Palatable Food Intake Research Articles

Maternal high-fat diet and obesity impact palatable food intake and dopamine signaling in nonhuman primate offspring.

ObjectiveTo utilize a nonhuman primate model to examine the impact of maternal high-fat diet (HFD) consumption and pre-pregnancy obesity on offspring intake of palatable food. We will also examine whether maternal HFD consumption impaired development of the dopamine system, critical for the regulation of hedonic feeding.MethodsThe impact of exposure to maternal HFD and obesity on offspring consumption of diets of varying composition was assessed after weaning. We also examined the influence of maternal HFD consumption on the development of the prefrontal cortex-dopamine system at 13 months of age.ResultsDuring a preference test, offspring exposed to maternal obesity and HFD consumption displayed increased intake of food high in fat and sugar content relative to offspring from lean control mothers. Maternal HFD consumption suppressed offspring dopamine signaling (as assessed by immunohistochemistry) relative to control offspring. Specifically, there was decreased abundance of dopamine fibers and of dopamine receptor 1 and 2 protein.ConclusionOur findings reveal that offspring exposed to both maternal HFD consumption and maternal obesity during early development are at increased risk for obesity due to overconsumption of palatable energy-dense food, a behavior that may be related to reduced central dopamine signaling.

The role of the opioid system in binge eating disorder.

Binge eating disorder is characterized by excessive, uncontrollable consumption of palatable food within brief periods of time. Excessive intake of palatable food is thought to be driven by hedonic, rather than energy homeostatic, mechanisms. However, reward processing does not only comprise consummatory actions; a key component is represented by the anticipatory phase directed at procuring the reward. This phase is highly influenced by environmental food-associated stimuli, which can robustly enhance the desire to eat even in the absence of physiological needs. The opioid system (endogenous peptides and their receptors) has been strongly linked to the rewarding aspects of palatable food intake, and perhaps represents the key system involved in hedonic overeating. Here we review evidence suggesting that the opioid system can also be regarded as one of the systems that regulates the anticipatory incentive processes preceding binge eating hedonic episodes.

Neurotensin Is Coexpressed, Coreleased, and Acts Together With GLP-1 and PYY in Enteroendocrine Control of Metabolism

The 2 gut hormones glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) are well known to be coexpressed, costored, and released together to coact in the control of key metabolic target organs. However, recently, it became clear that several other gut hormones can be coexpressed in the intestinal-specific lineage of enteroendocrine cells. Here, we focus on the anatomical and functional consequences of the coexpression of neurotensin with GLP-1 and PYY in the distal small intestine. Fluorescence-activated cell sorting analysis, laser capture, and triple staining demonstrated that GLP-1 cells in the crypts become increasingly multihormonal, ie, coexpressing PYY and neurotensin as they move up the villus. Proglucagon promoter and pertussis toxin receptor-driven cell ablation and reappearance studies indicated that although all the cells die, the GLP-1 cells reappear more quickly than PYY- and neurotensin-positive cells. High-resolution confocal fluorescence microscopy demonstrated that neurotensin is stored in secretory granules distinct from GLP-1 and PYY storing granules. Nevertheless, the 3 peptides were cosecreted from both perfused small intestines and colonic crypt cultures in response to a series of metabolite, neuropeptide, and hormonal stimuli. Importantly, neurotensin acts synergistically, ie, more than additively together with GLP-1 and PYY to decrease palatable food intake and inhibit gastric emptying, but affects glucose homeostasis in a more complex manner. Thus, neurotensin is a major gut hormone deeply integrated with GLP-1 and PYY, which should be taken into account when exploiting the enteroendocrine regulation of metabolism pharmacologically.

The fetal programming of food preferences: current clinical and experimental evidence.

