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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 non bulimic 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) (t 54 = - 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), non abused bulimic women (5. 62 3. 95), and abused women who were normal eaters (5. 73 5. 19) compared with non abused women who were normal eaters (13. 57 9. 94) (F 3, 51 = 3. 04, P = . 04). Furthermore, individuals reporting childhood abuse showed decreased plasma cortisol levels relative to non abused 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. 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 ([ 3 H]-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 [ 3 H]-paroxetine, 6 and blunted prolactin responses to m-CPP. 7 Suggesting altered cortisol function, one study 8 links atypical depression (ie, with hyperphagia and hyper somnolence) in BN to reduced plasma cortisol; another 9 links BN, in general, to decreased nocturnal and post glucose 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, 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-IV 13 criteria for BN purging subtype, 5 (14 %) for BN non purging 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 non student proportions among bulimic women), were aged 18 to 40 years, had relatively normal Bmi's 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 non bulimic differences on age or BMI. ASSESSMENTS To assess ED symptoms, we used the Eating Disorders Examination 12 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 (DIS 4), 15, 16 a DSM-IV version of the National Institute of Mental Health Diagnostic Interview Schedule, 17 and the well-validated 18 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. Integrated checks on 12 pseudo randomly selected interview pairs yielded 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 suicidal ity.
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 non bulimic 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 "non contact" experiences, such as being made to observe an adult masturbate, or lesser "contact" experiences, such as being held in a serialized 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 serialized way" or "pushed, but not pushed down") indicated abuse too ambiguously. Given a bilingual sample, we used official French versions of scales (DIS 4, 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 -HT 2 c 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 [ 3 H]-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 non bulimic 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. 052. 26, respectively).
Groups were compared on eating and psychopathological symptoms using ANOVAs, with Newman-Kelly 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 non abused bulimic women only. Depending on frequencies obtained, childhood abuse and psychiatric comorbidity indices were analyzed using &# 61539; 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 (Anovas; 4 9) to test for group effects on serial prolactin and cortisol indices. Anovas 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 binding 29 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...
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