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Night eating syndrome : diagnosis, epidemiology and management.

Night eating syndrome (NES) is an eating disorder characterised by the clinical features of morning anorexia, evening hyperphagia, and insomnia with awakenings followed by nocturnal food ingestion. The core clinical feature appears to be a delay in the circadian timing of food intake. Energy intake is reduced in the first half of the day and greatly increased in the second half, such that sleep is disrupted in the service of food intake. The syndrome can be distinguished from bulimia nervosa and binge eating disorder by the lack of associated compensatory behaviours, the timing of food intake and the fact that the food ingestions are small, amounting to repeated snacks rather than true binges. NES also differs from sleep-related eating disorder by the presence of full awareness, as opposed to parasomnic nocturnal ingestions. NES is of importance clinically because of its association with obesity. Its prevalence rises with increasing weight, and about half of those diagnosed with it report a normal weight status before the onset of the syndrome. The recognition and effective treatment of NES may be an increasingly important way to treat a subset of the obese population. Treatment of the syndrome, however, is still in its infancy. One clinical trial has reported efficacy with the SSRI sertraline. Other treatments, such as the anticonvulsant topiramate, phototherapy and other SSRIs, may also offer future promise.

Feeding and Eating Disorders↗

Effect of fiber on cholesterol metabolism in the Coturnix quail.

This experiment involving 288 Coturnix quail was conducted to determine the effects of various fiber sources (alfalfa, wheat bran, dried brewer's grain, cellulose, and pectin) on serum, liver and egg yolk cholesterol, and egg production. The fiber sources were added at a rate to provide 6.25% fiber to a corn-soybean meal diet and fed for a 28-day experimental period. Serum, liver, and egg cholesterol levels were measured as pen composite samples at the end of the experimental period. No difference was exhibited in egg yolk cholesterol among any of the groups (P greater than .10). Liver and serum cholesterol levels were elevated in the birds fed the pectin and wheat brain diets as compared with that in birds fed the other fiber source; also, metabolizable energy intakes and eggs per hen day (EHD) were decreased for both groups. When data were adjusted for EHD by covariance analysis, the treatment differences no longer appeared (P greater than .05). These results indicate that 1) there is a basal quantity of cholesterol deposited in the egg on which fiber intake, energy consumed, or egg production have very little effect and that 2) there is an inverse relationship between serum and tissue cholesterol levels and the total quantity of cholesterol excreted via the egg.

Animal Feed↗

The changing lifestyle in the world. Body weight and what else?

Body weight and the prevalence of obesity are rising so rapidly in many countries that the World Health Organization has recognized that there is a "global epidemic of obesity." The prevalence of type 2 diabetes is rising in parallel. In view of its associated cardiovascular complications, we are facing a severe public health problem. Both obesity and type 2 diabetes have a combined genetic and environmental background, but the epidemic must be due to major changes in the environment. By definition, obesity is a result of a positive energy balance, which usually amounts to a tiny proportion of the total energy turnover. Energy intake, energy expenditure, and energy accumulation (as fat) may all be primarily disturbed. There is a great, and still insufficiently understood, variation in prevalence of obesity and in the rate of change of the prevalence. The prevailing contention is that the epidemic is due to the changes in the society--the so-called modernization--leading to overnutrition and a sedentary life. These factors are likely contributors, but it has been difficult to provide consistent evidence for their effects. In Denmark, a steep rise has taken place in the prevalence of obesity among schoolboys and young men in two phases linked to the birth cohorts of the 1940s and of the mid-1960s and later. This rise suggests that environmental influences operating early in life are involved. In conclusion, a global obesity epidemic is developing, but the causes of the epidemic are not yet clear and more research is needed to establish the grounds for prevention.

Adipose Tissue↗

Human immunodeficiency virus-associated wasting and mechanisms of cachexia associated with inflammation.

