Showing papers in "Obesity in 2009"

The stigma of obesity: a review and update.

Abstract: Obese individuals are highly stigmatized and face multiple forms of prejudice and discrimination because of their weight (1,2). The prevalence of weight discrimination in the United States has increased by 66% over the past decade (3), and is comparable to rates of racial discrimination, especially among women (4). Weight bias translates into inequities in employment settings, health-care facilities, and educational institutions, often due to widespread negative stereotypes that overweight and obese persons are lazy, unmotivated, lacking in selfdiscipline, less competent, noncompliant, and sloppy (2,5–7). These stereotypes are prevalent and are rarely challenged in Western society, leaving overweight and obese persons vulnerable to social injustice, unfair treatment, and impaired quality of life as a result of substantial disadvantages and stigma. In 2001, Puhl and Brownell published the first comprehensive review of several decades of research documenting bias and stigma toward overweight and obese persons (2). This review summarized weight stigma in domains of employment, health care, and education, demonstrating the vulnerability of obese persons to many forms of unfair treatment. Despite evidence of weight bias in important areas of living, the authors noted many gaps in research regarding the nature and extent of weight stigma in various settings, the lack of science on emotional and physical health consequences of weight bias, and the paucity of interventions to reduce negative stigma. In recent years, attention to weight bias has increased, with a growing recognition of the pervasiveness of weight bias and stigma, and its potential harmful consequences for obese persons. The aim of this article is to provide an update of scientific evidence on weight bias toward overweight and obese adults through a systematic review of published literature since the 2001 article by Puhl and Brownell. This review expands upon previous findings of weight bias in major domains of living, documents new areas where weight bias has been studied, and highlights ongoing research questions that need to be addressed to advance this field of study. A systematic literature search of studies published between January 2000 and May 2008 was undertaken on computerized psychological, medical, social science, sport, and education databases including PsycINFO, PubMed, SCOPUS, ERIC, and SPORTDiscus. The following keyword combinations were used: weight, obese, obesity, overweight, BMI, fat, fatness, size, heavy, large, appearance, big, heavyweight, bias, biased, discrimination, discriminatory, discriminate, stigma, stigmatized, stigmatization, prejudice, prejudicial, stereotype(s), stereotypical, stereotyping, victimization, victimize(d), blame(d), blaming, shame(d), shaming, teasing, tease(d), unfair, bully, bullying, harassment, assumptions, attributions, education, health, health care, sales, employment, wages, promotion, adoption, jury, customer service, housing, media, television. Reference lists of retrieved articles and books were also reviewed, and manual searches were conducted in the databases and journals for authors who had published in this field. Most studies retrieved for this review were published in the United States. Any articles published internationally are noted with their country of origin. Research on weight stigma in adolescents and children was excluded from this review, as this literature was recently reviewed elsewhere (8). Unpublished manuscripts and dissertations were also excluded. In addition, issues pertaining to measurement of weight stigmatization, and demographic variables affecting vulnerability to weight bias such as gender, age, race, and body weight are not addressed in this review. This article instead primarily reviews the evidence of specific areas where weight bias occurs toward adults and its consequences for those affected. This article is organized similarly to the first review published by Puhl and Brownell (2), with sections on weight bias in settings of employment, health care, and education. New sections have been added including weight bias in interpersonal relationships and the media, as well as psychological and physical health consequences of weight bias, and the status of stigma-reduction research. As with the 2001 article, this review also provides an update on legal initiatives to combat weight discrimination, and outlines specific questions for future research.

Circadian Timing of Food Intake Contributes to Weight Gain

Abstract: Studies of body weight regulation have focused almost entirely on caloric intake and energy expenditure. However, a number of recent studies in animals linking energy regulation and the circadian clock at the molecular, physiological, and behavioral levels raise the possibility that the timing of food intake itself may play a significant role in weight gain. The present study focused on the role of the circadian phase of food consumption in weight gain. We provide evidence that nocturnal mice fed a high-fat diet only during the 12-h light phase gain significantly more weight than mice fed only during the 12-h dark phase. A better understanding of the role of the circadian system for weight gain could have important implications for developing new therapeutic strategies for combating the obesity epidemic facing the human population today.

Serum Bile Acids Are Higher in Humans With Prior Gastric Bypass: Potential Contribution to Improved Glucose and Lipid Metabolism

Abstract: The multifactorial mechanisms promoting weight loss and improved metabolism following Roux-en-Y gastric bypass (GB) surgery remain incompletely understood. Recent rodent studies suggest that bile acids can mediate energy homeostasis by activating the G-protein coupled receptor TGR5 and the type 2 thyroid hormone deiodinase. Altered gastrointestinal anatomy following GB could affect enterohepatic recirculation of bile acids. We assessed whether circulating bile acid concentrations differ in patients who previously underwent GB, which might then contribute to improved metabolic homeostasis. We performed cross-sectional analysis of fasting serum bile acid composition and both fasting and post-meal metabolic variables, in three subject groups: (i) post-GB surgery (n = 9), (ii) without GB matched to preoperative BMI of the index cohort (n = 5), and (iii) without GB matched to current BMI of the index cohort (n = 10). Total serum bile acid concentrations were higher in GB (8.90 ± 4.84 µmol/l) than in both overweight (3.59 ± 1.95, P = 0.005, Ov) and severely obese (3.86 ± 1.51, P = 0.045, MOb). Bile acid subfractions taurochenodeoxycholic, taurodeoxycholic, glycocholic, glycochenodeoxycholic, and glycodeoxycholic acids were all significantly higher in GB compared to Ov (P < 0.05). Total bile acids were inversely correlated with 2-h post-meal glucose (r = −0.59, P < 0.003) and fasting triglycerides (r = −0.40, P = 0.05), and positively correlated with adiponectin (r = −0.48, P < 0.02) and peak glucagon-like peptide-1 (GLP-1) (r = 0.58, P < 0.003). Total bile acids strongly correlated inversely with thyrotropic hormone (TSH) (r = −0.57, P = 0.004). Together, our data suggest that altered bile acid levels and composition may contribute to improved glucose and lipid metabolism in patients who have had GB.

