Relatively enriched housing conditions delay binge onset but do not attenuate binge size.

Housing and enrichment conditions are essential factors to consider when using animal models of behavior, as they can alter the behavior that is under investigation. The goal of this study was to determine the impact of the relatively enriched environment recommended by current animal care guidelines on development and maintenance of binge-type behavior in rats, using the limited access (LA) binge model. Non-food-deprived rats were divided into two groups, enriched and nonenriched, with all rats housed in shoebox cages. Bedding, nesting material, toys, and a solid floor were provided only to the enriched group to create a state of relative enrichment, or RE, compared to the nonenriched conditions historically used in the LA model. Enriched and nonenriched groups were further divided into control and experimental groups. Control rats received access to an optional source of fat (vegetable shortening) for 30min each day (daily access) while experimental rats received 30-min optional fat access on Monday, Wednesday, and Friday only (intermittent access). The four groups were designated C-E (Control-Enriched), C-NE (Control-Nonenriched), I-E (Intermittent-Enriched), and I-NE (Intermittent-Nonenriched). Bingeing in the LA model is established when a group with intermittent access (i.e., the I-E or I-NE group) consumes significantly more vegetable shortening during the limited access period than a group with daily access (i.e., the C-E or C-NE group). Access sessions continued for 8weeks under these conditions, at which time the housing conditions of the I-E and I-NE groups were reversed for an additional 8weeks of access sessions. Intakes of the C-E and C-NE groups were similar and data from these two groups were combined. Relative to this Combined Control Group (CCG), the I-NE group began bingeing in week 3 while the I-E group binged during weeks 6 and 8. Following the reversal at the beginning of week 9, the newly enriched I-NE group ceased bingeing in week 9 but resumed bingeing in weeks 10-16. The newly nonenriched I-E group continued bingeing through the remainder of the study. Intakes of the I-E and I-NE groups were not significantly different at any time during the study. These results indicate that RE delays binge onset; that is, RE increases the time between the first fat access session and the first occurrence of bingeing. However, RE does not significantly alter the amount of fat consumed during binge sessions. Furthermore, addition of RE to a nonenriched group of animals (I-NE) does not reverse established binge behavior. Thus it appears that regardless of enrichment condition, intermittent access to vegetable shortening induces greater consumption of fat than does daily access. However, it is clear that a certain level of austerity in housing conditions is required for rapid development of lasting binge-type eating to occur. In addition, results suggest that it is unlikely that enrichment, to the degree provided in this study, can prevent or reverse binge-type eating in rats.

Binge-type eating disrupts dopaminergic and GABAergic signaling in the prefrontal cortex and ventral tegmental area.

OBJECTIVE: Binge eating is characterized by repeated intermittent bouts of compulsive overconsumption of food. Treatment is challenging given limited understanding of the mechanisms underlying this type of disordered eating. The hypothesis that dysregulation of mesocortical dopaminergic and GABAergic systems underlie binge eating was tested. METHODS: Analysis of gene expression within the ventral tegmental area and its terminal mesocortical regions was examined in bingeing rats before and after bingeing occurred. In addition, alterations in binge-type behavior induced by pharmacological inactivation of subnuclei of the prefrontal cortex (PFC) and by pharmacological activation and inhibition of cortical D1 and D2 receptors were examined. RESULTS: Correlative and functional evidence demonstrates dysregulated neurotransmitter processing by the PFC and ventral tegmental area, but not the amygdala or nucleus accumbens, in bingeing rats. Either GABAergic inactivation or D2-like receptor activation within the PFC increased consumption in bingeing rats, but not controls, suggesting that the PFC, and D2 receptors in particular, functions as a behavioral brake to limit bingeing. CONCLUSIONS: The act of bingeing resolved some gene expression differences that preceded binge onset, further suggesting that bingeing may partially serve to self-medicate a system driving this maladaptive behavior. However, the failure of bingeing to resolve other dopaminergic/GABAergic differences may render individuals vulnerable to future binge episodes.

Factors affecting the ability of baclofen to reduce fat intake in rats.

