We examined prevalence of substance use disorders (SUD) in women with: (1) anorexia nervosa (AN) restricting type (RAN); (2) AN with purging only (PAN); (3) AN with binge eating only (BAN); and (4) lifetime AN and bulimia nervosa (ANBN). Secondary analyses examined SUD related to lifetime purging behavior and lifetime binge eating.
Participants (N = 731) were drawn from the International Price Foundation Genetic Studies.
The prevalence of SUD differed across AN subtypes, with more in the ANBN group reporting SUD than those in the RAN and PAN groups. Individuals who purged were more likely to report substance use than those who did not purge. Prevalence of SUD differed across lifetime binge eating status.
SUD are common in AN and are associated with bulimic symptomatology. Results underscore the heterogeneity in AN, highlighting the importance of screening for SUD across AN subtypes.
eating disorders; anorexia nervosa; bulimia nervosa; drug use; alcohol related disorders; cannabis
In spite of the role of some psychosomatic factors as alexithymia, mood intolerance, and somatization in both pathogenesis and maintenance of anorexia nervosa (AN), few studies have investigated the prevalence of psychosomatic syndromes in AN. The aim of this study was to use the Diagnostic Criteria for Psychosomatic Research (DCPR) to assess psychosomatic syndromes in AN and to evaluate if psychosomatic syndromes could identify subgroups of AN patients.
108 AN inpatients (76 AN restricting subtype, AN-R, and 32 AN binge-purging subtype, AN-BP) were consecutively recruited and psychosomatic syndromes were diagnosed with the Structured Interview for DCPR. Participants were asked to complete psychometric tests: Body Shape Questionnaire, Beck Depression Inventory, Eating Disorder Inventory–2, and Temperament and Character Inventory. Data were submitted to cluster analysis.
Illness denial (63%) and alexithymia (54.6%) resulted to be the most common syndromes in our sample. Cluster analysis identified three groups: moderate psychosomatic group (49%), somatization group (26%), and severe psychosomatic group (25%). The first group was mainly represented by AN-R patients reporting often only illness denial and alexithymia as DCPR syndromes. The second group showed more severe eating and depressive symptomatology and frequently DCPR syndromes of the somatization cluster. Thanatophobia DCPR syndrome was also represented in this group. The third group reported longer duration of illness and DCPR syndromes were highly represented; in particular, all patients were found to show the alexithymia DCPR syndrome.
These results highlight the need of a deep assessment of psychosomatic syndromes in AN. Psychosomatic syndromes correlated differently with both severity of eating symptomatology and duration of illness: therefore, DCPR could be effective to achieve tailored treatments.
Anorexia nervosa; Eating disorders; Psychosomatic syndromes; Illness denial; Alexithymia
The current study tested a psychosocial interactive model of perfectionism, self-efficacy, and weight/shape concern within a sample of women with clinically significant bulimic symptoms, examining how different dimensions of perfectionism operated in the model. Individuals with bulimia nervosa (full diagnostic criteria or subthreshold) completed measures of bulimic symptoms, multidimensional perfectionism, self-efficacy, and weight/shape concern. Among those who were actively binge eating (n = 180), weight/shape concern was associated with binge eating frequency in the context of high perfectionism (either maladaptive or adaptive) and low self-efficacy. Among those who were actively vomiting (n = 169), weight/shape concern was associated with vomiting frequency only in the context of high adaptive perfectionism and low self-efficacy. These findings provide support for the value of this psychosocial interactive model among actively binge eating and purging samples and for the importance of considering different dimensions of perfectionism in research and treatment related to bulimia nervosa.
Perfectionism; Self-efficacy; Body dissatisfaction; Binge eating; Vomiting
In a randomised controlled trial of different types of psychotherapy for bulimia 92 women were assigned to receive cognitive-behaviour therapy (n=32), behaviour therapy (30), or group therapy (30) for 15 weeks and a further 20 (controls) assigned to remain on a waiting list for 15 weeks. Eating behaviour and psychopathology were assessed by standard methods. At the end of the trial the controls had significantly higher scores than the treated groups on all measures of bulimic behaviour. In terms of behavioural change all three treatments were effective, 71 (77%) of the 92 women having stopped bingeing. In addition, scores on eating and depression questionnaires were reduced and self esteem improved. Follow up was continuing, but of 24 women available at one year, 21 were not bingeing and had maintained their improved scores on psychometric scales.