One-year weight losses in the Look AHEAD study: factors associated with success.

Abstract: This report provides a further analysis of the first year weight losses in the Look AHEAD (Action for Health in Diabetes) study and identifies factors associated with success. Participants were a total of 5,145 men and women with type 2 diabetes who were recruited at 16 sites and randomly assigned to an intensive lifestyle intervention (ILI) or a control condition, Diabetes Support and Education (DSE). During year 1, participants in ILI received comprehensive diet and physical activity counseling in a total of 42 group and individual sessions, compared with three educational sessions for DSE participants. As reported previously, at the end of the year, ILI participants lost 8.6% of initial weight, compared to 0.7% for DSE (P 5.5%), although there were significant differences among groups. For the year, ILI participants attended an average of 35.4 treatment sessions and reported exercising a mean of 136.6 min/week and consuming a total of 360.9 meal replacement products. Greater self-reported physical activity was the strongest correlate of weight loss, followed by treatment attendance and consumption of meal replacements. The use of orlistat, during the second half of the year, increased weight loss only marginally in those ILI participants who had lost <5% of initial weight during the first 6 months and chose to take the medication thereafter as a toolbox option. The lifestyle intervention was clinically effective in all subsets of an ethnically and demographically diverse population.

Interplay Between Weight Loss and Gut Microbiota Composition in Overweight Adolescents

Abstract: The aim of this study was to determine the influence of an obesity treatment program on the gut microbiota and body weight of overweight adolescents. Thirty-six adolescents (13-15 years), classified as overweight according to the International Obesity Task Force BMI criteria, were submitted to a calorie-restricted diet (10-40%) and increased physical activity (15-23 kcal/kg body weight/week) program over 10 weeks. Gut bacterial groups were analyzed by quantitative real-time PCR before and after the intervention. A group of subjects (n=23) experienced >4.0 kg weight loss and showed significant BMI (P=0.030) and BMI z-score (P=0.035) reductions after the intervention, while the other group (n=13) showed <2.0 kg weight loss. No significant differences in dietary intake were found between both groups. In the whole adolescent population, the intervention led to increased Bacteroides fragilis group (P=0.001) and Lactobacillus group (P=0.030) counts, and to decreased Clostridium coccoides group (P=0.028), Bifidobacterium longum (P=0.031), and Bifidobacterium adolescentis (P=0.044) counts. In the high weight-loss group, B. fragilis group and Lactobacillus group counts also increased (P=0.001 and P=0.007, respectively), whereas C. coccoides group and B. longum counts decreased (P=0.001 and P=0.044, respectively) after the intervention. Total bacteria, B. fragilis group and Clostridium leptum group, and Bifidobacterium catenulatum group counts were significantly higher (P<0.001-0.036) while levels of C. coccoides group, Lactobacillus group, Bifidobacterium, Bifidobacterium breve, and Bifidobacterium bifidum were significantly lower (P<0.001-0.008) in the high weight-loss group than in the low weight-loss group before and after the intervention. These findings indicate that calorie restriction and physical activity have an impact on gut microbiota composition related to body weight loss, which also seem to be influenced by the individual's microbiota.

Cancer incidence and mortality after gastric bypass surgery.

Abstract: Despite weight loss recommendations to prevent cancer, cancer outcome studies after intentional weight loss are limited. Recently, reduced cancer mortality following bariatric surgery has been reported. This study tested whether reduced cancer mortality following gastric bypass was due to decreased incidence. Cancer incidence and mortality data through 2007 from the Utah Cancer Registry (UCR) were compared between 6,596 Utah patients who had gastric bypass (1984-2002) and 9,442 severely obese persons who had applied for Utah Driver's Licenses (1984-2002). Study outcomes included incidence, case-fatality, and mortality for cancer by site and stage at diagnosis of all gastric bypass patients, compared to nonoperated severely obese controls. Follow-up was over a 24-year period (mean 12.5 years). Total cancer incidence was significantly lower in the surgical group compared to controls (hazard ratio (HR) = 0.76; confidence interval (CI) 95%, 0.65-0.89; P = 0.0006). Lower incidence in surgery patients vs. controls was primarily due to decreased incidence of cancer diagnosed at regional or distant stages. Cancer mortality was 46% lower in the surgery group compared to controls (HR = 0.54; CI 95%, 0.37-0.78; P = 0.001). Although the apparent protective effect of surgery on risk of developing cancer was limited to cancers likely known to be obesity related, the inverse association for mortality was seen for all cancers. Significant reduction in total cancer mortality in gastric bypass patients compared with severely obese controls was associated with decreased incidence, primarily among subjects with advanced cancers. These findings suggest gastric bypass results in lower cancer risk, presumably related to weight loss, supporting recommendations for reducing weight to lower cancer risk.

American association of clinical endocrinologists, the obesity society, and american society for metabolic & bariatric surgery medical guidelines for clinical practice for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric surgery patient

Abstract: American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery Medical Guidelines for Clinical Practice are systematically developed statements to assist health-care professionals in medical decision making for specific clinical conditions. Most of the content herein is based on literature reviews. In areas of uncertainty, professional judgment was applied. These guidelines are a working document that reflects the state of the field at the time of publication. Because rapid changes in this area are expected, periodic revisions are inevitable. We encourage medical professionals to use this information in conjunction with their best clinical judgment. The presented recommendations may not be appropriate in all situations. Any decision by practitioners to apply these guidelines must be made in light of local resources and individual patient circumstances. The American Society for Parenteral & Enteral Nutrition fully endorses sections of these guidelines that address the metabolic and nutritional management of the bariatric surgical patient.