The GABA-B agonist baclofen has been reported to reduce the consumption of vegetable shortening, but not lard, in rats. This study sought to examine some of the factors that could account for these differences. Baclofen (0, 1.0, 1.8, 3.2 mg/kg, intraperitoneal) was tested: (i) on shortening and lard intake, (ii) under 'binge-type' and non-'binge-type' conditions, (iii) when each fat was presented alone or simultaneously, and (iv) with a 30-min or no pretreatment time. With a 30-min pretreatment time, baclofen (3.2 mg/kg, intraperitoneal) consistently reduced shortening intake under 'binge-type' and non-'binge-type' conditions, as well as when shortening was presented alone or when lard was simultaneously available. Baclofen also reduced lard intake under 'binge-type' and non-'binge-type' conditions, but only when lard was presented alone. Baclofen had no effect on chow intake. When each fat was presented alone, and with no pretreatment time, the results were less consistent; baclofen reduced shortening intake only under non-'binge-type' conditions, and lard intake only under 'binge-type' conditions, and also stimulated chow intake. In summary, the type of fat, the presentation mode (one fat presented alone or two fats simultaneously), and the time between baclofen administration and intake all influence the ability of baclofen to reduce fat intake.

Baclofen reduces binge eating in a double-blind, placebo-controlled, crossover study.

Baclofen has shown promise in treating substance use disorders and also reduced binge frequency in an open-label trial. This placebo-controlled, double-blind, crossover study further assessed the effects of baclofen on binge eating. Twelve individuals who self-reported binge eating completed the study. Data were collected during a run-in period (no drug or placebo), placebo phase (48 days), and baclofen phase (titrated up to 60 mg daily or the maximum tolerated dose, 48 days). All the participants were exposed to all conditions. Participants completed a binge diary daily, and the Binge Eating Scale (BES), Food Craving Inventory-II (FCI-II), and Hospital Anxiety and Depression Scale (HADS) at regular intervals throughout the study. Baclofen significantly reduced binge frequency relative to placebo and run-in (P<0.05). This confirms results from the previous open-label trial. Baclofen also produced slight, but significant, increases in depression symptomatology as assessed by the HADS. Binge severity (BES scores) and craving (FCI-II scores) were significantly reduced during placebo and baclofen phases, that is both measures exhibited significant placebo effects. Tiredness, fatigue, and upset stomach were the most commonly reported side-effects. These results indicate that baclofen may be a useful treatment for binge eating in some patients.

Rodent models of binge eating: are they models of addiction?

Are recently developed rodent models of binge eating also models of food addiction? Valid models should meet human criteria for both bingeing and substance dependence as described in the 4th edition and proposed for the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM). Similarly, behavioral profiles of bingeing animals should share characteristics with those of animal models of drug addiction. We evaluate and discuss current rodent models of bingeing, their contributions to scientific understanding of bingeing, their validity with respect to DSM criteria, and their overlap with models of addiction. The models described indicate that repeated intermittent bouts in which large quantities of fatty or sugary foods are consumed (binges) are associated with behavioral changes similar to those described for drugs of abuse. In contrast, control groups consuming the same foods in a nonbinge-type manner do not exhibit an "addiction-like" behavioral profile. Thus, fatty/sugary foods in and of themselves do not appear to have addictive qualities. Rather, the manner in which they are consumed appears to be critical. In addition, while rodent models of bingeing and drug self-administration share similarities, we do not support reclassifying the bingeing-related eating disorders as substance use disorders because of differences that distinguish such disorders in humans.

A history of bingeing on fat enhances cocaine seeking and taking.

Binge eating and substance dependence are disorders characterized by a loss of control over consummatory behaviors. Given the common characteristics of these two types of disorders, it is not surprising that the comorbidity between eating disorders and substance abuse disorders is high (20-40%; Conason et al., 2006). It is unknown, however, whether loss of control in one disorder predisposes an individual to loss of control in the other. The present study, therefore, used a rodent model to test whether a history of binge eating would augment subsequent responding for cocaine. Using the limited access protocol described by Corwin et al. (1998), 45 adult male Sprague-Dawley rats were maintained on one of four dietary protocols for a period of six weeks: chow only (Chow; n = 9), continuous access to an optional source of dietary fat (Ad Lib; n = 12), 1-h access to an optional source of dietary fat daily (Daily; n = 12), or 1-h access to an optional source of dietary fat on Monday, Wednesday, and Friday (MWF; n = 12). All four groups also had unrestricted access to a nutritionally complete diet of chow and water. Fat-bingeing behaviors developed in the MWF rats, the group with the most restricted access to the optional fat. Thereafter, cocaine-seeking and -taking behaviors were assessed in all rats using a self-administration protocol modified from that described by Deroche-Gamonet et al. (2004), which focused on the motivation for and preoccupation with obtaining and consuming drug (assessed using a progressive ratio [PR] schedule of reinforcement) and persistence in responding for drug during periods of signaled drug non-availability (SNA). Rats with the MWF history tended to take more cocaine late in fixed ratio (FR) training, they persisted in their efforts to obtain cocaine in the face of signaled non-availability, worked harder for cocaine on a PR schedule of reinforcement, and exhibited more goal-directed behavior toward the cocaine-associated operandum. These results demonstrate a link between binge-type intake of fat and the development of drug-seeking and -taking behaviors, suggesting that a history of fat bingeing may predispose individuals to exhibit more robust "addiction-like" behaviors toward a substance of abuse. Thus, it appears that conditions promoting excessive behavior toward one substance (e.g., a palatable fatty food) beget excessive behavior toward another (e.g., cocaine).

