Exploring Patterns of Disturbed Eating in Psychosis: A Scoping Review.

Disturbed eating behaviours have been widely reported in psychotic disorders since the early 19th century. There is also evidence that antipsychotic (AP) treatment may induce binge eating or other related compulsive eating behaviours. It is therefore possible that abnormal eating patterns may contribute to the significant weight gain and other metabolic disturbances observed in patients with psychosis. In this scoping review, we aimed to explore the underlying psychopathological and neurobiological mechanisms of disrupted eating behaviours in psychosis spectrum disorders and the role of APs in this relationship. A systematic search identified 35 studies that met our eligibility criteria and were included in our qualitative synthesis. Synthesizing evidence from self-report questionnaires and food surveys, we found that patients with psychosis exhibit increased appetite and craving for fatty food, as well as increased caloric intake and snacking, which may be associated with increased disinhibition. Limited evidence from neuroimaging studies suggested that AP-naïve first episode patients exhibit similar neural processing of food to healthy controls, while chronic AP exposure may lead to decreased activity in satiety areas and increased activity in areas associated with reward anticipation. Overall, this review supports the notion that AP use can lead to disturbed eating patterns in patients, which may contribute to AP-induced weight gain. However, intrinsic illness-related effects on eating behaviors remain less well elucidated, and many confounding factors as well as variability in study designs limits interpretation of existing literature in this field and precludes firm conclusions from being made.

Amphetamine Dose-Dependently Decreases and Increases Binge Intake of Fat and Sucrose Independent of Sex.

OBJECTIVE: Amphetamine was formerly used as a treatment to combat obesity, but amphetamine's use as an appetite suppressant was discontinued because of its significant abuse potential. Most of the rewarding and reinforcing effects of amphetamine differ by sex, with females showing higher levels of drug intake and amphetamine-induced motivation, relapse, and locomotion, but it is unknown whether amphetamine's effects on feeding also differ by sex. Furthermore, previous research on the anorectic effects of amphetamine has been focused primarily on its effects on baseline homeostatic feeding, but it is unknown whether amphetamine also affects hedonic, reward-related feeding, which is an important factor driving the rise in obesity levels. METHODS: This study tested whether amphetamine alters food intake in a sex-dependent manner in two reward-related feeding paradigms: a sucrose two-bottle choice test and a high-fat/high-sugar binge intake model. RESULTS: Amphetamine altered food intake equally in males and females in both paradigms, with higher doses significantly inhibiting feeding and low doses of amphetamine increasing feeding at later time points. CONCLUSIONS: Amphetamine's effects on feeding and drug reward may be mediated by distinct mechanisms, which could allow for the development of new approaches to combat obesity with limited abuse and addiction-related side effects.

Nonmedical prescription stimulant use for suppressing appetite and controlling body weight is uniquely associated with more severe eating disorder symptomatology.

OBJECTIVE: Nonmedical prescription stimulant use (NPS; i.e., use without a prescription or in ways other than prescribed) to suppress appetite or control weight appears to be associated with eating disorder (ED) symptomatology among college students. However, it remains unknown if this relationship is motive-specific and uniquely related to ED symptomatology. This research examined whether engaging in NPS specifically for appetite/weight-related purposes is associated with ED symptomatology and a unique indicator of more severe symptomatology. METHOD: A nonclinical sample of college students (N = 668; 79% female) reported eating disorder symptoms via the Eating Pathology Symptoms Inventory and Eating Disorder Examination-Questionnaire, and lifetime history of NPS and corresponding motives. RESULTS: Binge eating, body dissatisfaction, negative attitudes towards obesity, restricting, purging, and cognitive restraint were reported more frequently by students who endorsed NPS for weight/appetite-related purposes than by those who used for other purposes or denied lifetime NPS. Additionally, NPS for appetite/weight-related purposes was uniquely associated with ED symptomatology after adjusting for gender, lifetime NPS, and past-month binge eating and purging. DISCUSSION: Engaging in NPS for appetite/weight-related purposes is a unique indicator of ED symptomatology, highlighting the need to query for this behavior among individuals with an ED. © 2016 Wiley Periodicals, Inc. (Int J Eat Disord 2016; 49:813-816).