Profound weight loss and progressive depletion of muscle mass is a common sequela of chronic diseases such as cancer, tuberculosis, and human immunodeficiency virus (HIV) infection. Studies of HIV-associated wasting have revealed several possible mechanisms. Alterations in anabolic hormones, energy intake, energy expenditure, and production of proinflammatory cytokines, which cause cachexia, may contribute to wasting in HIV-infected patients. These studies have revealed the complexity of the interactions between cytokines and the hormones that typically regulate catabolic-anabolic homeostasis. Despite this complexity, HIV-associated wasting should be manageable. Several strategies are currently under investigation, including anabolic steroid and human growth hormone therapy, appetite stimulants, nutritional supplementation, and cytokine antagonists. Some of these approaches have shown early promise. Further research in these areas should facilitate development of effective intervention strategies and lead to improvements in quality of life for patients suffering from wasting syndromes.

Cachexia↗

Fat and energy balance.

In summary, an imbalance between energy intake and energy expenditure can explain approximately 80% of the variance in body weight gain in this dietary model of obesity. Several metabolic variables appear to contribute to differences in energy balance. A high RQ and an inappropriate suppression of glucose production by insulin appear to be linked to the increase in energy intake that occurs when obesity-prone rats are provided with the high-fat diet. In addition, early tissue enzymatic differences in obesity-prone versus obesity-resistant rats may contribute to differences in energy expenditure and/or to differences in nutrient partitioning. In this dietary model, susceptibility to dietary obesity involves a metabolic environment that includes a high RQ and a reduced ability of insulin to suppress glucose appearance (FIG. 9). However, this environment does not lead to obesity nor to a measurable difference in body weight gain when the susceptible rats are eating a low-fat diet. The high-fat diet is a necessary catalyst for the observed variability in body weight gain and the development of obesity. As a catalyst, the high-fat diet results in an imbalance between energy intake and energy expenditure in some, but not all, rats. This imbalance interacts with the permissive metabolic environment (tissue enzymatic profile favoring carbohydrate utilization and lipid storage) to produce obesity on the high-fat diet. Later, in the HFD feeding period, the rate of weight gain is not significantly different between OP and OR rats, although net fat accumulation remains greater in the former group. It is interesting that this later period is characterized by a reduction in the difference in both RQ and energy intake between OP and OR rats. Thus, during the later stages of HFD feeding, the discrepancy in both energy balance and nutrient balance between OP and OR rats is reduced. This dietary model of obesity is relevant to human obesity. While the prevalence of obesity is high, the majority of people are not obese. The high prevalence of obesity may be due to environmental catalysts that interact with inherent behavioral and metabolic characteristics that favor nutrient retention. Resistance to obesity can be achieved by avoiding these environmental catalysts, by having inherent characteristics that prevent nutrient retention, or both. Our work suggests that the complete understanding of obesity will require not only the identification and functional significance of the genes that determine the inherent capacity of the behavioral and metabolic systems, but also the role of environmental catalysts in determining where and how these systems operate.

Animals↗

Energy expenditure in patients with chronic renal failure.

Although nondialyzed, chronically uremic patients and patients undergoing maintenance hemodialysis often show evidence for wasting and calorie malnutrition and have low dietary energy intakes, their energy expenditure has never been systematically evaluated. It is possible that low energy intakes are an adaptive response to reduced energy needs; alternatively, energy expenditure could be normal or high and the low energy intakes would be inappropriate. Energy expenditure was therefore measured by indirect calorimetry in 12 normal individuals, 10 nondialyzed patients with chronic renal failure, and 16 patients undergoing maintenance hemodialysis. Energy expenditure was measured in the resting state, during quiet sitting, during controlled exercise on an exercise bicycle, and for four hours after ingestion of a test meal. Resting energy expenditure (kcal/min/1.73 m2) in the normal subjects, chronically uremic patients and hemodialysis patients was, respectively, 0.94 +/- 0.24 (SD), 0.91 +/- 0.20, and 0.97 +/- 0.10. There was also no difference among the three groups in energy expenditure during sitting, exercise, or the postprandial state. Within each group, energy expenditure during resting and sitting was directly correlated. During bicycling, energy expenditure was directly correlated with work performed, and the regression equation for this relationship was similar in each of the three groups. These findings suggest that for a given physical activity, energy expenditure in nondialyzed, chronically uremic patients and maintenance hemodialysis patients is not different from normal. The low energy intakes of many of these patients may be inadequate for their needs.

Adult↗

Prediction of body weight changes caused by changes in energy balance.