Bulimia nervosa is amenable to treatment by once weekly structured psychotherapy in either individual or group form.
Food intake is mediated, in part, through brain pathways for motivation and reinforcement. Dysregulation of these pathways may underlay some of the behaviors exhibited by patients with eating disorders. Research using animal models of eating disorders has greatly contributed to the detailed study of potential brain mechanisms that many underlie the causes or consequences of aberrant eating behaviors. This review focuses on neurochemical evidence of reward-related brain dysfunctions obtained through animal models of binge eating, bulimia nervosa, or anorexia nervosa. The findings suggest that alterations in dopamine (DA), acetylcholine (ACh) and opioid systems in reward-related brain areas occur in response to binge eating of palatable foods. Moreover, animal models of bulimia nervosa suggest that while bingeing on palatable food releases DA, purging attenuates the release of ACh that might otherwise signal satiety. Animal models of anorexia nervosa suggest that restricted access to food enhances the reinforcing effects of DA when the animal does eat. The activity-based anorexia model suggests alterations in mesolimbic DA and serotonin occur as a result of starvation coupled with excessive wheel running. These findings with animal models complement data obtained through neuroimaging and pharmacotherapy studies of clinical populations. Finally, information on the neurochemical consequences of the behaviors associated with these eating disorders will be useful in understanding these complex disorders and may inform future therapeutic approaches, as discussed here.
acetylcholine; binge eating; clinical studies; dopamine; eating disorders; opioids; rat; serotonin
Fibroblast growth factor (FGF) 23, a circulating 26-kDa peptide produced by osteogenic cells, is a novel phosphaturic factor. In our previous study, binge-eating/purging type anorexia nervosa (AN-BP) patients had elevated plasma intact FGF23 (iFGF23) levels, while restricting type (AN-R) patients had plasma iFGF23 levels similar to healthy controls. Although bulimia nervosa (BN) patients as well as some patients with AN-BP regularly engage in binge eating, there have been no studies regarding plasma iFGF23 levels in BN patients. Therefore, this study was performed to determine plasma iFGF23 concentrations in BN patients and healthy controls. The study population consisted of 13 female BN patients and 11 healthy female controls. Blood samples were collected from all subjects after overnight fasting. Plasma iFGF23 was measured using an ELISA kit in a cross-sectional manner. The two-tailed Mann-Whitney U-test was used to assess differences between BN patients and healthy controls. In addition, BN patients were divided into two groups based on questionnaire-reported binge eating frequency immediately prior to participation in this study: high frequency of binge eating (once a week or more; HF group; n = 8) and low frequency of binge eating (less than once a week; LF group; n = 5). Two-tailed Mann-Whitney U-test with Bonferroni's correction was performed after the Kruskal-Wallis test to assess differences between HF group, LF group, and healthy controls. Median (quartiles) plasma iFGF23 levels were greater in BN patients (35.5 [14.8-65.0] pg/ml) than in controls (3.8 [not detected-5.3] pg/ml; p = 0.002). In addition, median (quartiles) plasma iFGF23 levels were greater in the HF group (62.3 [44.4-73.4] pg/ml) than in controls (p < 0.001) and in the LF group (12.9 [not detected-30.3] pg/ml; p = 0.011), while there were no differences between the LF group and controls (p = 0.441). This is the first study to show that BN patients have elevated plasma iFGF23 levels. Moreover, this study showed that BN patients with a high frequency of binge eating have elevated plasma iFGF23 levels, while iFGF23 levels are similar to healthy controls in those with a low frequency of binge eating. Plasma iFGF23 level may be a suitable indicator of binge eating in BN patients.
