Healthy Weight Individuals Research Articles

Intranasal oxytocin reduces attentional bias to food stimuli

Attentional biases to food-related stimuli have been demonstrated in response to hunger as well as during restrained eating. Such biases are often associated with obesity, but healthy-weight individuals who do not self-report hunger have also demonstrated attentional biases to stimuli signalling food using laboratory-based cognitive tasks. Levels of the anorectic neuropeptide oxytocin are elevated by food intake and, when administered intranasally, oxytocin inhibits food intake in the laboratory. To investigate whether oxytocin can affect appetite via an action on attentional processes, 40 adults (29 women; mean age 24.0 years old) self-administered 24 IU of oxytocin or placebo intranasally. Forty minutes after administration, participants ate a small snack to maintain alertness and ameliorate deprivation-induced hunger before starting a computerized dot-probe attentional bias task that presented 180 trials of paired visual stimuli comprising neutral, food, social and/or romantic images (500 ms presentation time). Reaction times to probe stimuli that appeared after the offset of the visual images indicated a significant attentional bias to food pictures after placebo; this effect was significantly attenuated by oxytocin, p < .001. The effect of oxytocin on attentional bias to the food pictures was not altered by the type of stimulus paired with the food image, and was independent of BMI, age, sex, self-rated eating behaviour, and self-reported parental bonding; however, the effect was modulated by self-reported food cravings and trait stress. The findings support and extend previous work which has suggested that oxytocin can counteract attentional biases to food-related stimuli in a sample with anorexia by demonstrating the same effect for the first time in a cohort who do not have an eating disorder.

Pain sensitivity does not differ between obese and healthy weight individuals.

There is emerging evidence suggesting a relationship between obesity and chronic pain. The aim of this study was to determine whether pain-free obese individuals display altered pain responses to acute noxious stimuli, thus raising the possibility of greater pain sensitivity and potential susceptibility for chronic pain development. Psychophysical and anthropometric data were collected from 38 individuals with an obese body mass index (BMI) classification (BMI ≥ 30) and 41 age/sex-matched individuals of a healthy BMI (BMI < 24.9). Because BMI may be an inaccurate index of obesity, additional anthropometric parameters of central adiposity and percent body fat were examined. Pain responses to suprathreshold noxious heat and cold stimuli were examined. Subjects provided pain intensity and unpleasantness ratings to noxious heat (49°C) applied at varying durations and locations (ventral forearm/lower leg). Cold pain ratings, thresholds, and tolerances were obtained after immersion of the hand in a cold-water bath (0-2°C). Between-group differences in pain responses, as well as relationships between pain responses and obesity parameters, were examined. Importantly, confounds that may influence pain such as anxiety, depression, impulsivity, sleepiness, and quality of life were assessed. No between-group differences in pain sensitivity to noxious heat and cold stimuli were found. No relationships were found between central adiposity or body fat (percentage or distribution) and pain responses to noxious heat or cold stimuli. Obesity has minimal influence on pain sensitivity. Accordingly, it is unlikely that obesity alone increases susceptibility for chronic pain development through amplification of nociceptive processes.

A Cohort Study Comparing Pediatric Patients with Overweight and Obesity in the Military Health System.

