Eating tasty food to cope. Longitudinal association with BMI.

The goals of this study were to determine if a change in certain motives to eat highly palatable food, as measured by the Palatable Eating Motives Scale (PEMS), could predict a change in body mass index (BMI) over time, to assess the temporal stability of these motive scores, and to test the reliability of previously reported associations between eating tasty foods to cope and BMI. BMI, demographics, and scores on the PEMS and the Binge Eating Scale were obtained from 192 college students. Test-retest analysis was performed on the PEMS motives in groups varying in three gap times between tests. Regression analyses determined what PEMS motives predicted a change in BMI over two years. The results replicated previous findings that eating palatable food for Coping motives (e.g., to forget about problems, reduce negative feelings) is associated with BMI. Test-retest correlations revealed that motive scores, while somewhat stable, can change over time. Importantly, among overweight participants, a change in Coping scores predicted a change in BMI over 2 years, such that a 1-point change in Coping predicted a 1.76 change in BMI (equivalent to a 10.5 lb. change in body weight) independent of age, sex, ethnicity, and initial binge-eating status (Cohen's f(2) effect size = 1.44). The large range in change of Coping scores suggests it is possible to decrease frequency of eating to cope by more than 1 scale point to achieve weight losses greater than 10 lbs. in young overweight adults, a group already at risk for rapid weight gain. Hence, treatments aimed specifically at reducing palatable food intake for coping reasons vs. for social, reward, or conformity reasons, should help achieve a healthier body weight and prevent obesity if this motive-type is identified prior to significant weight gain.

Motives for eating tasty foods associated with binge-eating. Results from a student and a weight-loss seeking population.

The aim of this study was to use the Palatable Eating Motives Scale (PEMS) to determine if and what motives for eating tasty foods (e.g., junk food, fast food, and desserts) are associated with binge-eating in two diverse populations. BMI and scores on the PEMS, Yale Food Addiction Scale (YFAS), and Binge-eating Scale (BES) were obtained from 247 undergraduates at the University of Alabama at Birmingham (UAB) and 249 weight-loss seeking patients at the UAB EatRight program. Regression analyses revealed that eating tasty foods to forget worries and problems and help alleviate negative feelings (i.e., the 4-item Coping motive) was associated with binge-eating independently of any variance in BES scores due to sex, age, ethnicity, BMI, other PEMS motives, and YFAS scores in both students (R² = .57) and patients (R² = .55). Coping also was associated with higher BMI in students (p < 0.01), and in patients despite their truncated BMI range (p < 0.05). Among students, the motives Conformity and Reward Enhancement were also independently associated with binge-eating. For this younger sample with a greater range of BES scores, eating for these motives, but not for Social ones, may indicate early maladaptive eating habits that could later develop into disorders characterized by binge-eating if predisposing factors are present. Thus, identifying one's tasty food motive or motives can potentially be used to thwart the development of BED and obesity, especially if the motive is Coping. Identifying one's PEMS motives should also help personalize conventional treatments for binge-eating and obesity toward improved outcomes.

Profiling motives behind hedonic eating. Preliminary validation of the Palatable Eating Motives Scale.

The purpose of this study was to validate a new scale designed to measure individual motives for eating tasty foods and determine if any specific motive(s) are associated with obesity. The "Palatable Eating Motives Scale" (PEMS) is a self-report measure adapted from the Drinking Motives Questionnaire Revised (DMQ-R). N=150 racially-diverse college students (mean age: 24.4, BMI: 16-51kg/m(2)) were administered the PEMS along with the Binge-Eating Scale (BES) and the Yale Food Addiction Scale (YFAS) to test for convergent and incremental validity and the Sensitivity to Punishment and Reward Questionnaire (SPSRQ) for discriminant validity. The PEMS identified four motives for eating tasty food, the same ones found with the DMQ-R for alcohol intake: Social, Conformity, Enhancement, and Coping motives. The scales had good convergent validity with BES and YFAS scores but discriminated from the broader motivational constructs of inhibition and activation measured by the SPSRQ. Of the PEMS motives, Coping (eating tasty food to deal with problems and negative feelings) accounted for unique variance in BMI, and added to variance in BMI contributed by BES scores, showing incremental validity. YFAS scores did not contribute to BMI after controlling for binge-eating. Coping subscale scores were also significantly higher (p<0.001) among the severely obese (BMI>40). Motives behind palatable food intake are not homogenous and should be considered in personalized weight-loss strategies in future studies. In normal weight individuals, knowing one's dominant motive for eating tasty foods may help promote healthier food choices in times and places where they are most vulnerable to do otherwise.