BACKGROUND: Experimental difficulties have so far restricted knowledge of the effects of energy imbalance on change in body weight. Direct measurement requires that the subjects are kept under dietary supervision for several months while the activity is being measured. MATERIALS AND METHODS: The effects of energy balance can be calculated using a combination of fundamental principles and directly measurable data: the law of energy conservation (increase in combustible energy equals the difference between energy intake and energy expenditure); data on energy expenditure of fat and lean tissues; and data on the composition of added/removed tissue during weight change. RESULTS AND CONCLUSIONS: We obtained an explicit differential equation describing the development of body weight over time, with energy intake and energy expenditure as control variables. Using this model it is possible to isolate and analyse the measured effects of parameters not included in the model, such as age or 'adaptivity' of the body.

Adaptation, Physiological↗

Leptin resistance and obesity.

The prevalence of obesity, and the human and economic costs of the disease, creates a need for better therapeutics and better understanding of the physiological processes that balance energy intake and energy expenditure. Leptin is the primary signal from energy stores and exerts negative feedback effects on energy intake. In common obesity, leptin loses the ability to inhibit energy intake and increase energy expenditure; this is termed leptin resistance. This review discusses the evidence in support of leptin resistance in mouse models and humans and the possible mechanisms of leptin resistance.

Adipose Tissue↗

Intestinal cell proliferation is influenced by intakes of protein and energy, aflatoxin, and whole-body radiation.

Intestinal epithelial cell proliferation in young male F344 rats was measured in response to dietary protein content (5%, 10%, and 20% casein diets), energy restriction (energy intake was 60% of ad libitum energy intakes of animals consuming the 20% casein diet), total diet restriction (dietary intake was 60% of the ad libitum intake of 20% casein diet group), aflatoxin administration, and whole body irradiation. Cellular proliferation was measured in sections of jejunum, ileum, proximal colon, and distal colon with the [3H]thymidine technique. Restricting energy or total diet intakes by 40% from ad libitum levels reduced proliferation in epithelial cells throughout the intestine. In comparison to the 5% casein diet, the 20% casein diet resulted in modestly lower cellular proliferation in all intestinal segments. Radiation induced a decrease in cellular proliferation in the jejunum and ileum; this decrease was prevented by a 20% casein diet. Pretreatment with aflatoxin B1 decreased intestinal cell proliferation throughout the intestine, and this decrease was not influenced by the protein content of the diet.

Aflatoxins↗

Energy balance, insulin-related genes and risk of colon and rectal cancer.

Energy balance, or the ability to maintain body weight by balancing energy intake with energy expenditure, appears to be important in the etiology of colon cancer. One possible mechanism whereby energy balance may be associated with colorectal cancer is through its association with insulin. In our study, we evaluate the interaction between polymorphisms in 4 genes thought to be involved in insulin-related functions and components of energy balance with risk of colorectal cancer. Data from 2 population-based case-control studies of colon and rectal cancer conducted in Utah and Northern California were used to evaluate associations between body mass index (BMI), physical activity, energy intake and sucrose-to-fiber ratio and a CA repeat polymorphism of the IGF1 gene, the A/C polymorphism at nucleotide -202 of the IGFBP3, the G972R polymorphism of the IRS1 gene and the G1057D polymorphism of the IRS2 gene. A total of 1,346 incident colon cancer cases and 1,544 population-based controls and 952 incident rectal cancer cases and 1,205 controls were available for analysis. Inconsistent associations were identified between BMI, physical activity, energy intake and insulin-related genes. The 192/192 IGF1 genotype was associated with significant reduction in colon cancer risk among those with high physical activity (odds ratio [OR] 0.57; 95% confidence interval [CI] 0.39-0.83; p interaction 0.01). Although there was no significant pattern of interaction between either BMI or energy intake and polymorphisms assessed, specific sources of energy did appear to be more related to colon cancer risk in the presence of specific IRS2 and IGF1 genotypes. A high sucrose-to-fiber ratio increased risk of colon cancer in men who had the IRS2 DD genotype and among men who did not have the 192/192 IGF1 genotype. In summary, these data support the importance of components of energy balance in risk of colorectal cancer. Obesity, physical activity and energy intake appear to alter risk of colorectal cancer; however, the risk appears to be minimally influenced by genetic variants evaluated.

