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Persistence of binge-eating patterns after a history of restriction with intermittent bouts of refeeding on palatable food in rats: Implications for bulimia nervosa
Abstract
To test the hypothesis that experience with food restriction produces persistent binge eating. The Minnesota semistarvation experiment and studies of prisoners-of-war show that chronic food restriction produces dramatic changes in eating behavior (including binge eating) that endure decades after restriction has ceased. Bulimia nervosa patients who restrict also binge. Restriction may be a risk factor in the etiology of binge eating and bulimia.
Animals were subjected to four different patterns of 12-week restriction-refeeding cycles. The rats were either food restricted (dieting) or not restricted and refed regular or palatable food (binging).
Thirty days after normalization (full feeding, no restriction cycling), rats with a history of cycles of restriction and hyperphagia continued to exhibit persistent binge eating. This effect was shown particularly with palatable food, in stated conditions, and in response to acute 24-hr deprivation.
Results from this animal model implicate restriction and overeating on palatable food as biological determinants of binge-eating behaviors, including bulimia nervosa.
... The causal relationship between previous experience with food restriction and subsequent change in food-related behaviors, such as choice and meal size, is well documented in the animal literature [21][22][23][24][25]. Food restriction in humans, whether voluntary as when dieting or compelled during starvation as a consequence of famine or war [26], can lead to compulsive overeating or binge eating that endures for years after the experience. ...
... The causal relationship between previous experience with food restriction and subsequent change in food-related behaviors, such as choice and meal size, is well documented in the animal literature [21][22][23][24][25]. Food restriction in humans, whether voluntary as when dieting or compelled during starvation as a consequence of famine or war [26], can lead to compulsive overeating or binge eating that endures for years after the experience. Subsequently, a study in rats demonstrated that persistent patterns of binge eating can be triggered by several brief episodes of compensatory overeating (i.e., binge-eating) during prolonged experience with food restriction [24]. Consumption of a highly preferred food (i.e., cookies) during binge periods further intensified the hyperphagic effects. ...
... In their study with rats mimicking binge-eating patterns of bulimic patients, Hagan and Moss [24] presented preliminary evidence that the resulting hyperphagia appeared to be linked to impaired control of food intake by disrupted sensory-specific satiety. Accordingly, we hypothesize that rats exposed to repeated food restriction-binge cycles will display decreased sensory-specific satiety in a formal test of this phenomenon. ...
The relationship between food restriction and subsequent dysregulation of food intake is complex, variable and long-lasting. The present study investigated in rats whether repeated cycles of food restriction and binge feeding opportunities may alter regulation of food intake by employing a test for sensory-specific satiety. Rats that experienced repeated food restriction-binge cycles maintained heavier body weights compared to rats that remained on continuous food restriction. In contrast to the control subjects, rats that alternated between food restriction and binge feeding failed to display sensory-specific satiety. During the first meal, there was a gradual decrease in the amount of food intake over a 40 min period. When presented with a second meal of the same food, these rats responded to the familiar food in a manner similar as to a novel food (i.e., comparable quantities of both types of food were consumed). Food restriction-binge feeding cycles may be considered as a form of stress, which in turn is associated with cross-sensitization to numerous behavioral responses. Therefore, we propose that stress-induced disruption of sensory-specific satiety reflects a sensitized response to food, in which the interaction between sensory and satiety factors are no longer the key regulators of food choice and meal cessation. Furthermore, a role for sensory-specific satiety in terminating food intake appeared to decline with the progression of the cycles, thereby contributing to a steady increase in body weight of rats that experienced restriction with bouts of binge feeding opportunities.
... In recent years, preclinical research has focused on the development of animal models that can mimic the maladaptive patterns of food intake observed in certain forms of disordered eating. A widely accepted approach to induce overeating is to provide intermittent access to highly palatable diets in free-fed experimental animals (Hagan and Moss, 1997;Avena et al, 2006;Cifani et al, 2009;Cottone et al, 2009b;Corwin et al, 2011;Parylak et al, 2012;Velazquez-Sanchez et al, 2014). This strategy allows the development of excessive intake of highly palatable food as well as undereating of safer alternatives. ...
... In summary, we have shown the consummatory and emotional effects of a shortened diet alternation procedure in female rats. The procedure described here in female rats has the advantage of being considerably faster than previously established protocols of palatable diet alternation (Hagan et al, 1997;Cifani et al, 2009;Cottone et al, 2009b;Rossetti et al, 2013). In addition, our results show that withdrawal from alternating access to the palatable diet makes individuals vulnerable to the anxiogenic effects of rimonabant. ...
The prevalence of eating disorders and obesity in western societies is epidemic and increasing in severity. Preclinical research has focused on the development of animal models that can mimic the maladaptive patterns of food intake observed in certain forms of eating disorders and obesity. This study was aimed at characterizing a recently established model of palatable diet alternation in female rats. For this purpose, females rats were fed either continuously with a regular chow diet (Chow/Chow) or intermittently with a regular chow diet for 2 days and a palatable, high-sucrose diet for 1 day (Chow/Palatable). Following diet cycling, rats were administered rimonabant (0, 0.3, 1, 3 mg/kg intraperitoneally) during access to either palatable diet or chow diet and were assessed for food intake and body weight. Finally, rats were pretreated with rimonabant (0, 3 mg/kg, intraperitoneally) and tested in the elevated plus maze during withdrawal from the palatable diet. Female rats with alternating access to palatable food cycled their intake, overeating during access to the palatable diet and undereating upon returning to the regular chow diet. Rimonabant treatment resulted in increased chow hypophagia and anxiety-like behavior in Chow/Palatable rats. No effect of drug treatment was observed on the compulsive eating of palatable food in the diet-cycled rats. The results of this study suggest that withdrawal from alternating access to the palatable diet makes individuals vulnerable to the anxiogenic effects of rimonabant and provides etiological factors potentially responsible for the emergence of severe psychiatric side-effects following rimonabant treatment in obese patients.
... The long-term effects of diet cycling in rodents are also unclear. Again, some studies have found that cycling between low-and highcalorie diets results in binge-eating when the animals are shifted to the high calorie diet, as well as increased weight, fat intake, and ghrelin levels, relative to continuous access to a high-calorie diet [13][14][15][16]. Other studies have reported that a history of diet cycling and the accompanying changes in body weight do not lead to obesity, decreased lifespan, changes in metabolic rate, or chronically elevated blood pressure [14,[17][18][19][20]. ...
... In addition, results in the present cycled rats support past work showing that switching between a low-and high-calorie diet may increase the probability of future overeating. For example, Hagan and Moss allowed rats four days of restricted access to chow followed by two days of unlimited access to palatable cookies [15]. Following 12 such cycles, rats were then fed chow alone for 44 days, and tested with cookies. ...
... . Algunos de los cambios que se han identificado en los patrones de consumo de agua o comida bajo estas condiciones han sido reportados como el binge eating o gran comilona en el primer día de acceso al alimento o al agua después de la privación de alimento o agua (Corwin& Buda-Levin, 2004;Hagan & Moss, 1997) ...
... . Diversos estudios también han mostrado los efectos de la modificación del patrón alimentario aumentando el consumo de alimento posterior a la restricción de comida (Hagan & Moss, 1997;López-Espinoza & Martínez, 2001, 2005Dimitriou, Rice, & Corwin, 2000;Linseman & Harding, 1989;López-Espinoza & Martínez, 2001, 2005Sclafani & Gorman, 1977) o el consumode alcohol (Soderpalm & Hansen, 1999Soderpalm & Hansen, 1999).Linseman & Harding, 1989;} Soderpalm & Hansen, 1999Tabla 2), Caton, & Hetherington, 2003). Richter (1926Egli, 2003;Yeomans, 2004;Yeomans et al.,2003). ...
Different methods were explored to induce alcohol intake in rats and subsequent cycles of food deprivation on the consumption of alcohol, food, water, and body weight when alcohol was available. Rats were assigned to four groups and a different procedure to induce alcohol intake was used over 12 days a) gradual forced alcohol (4% -10% v / v); b) forced alcohol (10% v / v /); c) water and alcohol (6% - 10% v / v) only during the induction period; or, d) water and alcohol (6% - 10% v / v) throughout the experiment. After the induction period all groups of rats had free access to food and alcohol for ten subsequent days, followed by two alternating cycles of three days of total food restriction and then ten days of free access to food. After the induction period, alcohol (10% v / v) always was available for all groups. Body weight, food and fluid intake were recorded daily. The induction procedures had differential effects on body weight and alcohol intake. For the rats that had water and alcohol available throughout the experiment, food intake increased and alcohol intake decreased during the days in which food was freely available. A “self-imposed” water deprivation was observed for this group during the food restriction period, and binge drinking occurred when food was available again. The interaction between eating, drinking and body weight under conditions of food restriction and alcohol availability is discussed. © 2013, Sociedad Mexicana de Analisis de la Conducta. All rights reserved.
... Animal models of binge-like eating in humans show that intermittent feeding causes a range of abnormalities in consummatory behavior. For example, repeated cycles of restriction and refeeding of maintenance chow promote binge-like eating that persists after the cessation of restriction-refeeding cycles (Hagan & Moss, 1997) and, moreover, binge-eating prone rats subjected to restriction-refeeding cycles of chow and palatable food are more likely to tolerate foot-shock in order to gain access to palatable foods than non-cycled rats (Oswald, Murdaugh, King, & Boggiano, 2011). Sensory-specific satiety is also disrupted following bingelike feeding in rats (Ahn & Phillips, 2012). ...
... Following instrumental training, rats were allocated to either an Intermittent group (n ¼ 23) or a Control group (n ¼ 23). Similar to previous studies (Ahn & Phillips, 2012;Hagan & Moss, 1997;Oswald et al., 2011), rats in group Intermittent received four days of restricted access (10 g per day) to their home-cage chow followed by two days of unrestricted chow. This pattern repeated for five cycles. ...
... Corwin & Buda-Levin, 2004;Martínez & Gómez, 2009). Algunos de los cambios que se han identificado en los patrones de consumo de agua o comida bajo estas condiciones han sido reportados como el binge eating o gran comilona en el primer día de acceso al alimento o al agua después de la privación de alimento o agua (Corwin & Buda-Levin, 2004;Hagan & Moss, 1997). Verplanck y Hayes (1953) reportaron que durante el periodo de privación de alimento en ratas con acceso libre al agua, se produjo una disminución del consumo de agua comparado con el consumo de agua previo al periodo de privación y durante la privación de agua estando el alimento en acceso libre se produjo una disminución del consumo de alimento. ...
... Se ha mostrado que mientras mayor sea el tiempo de restricción de alimento o agua, el consumo posterior a la restricción será proporcional al periodo de ausencia del agua o alimento restringido (Siegel & Talantis, 1948). Diversos estudios también han mostrado los efectos de la modificación del patrón alimentario aumentando el consumo de alimento posterior a la restricción de comida (Hagan & Moss, 1997;López-Espinoza & Martínez, 2001, 2005 incluyendo el consumo de agua, aún cuando ésta no haya sido restringida (Dimitriou, Rice, & Corwin, 2000;Linseman & Harding, 1989;López-Espinoza & Martínez, 2001, 2005Sclafani & Gorman, 1977) o el consumo de alcohol (Soderpalm & Hansen, 1999). La restricción de agua o comida es considerada una variable motivacional, ya que incrementa los patrones de la búsqueda de agua y alimento en ratas (Bindra, 1947). ...
