The effects of overnight nutrient intake on hypothalamic inflammation in a free-choice diet-induced obesity rat model.

Consumption of fat and sugar induces hyperphagia and increases the prevalence of obesity and diabetes type 2. Low-grade inflammation in the hypothalamus, a key brain area involved in the regulation of energy homeostasis is shown to blunt signals of satiety after long term high fat diet. The fact that this mechanism can be activated after a few days of hyperphagia before apparent obesity is present led to our hypothesis that hypothalamic inflammation is induced with fat and sugar consumption. Here, we used a free-choice high-fat high-sugar (fcHFHS) diet-induced obesity model and tested the effects of differential overnight nutrient intake during the final experimental night on markers of hypothalamic inflammation. Male Wistar rats were fed a control diet or fcHFHS diet for one week, and assigned to three different feeding conditions during the final experimental night: 1) fcHFHS-fed, 2) fed a controlled amount of chow diet, or 3) fasted. RT-qPCR and Western blot were utilized to measure hypothalamic gene and protein expression, of cytokines and intermediates of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway. Lastly, we investigated the effects of acute fat intake on markers of hypothalamic inflammation in fat-naïve rats. fcHFHS-fed rats consumed more calories, increased adipose tissue, and showed elevated expression of hypothalamic inflammation markers (increased phosphorylation of NF-κB protein, Nfkbia and Il6 gene expression) compared to chow-fed rats. These effects were evident in rats consuming relative high amounts of fat. Removal of the fat and sugar, or fasting, during the final experimental night ameliorated hypothalamic inflammation. Finally, a positive correlation was observed between overnight acute fat consumption and hypothalamic NF-κB phosphorylation in fat-naïve rats. Our data indicate that one week of fcHFHS diet, and especially the fat component, promotes hypothalamic inflammation, and removal of the fat and sugar component reverses these detrimental effects.

Passive and active roles of fat-free mass in the control of energy intake and body composition regulation.

While putative feedback signals arising from adipose tissue are commonly assumed to provide the molecular links between the body's long-term energy requirements and energy intake, the available evidence suggests that the lean body or fat-free mass (FFM) also plays a role in the drive to eat. A distinction must, however, be made between a 'passive' role of FFM in driving energy intake, which is likely to be mediated by 'energy-sensing' mechanisms that translate FFM-induced energy requirements to energy intake, and a more 'active' role of FFM in the drive to eat through feedback signaling between FFM deficit and energy intake. Consequently, a loss of FFM that results from dieting or sedentarity should be viewed as a risk factor for weight regain and increased fatness not only because of the impact of the FFM deficit in lowering the maintenance energy requirement but also because of the body's attempt to restore FFM by overeating-a phenomenon referred to as 'collateral fattening'. A better understanding of these passive and active roles of FFM in the control of energy intake will necessitate the elucidation of peripheral signals and energy-sensing mechanisms that drive hunger and appetite, with implications for both obesity prevention and its management.

Dietary Intake and Eating Behaviours of Obese New Zealand Children and Adolescents Enrolled in a Community-Based Intervention Programme.

OBJECTIVES: The aim of this study was to describe dietary intake and eating behaviours of obese children and adolescents, and also to determine how these differ in Indigenous versus non-Indigenous children at enrolment in an obesity programme. METHODS: Baseline dietary intake and eating behaviour records were assessed from those enrolled in a clinical unblinded randomised controlled trial of a multi-disciplinary intervention. The setting was a community-based obesity programme in Taranaki, New Zealand. Children or adolescents who were enrolled from January 2012 to August 2014, with a BMI ≥98th percentile or >91st centile with weight-related comorbidities were eligible. RESULTS: 239 participants (45% Maori, 45% NZ Europeans, 10% other ethnicities), aged 5-17 years were assessed. Two-thirds of participants experienced hyperphagia and half were not satiated after a meal. Comfort eating was reported by 62% of participants, and daily energy intake was above the recommended guidelines for 54%. Fruit and vegetable intake was suboptimal compared with the recommended 5 servings per day (mean 3.5 [SD = 1.9] servings per day), and the mean weekly breakfasts were less than the national average (5.9 vs 6.5; p<0.0001). Median sweet drink intake amongst Maori was twice that of NZ Europeans (250 vs 125 ml per day; p = 0.0002). CONCLUSIONS: There was a concerning prevalence of abnormal eating behaviours and significant differences in dietary intake between obese participants and their national counterparts. Ethnic differences between Indigenous and non-Indigenous participants were also present, especially in relation to sweet drink consumption. Eating behaviours, especially sweet drink consumption and fruit/vegetable intake need to be addressed.

