2 dummy variables as covariates,
which compared samplings obtained in summer (and then fall and spring) to
those obtained in winter. Consistent with published findings,31
our data showed contraceptive users to show strongly higher range of cortisol
values and weakly higher peak prolactin levels. Even though proportions of
contraceptive users did not differ significantly across groups, we introduced
a covariate to code for being "on" or "off" oral contraceptives. Statistical
tests were 2-tailed and conducted at the .05 level of significance. To balance
type I and type II errors, we report pairwise group comparisons with and without
Bonferroni corrections.
RESULTS
CHILDHOOD ABUSE
Abuse was reported by 26 (76%) of 34 bulimic women and 12 (52%) of 23
nonbulimic women. Significant bulimic and nonbulimic differences were indicated
for physical abuse (21 [62%] of 34 vs 7 [30%] of 23, respectively; 21 = 5.39; P = .02), but not for
sexual abuse (14 [41%] of 34 vs 8 [33%] of 24, respectively). Among sexually
abused bulimic and sexually abused nonbulimic participants, mean ±
SD severities (3.21 ± 0.89 vs 2.75 ± 1.04, respectively) and
ages of abuse onset (9.50 ± 3.46 vs 9.63 ± 3.11 years, respectively)
did not differ (t20 = 1.11, P>.25 and t20 = -0.08, P>.50, respectively). Corresponding mean ± SD physical
abuse severities (3.62 ± 0.92 vs 3.71 ± 0.76) and ages of onset
(7.43 ± 3.68 vs 5.86 ± 2.19 years) did not differ (t26 = -0.25, P>.50 and t26 = 1.06, P>.25,
respectively).
EATING SYMPTOMS AND PSYCHOPATHOLOGICAL INDICES
Table 1 shows mean ±
SD values on measures of eating and psychopathological symptoms for each of
the groups. On most indices bulimic women showed expected elevations relative
to nonbulimic women. Abused bulimic women reported significantly more self-injuriousness
than did nonabused bulimic women or women who were normal eaters.
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Table 1. Mean (SD) Findings in Bulimic (BN), Abused Bulimic (BN/CA),
Normal Eater (NE), and Abused Normal Eater (NE/CA) Groups on Eating Symptoms
and Psychopathological Indices*
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Prevalences of major depression, PTSD, and BPD obtained in different
groups are shown in Table 2. (DIS4
values were nonsystematically missing for 4 bulimic women and 1 nonbulimic
woman.) Results (tested with Fisher exact tests) indicate lifetime major depression
to coaggregate, regardless of abuse, with BN. In contrast, PTSD (lifetime
or current) occurred especially often in abused bulimic women. Statistically
significant differences were not obtained on BPD.
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Table 2. Count of Comorbid Psychiatric Syndromes in Bulimic (BN), Abused
Bulimic (BN/CA), Normal Eater (NE), and Abused Normal Eater (NE/CA) Groups
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SEROTONERGIC AND NEUROENDOCRINE MEASURES
Results on paroxetine-binding tests were evaluated using analyses of
covariance (ANCOVAs) to compare transporter density (Bmax) and
binding affinity (Kd) indices across groups,
with dummy variables for seasonal effects (Table 3 presents unadjusted means and SDs). The analysis on Bmax indicated expected winter vs summer (F1,50
= 7.26, P<.02) and spring or fall vs summer (F1,50 = 5.93, P<.03) effects, with higher
Bmax in the summer. Once removed, a significant group effect remained
(F3,50 = 4.61, P<.01). Covariate-adjusted
group contrasts (with or without Bonferroni corrections) generally indicate
lower Bmax in bulimic women, but no differences attributable to
childhood abuse (Table 3). No
effects were obtained on Kd.
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Table 3. Mean (SD) Platelet Paroxetine-Binding Density (Bmax)
and Affinity in Bulimic (BN), Abused Bulimic (BN/CA), Normal Eater (NE), and
Abused Normal Eater (NE/CA) Groups*
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We analyzed serial prolactin findings (Figure 1, plotting unadjusted means and SEs) using a 2-way repeated-measures
analysis of covariance (RANCOVA), with covariates for contraceptive and seasonal
effects. The RANCOVA yielded a significant time x contraceptive interaction
(F8,400 = 2.83, P<.01), indicative
of earlier "peaking" in contraceptive users, which remained significant after
Greenhouse-Geisser correction (F2,77 = 2.83, P<.05). Examination of resulting curves and proportions of contraceptive
users across groups indicated that the interaction could not have confounded
group and time effects of main interest. There was no main effect of contraceptives
or main or interaction effects implicating season of testing. A main effect
of time of sampling (F8,400 = 5.17, P<.005),
showing expected stimulation of prolactin after m-CPP
administration, remained significant after Greenhouse-Geisser correction (F2.77,138.63 = 5.17, P<.005). More important,
after removal of covariates, a significant group x time interaction
effect was obtained (F24,400 = 2.10, P<.005),
which remained after Greenhouse-Geisser correction (F8.32,138.63
= 2.10, P<.04). Simple effects of group were indicated
at 180 (F3,50 = 4.50, P<.01) and 210
(F3,50 = 3.52, P<.025), and, as a trend,
at 240 minutes (F3,50 = 2.74, P<.055).