... However, research with children suggests that intermittent access to palatable foods itself may alter the acceptance (1-choice intake) and preferredness (multiple-choice relative intake) of foods (Birch and Davidson, 2001;Fisher and Birch, 1999). Consistent with this possibility, control subjects in the binge model show long-lasting reductions in deprivation-induced chow intake compared with rats that never tasted cookies (Hagan and Moss, 1997). The present studies therefore sought to test explicitly the hypothesis that shortterm food intake by rats receiving alternating access to differently preferred highcarbohydrate foods becomes more controlled by relative diet palatability over cycles of access. ...
... For brevity, the first 5 days (chow only) of weekly diet cycles will be referred to as C phases and the last 2 days (chow or preferred per experimental group) will be referred to as P phases. The length of diet cycles (7 days) reduces the likelihood that the estrous cycle (4-5 days) accounts for observed effects and resembles designs used in previous diet cycling studies of female rats (Hagan and Moss, 1997). ...
Avoidance of and relapse to palatable foods is a qualitative aspect of dieting, a putative risk factor for eating disorders or obesity. The present studies tested the hypotheses that rats with alternating access to highly preferred foods would show: (1) hypophagia, a function of the relative hedonic value of the underaccepted diet, (2) increased anxiety-like behavior and psychomotor arousal when preferred diet was unavailable, (3) obesity-like changes, and (4) stable individual differences in diet-switch-induced hypophagia. Preferences among three high-carbohydrate diets were determined in female Wistar rats (n = 16). Adolescent rats (n = 162) received the following weekly diet schedules: (1) continuous regular chow (7 days/week), (2) chow (5 days/week) followed by a more preferred diet (2 days/week), or (3) chow (5 days/week) followed by a less preferred chow (2 days/week). Some animals were yoke-restricted (75% calories) when provided chow to increase its rewarding properties. Diurnal locomotor activity was measured in a familiar environment, and anxiety-like behavior was assessed in the elevated plus-maze and defensive withdrawal tests. Rats withdrawn from the preferred diet showed hypophagia, anxiogenic-like behavior, increased locomotion, and weight loss. Chow hypophagia was progressive, individual-specific in magnitude, (partly) non-homeostatic in nature, and blunted by previous chow restriction. Despite eating less, rats cycled with the preferred diet became heavier, fatter, and diurnally less active, with greater feed efficiency and proinflammatory adipokine levels than chow controls. The present diet cycling procedure may model consummatory, anxiety-related, and metabolic effects of qualitative dieting in humans.
... Factors that can influence binge eating episodes are thought to include environmental and physiological stress, dietary restraint, and intermittent exposure to energy-rich palatable food [2]. Many animal models of binge eating disorder have successfully employed these factors to mimic characteristics of human binge eating [3][4][5][6][7]. Regarding the food content of binges, clinical data suggests that binge eating disorder patients consume significantly more energy from fats than proteins during a binge meal [8,9]. ...
... Therefore, several rodent models of BED have been developed. Some use food restriction and refeeding [3], while others employ various stressors at the end of food restriction-refeeding cycles to drive escalation in PF intake [4,52]. In this study, we employed a previously described limited access model of BED, which involves intermittent exposure to a fat source (vegetable shortening) to induce binge eating episodes [6]. ...
Binge eating disorder (BED) is defined as recurrent, distressing over-consumption of palatable food (PF) in a short time period. Clinical studies suggest that individuals with BED may have impairments in cognitive processes, executive functioning, impulse control, and decision-making, which may play a role in sustaining binge eating behavior. These clinical reports, however, are limited and often conflicting. In this study, we used a limited access rat model of binge-like behavior in order to further explore the effects of binge eating on cognition. In binge eating prone (BEP) rats, we found novel object recognition (NOR) as well as Barnes maze reversal learning (BM-RL) deficits. Aberrant gene expression of brain derived neurotrophic factor (Bdnf) and tropomyosin receptor kinase B (TrkB) in the hippocampus (HPC)-prefrontal cortex (PFC) network was observed in BEP rats. Additionally, the NOR deficits were correlated with reductions in the expression of TrkB and insulin receptor (Ir) in the CA3 region of the hippocampus. Furthermore, up-regulation of serotonin-2C (5-HT2C) receptors in the orbitoprefrontal cortex (OFC) was associated with BM-RL deficit. Finally, in the nucleus accumbens (NAc), we found decreased dopamine receptor 2 (Drd2) expression among BEP rats. Taken together, these data suggest that binge eating vegetable shortening may induce contextual and reversal learning deficits which may be mediated, at least in part, by the altered expression of genes in the CA3-OFC-NAc neural network.
... Four different diets were used in this study, and animals were exposed to the respective diets for 8 weeks. [39,50]. Tap water was available at all times, except during testing. ...
... We did, however, observe an increase in body weight gain after exposure to the binge model. The current diet is based on a study by Hagan et al., who showed increased bingeing on palatable food of animals who had been exposed to a comparable diet even after they had been withdrawn from this diet for 30 days [50]. In contrast to Hagan et al., we used male rats. ...
The worldwide obesity epidemic poses an enormous and growing threat to public health. However, the neurobehavioral mechanisms of overeating and obesity are incompletely understood. It has been proposed that addiction-like processes may underlie certain forms of obesity, in particular those associated with binge eating disorder. To investigate the role of addiction-like processes in obesity, we adapted a model of cocaine addiction-like behavior in rats responding for highly palatable food. Here, we tested whether rats responding for highly palatable chocolate Ensure would come to show three criteria of addiction-like behavior, i.e., high motivation, continued seeking despite signaled non-availability and persistence of seeking despite aversive consequences. We also investigated whether exposure to a binge model (a diet consisting of alternating periods of limited food access and access to highly palatable food), promotes the appearance of food addiction-like behavior. Our data show substantial individual differences in control over palatable food seeking and taking, but no distinct subgroup of animals showing addiction-like behavior could be identified. Instead, we observed a wide range extending from low to very high control over palatable food intake. Exposure to the binge model did not affect control over palatable food seeking and taking, however. Animals that showed low control over palatable food intake (i.e., scored high on the three criteria for addiction-like behavior) were less sensitive to devaluation of the food reward and more prone to food-induced reinstatement of extinguished responding, indicating that control over palatable food intake is associated with habitual food intake and vulnerability to relapse. In conclusion, we present an animal model to assess control over food seeking and taking. Since diminished control over food intake is a major factor in the development of obesity, understanding its behavioral and neural underpinnings may facilitate improved management of the obesity epidemic.
... The large amount of palatable food consumed within a short period of time is 72% higher than control animals and is reminiscent of an acute emotional binge, lending face and construct validity to this model. 1,[29][30][31][32] It should be noted that 2 cycles of intermittent access to the highly palatable food was required in order to see this effect with no differences being observed Furthermore, our results show that the repetition of the stressful situation led to an increased binge-like behavior and highly palatable food consumption, which is agreement with rodents literature on how subchronic and chronic can induce hyperphagia and susceptibility to food addiction. 6,33,34 This data is also supported by the human literature on vulnerability to obesity, eating disorders and addiction in those submitted to chronic stressful episodes. ...
... This is in agreement with previous studies performed in rats. 10,29,30 Conversely, in male mice that were not food-restricted no stress-induced binge behavior was observed. This may be attributed to the predominance of homeostatic drivers responding to metabolic challenges (history of food restriction) over the hedonic or rewarding characteristics of the palatable food in male compared with female animals. ...
Overeating is a major contributing factor to obesity and related health complications. For women in particular, negative emotions such as stress strongly influence eating behavior and bingeing episodes. Modelling this type of binge eating in rodents presents challenges: firstly, stress‐induced anorexia is commonly observed in rodents therefore a mild stressor is required in order to observe an orexigenic effect. Second, many studies report using calorie restriction to observe the required behavior; yet this does not necessarily reflect the human condition. Thus, the aim of this study was to develop a model of emotional stress‐induced bingeing independent of caloric restriction. Female and male C57BL/6J mice were divided into ad libitum (n = 20 per sex) and food‐restricted (n = 20 per sex) groups which were both further split into a control group and a group exposed to frustration stress (n = 10 per group). All mice were provided intermittent access to a highly palatable food in 2 cycles. At the end of each cycle the stress group was subjected to a 15‐min frustration episode where highly palatable food was within the home cage but inaccessible. Both groups were then given free access for 15 min. Frustrated female mice from the ad libitum displayed binge‐like behavior compared to controls (P = 0.0001). Notably, this behavior was absent in males. Ovariectomy had no impact on binge‐like behavior. Collectively, these data validate a novel model of emotional stress‐induced binge eating specific to female mice which does not require caloric restriction and is not driven by ovarian hormones. This article is protected by copyright. All rights reserved. Enhanced binge eating of palatable food in female mice when exposed to frustration stress in the absence of a history of caloric restriction
... The second, chow-and-Ensure-fed rat cohort had 2-h access to Ensure immediately after stress, in a non-hungry state, and on the first and second days of refeeding after 2 days of food restriction. Intermittent access to a palatable diet, such as sugar, sweet cookies or lard, may trigger development of binge-like eating of palatable foods, and repeated food restriction and stress may exacerbate this behavior (Avena et al. 2008b;Boggiano & Chandler 2006;Corwin 2004;Corwin & Buda-Levin 2004;Cottone et al. 2008Cottone et al. , 2012Hagan & Moss 1997;Hagan et al. 2002;Martin & Timofeeva 2010). In agreement with the previous reports (Kinzig et al. 2008;Martin & Timofeeva 2010), adding palatable Ensure to the diets effectively blunted the anorectic effects of stress in male rats. ...
This study investigated sex-specific effects of repeated stress and food restriction on food intake, body weight, corticosterone plasma levels and expression of corticotropin-releasing factor (CRF) in the hypothalamus and relaxin-3 in the nucleus incertus (NI). CRF and relaxin-3 expression is affected by stress, and these neuropeptides produce opposite effects on feeding (anorexigenic and orexigenic, respectively), but sex-specific regulation of CRF and relaxin-3 by chronic stress is not fully understood. EXPERIMENTAL CONDITIONS: Male and female rats were fed ad libitum chow (AC) or ad libitum chow and intermittent palatable liquid Ensure without food restriction (ACE), or combined with repeated food restriction (60% chow, 2 days per week; RCE). Half of the rats were submitted to 1-h restraint stress once a week. In total, 7 weekly cycles were applied. RESULTS: The body weight of the RCE stressed male rats significantly decreased while the body weight of the RCE stressed female rats significantly increased compared to the respective control groups. The stressed female RCE rats considerably overate chow during recovery from stress and food restriction. The RCE female rats demonstrated elevated plasma corticosterone levels and low expression of CRF mRNA in the paraventricular hypothalamic nucleus but not in the medial preoptic area. The NI expression of relaxin-3 mRNA was significantly higher in the stressed RCE female rats compared to other groups. CONCLUSION: An increase in the expression of orexigenic relaxin-3 and misbalanced HPA axis activity may contribute to the overeating and increased body weight seen in chronically stressed and repeatedly food-restricted female rats.
... Animal studies indicate that food restriction (FR) increases sensitivity to drugs of abuse in self-administration (Carroll and Meisch 1984), conditioned place preference (Bell et al. 1997;Stuber et al. 2002;Liu et al. 2011;Zheng et al. 2012), motor activity (Deroche et al. 1995;Carr et al. 2003), and electrical brain stimulation reward paradigms (Cabeza de Vaca and Carr 1998;Cabeza de Vaca et al. 2004). In addition, FR interacts with episodic access to palatable food to generate enduring binge-like patterns of intake (Hagan and Moss 1997;Avena et al. 2008;Consoli et al. 2009). Most recently, it was observed that FR increases the incentive effects of an environment paired with cocaine during a prior ad libitum fed state (Zheng et al. 2012) and enhances cue-induced reinstatement of heroin seeking (D'Cunha et al. 2013). ...