Increased energy consumption is one of the major factors implicated in the epidemic of obesity. There is compelling evidence, both clinical and experimental, that fetal paucity of nutrients may have programming effects on feeding preferences and behaviors that can contribute to the development of diseases. Clinical studies in different age groups show that individuals born small for their gestational age (SGA) have preferences towards highly caloric foods such as carbohydrates and fats. Some studies have also shown altered eating behaviors in SGA children. Despite an apparent discrepancy in different age groups, all studies seem to converge to an increased intake of palatable foods in SGA individuals. Small nutrient imbalances across lifespan increase the risk of noncommunicable diseases in adult life. Homeostatic factors such as altered responses to leptin and insulin and alterations in neuropeptides associated with appetite and satiety are likely involved. Imbalances between homeostatic and hedonic signaling are another proposed mechanism, with the mesocorticolimbic dopaminergic pathway having differential reward and pleasure responses when facing palatable foods. Early exposure to undernutrition also programs hypothalamic-pituitary-adrenal axis, with SGA having higher levels of cortisol in different ages, leading to chronic hyperactivity of this neuroendocrine axis. This review summarizes the clinical and experimental evidence related to fetal programming of feeding preferences by SGA.

Alternatives to restrictive feeding practices to promote self-regulation in childhood: a developmental perspective.

Intake of energy-dense snack foods is high among US children. Although the use of restrictive feeding practices has been shown to be counterproductive, there is very limited evidence for effective alternatives to restriction that help children moderate their intake of these foods and that facilitate the development of self-regulation in childhood. The developmental literature on parenting and child outcomes may provide insights into alternatives to restrictive feeding practices. This review paper uses a model of parental control from the child development and parenting literatures to (i) operationally define restrictive feeding practices; (ii) summarize current evidence for antecedents and effects of parental restriction use on children's eating behaviours and weight status, and (iii) highlight alternative feeding practices that may facilitate the development of children's self-regulation and moderate children's intake of palatable snack foods. We also discuss recent empirical evidence highlighting the role of child temperament and food motivation related behaviours as factors that prompt parents to use restrictive feeding practices and, yet, may increase children's dysregulated intake of forbidden foods.

Musical intervention and food preferences in girls born with lower birth weight

BackgroundChildren born after intrauterine growth restriction (IUGR), especially girls, show an increased intake of palatable foods in several developmental stages, which likely contributes to their increased risk for obesity later. Recently, neuroimaging studies suggested that musical exposure activates the mesolimbic region, which is also involved in the processing of food rewards. AimsWe evaluated the impact of musical intervention in mother/infant pairs on feeding behavior during childhood with regard to birth weight. Study DesignCohort study. SubjectsA total of 28 children exposed to a structured musical intervention in early life were invited for an anthropometric and nutritional evaluation, and were compared to a communitarian age-matched sample. Outcome MeasuresA series of general linear models adjusted for socioeconomic status and maternal education were constructed to evaluate the interaction between music exposure, birth weight, and sex on the consumption of different types of foods, measured using a food frequency questionnaire. ResultsThere was an interaction between birth weight, sex, and musical intervention on the consumption of sugar during childhood (Wald=7.87, df=2, p=0.02); control participants consumed more sugar as birth weight decreased (B=−8.673, p<0.0001). No such effect was found for the girls exposed to musical intervention (B=3.352, p=0.15) or for boys (exposed B=2.870, p=0.44; non-exposed B=3.706, p=0.236). The absence of other effects suggests that this finding is specific for sweet foods. ConclusionEarly music intervention in mother/infant pairs may moderate the effects of IUGR on palatable food preference in girls.

Ghrelin and GHS-R1A signaling within the ventral and laterodorsal tegmental area regulate sexual behavior in sexually naïve male mice

In addition to food intake and energy balance regulation, ghrelin mediate the rewarding and motivational properties of palatable food as well as addictive drugs. The ability of ghrelin to regulate reinforcement involves the cholinergic-dopaminergic reward link, which encompasses a cholinergic projection from the laterodorsal tegmental area (LDTg) to the ventral tegmental area (VTA) together with mesolimbic dopaminergic projections from the VTA to the nucleus accumbens (NAc). Recently, systemic ghrelin was shown to regulate sexual behavior and motivation in male mice via dopamine neurotransmission. The present study therefore elucidates the role of ghrelin and ghrelin receptor (GHS-R1A) antagonist treatment within NAc, VTA or LDTg for sexual behavior in sexually naïve male mice. Local administration of the GHSR-1A antagonist, JMV2959, into the VTA or LDTg was found to reduce the preference for female mice, the number of mounts and the duration of mounting as well as to prolong the latency to mount. This was further substantiated by the findings that ghrelin administration into the VTA or LDTg increased the number of mounts and the duration of mounting and decreased the latency to mount. Moreover, ghrelin administered into the LDTg increased the preference for female mice. Accumbal administration of ghrelin increased whereas GHS-R1A antagonist decreased the intake of palatable food, but did not alter sexual behavior. In males exposed to sexual interaction, systemic administration of ghrelin increases whereas JMV2959 decreases the turnover of dopamine in the VTA. These data suggest that ghrelin signaling within the tegmental areas is required for sexual behavior in sexually naïve male mice.