fibroblast growth factor 23 (FGF23); intact fibroblast growth factor 23 (iFGF23); eating disorders; bulimia nervosa (BN); binge eating; frequency of binge eating; dietary phosphate; plasma phosphate; 1,25-dihydroxyvitamin D (1,25-(OH)2D)
No definitive therapy exists for anorexia nervosa (AN) or bulimia nervosa (BN). Nevertheless, biologic and psychologic research into these disorders has increased over the last decade. We examine the various drugs available for treatment. Advances in pharmacotherapy for AN have been modest and have reflected efforts either to stimulate hunger and weight gain or to control complications of the starvation process. Food remains the "drug" of choice. Antidepressants have been found to be beneficial in the treatment of BN. The meaning of this in the context of a relation between BN and mood disorders remains unclear, since coexistent depression does not predict a positive response to these drugs. Pharmacotherapy represents a single but important dimension of the management of patients with eating disorders. The optimal integration of drug therapy and psychotherapy and the identification of predictors of a positive response to drugs have yet to be addressed by clinical research.
A patient presented with severe hypophosphataemia that had been precipitated during binge eating. It was corrected by restricting the binges, and by hyperalimentation through a duodenal tube together with intravenous supplementation with sodium phosphate for a short period. Phosphate concentrations should be monitored in patients with severe anorexia complicated by bulimic episodes.
Despite a number of studies in the past decades, the role of Cholecystokinin (CCK) in anorexia nervosa (AN) has remained uncertain. In this study a highly specific assay for the biologically active part of CCK was used in patients with bulimic as well as with the restricting type of AN who were followed over the course of weight gain.
Ten patients with restricting and 13 with bulimic AN were investigated upon admission (T0), after a weight gain of at least 2 kg on two consecutive weighting dates (T1), and during the last week before discharge (T2) from inpatient treatment in a specialized clinic. Blood samples were drawn under fasting conditions and 20 and 60 minutes following a standard meal (250 kcal). Data were compared to those of eight controls matched for sex and age. Gastrointestinal complaints of patients were measured by a questionnaire at each of the follow-up time points.
At admission, AN patients exhibited CCK-levels similar to controls both prior to and after a test meal. Pre and post-meal CCK levels increased significantly after an initial weight gain but decreased again with further weight improvement. CCK release was somewhat lower in bulimic than in restricting type AN but both subgroups showed a similar profile. There was no significant association of CCK release to either initial weight or BMI, or their changes, but CCK levels at admission predicted gastrointestinal symptom improvement during therapy.
Normal CCK profiles in AN at admission indicates hormonal responses adapted to low food intake while change of eating habits and weight gain results in initially increased CCK release (counteracting the attempts to alter eating behavior) that returns towards normal levels with continuous therapy.
We present a rare case of abdominal compartment syndrome due to a bulimic attack in a 19-year-old female patient with bulimia nervosa. She was admitted to our emergency room with complaints of progressive abdominal pain following bulimia. Computed tomography showed dilated stomach with food and air pressed other visceral organs and major abdominal vessels. Decompression using nasogastric tube or gastric lavage tube failed. At laparotomy, we performed gastrotomy and decompression was performed. After decompression, she fell into hypovolemic shock due to bleeding in the intra-gastric and peritoneal cavity. Twelve hours after the operation, the patient died due to refractory hypovolemic shock from uncontrolled bleeding following decompression of abdominal compartment. It should keep in mind that binge-eating habits in patients with bulimic nervosa could cause abdominal compartment syndrome due to gastric distension and this may be a potentially fatal condition.
Compartment syndromes; Bulimia; Reperfusion injury
The purpose of this study was to determine if early response predicted remission at the end of a controlled trial.
80 adolescents with bulimia nervosa participated in an RCT comparing family-based treatment and individual supportive psychotherapy. Response to treatment was assessed via self-report of bingeing and purging. Remission was defined as abstinence from bingeing and purging for the last 28 days and measured by investigator-based interview, i.e., the Eating Disorder Examination.