Chronic food restriction (FR) increases behavioral responsiveness to drugs of abuse and associated environments. Pre- and postsynaptic neuroadaptations have been identified in the mesoaccumbens dopamine pathway of FR subjects but the mechanistic basis of increased drug reward magnitude remains unclear.
Effects of FR on basal and D-amphetamine-induced trafficking of AMPA receptor subunits to the nucleus accumbens (NAc) postsynaptic density (PSD) were examined, and AMPA receptor involvement in augmentation of D-amphetamine reward was tested.
FR and ad libitum fed (AL) rats were injected with D-amphetamine (2.5 mg/kg, i.p.) or vehicle. Brains were harvested and subcellular fractionation and Western analyses were used to assess AMPA receptor abundance in NAc homogenate and PSD fractions. A follow-up experiment used a curve-shift protocol of intracranial self-stimulation to assess the effect of 1-naphthylacetyl spermine (1-NASPM), a blocker of Ca(2+)-permeable AMPA receptors, on rewarding effects of D-amphetamine microinjected in NAc shell.
FR increased GluA1 in the PSD, and D-amphetamine increased p-Ser845-GluA1, GluA1, GluA2, but not GluA3, with a greater effect in FR than AL rats. D-amphetamine lowered reward thresholds, with greater effects in FR than AL rats, and 1-NASPM selectively reversed the enhancing effect of FR.
Results suggest that FR leads to increased synaptic incorporation of GluA1 homomers to potentiate rewarding effects of appetitive stimuli and, as a maladaptive byproduct, D-amphetamine. The D-amphetamine-induced increase in synaptic p-Ser845-GluA1, GluA1, and GluA2 may contribute to the rewarding effect of D-amphetamine, but may also be a mechanism of synaptic strengthening and behavior modification.
... All rats were diet cycled for at least 7 weeks (ranging from 8 to 11) and the number of weeks was equally represented in all the experimental groups. The length of diet cycles (7 days) reduces the likelihood that the estrous cycle (4–5 days) accounts for observed effects and resembles designs used in previous diet-cycling studies of female rats (Cottone et al, 2009b; Hagan and Moss, 1997). ...
... All rats were diet cycled for at least 7 weeks (ranging from 8 to 11) and the number of weeks was equally represented in all the experimental groups. The length of diet cycles (7 days) reduces the likelihood that the estrous cycle (4-5 days) accounts for observed effects and resembles designs used in previous diet-cycling studies of female rats (Cottone et al, 2009b;Hagan and Moss, 1997). ...
The anti-obesity medication rimonabant, an antagonist of cannabinoid type-1 (CB(1)) receptor, was withdrawn from the market because of adverse psychiatric side effects, including a negative affective state. We investigated whether rimonabant precipitates a negative emotional state in rats withdrawn from palatable food cycling. The effects of systemic administration of rimonabant on anxiety-like behavior, food intake, body weight, and adrenocortical activation were assessed in female rats during withdrawal from chronic palatable diet cycling. The levels of the endocannabinoids, anandamide and 2-arachidonoylglycerol (2-AG), and the CB(1) receptor mRNA and the protein in the central nucleus of the amygdala (CeA) were also investigated. Finally, the effects of microinfusion of rimonabant in the CeA on anxiety-like behavior, and food intake were assessed. Systemic administration of rimonabant precipitated anxiety-like behavior and anorexia of the regular chow diet in rats withdrawn from palatable diet cycling, independently from the degree of adrenocortical activation. These behavioral observations were accompanied by increased 2-AG, CB(1) receptor mRNA, and protein levels selectively in the CeA. Finally, rimonabant, microinfused directly into the CeA, precipitated anxiety-like behavior and anorexia. Our data show that (i) the 2-AG-CB(1) receptor system within the CeA is recruited during abstinence from palatable diet cycling as a compensatory mechanism to dampen anxiety, and (ii) rimonabant precipitates a negative emotional state by blocking the beneficial heightened 2-AG-CB(1) receptor signaling in this brain area. These findings help elucidate the link between compulsive eating and anxiety, and it will be valuable to develop better pharmacological treatments for eating disorders and obesity.
... Despite its clinical relevance, finding appropriate animal models for studying binge eating episodes has been challenging due to the fact that its etiology in humans is currently unclear [62]. In order to trigger acute food overconsumption, many animal models of binge eating involve a previous period of imposed food restriction, which also affects brain circuits regulating homeostatic aspects of food intake [55,63,64]. However, some evidences suggest that binge-eating episodes mainly involve hedonic-related feeding circuits [65]. ...
Overconsumption of palatable energy-dense foods has negative health implications and it is associated with obesity and several eating disorders. Currently, little is known about the neuronal circuitries activated by the acute ingestion of a rewarding stimulus. Here, we used a combination of immunohistochemistry, pharmacology and neuronal tracing analyses to examine the role of the mesolimbic system in general, and the orexin neurons in particular, in a simple experimental test in which naïve mice are allowed to spontaneously eat a pellet of a high fat diet (HFD) for 2 h. We found that acute HFD activates c-Fos expression in several reward-related brain areas, including the ventral tegmental area (VTA), nucleus accumbens, central amygdala and lateral hypothalamic area. We also found that: i- HFD-mediated orosensory stimulation was required for the mesolimbic pathway activation, ii- acute HFD differentially activates dopamine neurons of the paranigral, parabrachial pigmented and interfascicular sub-regions of the VTA, and iii- orexin neurons of the lateral hypothalamic area are responsive to acute HFD. Moreover, orexin signaling blockade, with the orexin 1 receptor antagonist SB-334867, reduces acute HFD consumption and c-Fos induction in the VTA but not in the other mesolimbic nuclei under study. Finally, we found that most orexin neurons responsive to acute HFD innervate the VTA. Our results show that acute HFD consumption recruits the mesolimbic system and that the full manifestation of this eating behavior requires the activation of orexin signaling.
... Two of the measures that have been used to distinguish binge-type from normal intake in animal studies are: (1) comparing intake at a given point in time between groups, and (2) assessing escalation of intake across time within groups. When using the first measure, "normal" eating is represented by a control group, while "binge-type" eating is represented by an experimental group (Boggiano & Chandler, 2006;Cifani et al., 2010;Cifani, Polidori, Melotto, Ciccocioppo, & Massi, 2009;Corwin, 2004;Corwin, Boan, Peters, Walsh, & Ulbrecht, 2010;Corwin et al., 1998;Czyzyk, Sahr, & Statnick, 2010;Davis et al., 2007;Dimitriou, Rice, & Corwin, 2000;Hagan & Moss, 1997;Hagan et al., 2002;Hancock, Menard, & Olmstead, 2005;Kinzig, Hargrave, & Honors, 2008;Placidi et al., 2004;Thomas, Rice, Weinstock, & Corwin, 2002;Wojnicki, Charny, & Corwin, 2008;Wojnicki, Johnson, & Corwin, 2008;Wojnicki, Stine, & Corwin, 2007;Wong, Wojnicki, & Corwin, 2009;Yu, Geary, & Corwin, 2008. This establishes "normal" intake for a given "brief period of time" and contrasts it with "higher than normal" intake, i.e. bingeing. ...
As interest in the study of binge eating has increased, several measures of bingeing have been developed for use in animal models. Two of the measures that have been used to distinguish binge-type from normal intake in animal studies are: (1) comparing intake at a given point in time between groups, and (2) assessing escalation of intake across time within groups. Here we use both of these measures to reanalyze data from 10 previous bingeing experiments conducted in our lab. Additionally, the data from two of these studies were then restructured in order to evaluate the use of these measures in binge eating prone (BEP) and resistant (BER) rats, as described by others. Analyses comparing intake at a given point in time indicated bingeing in all 10 studies, while comparisons of escalation indicated bingeing in 9 out of 10 studies. The goal of this study was to compare and contrast the two measures, identify the strengths and weaknesses of each, and determine their appropriateness for a given set of potential outcomes. The results indicate that both intake and escalation are useful measures. However, their limitations need to be taken into consideration when attempting to operationalize binge-type eating in animal models.
... A few reports in animals and one report in children indicated that limiting access to preferred foods can increase consumption during a test meal (Fisher & Birch, 1999b;Hagan & Moss, 1997) or shift circadian intake patterns (Hirsch & Walsh, 1982;Panksepp & Krost, 1975) even under non-energy-deprived conditions. Additionally, recent results from our laboratory using non-energy-deprived male rats showed that, across a 6-week period of time, consumption of an optional source of dietary fat increased as access to the fat decreased (Corwin et al., 1998). ...
Objective
The present investigation sought to determine if limiting access to an optional fatty food would induce binge-type behavior patterns in non–energy-deprived female rats.Method
Four groups of rats had continuous access to a commercial rodent diet throughout the 8-week study. In addition: (1) the control group had no access to vegetable shortening; (2) the high limitation group had access to shortening for 2 hr for 3 days each week; (3) the low limitation group had access to shortening for 2 hr every day; and (4) the no limitation group had continuous access to shortening.ResultsAs access to the shortening decreased, intake during the 2-hr access period increased. Total energy intake and body weight did not differ among groups. Body fat was greatest in the rats that ate the most cumulative shortening.DiscussionThese results indicate that, even under non–energy-deprived conditions, limiting access to a preferred fatty food can induce binge-type behavior in female rats. © 2000 by John Wiley & Sons, Inc. Int J Eat Disord 28: 436–445, 2000.
... ex., une personne peut se sentir mieux après avoir consommé des aliments plus sains ou évité de consommer des aliments moins bons pour la santé, ou après avoir consommé un aliment « réconfortant » dans le but de soulager sa détresse) 4 . Le fait de s'imposer des privations alimentaires, qu'on appelle communément « se mettre au régime », pousse à trop manger, même chez les animaux 32 . Ainsi, on observe souvent de la boulimie chez les personnes qui ont traversé des périodes de demi jeûne en raison de la guerre ou d'une famine, ou encore après avoir participé volontairement à certaines expériences 33 . ...
RÉSUMÉ Contexte : Les fluctuations observées au niveau de la santé mentale peuvent aussi bien contribuer à la saine alimentation qu'aller à l'encontre de celle-ci. On observe en effet une relation bidirectionnelle entre l'alimentation et la santé mentale. Ainsi, l'humeur ou l'état psychologique peuvent influencer ce qu'on mange, de même que les quantités consommées, tandis que l'alimentation influence également l'humeur et le bien-être psychologique. Par conséquent, dans une optique de promotion de la saine alimentation et d'élaboration de stratégies en ce sens, il est important de bien comprendre les diverses connexions entre la santé mentale et la saine alimentation. Méthodologie : De façon à mieux comprendre le sujet en titre, nous avons examiné, d'une part, les études portant sur les différentes réactions individuelles face à l'alimentation ainsi que les influences de l'humeur, de divers facteurs émotionnels, sociaux et collectifs sur le choix des aliments et les quantités consommées, dans le but de vérifier comment la santé mentale influence l'alimentation, plus particulièrement chez les adolescents et les adultes. D'autre part, nous avons examiné les études portant sur la relation entre l'alimentation et la santé mentale, c.-à-d. sur la façon de se sentir dans sa peau (bien ou mal) suite à l'ingestion de certains aliments ou de quantités spécifiques d'aliments. Conclusions : Aussi bien le fait de trop manger que de ne pas manger suffisamment entraîne des effets complexes, ces deux comportements pouvant procurer un meilleur sentiment de bien-être ou, au contraire, engendrer de la culpabilité ou un sentiment de manque, de dépression ou d'anxiété. Nous avons tenté d'identifier à la fois l'état actuel des connaissances et les lacunes à combler à cet égard par rapport à ces deux types de comportements opposés.