Inverse Association Between BMI and Prefrontal Metabolic Activity in Healthy Adults

Abstract: Obesity has been associated with a higher risk for impaired cognitive function, which most likely reflects associated medical complications (i.e., cerebrovascular pathology). However, there is also evidence that in healthy individuals excess weight may adversely affect cognition (executive function, attention, and memory). Here, we measured regional brain glucose metabolism (using positron emission tomography (PET) and 2-deoxy-2[ 18 F]fluoro-D-glucose (FDG)) to assess the relationship between BMI and brain metabolism (marker of brain function) in 21 healthy controls (BMI range 19–37 kg/m 2 ) studied during baseline (no stimulation) and during cognitive stimulation (numerical calculations). Statistical parametric mapping (SPM) revealed a significant negative correlation between BMI and metabolic activity in prefrontal cortex (Brodmann areas 8, 9, 10, 11, 44) and cingulate gyrus (Brodmann area 32) but not in other regions. Moreover, baseline metabolism in these prefrontal regions was positively associated with performance on tests of memory (California Verbal Learning Test) and executive function (Stroop Interference and Symbol Digit Modality tests). In contrast, the regional brain changes during cognitive stimulation were not associated with BMI nor with neuropsychological performance. The observed association between higher BMI and lower baseline prefrontal metabolism may underlie the impaired performance reported in healthy obese individuals on some cognitive tests of executive function. On the other hand, the lack of an association between BMI and brain metabolic activation during cognitive stimulation indicates that BMI does not influence brain glucose utilization during cognitive performance. These results further highlight the urgency to institute public health interventions to prevent obesity.

The impact of obesity on health service utilization and costs in childhood.

Abstract: Most studies of the economic costs of childhood obesity have focused upon hospitalization for comorbidities of obesity, whereas increased expenditures may also be the result of additional outpatient/emergency room visits or prescription drug expenditures. To quantify the magnitude of increased health-care utilization and expenditures among overweight and obese children, we performed descriptive, bivariate, and multivariable analyses on data from 6- to 19-year olds in the 2002-2005 Medical Expenditure Panel Survey (MEPS), a national probability survey of the noninstitutionalized civilian population in the United States. Compared with normal/underweight children, we found that children who were obese during both years of the MEPS had USD194 higher outpatient visit expenditures, USD114 higher prescription drug expenditures, and USD12 higher emergency room expenditures. Children who were overweight during both years, or overweight in one year and obese in the other had USD79 higher outpatient visit expenditures, USD64 higher prescription drug expenditures, and USD25 higher emergency room expenditures than normal/underweight children. Significantly, increased utilization was noted for outpatient visits, prescription drug use, and emergency room visits. Increased costs and utilization were concentrated among adolescents, though 6-11-year-old children who were obese in both years did have more outpatient visits and expenditures than other children. Extrapolated to the nation, elevated BMI in childhood was associated with USD14.1 billion in additional prescription drug, emergency room, and outpatient visit costs annually. Although further research is needed to identify effective interventions, the immediate economic consequences of childhood obesity are much greater than previously realized, and further reinforce efforts to prevent this major comorbidity are needed.

Dopamine for "wanting" and opioids for "liking": a comparison of obese adults with and without binge eating.

Abstract: Obesity research suffers from an overinclusion paradigm whereby all participants with a BMI beyond a certain cutoff value (e.g., 30) are typically combined in a single group and compared to those of normal weight. There has been little attempt to identify meaningful subgroups defined by their salient biobehavioral differences. In order to address this limitation, we examined genetic and psychological indicators of hedonic eating in obese adults with (n=66) and without (n=70) binge eating disorder (BED). Our analyses focused on dopamine (DA) and opioid genetic markers because of their conjoint association with the functioning of brain reward mechanisms. We targeted three functional polymorphisms related to the D2 receptor (DRD2) gene, as well as the functional A118G polymorphism of the mu-opioid receptor (OPRM1) gene. We found that significantly more obese controls had the "loss-of-function" A1 allele of Taq1A compared to their BED counterparts, whereas the "gain-of-function" G allele of A118G occurred with greater frequency in the BED group. A significant gene-gene combination chi2 analysis also indicated that of those participants with the gain-gain genotype (G+ and A1), 80% were in the BED group whereas only 35% with the loss-loss genotype (G- and A1+) were in this group. Finally, BED subjects had significantly higher scores on a self-report measure of hedonic eating. Our findings suggest that BED is a biologically based subtype of obesity and that the proneness to binge eating may be influenced by a hyper-reactivity to the hedonic properties of food--a predisposition that is easily exploited in our current environment with its highly visible and easily accessible surfeit of sweet and fatty foods.

Best practice updates for pediatric/adolescent weight loss surgery.

Abstract: The objective of this study is to update evidence-based best practice guidelines for pediatric/adolescent weight loss surgery (WLS). We performed a systematic search of English-language literature on WLS and pediatric, adolescent, gastric bypass, laparoscopic gastric banding, and extreme obesity published between April 2004 and May 2007 in PubMed, MEDLINE, and the Cochrane Library. Keywords were used to narrow the search for a selective review of abstracts, retrieval of full articles, and grading of evidence according to systems used in established evidence-based models. In light of evidence on the natural history of obesity and on outcomes of WLS in adolescents, guidelines for surgical treatment of obesity in this age group need to be updated. We recommend modification of selection criteria to include adolescents with BMI ≥ 35 and specific obesity-related comorbidities for which there is clear evidence of important short-term morbidity (i.e., type 2 diabetes, severe steatohepatitis, pseudotumor cerebri, and moderate-to-severe obstructive sleep apnea). In addition, WLS should be considered for adolescents with extreme obesity (BMI ≥ 40) and other comorbidities associated with long-term risks. We identified >1,085 papers; 186 of the most relevant were reviewed in detail. Regular updates of evidence-based recommendations for best practices in pediatric/adolescent WLS are required to address advances in technology and the growing evidence base in pediatric WLS. Key considerations in patient safety include carefully designed criteria for patient selection, multidisciplinary evaluation, choice of appropriate procedure, thorough screening and management of comorbidities, optimization of long-term compliance, and age-appropriate fully informed consent.

