Showing papers in "International Journal of Obesity in 2010"

Diagnostic performance of body mass index to identify obesity as defined by body adiposity: a systematic review and meta-analysis.

Abstract: We performed a systematic review and meta-analysis of studies that assessed the performance of body mass index (BMI) to detect body adiposity. Data sources were MEDLINE, EMBASE, Cochrane, Database of Systematic Reviews, Cochrane CENTRAL, Web of Science, and SCOPUS. To be included, studies must have assessed the performance of BMI to measure body adiposity, provided standard values of diagnostic performance, and used a body composition technique as the reference standard for body fat percent (BF%) measurement. We obtained pooled summary statistics for sensitivity, specificity, positive and negative likelihood ratios (LRs), and diagnostic odds ratio (DOR). The inconsistency statistic (I2) assessed potential heterogeneity. The search strategy yielded 3341 potentially relevant abstracts, and 25 articles met our predefined inclusion criteria. These studies evaluated 32 different samples totaling 31 968 patients. Commonly used BMI cutoffs to diagnose obesity showed a pooled sensitivity to detect high adiposity of 0.50 (95% confidence interval (CI): 0.43–0.57) and a pooled specificity of 0.90 (CI: 0.86–0.94). Positive LR was 5.88 (CI: 4.24–8.15), I2=97.8%; the negative LR was 0.43 (CI: 0.37–0.50), I2=98.5%; and the DOR was 17.91 (CI: 12.56–25.53), I2=91.7%. Analysis of studies that used BMI cutoffs ⩾30 had a pooled sensitivity of 0.42 (CI: 0.31–0.43) and a pooled specificity of 0.97 (CI: 0.96–0.97). Cutoff values and regional origin of the studies can only partially explain the heterogeneity seen in pooled DOR estimates. Commonly used BMI cutoff values to diagnose obesity have high specificity, but low sensitivity to identify adiposity, as they fail to identify half of the people with excess BF%.

Gluteofemoral body fat as a determinant of metabolic health

Abstract: Body fat distribution is an important metabolic and cardiovascular risk factor, because the proportion of abdominal to gluteofemoral body fat correlates with obesity-associated diseases and mortality. Here, we review the evidence and possible mechanisms that support a specific protective role of gluteofemoral body fat. Population studies show that an increased gluteofemoral fat mass is independently associated with a protective lipid and glucose profile, as well as a decrease in cardiovascular and metabolic risk. Studies of adipose tissue physiology in vitro and in vivo confirm distinct properties of the gluteofemoral fat depot with regards to lipolysis and fatty acid uptake: in day-to-day metabolism it appears to be more passive than the abdominal depot and it exerts its protective properties by long-term fatty acid storage. Further, a beneficial adipokine profile is associated with gluteofemoral fat. Leptin and adiponectin levels are positively associated with gluteofemoral fat while the level of inflammatory cytokines is negatively associated. Finally, loss of gluteofemoral fat, as observed in Cushing's syndrome and lipodystrophy is associated with an increased metabolic and cardiovascular risk. This underlines gluteofemoral fat's role as a determinant of health by the long-term entrapment of excess fatty acids, thus protecting from the adverse effects associated with ectopic fat deposition.

The association between obesity and anxiety disorders in the population: a systematic review and meta-analysis.

Abstract: Anxiety disorders are the most prevalent mental disorders in developed countries. Obesity is hypothesized to be a risk factor for anxiety disorders but evidence supporting an association between these two conditions is not clear. The objectives of this paper were to systematically review the literature for a link between obesity and anxiety disorders in the general population, and to present a pooled estimate of association. We performed a systematic search for epidemiological articles reporting on obesity (explanatory variable) and anxiety disorders (outcome variable) in seven bibliographical databases. Two independent reviewers abstracted the data and assessed study quality. We found 16 studies (2 prospective and 14 cross-sectional) that met the selection criteria. Measures of effect from prospective data were mixed but cross-sectional evidence suggested a positive association between obesity and anxiety. The pooled odds ratio from cross-sectional studies was 1.4 (confidence interval: 1.2-1.6). Subgroup analyses revealed a positive association in men and women. Overall, a moderate level of evidence exists for a positive association between obesity and anxiety disorders. Questions remain regarding the role of obesity severity and subtypes of anxiety disorders. The causal relationship from obesity to anxiety disorders could not be inferred from current data; future etiologic studies are recommended.

The genetic and environmental influences on childhood obesity: a systematic review of twin and adoption studies

Abstract: In this systematic review, we aimed to collect together all previous twin and adoption studies on childhood and adolescent obesity up to the age of 18 years. Using several sources, we identified nine twin and five adoption studies; all of these studies had used relative weight as an indicator of obesity. Except the two twin studies from the Korean population, all studies represented Caucasian populations. In a meta-analysis of these twin studies, we found that genetic factors had a strong effect on the variation of body mass index (BMI) at all ages. The common environmental factors showed a substantial effect in mid-childhood, but this effect disappeared at adolescence. Adoption studies supported the role of family environment in childhood obesity as correlations were found between adoptees and adoptive parents; however, correlations were substantially stronger between parents and their biological offspring, further supporting the importance of genetic factors. In the future, more studies implementing genetic and environmental measures into twin models are needed as they allow estimation of the proportion of total genetic variation explained by candidate genes and analyses of gene-environment interactions. More studies of genetic architecture in non-Caucasian populations, of gene-environment interactions, and of body composition and body fat distribution are needed.