Adult↗

Nutrition and aging: changes in the regulation of energy metabolism with aging.

Changes in energy regulation occur during normal aging and contribute to the common phenomenon of weight and fat losses late in life. This review synthesizes data on aging-related changes in energy intake and energy expenditure and on the regulation of energy intake and expenditure. The ability of older adults to accurately regulate energy intake is impaired, with a number of possible explanations including delayed rate of absorption of macronutrients secondary to reductions in taste and smell acuity and numerous hormonal and metabolic mediators of energy regulation that change with aging. There are also changes in patterns of dietary intake and a reduction in the variety of foods consumed in old age that are thought to further reduce energy intake. Additionally, all components of energy expenditure decrease with aging, in particular energy expenditure for physical activity and basal metabolic rate, and the ability of energy expenditure to increase or decrease to attenuate energy imbalance during overeating or undereating also decreases. Combined, these changes result in an increased susceptibility to energy imbalance (both positive and negative) in old age that is associated with deteriorations in health. Practical interventions for prevention of weight and fat fluctuations in old age are anticipated here based on emerging knowledge of the role of such factors as dietary variety, taste, and palatability in late-life energy regulation.

Aging↗

Growth, nutrient retention, and metabolic response in low birth weight infants fed varying intakes of protein and energy.

Growth, nutrient retention, and metabolic response were determined in low birth weight (LBW) infants fed daily protein and energy intakes, respectively, of 2.8 gm/kg and 119 kcal/kg (group 1), 3.8 gm/kg and 120 kcal/kg (group 2), and 3.9 gm/kg and 142 kcal/kg (group 3). The mean rates of both weight gain and nitrogen retention in group 1 were somewhat greater than intrauterine rates; plasma concentrations of transthyretin and albumin also were acceptable. Thus the lower protein intake appeared to be adequate. On the other hand, the rates of weight gain and nitrogen retention in groups 2 and 3 were greater than those in group 1, supporting the efficacy of the higher protein intake with respect to growth. However, blood urea nitrogen and plasma amino acid concentrations also were higher in groups 2 and 3; both were higher in group 2 than in group 3, reflecting the positive effect of the higher energy intake on protein utilization. This observation, combined with data from an earlier study, indicates that protein intakes in excess of 3 gm/100 kcal will not be utilized completely. Energy expenditure in group 3 was greater than in group 1 but not group 2, raising the possibility that protein intakes not utilized completely contribute to diet-induced thermogenesis. The higher energy intake in group 3 vs group 2 did not affect rate of weight gain significantly, but energy storage in group 3, and hence fat accretion, was greater than that of other groups. In all groups the ratio of protein accretion to fat accretion reflected dietary proportions of protein and energy.

Child Development↗

The effects of enterostatin intake on food intake and energy expenditure.

Enterostatin (ENT) has been found to inhibit food intake and selectively inhibit fat intake in rats. Both peripheral and central mechanisms have been proposed. It also has been suggested that ENT may increase thermogenesis. The present study investigated the effects of oral ENT administration on food intake, energy expenditure and body weight in subjects with a preference for a high-fat diet. In a double-blind, placebo-controlled, randomized and crossover design, nine female and three male healthy subjects (age 34 (sd 11) years, BMI 24.5 (sd 2.5) kg/m(2)) with a preference for a high-fat diet ingested ENT (3 x 15 mg/d) or placebo (PLA) while consuming a high-fat diet ad libitum for 4 d. Eight subjects ended each intervention with a 36 h stay in the respiration chamber, continuing the diet and treatment. Body-weight loss was significant (ENT 0.8 (se 0.3) kg, P<0.05; PLA 1.3 (se 0.3) kg, P<0.001), but not different between treatments. There was no difference between treatments in total energy intake (ENT 37.1 (se 2.6), PLA 35.9 (se 3.2) MJ), macronutrient composition, hunger, satiety and hedonic scores during the 4 d high-fat diet. Energy expenditure (24 h) (ENT 9.6 (se 0.4), PLA 9.5 (se 0.4) MJ), sleeping and resting metabolic rate, diet-induced thermogenesis, activity-induced energy expenditure and 24 h RQ (ENT 0.77 (se 0.01), PLA 0.77 (se 0.01)) were similar for both treatments. We conclude that oral ENT administration did not affect food intake, energy expenditure or body weight in subjects with a preference for a high-fat diet experiencing a negative energy and fat balance.