The Pavlovian power of palatable food: lessons for weight-loss adherence from a new rodent model of cue-induced overeating.

OBJECTIVE: Relapsing to overeating is a stubborn problem in obesity treatment. We tested the hypothesis that context cues surrounding palatable food (PF) intake have the power to disrupt caloric regulation even of less PF. Context cues are non-food cues that are in the environment where PF is habitually eaten. DESIGN: Rats were conditioned to associate intake of Oreo cookies as the PF to cages with distinct context cues that differed from cues in cages where they were only given chow. PF naturally stimulated greater caloric intake. The rats were then tested in the PF cage with only chow available to determine whether the PF-paired cues, alone, could elicit overeating of plain chow. SUBJECTS: Non-food-deprived female Sprague-Dawley rats. MEASUREMENTS: Intake of plain chow under PF-paired cues vs chow-paired cues was compared. This was also measured in tests that included a morsel of PF as a priming stimulus. We also controlled for any effect of binge-prone vs binge-resistant status to predict cued-overeating. RESULTS: Rats consumed significantly more chow when exposed to context cues paired earlier with PF than with chow (P<0.01). This effect occurred using various cues (for example, different types of bedding or wallpaper). The effect was strengthened by priming with a morsel of PF (P<0.001) and was unaffected by baseline differences in propensity to binge on PF. CONCLUSION: Context-cues associated with PF intake can drive overeating even of a less PF and abolish the ability of rats to compensate for the calories of a PF primer. Just as drug-associated context cues can reinstate drug-addiction relapse, PF-paired cues may trigger overeating relapses linked to weight regain and obesity. This model should help identify the reflex-like biology that sabotages attempts to adhere to healthy reduced calorie regimens and call greater attention to the cue-factor in the treatment of binge eating and obesity.

Effect of a cage divider permitting social stimuli on stress and food intake in rats.

The need to obtain data from individual laboratory animals has forced many researchers to singly-house small animals. This is costly to the researcher and isolation can adversely affect animal physiology and behavior which in turn may threaten the validity and generalization of experiment results to humans. We assessed the practical use of a housing device - dubbed "Buddy Barrier" (BB) - that allows social stimulation in a paired-housing situation while at the same time permitting the collection of individual measures that traditionally require individual-housing. To assess stress responses to the BB, adult male rats were single or pair-housed for several days with and without a BB in the cage. Fecal corticosterone metabolites (fCORT), food intake and body weight were monitored daily. Plasma CORT and adrenal catecholamine levels were assessed at the end of the housing manipulation. Stress hormone measures did not differ in paired vs. singly-housed rats and paired rats quickly habituated to introduction and removal of the BB. Barring a trend for paired rats to eat more in the first 4 h of the dark, there was no difference in 24 h intakes or body weight gain between singly and paired-housed rats. While the BB attenuated 24 h intakes in both groups, intakes normalized to non-BB conditions by the third BB reintroduction. A device such as the BB can enhance the welfare of animals by providing social enrichment without compromising the integrity of experimental protocols traditionally requiring single-housing. In times of lagging research funding it can also substantially reduce housing costs.

Body composition and endocrine status of long-term stress-induced binge-eating rats.

