A model of emotional stress‐induced binge eating in female mice with no history of food restriction

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. Modeling 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‐minute frustration episode where highly palatable food was within the home cage but inaccessible. Both groups were then given free access for 15 minutes. Frustrated female mice from the ad libitum displayed binge‐like behavior compared with controls (P = .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.     

Comparisons of energy intake and energy expenditure in overweight and obese women with and without binge eating disorder

The purpose of this study was to determine whether there are differences in energy intake or energy expenditure that distinguish overweight/obese women with and without binge eating disorder (BED). Seventeen overweight/obese women with BED and 17 overweight/obese controls completed random 24-h dietary recall interviews, and had total daily energy expenditure (TDEE) assessed by the doubly labeled water (DLW) technique with concurrent food log data collection. Participants received two baseline dual-energy X-ray absorptiometry (DXA) scans and had basal metabolic rate (BMR) and thermic effect of food (TEF) measured using indirect calorimetry. Results indicated no between group differences in TDEE, BMR, and TEF. As in our previous work, according to dietary recall data, the BED group had significantly higher caloric intake on days when they had binge eating episodes than on days when they did not (3,255 vs. 2,343 kcal). There was no difference between BED nonbinge day intake and control group intake (2,233 vs. 2,140 kcal). Similar results were found for food log data. Dietary recall data indicated a trend toward higher average daily intake in the BED group (2,587 vs. 2,140 kcal). Furthermore, when comparing TDEE to dietary recall and food log data, both groups displayed significant under-reporting of caloric intake of similar magnitudes ranging from 20 to 33%. Predicted energy requirements estimated via the Harris-Benedict equation (HBE) underestimated measured TDEE by 23-24%. Our data suggest that increased energy intake reported by BED individuals is due to increased food consumption and not metabolic or under-reporting differences.     

Energy Intake Patterns in Obese Women with Binge Eating Disorder

Objective: For binge eating disorder (BED) to be accepted as a distinct diagnostic category in the Diagnostic and Statistical Manual for Mental Disorders, Fifth Edition, it must be demonstrated that the criteria identify a diagnostic entity that is distinct from bulimia nervosa and obesity. This study examined the difference in total energy intake per day, patterns of energy intake throughout the day, and nutrient content of foods consumed in obese individuals who met the criteria for BED (on binge and non‐binge days) and those who did not. Research Methods and Procedures: Twenty women, 12 who met Diagnostic and Statistical Manual for Mental Disorders, Fourth Edition, criteria for BED and 8 matched obese controls, participated in the study. All participants underwent six random 24‐hour dietary recall telephone interviews conducted by experienced interviewers using the Nutrition Data Software System. Results: The BED group ingested significantly more kilocalories on days when they had binge eating episodes than the obese control group on average. The BED group ate significantly more in the evening on binge days than their control group counterparts. There is some indication in the data that those with BED may be restricting caloric intake. Finally, data indicated that the BED group ate significantly more protein, carbohydrate, and fat on binge days than on non‐binge days. However, the proportion of kilocalories from each nutrient shifted on BED binge days compared with non‐binge days to favor consumption of fat over carbohydrates. Discussion: More research needs to be done to determine if these findings are reproducible. Then, the neurobiological underpinnings of these differences in nutrient intake patterns and nutrient selection can be studied to help to determine the biological basis of the disorder.     

Use of an operant task to estimate food reinforcement in adult humans with and without BED