Adult↗

Skipping of meals has a significant impact on dietary intake and nutritional status of old (65+ y) nursing home residents.

BACKGROUND: In spite of a high prevalence of undernutrition among old nursing home residents, studies have generally reported a mean intake of energy sufficient to cover the mean estimated energy requirement. This discrepancy could be due to skipping of meals and hence periods of insufficient energy intake too intermittent to be identified, when mean results are presented. OBJECTIVE: To examine the significance of skipping of (part of) meals on dietary intake and nutritional status of old (65+y) nursing home residents. DESIGN: Participants were 132 nursing home residents (84 (82-85) y). They were characterised according to activity of daily living-functions (ADL-functions), cognitive performance, intake of energy and protein (4-days dietary record), skipping of meals, energy and protein balance, and nutritional status (body mass index (BMI)). RESULTS: The participants had an energy intake, which was significantly higher than the estimated energy requirement (p <0.001). However, 41 (31%) had nothing to eat or only had desert at one or more meals during the 4-day registration period. Participants who were skipping meals had a lower BMI, energy and protein intake (all p <0.001) and a higher prevalence of negative protein balance (p <0.01), than the other residents. CONCLUSION: More focus should be given to individualized nutritional assessment in order to discover the cause to this problem and target individuals who could be helped by nutritional intervention.

Activities of Daily Living↗

Dietary intake, physical activity and energy expenditure of Malaysian adolescents.

INTRODUCTION: Paediatric obesity is a public health concern worldwide as it can track into adulthood and increase the risk of adult morbidity and mortality. While the aetiology of obesity is multi-factorial, the roles of diet and physical activity are controversial. Thus, the purpose of this study was to report on the differences in energy intake, diet composition, time spent doing physical activity and energy expenditure among underweight (UW), normal weight (NW) and at-risk of overweight (OW) Malaysian adolescents (317 females and 301 males) aged 11-15 years. METHODS: This was a cross-sectional study with 6,555 adolescents measured for weights and heights for body mass index (BMI) categorisation. A total of 618 subjects were randomly selected from each BMI category according to gender. The subjects' dietary intake and physical activity were assessed using self-reported three-day food and activity records, respectively. Dietary intake components included total energy and macronutrient intakes. Energy expenditure was calculated as a sum of energy expended for basal metabolic rate and physical activity. Time spent (in minutes) in low, medium and high intensity activities was also calculated. RESULTS: The OW adolescents had the highest crude energy intake and energy expenditure. However, after adjusting for body weight, the OW subjects had the lowest energy intake and energy expenditure (p-value is less than 0.001). The study groups did not differ significantly in time spent for low, medium and high intensity activities. Macronutrient intakes differed significantly only among the girls where the OW group had the highest intakes compared to UW and NW groups (p-value is less than 0.05). All study groups had greater than 30 percent and less than 55 percent of energy intake from fat and carbohydrate, respectively. CONCLUSION: The data suggested that a combination of low energy expenditure adjusted for body weight and high dietary fat intake may be associated with overweight and obesity among adolescents. To prevent overweight and obesity among children and adolescents, strategies that address eating behaviours and physical activity are required. Various segments of the society must be involved in efforts to promote healthful dietary intakes and active lifestyle in children and adolescents.

Adolescent↗

Practical aspects of achieving positive energy balance in low birth weight infants.