The face of uncertainty eats.

The idea that foods rich in fat and sugar may be addictive has generated much interest, as well as controversy, among both scientific and lay communities. Recent research indicates that fatty and sugary food in-and-of itself is not addictive. Rather, the food and the context in which it is consumed interact to produce an addiction-like state. One of the contexts that appears to be important is the intermittent opportunity to consume foods rich in fat and sugar in environments where food is plentiful. Animal research indicates that, under these conditions, intake of the fatty sugary food escalates across time and binge-type behavior develops. However, the mechanisms that account for the powerful effect of intermittency on ingestive behavior have only begun to be elucidated. In this review, it is proposed that intermittency stimulates appetitive behavior that is associated with uncertainty regarding what, when, and how much of the highly palatable food to consume. Uncertainty may stimulate consumption of optional fatty and sugary treats due to differential firing of midbrain dopamine neurons, activation of the stress axis, and involvement of orexin signaling. In short, uncertainty may produce an aversive state that bingeing on palatable food can alleviate, however temporarily. "Food addiction" may not be "addiction" to food at all; it may be a response to uncertainty within environments of food abundance.

Individual effects of estradiol and progesterone on food intake and body weight in ovariectomized binge rats.

The individual roles of estradiol (E) and progesterone (P) in the control of food intake and body weight in ovariectomized (OVX) rats were investigated. Six groups of OVX Sprague-Dawley rats (n=9/group) were assigned to one of three 4-day cyclic hormone treatments: two groups were treated with E benzoate; two groups were treated with P; two groups were treated with both (EP). All rats had continuous access to chow and water throughout this 4-week study. One group of rats within each hormone treatment condition was fed chow ad libitum, and the second was subjected to a binge schedule: chow ad libitum plus 1-h access to an optional fat source on Monday, Wednesday, and Friday. A seventh OVX group (n=8) received the oil vehicle and chow. This group was included to monitor body weight and to verify hormone efficacy. The main findings were: (1) relative to rats receiving only P, E alone or EP attenuated 24-h chow intake tonically and cyclically, i.e. intake on Day 4, which models estrus, was lower in E and EP than in P, and also was lower than intake on Day 2, which models diestrus. In contrast, (2) neither E nor EP detectably affected optional fat intake during the 1-h fat access period relative to rats receiving only P when data were collapsed across the entire study. However, (3) E and EP had large effects on fat intake relative to P during the 1-h fat access period at the start of the study, but not at the end, when bingeing was fully established. (4) E and EP led to lower and apparently normal levels of body weight compared to rats receiving only the oil vehicle or only P. These results indicate that (1) administration of E alone has similar effects as co-administration of E and P on feeding and body weight in rats bingeing on fat, (2) with or without P, the inhibitory effects of E on meal size are compromised when bingeing on fat, and (3) the effects of E on binge size change dynamically as bingeing develops.

Feeding and reward: perspectives from three rat models of binge eating.