... Significant effort has been made in attempting to isolate the factors which contribute to the development of binge eating (Cottone et al, 2008b;Hagan and Moss, 1997). A widely accepted hypothesis on the etiology of binge eating is based on the qualitative alternation of food palatability. ...
Binge eating disorder is an addiction-like disorder characterized by excessive food consumption within discrete periods of time. This study was aimed at understanding the role of the opioid system within the medial prefrontal cortex (mPFC) in the consummatory and motivational aspects of binge-like eating. For this purpose, we trained male rats to obtain either a sugary, highly palatable diet (Palatable rats) or a chow diet (Chow rats) for 1 hour/day. We then evaluated the effects of the opioid receptor antagonist, naltrexone, given either systemically or site-specifically into the nucleus accumbens (NAcc) or the mPFC on a fixed ratio 1 (FR1) and a progressive ratio schedule of reinforcement for food. Finally, we assessed the expression of the genes proopiomelanocortin (POMC), pro-dynorphin (PDyn) and pro-enkephalin (PEnk), coding for the opioids peptides in the NAcc and the mPFC in both groups. Palatable rats rapidly escalated their intake by four times. Naltrexone, when administered systemically and into the NAcc, reduced FR1 responding for food and motivation to eat under a progressive ratio in both Chow and Palatable rats; conversely, when administered into the mPFC, the effects were highly selective for binge eating rats. Furthermore, we found a twofold increase in POMC and a ∼50% reduction in PDyn gene expression in the mPFC of Palatable rats, when compared to control rats; however, no changes were observed in the NAcc. Our data suggest that neuroadaptations of the opioid system in the mPFC occur following intermittent access to highly palatable food, which may be responsible for the development of binge-like eating.
... For example, rats can be trained to "binge" on chow or sugar solution by limiting the amount of time each day in which they have access to it. The time-restricted animals take in much more food than those that have unlimited access, and they develop concurrent brain changes closely resembling those found in drug-dependent animals, including naloxone-precipitable withdrawal signs (Avena, Rada, & Hoebel, 2008;Hagan & Moss, 1997;Hoebel, Avena, Bocarsly, & Rada, 2009;Rada, Avena, & Hoebel, 2005). The stimulus strength of very sweet solutions, as reflected in the preference for either saccharine or sugar solution, exceeds that of cocaine solution, even in cocaine-dependent animals (Lenoir, Serre, Cantin, & Ahmed, 2007). ...
Kalant, H. (2015). Neurobiological research on addiction: What value has it added to the concept?. The International Journal Of Alcohol And Drug Research, 4 (1), 53-59. doi: http://dx.doi.org/10.7895/ijadr.v4i1.196 The initial goal of neurobiological research on addiction was to identify the neural mechanisms involved in the mediation and expression of addictive behavior. More recently, however, it has attributed causal roles to these mechanisms, as illustrated by the definition of addiction as a brain disease caused by chronic exposure to a drug. This concept carries a number of implications that can be assessed experimentally and clinically. None of these implications is borne out by the currently available evidence. The interactions of neuronal systems involved in addiction are also involved in adaptation to experience and environmental change. Much of the neurobiological research to date has not differentiated between causes of addiction, neuronal mechanisms that are activated by them, and risk factors that contribute to individual vulnerability. It has largely ignored the important experiential and environmental influences known to affect the prevalence of addiction in different populations or different times, and it has so far directed much less attention to other forms of addiction-like behavior that do not involve drugs. These failures are not inherent in neurobiological research but require reorientation of objectives, including more emphasis on the study of mechanisms by which environment and experience, including drug experience, can determine whether genetic risk factors are expressed or remain dormant and can direct neuroadaptive mechanisms toward alternative outcomes.
... Corwin & Buda-Levin, 2004;Martínez & Gómez, 2009). Algunos de los cambios que se han identificado en los patrones de consumo de agua o comida bajo estas condiciones han sido reportados como el binge eating o gran comilona en el primer día de acceso al alimento o al agua después de la privación de alimento o agua (Corwin & Buda-Levin, 2004;Hagan & Moss, 1997). Verplanck y Hayes (1953) reportaron que durante el periodo de privación de alimento en ratas con acceso libre al agua, se produjo una disminución del consumo de agua comparado con el consumo de agua previo al periodo de privación y durante la privación de agua estando el alimento en acceso libre se produjo una disminución del consumo de alimento. ...
Different methods were explored to induce alcohol intake in rats and subsequent cycles of food deprivation on the consumption of alcohol, food, water, and body weight when alcohol was available. Rats were assigned to four groups and a different procedure to induce alcohol intake was used over 12 days a) gradual forced alcohol (4% -10% v / v); b) forced alcohol (10% v / v /); c) water and alcohol (6% - 10% v / v) only during the induction period; or, d) water and alcohol (6% - 10% v / v) throughout the experiment. After the induction period all groups of rats had free access to food and alcohol for ten subsequent days, followed by two alternating cycles of three days of total food restriction and then ten days of free access to food. After the induction period, alcohol (10% v / v) always was available for all groups. Body weight, food and fluid intake were recorded daily. The induction procedures had differential effects on body weight and alcohol intake. For the rats that had wa- ter and alcohol available throughout the experiment, food intake increased and al- cohol intake decreased during the days in which food was freely available. A “self-imposed” water deprivation was observed for this group during the food restric- tion period, and binge drinking occurred when food was available again. The inter- action between eating, drinking and body weight under conditions of food restriction and alcohol availability is discussed.
... All rats were diet cycled for at least 7 weeks (ranging from 8 to 11) and the number of weeks was equally represented in all the experimental groups. The length of diet cycles (7 days) reduces the likelihood that the estrous cycle (4-5 days) accounts for observed effects and resembles designs used in previous diet-cycling studies of female rats (Cottone et al, 2009b;Hagan and Moss, 1997). ...
The anti-obesity medication rimonabant, an antagonist of cannabinoid type-1 (CB1) receptor, was withdrawn from the market because of adverse psychiatric side effects, including a negative affective state. We investigated whether rimonabant precipitates a negative emotional state in rats withdrawn from palatable food cycling. The effects of systemic administration of rimonabant on anxiety-like behavior, food intake, body weight, and adrenocortical activation were assessed in female rats during withdrawal from chronic palatable diet cycling. The levels of the endocannabinoids, anandamide (AEA) and 2-arachidonoylglycerol (2-AG) and the CB1 receptor mRNA and the protein in the central nucleus of the amygdala (CeA) were also investigated. Finally, the effects of microinfusion of rimonabant in the CeA on anxiety-like behavior, and food intake were assessed. Systemic administration of rimonabant precipitated anxiety-like behavior and anorexia of the regular chow diet in rats withdrawn from palatable diet cycling, independently from the degree of adrenocortical activation. These behavioral observations were accompanied by increased 2-AG, CB1 receptor mRNA, and protein levels selectively in the CeA. Finally, rimonabant, microinfused directly into the CeA, precipitated anxiety-like behavior and anorexia. Our data shows that (i) the 2-AG-CB1 receptor system within the CeA is recruited during abstinence from palatable diet cycling as a compensatory mechanism to dampen anxiety, and (ii) rimonabant precipitates a negative emotional state by blocking the beneficial heightened 2-AG-CB1 receptor signaling in this brain area. These findings help elucidate the link between compulsive eating and anxiety, and it will be valuable to develop better pharmacological treatments for eating disorders and obesity
... It is well known that food deprivation has powerful effects on anticipatory and consummatory food related behavior. Acute food deprivation (ranging from 1 48 h) is associated with increased food consumption in animals and humans (Grill and Berridge, 1985;DiBattista, 1987;Spiegel et al., 1989;Hagan and Moss, 1997;Drobes et al., 2001;Mauler et al., 2006). Using behavioral economics and choice paradigms, it was shown that food deprivation enhanced the reinforcing value of food (Bulik and Brinded, 1994;Epstein and Saelens, 2000;Raynor and Epstein, 2003). ...
The present study used event-related brain potentials to examine deprivation effects on visual attention to food stimuli at the level of distinct processing stages. Thirty-two healthy volunteers (16 females) were tested twice 1 week apart, either after 24 h of food deprivation or after normal food intake. Participants viewed a continuous stream of food and flower images while dense sensor ERPs were recorded. As revealed by distinct ERP modulations in relatively earlier and later time windows, deprivation affected the processing of food and flower pictures. Between 300 and 360 ms, food pictures were associated with enlarged occipito-temporal negativity and centro-parietal positivity in deprived compared to satiated state. Of main interest, in a later time window (∼ 450–600 ms), deprivation increased amplitudes of the late positive potential elicited by food pictures. Conversely, flower processing varied by motivational state with decreased positive potentials in the deprived state. Minimum-Norm analyses provided further evidence that deprivation enhanced visual attention to food cues in later processing stages. From the perspective of motivated attention, hunger may induce a heightened state of attention for food stimuli in a processing stage related to stimulus recognition and focused attention.
... Moreover, these mice ate roughly 21% more, drank 15% more, gained roughly 5% more body weight, and worked harder for a sweet reward. Upon sucrose consumption after fasting, an exaggerated release of dopamine was observed (Polivy and Herman, 1985;Hagan and Moss, 1997;Bello et al., 2003). Given this information, Drosophila with impaired DAT function are expected to experience higher levels of dopamine signaling. ...
Feeding is a complex behavior that is regulated by several internal mechanisms. Neuropeptides are able to survey quantities of stored energy and inform the organism if nutrient intake is required. In addition to this homeostatic regulation, a post-feeding reward system positively reinforces feeding. Slight adjustments to either system can tilt the balance to affect the energy reserves and survivorship in times of nutrient adversity. Neuropeptide F (NPF), a homolog of the mammalian neuropeptide Y, acts to induce feeding within the homeostatic regulation of this behavior. Drosophila and other insects bear a shorter form of NPF known as short NPF (sNPF) that can influence feeding. A neural hormone regulator, the dopamine transporter (DAT), works to clear dopamine from the synapses. This action may manipulate the post-feeding reward circuit in that lowered dopamine levels depress feeding, and excess dopamine levels encourage feeding. Here, we have overexpressed and impaired the activities of NPF, sNPF, and DAT in Drosophila, and we examined their ability to survive during conditions of amino acid starvation. Too much or too little NPF or sNPF, which are key players in homeostatic feeding regulation, leads to increased sensitivity to amino acid starvation and diminished survivorship when compared to controls. When DAT, a member of the post-feeding reward system, is either overexpressed or reduced via mutation, Drosophila has increased sensitivity to amino acid starvation. Taken together, these results indicate that subtle variation in the expression of key components of these systems impacts survivorship during adverse nutrient conditions.
... There are three key design aspects used to create this desired experimental condition. First, subjects were restrict fed for 2 h; these conditions do not result in overt increases in stress hormones (Choi et al., 1998) and has previously been used by numerous others to enhance hungerdriven feeding (Hagan and Moss, 1997;Denis et al., 2015;Wei et al., 2015;Baldo et al., 2016). Confounding interactions stemming from malnourishment in these animals is extremely unlikely since rats with similar long-term caloric restriction paradigms (25% reduction) show improved life expectancy and health outcomes (Keenan et al., 1996(Keenan et al., , 2013. ...