Sympathetic and sensory innervation of brown adipose tissue

Abstract: The innervation of brown adipose tissue (BAT) by the sympathetic nervous system (SNS) is incontrovertible and, with its activation, functions as the principal, if not exclusive, stimulator of BAT thermogenesis. The parasympathetic innervation of BAT only appears in two minor BAT depots, but not in the major interscapular BAT (IBAT) depot. BAT thermogenesis is triggered by the release of norepinephrine from its sympathetic nerve terminals, stimulating β3-adrenoceptors that turns on a cascade of intracellular events ending in activation of uncoupling protein-1 (UCP-1). BAT also has sensory innervation that may function to monitor BAT lipolysis, a response necessary for activation of UCP-1 by fatty acids, or perhaps responding in a feedback manner to BAT temperature changes. The central sympathetic outflow circuits ultimately terminating in BAT have been revealed by injecting the retrograde viral transneuronal tract tracer, pseudorabies virus, into the tissue; moreover, there is a high degree of colocalization of melanocortin 4-receptor mRNA on these neurons across the neural axis. The necessary and sufficient central BAT SNS outflow sites that are activated by various thermogenic stimuli are not precisely known. In a chronic decerebration procedure, IBAT UCP-1 gene expression can be triggered by fourth ventricular injections of melanotan II, the melanocortin 3/4 receptor agonist, suggesting that there is sufficient hindbrain neural circuitry to generate thermogenic responses with this stimulation. The recent recognition of BAT in normal adult humans suggests a potential target for stimulation of energy expenditure by BAT to help mitigate increased body fat storage.

Childhood obesity and overweight prevalence trends in England: evidence for growing socioeconomic disparities.

Abstract: Objective: Previous data indicate a rapidly increasing prevalence of obesity and overweight among English children and an emerging socioeconomic gradient in prevalence. The main aim of this study was to update the prevalence trends among school-age children and assess the changing socioeconomic gradient.

A nationally representative study of maternal obesity in England, UK: trends in incidence and demographic inequalities in 619 323 births, 1989–2007

Abstract: A nationally representative study of maternal obesity in England, UK: trends in incidence and demographic inequalities in 619 323 births, 1989–2007

Parental influence on children's early eating environments and obesity risk: implications for prevention.

Abstract: Most childhood obesity prevention efforts have focused on school-age children and adolescents and have had limited success. We argue that the first years of life, including the prenatal period, the postnatal suckling period and the transition to the modified adult diet, may provide opportunities for preventive interventions. These early periods are characterized by high plasticity and rapid transitions, and parents have a high degree of control over children's environments and experiences. Observational and experimental evidence reveal persistent effects of early environments on eating behavior and obesity risk, suggesting that interventions should be tested during these early periods. The central task parents have in early development points to their potential as key targets and agents of change in early preventive interventions. In this paper, we review evidence of early environmental effects on children's eating and obesity risk, highlighting ways that parental feeding practices and parents' own behaviors impact these outcomes and calling for further experimental research to elucidate whether these factors are indeed promising targets for childhood obesity preventive interventions.

Long-term weight loss maintenance in the United States

Abstract: Although the rise in overweight and obesity in the United States is well documented, long-term weight loss maintenance (LTWLM) has been minimally explored. The aim of this study is to estimate the prevalence and correlates of LTWLM among US adults. We examined weight data from 14 306 participants (age 20–84 years) in the 1999–2006 National Health and Nutrition Examination Survey (NHANES). We defined LTWLM as weight loss maintained for at least 1 year. We excluded individuals who were not overweight or obese at their maximum weight. Among US adults who had ever been overweight or obese, 36.6, 17.3, 8.5 and 4.4% reported LTWLM of at least 5, 10, 15 and 20%, respectively. Among the 17.3% of individuals who reported an LTWLM of at least 10%, the average and median weight loss maintained was 19.1 kg (42.1 pounds) and 15.5 kg (34.1 pounds), respectively. LTWLM of at least 10% was higher among adults of ages 75–84 years (vs ages 20–34, adjusted odds ratio (OR): 1.5; 95% confidence interval (CI): 1.2, 1.8), among those who were non-Hispanic white (vs Hispanic, adjusted OR: 1.6; 95% CI: 1.3, 2.0) and among those who were female (vs male, adjusted OR: 1.2; 95% CI: 1.1, 1.3). More than one out of every six US adults who has ever been overweight or obese has accomplished LTWLM of at least 10%. This rate is significantly higher than those reported in clinical trials and many other observational studies, suggesting that US adults may be more successful at sustaining weight loss than previously thought.