Nutritional intervention with hypocaloric diet for weight control in children and adolescents with Prader-Willi Syndrome.

Prader-Willi Syndrome (PWS) is a genetic disorder caused by the lack of expression of paternal alleles in the proximal region of the long arm of chromosome 15. Low inhibitory control and hyperphagia are two of the most severe neurobehavioral symptoms of the syndrome. The aim of the present study was to assess the efficiency of nutritional training program with the use hypocaloric diet for weight control in a group of five children and adolescents with PWS. The intervention program consisted of 10 sessions for parents' orientation during 8months. Patients had their anthropometric measures assessed (weight, height and body mass index - BMI). The main results indicate weight maintenance, height increase, and BMI decrease after intervention. These results were considered indicators of the program's efficiency.

Violation of eating expectancies does not reduce conditioned desires for chocolate.

Although eating desires can be easily learned, their extinction appears more difficult. The present two-session study aimed to investigate the role of eating expectancies in the short and longer-term extinction of eating desires. In addition, the relationship between eating desires and conditioned evaluations was examined to test whether they might share a similar mechanism. It was hypothesized that the short-term extinction of eating desires would be more successful after the disconfirmation of eating expectancies (instructed extinction or IE), while resulting in worse longer-term extinction because omission of the food reward during extinction is not surprising. In contrast to the hypotheses, it was found that IE had no effect on the short-term and longer-term extinction of eating desires. Eating desires correlated with conditioned evaluations only to some extent. It is concluded that eating expectancies do not mediate the short-term extinction of conditioned eating desires. In addition, their longer-term extinction does not appear to be facilitated by a greater violation of eating expectancies. This suggests that it might not be necessary to focus on expectancy violation in cue exposure therapy to reduce eating desires.

Reduced reward-driven eating accounts for the impact of a mindfulness-based diet and exercise intervention on weight loss: Data from the SHINE randomized controlled trial.

Many individuals with obesity report over eating despite intentions to maintain or lose weight. Two barriers to long-term weight loss are reward-driven eating, which is characterized by a lack of control over eating, a preoccupation with food, and a lack of satiety; and psychological stress. Mindfulness training may address these barriers by promoting awareness of hunger and satiety cues, self-regulatory control, and stress reduction. We examined these two barriers as potential mediators of weight loss in the Supporting Health by Integrating Nutrition and Exercise (SHINE) randomized controlled trial, which compared the effects of a 5.5-month diet and exercise intervention with or without mindfulness training on weight loss among adults with obesity. Intention-to-treat multiple mediation models tested whether post-intervention reward-driven eating and psychological stress mediated the impact of intervention arm on weight loss at 12- and 18-months post-baseline among 194 adults with obesity (BMI: 30-45). Mindfulness (relative to control) participants had significant reductions in reward-driven eating at 6 months (post-intervention), which, in turn, predicted weight loss at 12 months. Post-intervention reward-driven eating mediated 47.1% of the total intervention arm effect on weight loss at 12 months [ß = -0.06, SE(ß) = 0.03, p = .030, 95% CI (-0.12, -0.01)]. This mediated effect was reduced when predicting weight loss at 18 months (p = .396), accounting for 23.0% of the total intervention effect, despite similar weight loss at 12 months. Psychological stress did not mediate the effect of intervention arm on weight loss at 12 or 18 months. In conclusion, reducing reward-driven eating, which can be achieved using a diet and exercise intervention that includes mindfulness training, may promote weight loss (clinicaltrials.gov registration: NCT00960414).