For the low birth weight (LBW) infant, energy balance during the first several days of life usually is equated to absorption of sufficient energy to match energy expenditure. Most studies show that energy expenditure of nongrowing LBW infants is 45 to 55 kcal/kg/day. Hence, for energy equilibrium, energy intake minus energy losses (i.e., metabolizable energy intake) must be at least 50 kcal/kg/day. Intakes above this amount result in energy storage or positive energy balance, whereas lesser intakes necessitate mobilization of endogenous energy stores (negative energy balance). Some of the problems of achieving positive energy balance in LBW infants (e.g., feeding intolerance and fear of necrotizing enterocolitis) can be circumvented by use of parenterally delivered nutrients. On balance, virtually all LBW infants will tolerate parenteral amino acid, glucose, and lipid intakes, respectively, of 2, 5, and 1 gm/kg/day or an energy intake of about 40 kcal/kg/day. It usually is possible to increase energy intake of most infants by an additional 10 kcal/kg/day. Whether this is achieved with enterally delivered nutrients or additional parenteral glucose or lipid intake, including the necessary modifications to enhance tolerance (e.g., insulin, 20% vs 10% lipid emulsions, and lipid emulsions containing medium-chain fatty acids), must be decided for each infant based on his or her underlying condition, likelihood of tolerating either substrate, and the impact of intolerance on the underlying condition. The consequences of not providing an essential nutrient during the immediate postnatal period also must be considered. The fact that essential fatty acid deficiency develops more rapidly in infants receiving isocaloric (60 kcal/kg/day) parenteral intakes with versus without amino acids, the likelihood that brain growth continues despite negative energy balance, and the possibility that LBW infants may not be able to desaturate/elongate linoleic and linolenic acids to the more unsaturated, longer-chain fatty acids that are deposited in the developing brain suggest that these infants may require exogenous intakes of specific fatty acids.

Energy Intake↗

Conjugated linoleic acid persistently increases total energy expenditure in AKR/J mice without increasing uncoupling protein gene expression.

AKR/J mice fed a high fat diet were treated with a 1% (1 g/100 g) admixture of conjugated linoleic acids (CLA) for 5 wk and compared with control mice. Body weights, energy intakes and energy expenditure (EE) determined by indirect calorimetry were measured weekly. CLA treatment reduced adipose depot weights by approximately 50% but had no significant effects on either body weight or energy intake. CLA increased EE persistently by an average of 7.7% throughout the 5-wk experiment. This greater EE, despite no difference in energy intake, was sufficient to account for the lower body fat stores in the CLA-treated mice. De novo fatty acid biosynthesis in adipose tissue, measured by incorporation of deuterium-labeled water, was not decreased by CLA treatment and therefore did not explain the lower adipose lipid in these mice. Expression of uncoupling protein (UCP) in skeletal muscle, white adipose tissue and kidney was not affected by CLA treatment. In brown adipose tissue, UCP1 expression was not affected by CLA treatment. However, UCP2 expression, although quite low, was significantly greater in CLA-fed mice. We conclude that CLA acts to reduce body fat stores by chronically increasing metabolic rate. This effect on metabolic rate is likely not due to increased UCP gene expression. Furthermore, the reduced body fat is not due to decreased de novo fatty acid synthesis in white adipose tissue.

Adipose Tissue↗

Energy, nutrient intake and prostate cancer risk: a population-based case-control study in Sweden.

The role of diet in the etiology of prostate cancer remains unclear, because results from several case-control and cohort studies on fat intake and risk of prostate cancer have been inconsistent; few of the studies have adjusted the results for caloric intake. To examine the relationship between energy, intake of several nutrients and risk of prostate cancer (all stages combined and advanced stages separately), we conducted a population-based case-control study in Orebro County, Sweden, from 1989 through 1994. A total of 526 patients with newly diagnosed prostate cancer and 536 controls, randomly selected from the population register and frequency-matched by age, were included in the analyses. Information about dietary intake was obtained from a self-administered semi-quantitative food frequency questionnaire. Odds ratios with 95% confidence intervals were estimated by unconditional logistic regression. In age-adjusted analyses, there were positive associations of prostate cancer (all stages combined) risk with total energy intake as well as intake of total fat (saturated and monounsaturated), protein, retinol and zinc. The positive association with energy intake was stronger for advanced cancer, with an excess risk of 70% for the highest quartile vs. the lowest. After adjustment for energy intake, there was no apparent association of prostate cancers (all stages combined) with any of the investigated nutrients. However, a weak positive association between intake of retinol and advanced cancer was observed. We conclude that our results provide some evidence that total energy intake is a risk factor for prostate cancer.

Adult↗