Excessive fructose intake induces the features of metabolic syndrome in healthy adult men: role of uric acid in the hypertensive response

Abstract: Excessive fructose intake causes metabolic syndrome in animals and can be partially prevented by lowering the uric acid level. We tested the hypothesis that fructose might induce features of metabolic syndrome in adult men and whether this is protected by allopurinol. A randomized, controlled trial of 74 adult men who were administered 200 g fructose daily for 2 weeks with or without allopurinol. Primary measures included changes in ambulatory blood pressure (BP), fasting lipids, glucose and insulin, homeostatic model assessment (HOMA) index, body mass index and criteria for metabolic syndrome. The ingestion of fructose resulted in an increase in ambulatory BP (7±2 and 5±2 mm Hg for systolic (SBP) and diastolic BP (DBP), P<0.004 and P<0.007, respectively). Mean fasting triglycerides increased by 0.62±0.23 mmol l−1 (55±20 mg per 100 ml), whereas high-density lipoprotein cholesterol decreased by 0.06±0.02 mmol l−1 (2.5±0.7 mg per 100 ml), P<0.002 and P<0.001, respectively. Fasting insulin and HOMA indices increased significantly, whereas plasma glucose level did not change. All liver function tests showed an increase in values. The metabolic syndrome increased by 25–33% depending on the criteria. Allopurinol lowered the serum uric acid level (P<0.0001) and prevented the increase in 24-h ambulatory DBP and daytime SBP and DBP. Allopurinol treatment did not reduce HOMA or fasting plasma triglyceride levels, but lowered low-density lipoprotein cholesterol relative to control (P<0.02) and also prevented the increase in newly diagnosed metabolic syndrome (0–2%, P=0.009). High doses of fructose raise the BP and cause the features of metabolic syndrome. Lowering the uric acid level prevents the increase in mean arterial blood pressure. Excessive intake of fructose may have a role in the current epidemics of obesity and diabetes.

Trends in the prevalence of childhood overweight and obesity in Australia between 1985 and 2008

Abstract: Popular media, health experts and researchers talk about a paediatric ‘obesity epidemic’ with exponentially increasing rates of obesity and overweight. However, some recent reports suggest that prevalence may have plateaued. This study examined trends in the prevalence of Australian childhood overweight and obesity since 1985. Specifically, it aimed to determine whether there have been (a) overall increases in average body mass index (BMI), (b) differential patterns of change within age groups and (c) increases in BMI within each weight-status category. Forty-one Australian studies of childhood weight status conducted between 1985 and 2008 were reviewed. The studies included data on 264 905 Australians aged 2–18 years, with raw data being available on 70 758 children (27%). Children were classified as overweight or obese based on BMI using the criteria of Cole et al. (BMJ, 2000). The prevalence estimates were adjusted for age and sex, and plotted against measurement year using Lowess plots and two-linear-segment models. Where raw data were available, BMI z-scores (UK 1990 standard) were plotted against measurement year for all children and children in various age groups. Lowess plots and two-linear-segment models were used to assess secular trends in BMI z-scores pre- and post-1996 within age, gender and weight-status categories. There has been a plateau, or only slight increase, in the percentage of boys and girls classified as overweight or obese, with almost no change over the last 10 years. In boys and girls, prevalence rates have settled around 21–25% for overweight and obesity together, and 5–6% for obesity alone. Similar trends were found for BMI z-scores. These patterns were fairly consistent across the age span. Within each weight-status category, average BMI has not increased. Although levels of Australian paediatric overweight remain high, the prevalence of overweight and obesity seems to have flattened and has not followed the anticipated exponential trajectory.

Psychological correlates of childhood obesity

Abstract: To enhance the prevention and intervention efforts of childhood obesity, there is a strong need for the early detection of psychological factors contributing to its development and maintenance. Rather than a stable condition, childhood obesity represents a dynamic process, in which behavior, cognition and emotional regulation interact mutually with each other. Family structure and context, that is, parental and familial attitudes, activity, nutritional patterns as well as familial stress, have an important role with respect to the onset and maintenance of overweight and obesity. Behavioral and emotional problems are found in many, though not all, obese children, with a higher prevalence in clinical, treatment-seeking samples. The interrelatedness between obesity and psychological problems seems to be twofold, in that clinically meaningful psychological distress might foster weight gain and obesity may lead to psychosocial problems. The most frequently implicated psychosocial factors are externalizing (impulsivity and attention-deficit hyperactivity disorder) and internalizing (depression and anxiety) behavioral problems and uncontrolled eating behavior. These findings strengthen the need to further explore the interrelatedness between psychological problems and childhood obesity.

The impact of perinatal probiotic intervention on the development of overweight and obesity: follow-up study from birth to 10 years.