High-fat feeding impairs nutrient sensing and gut brain integration in the caudomedial nucleus of the solitary tract in mice.

Hyperphagic obesity is characterized in part by a specific increase in meal size that contributes to increased daily energy intake, but the mechanisms underlying impaired activity of meal size regulatory circuits, particularly those converging at the caudomedial nucleus of the solitary tract in the hindbrain (cmNTS), remain poorly understood. In this paper, we assessed the consequences of high-fat (HF) feeding and diet-induced obesity (DIO) on cmNTS nutrient sensing and metabolic integration in the control of meal size. Mice maintained on a standard chow diet, low-fat (LF) diet or HF diet for 2 weeks or 6 months were implanted with a bilateral brain cannula targeting the cmNTS. Feeding behavior was assessed using behavioral chambers and meal-pattern analysis following cmNTS L-leucine injections alone or together with ip CCK. Molecular mechanisms implicated in the feeding responses were assessed using western blot, immunofluorescence and pharmacological inhibition of the amino acid sensing mTORC1 pathway (mammalian target of rapamycin complex 1). We found that HF feeding blunts the anorectic consequences of cmNTS L-leucine administration. Increased baseline activity of the L-leucine sensor P70 S6 kinase 1 and impaired L-leucine-induced activation of this pathway in the cmNTS of HF-fed mice indicate that HF feeding is associated with an impairment in cmNTS mTOR nutritional and hormonal sensing. Interestingly, the acute orexigenic effect of the mTORC1 inhibitor rapamycin was preserved in HF-fed mice, supporting the assertion that HF-induced increase in baseline cmNTS mTORC1 activity underlies the defect in L-leucine sensing. Last, the synergistic feeding-suppressive effect of CCK and cmNTS L-leucine was abrogated in DIO mice. These results indicate that HF feeding leads to an impairment in cmNTS nutrient sensing and metabolic integration in the regulation of meal size.

Probiotic supplementation prevents high-fat, overfeeding-induced insulin resistance in human subjects.

The purpose of the present study was to determine whether probiotic supplementation (Lactobacillus casei Shirota (LcS)) prevents diet-induced insulin resistance in human subjects. A total of seventeen healthy subjects were randomised to either a probiotic (n 8) or a control (n 9) group. The probiotic group consumed a LcS-fermented milk drink twice daily for 4 weeks, whereas the control group received no supplementation. Subjects maintained their normal diet for the first 3 weeks of the study, after which they consumed a high-fat (65 % of energy), high-energy (50 % increase in energy intake) diet for 7 d. Whole-body insulin sensitivity was assessed by an oral glucose tolerance test conducted before and after overfeeding. Body mass increased by 0·6 (SE 0·2) kg in the control group (P< 0·05) and by 0·3 (SE 0·2) kg in the probiotic group (P>0·05). Fasting plasma glucose concentrations increased following 7 d of overeating (control group: 5·3 (SE 0·1) v. 5·6 (SE 0·2) mmol/l before and after overfeeding, respectively, P< 0·05), whereas fasting serum insulin concentrations were maintained in both groups. Glucose AUC values increased by 10 % (from 817 (SE 45) to 899 (SE 39) mmol/l per 120 min, P< 0·05) and whole-body insulin sensitivity decreased by 27 % (from 5·3 (SE 1·4) to 3·9 (SE 0·9), P< 0·05) in the control group, whereas normal insulin sensitivity was maintained in the probiotic group (4·4 (SE 0·8) and 4·5 (SE 0·9) before and after overeating, respectively (P>0·05). These results suggest that probiotic supplementation may be useful in the prevention of diet-induced metabolic diseases such as type 2 diabetes.

Maternal diet, bioactive molecules, and exercising as reprogramming tools of metabolic programming.