Background: National Health and Nutrition Examination Survey data from the 1960s to 2010s confirm that pediatric obesity rates are increasing. To assess obesity in the Military Health System (MHS), we evaluated a pediatric cohort's trends in BMI categorization from 2009 to 2016.Methods: We identified two age-based pediatric cohorts in the United States using the MHS Data Repository. We tracked them for BMI from 2009 to 2016. We calculated BMI percentiles and z-scores using validated growth charts, and biologically implausible BMI z-scores were removed from analyses. Using the Stuart-Maxwell test, we assessed the percent change in BMI categorization from 2009 to 2016 and stratified by age group.Results: Our cohort consisted of 130,675 pediatric patients (52.2% males and 47.8% females). The proportion in each BMI categorization changed significantly from 2009 to 2016 in all groups (p < 0.001). Increases in the Overweight and Moderate or Severe Obesity categories were observed in all age groups (2–5, 6–10, and 2–10), and increases in Obese were observed in 6–10-year olds. Most shifts occurred from healthy-weight individuals increasing in BMI category.Conclusions: We observed a significant increase in the proportion of children with overweight and obesity in a nationally representative MHS cohort from 2009 to 2016. The prevalence of obesity, but not overweight, in our cohort mirrored the civilian population. Increasingly heavier MHS and civilian children have implications for our future military force, as they are ineligible for military service if unable to meet weight standards.

Alterations in Brain Network Organization in Adults With Obesity as Compared With Healthy-Weight Individuals and Seniors.

Life expectancy and obesity rates have drastically increased in recent years. An unhealthy weight is related to long-lasting medical disorders that might compromise the normal course of aging. The aim of the current study of brain connectivity patterns was to examine whether adults with obesity would show signs of premature aging, such as lower segregation, in large-scale networks. Participants with obesity (n = 30, mean age = 32.8 ± 5.68 years) were compared with healthy-weight controls (n = 33, mean age = 30.9 ± 6.24 years) and senior participants who were stroke-free and without dementia (n = 30, mean age = 67.1 ± 6.65 years) using resting-state magnetic resonance imaging and graph theory metrics (i.e., small-world index, clustering coefficient, characteristic path length, and degree). Contrary to our hypothesis, participants with obesity exhibited a higher clustering coefficient compared with senior participants (t = 5.06, p < .001, d = 1.23, 95% CIbca = 0.64 to 1.88). Participants with obesity also showed lower global degree relative to seniors (t = -2.98, p = .014, d = -0.77, 95% CIbca = -1.26 to -0.26) and healthy-weight controls (t = -2.92, p = .019, d = -0.72, 95% CIbca = -1.19 to -0.25). Regional degree alterations in this group were present in several functional networks. Participants with obesity displayed greater network clustering than did seniors and also had lower degree compared with seniors and individuals with normal weight, which is not consistent with the notion that obesity is associated with premature aging of the brain. Although the cross-sectional nature of the study precludes causal inference, the overly clustered network patterns in obese participants could be relevant to age-related changes in brain function because regular networks might be less resilient and metabolically inefficient.

Metabolically Healthy/Unhealthy Overweight/Obesity Associations With Incident Heart Failure in Postmenopausal Women: The Women's Health Initiative.

Obesity is associated with an increased risk of heart failure (HF); however, how metabolic weight groups relate to HF risk, especially in postmenopausal women, has not been demonstrated. We included 19 412 postmenopausal women ages 50 to 79 without cardiovascular disease from the Women's Health Initiative. Normal weight was defined as a body mass index ≥18.5 and <25 kg/m2 and waist circumference <88 cm and overweight/obesity as a body mass index ≥25 kg/m2 or waist circumference ≥88 cm. Metabolically healthy was based on <2 and unhealthy ≥2 cardiometabolic traits: triglycerides ≥150 mg/dL, systolic blood pressure ≥130 mm Hg or diastolic blood pressure ≥85 mm Hg or blood pressure medication, fasting glucose ≥100 mg/dL or diabetes medication, and HDL-C (high-density lipoprotein cholesterol) <50 mg/dL. Risk factor-adjusted Cox regression examined the hazard ratios (HRs) for incident hospitalized HF among metabolically healthy normal weight (reference), metabolically unhealthy normal weight, metabolically healthy overweight/obese, and metabolically unhealthy overweight/obese. Among our sample, 455 (2.34%) participants experienced HF hospitalizations over a mean follow-up time of 11.3±1.1 years. Compared with metabolically healthy normal weight individuals, HF risk was greater in metabolically unhealthy normal weight (HR, 1.66 [95% CI, 1.01-2.72], P=0.045) and metabolically unhealthy overweight/obese individuals (HR, 1.95 [95% CI, 1.35-2.80], P=0.0004), but not metabolically healthy overweight/obese individuals (HR, 1.15 [95% CI, 0.78-1.71], P=0.48). Subdividing the overweight/obese into separate groups showed HRs for metabolically unhealthy obese of 2.62 (95% CI, 1.80-3.83; P<0.0001) and metabolically healthy obese of 1.52 (95% CI, 0.98-2.35; P=0.06). Metabolically unhealthy overweight/obese and metabolically unhealthy normal weight are associated with an increased risk of HF in postmenopausal women.