Abstract: The achievements in combating the increasing trend of overweight and obesity have thus far been inadequate. The recently discovered instrumental role of the gut microbiota in host metabolism may offer a novel target in the prevention and management of obesity. To evaluate the impact of perinatal probiotic intervention on childhood growth patterns and the development of overweight during a 10-year follow-up. Altogether 159 women were randomized and double-blinded to receive probiotics (1 × 1010 colony-forming units of Lactobacillus rhamnosus GG, ATCC 53103) or placebo 4 weeks before expected delivery; the intervention extending for 6 months postnatally. Anthropometric measurements of the children were taken at the ages of 3, 6, 12 and 24 months and at 4, 7 and 10 years in 113 (72%) children. The excessive weight gain was detected to be two-parted; the initial phase of excessive weight gain initiating during fetal period and continuing until 24–48 months of age and a second phase of excessive weight gain starting after the age of 24–48 months. The perinatal probiotic intervention appeared to moderate the initial phase of excessive weight gain, especially among children who later became overweight, but not the second phase of excessive weight gain, the impact being most pronounced at the age of 4 years (P=0.063, analysis of variance for repeated measures). The effect of intervention was also shown as a tendency to reduce the birth-weight-adjusted mean body mass index at the age of 4 years (P=0.080, analysis of covariance). Early gut microbiota modulation with probiotics may modify the growth pattern of the child by restraining excessive weight gain during the first years of life. This novel observation calls for further epidemiological and clinical trials, with precise data on early growth patterns and on confounding factors influencing weight development.

Gestational weight gain in relation to offspring body mass index and obesity from infancy through adulthood

Abstract: Gestational weight gain (GWG) is associated with childhood obesity. We analyzed whether this effect persists into adulthood and is mediated by effects in childhood. The design of the study a prospective birth cohort study established in 1959–1961. The subjects were offspring (n=4234 of whom 2485 had information from the last follow-up) of mothers included in ‘The Copenhagen Perinatal Cohort’ during pregnancy or at birth. Information on maternal pre-pregnancy body mass index (BMI), GWG and several potential confounders were collected around delivery. Information on offspring BMI was available from various follow-up examinations from 1 to 42 years of age. The association of GWG with offspring BMI was analyzed by regression models including confounders. Using path analysis, the association of GWG with adult BMI was disentangled into an association mediated through childhood BMI and one independent hereof. GWG was associated with offspring BMI at all ages. At the age of 42 years (n=1540), there was an increasing risk of obesity (odds ratio (OR) 1.08, 95% confidence interval (CI) 1.03–1.14 per kg GWG, P=0.003). Only half of the association of GWG on offspring adult BMI was mediated through birth weight and BMI up to 14 years of age. Greater GWG is associated with an increased BMI in childhood through adulthood and with an increased risk of obesity in adults. Only part of the association with adult BMI is mediated by childhood BMI, suggesting that excessive GWG induces a persisting susceptibility to obesogenic environments. As GWG is greater in women with small pre-pregnancy body weight, this implies a reinforcement of the obesity epidemic in the next generation. Our findings provide support for avoiding excessive GWG.

Adaptive thermogenesis in humans

Abstract: The increasing prevalence of obesity and its comorbidities reflects the interaction of genes that favor the storage of excess energy as fat with an environment that provides ad libitum availability of energy-dense foods and encourages an increasingly sedentary lifestyle. Although weight reduction is difficult in and of itself, anyone who has ever lost weight will confirm that it is much harder to keep the weight off once it has been lost. The over 80% recidivism rate to preweight loss levels of body fatness after otherwise successful weight loss is due to the coordinate actions of metabolic, behavioral, neuroendocrine and autonomic responses designed to maintain body energy stores (fat) at a central nervous system-defined 'ideal'. This 'adaptive thermogenesis' creates the ideal situation for weight regain and is operant in both lean and obese individuals attempting to sustain reduced body weights. Much of this opposition to sustained weight loss is mediated by the adipocyte-derived hormone 'leptin'. The multiple systems regulating energy stores and opposing the maintenance of a reduced body weight illustrate that body energy stores in general and obesity in particular are actively 'defended' by interlocking bioenergetic and neurobiological physiologies. Important inferences can be drawn for therapeutic strategies by recognizing obesity as a disease in which the human body actively opposes the 'cure' over long periods of time beyond the initial resolution of symptomatology.

Acute effects of gastric bypass versus gastric restrictive surgery on β-cell function and insulinotropic hormones in severely obese patients with type 2 diabetes

Abstract: Acute effects of gastric bypass versus gastric restrictive surgery on β-cell function and insulinotropic hormones in severely obese patients with type 2 diabetes

Toddler self-regulation skills predict risk for pediatric obesity

Abstract: To investigate the role of early self-regulation skills, including emotion regulation, sustained attention and inhibitory control/reward sensitivity, in predicting pediatric obesity in early childhood. Participants for this study included 57 children (25 girls) obtained from three different cohorts participating in a larger ongoing longitudinal study. At 2 years of age, participants participated in several laboratory tasks designed to assess their self-regulation skills. Height and weight measures were collected when children were 2 and 5.5 years of age. Self-regulation skills in toddlerhood were predictive of both normal variations in body mass index (BMI) development and pediatric obesity. Specifically, emotion regulation was the primary self-regulation skill involved in predicting normative changes in BMI as no effects were found for sustained attention or inhibitory control/reward sensitivity. However, both emotion regulation and inhibitory control/reward sensitivity predicted more extreme weight problems (that is, pediatric obesity), even after controlling for 2-year BMI. Thus, toddlers with poor emotion regulation skills and lower inhibitory control skills/higher reward sensitivity were more likely to be classified as overweight/at risk at 5.5 years of age. Early self-regulation difficulties across domains (that is, behavioral and emotional) represent significant individual risk factors for the development of pediatric obesity. Mechanisms by which early self-regulation skills may contribute to the development of pediatric obesity are discussed.