Nutrition and lifestyle, particularly over-nutrition and lack of exercise, promote the progression and pathogenesis of obesity and metabolic diseases. Nutrition is likely the most important environmental factor that modulates the expression of genes involved in metabolic pathways and a variety of phenotypes associated with obesity and diabetes. During pregnancy, diet is a major factor that influences the organ developmental plasticity of the foetus. Experimental evidence shows that nutritional factors, including energy, fatty acids, protein, micronutrients, and folate, affect various aspects of metabolic programming. Different epigenetic mechanisms that are elicited by bioactive factors in early critical developmental ages affect the susceptibility to several diseases in adulthood. The beneficial effects promoted by exercise training are well recognised, and physical exercise may be considered one of the more prominent non-pharmacological tools that can be used to attenuate metabolic programming and to consequently ameliorate the illness provoked by metabolic diseases and reduce the prevalence of obesity, type 2 diabetes, and cardiovascular diseases. Literature on the different outcomes of unbalanced diets and the beneficial effects of some bioactive molecules during gestation and lactation on the metabolic health of offspring, as well as the potential mechanisms underlying these effects, was reviewed. The importance of the combined effects of functional nutrition and exercise as reprogramming tools of metabolic programming is discussed in depth. Finally, this review provides recommendations to healthcare providers that may aid in the control of early programming in an attempt to optimise the health of the mother and child.

Slimming starters. Intake of a diet-congruent food reduces meal intake in active dieters.

Dietary restraint is known to break down in the face of tempting foods. Previous research suggests exposure to cues associated with slimming such as images or odours act as prompts to restrict intake of a tempting snack in dieters. The effects of consuming diet-congruent foods on subsequent intake of a meal have not yet been investigated. Thus, using a repeated measures design 26 female participants (dieters or non-dieters) consumed a diet-congruent (100 kcal salad), hedonic (100 kcal garlic bread) or neutral (0 kcal water) preload. A lexical decision task measured the salience of diet and hedonic thoughts and participants were then offered pizza as a main meal. Appetite sensations were measured throughout the study. Compared to the hedonic and neutral preload, a diet-congruent preload reduced dieters' entire meal intake by 21%. In contrast, non-dieters consumed 9% more in the hedonic preload condition compared to the neutral preload, yet showed no differences between the diet-congruent and other conditions. Salad lowered participants desire to eat and increased fullness compared to garlic bread and water preloads. Dieters were also less hungry after the salad compared to the garlic bread and water preloads. Consuming a diet-congruent first course may prompt lower intake at a meal, in part due to facilitating resolve to refrain from overeating a tempting second course.

Influência da grelina sobre o processo de estímulo-secreção de insulina in vitro em camundongos Swiss adultos hiperalimentados na lactação / Ghrelin influence on the process of insulin secretion stimulus-vitro in mice Swiss adults overfeeding in lactation

O excesso ou a privação de nutrientes em períodos específicos do desenvolvimento, tais como a lactação, estimulam alterações no metabolismo celular, por exemplo. Estas modificações perpetuam-se ao longo da vida e em conseqüência tornam o organismo mais suscetível ao aparecimento de patologias na idade adulta (Programação Metabólica). Estudamos a influência da grelina na secreção de insulina em camundongos Swiss de 120 dias submetidos à hiperalimentação na lactação. Para induzir a hiperalimentação as ninhadas foram reduzidas a 3 filhotes machos por lactante no 3o dia de vida pós-natal. As ninhadas controle foram ajustadas para 9 filhotes machos por lactante. Na idade adulta os animais hiperalimentados (AH) exibiram em comparação aos animais controle (AC) um incremento de 20% no peso corporal, maior índice de Lee (1705,63 g/mm + 29,3 vs 1374,10 g/mm + 54,9; p< 0,001), elevação da gordura corporal (31,0% + 4,6 vs 21,5% + 3,6; p< 0,01), aumento da gordura retroperitoneal (0,79 g + 0,1 vs 0,44 g + 0,1; p< 0,001), hiperglicemia de jejum (151,83 mg/ dl + 8,3 vs 118,0 mg/ dl + 1,0; p< 0,001), hiperinsulinemia de jejum (54,06 µUI/ml + 2,3 vs 19,28 µUI/ml + 1,53; p< 0,001) e hipogrelinemia de jejum (98,64 pg/ml + 56,5 vs 201,14 pg/ml + 46,4; p< 0,05). Os AH apresentaram maior secreção de insulina in vitro em presença de glicose aos 10 minutos (209,66 µUI/ml + 46,5; p< 0,05), 30 minutos (441,88 µUI/ml + 30,2; p< 0,05) e 60 minutos (214,34 µUI/ml + 29,8) em comparação aos AC, respectivamente 86,90 µUI/ml + 9,5; 74,31 µUI/ml + 7,7 vs 27,45 µUI/ml + 6,1; p< 0,05. As ilhotas pancreáticas dos AH adultos demonstraram em relação aos AC diminuição do consumo de O2 (1,76 pmols O2/ s. ilhota-1 + 0,4 vs 4,85 pmols O2/ s. ilhota-1 + 1,5; p< 0,001) e elevação do conteúdo do receptor de grelina GHSR1A (3,05 % + 2,13 vs 0,95 % + 0,1; p< 0,05)...