Receiver operating characteristic analyses showed that, regardless of treatment, symptom reduction at session 6 predicted remission at post-treatment (AUC = .814 (p<.001)) and 6-month follow-up (AUC = .811 (p<.001)).
Results suggest that adolescents with BN who do not show early reductions in bulimic symptoms are unlikely to remit at post-treatment or follow-up.
adolescent bulimia nervosa; psychotherapy; early treatment response; receiver operating characteristics curves
Prospectively investigate whether weight gain or weight loss increases risk for onset of binge eating and purging in adolescent women.
Diagnostic interviews and direct measures of body mass were completed by 496 adolescent women annually for eight years.
Substantial weight gain or weight loss during the study produced a 7-fold increase in risk for future onset of threshold or subthreshold bulimia nervosa (BN) relative to weight-stable participants, though the low incidence rate limited statistical power. Those who showed onset of threshold/subthreshold BN experienced greater increases in weight in the two years before onset of their eating disorder relative to healthy comparison participants.
This is the first prospective study to demonstrate that weight gain and weight loss may both increase risk for future onset of bulimic pathology. Results suggest that young women who have difficulty limiting their dietary intake are at increased risk for BN, an eating disorder characterized by loss of control over eating.
The purpose of this investigation was to examine differences in personality dimensions among individuals with bulimia nervosa, binge eating disorder, non-binge eating obesity and a normal weight comparison group as well as to determine the extent to which these differences were independent of self-reported depressive symptoms.
Personality dimensions were assessed using the Multidimensional Personality Questionnaire in 36 patients with bulimia nervosa, 54 patients with binge eating disorder, 30 obese individuals who did not binge eat, and 77 normal weight comparison participants.
Participants with bulimia nervosa reported higher scores on measures of stress reaction and negative emotionality compared to the other three groups, and lower well-being scores compared to the normal weight comparison and the obese samples. Patients with binge eating disorder scored lower on well-being and higher on harm avoidance than the normal weight comparison group. In addition, the bulimia nervosa and binge eating disorder groups scored lower than the normal weight group on positive emotionality. When personality dimensions were re-analyzed using depression as a covariate, only stress reaction remained higher in the bulimia nervosa group compared to the other three groups and harm avoidance remained higher in the binge eating disorder than the normal weight comparison group.
The higher levels of stress reaction in the bulimia nervosa sample and harm avoidance in the binge eating disorder sample after controlling for depression indicate that these personality dimensions are potentially important in the etiology, maintenance, and treatment of these eating disorders. Although the extent to which observed group differences in well-being, positive emotionality and negative emotionality reflect personality traits, mood disorders, or both is unclear, these features clearly warrant further examination in understanding and treating bulimia nervosa and binge eating disorder.
The purpose of this study was to examine the relationship between caloric restriction (CR) and binge eating (BE) using ecological momentary assessment (EMA). Participants included 133 women with bulimia nervosa (BN) who completed an EMA protocol for 2 weeks. Logistic regression analyses tested whether CR increased the probability of BE episodes. The results revealed that the odds of BE increased on the day that restriction occurred as well as on the following day. In addition, both restriction and BE on one day predicted the likelihood of BE the subsequent day, but restriction for two days prior to the episode failed to add additional information for predicting BE. These findings support the cognitive-behavioral therapy (CBT) model of BN, suggesting that self-reported dietary restriction is predictive of subsequent BE episodes, and that reducing dietary restriction in treatment may lead to improvements in bulimic symptoms.