Obese children show hyperactivation to food pictures in brain networks linked to motivation, reward and cognitive control

Abstract: To investigate the neural mechanisms of food motivation in children and adolescents, and examine brain activation differences between healthy weight (HW) and obese participants. Ten HW children (ages 11–16; BMI 95%ile) matched for age, gender and years of education. Functional magnetic resonance imaging (fMRI) scans were conducted twice: when participants were hungry (pre-meal) and immediately after a standardized meal (post-meal). During the fMRI scans, the participants passively viewed blocked images of food, non-food (animals) and blurred baseline control. Both groups of children showed brain activation to food images in the limbic and paralimbic regions (PFC/OFC). The obese group showed significantly greater activation to food pictures in the PFC (pre-meal) and OFC (post-meal) than the HW group. In addition, the obese group showed less post-meal reduction of activation (vs pre-meal) in the PFC, limbic and the reward-processing regions, including the nucleus accumbens. Limbic and paralimbic activation in high food motivation states was noted in both groups of participants. However, obese children were hyper-responsive to food stimuli as compared with HW children. In addition, unlike HW children, brain activations in response to food stimuli in obese children failed to diminish significantly after eating. This study provides initial evidence that obesity, even among children, is associated with abnormalities in neural networks involved in food motivation, and that the origins of neural circuitry dysfunction associated with obesity may begin early in life.

The chronobiology, etiology and pathophysiology of obesity

Abstract: The effect of CD on human health is an emerging issue. Many records link CD with diseases such as cancer, cardiovascular, cognitive impairment and obesity, all of them conducive to premature aging. The amount of sleep has declined by 1.5 h over the past century, accompanied by an important increase in obesity. Shift work, sleep deprivation and exposure to bright light at night increase the prevalence of adiposity. Animal models have shown that mice with Clock gene disruption are prone to developing obesity and MetS. This review summarizes the latest developments with regard to chronobiology and obesity, considering (1) how molecular clocks coordinate metabolism and the specific role of the adipocyte; (2) CD and its causes and pathological consequences; (3) the epidemiological evidence of obesity as a chronobiological illness; and (4) theories of circadian disruption and obesity. Energy intake and expenditure, relevance of sleep, fat intake from a circadian perspective and psychological and genetic aspects of obesity are examined. Finally, ideas about the use of chronobiology in the treatment of obesity are discussed. Such knowledge has the potential to become a valuable tool in the understanding of the relationship between the chronobiology, etiology and pathophysiology of obesity.

Body composition phenotypes in pathways to obesity and the metabolic syndrome.

Abstract: Dynamic changes in body weight have long been recognized as important indicators of risk for debilitating diseases. While weight loss or impaired growth can lead to muscle wastage, as well as to susceptibility to infections and organ dysfunctions, the development of excess fat predisposes to type 2 diabetes and cardiovascular diseases, with insulin resistance as a central feature of the disease entities of the metabolic syndrome. Although widely used as the phenotypic expression of adiposity in population and gene-search studies, body mass index (BMI), that is, weight/height(2) (H(2)), which was developed as an operational definition for classifying both obesity and malnutrition, has considerable limitations in delineating fat mass (FM) from fat-free mass (FFM), in particular at the individual level. After an examination of these limitations within the constraints of the BMI-FM% relationship, this paper reviews recent advances in concepts about health risks related to body composition phenotypes, which center upon (i) the partitioning of BMI into an FM index (FM/H(2)) and an FFM index (FFM/H(2)), (ii) the partitioning of FFM into organ mass and skeletal muscle mass, (iii) the anatomical partitioning of FM into hazardous fat and protective fat and (iv) the interplay between adipose tissue expandability and ectopic fat deposition within or around organs/tissues that constitute the lean body mass. These concepts about body composition phenotypes and health risks are reviewed in the light of race/ethnic variability in metabolic susceptibility to obesity and the metabolic syndrome.

Childhood obesity and adult cardiovascular disease risk: a systematic review.