Excess or lack of nutrients at specific times of development generates adaptive responses that can change the body causing the onset of chronic diseases in adulthood (Metabolic Programming). We studied the influence of the hormone ghrelin in insulin secretion of adult Swiss mice overfed during lactation. To induce early postnatal overnutrition, the litter size was reduced to 3 pups per litter at the 3rd day after birth. In the control group, the litter size was adjusted to 9 pups per litter. In adulthood, overfed group (OG) had an increase of 20% in body weight compared to control group (CG). OG had increased in Lee index (1705.63 g/mm + 29.3 vs 1374.10 g/mm + 54.9; p< 0.001), high body fat (31.0% + 4.6 vs 21.5% + 3.6; p< 0.01), and an elevated retroperitoneal fat (0.79 g + 0.1 vs 0.44 g + 0.1; p< 0.001), fasting hyperglycemia (151.83 mg/ dl + 8.3 vs 118.0 mg/ dl + 1.0; p< 0.001), high fasting insulinemia (54.06 µUI/ml + 2.3 vs 19.28 µUI/ml + 1.53; p< 0.001), and low fasting plasma ghrelin (98.64 pg/ml + 56.5 vs 201.14 pg/ml + 46.4; p< 0.05) compared to CG at 120 days. OG exhibited high insulin secretion in vitro at 10 minutes (209.66 µUI/ml + 46.5), 30 minutes (441.88 µUI/ml + 30.2), and 60 minutes (214.34 µUI/ml + 29.8) compared to CG, respectively 86.90 µUI/ml + 9.5; 74.31 µUI/ml + 7.7 vs 27.45 µUI/ml + 6.1; p< 0.05. Pancreatic islets from OG had a decrease of O2 consumption compared to CG (1.76 pmols O2/ s. islets-1 + 0.4 vs 4.85 pmols O2/ s. islets-1 + 1.5; p< 0.001) and an increased of GHSR1A content (3.05 % + 2.13 vs 0.95 % + 0.1; p< 0.05). Acylated ghrelin increased control group’s insulin secretion in vitro at 30 minutes (CG with ghrelin: 208.50 µUI/ml + 40.85 vs CG without ghrelin 74.31 µUI/ml + 7,7; p< 0.05) and decreased the respiratory control ration (CG with ghrelin: 1.45 + 0.2 vs CG without ghrelin: 2.51 + 0.7; p< 0.05)...

Dietary restraint and disinhibition are associated with increased alcohol use behaviours and thoughts in young women social drinkers.

Previous studies have identified a positive relationship between dietary restraint and alcohol use. However, it is unclear whether heavier drinking is associated with higher dietary restraint per se, or restraint combined with a tendency towards disinhibition. The aim of the present study was to examine alcohol use behaviours in women classified using both restraint and disinhibition scores. Forty-four young female social drinkers gave self-reported measures of their drinking behaviour, including frequency and quantity of alcohol consumed and frequency of drunkenness and binge drinking. Attentional bias for alcohol-related stimuli was also assessed using a dot probe detection task. Finally, the Temptation and Restraint Inventory was used to investigate whether preoccupation with drinking might underlie the relationship between dietary and drinking behaviours. Women classified as both highly restrained and disinhibited tended to report more episodes of drunkenness, showed an attentional bias for alcohol-related words, and had greater cognitive preoccupation with drinking compared to other dietary groups. These data suggest that a tendency towards overeating (disinhibition) combined with attempts at restriction is associated with increased alcohol use behaviours, perhaps due to a greater preoccupation with alcohol.