Metabolically healthy obesity and risk of stroke: a meta-analysis of prospective cohort studies.

BackgroundMetabolic healthy obesity (MHO) is a unique subgroup of overweight and obese individuals with normal metabolic characteristics. Its association with the risk of stroke remains unclear. We aimed to examine the risk of stroke in MHO individuals and the further associations between stroke and metabolic abnormalities under different bodyweight conditions.MethodsWe systematically searched PubMed, Embase and Cochrane Library from December 1946 to January 2019, and only included prospective cohort studies. Random effects models were used to evaluate the pooled risk ratios (RR) and 95% confidence intervals (95% CI) of incident stroke.ResultsA total of eight studies comprising 4,256,888 participants were included in the meta-analysis. MHO individuals had an increased risk of stroke compared with metabolically healthy normal weight (MH-NW) individuals (RR =1.17, 95% CI: 1.11–1.23). However, the stroke risk of metabolically healthy overweight individuals was the same (RR =1.02, 95% CI: 0.84–1.23). All groups with unhealthy metabolism had a similarly elevated risk: normal weight (RR =1.83, 95% CI: 1.57–2.14), overweight (RR =1.93, 95% CI: 1.44–2.58), and obesity (RR =2.00, 95% CI: 1.40–2.87).ConclusionsThe meta-analysis confirms a positive association between MHO phenotype and the risk of stroke. Individuals with metabolic abnormalities under different bodyweight conditions are at elevated risk.

The self-perceived body size in obesity: Evidence from the implicit representation of the hand.

To locate our body in the space, we rely on an implicit representation of body size and shape: the body model. Evidence about the implicit representation of bodily dimensions in obesity is rare. Nevertheless, it seems to suggest that such representation is not altered in obesity compared to healthy weight individuals. To probe further this hypothesis, we investigated the implicit representation of hand dimensions with a landmark localisation task, comparing individuals with obesity and healthy weight individuals. Furthermore, as body model distortions may be related to tactile acuity, the tactile acuity threshold was measured using a two-point discrimination task. In accordance with the previous evidence, we observed that healthy weight participants showed a significant underestimation of finger length and overestimation of hand width. Interestingly, comparable body model distortions were shown also in participants with obesity. No differences in tactile acuity emerged between the two groups; also, when considering the whole sample, as tactile acuity decreases hand width overestimation increases. Thus, obesity seems to have no effect on the characteristics of the body model relative to the hand. Accordingly, the physiological mechanisms supporting the development of the implicit representation of hand dimensions in the healthy weight population may be preserved in obesity.

Dysregulation of endocannabinoid concentrations in human subcutaneous adipose tissue in obesity and modulation by omega-3 polyunsaturated fatty acids.