Objective: The purpose of this study was to demonstrate the utility of food‐reinforced operant task performance in modeling binge‐eating disorder (BED). We hypothesized that food reinforcement after a caloric preload would be related to BED status, but not hunger. Methods and Procedures: We investigated the association between reports of hunger, binge tendency, and food reinforcement in a sample of 18 women (12 non‐BED, 7 lean, 5 obese, and 6 obese BED). Participants completed two sessions of operant task performance after consuming 600 ml of flavored water or 600 ml of a 1 kcal/ml liquid meal. Results: Under the water condition, food reinforcement did not differ between the non‐BED and BED groups, and was positively correlated with hunger ratings across all participants (r = 0.55, P = 0.023). Under the liquid meal condition, food reinforcement was significantly decreased compared with the water condition in the non‐BED group (t = ?2.6, P = 0.026). There was also a significant difference between the non‐BED and BED groups in the fed condition (41 ± 40, 117 ± 60, F = 10.3, P = 0.005, non‐BED vs. BED, respectively, mean ± s.d.). The correlation between food reinforcement and hunger remained significant only in the non‐BED group (r = 0.69, P = 0.011). Discussion: Our results support the hypothesis that food reinforcement measured after a caloric preload is related to BED status but not hunger in those subjects with BED. The data also suggest that operant task performance can be useful in modeling BED criteria such as “eating when not physically hungry.”     

Pramlintide treatment reduces 24-h caloric intake and meal sizes and improves control of eating in obese subjects: a 6-wk translational research study

Evidence from rodent studies indicates that the beta-cell-derived neurohormone amylin exerts multiple effects on eating behavior, including reductions in meal size, intake of highly palatable foods, and stress-induced sucrose consumption. To assess the effect of amylin agonism on human eating behavior we conducted a randomized, blinded, placebo-controlled, multicenter study investigating the effects of the amylin analog pramlintide on body weight, 24-h caloric intake, portion sizes, "fast food" intake, and perceived control of eating in 88 obese subjects. After a 2-day placebo lead-in, subjects self-administered pramlintide (180 microg) or placebo by subcutaneous injection 15 min before meals for 6 wk without concomitant lifestyle modifications. Compared with placebo, pramlintide treatment elicited significant mean reductions from baseline in body weight on day 44 (-2.1 +/- 0.3 vs. +0.1 +/- 0.4%, P < 0.001), 24-h caloric intake (-990 +/- 94 vs. -243 +/- 126 kcal on day 3, P < 0.0001; -680 +/- 86 vs. -191 +/- 161 kcal on day 43, P < 0.01), portion sizes, and caloric intake at a "fast food challenge" (-385 +/- 61 vs. -109 +/- 88 kcal on day 44, P < 0.05). Pramlintide treatment also improved perceived control of eating, as demonstrated by a 45% placebo-corrected reduction in binge eating scores (P < 0.01). The results of this translational research study confirm in humans various preclinical effects of amylin agonism, demonstrating that pramlintide-mediated weight loss in obese subjects is accompanied by sustained reductions in 24-h food intake, portion sizes, fast food intake, and binge eating tendencies.     

Enhanced striatal dopamine release during food stimulation in binge eating disorder

Subjects with binge eating disorder (BED) regularly consume large amounts of food in short time periods. The neurobiology of BED is poorly understood. Brain dopamine, which regulates motivation for food intake, is likely to be involved. We assessed the involvement of brain dopamine in the motivation for food consumption in binge eaters. Positron emission tomography (PET) scans with [(11)C]raclopride were done in 10 obese BED and 8 obese subjects without BED. Changes in extracellular dopamine in the striatum in response to food stimulation in food-deprived subjects were evaluated after placebo and after oral methylphenidate (MPH), a drug that blocks the dopamine reuptake transporter and thus amplifies dopamine signals. Neither the neutral stimuli (with or without MPH) nor the food stimuli when given with placebo increased extracellular dopamine. The food stimuli when given with MPH significantly increased dopamine in the caudate and putamen in the binge eaters but not in the nonbinge eaters. Dopamine increases in the caudate were significantly correlated with the binge eating scores but not with BMI. These results identify dopamine neurotransmission in the caudate as being of relevance to the neurobiology of BED. The lack of correlation between BMI and dopamine changes suggests that dopamine release per se does not predict BMI within a group of obese individuals but that it predicts binge eating.     