While pituitary adenylate cyclase activating polypeptide (PACAP) signaling in the hypothalamic ventromedial nuclei (VMN) has been shown to regulate feeding, a challenge in unmasking a role for this peptide in obesity is that excess feeding can involve numerous mechanisms including homeostatic (hunger) and hedonic-related (palatability) drives. In these studies, we first isolated distinct feeding drives by developing a novel model of binge behavior in which homeostatic-driven feeding was temporally separated from feeding driven by food palatability. We found that stimulation of the VMN, achieved by local microinjections of AMPA, decreased standard chow consumption in food-restricted rats (e.g., homeostatic feeding); surprisingly, this manipulation failed to alter palatable food consumption in satiated rats (e.g., hedonic feeding). In contrast, inhibition of the nucleus accumbens (NAc), through local microinjections of GABA receptor agonists baclofen and muscimol, decreased hedonic feeding without altering homeostatic feeding. PACAP microinjections produced the site-specific changes in synaptic transmission needed to decrease feeding via VMN or NAc circuitry. PACAP into the NAc mimicked the actions of GABA agonists by reducing hedonic feeding without altering homeostatic feeding. In contrast, PACAP into the VMN mimicked the actions of AMPA by decreasing homeostatic feeding without affecting hedonic feeding. Slice electrophysiology recordings verified PACAP excitation of VMN neurons and inhibition of NAc neurons. These data suggest that the VMN and NAc regulate distinct circuits giving rise to unique feeding drives, but that both can be regulated by the neuropeptide PACAP to potentially curb excessive eating stemming from either drive.
... Moreover, the prevalence of drug abuse among individuals with eating disorders is disproportionately high (Jonas et al., 1987;Pisetsky et al., 2008;Root et al., 2010). The causal relation between food restriction and binge eating, drug reward sensitivity, and incentive effects of drug-associated cues and contexts have been confirmed in animal models (Carroll et al., 1979;Hagan & Moss, 1997;Cabeza de Vaca & Carr, 1998;Zheng et al., 2012;D'Cunha et al., 2013). ...
Chronic food restriction potentiates behavioral and cellular responses to drugs of abuse and D-1 dopamine receptor agonists administered systemically or locally in the nucleus accumbens (NAc). However, the alterations in NAc synaptic transmission underlying these effects are incompletely understood. AMPA receptor trafficking is a major mechanism for regulating synaptic strength, and previous studies have shown that both sucrose and d-amphetamine rapidly alter the abundance of AMPA receptor subunits in the NAc postsynaptic density (PSD) in a manner that differs between food-restricted and ad libitum fed rats. The present study examined whether food restriction, in the absence of reward stimulus challenge, alters AMPAR subunit abundance in the NAc PSD. Food restriction was found to increase surface expression and, specifically, PSD abundance, of GluA1 but not GluA2, suggesting synaptic incorporation of GluA2-lacking Ca2+-permeable AMPARs (CP-AMPARs). Naspm, an antagonist of CP-AMPARs, decreased the amplitude of evoked EPSCs in Nac shell, and blocked the enhanced locomotor response to local microinjection of the D-1 receptor agonist, SKF-82958, in food-restricted, but not ad libitum fed, subjects. Although microinjection of the D-2 receptor agonist, quinpirole, also induced greater locomotor activation in food-restricted than ad libitum fed rats, this effect was not decreased by Naspm. Taken together, the present findings are consistent with synaptic incorporation of CP-AMPARs in D-1 receptor expressing medium spiny neurons in NAc as a mechanistic underpinning of the enhanced responsiveness of food-restricted rats to natural rewards and drugs of abuse. This article is protected by copyright. All rights reserved.
... Indeed, past prolonged bouts of CR have been associated with the onset of binge eating Physiology & Behavior 174 (2017) [49][50][51][52][53][54][55][56] pathologies [15][16][17]. In order to mimic the metabolic and motivational drive to overeat, intermittent bouts of CR are also routinely incorporated into some animal models of binge eating [18][19][20][21]. The notion that prolonged CR or IMF protocols contribute to eating pathologies, however, has not been supported by clinical studies [22,23]. ...
Alternate day, intermittent fasting (IMF) can be an effective weight loss strategy. However, the effects of IMF on eating behaviors are not well characterized. We investigated the acute and residual effects of IMF for weight loss on meal patterns in adult obese male C57BL/6 mice. After 8 weeks of ad libitum high-fat diet to induce diet-induced obesity (DIO), mice were either continued on ad libitum high-fat diet (HFD) or placed on one of 5 diet strategies for weight loss: IMF of high-fat diet (IMF-HFD), pair-fed to IMF-HFD group (PF-HFD), ad libitum low-fat diet (LFD), IMF of low-fat diet (IMF-LFD), or pair-fed to IMF-LFD group (PF-LFD). After the 4-week diet period, all groups were refed the high-fat diet for 6 weeks. By the end of the diet period, all 5 groups had lost weight compared with HFD group, but after 6 weeks of HFD re-feeding all groups had similar body weights. On (Day 2) of the diet period, IMF-HFD had greater first meal size and faster eating rate compared with HFD. Also, first meal duration was greater in LFD and IMF-LFD compared with HFD. At the end of the diet period (Day 28), the intermittent fasting groups (IMF-HFD and IMF-LFD) had greater first meal sizes and faster first meal eating rate compared with their respective ad libitum fed groups on similar diets (HFD and LFD). Also, average meal duration was longer on Day 28 in the low-fat diet groups (LFD and IMF-LFD) compared with high-fat diet groups (HFD and IMF-HFD). After 6 weeks of HFD re-feeding (Day 70), there were no differences in meal patterns in groups that had previously experienced intermittent fasting compared with ad libitum fed groups. These findings suggest that meal patterns are only transiently altered during alternate day intermittent fasting for weight loss in obese male mice.
... La gran comilona ha sido descrita como un evento conductual caracterizado por un consumo excesivo de alimento durante el periodo post-privación. Esta modificación conductual se ha relacionado directamente con la génesis de enfermedades como obesidad, bulimia, o anorexia (Corwin, 2000;Hagan & Moss, 1997;López-Espinoza & Martínez, 2001 a, b;Polivy & Herman, 1985). ...
El presente trabajo tiene como objetivo principal cuestionar el uso de dietas como estrategia para mantener el control de peso corporal. Existe evidencia experimental que demuestra que los organismos recuperan o aumentan de peso después de un periodo de restricción. Para el análisis de este fenómeno se aborda el término ¿causa¿ en el marco de las principales aproximaciones filosóficas y se utilizó el modelo de causalidad de análisis contrafáctico propuesto por Von Wright. El resultado confirmó que la exposición a un periodo de restricción es una condición suficiente para producir un aumento de peso al retornar a condiciones de libre acceso.
... Binge eating in humans can occur in sated and hungry individuals (Marcus and Kalarchian, 2003). Periods of food restriction and bingeing have been shown in laboratory animal models to impact food consumption long after restriction has ceased (Hagan and Moss, 1997), a finding that models reports in humans (Polivy, 1996). There is also a connection between stress and binge-type eating in humans (Cattanach et al., 1988) similar to that observed in animal models. ...
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 restricted eating coupled with excessive wheel running. These findings with animal models complement data obtained through neuroimaging and pharmacotherapy studies of clinical populations. 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. This article is part of a Special Issue entitled 'Central Control of Food Intake'.
... Understanding the physiological consequences of dietary conditions will help elucidate the pathophysiology of eating disorders and related pathologies [23][24][25][26][27]. Prolonged periods of calorie restriction, repeated failed dieting attempts, and body weight suppression are often antecedent to and/or involved in the maintenance of clinical eating pathologies [28][29][30][31][32]. ...
Endogenous cannabinoid signaling, mediated predominately by CB1 receptor activation, is involved in food intake control and body weight regulation. Despite advances in determining the role of the CB1 receptor in obesity, its involvement in the driven nature of eating pathologies has received little attention. The present study examined CB1 receptor alterations as a consequence of dietary-induced binge eating in female Sprague Dawley rats. Four control groups were used to control for calorie restriction and highly palatable food variables characterizing this behavioral model. All groups were kept on their respective feeding schedules for 6-weeks and were given a uniform 33% calorie restriction (~22 h food deprivation) prior to sacrifice. Our findings indicate that regional CB1 mRNA and density were influenced by dietary conditions, but were not specific to the dietary-induced binge eating paradigm used. An increase of approximately 50% (compared with naive controls) in CB1 receptor mRNA levels in the nucleus of the solitary tract as measured by in situ hybridization was found in animals receiving continuous access to a highly palatable food (i.e., vegetable shortening with 10% sucrose). This group also had a significant increase in body weight and adiposity. An approximate 20% reduction in CB1 mRNA was observed in the cingulate cortex (areas 1 and 2) in animals exposed to an intermittent schedule of feeding, compared with groups that had ad libitum feeding schedules (i.e., continuous access and naive controls). Receptor density as measured by [(3)H]CP55,940 autoradiography, was reduced by approximately 30% in the nucleus accumbens shell region in groups receiving repeated access to the highly palatable food. Taken together, these findings indicate that dietary conditions can differentially influence CB1 receptors in forebrain and hindbrain regions.
... Instead, the SS rats demonstrated a gradual significant escalation of their daily sucrose intake over all 3 weeks of the experiment. This differential sucrose and chow intake may be explained by the fact that intermittent access to palatable food promotes the increased intake of palatable ingredients of food (Hagan and Moss, 1997; Martin and Timofeeva, 2010), while reducing the reinforcing efficacy of regular chow (Cottone et al., 2008). The SC and SS rats demonstrated fairly similar activation of the anterior PVT during food anticipation and following feeding. ...
Food intake is regulated according to circadian activity, metabolic needs and the hedonic value of food. Rodents placed on a fixed feeding schedule show behavioral and physiological anticipation of mealtime referred to as food-anticipatory activity (FAA). FAA is driven by the food-entrainable oscillator (FEO), whose anatomical substrate is not yet known. Recent data have shown that restricted feeding schedules for regular chow and daily limited access to palatable food in free-feeding rats activate distinct brain regions during FAA. The combination of a deprivation regimen and scheduled access to palatable food may give rise to a more global anticipatory mechanism because the temporal cycles of energy balance would be strongly modulated by the incentive properties of palatable food; however, the neuronal response to this combined treatment is not yet known. The present study investigated how adding palatable sucrose to feeding schedules affects the pattern of brain c-fos mRNA expression during FAA (0-3 h) and 1 h following feeding. The rats maintained on scheduled chow access increased their daily chow intake, while the rats maintained on scheduled sucrose and chow mainly increased their daily sucrose intake. Adding sucrose to scheduled feeding displaced c-fos mRNA expression from the dorsomedial and paraventricular hypothalamic nuclei and posterior lateral hypothalamus (LH) to the prefrontal cortex, lateral septum, nucleus accumbens and anterior LH. During refeeding, the rats on scheduled sucrose demonstrated higher activation of the nucleus of the solitary tract. The present results suggest that palatable sucrose combined with restricted feeding schedules activate a distinct neuronal network compared to neuronal activation produced by scheduled access to regular chow. These data provide evidence that the brain may contain different food-oscillatory systems and that food palatability may shift the neuronal activity from the medial hypothalamus to the limbic and reward-related areas even at the negative metabolic state.
... These factors, e.g. the reaction to war experience, underline the increased vulnerability to the effects of stress in some individuals, which combined with food restriction or deprivation, may lead to developing an ED. This has been shown in experiments with rats: after having undergone repeated stress with cycles of restriction and hyperphagia, animals continued binge eating even after normalization of feeding cycles [45]. The amount and repetition of stress also seems to play a role. ...