ecological momentary assessment; bulimia nervosa; binge eating; caloric restriction
Previous studies showed that symptoms of oesophageal motor disorders can be misinterpreted as indicating anorexia nervosa and that in primary anorexia nervosa gastric motility is frequently impaired. We investigated in 32 women with bulimia nervosa whether symptoms of oesophageal motor disorders could be obscured by or be mistaken as forming part of bulimic behaviour, and whether impaired gastric motility was frequent as well. Oesophageal motility was normal in 18 of 26 patients studied, another four had incomplete lower oesophageal sphincter relaxation. Two patients had vigorous achalasia and each one achalasia and diffuse oesophageal spasm, all of whom experienced two types of vomiting: one self-induced and one involuntary, in which the vomit was non-acidic and tasted as the preceding meal. Gastric emptying of a semisolid meal was studied in all patients except of the eight with oesophageal motor abnormalities. Emptying was significantly slower than in healthy controls and grossly delayed in nine of 24 patients. Antral contraction amplitudes were lower and increased less postcibally than in controls. In conclusion (i) bulimic behaviour can obscure symptoms of oesophageal motor disorders and (ii) gastric emptying is frequently delayed in bulimia nervosa.
This case report details the therapeutic effects of tandospirone on two patients with anorexia nervosa, one with the restricting subtype (ANR), and another with the binge-eating/purging subtype (ANBP). A 22-year-old female patient with ANR and a 23-year-old female patient with ANBP were treated successfully with the 5-HT1A partial agonist tandospirone. After treatment, not only did both patients gain weight, they also showed improved scores on the Eating Disorder Examination Questionnaire. In addition, a 6-month follow-up showed maintenance of these effects. In this disorder, tandospirone may be an effective drug for long-term use with good patient compliance.
Anorexia nervosa; Pharmacotherapy; Treatment; Serotonin 1A receptor; Tandospirone
Disordered eating behavior and body dissatisfaction affect a large proportion of the Dutch population and account for severe psychological, physical and social morbidity. Yet, the threshold for seeking professional care is still high. In the Netherlands, only 7.5% of patients with bulimia nervosa and 33% of patients with anorexia nervosa are treated within the mental health care system. Easily accessible and low-threshold interventions, therefore, are needed urgently. The internet has great potential to offer such interventions. The aim of this study is to determine whether a web-based treatment program for patients with eating disorders can improve eating disorder psychopathology among female patients with bulimia nervosa, binge eating disorder and eating disorders not otherwise specified.
This randomized controlled trial will compare the outcomes of an experimental treatment group to a waiting list control group. In the web-based treatment program, participants will communicate personally and asynchronously with their therapists exclusively via the internet. The first part of the program will focus on analyzing eating attitudes and behaviors. In the second part of the program participants will learn how to change their attitudes and behaviors. Participants assigned to the waiting list control group will receive no-reply email messages once every two weeks during the waiting period of 15 weeks, after which they can start the program. The primary outcome measure is an improvement in eating disorder psychopathology as determined by the Eating Disorder Examination Questionnaire. Secondary outcomes include improvements in body image, physical and mental health, body weight, self-esteem, quality of life, and social contacts. In addition, the participants’ motivation for treatment and their acceptability of the program and the therapeutic alliance will be measured. The study will follow the recommendations in the CONSORT statement relating to designing and reporting on RCTs.
This study protocol presents the design of a RCT for evaluating the effectiveness of a web-based treatment program using intensive therapeutic support for female patients with bulimia nervosa, binge eating disorder and eating disorders not otherwise specified.
The protocol for this study is registered with the Netherlands Trial Registry NTR2415.
Eating disorders; Bulimia nervosa; Binge eating disorder; Eating disorders not otherwise specified; Randomized controlled trial; Web-based treatment program; e-health; Intensive therapeutic support; Asynchronous support
Elucidation of clinically relevant subtypes has been proposed as a means of advancing treatment research, but classifying anorexia nervosa (AN) patients into restricting and binge-eating/purging types has demonstrated limited predictive validity. This study aimed to evaluate whether an approach to classifying eating disorder patients based on comorbid personality psychopathology has utility in predicting treatment response and readmission in patients with AN.
Data were collected from 154 AN patients (M[SD] age = 25.6[9.4] years; 95.5% female; 96.8% Caucasian) at admission, discharge, and three months post-discharge from intensive treatment. Latent profile analysis of personality traits assessed at admission was performed to classify participants into personality subtypes, which were then used to predict outcomes at discharge and risk of readmission.