Obesity is believed to be associated with a dysregulated endocannabinoid system which may reflect enhanced inflammation. However, reports of this in human white adipose tissue (WAT) are limited and inconclusive. Marine long-chain omega-3 polyunsaturated fatty acids (LC n-3 PUFAs) have anti-inflammatory actions and therefore may improve obesity-associated adipose tissue inflammation. Therefore, fatty acid (FA) concentrations, endocannabinoid concentrations, and gene expression were assessed in subcutaneous WAT (scWAT) biopsies from healthy normal weight individuals (BMI 18.5-25 kg/m2) and individuals living with metabolically healthy obesity (BMI 30-40 kg/m2) prior to and following a 12-week intervention with 3 g fish oil/day (1.1 g eicosapentaenoic acid (EPA) + 0.8 g DHA) or 3 g corn oil/day (placebo). WAT from individuals living with metabolically healthy obesity had higher n-6 PUFAs and EPA, higher concentrations of two endocannabinoids (anandamide (AEA) and eicosapentaenoyl ethanolamide (EPEA)), higher expression of phospholipase A2 Group IID (PLA2G2D) and phospholipase A2 Group IVA (PLA2G4A), and lower expression of CNR1. In response to fish oil intervention, WAT EPA increased to a similar extent in both BMI groups, and WAT DHA increased by a greater extent in normal weight individuals. WAT EPEA and docosahexaenoyl ethanolamide (DHEA) increased in normal weight individuals only and WAT 2-arachidonyl glycerol (2-AG) decreased in individuals living with metabolically healthy obesity only. Altered WAT fatty acid, endocannabinoid, and gene expression profiles in metabolically healthy obesity at baseline may be linked. WAT incorporates n-3 PUFAs when their intake is increased which affects the endocannabinoid system; however, effects appear greater in normal weight individuals than in those living with metabolically healthy obesity.

Impact of obesity and SARS-CoV-2 infection: implications for host defence - a living review.

The role of obesity in the pathophysiology of respiratory virus infections has become particularly apparent during the current severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, where obese patients are twice as likely to suffer from severe coronavirus disease 2019 (COVID-19) than healthy weight individuals. Obesity results in disruption of systemic lipid metabolism promoting a state of chronic low-grade inflammation. However, it remains unclear how these underlying metabolic and cellular processes promote severe SARS-CoV-2 infection. Emerging data in SARS-CoV-2 and Influenza A virus (IAV) infections show that viruses can further subvert the host’s altered lipid metabolism and exploit obesity-induced alterations in immune cell metabolism and function to promote chronic inflammation and viral propagation. In this review, we outline the systemic metabolic and immune alterations underlying obesity and discuss how these baseline alterations impact the immune response and disease pathophysiology. A better understanding of the immunometabolic landscape of obese patients may aid better therapies and future vaccine design.

MiR-125b-2 knockout increases high-fat diet-induced fat accumulation and insulin resistance

Obese individuals are more susceptible to comorbidities than individuals of healthy weight, including cardiovascular disease and metabolic disorders. MicroRNAs are a class of small and noncoding RNAs that are implicated in the regulation of chronic human diseases. We previously reported that miR-125b plays a critical role in adipogenesis in vitro. However, the involvement of miR-125b-2 in fat metabolism in vivo remains unknown. In the present study, miR-125b-2 knockout mice were generated using CRISPR/CAS9 technology, resulting in mice with a 7 bp deletion in the seed sequence of miR-125b-2. MiR-125b-2 knockout increased the weight of liver tissue, epididymal white fat and inguinal white fat. MiR-125b-2 knockout also increased adipocyte volume in HFD-induced obese mice, while there were no significant differences in body weight and feed intake versus mice fed a normal diet. Additionally, qRT-PCR and western blot analysis revealed that the expression of the miR-125b-2 target gene SCD-1 and fat synthesis-associated genes, such as PPARγ and C/EBPα, were significantly up-regulated in miR-125b-2KO mice (P < 0.05). Moreover, miR-125b-2KO altered HFD-induced changes in glucose tolerance and insulin resistance. In conclusion, we show that miR-125b-2 is a novel potential target for regulating fat accumulation, and also a candidate target to develop novel treatment strategies for obesity and diabetes.