Research has focused on understanding how overeating can affect brain reward mechanisms and subsequent behaviors, both preclinically and in clinical research settings. This work is partly driven by the need to uncover the etiology and possible treatments for the ongoing obesity epidemic. However, overeating, or non-homeostatic feeding behavior, can occur independent of obesity. Isolating the variable of overeating from the consequence of increased body weight is of great utility, as it is well known that increased body weight or obesity can impart its own deleterious effects on physiology, neural processes, and behavior. In this review, we present data from three selected animal models of normal-weight non-homeostatic feeding behavior that have been significantly influenced by Bart Hoebel's 40+-yr career studying motivation, feeding, reinforcement, and the neural mechanisms that participate in the regulation of these processes. First, a model of sugar bingeing is described (Avena/Hoebel), in which animals with repeated, intermittent access to a sugar solution develop behaviors and brain changes that are similar to the effects of some drugs of abuse, serving as the first animal model of food addiction. Second, another model is described (Boggiano) in which a history of dieting and stress can perpetuate further binge eating of palatable and non-palatable food. In addition, a model (Boggiano) is described that allows animals to be classified as having a binge-prone vs. binge-resistant behavioral profile. Lastly, a limited access model is described (Corwin) in which non-food deprived rats with sporadic limited access to a high-fat food develop binge-type behaviors. These models are considered within the context of their effects on brain reward systems, including dopamine, the opioids, cholinergic systems, serotonin, and GABA. Collectively, the data derived from the use of these models clearly show that behavioral and neuronal consequences of bingeing on a palatable food, even when at a normal body weight, are different from those that result from simply consuming the palatable food in a non-binge manner. These findings may be important in understanding how overeating can influence behavior and brain chemistry.

Baclofen, raclopride, and naltrexone differentially affect intake of fat and sucrose under limited access conditions.

Gamma-aminobutyric acid (GABA), dopamine, and opioids are implicated in impulse control, addiction and binge eating. Recent evidence suggests that sucrose alters the effects of GABAergic, dopaminergic, and opioid receptor ligands on consumption of a fatty food in a rat limited-access binge protocol. This study determined the independent effects of fat and sucrose on the efficacy of these ligands under limited-access conditions. Nonfood-deprived male Sprague-Dawley rats had 1 h access to fat (vegetable shortening) or sucrose (3.2, 10, or 32% w/v). Half had intermittent access (Monday, Wednesday, Friday) and half had daily access. Effects of baclofen (GABAB agonist), SCH 23390 (D1 antagonist), raclopride (D2 antagonist), and naltrexone (opioid antagonist) were assessed. Baclofen and naltrexone reduced fat intake regardless of the access schedule. Baclofen had no effect on sucrose intake; naltrexone reduced sucrose intake at higher doses than were required to reduce fat intake. Raclopride stimulated fat intake in intermittent-access rats and had no effect in daily-access rats; raclopride reduced sucrose intake in all groups. SCH 23390 reduced intake in a nonspecific manner. The results indicate the involvement of GABAB receptors in fat but not sucrose intake, and of D2 receptor dysfunction in rats with a history of bingeing on fat.

Symposium overview--Food addiction: fact or fiction?

Food addiction is a pervasive, yet controversial, topic that has gained recent attention in both lay media and the scientific literature. The goal of this series of articles is to use a combination of preclinical and clinical data to determine whether foods, like drugs of abuse, can be addictive, the conditions under which the addiction develops, and the underlying neurophysiological substrates. Operational definitions of addiction that have been used in the treatment of human disorders and to guide research in both humans and animals are presented, and an overview of the symposium articles is provided. We propose that specific foods, especially those that are rich in fat and/or sugar, are capable of promoting "addiction"-like behavior and neuronal change under certain conditions. That is, these foods, although highly palatable, are not addictive per se but become so following a restriction/binge pattern of consumption. Such consummatory patterns have been associated with increased risk for comorbid conditions such as obesity, early weight gain, depression, anxiety, and substance abuse as well as with relapse and treatment challenges. The topic of food addiction bears study, therefore, to develop fresh approaches to clinical intervention and to advance our understanding of basic mechanisms involved in loss of control.

Ovarian hormones inhibit fat intake under binge-type conditions in ovariectomized rats.

Binge eating is more common in females than in males. This study investigated the effects of ovarian hormones on binge-eating behavior in a diet-related rat model. Six groups of ovariectomized Sprague-Dawley rats were used (n=13/group). All rats had continuous access to chow and water throughout the study. One half of the rats were injected every fourth day with estradiol benzoate (2 microg/100 microl sesame oil) and progesterone (500 microg/100 microl sesame oil); the other half received only the sesame oil vehicle. Three feeding protocols were tested in each hormone injection condition: (1) chow only: no additional dietary fat access; (2) low-restriction: 1-h fat access every day; (3) high-restriction: 1-h fat access on Monday, Wednesday, and Friday. As previously reported in intact male and female rats, the high-restriction groups exhibited binge-like increases in 1-h energy intake during fat access. The major new finding of this study is that 1-h energy intake was tonically, but not cyclically, reduced in the hormone-treated high-restriction (binge) rats. Specifically, both low- and high-restriction hormone-treated rats consumed significantly less energy than did the oil-treated rats during the 1-h fat period (p<0.0001) and overall (p<0.0001), indicating a tonic inhibition of eating. However, food intake during the 1-h fat access period was also cyclically reduced in the hormone-treated low-restriction rats, but not in the hormone-treated high-restriction rats. These results indicate that the normal cyclic inhibitory influence of ovarian hormones on eating, but not their normal tonic inhibitory influence, is disrupted by conditions leading to binge-type eating.