Dietary-induced binge eating increases prefrontal cortex neural activation to restraint stress and increases binge food consumption following chronic guanfacine.

Binge eating is a prominent feature of bulimia nervosa and binge eating disorder. Stress or perceived stress is an often-cited reason for binge eating. One notion is that the neural pathways that overlap with stress reactivity and feeding behavior are altered by recurrent binge eating. Using young adult female rats in a dietary-induced binge eating model (30 min access to binge food with or without 24-h calorie restriction, twice a week, for 6 weeks) we measured the neural activation by c-Fos immunoreactivity to the binge food (vegetable shortening mixed with 10% sucrose) in bingeing and non-bingeing animals under acute stress (immobilization; 1 h) or no stress conditions. There was an increase in the number of immunopositive cells in the dorsal medial prefrontal cortex (mPFC) in stressed animals previously exposed to the binge eating feeding schedules. Because attention deficit hyperactive disorder (ADHD) medications target the mPFC and have some efficacy at reducing binge eating in clinical populations, we examined whether chronic (2 weeks; via IP osmotic mini-pumps) treatment with a selective alpha-2A adrenergic agonist (0.5 mg/kg/day), guanfacine, would reduce binge-like eating. In the binge group with only scheduled access to binge food (30 min; twice a week; 8 weeks), guanfacine increased total calories consumed during the 30-min access period from the 2-week pre-treatment baseline and increased binge food consumption compared with saline-treated animals. These experiments suggest that mPFC is differentially activated in response to an immobilization stress in animals under different dietary conditions and chronic guanfacine, at the dose tested, was ineffective at reducing binge-like eating.

Lesson of the month (1): cabergoline - 'i eat funny on that'.

We present the case of a patient treated for hyperprolactinaemia with weekly doses of cabergoline for 12 years. Over this time she had suffered from binge eating and compulsive shopping which impacted on her weight and made her finances precarious. We discuss the features of impulse control disorders and suggest that seeking out these side effects in patients taking such agents is important. The behaviours may be embarrassing and patients may not volunteer them, likewise if the doctor dismisses them they may continue unabated, causing significant social harm.

Common psychiatric disorders and caffeine use, tolerance, and withdrawal: an examination of shared genetic and environmental effects.

BACKGROUND: Previous studies examined caffeine use and caffeine dependence and risk for the symptoms, or diagnosis, of psychiatric disorders. The current study aimed to determine if generalized anxiety disorder (GAD), panic disorder, phobias, major depressive disorder (MDD), anorexia nervosa (AN), or bulimia nervosa (BN) shared common genetic or environmental factors with caffeine use, caffeine tolerance, or caffeine withdrawal. METHOD: Using 2,270 women from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders, bivariate Cholesky decomposition models were used to determine if any of the psychiatric disorders shared genetic or environmental factors with caffeine use phenotypes. RESULTS: GAD, phobias, and MDD shared genetic factors with caffeine use, with genetic correlations estimated to be 0.48, 0.25, and 0.38, respectively. Removal of the shared genetic and environmental parameter for phobias and caffeine use resulted in a significantly worse fitting model. MDD shared unique environmental factors (environmental correlation=0.23) with caffeine tolerance; the genetic correlation between AN and caffeine tolerance and BN and caffeine tolerance were 0.64 and 0.49, respectively. Removal of the genetic and environmental correlation parameters resulted in significantly worse fitting models for GAD, phobias, MDD, AN, and BN, which suggested that there was significant shared liability between each of these phenotypes and caffeine tolerance. GAD had modest genetic correlations with caffeine tolerance, 0.24, and caffeine withdrawal, 0.35. CONCLUSIONS: There was suggestive evidence of shared genetic and environmental liability between psychiatric disorders and caffeine phenotypes. This might inform us about the etiology of the comorbidity between these phenotypes.

Effects of CB1 and CRF1 receptor antagonists on binge-like eating in rats with limited access to a sweet fat diet: lack of withdrawal-like responses.