Branched-Chain Amino Acid Oxidation Is Elevated in Adults with Morbid Obesity and Decreases Significantly after Sleeve Gastrectomy

Plasma concentrations of branched-chain amino acids (BCAAs) are elevated in obese individuals with insulin resistance (IR) and decrease after bariatric surgery. However, the metabolic mechanisms are unclear. Our objectives are to compare leucine kinetics between morbidly obese and healthy-weight individuals cross-sectionally, and to prospectively evaluate changes in the morbidly obese after sleeve gastrectomy. We hypothesized that leucine oxidation is slower in obese individuals and increases after surgery. Ten morbidly obese [BMI (in kg/m2)≥32.5, age 21-50 y] and 10 healthy-weight participants (BMI <25), matched for age (median ∼30 y) but not gender, were infused with [U-13C6] leucine and [2H5] glycerol to quantify leucine and glycerol kinetics. Morbidly obese participants were studied again 6 mo postsurgery. Primary outcomes were kinetic parameters related to BCAA metabolism. Data were analyzed by nonparametric methods and presented as median (IQR). Participants with obesity had IR with an HOMA-IR (4.89; 4.36-8.76) greater than that of healthy-weight participants (1.32; 0.99-1.49; P <0.001) and had significantly faster leucine flux [218; 196-259 compared with 145; 138-149 μmol · kg fat-free mass (FFM)-1 · h-1], oxidation (24.0; 17.9-29.8 compared with 16.1; 14.3-18.5 μmol · kg FFM-1 · h-1), and nonoxidative disposal (204; 190-247 compared with 138; 129-140 μmol · kg FFM-1 · h-1) (P <0.017 for all). After surgery, the morbidly obese had a marked improvement in IR (3.54; 3.06-6.08; P=0.008) and significant reductions in BCAA concentrations (113; 95-157 μmol/L) and leucine oxidation (9.37; 6.85-15.2 μmol · kg FFM-1 · h-1) (P=0.017 for both). Further, leucine flux in this group correlated significantly with IR (r=0.78, P <0.001). BCAA oxidation is not impaired but elevated in individuals with morbid obesity. Plasma BCAA concentrations are lowered after surgery owing to slower breakdown of body proteins as insulin's ability to suppress proteolysis is restored. These findings suggest that IR is the underlying cause and not the consequence of elevated BCAAs in obesity.

Copy number variant analysis and expression profiling of the olfactory receptor-rich 11q11 region in obesity predisposition

Genome-wide copy number surveys associated chromosome 11q11 with obesity. As this is an olfactory receptor-rich region, we hypothesize that genetic variation in olfactory receptor genes might be implicated in the pathogenesis of obesity. Multiplex Amplicon Quantification analysis was applied to screen for copy number variants at chromosome 11q11 in 627 patients with obesity and 330 healthy-weight individuals. A ± 80 kb deletion with an internally 1.3 kb retained segment was identified, covering the three olfactory receptor genes OR4C11, OR4P4, and OR4S2. A significant increase in copy number loss(es) was perceived in our patient cohort (MAF = 27%; p = 0.02). Gene expression profiling in metabolic relevant tissues was performed to evaluate the functional impact of the obesity susceptible locus. All three 11q11 genes were present in visceral and subcutaneous adipose tissue while no expression was perceived in the liver. These results support the ‘metabolic system’ hypothesis and imply that gene disruption of OR4C11, OR4P4, and OR4S2 will negatively influence energy metabolism, ultimately leading to fat accumulation and obesity. Our study thus demonstrates a role for structural variation within olfactory receptor-rich regions in complex diseases and defines the 11q11 deletion as a risk factor for obesity.

Prior ingestion of a ketone monoester supplement reduces postprandial glycemic responses in young healthy-weight individuals.