The best-fitting model identified three personality subtypes (undercontrolled, overcontrolled, low psychopathology) that contributed significantly to multivariate models predicting study outcomes. Undercontrolled patients were more likely to have a poor outcome at discharge than overcontrolled (OR = 3.56, p = .01) and low psychopathology patients (OR = 11.23, p <.001). Undercontrolled patients also had a greater risk of discharge against medical advice (HR = 2.08, p = .02) and readmission than overcontrolled patients (HR = 3.76, p = .009). Binge-eating/purging versus restricting subtypes did not predict discharge against medical advice or readmission in the multivariate models.
Findings support the clinical utility of personality subtypes in AN. Future work is needed to identify mechanisms that explain diminished treatment response in undercontrolled patients and to develop interventions for this high-risk group.
anorexia nervosa; subtypes; personality; latent profile analysis; treatment
Fibroblast growth factor (FGF)23 is a novel phosphaturic factor associated with inorganic phosphate homeostasis. Previous human studies have shown that serum FGF23 levels increase in response to a high phosphate diet. For anorexia nervosa (AN) patients, inorganic phosphate homeostasis is important in the clinical course, such as in refeeding syndrome. The purpose of this study was to determine plasma levels of intact FGF23 (iFGF23) in restricting-type AN (AN-R) patients, binge-eating/purging-type AN (AN-BP) patients, and healthy controls.
The subjects consisted of 6 female AN-R patients, 6 female AN-BP patients, and 11 healthy female controls; both inpatients and outpatients were included. Plasma iFGF23, 1,25-dihydroxyvitamin D (1,25-(OH)2D), and 25-hydroxyvitamin D (25-OHD) levels were measured. Data are presented as the median and the range. A two-tailed Mann-Whitney U-test with Bonferroni correction was used to assess differences among the three groups, and a value of p < 0.017 was considered statistically significant.
There were no differences between AN-R patients and controls in the iFGF23 and 1,25-(OH)2D levels. In AN-BP patients, the iFGF23 level (41.3 pg/ml; range, 6.1–155.5 pg/ml) was significantly higher than in controls (3.8 pg/ml; range, not detected-21.3 pg/ml; p = 0.001), and the 1,25-(OH)2D was significantly lower in AN-BP patients (7.0 pg/ml; range, 4.2–33.7 pg/ml) than in controls (39.7 pg/ml; range, 6.3–58.5 pg/ml; p = 0.015). No differences in plasma 25-OHD levels were observed among the groups.
This preliminary study is the first to show that plasma iFGF23 levels are increased in AN-BP patients, and that these elevated plasma FGF23 levels might be related to the decrease in plasma 1,25-(OH)2D levels.
Extremely low body mass index (BMI) values are associated with increased risk for death and poor long-term prognosis in individuals with AN. The present study explores childhood personality characteristics that could be associated with the ability to attain an extremely low BMI.
Participants were 326 women from the Genetics of Anorexia Nervosa (GAN) Study who completed the Structured Interview for Anorexia Nervosa and Bulimic Syndromes and whose mother completed the Child Behavioral Check List and/or Revised Dimensions of Temperament Survey.
Children who were described as having greater fear or anxiety by their mothers attained lower BMIs during AN (p <0.02). Path analysis in the GAN and a validation sample, Price Foundation Anorexia Nervosa Trios Study, confirmed the relation between early childhood anxiety, caloric restriction, qualitative food item restriction, excessive exercise, and low BMI. Path analysis also confirmed a relation between childhood anxiety and caloric restriction, which mediated the relation between childhood anxiety and low BMI in the GAN sample only.
Fearful or anxious behavior as a child was associated with the attainment of low BMI in AN and childhood anxiety was associated with caloric restriction. Measures of anxiety and factors associated with anxiety-proneness in childhood may index children at risk for restrictive behaviors and extremely low BMIs in AN.