Clinical binge eating runs a protracted course. The etiology of binge eating remains perplexing in part because, in humans, it is difficult to isolate and assess the independent and aggregate impact of various contributing variables. Using rats, we found that footshock stress and a history of caloric restriction (S+R), combine synergistically to induce binge eating. Stress and dieting are also strong antecedents and relapse factors in human eating disorders. Here we report further behavioral and physiological parallels to human binge eating. Like the protracted course of human binge eating, young female Sprague-Dawley rats continued to binge eat after 23 restriction/stress cycles (7 months) and this despite experiencing no significant weight loss during the restriction phases. Stress alone reduced adiposity by 35% (p<0.001) but S+R rats had no significant fat loss. An endocrine profile of normal plasma leptin and insulin levels but marked elevation of plasma corticosterone levels was found only in the binge-eating (S+R) rats (p<0.01), also paralleling endocrine profiles reported in clinical binge-eating studies. These behavioral and physiological similarities between this animal model and clinical binge eating increase its utility in understanding binge eating. Importantly, our findings also highlight the stubborn nature of binge eating: once a critical experience with dieting and stress is experienced, little if any further weight loss or food restriction is necessary to sustain it.

A history of caloric restriction induces neurochemical and behavioral changes in rats consistent with models of depression.

A history of dieting is common in individuals suffering from eating disorders for which depression and mood disturbances are also comorbid. We investigated the effect of a history of caloric restriction (HCR) in rats that involved cyclic food restriction and refeeding with varying levels of access to palatable food (PF) on: 1) responses to the SSRI, fluoxetine; 2) monoamine levels in brain regions central to the control of feeding, reward, and mood regulation; and 3) behavioral tests of anxiety and depression. HCR coupled with intermittent but not daily access to PF exaggerated rats' anorectic response to fluoxetine (p<0.05); was associated with a significant 71% and 58% reduction of 5-HT and dopamine, respectively, in the medial prefrontal cortex; and induced behaviors consistent with models of depression. HCR, irrespective of access to PF, abolished the strong association between 5-HT and dopamine turnover in the nucleus accumbens in control rats (r=0.71 vs. -0.06, p<0.01). Access to PF, irrespective of HCR, reduced hypothalamic dopamine. Together, these findings suggest that a history of frequent food restriction-induced weight fluctuation imposes neurochemical changes that negatively impact feeding and mood regulation.

High intake of palatable food predicts binge-eating independent of susceptibility to obesity: an animal model of lean vs obese binge-eating and obesity with and without binge-eating.

OBJECTIVE: To determine the stability of individual differences in non-nutritive 'junk' palatable food (PF) intake in rats; assess the relationship of these differences to binge-eating characteristics and susceptibility to obesity; and evaluate the practicality of using these differences to model binge-eating and obesity. DESIGN: Binge-eating prone (BEP) and resistant (BER) groups were identified. Differential responses to stress, hunger, macronutrient-varied PFs, a diet-induced obesity (DIO) regimen and daily vs intermittent access to a PF+chow diet, were assessed. SUBJECTS: One hundred and twenty female Sprague-Dawley rats. MEASUREMENTS: Reliability of intake patterns within rats; food intake and body weight after various challenges over acute (1, 2, 4 h), 24-h and 2-week periods. RESULTS: Although BEP and BER rats did not differ in amount of chow consumed, BEPs consumed >50% more intermittent PF than BERs (P<0.001) and consistently so (alpha=0.86). BEPs suppressed chow but not PF intake when stressed, and ate as much when sated as when hungry. Conversely, BERs were more affected by stress and ate less PF, not chow, when stressed and were normally hyperphagic to energy deficit. BEP overeating generalized to other PFs varying in sucrose, fat and nutrition content. Half the rats in each group proved to be obesity prone after a no-choice high fat diet (DIO diet) but a continuous diet of PF+chow normalized the BEPs high drive for PF. CONCLUSION: Greater intermittent intake of PF predicts binge-eating independent of susceptibility to weight gain. Daily fat consumption in a nutritious source (DIO-diet; analogous to a fatty meal) promoted overeating and weight gain but limiting fat to daily non-nutritive food (PF+chow; analogous to a snack with a low fat meal), did not. The data offer an animal model of lean and obese binge-eating, and obesity with and without binge-eating that can be used to identify the unique physiology of these groups and henceforth suggest more specifically targeted treatments for binge-eating and obesity.