The pattern of results on covariate-adjusted pairwise comparisons, conducted
with and without Bonferroni corrections (Figure 1), indicates "blunted" prolactin response in both bulimic
and abused participants. An adjunctive analysis, conducted using 1-way ANCOVA
(with covariates controlling for seasonal effects) testing group differences
on an index of change (-peak) on prolactin (ie, peak minus baseline
at each time point for each subject), indicated no seasonal effects, but a
significant overall group effect (F3,55 = 3.15, P<.04). Covariate-adjusted contrasts showed mean -peak prolactin
for bulimic women (5.62 ± 3.95), abused bulimic women (7.26 ±
7.06), and abused women who were normal eaters (5.73 ± 5.19) to always
be lower than the score obtained in the group of nonabused women who were
normal eaters (13.57 ± 9.94).
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Figure 1. Means (and SEs) obtained at each
moment of the serial sampling for prolactin in nonabused bulimic, abused bulimic,
nonabused normal eater, and abused normal eater groups. Significant pairwise
differences between nonabused women who were normal eaters and (A) abused
bulimic women, (B) nonabused bulimic women, and (C) abused women who were
normal eaters at P<.05 on covariate-adjusted pairwise
contrast; asterisk indicates corresponding contrast differs at P<.05 after Bonferroni correction for family-wise error.
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The combination of downward diurnal cortisol variations with upward
shifts (presumably) due to m-CPP administration complicated
determination of -peak values on cortisol. We therefore analyzed serial
cortisol findings using 2-way RANCOVA, with covariates for contraceptive and
seasonal effects (Figure 2, which
plots unadjusted means and SEs). The RANCOVA indicated a significant time
x contraceptive effect (F8,392 = 2.58, P<.01), even after Greenhouse-Geisser correction (F4.16,203.71 = 2.58, P<.04), and an even stronger main
effect of contraceptive use (F1,49 = 27.43, P<.001). Average ± SE cortisol level was higher in contraceptive
users (21.08 ± 1.18) than in nonusers (11.25 ± 0.99) (and downward
diurnal shifts in these individuals were, correspondingly, somewhat larger).
Examination of curves suggested that the interaction of time and contraceptive
variables could not have confounded effects of main interest. Moreover, after
removal of covariate effects, a significant group x time interaction
was obtained (F24,392 = 2.03, P<.005),
even after Greenhouse-Geisser correction (F12.47,203.71 = 2.03, P<.03). There was no main time or group effect. Simple
effects of group were indicated at 210 minutes (F3,49 = 2.89, P<.05) and 240 minutes (F3,49 = 3.15, P<.04). Covariate-adjusted pairwise group comparisons
indicated significantly lower means at these time points in samples of abused
bulimic women and abused women who were normal eaters (Figure 2). However, after Bonferroni corrections, pairwise differences
remained significant in abused bulimic women only.
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Figure 2. Means (and SEs) obtained at each
moment of the serial sampling for cortisol in nonabused bulimic, abused bulimic,
nonabused normal eater, and abused normal eater groups. Significant pairwise
differences between nonabused normal eaters and (A) abused bulimic women and
(B) abused women who were normal eaters at P<.05
on covariate-adjusted pairwise contrast; asterisk indicates corresponding
contrast differs atP<.05 after Bonferroni correction
for family-wise error. To convert cortisol levels from micrograms per deciliter
to nanomoles per liter, multiply by 27.59.
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COMMENT
This study shows intriguing patterns of association, in bulimic and
nonbulimic women, between childhood abuse, on the one hand, and eating pathology,
general psychopathology, and 5-HT and cortisol functioning, on the other.
Although we found no systematic association between childhood abuse and expression
of eating or affective or impulsive symptoms, we did note symptoms of PTSD
and self-destructiveness to be elevated in abused bulimic women compared with
levels obtained in other groups. This pattern links abuse (in at least the
presumably more vulnerable bulimic individuals in our sample) with symptoms
that are believed to sometimes represent posttraumatic sequelae.
On neurobiological indices, different findings were obtained on different
measures. We observed reduced platelet paroxetine binding (Bmax)
in bulimic women relative to that in nonbulimic women (with no apparent effects
due to childhood abuse). These findings replicate our previous finding in
40 bulimic women (16 of whom were in the present sample) of reduced platelet
[3H]-paroxetine binding.6 If paroxetine
binding models the central 5-HT transporter, then such findings would indicate
reduced 5-HT reuptake at central presynaptic sites. Regardless, our findings
link reduced paroxetine binding more strongly to BN than to developmental
abuse.
