Correction: Appetite disinhibition rather than hunger explains genetic effects on adult BMI trajectory.
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ABSTRACT:
SUBMITTER: Brunner EJ
PROVIDER: S-EPMC7906901 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Background/objectivesThe mediating role of eating behaviors in genetic susceptibility to weight gain during mid-adult life is not fully understood. This longitudinal study aims to help us understand contributions of genetic susceptibility and appetite to weight gain.Subjects/methodsWe followed the body-mass index (BMI) trajectories of 2464 adults from 45 to 65 years of age by measuring weight and height on four occasions at 5-year intervals. Genetic risk of obesity (gene risk score: GRS) was ascertained, comprising 92 BMI-associated single-nucleotide polymorphisms and split at a median (=high and low risk). At the baseline, the Eating Inventory was used to assess appetite-related traits of 'disinhibition', indicative of opportunistic eating or overeating and 'hunger' which is susceptibility to/ability to cope with the sensation of hunger. Roles of the GRS and two appetite-related scores for BMI trajectories were examined using a mixed model adjusted for the cohort effect and sex.ResultsDisinhibition was associated with higher BMI (β = 2.96; 95% CI: 2.66-3.25 kg/m2), and accounted for 34% of the genetically-linked BMI difference at age 45. Hunger was also associated with higher BMI (β = 1.20; 0.82-1.59 kg/m2) during mid-life and slightly steeper weight gain, but did not attenuate the effect of disinhibition.ConclusionsAppetite disinhibition is most likely to be a defining characteristic of genetic susceptibility to obesity. High levels of appetite disinhibition, rather than hunger, may underlie genetic vulnerability to obesogenic environments in two-thirds of the population of European ancestry.
| S-EPMC8005371 | biostudies-literature
Project description:BackgroundHigher energy expenditure (EE) is associated with greater food intake, possibly because the human body senses EE and modifies eating behaviors to regulate food intake and ultimately achieve energy balance. As eating behaviors are also influenced by social and cultural factors, any association between EE and eating behavior may differ between ethnicities and sexes.ObjectiveTo assess relationships between EE and eating behavior constructs of the Three-Factor Eating Questionnaire (TFEQ).Subjects/methodsIn all, 307 healthy adults (201 M/106 F, 160 Native Americans) completed the TFEQ and had measures of 24-h EE in a whole-room calorimeter during energy balance. Body composition was assessed by DXA.ResultsOn average, adjusted 24-h EE was lower (β = -229 kcal/day, CI: -309 to -148, p < 0.001) but cognitive restraint (Δ = + 1.5; CI: 0.5 to 2.5, p = 0.003) and disinhibition (Δ = + 2.1, CI: 1.3 to 2.8, p < 0.001) scores were higher in women compared with men. In Native Americans, adjusted 24-h EE (β = + 94 kcal/day, CI: 48 to 139, p < 0.001) and disinhibition scores (Δ = + 1.0, CI: 0.1 to 2.0, p = 0.003) were higher compared with other ethnicities. Higher 24-h EE associated with lower cognitive restraint in women (ρ = -0.20, p = 0.04), but not men (p = 0.71; interaction term p = 0.01) with no ethnic differences. Greater 24-h EE associated with higher disinhibition (ρ = 0.20, p = 0.001) and hunger cues (ρ = 0.16, p = 0.004) with no gender differences. These associations were primarily present in non-Native Americans (ρ = 0.23, p = 0.006 and ρ = 0.25, p = 0.003) but not observed in Native Americans (both p > 0.40).ConclusionsHigher EE is associated with psychological constructs of eating behaviors that favors overeating including lower cognitive restraint, higher dietary disinhibition, and greater susceptibility to hungers cues, supporting the existence of energy-sensing mechanisms influencing human eating behavior. These associations were observed in ethnicities other than Native Americans, possibly explaining the contradictory relationships reported between EE and weight change in different ethnic groups. We propose that increased EE may alter eating behaviors, potentially leading to uncontrolled overeating and weight gain.
| S-EPMC6610661 | biostudies-literature
Project description:Little is known about the genetic influence on BMI trajectory throughout adulthood. We created a genetic risk score (GRS) comprising 97 adult BMI-associated variants among 9,971 women and 6,405 men of European ancestry. Serial measures of BMI were assessed from 18 (women) or 21 (men) years to 85 years of age. We also examined BMI change in early (from 18 or 21 to 45 years of age), middle (from 45 to 65 years of age), and late adulthood (from 65 to 80 years of age). GRS was positively associated with BMI across all ages, with stronger associations in women than in men. The associations increased from early to middle adulthood, peaked at 45 years of age in men and at 60 years of age in women (0.91 and 1.35 kg/m2 per 10-allele increment, respectively) and subsequently declined in late adulthood. For women, each 10-allele increment in the GRS was associated with an average BMI gain of 0.54 kg/m2 in early adulthood, whereas no statistically significant association was found for BMI change in middle or late adulthood or for BMI change in any life period in men. Our findings indicate that genetic predisposition exerts a persistent effect on adiposity throughout adult life and increases early adulthood weight gain in women.