Eating disorders and drug addiction share many common traits. This includes biological and environmental factors that predispose
individuals to develop either disorder, an increased risk for anxiety and depression when the disorders are present, and heightened
trait levels of impulsivity and compulsion. Animal models of eating disorders are not as well established as those that model
drug addiction, but the research in this area is progressing rapidly. In this chapter, we discuss anorexia nervosa, bulimia
nervosa, binge eating disorder, and obesity as these encompass the majority of maladaptive eating behaviors in humans. We
begin by outlining the important features that characterize each disorder and that should thereby be present in an animal
model. An overview of peptide control of feeding is provided to help the reader evaluate the animal models presented. These
are based principally on genetic variation and stressful life events. In general, most animal models based on genetic alterations
have limited applicability to humans, at least to date. Those based on stressful life events appear more promising in that
they more accurately reproduce alterations in feeding and neuroendocrine function that are characteristic of each disorder.
The next obvious step in eating disorder research is to combine the two approaches to determine how genetic alterations and
stressful events interact to produce maladaptive eating and physiological changes.
Key wordsAnorexia nervosa–Bulimia nervosa–Binge eating disorder–Obesity–Stress–Genetics–Neuroendocrine function–Feeding peptides–Hypothalamus
The dramatically increasing prevalence of obesity, associated with potentially life-threatening health problems, including cardiovascular diseases and type II diabetes, poses an enormous public health problem. It has been proposed that the obesity epidemic can be explained by the concept of 'food addiction'. In this review we focus on possible similarities between binge eating disorder (BED), which is highly prevalent in the obese population, and drug addiction. Indeed, both behavioral and neural similarities between addiction and BED have been demonstrated. Behavioral similarities are reflected in the overlap in DSM-IV criteria for drug addiction with the (suggested) criteria for BED and by food addiction-like behavior in animals after prolonged intermittent access to palatable food. Neural similarities include the overlap in brain regions involved in food and drug craving. Decreased dopamine D2 receptor availability in the striatum has been found in animal models of binge eating, after cocaine self-administration in animals as well as in drug addiction and obesity in humans. To further explore the neurobiological basis of food addiction, it is essential to have an animal model to test the addictive potential of palatable food. A recently developed animal model for drug addiction involves three behavioral characteristics that are based on the DSM-IV criteria: i) extremely high motivation to obtain the drug, ii) difficulty in limiting drug seeking even in periods of explicit non-availability, iii) continuation of drug-seeking despite negative consequences. Indeed, it has been shown that a subgroup of rats, after prolonged cocaine self-administration, scores positive on these three criteria. If food possesses addictive properties, then food-addicted rats should also meet these criteria while searching for and consuming food. In this review we discuss evidence from literature regarding food addiction-like behavior. We also suggest future experiments that could further contribute to our understanding of behavioral and neural commonalities and differences between obesity and drug addiction. Copyright © 2012 S. Karger GmbH, Freiburg.
During the past few centuries humans have transformed themselves from rear to voracious consumers of sugar. The present chapter sheds light on the questions of why we increased our consumption of sugar and what effects sucrose intake may produce on our mood and mind. Once consumed, sucrose signals to the brain via the specialized taste receptors and glucosensing mechanisms. In the brain, sucrose intake activates the primary gustatory pathway and the brain reward system, which recognizes sweet taste of sucrose as rewarding. The role of the sweet taste system is to detect the potentially high-energy sweet foods that normally are relatively rare in the nature. The glucosensing mechanisms stimulate or inhibit food intake according to the energy needs. Because of the scarcity of sweet foods in nature, seeking these foods requires some effort. Therefore, once these foods are found and consumed, this effort would be awarded by the brain reward system. These sophisticated systems work properly when their functions are not compromised by the unlimited availability of sweet palatable food, which may counteract the precise mechanisms controlling food intake. The experimental results obtained in animal models have shown that seeking and consumption of the regular non-sweet foods activate the medial hypothalamus directly related to the control of energy homeostasis and stress response. In contrast, seeking and consumption of sucrose inhibit the activity of the medial hypothalamus, but strongly activate the brain reward area. This sucrose-induced shift in neuronal activity results in consumption of more and more palatable sweet foods at the expense of regular low-energy foods. Repeated overeating of sucrose may alter the neurochemistry in the brain reward regions promoting sucrose craving and triggering sucrose binge-eating episodes. On the other hand, sucrose-induced decrease in the activity of the medial hypothalamus directly affects the response of the neuroendocrine system to stress. The stress-induced neuronal expressions of stress neuropeptides as well as the release of plasma stress hormones are blunted by consumption of sucrose. This ‘anti-stress’ effect of sucrose may explain overconsumption of sweets during stress even in the absence of hunger or needs for calories. This chapter reviews the neuronal effects of sucrose that may be beneficial by giving us energy and helping to relieve stress, or, when sucrose is over consumed, may be detrimental by leading to uncontrolled craving for sucrose, eating disorders and obesity.
While studies in humans suggest a role for psychosocial factors as well as biological and genetic processes in the development of eating disorders, the specific etiologic mechanisms remain largely unknown. In this virtual issue, we present a collection of 14 archived articles from the International Journal of Eating Disorders to highlight the utility of animal studies of eating disorders to advance our understanding of eating disorder etiology. Selected articles establish animal studies as valid tools to study disordered eating behavior, offer insight into potential neurobiological mechanisms, and highlight novel targets for future pharmacological treatments. Clinical implications of each article's findings are included to demonstrate the translational value of animal studies for the eating disorders field. We hope that the exciting concepts and findings in this issue inspire future animal studies of eating disorders.
Zusammenfassung. Theoretischer Hintergrund: Ergebnisse tierexperimenteller Studien lassen darauf schließen, dass Fastenperioden mit reduzierter sympathischer Aktivierung verbunden sind, während Zeiten der normalen Ernährung oder des Überessens mit einer erhöhten sympathischen Aktivierung einhergehen. Fragestellung: In der vorliegenden Studie wurden Parameter der kardialen sympatho-vagalen Balance zu endokrinologischen Variablen des Ernährungszustandes in Beziehung gesetzt. Methode: Sechzehn Frauen mit der Diagnose Bulimia nervosa wurden anhand ihres Serum-Profils in verschiedenen endokrinologischen Parametern (Glukose, Prä-Albumin, Somatomedin-C, TSH, Leptin) in zur Zeit mangelernährt (fastend) und nicht-mangelernährt (nicht-fastend) kategorisiert und mit 14 alters- und BMI-parallelisierten gesunden Frauen verglichen. Zur Bestimmung der sympatho-vagalen Erregungslage wurden die spektralanalytischen Komponenten der Herzfrequenzvariabilität mit autoregressiven Analysen von Ruhedaten berechnet. Ergebnisse: Wie erwartet war die Ruhepulsfrequenz bei fastenden Bulimikerinnen signifikant niedriger als bei nicht-fastenden Bulimikerinnen oder Kontrollpersonen. Nicht-fastende Bulimikerinnen zeigten die niedrigsten vagalen und die höchsten sympathischen Frequenzkomponenten in der Herzfrequenzvariabilität. Schlussfolgerungen: Diese Ergebnisse bestätigen die Hypothese kardialer sympathischer Hemmung während des Fastens und der erhöhten sympathischen Aktivierung bei normaler Ernährung oder Überessen.
Bulimia nervosa (BN) is highly comorbid with substance abuse and shares common phenotypic and genetic predispositions with drug addiction. Although treatments for the two disorders are similar, controversy remains about whether BN should be classified as addiction.
Here, we review the animal and human literature with the goal of assessing whether BN and drug addiction share a common neurobiology.
Similar neurobiological features are present following administration of drugs and bingeing on palatable food, especially sugar. Specifically, both disorders involve increases in extracellular dopamine (DA), D1 binding, D3 messenger RNA (mRNA), and ΔFosB in the nucleus accumbens (NAc). Animal models of BN reveal increases in ventral tegmental area (VTA) DA and enzymes involved in DA synthesis that resemble changes observed after exposure to addictive drugs. Additionally, alterations in the expression of glutamate receptors and prefrontal cortex activity present in human BN or following sugar bingeing in animals are comparable to the effects of addictive drugs. The two disorders differ in regards to alterations in NAc D2 binding, VTA DAT mRNA expression, and the efficacy of drugs targeting glutamate to treat these disorders.
Although additional empirical studies are necessary, the synthesis of the two bodies of research presented here suggests that BN shares many neurobiological features with drug addiction. While few Food and Drug Administration-approved options currently exist for the treatment of drug addiction, pharmacotherapies developed in the future, which target the glutamate, DA, and opioid systems, may be beneficial for the treatment of both BN and drug addiction.
The prevalence of obesity continues to rise despite advances in behavioral, pharmacological, and surgical treatments. This is likely in part due to the overabundance of highly caloric food, which has extremely rewarding properties associated with dopaminergic neurotransmission in the ventral striatum where the nucleus accumbens (NAc) is located. The NAc has been repeatedly implicated in reward-seeking disorders, including binge eating, a common feature of obesity. Altered expression of dopaminergic receptors in the NAc has been associated with binge eating both in animals and humans. The application of deep brain stimulation (DBS) to the NAc to suppress binge eating in mice may further implicate the dopamine system in aberrant eating behavior. Molecular, biochemical, and optogenetic studies of the mechanism of DBS may also shed light on future treatment strategies for binge eating. Furthermore, given that DBS is a commonly used surgical therapy for multiple neurological disorders, this work may also pave the way for expanding the application of DBS to obesity.
Eating-disorder patients exhibit not only abnormal eating attitudes but also pathologic anxiety-like behaviors. The specific nature of the relationship between dieting and anxiety-like behavior is unknown.Methods
To investigate the adaptational changes that resulted from chronic restricted scheduled feeding (2-hour access per day for 2 weeks) and subsequent free refeeding, longitudinal changes in the microstructure of feeding behavior were studied in male rats. To study the relationship between restricted feeding and anxiety-like behavior, separate rats were tested in the elevated plus-maze under the following conditions: 1) free feeding; 2) acute food restriction (2-hour access for 1 day); 3) chronic food restriction (for 10 days); or 4) postrecovery (after 10 days of free feeding subsequent to chronic food restriction).ResultsThe effects of chronic food restriction on meal structure diminished within a few days after refeeding. Decreased anxiety-like behavior was seen during acute and chronic food restriction and did not reflect nonspecific behavioral activation. Anxiolytic-like effects persisted after 10 days of refeeding.Conclusions
Chronic food restriction produced reductions in anxiety-like behavior that persisted beyond the normalization of food intake patterns. The findings might have etiologic and pathophysiologic relevance for the restrained eating pattern in eating-disorder patients with comorbid anxious symptoms.
Preclinical models are needed to investigate the neuro- and psycho-biology of binge eating (BE) and to identify innovative pharmacotherapeutic strategies. A new model, based on the combination of cyclic caloric restriction and acute stress, has been recently developed in our laboratory to induce BE of highly palatable food (HPF) in female rats. Rats were exposed to three cycles of food restriction/refeeding and then stressed on the test day. Acute stress was elicited by exposing rats to HPF, but preventing them from accessing it for 15 min. This experimental procedure induces a marked binge-type intake of HPF. Interestingly, in this model BE does not occur during the estrus phase of the ovarian cycle; if data from female rats in estrus are not included in the statistical analysis, the variability of the BE response is very low. Topiramate, sibutramine, and fluoxetine potently inhibited HPF intake in this model, providing evidence for its predictive validity. The model has been used to investigate the effect of drugs targeting stress mechanisms. The corticotrophin-releasing factor (CRF)-1 receptor antagonist R121919 selectively inhibited BE, indicating that CRF is involved in the BE response. Its effect is likely exerted in extra-hypothalamic sites rather than in hypothalamic sites controlling the hypothalamic–pituitary–adrenal axis. In addition, orexin-1 receptor antagonists selectivity inhibit BE; studies are under way to evaluate whether their effects are related to influences on stress or on reward mechanisms. This preclinical model appears to be highly reliable and reproducible; it may represent a valid model to identify novel pharmacological treatments of BE disorder and bulimia nervosa.