Bingeing,Self‐restriction,and Increased Body Weight in Rats With Limited Access to a Sweet‐fat Diet

Objective: Prior research has shown that fasting alternated with a diet of standard rodent chow and a 10% sucrose solution produces bingeing on the sucrose, but animals remain at normal body weight. The present study investigated whether restricted access to a highly palatable combination of sugar and fat, without food deprivation, would instigate binge eating and also increase body weight. Methods and Procedures: Male rats were maintained for 25 days on one of four diets: (i) sweet‐fat chow for 2 h/day followed by ad libitum standard chow, (ii) 2‐h sweet‐fat chow only 3 days/week and access to standard chow the rest of the time, (iii) ad libitum sweet‐fat chow, or (iv) ad libitum standard chow. Results: Both groups with 2‐h access to the sweet‐fat chow exhibited bingeing behavior, as defined by excessively large meals. The body weight of these animals increased due to large meals and then decreased between binges as a result of self‐restricted intake of standard chow following binges. However, despite these fluctuations in body weight, the group with 2‐h access to sweet‐fat chow every day gained significantly more weight than the control group with standard chow available ad libitum. Discussion: These findings may have implications for the body weight fluctuations associated with binge‐eating disorder, as well as the relationship between binge eating and the obesity epidemic.     

Cognitive behavioral therapy and fluoxetine for binge eating disorder: two-year follow-up

Objective: This study assessed the long‐term effects of group behavioral treatment plus individual cognitive behavioral therapy (CBT) and/or fluoxetine in binge eating disorder (BED) patients. Research Methods and Procedures: A total of 116 individuals were randomized to an initial five‐month trial and were followed up over two years. Assessments, including binge frequency, weight, and self‐report measures, were administered at pre‐treatment, post‐treatment, and ～6, 12, 18, and 24 months after initial treatment. Results: Across treatment groups, there was overall improvement over 29 months in binge frequency and in binge abstinence. The odds of binge abstinence 2 years post‐treatment were 1.373 times the odds of binge abstinence immediately post‐treatment. There was no significant change in weight over the two‐year period. Subjects who received individual CBT evidenced lower binge frequency over the two‐year follow‐up period than patients who had not received individual CBT. Similarly, CBT was associated with increased rates of binge abstinence. There were no main effects of treatment assignment on weight over the two‐year follow‐up period. There was a significant advantage for fluoxetine assignment over the two‐year follow‐up period on depressive symptoms. Discussion: The major significance of the study rests in its examination of the long‐term effects of standardized interventions for BED. Our findings provide support for the ideas that short‐term treatment may confer long‐term benefit and that not all treatments are equivalent in the benefits they confer.     

Loss of control is central to psychological disturbance associated with binge eating disorder

Objective: Binge eating disorder (BED) is positively associated with obesity and psychological distress, yet the behavioral features of BED that drive these associations are largely unexplored. The primary aim of this study was to investigate which core behavioral features of binge eating are most strongly related to psychological disturbance. Methods and Procedures: A cross‐sectional study involved 180 bariatric surgery candidates, 93 members of a non‐surgical weight loss support group, and 158 general community respondents (81 men/350 women, mean age 45.8 ± 13.3, mean BMI 34.8 ± 10.8, BMI range 17.7–66.7). Validated questionnaires assessed BED and binge eating, symptoms of depression, appearance dissatisfaction (AD), quality of life (QoL) and eating‐related behaviors. Features of binge eating were confirmed by interview. BMI was determined by clinical assessment and self‐report. Results: The loss of control (LOC) over eating, that is, being unable to stop eating or control what or how much was consumed was most closely related to psychological markers of distress common in BED. In particular, those who experienced severe emotional disturbance due to feelings of LOC reported higher symptoms of depression (P < 0.001), AD (P = 0.009), and poorer mental health–related QoL (P = 0.027). Discussion: Persons who report subjective binge episodes or do not meet BED frequency criteria for objective binge episodes may still be at elevated risk of psychological disturbance and benefit from clinical intervention. Feelings of LOC could drive binge eaters to seek bariatric surgery in an attempt to gain control over body weight and psychologically disturbing eating behavior.     