Palatability Can Drive Feeding Independent of AgRP Neurons

Feeding behavior is exquisitely regulated by homeostatic and hedonic neural substrates that integrate energy demand as well as the reinforcing and rewarding aspects of food. Understanding the net contribution of homeostatic and reward-driven feeding has become critical because of the ubiquitous source of energy-dense foods and the consequent obesity epidemic. Hypothalamic agouti-related peptide-secreting neurons (AgRP neurons) provide the primary orexigenic drive of homeostatic feeding. Using models of neuronal inhibition or ablation, we demonstrate that the feeding response to a fast ghrelin or serotonin receptor agonist relies on AgRP neurons. However, when palatable food is provided, AgRP neurons are dispensable for an appropriate feeding response. In addition, AgRP-ablated mice present exacerbated stress-induced anorexia and palatable food intake--a hallmark of comfort feeding. These results suggest that, when AgRP neuron activity is impaired, neural circuits sensitive to emotion and stress are engaged and modulated by food palatability and dopamine signaling.

DRD4 and SLC6A3 gene polymorphisms are associated with food intake and nutritional status in children in early stages of development

Variants of dopamine system genes such as the DRD4 and the SLC6A3 genes may be involved in food intake regulation because the dopaminergic system influences food reward. We investigated an association of polymorphisms in the DRD4 (exon 3 VNTR) and SLC6A3 (3′UTR VNTR, rs2550948, rs2652511 and rs1048953) genes with food intake and nutritional status in children. This prospective cohort study recruited 359 children at birth. Dietary data and nutritional status were collected at 1 year, 3–4 years, and 7–8 years of age. The polymorphisms were analyzed using polymerase chain reaction based techniques. Food intake and nutritional status were compared among the different SNP genotypes. In the first year of life, DRD4.7R− children showed higher BMI Z-scores (P=.019) than the DRD4.7R+ cohort. At 3–4 years old, DRD4.7R− and SLC6A3.10R/10R children showed a higher intake of palatable foods (P=.024) and a higher waist circumference (P=.017). The rs1048953 SLC6A3 polymorphism was associated with average daily energy intake (P=.003) at 3–4 years and with a waist-to-height ratio of children at 7–8 years (P=.041). Carriers of high dopamine activity alleles of the VNTRs studied in DRD4 and SLC6A3 genes and carriers of T/T genotype of the variant rs1048953 SLC6A3 can present an increased risk for obesity related to overeating because high dopamine activity can increase the perceived incentive value of food reward.

Endogenous Glucagon-like Peptide-1 Suppresses High-Fat Food Intake by Reducing Synaptic Drive onto Mesolimbic Dopamine Neurons.

Glucagon-like peptide-1 (GLP-1) and its analogs act as appetite suppressants and have been proven to be clinically efficacious in reducing body weight in obese individuals. Central GLP-1 is expressed in a small population of brainstem cells located in the nucleus tractus solitarius (NTS), which project to a wide range of brain areas. However, it remains unclear how endogenous GLP-1 released in the brain contributes to appetite regulation. Using chemogenetic tools, we discovered that central GLP-1 acts on the midbrain ventral tegmental area (VTA) and suppresses high-fat food intake. We used integrated pathway tracing and synaptic physiology to further demonstrate that activation of GLP-1 receptors specifically reduces the excitatory synaptic strength of dopamine (DA) neurons within the VTA that project to the nucleus accumbens (NAc) medial shell. These data suggest that GLP-1 released from NTS neurons can reduce highly palatable food intake by suppressing mesolimbic DA signaling.