Putative contributors to the secular increase in obesity: exploring the roads less traveled.

OBJECTIVE: To investigate plausible contributors to the obesity epidemic beyond the two most commonly suggested factors, reduced physical activity and food marketing practices. DESIGN: A narrative review of data and published materials that provide evidence of the role of additional putative factors in contributing to the increasing prevalence of obesity. DATA: Information was drawn from ecological and epidemiological studies of humans, animal studies and studies addressing physiological mechanisms, when available. RESULTS: For at least 10 putative additional explanations for the increased prevalence of obesity over the recent decades, we found supportive (although not conclusive) evidence that in many cases is as compelling as the evidence for more commonly discussed putative explanations. CONCLUSION: Undue attention has been devoted to reduced physical activity and food marketing practices as postulated causes for increases in the prevalence of obesity, leading to neglect of other plausible mechanisms and well-intentioned, but potentially ill-founded proposals for reducing obesity rates.

PYY3-36 as an anti-obesity drug target.

The neuropeptide Y (NPY)/peptide YY (PYY) system has been implicated in the physiology of obesity for several decades. More recently ignited enormous interest in PYY3-36, an endogenous Y2-receptor agonist, as a promising anti-obesity compound. Despite this interest, there have been remarkably few subsequent reports reproducing or extending the initial findings, while at the same time studies finding no anti-obesity effects have surfaced. Out of 41 different rodent studies conducted (in 16 independent labs worldwide), 33 (83%) were unable to reproduce the reported effects and obtained no change or sometimes increased food intake, despite use of the same experimental conditions (i.e. adaptation protocols, routes of drug administration and doses, rodent strains, diets, drug vendors, light cycles, room temperatures). Among studies by authors in the original study, procedural caveats are reported under which positive effects may be obtained. Currently, data speak against a sustained decrease in food intake, body fat, or body weight gain following PYY3-36 administration and make the previously suggested role of the hypothalamic melanocortin system unlikely as is the existence of PYY deficiency in human obesity. We review the studies that are in the public domain which support or challenge PYY3-36 as a potential anti-obesity target.

Feeding response to melanocortin agonist predicts preference for and obesity from a high-fat diet.

Overconsumption and increased selection of high fat (HF) foods contribute to the development of common obesity. Because the hypothalamic melanocortin (MC) system plays an integral role in the regulation of food intake and dietary choice, we tested the hypothesis that proneness (-P) or resistance (-R) to dietary-induced obesity (DIO) may be due to differences in MC function. We found that prior to developing obesity and while still maintained on chow, acute, central administration of MTII, an MC agonist, produced a greater anorectic response in DIO-P rats than in DIO-R rats. However, after only 5 days of exclusive HF feeding, the DIO-R rats had significantly greater suppression of intake after MTII treatment than they did when maintained on chow. In addition, the DIO-P rats were much less responsive to MTII treatment than the DIO-R rats after only 5 days of the HF diet. In fact, MTII-induced anorexia during HF feeding correlated negatively with body weight gained on the HF diet. These results suggest that the voluntary decrease of HF feeding in DIO-R rats may be mediated by increased endogenous MC signaling, a signal likely compromised in DIO-P rats. Differences in MC regulation may also explain the observed preference for HF over a lower fat food choice in DIO-P rats. Finally, the results indicate that responses to exogenous MC challenge can be used to predict proneness or resistance to DIO.