Abstract: Although the relationship between adult obesity and cardiovascular disease (CVD) has been shown, the relationship with childhood obesity remains unclear. Given the evidence of tracking of body mass index (BMI) from childhood to adulthood, this systematic review investigated the independent relationship between childhood BMI and adult CVD risk. To investigate the association between childhood BMI and adult CVD risk, and whether the associations observed are independent of adult BMI. Electronic databases were searched from inception until July 2008 for studies investigating the association between childhood BMI and adult CVD risk. Two investigators independently reviewed studies for eligibility according to inclusion/exclusion criteria, extracted the data and assessed study quality using the Newcastle–Ottawa Scale. Positive associations between childhood BMI and adult blood pressure or carotid intima-media thickness were generally attenuated once adjusted for adult BMI. Associations between childhood BMI and CVD morbidity/mortality had not been adjusted and do not provide evidence of an independent relationship. Negative associations between childhood BMI and blood pressure were observed in several adjusted data sets. Little evidence was found to suggest that childhood obesity is an independent risk factor for CVD risk. Instead, the data suggest that relationships observed are dependent on the tracking of BMI from childhood to adulthood. Importantly, evidence suggests that risk of raised blood pressure is highest in those who are at the lower end of the BMI scale in childhood and overweight in adulthood. The findings challenge the widely accepted view that the presence of childhood obesity is an independent risk factor for CVD and that this period should be a priority for public health intervention. Although interventions during childhood may be important in prevention of adult obesity, it is important to avoid the potential for negative consequences when the timing coincides with critical stages of neurological, behavioural and physical development.

Measuring dietary intake in children and adolescents in the context of overweight and obesity

Abstract: Dietary intake throughout childhood is a key determinant of growth and development and has an important role in both the prevention and treatment of childhood overweight and obesity. Although dietary intake assessment is fraught with challenges and limitations, reporting intake remains an important research outcome if dietary recommendations to promote healthy weight are to be refined. The aims of this paper are to review current dietary intake assessment methodologies for children, to identify their biases and provide guidance on how these can be addressed to improve reporting of dietary intakes of overweight children in the literature and to identify future research priorities. Knowledge of the methodological aspects of studies examining dietary intake a priori in the context of obesity will assist researchers in improving the quality of dietary data collected and reported and facilitate publication of both dietary intake and nutrition outcomes in the context of body weight. This will help to develop a strong evidence base against which to evaluate the effectiveness of nutrition interventions for both the prevention and treatment of pediatric obesity.

Gut microbiome-derived metabolites characterize a peculiar obese urinary metabotype

Abstract: Obesity is a complex multifactorial disease involving genetic and environmental factors and influencing several different metabolic pathways. In this regard, metabonomics, that is the study of complex metabolite profiles in biological samples, may provide a systems approach to understand the global metabolic regulation of the organism in relation to this peculiar pathology. In this pilot study, we have applied a nuclear magnetic resonance (NMR)-based metabolomic approach on urinary samples of morbidly obese subjects. Urine samples of 15 morbidly obese insulin-resistant (body mass index>40; homeostasis assessment model of insulin resistance>3) male patients and 10 age-matched controls were collected, frozen and analyzed by high-resolution (1)H-NMR spectroscopy combined with partial least squares-discriminant analysis. Furthermore, two obese patients who underwent bariatric surgery (biliopancreatic diversion and gastric bypass, respectively) were monitored during the first 3 months after surgery and their urinary metabolic profiles were characterized. NMR-based metabolomic analysis allowed us to identify an obesity-associated metabolic phenotype (metabotype) that differs from that of lean controls. Gut flora-derived metabolites such as hippuric acid, trigonelline, 2-hydroxyisobutyrate and xanthine contributed most to the classification model and were responsible for the discrimination. These preliminary results confirmed that in humans the gut microflora metabolism is strongly linked to the obesity phenotype. Moreover, the typical obese metabotype is lost after weight loss induced by bariatric surgery.

Getting heavier, younger: trajectories of obesity over the life course

Abstract: Although recent trends in obesity have been well documented, generational patterns of obesity from early childhood through adulthood across birth cohorts, which account for the recent epidemic of childhood obesity, have not been well described Such trends may have implications for the prevalence of obesity-associated conditions among population subgroups, including type 2 diabetes Our objective was to evaluate trajectories of obesity over the life course for the US population, overall and by gender and race We conducted an age, period and birth cohort analysis of obesity for US individuals who participated in the National Health and Nutrition Examination Surveys (NHANES) (1971–2006) Obesity was defined as a body mass index ⩾95th percentile for individuals aged 2–16 years or ⩾30 kg m–2 among individuals older than 16 years Age was represented by the age of the individual at each NHANES, period was defined by the year midpoint of each survey, and cohort was calculated by subtracting age from period Recent birth cohorts are becoming obese in greater proportions for a given age, and are experiencing a greater duration of obesity over their lifetime For example, although the 1966–1975 and 1976–1985 birth cohorts had reached an estimated obesity prevalence of at least 20% by 20–29 years of age, this level was only reached by 30–39 years for the 1946–1955 and 1956–1965 birth cohorts, by 40–49 years for the 1936–1945 birth cohort and by 50–59 years of age for the 1926–1935 birth cohort Trends are particularly pronounced for female compared with male, and black compared with white cohorts The increasing cumulative exposure to excess weight over the lifetime of recent birth cohorts will likely have profound implications for future rates of type 2 diabetes, and mortality within the US population

A microarray analysis of sexual dimorphism of adipose tissues in high-fat-diet-induced obese mice.