Enhanced weight loss with pramlintide/metreleptin: an integrated neurohormonal approach to obesity pharmacotherapy.

Abstract: The neurohormonal control of body weight involves a complex interplay between long-term adiposity signals (e.g., leptin), and short-term satiation signals (e.g., amylin). In diet-induced obese (DIO) rodents, amylin/leptin combination treatment led to marked, synergistic, fat-specific weight loss. To evaluate the weight-lowering effect of combined amylin/leptin agonism (with pramlintide/metreleptin) in human obesity, a 24-week, randomized, double-blind, active-drug-controlled, proof-of-concept study was conducted in obese or overweight subjects (N = 177; 63% female; 39 +/- 8 years; BMI 32.0 +/- 2.1 kg/m(2); 93.3 +/- 13.2 kg; mean +/- s.d.). After a 4-week lead-in period with pramlintide (180 microg b.i.d. for 2 weeks, 360 microg b.i.d. thereafter) and diet (40% calorie deficit), subjects achieving 2-8% weight loss were randomized 1:2:2 to 20 weeks of treatment with metreleptin (5 mg b.i.d.), pramlintide (360 microg b.i.d.), or pramlintide/metreleptin (360 microg/5 mg b.i.d.). Combination treatment with pramlintide/metreleptin led to significantly greater weight loss from enrollment to week 20 (-12.7 +/- 0.9%; least squares mean +/- s.e.) than treatment with pramlintide (-8.4 +/- 0.9%; P < 0.001) or metreleptin (-8.2 +/- 1.3%; P < 0.01) alone (evaluable, N = 93). The greater reduction in body weight was significant as early as week 4, and weight loss continued throughout the study, without evidence of a plateau. The most common adverse events with pramlintide/metreleptin were injection site events and nausea, which were mostly mild to moderate and decreased over time. These results support further development of pramlintide/metreleptin as a novel, integrated neurohormonal approach to obesity pharmacotherapy.

Rational Design of a Combination Medication for the Treatment of Obesity

Abstract: Existing obesity therapies are limited by safety concerns and modest efficacy reflecting a weight loss plateau. Here, we explore combination therapy with bupropion (BUP), a putative stimulator of melanocortin pathways, and an opioid antagonist, naltrexone (NAL), to antagonize an inhibitory feedback loop that limits sustained weight reduction. In vitro electrophysiologic experiments were conducted to determine the extent to which BUP+NAL stimulated hypothalamic pro-opiomelanocortin (POMC) neurons in mouse brain. A subsequent study further characterized the effect of combination BUP+NAL treatment on food intake in lean and obese mice. Finally, a randomized, blinded, placebo-controlled trial in obese adult subjects was conducted. Randomization included: BUP (300 mg) + NAL (50 mg), BUP (300 mg) + placebo (P), NAL (50 mg) + P or P+P for up to 24 weeks. BUP+NAL stimulated murine POMC neurons in vitro and caused a greater reduction in acute food intake than either monotherapy, an effect consistent with synergism. Combined BUP+NAL provided sustained weight loss without evidence of an efficacy plateau through 24 weeks of treatment. BUP+NAL completers diverged from NAL+P (P < 0.01) and P+P (P < 0.001) at week 16 and from BUP+P by week 24 (P < 0.05). The combination was also well tolerated. Translational studies indicated that BUP+NAL therapy produced synergistic weight loss which exceeded either BUP or NAL alone. These results supported the hypothesis that NAL, through blockade of β-endorphin mediated POMC autoinhibition, prevents the classic weight loss plateau observed with monotherapies such as BUP. This novel treatment approach (BUP+NAL) holds promise for the treatment of obesity.

Sarcopenic/obesity and physical capacity in older men and women: data from the Nutrition as a Determinant of Successful Aging (NuAge)-the Quebec longitudinal Study.

Abstract: Sarcopenia and obesity have been independently associated with physical capacity impairments. However, few studies have investigated the impact of sarcopenic/obesity on physical capacity in older individuals using objective measures of physical capacity and body composition. This study included 904 older individuals aged between 68 and 82 years old. Body composition (fat mass (FM) and lean body mass (LBM) by dual-energy X-ray absorptiometry (DXA)), physical capacity (timed up and go, chair stands, walking speed at normal and fastest pace, and one leg stand), sum of reported chronic conditions and physical activity level were measured. A global physical capacity score was then calculated giving a maximal score of 20. Finally, four groups were created within genders based on sarcopenia and obesity ((i) nonsarcopenic/nonobese; (ii) sarcopenic/nonobese; (iii) nonsarcopenic/obese; (iv) sarcopenic/obese). The four groups were significantly different for the sit-to-stand test and the one leg stand test (P < 0.05) and only for the one leg stand test in women (P < 0.05). In both genders results for the global physical capacity score revealed that both obese groups (sarcopenic and nonsarcopenic) were similar (P = 0.14 in men and P = 0.19 in women) and had a lower global physical capacity score compared to nonsarcopenic/nonobese individuals (P < 0.05). In addition, sarcopenic women displayed a higher score than both obese nonsarcopenic and obese sarcopenic groups (P < 0.01). Sarcopenic/obese men and women do not display lower physical capacity compared to nonsarcopenic/obese individuals in this cohort of well-functioning older men and women. Obesity per se appears to contribute more to lower physical capacity than sarcopenia.