Laboratory animal models are valuable in that they allow researchers to better understand the various biological and behavioral factors that may contribute to eating disorders and substance use disorders, as well as an opportunity to discover effective treatments for each. This chapter describes how animal models have been used to study features of anorexia nervosa, bulimia nervosa, and binge eating disorder, with a particular focus on the variables associated with the development of such behavior in animals. The second half of this chapter focuses on the various animal models that have been used to explore key characteristics of addiction. This chapter concludes with a brief discussion of the overlaps that exist between the two types of disorders and suggestions for future research directions.
We tested the hypothesis that perinatal undernourishment is a factor for binge eating. At 52days rats born from dams fed on 17% protein (Control) or 8% protein (Undernourished) were distributed into four groups, two of which continued to be fed ad. libitum chow and two were submitted to three consecutive Restricted/Refeeding (R/R) cycles. According to the following schedule: Control Naïve (from mothers fed 17% protein/no restriction phase); Control Restricted (from mothers fed 17% protein/restriction phase); Undernourished Naïve (from mothers fed 8% protein/no restriction phase); and Undernourished Restricted (from mothers fed 8% protein/restriction phase). Each cycle consisted of a restriction phase (in the first four days 40% of the mean daily individual chow intake was offered for consumption), followed by a refeeding phase (4days of chow ad.lib.). After the three cycles, all animals were subjected to a feeding test (chow diet and palatable food ad.lib. for 24h). During the feeding test, the Undernourished Restricted demonstrated rebound hyperphagia during 2, 4 and 6h. These results suggest the perinatal undernourishment cannot contribute to a binge eating phenotype.
This paper presents a critical review of diagnostic criteria and determination models of anorexia and bulimia, used in the International Journal of Eating Disorders. It is particularly questioning the notion of internal determination of these disorders, emphasizing this mode of interpretation with an analysis of the weight phobia (fat phobia). The recovery of this biobehavioral model of anorexia induced by physical activity, and the set of experiments that underlie it, aims to bring the consideration of alternative explanations for eating disorders without the need to appeal to emotional or cognitive variables as determinants of these disorders.
La práctica de restricción alimentaria intermitente (RAI) bien como sus variaciones, es utilizada por individuos con intensión de pérdida de masa corporal. Existen evidencias científicas favorables a esta práctica; no obstante, son insuficientes los estudios que muestren las consecuencias a largo plazo y sus repercusiones en el control de la homeostasis energética en el sistema nervioso central (SNC). Considerando su creciente utilización, tanto como su recomendación y además de la controversia existente en la bibliografía, la presente revisión tiene como objetivo mostrar los efectos de la RAI sobre la regulación central de la homeostasis energética registrados en la literatura.
Previous research has demonstrated significant associations between increased levels of ovarian hormones and increased rates of binge eating (BE) in women. However, whereas all women experience fluctuations in ovarian hormones across the menstrual cycle, not all women binge eat in response to these fluctuations, suggesting that other factors must contribute. Stress is one potential contributing factor. Specifically, it may be that hormone-BE associations are stronger in women who experience high levels of stress, particularly as stress has been shown to be a precipitant to BE episodes in women. To date, no studies have directly examined stress as a moderator of hormone-BE associations, but indirect data (that is, associations between BE and stress and between ovarian hormones and stress) could provide initial clues about moderating effects. Given the above, the purpose of this narrative review was to evaluate these indirect data and their promise for understanding the role of stress in hormone-BE associations. Studies examining associations between all three phenotypes (that is, ovarian hormones, stress, and BE) in animals and humans were reviewed to provide the most thorough and up-to-date review of the literature on the potential moderating effects of stress on ovarian hormone–BE associations. Overall, current evidence suggests that associations between hormones and BE may be stronger in women with high stress levels, possibly via altered hypothalamic–pituitary–adrenal axis response to stress and increased sensitivity to and altered effects of ovarian hormones during stress. Additional studies are necessary to directly examine stress as a moderator of ovarian hormone–BE associations and identify the mechanisms underlying these effects.
Background
Variations in mental health may contribute to or impair healthy eating. The relation between eating and mental health is bi-directional: one’s mood or psychological state can affect what and how much one eats, and eating affects one’s mood and psychological well-being. Thus, if we want to promote and develop strategies to encourage healthy eating, it is important to understand the connections between mental health and healthy eating.
Methods
To contribute to this understanding, we examine the research on individual differences in how people respond to food, as well as mood, and emotional, social and collective influences on what and how much is eaten; we then examine the implications of these connections for mental health, with a focus on adolescents and adults. Looking at the relation between eating and mental health from the other direction, we review research investigating whether the amount that one eats or particular foods one ingests can make one feel good or bad about oneself.
Conclusions
Overeating and undereating have complex effects, sometimes contributing to improved feelings of well-being and at other times leaving the individual feeling guilty, deprived, depressed and anxious. We attempt to identify both what we know and the gaps in our knowledge.
Given the frequency of transition from anorexia nervosa to bulimia nervosa, this study investigated whether a history of activity-based anorexia (ABA) during adolescence would promote binge eating during adulthood in female rats.
Adolescent rats were given 1-h unlimited access to chow and ad libitum access to a running wheel until body weight reached <80%, indicating the development of ABA. During adulthood, all groups were given 21 days of access to a palatable food for 2 h/day and ad libitum access to chow.
During adolescence, rats in the ABA paradigm developed increased wheel running and decreased food intake, reaching <80% of body weight after 3 days. However, there were no significant differences between groups in the amount of binge food consumed during adulthood.
A brief episode of ABA during adolescence did not lead to increased binge eating later in life. Longer-term models are needed to determine whether a propensity toward binge eating may result from more sustained ABA during adolescence.
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.
The relationship between depressive symptoms and starvation, reflected by body weight and biochemical parameters, was investigated in 64 patients fulfilling DSM-III criteria for anorexia nervosa or bulimia. Multiple regression analysis revealed significant effects of body weight and beta-hydroxybutyric acid, respectively, on such specific depressive symptoms as depressed or dysphoric mood when controlling for severity of psychopathology of the eating disorder.
Explores why women in general are more prone to develop bulimia than men and which women in particular have a higher risk of becoming bulimic. Risk factors for bulimia are discussed in terms of sociocultural variables, such as the central role of beauty in the female sex-role stereotype; developmental processes; psychological variables; and biological factors, including genetic determinants of weight, the disregulation of body weight and eating through dieting, affective instability, and family variables. The sociocultural and psychological mediators that contribute to the increased risk of bulimia in this era are discussed, including a shift toward an increased emphasis on thinness, the effects of media attention on dieting and bulimia, fitness, and shifting sex roles. Results indicate that female socialization is a major contributing factor in bulimia. Although significantly fewer men than women currently show evidence of bulimia, it is hypothesized that the general pressure on men to become conscious of physical fitness and appearance, together with certain male subcultures that emphasize weight standards, will lead to an increased incidence of bulimia in men. (5½ p ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Fifteen patients with bulimia (DSM-III) and 22 patients with anorexia nervosa (10 "restricters" and 12 "vomiters") were compared with 24 age- and sex-matched healthy controls. Serial blood samples were collected between 8:30 and 9:30 a.m. with patients in supine and standing positions. Elevated blood values of beta-hydroxybutyric acid and free fatty acids were observed in the majority of patients with bulimia and anorexia nervosa. These data indicate that many patients with bulimia showed the metabolic signs of starvation at the time of the study, a finding supported by the symptoms of endocrine adaptation to starvation, namely low triiodothyronine and a decreased noradrenaline response to an orthostatic test in many of these patients.
The eating behavior of 30 female bulimics was studied by a 24-hour dietary recall for 3 weeks. The patients showed a wide range of bulimic behavior as can be seen by the wide range of 0–54 bingings per patient during investigation. Binge-eating episodes favorably happened in the afternoon and at night, preferably following regular meals. The average total daily energy intake (including bingings) was 3100 kcal. When binging, the women chose high-calorie food, which is easy to handle. The nutrient (carbohydrates, protein, fat) content was high in fat. Despite consumption of high-calorie diets, there were still patients who did not reach the actual German recommendations for daily food intake, particularly for vitamins and minerals. In addition, nutritional depletion by vomiting and laxative abuse has to be taken into account.
Synopsis
Thirty patients were selected for a prospective study according to two criteria: (i) an irresistible urge to overeat (bulimia nervosa), followed by self-induced vomiting or purging; (ii) a morbid fear of becoming fat. The majority of the patients had a previous history of true or cryptic anorexia nervosa. Self-induced vomiting and purging are secondary devices used by the patients to counteract the effects of overeating and prevent a gain in weight. These devices are dangerous for they are habit-forming and lead to potassium loss and other physical complications. In common with true anorexia nervosa, the patients were determined to keep their weight below a self-imposed threshold. Its level was set below the patient‘s healthy weight, defined as the weight reached before the onset of the eating disorder. In contrast with true anorexia nervosa, the patients tended to be heavier, more active sexually, and more likely to menstruate regularly and remain fertile. Depressive symptoms were often severe and distressing and led to a high risk of suicide.
A theoretical model is described to emphasize the interdependence of the various symptoms and the role of self-perpetuating mechanisms in the maintenance of the disorder. The main aims of treatment are (i) to interrupt the vicious circle of overeating and self-induced vomiting (or purging), (ii) to persuade the patients to accept a higher weight. Prognosis appears less favourable than in uncomplicated anorexia nervosa.
This study was an investigation of personality factors associated with bulimic behaviors and attitudes in males. Various measures that have been noted as predictors of female bulimia were tested on 96 college students. Chronic dietary restraint and interoceptive awareness were the strongest predictors of more maladaptive eating patterns. The results suggest that maladaptive eating patterns in males and females may share a common set of features.
We characterized the naturalistic feeding patterns of 54 women with bulimia nervosa and 11 matched controls over a continuous 24-hr period in a feeding laboratory. Overall, bulimic women consumed more calories in 24 hr (4446 +/- 584 kcal) than did controls (1845 +/- 649 kcal). Bulimic women consumed a wide range of caloric intake, with 44% overeating and 19% undereating in comparison to the range of controls. In addition, bulimics showed a disruption of circadian feeding patterns. For overeating bulimic women, the majority of meals were of normal size and frequency. Increased caloric intake in the group of overeating bulimic women was mainly due to the fact that 37% of their meals were greater than 1000 calories. Large meals occurred predominantly during the afternoon and evening and consisted primarily of dessert and snack foods. Importantly, the percentage of fat, but not carbohydrates, consumed increased as meal size, and 24-hr caloric intake increased. This study is the first to describe the naturalistic feeding characteristics of a large number of bulimics by direct observation. These findings are consistent with previous self-reports and extend and replicate previous laboratory studies. We think that laboratory studies are a reasonable replica of naturalistic feeding and should facilitate further investigation of the psychological and physiological correlates of feeding behavior in eating disorders.
Eating behavior in eating-disordered subjects was investigated by recording food intake and subjective ratings following three preloads differing in calories, weight and connotation. Subjects were patients with a DSM-IIIR diagnosis of anorexia nervosa or bulimia nervosa and nonpatient volunteers (normal-weight or overweight dieters, and normal-weight nondieters). After all preloads, anorectics ate significantly less than all other subjects except normal-weight dieters, and anorectics rated hunger and desire to eat consistently lower and fullness greater than all other subjects. When analysis of intake was adjusted for body weight, anorectics and normal-weight dieters still consumed significantly less than controls. Anorectics selected foods that were lower in fat and carbohydrate and ate a larger proportion of calories as protein than the other subjects. All groups decreased subsequent intake after the high-calorie preload except bulimics. This study demonstrates that the regulatory capacity of eating-disordered individuals can be investigated and that aberrant eating behavior was observed.