Positive reinforcement (e.g., appetitive, rewarding properties) has often been hypothesized to maintain excessive intake of palatable foods. Recently, rats receiving intermittent access to high sucrose diets showed binge-like intake with withdrawal-like signs upon cessation of access, suggesting negative reinforcement mechanisms contribute as well. Whether intermittent access to high fat diets also produces withdrawal-like syndromes is controversial. The present study therefore tested the hypothesis that binge-like eating and withdrawal-like anxiety would arise in a novel model of binge eating based on daily 10-min access to a sweet fat diet (35% fat kcal, 31% sucrose kcal). Within 2-3 weeks, female Wistar rats developed binge-like intake comparable to levels seen previously for high sucrose diets (~40% of daily caloric intake within 10 min) plus excess weight gain and adiposity, but absent increased anxiety-like behavior during elevated plus-maze or defensive withdrawal tests after diet withdrawal. Binge-like intake was unaffected by pretreatment with the corticotropin-releasing factor type 1 (CRF(1)) receptor antagonist R121919, and corticosterone responses to restraint stress did not differ between sweet-fat binge rats and chow-fed controls. In contrast, pretreatment with the cannabinoid type 1 (CB(1)) receptor antagonist SR147778 dose-dependently reduced binge-like intake, albeit less effectively than in ad lib chow or sweet fat controls. A priming dose of the sweet fat diet did not precipitate increased anxiety-like behavior, but rather increased plus-maze locomotor activity. The results suggest that CB(1)-dependent positive reinforcement rather than CRF(1)-dependent negative reinforcement mechanisms predominantly maintain excessive intake in this limited access model of sweet-fat diet binges.

Reinforcing efficacy of fat, as assessed by progressive ratio responding, depends upon availability not amount consumed.

Intermittent limited access to an optional source of dietary fat can induce binge-type behavior in rats. However, the ability of such access to alter the reinforcing efficacy of fat has not been clearly demonstrated. In this study, performance under progressive ratio one (PR1) and three (PR3) schedules of shortening (fat) reinforcement was assessed in non-food deprived rats (n=15/group). One group of rats had intermittent access to a dietary fat option (INT, 1-hour shortening access in the home cage each Monday, Wednesday, and Friday), whereas the other group had daily access to the fat option (D, 1-hour shortening access daily). Chow and water were continuously available. After five weeks, the INT group consumed more shortening during the 1-hour access period than did the D group. Rats were then trained to lever press for a solid shortening reinforcer (0.1 gm). INT rats earned significantly more reinforcers than did D rats under PR1, but not under PR3. Subgroups of INT and D rats (n=7 each) were matched on the amount of shortening consumed in the home cage during week five of the protocol and the PR data were reanalyzed. The INT subgroup earned significantly more reinforcers than the D subgroup did under PR1, but not PR3. These results demonstrate that: (1) intermittent access to shortening in the home cage, but not the amount consumed during the access period (i.e. bingeing), increases the reinforcing efficacy of solid shortening; and (2) the type of PR schedule is critical in delineating differences between the groups.

Sugar bingeing in rats.

Bingeing behavior is characteristic of many eating disorders. This unit describes an animal model of sugar bingeing. This model has been used successfully to elicit behavioral and neurochemical signs of sugar dependence in rats, e.g., indices of bingeing, withdrawal, increased intake after abstinence (deprivation effect), cross-sensitization with amphetamine, and increases in dopamine release in the nucleus accumbens due to repeated bingeing.

Stress and hunger alter the anorectic efficacy of fluoxetine in binge-eating rats with a history of caloric restriction.

OBJECTIVE: We examined the effect of fluoxetine to suppress binge eating in rats with a history of caloric restriction (CR) and the extent to which this effect was altered by stress and hunger. METHOD: To detect heightened sensitivity to fluoxetine, young female rats were used to determine a subthreshold anorectic dose (2 mg/kg, intraperitonally). Another group of rats was either fed ad libitum or given multiple CR (to 90% body weight) and refeeding-to-satiety cycles. One half of the rats were then either spared or subjected to foot shock stress before fluoxetine treatment. RESULTS: A history of CR alone produced bingelike eating on palatable food (p < .001) and, although stress did not affect intake, it rendered CR rats hypersensitive to the satiety effect of fluoxetine. The feeding-suppression was mainly for chow (p < .05) and the effect was abolished if the rats were in negative energy balance. DISCUSSION: Results support the utility of this animal model to elucidate serotonergic changes linking dieting to binge eating. The diverse effects of fluoxetine on the type of food, and in hungry versus sated rats, suggest alternate brain mechanisms should be concomitantly targeted for improved treatment of binge eating disorders.