Abstract: A sexual dimorphism exists in body fat distribution; females deposit relatively more fat in subcutaneous/inguinal depots whereas males deposit more fat in the intra-abdominal/gonadal depot. Our objective was to systematically document depot- and sex-related differences in the accumulation of adipose tissue and gene expression, comparing differentially expressed genes in diet-induced obese mice with mice maintained on a chow diet. We used a microarray approach to determine whether there are sexual dimorphisms in gene expression in age-matched male, female or ovariectomized female (OVX) C57/BL6 mice maintained on a high-fat (HF) diet. We then compared expression of validated genes between the sexes on a chow diet. After exposure to a high fat diet for 12 weeks, females gained less weight than males. The microarray analyses indicate in intra-abdominal/gonadal adipose tissue in females 1642 genes differ by at least twofold between the depots, whereas 706 genes differ in subcutaneous/inguinal adipose tissue when compared with males. Only 138 genes are commonly regulated in both sexes and adipose tissue depots. Inflammatory genes (cytokine–cytokine receptor interactions and acute-phase protein synthesis) are upregulated in males when compared with females, and there is a partial reversal after OVX, where OVX adipose tissue gene expression is more ‘male-like’. This pattern is not observed in mice maintained on chow. Histology of male gonadal white adipose tissue (GWAT) shows more crown-like structures than females, indicative of inflammation and adipose tissue remodeling. In addition, genes related to insulin signaling and lipid synthesis are higher in females than males, regardless of dietary exposure. These data suggest that male and female adipose tissue differ between the sexes regardless of diet. Moreover, HF diet exposure elicits a much greater inflammatory response in males when compared with females. This data set underscores the importance of analyzing depot-, sex- and steroid-dependent regulation of adipose tissue distribution and function.

Morbid obesity exposes the association between PNPLA3 I148M (rs738409) and indices of hepatic injury in individuals of European descent.

Abstract: The PNPLA3 I148M variant (rs738409) is robustly associated with hepatic steatosis. Intriguingly, initial findings in cohorts with a mean body mass index (BMI) of 30 kg m−2 also suggested that it is associated with elevated liver enzymes but not with insulin resistance and dyslipidaemia. To determine whether the PNPLA3 variant alters the susceptibility of morbidly obese subjects to develop liver injury and metabolic sequelae. The study was carried out in 678 obese Italians (mean BMI=41 kg m−2) who were genotyped for the I148M variant. All participants provided fasting blood samples and then underwent oral glucose tolerance tests. Indices of liver injury (alanine transaminase (ALT), aspartate transaminase (AST)), glucose tolerance and insulin resistance were measured. Markers of hepatic injury such as ALT and AST were significantly higher in carriers of the 148M allele (P=2.2 × 10−5 and 0.001, respectively). In all, 50% of 148M risk allele homozygotes had pathological levels of ALT (>40 U l−1) compared with 25% of 148I allele homozygotes (P=0.005). Glucose tolerance and insulin sensitivity were similar in all three genotypes. Obese Southern Europeans carrying the 148M allele have increased indices of liver damage uncoupled from proxy measures of insulin resistance.

Metabolic consequences of the presence or absence of the thermogenic capacity of brown adipose tissue in mice (and probably in humans).

Abstract: Only with the development of the uncoupling protein 1 (UCP1)-ablated mouse has it become possible to strictly delineate the physiological significance of the thermogenic capacity of brown adipose tissue. Considering the presence of active brown adipose tissue in adult humans, these insights may have direct human implications. In addition to classical nonshivering thermogenesis, all adaptive adrenergic thermogeneses, including diet-induced thermogenesis, is fully dependent on brown adipocyte activity. Any weight-reducing effect of β(3)-adrenergic agonists is fully dependent on UCP1 activity, as is any weight-reducing effect of leptin (in excess of its effect on reduction of food intake). Consequently, in the absence of the thermogenic activity of brown adipose tissue, obesity develops spontaneously. The ability of brown adipose tissue to contribute to glucose disposal is also mainly related to thermogenic activity. However, basal metabolic rate, cold-induced thermogenesis, acute cold tolerance, fevers, nonadaptive adrenergic thermogenesis and processes such as angiogenesis in brown adipose tissue itself are not dependent on UCP1 activity. Whereas it is likely that these conclusions are also qualitatively valid for adult humans, the quantitative significance of brown adipose tissue for human metabolism--and the metabolic consequences for a single individual possessing more or less brown adipose tissue--awaits clarification.

The longitudinal influence of home and neighbourhood environments on children's body mass index and physical activity over 5 years: the CLAN study.