Anorexia Nervosa; Anxiety; Body Mass Index
The aim of our study was to determine the central and peripheral autonomic nervous system profiles underlying anorexia nervosa (AN) syndrome, given that affected patients present with the opposite clinical profile to that seen in the hyperinsulinism syndrome.
We measured blood pressure and heart rate, as well as circulating neurotransmitters (noradrenaline, adrenaline, dopamine, plasma serotonin, and platelet serotonin), using high-performance liquid chromatography with electrochemical detection, during supine resting, one minute of orthostasis, and after five minutes of exercise. In total, 22 AN patients (12 binge-eating/purging type and 10 restricting type) and age-, gender-, and race-matched controls (70 ± 10.1% versus 98 ± 3.0% of ideal body weight) were recruited.
We found that patients with AN had adrenal sympathetic overactivity and neural sympathetic underactivity, demonstrated by a predominance of circulating adrenaline over noradrenaline levels, not only during the supine resting state (52 ± 2 versus 29 ± 1 pg/mL) but also during orthostasis (67 ± 3 versus 32 ± 2 pg/mL, P < 0.05) and after exercise challenge (84 ± 4 versus 30 ± 3 pg/mL, P < 0.01).
Considering that this peripheral autonomic nervous system disorder depends on the absolute predominance of adrenomedullary C1 adrenergic nuclei over A5 noradrenergic pontine nucleus, let us ratify the abovementioned findings. The AN syndrome depends on the predominance of overwhelming adrenal sympathetic activity over neural sympathetic activity. This combined central and autonomic nervous system profile contrasts with that registered in patients affected by hyperinsulinism, hypoglycemia, and bulimia syndrome which depends on the absolute predominance of neural sympathetic activity.
anorexia nervosa; adrenal sympathetic activity; adrenaline; noradrenaline; eating disorders
Anorexia nervosa (AN) and bulimia nervosa (BN) are marked by longitudinal symptom fluctuations. DSM-IV-TR does not address how to classify eating disorder (ED) presentations in individuals who no longer meet full criteria for these disorders. To consider this issue, we examined subthreshold presentations in women with initial diagnoses of AN and BN.
A total of 246 women with AN or BN were followed for a median of 9 years; weekly symptom data were collected at frequent intervals using the Longitudinal Interval Follow-up Evaluation of Eating Disorders (LIFE-EAT-II). Outcomes were ED presentations that were subthreshold for ≥3 months, including those narrowly missing full criteria for AN or BN, along with binge eating disorder (BED) and purging disorder.
During follow-up, most women (77.6%) experienced a subthreshold presentation. Subthreshold presentation was related to intake diagnosis (Wald χ2 = 8.065, df = 2, p = 0.018). Individuals with AN most often developed subthreshold presentations resembling AN; those with BN were more likely to develop subthreshold BN. Purging disorder was experienced by half of those with BN and one-quarter of those with AN binge/purge type (ANBP); BED occurred in 20% with BN. Transition from AN or BN to most subthreshold types was associated with improved psychosocial functioning (p < 0.001).
Subthreshold presentations in women with lifetime AN and BN were common, resembled the initial diagnosis, and were associated with modest improvements in psychosocial functioning. For most with lifetime AN and BN, subthreshold presentations seem to represent part of the course of illness and to fit within the original AN or BN diagnosis.
Anorexia nervosa; bulimia nervosa; classification; eating disorder not otherwise specified; longitudinal
Acute gastric dilatation is a rare complication of anorexia nervosa binge/purge subtype that results from gastrointestinal abnormalities, including decreased gastric motility and delayed gastric emptying. Early diagnosis and intervention is critical since delay may result in gastric necrosis, perforation, shock, and death. We report a 26-year-old female with anorexia nervosa binge/purge subtype, who presented with abdominal pain and nausea after a binge episode. Abdominal radiography and computed tomography showed a grossly dilated stomach measuring 32 cm × 17.9 cm consistent with acute gastric dilatation. She underwent exploratory laparotomy with gastrotomy and gastric decompression, and recovered uneventfully. Initially, the patient denied the binge episode, as many patients with eating disorders do, but later revealed an extensive history of anorexia nervosa binge/purge subtype. This case stresses the importance of obtaining a thorough history of eating disorders and maintaining a high index of suspicion for acute gastric dilatation in young women who present with abdominal pain and distention.