Spectrum of binge eating symptomatology in patients treated with clozapine and olanzapine.

The authors explored the binge eating symptomatology in 74 patients receiving clozapine (N = 57) or olanzapine (N = 17), and compared body mass index (BMI, kg/m(2)) and weight gain in patients with and without binge eating symptomatology. Subjects who screened positively for binge eating were interviewed using a modified version of the Questionnaire on Eating and Weight Patterns (QEWP). Current BMIs were assessed cross-sectionally, BMIs at initiation of clozapine/olanzapine treatment retrospectively. Thirty-seven subjects (50%) screened positively. Taking clozapine and olanzapine together, 6/27 (22.2%) females and 3/47 (6.4%) males fulfilled criteria for binge eating disorder, 3/27 (11.1%) females and 2/47 (4.3%) males for bulimia nervosa. Patients who screened positively showed higher current BMIs (26.8 +/- 3.9 vs. 24.7 +/- 3.7 kg/m(2)) and higher BMI increments during clozapine/olanzapine treatment (3.9 +/- 3.1 vs. 2.6 +/- 3.4 kg/m(2)) than patients who screened negatively. We conclude that clozapine/olanzapine may induce binge eating and full blown eating disorders which may have predictive value for weight gain. For future research in this field we suggest a novel DSM-IV research classification "Medication-induced eating disorders".

Laxative misuse and behavioral disinhibition in bulimia nervosa.

OBJECTIVE: Various reports suggest that purging with laxatives is associated with greater behavioral impulsivity in bulimia nervosa (BN) patients. We investigated the extent to which laxative misuse corresponds to specific impulse-control problems. METHOD: Participants included bulimic women who misuse laxatives (BNL+; n = 12), bulimic women who do not misuse laxatives (BNL-; n = 33), and healthy normal eaters (NE; n = 26). Participants completed the Go/No-Go discrimination task (a well-validated computerized measure of response disinhibition), as well as self-report questionnaires of impulsivity, eating symptoms, and general psychopathology. RESULTS: Compared with the other groups, the BNL+ group made more commission errors on the Go/No-Go under cues for punishment, indicating they were more disinhibited when faced with possible negative outcomes. Compared with the BNL- group, the BNL+ group was also more likely to differ from the NE group on self-reported impulsivity. There were no differences between the two bulimic groups on eating symptoms and the three groups did not differ in terms of general psychopathology. DISCUSSION: Findings suggest that, controlling for eating symptoms and psychopathology, laxative misuse among BN patients is associated with difficulty inhibiting incorrect responses in the face of perceived threats.

Anorexia nervosa and steroid withdrawal.

We report a case of anorexia nervosa in a 14-year-old girl following withdrawal of oral prednisolone used in the treatment of asthma. The patient exhibited depressed affect and disturbance of body image prior to onset of anorexia. To the authors' knowledge this is the first report of anorexia nervosa precipitated by steroid withdrawal. The pathogenesis is discussed with reference to recent literature, considering both the physiological and psychological impact of steroid withdrawal.

An animal model of bulimia nervosa: opioid sensitivity to fasting episodes.

A group of female rats was deprived and maintained at 75-80% of body weight at three different times during development. Following recovery to normal weight, food intake was measured with and without butorphanol tartrate, a kappa-sigma agonist, 8 mg/kg SC. Animals with a history of deprivation (DEP) showed an increase in postrecovery feeding when they were tested at normal body weight and not food deprived. More importantly, butorphanol prolonged food intake in the 3-h eating test only in the rats with a developmental history of food restriction. A developmental history of fasting in eating disorders may trigger changes in opiate systems that result in atypical feeding behavior in the adult.