The main objective of this study was to determine whether acute ingestion of a ketone monoester (KME) supplement impacted mixed-meal tolerance test (MMTT) glucose area under the curve (AUC). Nineteen healthy young volunteers (10 males/9 females; age, 24.7 ± 4.9 years; body mass index, 22.7 ± 2.4 kg/m2) participated in a double-blind, placebo-controlled crossover study. Following overnight fasting (≥10 h), participants consumed 0.45 mL/kg of a KME supplement or taste-matched placebo followed by an MMTT 15 min later. Blood samples were collected every 15-30 min over 2.5 h. KME supplementation acutely raised β-hydroxybutyrate AUC (590%, P < 0.0001, d = 2.4) and resulted in decreases in blood glucose AUC (-9.4%, P = 0.03, d = 0.56) and nonesterified fatty acid (NEFA) AUC (-27.3%, P = 0.023, d = 0.68) compared with placebo. No differences were found for plasma insulin AUC (P = 0.70) or gastric emptying estimated by co-ingested acetaminophen AUC (P = 0.96) between ketone and placebo. Overall, results indicate that KME supplementation attenuates postprandial glycemic and NEFA responses when taken 15 min prior to a mixed meal in young healthy individuals. Future studies are warranted to investigate whether KME supplementation may benefit individuals with impaired glycemic control. Novelty: Acute ketone monoester supplementation 15 min prior to a mixed meal decreased postprandial glucose and NEFA levels without significantly impacting postprandial insulin or estimates of gastric emptying. Glucose- and NEFA-lowering effects of ketone monoester supplementation are apparently not mediated by changes in insulin release or gastric emptying.

Reduced Temporal Sensitivity in Obesity: Evidence From a Simultaneity Judgement Task.

Preliminary evidence showed a reduced temporal sensitivity (i.e., larger temporal binding window) to audiovisual asynchrony in obesity. Our aim was to extend this investigation to visuotactile stimuli, comparing individuals of healthy weight and with obesity in a simultaneity judgment task. We verified that individuals with obesity had a larger temporal binding window than healthy-weight individuals, meaning that they tend to integrate visuotactile stimuli over an extended range of stimulus onset asynchronies. We point out that our finding gives evidence in support of a more pervasive impairment of the temporal discrimination of co-occurrent stimuli, which might affect multisensory integration in obesity. We discuss our results referring to the possible role of atypical oscillatory neural activity and structural anomalies in affecting the perception of simultaneity between multisensory stimuli in obesity. Finally, we highlight the urgency of a deeper understanding of multisensory integration in obesity at least for two reasons. First, multisensory bodily illusions might be used to manipulate body dissatisfaction in obesity. Second, multisensory integration anomalies in obesity might lead to a dissimilar perception of food, encouraging overeating behaviours.

Variability of Sleep and Relations to Body Weight Among First-Year College Students.

Existing research suggests that greater sleep variability may increase risk for weight gain. College often marks a transition to a less consistent daily schedule, which may adversely impact sleep routines and further increase risk for weight gain. The current study is among the first to explore relations between nighttime sleep variability and daytime sleep (napping) and body weight among first-year college students. Using daily diary methods, first-year college students (N = 307; 84.7% female) self-reported their sleep for seven days. Several indices were created to capture sleep variability for reported bedtime, wake time, and sleep duration, including weekday versus weekend differences (WvW), day to day differences (D2D), and overall standard deviation (SD). Napping was also assessed. Based on body mass index (BMI), individuals were categorized as underweight, healthy weight, overweight, and obese. Across indices, students' sleep varied over an hour on average across the week. Hierarchical regressions revealed that greater differences in wake time D2D, wake time SD, and sleep duration WvW were all associated with higher BMI, after accounting for gender, depressive symptoms, and sleep duration. Longer napping was also associated with higher BMI, using the same covariates. Finally, greater sleep variability was reported by overweight and obese than healthy weight individuals. These findings suggest that sleep variability, particularly wake times and napping may be important modifiable sleep behaviors to investigate in future studies. More longitudinal research is needed to explore relations between multiple facets of sleep variability and weight gain, including possible mechanisms.