Abstract: To determine the independent contributions of family and neighbourhood environments to changes in youth physical activity and body mass index (BMI) z-score over 5 years. In 2001, 2004 and 2006, 301 children (10–12 years at baseline) had their height and weight measured (BMI was converted to z-scores using Centers for Disease Control and Prevention reference charts; see http://www.cdc.gov/growthcharts ) and moderate-to-vigorous physical activity (MVPA) assessed using accelerometers. In 2001, parents reported on the home environment (social support, role modelling, rules and restrictions, physical environment) and perceived neighbourhood environment (local traffic, road safety, sporting venues, public transport), and Geographic Information Systems were used to map features of the neighbourhood environment (destinations, road connectivity, traffic exposure). Generalized estimating equations were used to predict average BMI z-score and MVPA over time from baseline home and perceived and objective neighbourhood environment factors. Among boys, maternal education and heavy traffic were inversely associated, and sibling physical activity, maternal role modelling of MVPA and the presence of dead-end roads were positively associated with MVPA. Having unmarried parents, maternal MVPA role modelling and number of home sedentary items were positively associated with BMI z-score among boys. Among girls, having siblings, paternal MVPA role modelling, physical activity rules and parental physical activity co-participation were positively associated with MVPA. Having unmarried parents and maternal sedentary behaviour role modelling were positively associated, and number of sedentary behaviour rules and physical activity items were inversely associated with BMI z-score among girls. The home environment seems more important than the neighbourhood environment in influencing children's physical activity and BMI z-score over 5 years. Physical activity and weight gain programmes among youth should focus on parental role modelling, rules around sedentary and active pursuits, and parental support for physical activity. Intervention studies to investigate these strategies are warranted.

Acute stress and food-related reward activation in the brain during food choice during eating in the absence of hunger.

Abstract: Stress results in eating in the absence of hunger, possibly related to food reward perception. Stress decreases food reward perception. Determine the effect of acute stress on food choice and food choice reward-related brain activity. Nine females (BMI=21.5±2.2 kg/m2, age=24.3±3.5 years). Fasted subjects came twice to randomly complete either a rest or stress condition. Per session, two functional MRI scans were made, wherein the subjects chose the subsequent meal (food images). The rewarding value of the food was measured as liking and wanting. Food characteristics (for example, crispiness, fullness of taste and so on), energy intake, amount of each macronutrient chosen, plasma cortisol and Visual Analog Scale (VAS) hunger and satiety were measured. Fasted state was confirmed by high hunger (80±5 mm VAS). Breakfast energy intake (3±1 MJ) and liking were similar in all conditions. Wanting was lower postprandially (Δ=−0.3 items/category, P<0.01). Breakfast decreased hunger (−42 mm VAS, P<0.01). Postprandially, energy intake (−1.1 MJ), protein intake (−14.7 g) and carbohydrate intake (−32.7 g all P<0.05) were lower. Fat intake was not different (−7.3, P=0.4). Putamen activity was not lower postprandially. Cortisol levels were increased in the stress condition (Area under the curve of cortisol: ΔAUC=+2.2 × 104 nmol min−1 l−1, P<0.05). Satiety was lower after breakfast (−8 mm VAS, P<0.01). Postprandial energy intake, protein intake and carbohydrate intake were relatively higher compared with the rest condition, resulting from more choice for crispiness and fullness of taste (P<0.05). Brain activation was reduced in reward areas: amygdala, hippocampus and cingulate cortex (AUC=−13.33, −1.34, −2.56% blood oxygen level dependent (BOLD) s for choosing breakfast and AUC=−9.31, −1.25, −2.34%BOLD s<0.05 for choosing the second meal). Putamen activation was decreased postprandially (AUC=−1.2%BOLD s, P<0.05). Reward signaling and reward sensitivity were significantly lower under stress, coinciding with increased energy intake from food choice for more crispiness and fullness of taste. The changes in putamen activation may reflect specifically decreased reward prediction sensitivity.

Association between single-slice measurements of visceral and abdominal subcutaneous adipose tissue with volumetric measurements: the Framingham Heart Study

Abstract: Volumetric visceral abdominal adipose tissue (VAT) and subcutaneous abdominal adipose tissue (SAT) as measured by computed tomography (CT) are associated with metabolic risk factors. We sought to identify the correlations of VAT and SAT between area-based measures at different anatomic locations with volumetric measurements to identify the optimal anatomic site, and to relate measurements at this site with metabolic risk factors. We measured SAT and VAT volumes across the total imaging volume, whereas we measured SAT and VAT area at seven predefined anatomic landmarks in 200 participants from the Framingham Heart Study (mean age 54 years, 50% women) who underwent abdominal multi-detector CT. Correlation coefficients were used to assess the association between area measurements and volumes as well as metabolic risk factors stratified by gender. Area-based measurements of SAT and VAT obtained at all anatomic landmarks were strongly associated with SAT and VAT volumes (all r>0.93, P 0.87, P<0.0001, for women and men; respectively). Consistently, area-based measurements of SAT and VAT obtained at L3/4 were most strongly associated with volumetric measured VAT and SAT independent of age (both r=0.99 in men, r=0.96 for SAT and r=0.99 for VAT in women, all P-value <0.0001) and were similarly correlated with risk factors compared with SAT and VAT volumes (all P<0.05 for fasting plasma glucose, triglycerides, high-density lipoprotein, systolic blood pressure). Among area-based measurements of SAT and VAT, those obtained at the level of L3/4 were strongly associated with SAT and VAT volumes and cardio-metabolic risk factors in both men and women.