Reversal of behavioral and metabolic abnormalities, and insulin resistance syndrome, by dietary restriction in mice deficient in brain-derived neurotrophic factor.

Dietary restriction (DR) extends life span and improves glucose metabolism in mammals. Recent studies have shown that DR stimulates the production of brain-derived neurotrophic factor (BDNF) in brain cells, which may mediate neuroprotective and neurogenic actions of DR. Other studies have suggested a role for central BDNF signaling in the regulation of glucose metabolism and body weight. BDNF heterozygous knockout (BDNF+/-) mice are obese and exhibit features of insulin resistance. We now report that an intermittent fasting DR regimen reverses several abnormal phenotypes of BDNF(+/-) mice including obesity, hyperphagia, and increased locomotor activity. DR increases BDNF levels in the brains of BDNF(+/-) mice to the level of wild-type mice fed ad libitum. BDNF(+/-) mice exhibit an insulin-resistance syndrome phenotype characterized by elevated levels of circulating glucose, insulin, and leptin; DR reduces levels of each of these three factors. DR normalizes blood glucose responses in glucose tolerance and insulin tolerance tests in the BDNF(+/-) mice. These findings suggest that BDNF is a major regulator of energy metabolism and that beneficial effects of DR on glucose metabolism are mediated, in part, by BDNF signaling. Dietary and pharmacological manipulations of BDNF signaling may prove useful in the prevention and treatment of obesity and insulin resistance syndrome-related diseases.

Position of the American Dietetic Association: nutrition intervention in the treatment of anorexia nervosa, bulimia nervosa, and eating disorders not otherwise specified (EDNOS).

More than 5 million Americans suffer from eating disorders. Five percent of females and 1% of males have anorexia nervosa, bulimia nervosa, or binge eating disorder. It is estimated that 85% of eating disorders have their onset during the adolescent age period. Although Eating Disorders fall under the category of psychiatric diagnoses, there are a number of nutritional and medical problems and issues that require the expertise of a registered dietitian. Because of the complex biopsychosocial aspects of eating disorders, the optimal assessment and ongoing management of these conditions appears to be with an interdisciplinary team consisting of professionals from medical, nursing, nutritional, and mental health disciplines (1). Medical Nutrition Therapy provided by a registered dietitian trained in the area of eating disorders plays a significant role in the treatment and management of eating disorders. The registered dietitian, however, must understand the complexities of eating disorders such as comorbid illness, medical and psychological complications, and boundary issues. The registered dietitian needs to be aware of the specific populations at risk for eating disorders and the special considerations when dealing with these individuals.

Nondieting versus dieting treatment for overweight binge-eating women.

This study evaluated the effectiveness of nondieting versus dieting treatments for overweight, binge-eating women. Participants (N = 219) were randomly assigned to 1 of 3 groups: diet treatment (DT), nondiet treatment (NDT), or wait-list control (WLC). DT received a balanced-deficit diet reinforced with behavioral strategies. NDT received therapy designed to help participants break out of their dieting cycles. Treatment in both conditions was administered in weekly groups for 6 months, followed by 26 biweekly maintenance meetings, for a total of 18 months of contact. At 6 months posttreatment, DT lost 0.6 kg while NDT gained 1.3 kg. Both treatment groups reduced their Binge Eating Scale scores significantly more than WLC. At 18-month follow-up, both treatment groups experienced weight gain but maintained similar reductions in binge eating. Results indicate that neither intervention was successful in producing short- or long-term weight loss. Therapist biases, which may have affected treatment integrity, and other methodological issues are discussed in relation to the small weight losses achieved.

Fasting and postprandial cerebrospinal fluid glucose concentrations in healthy women and in an obese binge eater.