Compact Development and BMI for Young Adults

Problem, research strategy, and findings: The literature widely reports a statistical association between the built environment and obesity. What is less clear is the reason for the association. Is it environmental determinism—the effect of the built environment on individual behavior—with compact places inducing more physical activity and hence lower weight? Or is it self-selection, the tendency of healthy-weight individuals to select to live in compact places where they can be more physically active and possibly the tendency of overweight or obese individuals to opt for sprawling places? Both theories have been promoted in the literature. In this study we seek to address this issue using data from the National Longitudinal Survey of Youth. We study body mass indices (BMIs) of survey participants, all young adults, at two points in time and follow them longitudinally for 9 years as they move from place to place. We estimate models for the entire cohort and also for young adult movers and stayers separately. We find more evidence of self-selection than of environmental determinism. First, we find that compactness is not significantly associated with BMI in young adults for those staying in the same place for the entire period. Second, we find no significant association between changes in sprawl and the changes in BMI for the cohort of young adult movers. Third, our longitudinal analysis shows that young adults who are not overweight tend to move in the direction of greater neighborhood compactness, whereas overweight young adults tend to move in the direction of greater sprawl. Because young adults are at a unique stage in the life cycle, these findings cannot be generalized to other cohorts.Takeaway for practice: These findings do not suggest that place characteristics are unimportant; planners need to meet the growing demand for walkable, compact, and connected places, which are currently undersupplied. Still, they do not provide evidence that place characteristics influence the behaviors of young adults and hence their weight. Rather, they suggest that compact places appeal to more than half of the young adult population and that this latent demand should be met by providing dense, diverse, and well-designed residential options, even in the suburbs, through regional transportation plans and local planning and zoning. Education for primary and secondary school students, who are about to enter young adulthood, could also play a role.

Influence of hunger on attentional engagement with and disengagement from pictorial food cues in women with a healthy weight

Because of inconsistencies in the field of attentional bias to food cues in eating behavior, this study aimed to re-examine the assumption that hungry healthy weight individuals have an attentional bias to food cues, but satiated healthy weight individuals do not. Since attentional engagement and attentional disengagement have been proposed to play a distinct role in behavior, we used a performance measure that is specifically designed to differentiate between these two attentional processes. Participants were healthy weight women who normally eat breakfast. In the satiated condition (n = 54), participants were instructed to have breakfast just before coming to the lab. In the fasted condition (n = 50), participants fasted on average 14 h before coming into the lab. Satiated women showed no stronger attentional engagement or attentional disengagement bias to food cues than to neutral cues. Fasted women did show stronger attentional engagement to food cues than to neutral cues that were shown briefly (100 ms). They showed no bias in attentional engagement to food cues that were shown longer (500 ms) or in attentional disengagement from food cues. These findings are in line with the assumption that healthy weight individuals show an attentional bias to food cues when food stimuli are motivationally salient. Furthermore, the findings point to the importance of differentiating between attentional engagement and attentional disengagement.

Food cue recruits increased reward processing and decreased inhibitory control processing in the obese/overweight: An activation likelihood estimation meta-analysis of fMRI studies

IntroductionGrowing researches have shown that obese/overweight and healthy weight individuals exhibit different neural responses to food-related stimuli. Accordingly, researchers proposed several theories to explain these differences. Hereon, meta-analyses were conducted using activation likelihood estimation (ALE) to verify these theories and specify the reason of overeating from two aspects. Materials and MethodsPubmed, Web of Science and Neurosynth were searched for the current study and screened according to inclusion criteria. Firstly, neural responses to visual food cues versus non-food images were compared between obese/overweight and healthy weight individuals. Then, neural activation to high-calorie food images versus low-calorie food/non-food visual stimuli was further investigated among the two populations. Coordinates in included studies were recorded and analysed by Ginger ALE software under threshold at uncorrected p < 0.001 with cluster-level p < 0.05 (cFWE). ResultsEleven and seven studies were found in the first and second set of meta-analysis, respectively. The first meta-analysis showed that obese/overweight have hyper-responsivity in reward area and hypo-responsivity in both gustatory processing and inhibitory control area. The second meta-analysis indicated that the reward responsivity in the obese/overweight individuals was amplified and healthy weight individuals had higher activation in areas associated with gustatory processing in response to high-calorie food images. ConclusionsOur results showed that the obese/overweight exhibit hyper-responsivity in brain regions involved in reward processing for visual food cue which provide strong support for incentive-sensitization theory of obesity and healthy weight individuals showed higher response in inhibitory control region which support the inhibitory control deficit theory of obesity.