Acute stress-related changes in eating in the absence of hunger

Abstract: Obesity results from chronic deregulation of energy balance, which may in part be caused by stress. Our objective was to investigate the effect of acute and psychological stress on food intake, using the eating in the absence of hunger paradigm, in normal and overweight men and women (while taking dietary restraint and disinhibition into account). In 129 subjects (BMI = 24.5 +/- 3.4 kg/m(2) and age = 27.6 +/- 8.8 years), scores were determined on the Three Factor Eating Questionnaire (dietary restraint = 7.2 +/- 4.4; disinhibition = 4.5 +/- 2.6; feeling of hunger = 3.9 +/- 2.6) and State-Trait Anxiety Inventory (trait score = 31.7 +/- 24.2). In a randomized crossover design, the "eating in absence of hunger" protocol was measured as a function of acute stress vs. a control task and of state anxiety scores. Energy intake from sweet foods (708.1 kJ vs. 599.4 kJ, P < 0.03) and total energy intake (965.2 kJ vs. 793.8 kJ, P < 0.01) were significantly higher in the stress condition compared to the control condition. Differences in energy intake between the stress and control condition were a function of increase in state anxiety scores during the stress task (Delta state anxiety scores) (R(2) = 0.05, P < 0.01). This positive relationship was stronger in subjects with high disinhibition scores (R(2) = 0.12, P < 0.05). Differences in state anxiety scores were a function of trait anxiety scores (R(2) = 0.07, P < 0.05). We conclude that acute psychological stress is associated with eating in the absence of hunger, especially in vulnerable individuals characterized by disinhibited eating behavior and sensitivity to chronic stress.

Neurobehavioral inhibition of reward-driven feeding: implications for dieting and obesity.

Abstract: Overview The development of effective weight loss interventions requires a thorough understanding of the motivational factors that drive and inhibit the overconsumption of food. Obesity was once believed to result purely from disruptions of homeostatic mechanisms controlling food intake. However, it is increasingly recognized that much of the excess caloric intake in obesity is driven by pleasure or the rewarding properties of readily available palatable food (1,2). It is important to note that the motivation underlying this reward-driven or “hedonic” feeding appears to have a different neurophysiological basis than homeostatic controls over energy balance, though the hedonic and homeostatic systems do interact (3). Recently, a surge of research has linked the appetitive motivation to consume palatable food to activation of the mesolimbic dopaminergic system, a neural pathway also implicated in drug addiction and addictive behaviors such as gambling (4). As a result of these findings, a view of obesity as a “disorder of appetitive motivation” has gained prominence among a growing number of obesity researchers. However, a model of hedonic feeding based purely on appetitive motivation has limitations, including an inability to explain instances of feeding behavior parsimoniously in both dieters and nondieters. The aim of this review is to summarize the strengths and weaknesses of the appetitive model, present the extant literature linking control of hedonic feeding to inhibitory processes localized in the prefrontal cortex (PFC), and delineate a theoretical model in which hedonic feeding is viewed as the product of an interaction between appetitive motivation and inhibitory control.

A Catechin-rich Beverage Improves Obesity and Blood Glucose Control in Patients With Type 2 Diabetes

Abstract: We investigated the effects of continuous ingestion of a catechin-rich beverage in patients with type 2 diabetes who were not receiving insulin (Ins) therapy in a double-blind controlled study. The participants ingested green tea containing either 582.8 mg of catechins (catechin group; n = 23) or 96.3 mg of catechins (control group; n = 20) per day for 12 weeks. At week 12, the decrease in waist circumference was significantly greater in the catechin group than in the control group. Adiponectin, which is negatively correlated with visceral adiposity, increased significantly only in the catechin group. Although the increase in Ins at week 12 was significantly greater in the catechin group than in the control group, no apparent difference was noted between the two groups in glucose and hemoglobin A(1c). In patients treated with insulinotropic agents, the increase in Ins at week 12 was significantly greater in the catechin group than in the control group. This significant increase in Ins levels was observed only in the catechin group. In the catechin group receiving other treatments, Ins levels remained unchanged. In addition, in patients treated with insulinotropic agents, the decrease in hemoglobin A(1c) at week 12 was significantly greater in the catechin group than in the control group. These results suggest that a catechin-rich beverage might have several therapeutic uses: in the prevention of obesity; in the recovery of Ins-secretory ability; and, as a way to maintain low hemoglobin A(1c) levels in type 2 diabetic patients who do not yet require Ins therapy.

Neutrophil Activation in Morbid Obesity, Chronic Activation of Acute Inflammation

Abstract: Recent studies show that morbid obesity is associated with activation of the innate immune response. Neutrophil activation is a fundamental process in the innate immune response. Therefore, the activation state of neutrophils in severely obese subjects and the effect of bariatric surgery on neutrophil activation was evaluated. Neutrophil activation was assessed by measuring circulating concentrations of myeloperoxidase (MPO) and calprotectin in 37 severely obese and 9 control subjects (enzyme-linked immunosorbent assay). Moreover, membrane expression of CD66b on circulating neutrophils was measured using flow cytometry in a group of seven severely obese and six control subjects. Immunohistochemical detection of MPO was performed in adipose and muscle tissue. Plasma MPO and calprotectin levels were significantly increased in severely obese subjects as compared to healthy controls, 27.1 ± 10.8 vs. 17.3 ± 5.5 ng/ml (P < 0.001) and 115.5 ± 43.5 vs. 65.1 ± 23.1 ng/ml (P < 0.001) for MPO and calprotectin, respectively. In line, CD66b expression was significantly increased in severely obese individuals, 177.3 ± 43.7 vs. 129.7 ± 9.2 (mean fluorescence intensity) (P < 0.01). Bariatric surgery resulted in decreased calprotectin, but MPO plasma levels remained elevated. Adipose and muscle tissue did not contain increased numbers of MPO expressing cells in severely obese individuals. These results point out that circulating neutrophils are activated to a greater extent in severely obese subjects. Our data support the finding that the innate immune system is activated in severely obese individuals. Moreover, because neutrophils have a short life span, this indicates that the chronic inflammatory condition associated with morbid obesity is characterized by a continuous activation of the innate immune system.