OBJECTIVE: We hypothesized that abnormal entry of glucose into the central nervous system (CNS) might exist in some chronic binge eaters of carbohydrates, as either a cause or consequence of binge eating. The purpose of this study was thus to determine fasting and postprandial glucose concentrations in the cerebrospinal fluid (CSF) of healthy women, and to obtain similar data in an obese, irritable woman with chronic binge eating of postpartum onset. METHOD: CSF was sampled continuously at 0.1 ml/min from 1100 hr to 1700 hr from the binge eating patient, who consumed 5,000 to 10,000 calories per day (preferentially binging on refined carbohydrates), and 4 healthy women via an indwelling, flexible spinal canal catheter. CSF aliquots were obtained at 10-min intervals for measurement of glucose concentrations. Simultaneously, blood was withdrawn at 30-min intervals to obtain serum for glucose assay. A glucose-rich mixed liquid meal was consumed by participants at 1300 hr. RESULTS: In striking contrast to the normal women, our bulimic patient showed no postprandial rise whatever in CSF glucose concentrations. Fasting CSF glucose concentrations were slightly lower whereas fasting serum glucose levels were normal in the bulimic patient, compared with the normal women. After eating, serum glucose levels increased in all participants, but less so in our patient. DISCUSSION: This is the first description of a lack of postprandial elevation in CSF glucose concentration in a patient with a binge eating disorder. Defective transport of glucose across the blood-brain barrier might account for the observed abnormality. While considering other possibilities, we conjecture that our patient's binge eating was an attempt to compensate for impaired postprandial entry of glucose into her CNS.

Instability of restraint among clinical binge eaters: a methodological note.

The Three Factor Eating Questionnaire was administered to 47 clinical binge eaters at the end of days on which they had and had not binged. Scores on each of the subscales of the questionnaire differed significantly for binge versus nonbinge days. Implications for methodological improvements in future studies are suggested.

Recorded food intake of obese women with binge eating disorder before and after weight loss.

Because binge eating in obese individuals has been postulated to be a reaction to dietary restriction, we examined the recorded food intake of 17 obese women with and 16 obese women without binge eating disorder (BED) during 1-week periods before and 3 months after a very low calorie diet program in order to determine the effects of dietary restriction on binge eating frequency and severity. Before weight loss, rather than reporting severe caloric restriction, women with BED reported greater average energy intake than nonbinge eaters on both a total (2707 vs. 1869 k cal/day, p < .01) and weight-adjusted (25.1 vs. 18.1 kcal/kg, p < .01) basis, with both higher intake on nonbinge days and an increased frequency of binge days. After weight loss, there was no significant difference in energy intake, on either a total or weight-adjusted basis, between subjects with and without BED. Although average daily energy intake fell for both groups after weight loss, only subjects with BED reported significantly decreased energy intake when adjusted for change in body weight. This resulted from decreased intake on nonbinge days and a decreased frequency of binge days. Before weight loss, subjects with BED reported an average energy intake equivalent to 94% of their predicted energy expenditure. Whereas subjects without BED reported intake only 64% of predicted (p = .002). After weight loss, there was no significant difference between subjects with and without BED in the percentage of predicted energy expenditure reported as intake (64% vs. 58%). Restraint was similar in both groups before weight loss, but those with BED reported greater hunger and disinhibition. After weight loss treatment, restraint increased significantly, whereas disinhibition and hunger remained elevated in subjects with BED. Disinhibition, rather than restraint, appears to be a major contributor to the disordered eating of these individuals. Unlike normal-weight women with bulimia nervosa, dietary restriction does not appear to worsen symptoms of binge eating in obese women with BED. Over the short term, subjects with BED may respond to a standard weight loss treatment program with improvements in binge eating behaviors.

Assessment of binge eating in obese patients.

Obese patients entering a weight control program were classified as binge eaters if they reported uncontrolled consumption of what others would regard as an unusually large amount of food at least once a week for the previous month. Binge eaters differed significantly from nonbingers across a broad range of eating and weight-related characteristics assessed using a self-report version of the Eating Disorder Examination. Attitudinal differences were marked. The results provided no support for the view that obese binge eaters have a pattern of general "addictiveness" to psychoactive substances or other activities.