Acute gastric dilatation; anorexia; binge/purge; denial; eating disorder; gastric dysmotility
Anorexia nervosa (AN) is associated with behavioral traits that predate the onset of AN and persist after recovery. We identified patterns of behavioral traits in AN trios (proband plus two biological parents).
A total of 433 complete trios were collected in the Price Foundation Genetic Study of AN using standardized instruments for eating disorder (ED) symptoms, anxiety, perfectionism, and temperament. We used latent profile analysis and ANOVA to identify and validate patterns of behavioral traits.
We distinguished three classes with medium to large effect sizes by mothers’ and probands’ drive for thinness, body dissatisfaction, perfectionism, neuroticism, trait anxiety, and harm avoidance. Fathers did not differ significantly across classes. Classes were distinguished by degree of symptomatology rather than qualitative differences. Class 1 (~33 %) comprised low symptom probands and mothers with scores in the healthy range. Class 2 (~43 %) included probands with marked elevations in drive for thinness, body dissatisfaction, neuroticism, trait anxiety, and harm avoidance and mothers with mild anxious/perfectionistic traits. Class 3 (~24 %) included probands and mothers with elevations on ED and anxious/perfectionistic traits. Mother–daughter symptom severity was related in classes 1 and 3 only. Trio profiles did not differ significantly by proband clinical status or subtype.
A key finding is the importance of mother and daughter traits in the identification of temperament and personality patterns in families affected by AN. Mother–daughter pairs with severe ED and anxious/perfectionistic traits may represent a more homogeneous and familial variant of AN that could be of value in genetic studies.
Anorexia nervosa; eating disorder; genetics; temperament
We have demonstrated that anorexia nervosa is underpinned by overwhelming adrenal sympathetic activity which abolishes the neural sympathetic branch of the peripheral autonomic nervous system. This physiological disorder is responsible for gastrointestinal hypomotility, hyperglycemia, raised systolic blood pressure, raised heart rate, and other neuroendocrine disorders. Therefore, we prescribed neuropharmacological therapy to reverse this central and autonomic nervous system disorder, in order to normalize the clinical and neuroendocrine profile.
The study included 22 female patients with anorexia nervosa (10 restricted type, 12 binge-eating type) who received three months of treatment with amantadine 100 mg/day. We measured blood pressure, heart rate, and circulating neurotransmitters, (noradrenaline, adrenaline, dopamine, platelet serotonin, free plasma serotonin) during supine resting, one minute of orthostasis, and a five-minute exercise test before and after one, two, and three months of treatment with amantadine, a drug which abrogates adrenal sympathetic activity by acting at the C1(Ad) medullary nuclei responsible for this branch of the peripheral sympathetic activity.
We found the amantadine abolished symptoms of anorexia nervosa from the first oral dose onwards. Normalization of autonomic and cardiovascular parameters was demonstrated within the early days of therapy. Abrupt and sustained increases in the plasma noradrenaline:adrenaline ratio and disappearance of abnormal plasma glucose elevation were registered throughout the three-month duration of the trial. Significant and sustained increases in body weight were documented in all cases. No relapses were observed.
We have confirmed our previously published findings showing that the anorexia nervosa syndrome depends on the hypomotility of the gastrointestinal tract plus hyperglycemia, both of which are triggered by adrenal sympathetic hyperactivity. The above neuroendocrine plus neuroautonomic and clinical disorders which underpinned anorexia nervosa were abruptly suppressed since the first oral dose of amantadine, a drug able to revert the C1(Ad) over A5(NA) pontomedullary predominance responsible for adrenal and neural sympathetic activity, respectively.
amantadine; anorexia nervosa; adrenal sympathetic activity; hyperglycemia; hyperinsulinism; neural sympathetic activity