In order to examine the meal pattern characteristics associated with bulimia nervosa the meal patterns of 19 untreated bulimia nervosa, 12 recovered bulimics, and 21 normal controls spontaneously eating in their natural environments were compared. Subjects reported in a diary everything they either ate or drank for seven consecutive days. Meal pattern correlations included comparisons of the groups in regard to meal size (and binge size), meal frequency, premeal and postmeal intervals, deprivation ratios, satiety ratios, stomach contents, and composition of meals and binges. Results indicated that, although total reported intake was normal, only 33% of the total calories consumed by the untreated bulimia nervosa subjects were not followed immediately by purging. Both purged and unpurged binges were twice as large as their meal sizes which did not differ from normal. It is hypothesized that the caloric restriction of the untreated bulimics is binge/purge specific, and is used by them as a form of weight control. The recovered group showed a lack of responsivity to the signals that influence meal size and intermeal intervals in normals including impaired social facilitation of eating. They also had larger meal sizes, and greater frequency of meals. It is theorized that recovered bulimics employ other, as yet unspecified, means of food intake restriction resulting in an abnormal feeding pattern.
A correlation between dietary restraint and the occurrence of binge eating has been convincingly shown in several investigations. However, the mediating mechanisms have not yet been elaborated in detail nor linked to empirical evidence. This theoretical gap is addressed in the following. After a short review of behavioral and metabolic correlates of dietary restraint, potential effects of restrained eating on the psychophysiological regulation of food intake are described. These effects may lead to the disruption of intake regulation and therefore can be regarded as direct causes of binge eating.
The present study investigated cognitive processing in terms of vigilance performance in patients with bulimia nervosa. In particular, the relationship of vigilance performance to biological adaptation to starvation was examined
Naltrexone (0.05-5.0 mg/kg, SC) was administered to food-deprived rats prior to a 15-min food-preference test. Total food intake and feeding duration was reduced following administration of the opiate antagonist. However, while naltrexone reduced the consumption of the initially-preferred chocolate-coated cookies, the ingestion of the nonpreferred standard laboratory chow pellets was significantly enhanced. These data cannot be explained in terms of a general anorexic effect and nonspecific suppression of feeding responses. Instead, they indicate that naltrexone reduced preference for the highly palatable cookies, so that a feeding response to the chow pellets emerged. Under the conditions of test-familiarity, naltrexone did not reduce grooming, locomotion or rearing duration. An increase in locomotion may have been secondary to the reduction in feeding. The results agree with previous data from animal and human studies in suggesting that endogenous opioid peptide activity is involved in the palatability of preferred foods.
This report describes a standard procedure for studying the disordered eating behavior of bulimic patients in a laboratory setting. Test meals were given to eight normal weight women with bulimia under four different conditions on non-consecutive days. On day 1 they were asked to consume as much as they "would normally eat" by means of a straw from an opaque container holding 1500 g of a palatable liquid food. An eating monitor recorded the pattern of consumption. Five patients showed abnormalities of either excessive eating or acceleration of the rate of eating. On the second and third days they were given standardized amounts of an array of foods. They were instructed to eat normally on one of these days and to eat as much as they could on the other, in counterbalanced order. All patients ate to excess when they were asked, over a 28 to 90 min period, and consumed a mean of 4477 kcal (range 2083-8499 kcal) with a macronutrient composition similar to that of the typical American diet. They all vomited afterwards. On the day they were asked to eat normally, five patients overate and vomited, two ate very little, and one refused to participate. On the fourth day patients were asked to eat as much as they could of a single item, ice cream. Six patients consumed a mean of 1545 kcal (range 741-2919 kcal); one patient ate only 85 kcal; and one patient refused to participate. There were large and significant correlations among the sizes of the various meals consumed in excess.(ABSTRACT TRUNCATED AT 250 WORDS)
We first establish the association between binge eating and dieting and present sequence data indicating that dieting usually precedes binging, chronologically. We propose that dieting causes binging by promoting the adoption of a cognitively regulated eating style, which is necessary if the physiological defense of body weight is to be overcome. The defense of body weight entails various metabolic adjustments that assist energy conservation, but the behavioral reaction of binge eating is best understood in cognitive, not physiological, terms. By supplanting physiological regulatory controls with cognitive controls, dieting makes the dieter vulnerable to disinhibition and consequent overeating. Implications for therapy are discussed, as are the societal consequences of regarding dieting as a "solution" to the problem of binging.
SYNOPSIS
Thirty-two patients who complained of episodes of ravenous overeating which they felt unable to control (bulimia) were asked to describe their behaviour and symptoms. There was considerable variation both between and within individuals, but a number of factors were defined which appeared to be common to all with the complaint. It is difficult to set up strict criteria for the recognition of bulimia, and those that have recently been proposed are criticized in the light of our present findings.
A highly palatable diet (ordinary chow supplemented with 4 highly palatable items changes every day) (HPD) provokes hyperphagia and overweight in the rat. After 17 weeks of such a diet, naltrexone (0.5 or 2.5 mg/kg IP) and opiate antagonist, was injected at the beginning of the dark period, and a food intake test was performed during the 3 following hours. Naltrexone does not modify the energy intake in control rats receiving ordinary chow but suppresses HPD induced hyperphagia. The involvement of the beta-endorphin system in this type of hyperphagia is discussed.
Pharmacological treatments are one of several strategies used in the treatment of anorexia nervosa and bulimia nervosa. Many studies have found that antidepressants are effective in the treatment of bulimia nervosa and these drugs represent a mainstay of treatment for these patients. Over the past several years, selective serotonin reuptake inhibitors have become perhaps the most commonly used class of drugs. A variety of medications have been investigated for anorexia nervosa, but there is little consistent evidence that medications are effective. In both these illnesses it is important to diagnose and treat any comorbid conditions including mood and anxiety disorders; this may involve the administration of other medications, including anxiolytics such as benzodiazepines or buspirone or mood stabilising agents such as lithium, valproic acid (valproate sodium) or carbamazepine.
In this two-part study, an animal model of binge eating was first produced, then the rate of acquisition of cocaine self-administration was assessed. Initially, 16 female weanling rats were food deprived (DEPR) at 25, 95, and 143 days of age. Another group of 16 age-matched controls was allowed ad lib access to food. Each time the DEPR group was food deprived, they were allowed to recover to normal weight. They were then injected with butorphanol tartrate (BUTR), an opioid that stimulates feeding, and food intake was measured for 4 h. All rats given BUTR consumed significantly more food than those given saline. Animals with DEPR history consumed food over a longer period of time, and at h 4 after BUTR injection, they consumed significantly more food than controls. In the second part of the experiment, an autoshaping procedure was used to quantitatively evaluate the rate of acquisition of cocaine self-administration. By day 30, 86% of the DEPR and 69% of the control groups had acquired cocaine self-administration.
Food restriction is correlated with binge eating, but evidence that restriction leads to binge eating is scanty. In this study we investigated postwar binge eating in 67 World War II combat veterans and 198 former prisoners of war. As predicted, binge eating was relatively rare in combat veterans but was significantly more prevalent in veterans who, as prisoners in German prisoner of war camps, lost significant amounts of weight during their captivity. Our data thus support the contention that starvation or dieting seems to precede binge eating.
Food selection and macro nutrient content were evaluated in a group of bulimic subjects, both during the nonpurged intake and the bingeing. Dietary data was assessed by single 24-hour recall. As expected, energy distribution and food selection differed markedly between the nonpurged diet and the binges. The main differences were related to an inverse relationship in the order of macro nutrients, fat being the dominant and protein the least important source of macro nutrients during binge eating. The nutrient content during binges admittedly had a preponderance for fat. Nevertheless, the primary choice of food items during binges was carbohydrates, which was shown both by a greater quantity and by the subjects' own desires.
It has been suggested that opioids modify food intake by enhancing palatability. In the present series of studies we evaluated the effect of naloxone on food intake of a preferred food (chocolate chip cookies), normal rat chow, and an "aversive" food (high fiber chow). We found that naloxone decreased 18- and 48-h deprivation-induced intake of chocolate chip cookies much more potently than that of chow, when these foods were presented on separate occasions. When these foods were presented concurrently, this difference in naloxone's potency was no longer apparent. When rats were offered high fiber chow, only the 10 mg/kg dose of naloxone decreased intake. In these same rats naloxone significantly decreased normal chow intake at a dose of 0.1 mg/kg. Thus, naloxone's ability to decrease food intake appears to be dependent upon the palatability of the food.
The present study was designed to assess whether the pattern of meal feeding and the degree of caloric restriction have an effect on the body weights and refeeding patterns of restricted 4-month-old Long-Evans rats, relative to ad lib-fed controls. Four experimental groups of rats (n = 6 each) were put on different paradigms of food restriction, and a fifth group fed ad lib throughout served as controls. Twelve rats were restricted to receiving 50% of their mean baseline food intake, and 12 rats received only 70% of their baseline food intake. Each experimental group was further subdivided with one subgroup receiving all of their calories in one meal/day and the other with caloric intake equally divided into two meals/day. There was no statistical difference in the final body weights of the restricted groups. Although there appeared to be identical patterns of weight regain, none of the restricted groups ever reached the mean body weight of the controls because of an asymptotic leveling off of rate of body weight regain. Rats that had received 50% of baseline calories as two meals/day had significantly more adipose mass than did any other group. The present findings suggest that in the rat, refeeding and, hence, regulation, occurs to normalize rate of weight gain rather than absolute body weight.
It has been suggested that a new diagnostic category be added to the section on eating disorders in DSM-IV. This new diagnosis has been termed binge eating disorder. In this article we argue that for two main reasons it would be a mistake to include binge eating disorder in DSM-IV: first, too little is known about binge eating and other related forms of recurrent overeating to justify its inclusion in DSM-IV; and second, its inclusion would be a source of diagnostic confusion. We argue that it is premature to crystallize this specific subgroup from amongst those who recurrently overeat and that to do so would impede the acquisition of knowledge rather than enhance it. We advocate a research strategy that involves studying broad samples of those with recurrent overeating rather than narrow ones.
Peptide YY (PYY) administered centrally in rats induces powerful overeating. PYY also occurs endogenously in humans and is elevated in abstaining bulimic patients. To examine the effect of PYY in an environment that parallels some aspects of bulimia, rats were tested in a paradigm associated with approach-avoidance behavior, choosing a preferred (sweet) food paired with shock, over regular food safe from shock. PYY-treated rats chose to sustain shock to retrieve and consume the preferred food, at a significantly greater speed and quantity. The number of approaches that were met without retrieval of food due to anxiety after PYY treatment indicates that PYY increased motivation towards feeding, rather than anxiolysis. This effect of PYY in a model of conflict associated with food choice resembles aspects of bulimic binge-eating, which is characterized by the repetitive, rapid intake of food, despite anxiety associated with this behavior.
Behavioral models in psychopharmacology: Theoretical, industrial, and clinical perspectives
- D V Coscina
- P E Garfinkel
Coscina, D. V., & Garfinkel, P. E. (1991). In P. Willner (Ed.), Behavioral models in psychopharmacology: Theoretical,
industrial, and clinical perspectives. Cambridge: Cambridge University Press.
Eating disorders Adult abnormal psychology
- P J Cooper
- Z Cooper
Cooper, P. J., & Cooper, Z. (1988). Eating disorders. In E. Miller and P. J. Cooper (Eds.), Adult abnormal psychology.
London: Churchill Livingstone.
Diagnostic and statistical manual of mental disorders
American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author.