Racial/ethnic differences in weight perception.

Abstract: The objective of this research was to estimate the prevalence of weight misperception among adults using the most recent nationally representative data, according to measured weight category and to assess the relationship between weight misperception and race/ethnicity. Height and weight were measured as part of the 1999-2006 National Health and Nutrition Examination Survey. The study sample consisted of 17,270 adults aged >or=20 years. BMI was categorized as underweight (BMI or= 30). Subjects reported self-perception of weight status. Among study subjects, 31.7% of healthy weight adults, 38.1% of overweight adults, and 8.1% of obese adults incorrectly perceived their weight category. Among obese men, the odds of weight misperception were higher for non-Hispanic blacks (odds ratio (OR) = 3.0; 95% confidence interval (CI) = 2.0-4.5) compared to non-Hispanic whites and for persons with less than a high school education (OR = 2.1; 95% CI = 1.3-2.1), compared to those with some college education. Among obese women, the odds of weight misperception were higher for non-Hispanic blacks (OR = 3.4; 95% CI = 1.4, 3.1) and Mexican Americans (OR = 1.9; 95% CI = 1.2, 3.2) compared to non-Hispanic whites and for persons with less than high school education compared to those with some college education (OR = 5.5; 95% CI = 3.3-9.3). Weight misperception is highly prevalent in the US population, and more frequent in racial/ethnic minorities, males, and in persons with lower educational levels. Addressing the issue of weight misperception may help address the problem of obesity in the United States by increasing awareness of healthy weight levels, which may subsequently have an impact on weight-related behavior change.

Are Natural Killer Cells Protecting the Metabolically Healthy Obese Patient

Abstract: With the emerging obesity pandemic, identifying those who appear to be protected from adverse consequences such as type 2 diabetes and certain malignancies will become important. We propose that the circulating immune system plays a role in the development of these comorbidities. Clinical data and blood samples were collected from 52 patients with severe obesity attending a hospital weight-management clinic and 11 lean healthy controls. Patients were classified into metabolically "healthy obese" (n = 26; mean age 42.6 years, mean BMI 46.8 kg/m(2)) or "unhealthy obese" (n = 26; mean age 45 years, mean BMI 47.5 kg/m(2)) groups, based upon standard cutoff points for blood pressure, lipid profile, and fasting glucose. Circulating lymphoid populations and phenotypes were assessed by flow cytometry. Obese patients had significantly less circulating natural killer (NK) and cytotoxic T lymphocytes (CTL) compared to lean controls. There were significantly higher levels of NK cells and CTLs in the healthy obese group compared to the unhealthy obese group (NK: 11.7% vs. 6.5%, P < 0.0001, CD8 13.4% vs. 9.3%, P = 0.04), independent of age and BMI and these NK cells were also less activated in the healthy compared to the unhealthy group (CD69, 4.1% vs. 11.8%, P = 0.03). This is the first time that quantitative differences in the circulating immune system of obese patients with similar BMI but different metabolic profiles have been described. The significantly higher levels of CTLs and NK cells, which express fewer inhibitory molecules, could protect against malignancy, infection, and metabolic disease seen in obesity.

Inflammation and Race and Gender Differences in Computerized Tomography‐measured Adipose Depots

Abstract: A growing body of evidence has consistently shown a correlation between obesity and chronic subclinical inflammation. It is unclear whether the size of specific adipose depots is more closely associated with concentrations of inflammatory markers than overall adiposity. This study investigated the relationship between inflammatory markers and computerized tomography-derived abdominal visceral and subcutaneous fat and thigh intermuscular and subcutaneous fat in older white and black adults. Data were from 2,651 black and white men and women aged 70-79 years participating in the Health, Aging, and Body Composition (Health ABC) study. Inflammatory markers, interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-alpha (TNF-alpha) were obtained from serum samples. Abdominal visceral and subcutaneous fat and thigh intermuscular and subcutaneous fat were quantified on computerized tomography images. Linear regression analysis was used to evaluate the cross-sectional relationship between specific adipose depots and inflammatory markers in four race/gender groups. As expected, blacks have less visceral fat than whites and women less visceral fat than men. However, abdominal visceral adiposity was most consistently associated with significantly higher IL-6 and CRP concentrations in all race/gender groups (P < 0.05), even after controlling for general adiposity. Thigh intermuscular fat had an inconsistent but significant association with inflammation, and there was a trend toward lower inflammatory marker concentration with increasing thigh subcutaneous fat in white and black women. Despite the previously established differences in abdominal fat distribution across gender and race, visceral fat remained a significant predictor of inflammatory marker concentration across all four subgroups examined.

Low sympathetic tone and obese phenotype in oxytocin-deficient mice.

Abstract: Oxytocin (Oxt) is secreted both peripherally and centrally and is involved in several functions including parturition, milk let-down reflex, social behavior, and food intake. Recently, it has been shown that mice deficient in Oxt receptor develop late-onset obesity. In this study, we characterized a murin model deficient in Oxt peptide (Oxt(-/-)) to evaluate food intake and body weight, glucose tolerance and insulin tolerance, leptin and adrenaline levels. We found that Oxt(-/-) mice develop late-onset obesity and hyperleptinemia without any alterations in food intake in addition to having a decreased insulin sensitivity and glucose intolerance. The lack of Oxt in our murin model also results in lower adrenalin levels which led us to hypothesize that the metabolic changes observed are associated with a decreased sympathetic nervous tone. It has been shown that Oxt neurons in the paraventricular nucleus (PVN) are a component of a leptin-sensitive signaling circuit between the hypothalamus and caudal brain stem for the regulation of food intake and energy homeostasis. Nevertheless, the lack of Oxt in these mice does not have a direct impact on feeding behavior whose regulation is probably dependent on the complex interplay of several factors. The lack of hyperphagia evident in the Oxt(-/-) mice may, in part, be attributed to the developmental compensation of other satiety factors such as cholecystokinin or bombesin-related peptides which merits further investigation. These findings identify Oxt as an important central regulator of energy homeostasis.