Sensitivity to reward is associated with snack and sugar-sweetened beverage consumption in adolescents.

High intake of palatable foods, such as energy-dense snacks and sugar-sweetened beverages (SSBs), is common among adolescents. An individual's sensitivity to reward (SR) may influence these intakes. The main objective of this study was to investigate the association between SR and both snack and SSB intake among adolescents. A representative cross-sectional survey was conducted among 1104 14- to 16-year-olds (mean age=14.7±0.8years; 50.9% boys; 18.0% overweight) in Flanders. Daily intakes were measured by a food frequency questionnaire. SR was assessed using the behavioral activation system (BAS) scales. Multilevel regression analyses (two level: adolescent school) were conducted using STATA version 13. BAS drive was positively associated with daily intakes of SSBs (13.79%, p<0.01), unhealthy snacks (5.42%, p<0.001), and energy and nutrients derived from SSBs (p<0.001) and snacks (p<0.01). BAS reward responsiveness (RR) was only positively associated with intake of unhealthy snacks (3.85%, p<0.05), healthy snacks (6.41%, p<0.05), and fat (4.05%, p<0.01) and Na (3.89%, p<0.05) from snacks. Interaction effects of gender and BAS RR (p<0.05) were found. Significant positive associations between BAS RR and daily intakes of energy from snacks (6.48%, p<0.01) and fat from snacks (7.22%, p<0.001) were found only for girls. SR was associated with snack and SSB consumption in adolescents, especially in girls. These findings suggest that SR should be taken into account when designing interventions to improve the snack and SSB intake of adolescents.

Depressed affect and dietary restraint in adolescent boys' and girls' eating in the absence of hunger

Data suggest that depressed affect and dietary restraint are related to disinhibited eating patterns in children and adults. Yet, experimental research has not determined to what extent depressed affect acutely affects eating in the absence of physiological hunger (EAH) in adolescents. In the current between-subjects experimental study, we measured EAH in 182 adolescent (13–17 y) girls (65%) and boys as ad libitum palatable snack food intake after youth ate to satiety from a buffet meal. Just prior to EAH, participants were randomly assigned to view either a sad or neutral film clip. Dietary restraint was measured with the Eating Disorder Examination. Adolescents who viewed the sad film clip reported small but significant increases in state depressed affect relative to adolescents who viewed the neutral film clip (p < .001). Yet, there was no main effect of film condition on EAH (p = .26). Instead, dietary restraint predicted greater EAH among girls, but not boys (p < .001). These findings provide evidence that adolescent girls' propensity to report restrained eating is associated with their greater disinhibited eating in the laboratory. Additional experimental research, perhaps utilizing a more potent laboratory stressor and manipulating both affective state and dietary restraint, is required to elucidate how state affect may interact with dietary restraint to influence EAH during adolescence.

Perinatal malnutrition stimulates motivation through reward and enhances drd1a receptor expression in the ventral striatum of adult mice

AimThe aim of this study was to analyze the effects of protein perinatal malnutrition on the function of dopamine DRD1 and DRD2 receptors in regards to motivation and food consumption in adult mice. The study also analyzed the effect of protein perinatal malnutrition on the gene expression of these receptors in the ventral striatum. MethodsWistar lineage mice were divided into two groups according to maternal diet: control (17% casein), n=30 and low protein (8% casein), n=30. Between 30 and 120days of life, the following factors were measured: body weight; the effect of dopamine D1 and D2 agonists on the ingestion of palatable food; the motivational aspect under the action of the D1 (SKF 38393) and D2 Quinpirole dopaminergic agonists; and the gene expression of DRD1 and DRD2 receptors in the ventral striatum. ResultsThe body weights of the malnourished animals remained significantly lower than those of the control group from 30 to 120days of life. Malnourished animals ingested a greater quantity of palatable food. There was a decrease in palatable diet consumption in both the control and malnourished groups after the application of D1 and D2 agonists; however, the anorexic effect of the D1 agonist was understated in malnourished animals. Perinatal malnutrition increases the motivational behavior of the animal when food reward is used. There was an increase in gene expression of the DRD1a receptor in the ventral striatum of malnourished animals, and there were no significant changes concerning the DRD2 receptor. ConclusionsPerinatal protein malnutrition stimulates hedonic control of eating behavior by promoting increased intake of palatable foods, possibly due to increased expression of dopamine receptor DRD1a in the ventral striatum.