Divergent neural substrates of inhibitory control in binge eating disorder relative to other manifestations of obesity

Objective:

An important endeavor involves increasing our understanding of biobehavioral processes underlying different types of obesity. The current study investigated the neural correlates of cognitive control (involving conflict monitoring and response inhibition) in obese individuals with binge eating disorder (BED) as compared to BMI‐matched non‐BED obese (OB) individuals and lean comparison (LC) participants. Alterations in cognitive control may contribute to differences in behavioral control over eating behaviors in BED and obesity.

Design and Methods:

Participants underwent functional magnetic resonance imaging while completing the Stroop color‐word interference task.

Results and Conclusions:

Relative to the OB and LC groups, activity in the BED group was differentiated by relative hypoactivity in brain areas involved in self‐regulation and impulse control. Specifically, the BED group showed diminished activity in the ventromedial prefrontal cortex (vmPFC), inferior frontal gyrus (IFG), and insula during Stroop performance. In addition, dietary restraint scores were negatively correlated with right IFG and vmPFC activation in the BED group, but not in the OB or HC groups. Thus, BED individuals' diminished ability to recruit impulse‐control‐related brain regions appears associated with impaired dietary restraint. The observed differences in neural correlates of inhibitory processing in BED relative to OB and LC groups suggest distinct eurobiological contributions to binge eating as a subgroup of obese individuals.     

Momentary affect surrounding loss of control and overeating in obese adults with and without binge eating disorder

Research suggests that loss of control (LOC) while eating (the sense that one cannot control what or how much one is eating) is a more salient feature of binge eating than the amount of food consumed. This study examined the unique contributions of LOC and episode size to negative affect surrounding eating episodes in binge eating disorder (BED) and obesity. Twenty-two obese adults with (n = 9) and without (n = 13) BED completed daily records of eating patterns and mood using ecological momentary assessment (EMA). Linear mixed modeling revealed that across groups, greater premeal self-reported LOC was associated with higher premeal negative affect independent of episode size. For individuals with BED, greater premeal self-reported LOC was associated with higher postmeal negative affect, regardless of the amount of food eaten, whereas for obese controls, the combination of LOC and consumption of large amounts of food was associated with lower postmeal negative affect. Results indicate that LOC, but not the quantity of food consumed, is associated with momentary distress related to aberrant eating in BED. Findings also highlight the need for further research investigating the emotional context surrounding aberrant eating in obese individuals without BED.     

Hypothalamic‐specific proopiomelanocortin deficiency reduces alcohol drinking in male and female mice

Opioid receptor antagonist naltrexone reduces alcohol consumption and relapse in both humans and rodents. This study investigated whether hypothalamic proopiomelanocortin (POMC) neurons (producing beta‐endorphin and melanocortins) play a role in alcohol drinking behaviors. Both male and female mice with targeted deletion of two neuronal Pomc enhancers nPE1 and nPE2 (nPE?/?), resulting in hypothalamic‐specific POMC deficiency, were studied in short‐access (4‐h/day) drinking‐in‐the‐dark (DID, alcohol in one bottle, intermittent access (IA, 24‐h cycles of alcohol access every other day, alcohol vs. water in a two‐bottle choice) and alcohol deprivation effect (ADE) models. Wild‐type nPE+/+ exposed to 1‐week DID rapidly established stable alcohol drinking behavior with more intake in females, whereas nPE?/? mice of both sexes had less intake and less preference. Although nPE?/? showed less saccharin intake and preference than nPE+/+, there was no genotype difference in sucrose intake or preference in the DID paradigm. After 3‐week IA, nPE+/+ gradually escalated to high alcohol intake and preference, with more intake in females, whereas nPE?/? showed less escalation. Pharmacological blockade of mu‐opioid receptors with naltrexone reduced intake in nPE+/+ in a dose‐dependent manner, but had blunted effects in nPE?/? of both sexes. When alcohol was presented again after 1‐week abstinence from IA, nPE+/+ of both sexes displayed significant increases in alcohol intake (ADE or relapse‐like drinking), with more pronounced ADE in females, whereas nPE?/? did not show ADE in either sex. Our results suggest that neuronal POMC is involved in modulation of alcohol ‘binge’ drinking, escalation and ‘relapse’, probably via hypothalamic‐mediated mechanisms, with sex differences.     