Baclofen for binge eating: an open-label trial.

OBJECTIVE: Baclofen is a GABA-B agonist that may be useful in the treatment of substance use disorders, and also reduces 'binge-like' eating in rodents. We hypothesized that baclofen might be effective in reducing binge eating episodes in binge eating disorder (BED) and bulimia nervosa (BN). METHOD: Seven women with BED (n = 4) or BN (n = 3) took baclofen (60 mg/day) for 10 weeks. RESULTS: Six out of seven patients completed the full 10-week trial. Five out of seven participants (3 BED; 2 BN) demonstrated 50% or greater reduction of frequency of binge eating from beginning to end of the study. Three out of seven participants (2 BED; 1 BN) were free of binge eating at study end. Four out of seven participants elected to continue baclofen at study end. Baclofen was well tolerated by the participants. CONCLUSION: In this open-label trial, baclofen was associated with decreased binge eating frequency in patients with BED and BN.

An increase in dietary n-3 fatty acids decreases a marker of bone resorption in humans.

Human, animal, and in vitro research indicates a beneficial effect of appropriate amounts of omega-3 (n-3) polyunsaturated fatty acids (PUFA) on bone health. This is the first controlled feeding study in humans to evaluate the effect of dietary plant-derived n-3 PUFA on bone turnover, assessed by serum concentrations of N-telopeptides (NTx) and bone-specific alkaline phosphatase (BSAP). Subjects (n = 23) consumed each diet for 6 weeks in a randomized, 3-period crossover design: 1) Average American Diet (AAD; [34% total fat, 13% saturated fatty acids (SFA), 13% monounsaturated fatty acids (MUFA), 9% PUFA (7.7% LA, 0.8% ALA)]), 2) Linoleic Acid Diet (LA; [37% total fat, 9% SFA, 12% MUFA, 16% PUFA (12.6% LA, 3.6% ALA)]), and 3) alpha-Linolenic Acid Diet (ALA; [38% total fat, 8% SFA, 12% MUFA, 17% PUFA (10.5% LA, 6.5% ALA)]). Walnuts and flaxseed oil were the predominant sources of ALA. NTx levels were significantly lower following the ALA diet (13.20 +/- 1.21 nM BCE), relative to the AAD (15.59 +/- 1.21 nM BCE) (p < 0.05). Mean NTx level following the LA diet was 13.80 +/- 1.21 nM BCE. There was no change in levels of BSAP across the three diets. Concentrations of NTx were positively correlated with the pro-inflammatory cytokine TNFalpha for all three diets. The results indicate that plant sources of dietary n-3 PUFA may have a protective effect on bone metabolism via a decrease in bone resorption in the presence of consistent levels of bone formation.

Bingeing rats: a model of intermittent excessive behavior?

Intermittent excessive behaviors (IEB) characterize a variety human disorders including binge eating, drug abuse, alcoholism, aberrant sexual conduct, and compulsive gambling. Clinical co-morbidity exists among IEB, and limited treatment options are available. The use of behavioral models of bingeing and other feeding protocols is beginning to clarify neural similarities and differences that exist between IEB directed toward obtaining and consuming food and IEB directed toward obtaining and consuming drugs of abuse. Research from this laboratory using a limited access binge-type eating protocol may provide new insight into IEB.

Dietary saturated fat intake is inversely associated with bone density in humans: analysis of NHANES III.

Mounting evidence indicates that the amount and type of fat in the diet can have important effects on bone health. Most of this evidence is derived from animal studies. Of the few human studies that have been conducted, relatively small numbers of subjects and/or primarily female subjects were included. The present study assessed the relation of dietary fat to hip bone mineral density (BMD) in men and women using NHANES III data (n = 14,850). Multivariate models using SAS-callable SUDAAN were used to adjust for the sampling scheme. Models were adjusted for age, sex, weight, height, race, total energy and calcium intakes, smoking, and weight-bearing exercise. Data from women were further adjusted for use of hormone replacement therapy. Including dietary protein, vitamin C, and beta-carotene in the model did not influence the outcome. Analysis of covariance was used to generate mean BMD by quintile of total and saturated fat intake for 4 sex/age groups. Saturated fat intake was negatively associated with BMD at several hip sites. The greatest effects were seen among men < 50 y old (linear trend P = 0.004 for the femoral neck). For the femoral neck, adjusted mean BMD was 4.3% less among men with the highest compared with the lowest quintile of saturated fat intake (BMD, 95% CI: highest quintile: 0.922 g/cm2, 0.909-0.935; lowest quintile: 0.963 g/cm2, 95% CI: 0.950-0.976). These data indicate that BMD is negatively associated with saturated fat intake, and that men may be particularly vulnerable to these effects.