Preliminary validation and principal components analysis of the Control of Eating Questionnaire (CoEQ) for the experience of food craving.

The Control of Eating Questionnaire (CoEQ) comprises 21-items that are designed to assess the severity and type of food cravings an individual experiences over the previous 7 days. The CoEQ has been used in clinical trials as a multi-dimensional measure of appetite, craving and mood regulation however its underlying component structure has yet to be determined. The current paper has two aims; (1) to examine the psychometric properties, and internal consistency of the CoEQ; and (2) to provide a preliminary examination of the underlying components by exploring their construct and predictive validity. Data were pooled from four studies in which a total 215 adults (80% women; Age=29.7 ± 10.3; BMI=26.5 ± 5.2) had completed the CoEQ alongside measures of psychometric eating behaviour traits, ad libitum food intake, and body composition. A principal components analysis (PCA) and parallel analysis was conducted to examine the underlying structure of the questionnaire. The resulting subscales were tested for internal consistency (Cronbach's α=0.66-0.88). PCA revealed four components that explained 54.5% of the variance. The components were identified as: Craving Control, Positive Mood, Craving for Sweet, and Craving for Savoury. Associations between the underlying CoEQ subscales and measures of body composition and eating behaviour traits confirmed construct validity of the subscales. The associations between the subscales and snack food selection and intake of palatable snack foods supported the CoEQ's predictive validity. The CoEQ has good psychometric properties with a clear component structure and acceptable internal consistency. This preliminary validation supports the CoEQ as a measure of the experience of food cravings.

Sucrose Solution Intake and its Schedule of Access Affect the Response to Chronic Variable Stress in Mice

There is a strong relationship between the intake of calorically-dense palatable food and stress. Moreover, intake of sodas is an important contributory factor to obesity, and is often associated with palatable food consumption. We studied the effects of 2-hour intermittent access to sucrose-sweetened water (SSW, 12.3%, soda-like) and its schedule of administration on the response to chronic variable stress in mice fed a high-fat, high-sugar diet. C57BL/6 mice received access to water or to both water and 2-hour SSW access during 5 weeks, in addition to their diet. After the first two weeks, half of the animals from each group were stressed daily using a chronic variable stress (CVS) paradigm, while the other half were kept undisturbed. During the CVS exposure period, SSW access was either scheduled randomly, right before the stressors or right after the stressor The effects of SSW and its schedule of administration on stress hormones, adiposity and serum lipids were analyzed. Results showed that SSW access induced an increase in energy intake, body weight gain and abdominal fat as well as attenuation in the response to CVS compared to water access alone. Moreover, there was a greater stress-relieving effect when SSW was administered after exposure to the stressors, compared to random exposure and exposure before the stressors. The present study provides arguments that the availability of intermittent SSW access renders mice more resilient to the effects of CVS, particularly when SSW is provided after exposure to stress.

Seeking behavior, place conditioning, and resistance to conditioned suppression of feeding in rats intermittently exposed to palatable food.

Binge eating disorder is characterized by excessive consumption of highly palatable food within short periods of time accompanied by loss of control over eating. Extensive evidence provides support for the consideration of binge eating disorder as an addiction-like disorder. In this study, we wanted to determine whether rats undergoing an operant binge-like eating procedure could develop maladaptive forms of conditioned feeding behaviors. For this purpose, we trained male rats to self-administer either a sugary, highly palatable diet ("Palatable" rats) or a chow diet ("Chow" rats) for 1 hour a day. After escalation and stabilization of palatable food intake, we tested Chow and Palatable rats in (a) a conditioned place preference test, (b) a second-order schedule of reinforcement, (c) a cue-induced suppression of feeding test. In the conditioned place preference task, Palatable rats spent significantly more time in the compartment that was previously paired with the palatable food, compared to Chow controls. Furthermore, in the second-order schedule of reinforcement task, Palatable rats exhibited active lever responding 4- to 6-fold higher than Chow control rats. Finally, in the cue-induced suppression of feeding test, although Chow control subjects reduced responding by 32% in the presence of the conditioned punishment, Palatable rats persevered in responding despite the aversive cue. These results further characterize this animal model of binge-like eating and provide additional evidence for the addictive properties of highly palatable food.