On the Relation of Attempting to Lose Weight,Restraint, and Binge Eating in Outpatients with Binge Eating Disorder

Objective: To examine the relationship among attempts to lose weight, restraint, and eating behavior in outpatients with binge eating disorder (BED). Research Methods and Procedures: Participants were 93 consecutive outpatients evaluated for a clinical trial who met Diagnostic and Statistical Manual, Fourth edition criteria for BED. The Eating Disorder Examination Interview was administered to assess attempts at weight loss, restraint, different forms of overeating, and the attitudinal psychopathology of eating disorders (i.e., concerns regarding eating, shape, and weight). In addition, the Three‐Factor Eating Questionnaire was used to assess cognitive restraint, hunger, and disinhibition. Psychometrically established measures were given to assess body dissatisfaction, depression, and self‐esteem. Results: The majority of participants (75.3%; N = 70) reported attempting to lose weight, but only 37.6% (N = 35) reported dietary restraint on at least half the days of the month. Dietary restraint and cognitive restraint were not associated with any form of binge eating or overeating. Dietary restraint and cognitive restraint were positively correlated with weight concern, shape concern, and body dissatisfaction, and negatively correlated with body mass index. To further examine the interplay between attempting to lose weight and restraint, three study groups were created: unrestrained nonattempters (21.5%, N = 20), unrestrained attempters (40.9%; N = 38), and restrained attempters (34.4%; N = 32). The three groups did not differ significantly on binge eating or other eating behaviors; however, significant differences were observed for weight concern, shape concern, and body dissatisfaction. Discussion: Attempts to lose weight and restraint are not synonymous for patients with BED. Although 75.3% of BED patients reported that they were attempting to lose weight, only 37.6% reported dietary restraint on at least half the days of the previous month. While restraint was negatively associated with body mass index, it was not related to binge eating or overeating. Our findings raise questions about prevailing models that posit restraint as a predominant factor in the maintenance of binge eating in BED.     

Significance of Overvaluation of Shape/Weight in Binge‐eating Disorder: Comparative Study With Overweight and Bulimia Nervosa

Increasing empirical evidence supports the validity of binge‐eating disorder (BED) and its inclusion as a formal diagnosis in the Diagnostic and Statistical Manual of Mental Disorders (DSM‐V). Contention exists regarding the criteria for BED, including whether, like bulimia nervosa (BN), it should be characterized by overvaluation of shape/weight. This study examined the significance of overvaluation for BED using two complementary comparisons groups. Participants were 324 women who completed self‐report instruments as part of an Internet study. Analyses compared BMI, eating disorder (ED) features, and depressive levels in four groups: 123 overweight participants without ED, 47 BED participants who do not overvalue shape/weight, 101 BED participants who overvalue shape/weight, and 53 BN participants. Both BED groups had significantly greater ED psychopathology than the overweight group. Within BED, the group with overvaluation had significantly greater ED psychopathology and depressive levels despite no differences in binge eating. BED with overvaluation and BN groups differed little from each other but had significantly higher ED psychopathology and depressive levels than the other groups. Group differences existed despite similar age and BMI across the groups, as well as when controlling for group differences in depressive levels. These findings provide further support for the validity of BED and suggest that overvaluation of shape/weight, which provides important information about BED severity, warrants consideration as either a diagnostic specifier or as a dimensional severity rating. Although inclusion of overvaluation of shape/weight could be considered as a required criterion for BED, this would exclude a substantial proportion of BED patients with clinically significant problems.     