On prolactin, we obtained further evidence of abnormal 5-HT function
in BN (Figure 1), replicating well-known
tendencies for bulimic women to display smaller prolactin responses after m-CPP administration than nonbulimic women.7
Blunting of prolactin response after m-CPP administration
has been interpreted as indicating down-regulation of postsynaptic 5-HT receptors
on which m-CPP acts. Whether such findings reflect
"state" effects attributable to active BN (eg, due to sequelae of binge eating
on 5-HT mechanisms), "trait" effects related to some stable aspect of those
who develop BN, or some combination of the 2 remains unknown, however. Blunting
effects obtained in abused women who were normal eaters at some prolactin
sampling intervals are consistent with previous findings on prolactin after m-CPP administration in abused nonbulimic populations.2 Such findings would suggest that there may also be
an association between childhood abuse and reduced postsynaptic 5-HT activity.
However, further work is needed to clarify causal questions, since such effects
could constitute a simple correlate (vs consequence) of abuse. For example,
connection between 5-HT function and abuse could reflect association with
a trait (eg, impulsivity) that might be present in the abusive parent and
the vulnerable child, without implying a causal role of abuse.
Results on cortisol levels contrast with our other findings. Compared
with levels in nonabused women who were normal eaters, we obtained unequivocal
evidence of reduced plasma cortisol levels in abused bulimic women, weak evidence
of such reduction in abused women who were normal eaters, but no evidence
of such reduction in nonabused bulimic women (Figure 2). In other words, our data did not so much link decreased
cortisol levels with BN (as was the case for 5-HT indices such as prolactin
and paroxetine binding) as with abuse. Reduced cortisol activity has been
thought to represent an adaptation of the HPA axis to prolonged or particularly
intense stress.3, 4 From this perspective,
abnormally low cortisol values, especially evident in our abused bulimic patients,
could reflect a posttraumatic alteration of HPA axis function. Particularly
strong effects in the bulimic participants might be attributed to 1 (or both)
of the following. First, abused bulimic women more often reported a history
of PTSD (Table 2), perhaps indicating
that these participants underwent more intensely traumatic experiences than
did abused women who were normal eaters. Second, it may be that the same vulnerability
that rendered abused bulimic women susceptible to BN also rendered them vulnerable
to detrimental effects of abuse—manifested (at a neurobiologial level)
as cortisol alteration and (at a behavioral level) as PTSD symptoms. Although
we are unable to ascertain which of these explanations is correct, rated severities
of abuse did not differ significantly across abused bulimic and nonbulimic
women, and this argues in favor of an explanation couched in terms of susceptibility
to, rather than severity of, abuse. Regardless, it is striking to note effects,
in individuals who are on average in their mid-20s, of events that occurred
in childhood.
We note various limitations of our study. Our design did not include
measurement of serum estradiol levels and m-CPP concentrations
to ascertain hormonal and drug effects. It also lacked a placebo condition
by which to evaluate neuroendocrine responses under neutral circumstances.
Finally, without prospective measurements, we cannot interpret effects observed
as either consequences of active BN or stable "trait" antecedents. Regardless,
results obtained point to potentially important 5-HT and cortisol effects.
Direct and indirect effects of 5-HT and cortisol anomalies observed might
have various implications for affected individuals' stress tolerances, impulse
controls, capacities for mood regulation, and abilities to control eating
behavior (ie, to satiate). We therefore speculate that, here, we may be observing
neurobiological mediators of the link between developmental trauma and heightened
susceptibility to BN.
AUTHOR INFORMATION
Accepted for publication March 23, 2001.
This research was supported by grant 970917 from the Joint Program on
Mental Health Research of the Fonds de la Recherche en Santé du Québec,
Montreal, and the Conseil Québécois de la Recherche Sociale,
Quebec.
Preliminary findings from this study were presented at the International
Conference on Eating Disorders, New York, NY, May 5, 2000, and at the Annual
Meeting of the American Psychiatric Association, Chicago, Ill, May 17, 2000.
We are grateful to Kenneth R. Bruce, PhD, Marla Engelberg, BA, Cecile
Ladouceur, MSc, Philippe Lageix, MD, Sylvette Latouche, BA, Pascale Lehoux,
MA, Barbara Morse, MSc, Dunraj Ramdoyal, MSc, and Mira Thakur, MSc, for contributions
at various stages of this project.
From the Eating Disorders Program, Douglas Hospital, Verdun (Drs Steiger
and Israël and Ms Koerner); Department of Psychiatry, McGill University,
Montreal (Drs Steiger, Israël, Ng Ying Kin, Paris, and Young); Research
Centre, Douglas Hospital, Verdun (Drs Israël, Ng Ying Kin, Paris, and
Young); and Department of Social and Preventive Medicine and Groupe de Recherche
Interdisciplinaire en Santé (GRIS), University of Montreal, Montreal
(Dr Gauvin), Quebec.
Corresponding author and reprints: Howard Steiger, PhD, Eating Disorders
Program, Douglas Hospital, 6875 LaSalle Blvd, Verdun, Quebec, Canada H4H 1R3.
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