Differential Exposure to Chronic vs Acute Palatable Food Intake on Rat Renal Orexin Receptor 1 and NOX‐4 Liver Expression

Differential Exposure to Chronic vs Acute Palatable Food Intake on Rat <b>Renal Orexin Receptor 1 and NOX‐4 Liver Expression</b>

Activation of the GLP-1 receptors in the nucleus of the solitary tract reduces food reward behavior and targets the mesolimbic system.

The gut/brain peptide, glucagon like peptide 1 (GLP-1), suppresses food intake by acting on receptors located in key energy balance regulating CNS areas, the hypothalamus or the hindbrain. Moreover, GLP-1 can reduce reward derived from food and motivation to obtain food by acting on its mesolimbic receptors. Together these data suggest a neuroanatomical segregation between homeostatic and reward effects of GLP-1. Here we aim to challenge this view and hypothesize that GLP-1 can regulate food reward behavior by acting directly on the hindbrain, the nucleus of the solitary tract (NTS), GLP-1 receptors (GLP-1R). Using two models of food reward, sucrose progressive ratio operant conditioning and conditioned place preference for food in rats, we show that intra-NTS microinjections of GLP-1 or Exendin-4, a stable analogue of GLP-1, inhibit food reward behavior. When the rats were given a choice between palatable food and chow, intra-NTS Exendin-4 treatment preferentially reduced intake of palatable food but not chow. However, chow intake and body weight were reduced by the NTS GLP-1R activation if chow was offered alone. The NTS GLP-1 activation did not alter general locomotor activity and did not induce nausea, measured by PICA. We further show that GLP-1 fibers are in close apposition to the NTS noradrenergic neurons, which were previously shown to provide a monosynaptic connection between the NTS and the mesolimbic system. Central GLP-1R activation also increased NTS expression of dopamine-β-hydroxylase, a key enzyme in noradrenaline synthesis, indicating a biological link between these two systems. Moreover, NTS GLP-1R activation altered the expression of dopamine-related genes in the ventral tegmental area. These data reveal a food reward-suppressing role of the NTS GLP-1R and indicate that the neurobiological targets underlying food reward control are not limited to the mesolimbic system, instead they are distributed throughout the CNS.

Increased palatable food intake and response to food cues in intrauterine growth-restricted rats are related to tyrosine hydroxylase content in the orbitofrontal cortex and nucleus accumbens

Intrauterine growth restriction (IUGR) is associated with altered food preferences, which may contribute to increased risk of obesity. We evaluated the effects of IUGR on attention to a palatable food cue, as well as tyrosine hydroxylase (TH) content in the orbitofrontal cortex (OFC) and nucleus accumbens (NAcc) in response to sweet food intake. From day 10 of gestation and through lactation, Sprague–Dawley rats received either an ad libitum (Adlib) or a 50% food-restricted (FR) diet. At birth, pups were cross-fostered, generating four groups (gestation/lactation): Adlib/Adlib (control), FR/Adlib (intrauterine growth-restricted), Adlib/FR, and FR/FR. Adult attention to palatable food cues was measured using the Attentional Set-Shifting Task (ASST), which uses a sweet pellet as reward. TH content in the OFC and NAcc was measured at baseline and in response to palatable food intake. At 90 days of age, FR/Adlib males ate more sweet food than controls, without differences in females. However, when compared to Controls, FR/Adlib females needed fewer trials to reach criterion in the ASST (p=0.04) and exhibited increased TH content in the OFC in response to sweet food (p=0.03). In the NAcc, there was a differential response of TH content after sweet food intake in both FR/Adlib males and females (p<0.05). Fetal programming of adult food preferences involves the central response to palatable food cues and intake, affecting dopamine release in select structures of the brain reward system.

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 f2 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.