Definitions of Night Eating in Adolescent Girls

Objective: To describe the prevalence of night eating in a community cohort of black and white girls, using different definitions of night eating as described in the literature. Research Methods and Procedures: Three‐day food diaries collected as part of the National Growth and Health Study were examined to identify episodes of night eating, which was defined in five different ways: eating >25% of daily caloric intake after the last evening meal, eating >25% of daily caloric intake after 7 pm, eating >50% of daily caloric intake after the last evening meal, eating >50% of daily caloric intake after 7 pm, or eating between 11 pm and 4:59 am. Results: Frequency of night eating varied tremendously depending on how the behavior was defined. For the least restrictive definition (>25% of total intake after last meal), 50% to 70% of girls reported one night eating event; for the most restrictive (>50% of total intake after last meal), only 1.5% of 11‐year‐old girls' diaries and 3.5% of 19‐year‐old girls' diaries contained a night eating event. The frequency of night eating decreased dramatically (typically by a factor of 10) if the inclusion criteria required multiple night eating events in a given week. Discussion: A standard definition of night eating behavior is needed to advance the field. An agreed‐on operationalized definition that includes time of day, amount of calories consumed, and a frequency criterion would enable cross‐study comparisons and encourage the examination of developmental and clinical considerations of night eating behavior.     

Binge Eating Behavior in Patients with Eating Disorders

The purpose of this study was to determine whether the objectively observed binge eating behavior of obese subjects meeting the proposed DSM-IV criteria for binge eating disorder would be similar to that observed in patients with bulimia nervosa. Non-obese patients with bulimia nervosa (BN), obese subjects with binge eating disorder (BED), obese and non-obese women without eating disorders were each instructed to binge eat single- and multiple-item meals. In the multiple-item meal, the obese subjects with BED ate significantly more (1515 kcal) than obese subjects without BED (1115 kcal), but they ate less than the normal-weight bulimic patients (2680 kcal). The non-obese controls ate amounts similar to the obese non-binge-eating-disordered group (1093 and 1115.2 kcal, respectively). In the single-item meal, consisting of ice cream, patients with BN ate significantly more than any other group (1307 kcal), while obese subjects with or without binge-eating disorder ate significantly more (762 kcal) than non-obese controls (308 kcal). This study has demonstrated that although both BN and BED are characterized by recurrent episodes of binge eating, quantitatively there appear to be differences between the eating disturbances in the two disorders. Because single- and multiple-item meals differ in external cues, these results also suggest that the obese subjects with BED may be disinhibited by external cues, while obese subjects without BED may be inhibited by external cues.     

The Metabolic Syndrome and Behavioral Correlates in Obese Patients With Binge Eating Disorder

This study examined the frequency of the metabolic syndrome (MetSyn) and explored behavioral eating‐ and weight‐related correlates in obese patients with binge eating disorder (BED). Ninety‐three treatment‐seeking obese BED patients (22 men and 71 women) with and without the MetSyn were compared on demographic features and a number of current and historical eating and weight variables. Sixty percent of the obese patients with BED met criteria for the MetSyn, with men and whites having significantly higher rates than women and African Americans, respectively. Patients with vs. without coexisting MetSyn did not differ significantly in self‐reported frequency of binge eating or severity of eating disorder psychopathology. Multivariate hierarchical logistic regression analysis revealed that, after controlling for gender, ethnicity, and BMI, fewer episodes of weight cycling and regular meal skipping were significant predictors of the MetSyn. These findings suggest that lifestyle behaviors including weight loss attempts and regular meal consumption may be potential targets for prevention and/or treatment of the MetSyn in obese patients with BED.     