Associations between perceived weight discrimination and the prevalence of psychiatric disorders in the general population.

Abstract: Despite the increased prevalence of weight discrimination, few studies have examined the association between perceived weight discrimination and the prevalence of current psychiatric disorders in the general population. This study utilized a subsample of overweight and obese individuals (N = 22,231) from Wave 2 of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC), a cross-sectional nationally representative study of noninstitutionalized US adults. Perceived weight discrimination is associated with substantial psychiatric morbidity and comorbidity. These results remained significant after adjusting for a potential confound, perceived stress. Moreover, social support did not buffer against the adverse effects of perceived weight discrimination on mental health. Controlling for BMI did not diminish the associations, indicating that perceived weight discrimination is potentially harmful to mental health regardless of weight. These results highlight the urgent need for a multifaceted approach to address this important public health issue, including interventions to assist overweight individuals in coping with the mental health sequelae of perceived weight discrimination.

Roux-en-Y Gastric Bypass Enhances Energy Expenditure and Extends Lifespan in Diet-induced Obese Rats

Abstract: Gastrointestinal weight-loss surgery (GIWLS) is currently the most effective treatment for severe obesity, with Roux en-Y gastric bypass (RYGB) among the best of the available surgical options. Despite its widespread clinical use, the mechanisms by which RYGB induces its profound weight loss remain largely unknown. This procedure effects weight loss by altering the physiology of weight regulation and eating behavior rather than by simple mechanical restriction and/or malabsorption as previously thought. To study how RYGB affects the physiology of energy balance, we developed a rat model of this procedure. In this report, we demonstrate that RYGB in diet-induced obese (DIO) rats induces a 25% weight loss, prolongs mean survival by 45%, and normalizes glucose homeostasis and lipid metabolism. RYGB induced a 19% increase in total and a 31% increase in resting energy expenditure (REE). These effects, along with a 17% decrease in food intake and a 4% decrease in nutrient absorption account for the normalization of body weight after this procedure. These effects indicate that surgery acts by altering the physiology of weight regulation and help to explain the effectiveness of RYGB in comparison to restrictive dieting and other forms of dietary and pharmacological therapies for obesity. The clinical effectiveness of RYGB and its physiological effects on body weight regulation and energy expenditure (EE) suggest that this operation provides a unique opportunity to explore the mechanisms of energy homeostasis and to identify novel therapies for obesity and related metabolic diseases.

The role of obesity-associated loci identified in genome-wide association studies in the determination of pediatric BMI.

Abstract: The prevalence of obesity in children and adults in the United States has increased dramatically over the past decade. Besides environmental factors, genetic factors are known to play an important role in the pathogenesis of obesity. A number of genetic determinants of adult BMI have already been established through genome-wide association (GWA) studies. In this study, we examined 25 single-nucleotide polymorphisms (SNPs) corresponding to 13 previously reported genomic loci in 6,078 children with measures of BMI. Fifteen of these SNPs yielded at least nominally significant association to BMI, representing nine different loci including INSIG2, FTO, MC4R, TMEM18, GNPDA2, NEGR1, BDNF, KCTD15, and 1q25. Other loci revealed no evidence for association, namely at MTCH2, SH2B1, 12q13, and 3q27. For the 15 associated variants, the genotype score explained 1.12% of the total variation for BMI z-score. We conclude that among 13 loci that have been reported to associate with adult BMI, at least nine also contribute to the determination of BMI in childhood as demonstrated by their associations in our pediatric cohort.

Becoming physically active after bariatric surgery is associated with improved weight loss and health-related quality of life.

Abstract: The purpose of this study was to determine whether pre- to postoperative increases in physical activity (PA) are associated with weight loss and health-related quality of life (HRQoL) following bariatric surgery. Participants were 199 Roux-en-Y gastric bypass (RYGB) surgery patients. The International Physical Activity Questionnaire (IPAQ) was used to categorize participants into three groups according to their preoperative and /1-year postoperative PA level: (i) Inactive/Active ( or=200-min/week), (ii) Active/Active (>or=200-min/week/>or=200-min/week) and (iii) Inactive/Inactive (<200-min/week/<200-min/week). The Medical Outcomes Study Short Form-36 (SF-36) was used to assess HRQoL. Analyses of covariance were conducted to examine the effects of PA group on weight and HRQoL changes. Inactive/Active participants, compared with Inactive/Inactive individuals, had greater reductions in weight (52.5 +/- 15.4 vs. 46.4 +/- 12.8 kg) and BMI (18.9 +/- 4.6 vs. 16.9 +/- 4.2 kg/m(2)). Weight loss outcomes in the Inactive/Active and Active/Active groups were similar to each other. Inactive/Active and Active/Active participants reported greater improvements than Inactive/Inactive participants on the mental component summary (MCS) score and the general health, vitality and mental health domains (P < 0.01). Although the direction of causation is not clear, these findings suggest that RYGB patients who become active postoperatively achieve weight losses and HRQoL improvements that are greater than those experienced by patients who remain inactive and comparable to those attained by patients who stay active. Future randomized controlled trials should examine whether assisting patients who are inactive preoperatively to increase their PA postoperatively contributes to optimization of weight loss and HRQoL outcomes.

Pre- and postsurgery behavioral compliance, patient health, and postbariatric surgical weight loss.