A correlation-based network for biomarker discovery in obesity with metabolic syndrome

BackgroundObesity is associated with chronic activation of the immune system and an altered gut microbiome, leading to increased risk of chronic disease development. As yet, no biomarker profile has been found to distinguish individuals at greater risk of obesity-related disease. The aim of this study was to explore a correlation-based network approach to identify existing patterns of immune-microbiome interactions in obesity.ResultsThe current study performed correlation-based network analysis on five different datasets obtained from 11 obese with metabolic syndrome (MetS) and 12 healthy weight men. These datasets included: anthropometric measures, metabolic measures, immune cell abundance, serum cytokine concentration, and gut microbial composition. The obese with MetS group had a denser network (total number of edges, n = 369) compared to the healthy network (n = 299). Within the obese with MetS network, biomarkers from the immune cell abundance group was found to be correlated to biomarkers from all four other datasets. Conversely in the healthy network, immune cell abundance was only correlated with serum cytokine concentration and gut microbial composition. These observations suggest high involvement of immune cells in obese with MetS individuals. There were also three key hubs found among immune cells in the obese with MetS networks involving regulatory T cells, neutrophil and cytotoxic cell abundance. No hubs were present in the healthy network.ConclusionThese results suggest a more complex interaction of inflammatory markers in obesity, with high connectivity of immune cells in the obese with MetS network compared to the healthy network. Three key hubs were identified in the obese with MetS network, involving Treg, neutrophils and cytotoxic cell abundance. Compared to a t-test, the network approach offered more meaningful results when comparing obese with MetS and healthy weight individuals, demonstrating its superiority in exploratory analysis.

The association between obesity and lower working memory is mediated by inflammation: Findings from a nationally representative dataset of U.S. adults

Obesity is often accompanied by lower working memory (e.g., a lower ability to keep goal-relevant information in mind) relative to healthy weight individuals. Understanding this relative working memory impairment has important clinical implications, as working memory is thought to facilitate adherence to weight management programs. Theoretical models of obesity, self-regulation, and inflammation suggest that inflammation plays a role in obesity-related working memory impairments, but to date no study has tested this prediction. Therefore, the current study examined whether inflammation statistically mediated the relationship between obesity and working memory in a nationally representative dataset of U.S. adults from Wave IV of The National Longitudinal Study of Adolescent to Adult Health (N = 11,546, age range 25–34). Inflammation was quantified via C-reactive protein (CRP) level, and working memory was assessed using a modified digit span backward task. As expected, cross-sectional analyses showed that a body mass index (BMI) indicative of obesity—as well as greater BMI when BMI was analyzed continuously—and greater CRP were each related to lower working memory. Critically, we found that CRP levels statistically mediated the relationships between obesity/greater BMI and working memory, with CRP accounting for 44.1% of the variance explained in working memory by BMI. Moreover, these findings held both with and without controlling for relevant covariates, including demographic characteristics (e.g., age), socioeconomic status, and behavioral factors (e.g., smoking). Our results therefore point to inflammation as playing an important role in the relationship between obesity and working memory, and suggest that interventions aimed at reducing inflammation may help lessen the cognitive burden of obesity.