Eating disorder symptomatology in normal-weight vs. obese individuals with binge eating disorder

Although normal-weight individuals comprise a substantial minority of the binge eating disorder (BED) population, little is known about their clinical presentation. This study sought to investigate the nature and severity of eating disturbances in normal-weight adults with BED. We compared 281 normal-weight (n = 86) and obese (n = 195) treatment-seeking adults with BED (mean age = 31.0; s.d. = 10.8) on a range of current and past eating disorder symptoms using ANOVA and χ(2) analyses. After controlling for age and sex, normal-weight participants reported more frequent use of a range of healthy and unhealthy weight control behaviors compared to their obese peers, including eating fewer meals and snacks per day; exercising and skipping meals more frequently in the past month; and avoiding certain foods for weight control. They also endorsed more frequent attempts at dieting in the past year, and feeling more frequently distressed about their binge eating, at a trend level. There were no group differences in binge eating frequency in the past month, age at onset of binge eating, overvaluation of shape/weight, or likelihood of having used certain weight control behaviors (e.g., vomiting, laxative use) or having sought treatment for an eating disorder in the past. Based on our findings, normal-weight individuals appear to be a behaviorally distinct subset of the BED population with significantly greater usage of both healthy and unhealthy weight control behaviors compared to their obese peers. These results refute the notion that distress and impairment in BED are simply a result of comorbid obesity.     

Independent and combined effects of eating rate and energy density on energy intake,appetite, and gut hormones

Objective:

Energy density (ED) and eating rate (ER) influence energy intake; their combined effects on intake and on postprandial pancreatic and gut hormone responses are undetermined. To determine the combined effects of ED and ER manipulation on voluntary food intake, subjective appetite, and postprandial pancreatic and gut hormone responses.

Design and Methods:

Twenty nonobese volunteers each consumed high (1.6 kcal g^?1; HED) and low (1.2 kcal g^?1; LED) ED breakfasts slowly (20 g min^?1; SR) and quickly (80 g min^?1; FR) ad libitum to satiation. Appetite, and pancreatic and gut hormone concentrations were measured periodically over 3 h. Ad libitum energy intake during the subsequent lunch was then measured.

Results:

Main effects of ED and ER on energy intake and a main effect of ER, but not ED, on mass of food consumed were observed, FR and HED being associated with increased intake (P < 0.05). Across all conditions, energy intake was highest during FR‐HED (P ≤ 0.01). Area under the curve (AUC) of appetite ratings was not different between meals. Main effects of ED and ER on insulin, peptide‐YY, and glucagon‐like peptide‐1 AUC (P < 0.05) were observed, FR and HED being associated with larger AUC. No effects on active or total ghrelin AUC were documented. Total energy intake over both meals was highest during the FR‐HED trial with the greatest difference between FR‐HED and SR‐LED trials (P ≤ 0.01).

Conclusion:

Consuming an energy dense meal quickly compounds independent effects of ER and ED on energy intake. Energy compensation at the following meal may not occur despite altered gut hormone responses.

     

Depression‐like symptoms of withdrawal in a genetic mouse model of binge methamphetamine intake

Binge methamphetamine (MA) users have higher MA consumption, relapse rates and depression‐like symptoms during early periods of withdrawal, compared with non‐binge users. The impact of varying durations of MA abstinence on depression‐like symptoms and on subsequent MA intake was examined in mice genetically prone to binge‐level MA consumption. Binge‐level MA intake was induced using a multiple‐bottle choice procedure in which mice were offered one water drinking tube and three tubes containing increasing concentrations of MA in water, or four water tubes (control group). In two studies, depression‐like symptoms were measured using a tail‐suspension test and a subsequent forced‐swim test, after forced abstinence of 6 and 30 hours from a 28‐day course of chronic MA intake. An additional study measured the same depression‐like symptoms, as well as MA intake, after prolonged abstinence of 1 and 2 weeks. MA high drinking mice and one of their progenitor strains DBA/2J escalated their MA intake with increasing MA concentration; however, MA high drinking mice consumed almost twice as much MA as DBA/2J mice. Depression‐like symptoms were significantly higher early after MA access was withdrawn, compared to levels in drug‐naïve controls, with more robust effects of MA withdrawal observed in MA high drinking than DBA/2J mice. When depression‐like symptoms were examined after 1 or 2 weeks of forced abstinence in MA high drinking mice, depression‐like symptoms dissipated, and subsequent MA intake was high. The MA high drinking genetic mouse model has strong face validity for human binge MA use and behavioral sequelae associated with abstinence.