Abstract: This study investigated the relationship between weight loss from gastric bypass surgery, patient characteristics, and compliance with physician instructions before and after surgery. A chart review of psychiatric and medical files was conducted for an initial cohort of 172 patients in a postsurgical management program. A total of 112 patients (primarily women (85%), white (79%), and well educated) from this cohort had presurgical data. Of these 112 subjects, 67 (60%) had postsurgical compliance information and BMI at 24 months postsurgery. The relationships between weight loss and a number of demographic, psychiatric, comorbid, and behavioral compliance factors were examined for these 67 patients. Missed appointments and noncompliance with exercise and weight loss plan instructions were high before and after surgery (65% vs. 72% for missed appointments, 39% vs. 51% for exercise, 42% vs. 57% for weight loss instructions). Although poor food choices were not frequently a problem before surgery (11%), they increased significantly after surgery: 37%, chi(2)(1) = 25.00, P < 0.001. Participants who lost the least weight at 2 years postsurgery were more likely to be nonwhite (r = 0.27, P = 0.039), have a lower socioeconomic status (SES) (r = 0.285, P = 0.02), and have a diagnosis of binge eating before surgery (r = 0.25, P = 0.039). Having more contact with patients and requiring adherence to behavioral changes, especially with respect to exercise and dietary restrictions, may improve the long-term outcomes for bariatric procedures. In addition, those patients who are depressed and suffer from binge eating may need special attention from physicians during long-term postoperative follow-up.

Sedentary Behavior and Obesity in a Large Cohort of Children

Abstract: The purpose of this study was to examine the association between sedentary behavior and obesity among 12-year-old children, while adjusting for moderate-to-vigorous physical activity (MVPA) and other potential confounding variables. Cross-sectional analyses were carried out with data from 5,434 children who participated in the Avon Longitudinal Study of Parents and Children (ALSPAC). Fat mass was derived using dual-energy X-ray emission absorptiometry, and height and weight measurements were used to calculate BMI (kg/m(2)). The children wore an accelerometer for 7 days. The cut points for sedentary behavior and MVPA were or=3,600 counts per minute (cpm), respectively. Logistic regression analyses were performed to estimate odds ratios (ORs), adjusting for potential confounders of physical activity that included gender, social factors, early life factors, and maturation. The minimally adjusted association between sedentary behavior and obesity was positive, OR = 1.18 (1.08, 1.28). After adjusting for the series of potential confounders of physical activity the positive association remained, OR = 1.32 (1.14, 1.53). The crude association between 15 min of MVPA per day and obesity was negative, OR = 0.54 (0.48, 0.62). When 15 min of MVPA per day was additionally controlled for in the models, the positive associations between sedentary behavior and obesity were negated. Sedentary behavior was positively associated with obesity in the 12-year-old children, but this association was not independent of MVPA; low levels of MVPA among the sedentary children increased the odds of obesity. These findings support the importance of specifically engaging in MVPA during childhood to reduce the prevalence of obesity.

Epicardial and pericardial fat: Close, but very different

Abstract: TO THE EDITOR: I read the article by Ding et al. titled “The Association of Pericardial Fat With Calcified Coronary Plaque” recently published in Obesity with great interest (1). The authors showed that the volume of pericardial fat around the coronary arteries, newly measured by computed tomography (CT), is independently associated with calcified coronary plaque (1). Although this is undoubtedly a finding of remarkable note, it seems that Ding et al. indifferently discussed about pericardial and epicardial fat, as these should be the identical adipose tissue. In fact, when they cited our articles on echocardiographic measurement of epicardial fat thickness (2,3) and other reports on the biomolecular aspects of epicardial fat (4), they erroneously referred it as pericardial fat. This is not just a tedious matter of terminology, but it is an incorrect and misleading concept. Pericardial fat has to be distinguished from the epicardial fat. Anatomically, epicardial and pericardial adipose tissue are clearly different (5,6). Epicardial fat is located between the outer wall of the myocardium and the visceral layer of pericardium. Pericardial fat is anterior to the epicardial fat and therefore located between visceral and parietal pericardium. Much of the importance within the epicardial fat is its anatomical closeness to the myocardium and the fact that the two tissues share the same microcirculation. As we and others have shown that epicardial fat is metabolically active and source of several adipokines, potential interactions through paracrine or vasocrine mechanisms between epicardial fat and myocardium are strongly suggested (5,6). This is clearly not true for the pericardial fat. However, pericardial fat could really modulate coronary arteries, as Ding et al. suggested, but it should be more correctly considered as paracardiac or perivascular fat (7). Biochemically epicardial and pericardial fat are different. In humans the evidences that the epicardial adipose tissue is an active endocrine organ are robust (5,6), whereas the role pericardial fat as source of adipokines is still partially unknown. Echocardiographically epicardial and pericardial fat thickness are different (2). For the anatomical and biomolecular features that I briefly reported above, we first proposed to measure the epicardial fat rather than the pericardial fat thickness. Epicardial fat is identified as the echo-free space between the outer wall of the myocardium and the visceral layer of pericardium. Pericardial fat thickness can be identified as the hypoechoic space anterior to the epicardial fat and parietal pericardium and it does not significantly change size during the cardiac cycle (2). Clinically epicardial and pericardial fat are different. We largely demonstrated the role of echocardiographic epicardial fat in predicting metabolic syndrome (8), visceral adiposity (2,3), heart morphology (9,10), insulin resistance (11), fasting glucose (12), subclinical atherosclerosis (13), liver enzymes (14), and in serving as accurate therapeutic target (15). Pericardial fat has not yet shown all these features. The article by Ding et al. may definitively open new avenues on the role of pericardial fat (1). I agree that echocardiography can provide only a linear measurement of epicardial fat and may be not accurate as CT. However echocardiographic assessment of epicardial visceral fat would certainly be less expensive CT and as echocardiography is routinely performed in high-risk cardiac patients, this objective noninvasive measure may be readily available at no extra cost. For all these reasons, the need to distinguish between epicardial and pericardial fat was compelling. If a body of evidences is suggesting that epicardial fat could play an active role as cardiometabolic risk factor, diagnostic tool and therapeutic target, further studies will be necessary to strengthen the role of pericardial fat.