Binge eating in rats with limited access to vegetable shortening.

In this protocol, binge-type eating is induced in non-food-deprived rats by providing limited access to an optional source of dietary fat: vegetable shortening. The protocol is simple and inexpensive, and the binge behavior is robust, reliable, and maintainable across extended periods of time. Two peptides that normally affect fat intake in rats have no effect on fat intake under limited-access conditions. However, recent results with a GABA(B) receptor agonist and with progressive-ratio responding suggest that the behavior induced by the limited-access binge protocol may share similarities with substance abuse. This protocol is designed to model the kind of excessive behavior that characterizes bingeing-related eating disorders and certain addictions.

Baclofen reduces fat intake under binge-type conditions.

The GABA-B agonist baclofen reduces drug self-administration in rats and has shown promise clinically in the treatment of substance abuse. Baclofen generally does not reduce food intake in non-binge feeding protocols. In this study, baclofen was tested in a fat-binge protocol. Thirty male rats were divided into three groups (B: binge; FM: fat-matched; C: chow). B received a bowl of vegetable shortening for 2 h on Monday, Wednesday, and Friday (MWF) and continuous access to powdered chow (regular chow) in all phases. FM had continuous access to a regular chow+shortening mixture (FM chow) that provided the same proportion of shortening and regular chow that the B rats consumed in all phases. In addition, FM had the following: phase 1: no separate bowl of shortening; phase 2: 2-h MWF access to a separate bowl of shortening; phase 3, daily 2-h access to a separate bowl of shortening; C rats had continuous access to the regular chow in all phases. In addition, C had the following: phase 1: no separate bowl of shortening; phase 2: 2-h MWF access to a separate bowl of shortening; in phase 3, daily 2-h access to a separate bowl of shortening. Baclofen (1.0, 1.8 mg/kg, i.p.) reduced shortening intake regardless of access condition. Baclofen had no effect on, or stimulated, FM and regular chow intake. These results demonstrate that baclofen can reduce fat intake in rats under binge-type conditions. Furthermore, these results indicate that bingeing, as modeled in our protocol, is different from other forms of food intake and may share similarities with substance abuse.

Too much of a good thing: neurobiology of non-homeostatic eating and drug abuse.

In this paper, a framework involving four aspects to be considered when establishing an operational definition of non-homeostatic appetitive behavior is presented. The four aspects are (1) the quantity of the commodity consumed, (2) the quality or type of commodity consumed, (3) the context in which the behavior occurs, and (4) the specific kind of behavior that is directed toward obtaining and consuming the commodity of interest. This framework permits comparisons among a variety of non-homeostatic behaviors and accommodates different theoretical approaches reflected in the use of mechanistic, systems, behavioral, nutritional, and clinical experimental strategies. The speakers of this symposium were selected to emphasize the four aspects of non-homeostatic behavior, to represent several different approaches, and to facilitate discussion regarding neural similarities and differences between non-homeostatic eating and drug abuse. The various talks illustrated that boundaries need not exist among research fields, and that communication among the various areas enhances the research effort.

Behavioral models of binge-type eating.

PURPOSE: To describe and evaluate behavioral models of binge-type eating. DATA IDENTIFICATION: Studies were identified using Medline and hand searches of bibliographies of identified articles. STUDY SELECTION: Isomorphic studies were selected that were judged to have some measure of construct validity. DATA EXTRACTION: Face and construct validity were assessed, as well as simplicity and cost of use. RESULTS OF DATA SYNTHESIS: Several different models of binge-type eating exist, each with different strengths of validity and use. These include models using sham feeding, restriction/refeeding cycles and/or stress, limited access (LA) to optional foods, and eating induced by operant schedules of behavior. CONCLUSIONS: We concur with Harry Harlow, who was quoted by Gerry Smith as saying: "You'd be crazy to use animal models, but you'd also be crazy not to use them."