| S-EPMC5780056 | biostudies-literature
Project description:Chronic circadian disruption (CCD), such as occurs during rotating shiftwork, and insufficient sleep are each independently associated with poor health outcomes, including obesity and glucose intolerance. A potential mechanism for poor health is increased energy intake (i.e., eating), particularly during the circadian night, when the physiological response to energy intake is altered. However, the contributions of CCD and insufficient sleep to subjective hunger, appetite, food preference, and appetitive hormones are not clear. To disentangle the influences of these factors, we studied seventeen healthy young adults in a 32-day in-laboratory study designed to distribute sleep, wakefulness, and energy intake equally across all phases of the circadian cycle, thereby imposing CCD. Participants were randomized to the Control (1:2 sleep:wake ratio, n = 8) or chronic sleep restriction (CSR, 1:3.3 sleep:wake ratio, n = 9) conditions. Throughout each waking episode the participants completed visual analog scales pertaining to hunger, appetite, and food preference. A fasting blood sample was collected to assess appetitive hormones. CCD was associated with a significant decrease in hunger and appetite in a multitude of domains in both the Control and CSR groups. This change in hunger was significantly correlated with changes in the ghrelin/leptin ratio. These findings further our understanding of the contributions of CCD and insufficient sleep on subjective hunger and appetite as well as of their possible contributions to adverse health behaviors.
| S-EPMC9105437 | biostudies-literature
Project description:Food homeostatic states (hunger and satiety) influence the cognitive systems regulating impulsive responses, but the direction and specific mechanisms involved in this effect remain elusive. We examined how fasting, and satiety, affect cognitive mechanisms underpinning disinhibition using a novel framework and a gamified test-battery. Thirty-four participants completed the test-battery measuring three cognitive facets of disinhibition: attentional control, information gathering and monitoring of feedback, across two experimental sessions: one after overnight fasting and another after a standardised meal. Homeostatic state was assessed using subjective self-reports and biological markers (i.e., blood-derived liver-expressed antimicrobial protein 2 (LEAP-2), insulin and leptin). We found that participants who experienced greater subjective hunger during the satiety session were more impulsive in the information gathering task; results were not confounded by changes in mood or anxiety. Homeostatic state did not significantly influence disinhibition mechanisms linked to attentional control or feedback monitoring. However, we found a significant interaction between homeostatic state and LEAP-2 on attentional control, with higher LEAP-2 associated with faster reaction times in the fasted condition only. Our findings indicate lingering hunger after eating increases impulsive behaviour via reduced information gathering. These findings identify a novel mechanism that may underpin the tendency to overeat and/or engage in broader impulsive behaviours.
| S-EPMC8230368 | biostudies-literature
Project description:BackgroundBody mass index (BMI) has been shown to be associated with lung function. Recent findings showed that DNA methylation (DNAm) variation is likely to be a consequence of changes in BMI. However, whether DNAm mediates the association of BMI with lung function is unknown. We examined the mediating role of DNAm on the association of pre-adolescent BMI trajectories with post-adolescent and adulthood lung function (forced expiratory volume (FEV1), forced vital capacity (FVC), and FEV1/FVC).MethodsAnalyses were undertaken in the Isle of Wight birth cohort (IOWBC). Group-based trajectory modelling was applied to infer latent BMI trajectories from age 1 to 10 years. An R package, ttscreening, was applied to identify CpGs at 10 years potentially associated with BMI trajectories for each sex. Linear regressions were implemented to further screen CpGs for their association with lung function at 18 years. Path analysis, stratified by sex, was applied to each screened CpG to assess its role of mediation. Internal validation was applied to further examine the mediation consistency of the detected CpGs based on lung function at 26 years. Mendelian randomization (MR-base) was used to test possible causal effects of the identified CpGs.ResultsTwo BMI trajectories (high vs. low) were identified. Of the 442,475 CpG sites, 18 CpGs in males and 33 in females passed screening. Eight CpGs in males and 16 CpGs in females (none overlapping) were identified as mediators. For subjects with high BMI trajectory, high DNAm at all CpGs in males were associated with decreased lung function, while 8 CpGs in females were associated with increased lung function at 18 years. At 26 years, 6 CpGs in males and 14 CpGs in females showed the same direction of indirect effects as those at 18 years. DNAm at CpGs cg19088553 (GRIK2) and cg00612625 (HPSE2) showed a potential causal effect on FEV1.ConclusionsThe effects of BMI trajectory in early childhood on post-adolescence lung function were likely to be mediated by pre-adolescence DNAm in both males and females, but such mediation effects were likely to diminish over time.
| S-EPMC9335987 | biostudies-literature
Project description:IntroductionChildhood maltreatment is associated with later obesity, but the underlying mechanisms are unknown. The objective of this study was to estimate the extent to which depression mediates the associations between childhood maltreatment and BMI in adolescence through adulthood.MethodsData on a cohort of 13,362 adolescents in the National Longitudinal Study of Adolescent to Adult Health (Wave I [1994-1995] to Wave IV [2008-2009]) were analyzed in 2015-2016. Classes of maltreatment experienced prior to age 12 years were statistically identified using latent class analysis. Gender-stratified latent growth curve analysis was used to estimate total effects of maltreatment classes on latent BMI trajectory (aged 13-31 years) and indirect effects of maltreatment classes that occurred through latent depression trajectory (aged 12-31 years).ResultsFour latent maltreatment classes were identified: high abuse and neglect; physical abuse dominant; supervisory neglect dominant; and no/low maltreatment. In girls, compared with no/low maltreatment, supervisory neglect dominant (coefficient=0.3, 95% CI=0.0, 0.7) and physical abuse dominant (coefficient=0.6, 95% CI=0.1, 1.2) maltreatment were associated with faster gain in BMI. Change in depression over time fully mediated the association of BMI slope with physical abuse dominant maltreatment, but not with supervisory neglect dominant maltreatment. In boys, high abuse and neglect maltreatment was associated with marginally greater BMI at baseline (coefficient=0.7, 95% CI= -0.1, 1.5); this association was not mediated by depression.ConclusionsAlthough maltreatment was associated with depression and BMI trajectories from adolescence to adulthood, depression only mediated associations with physical abuse dominant maltreatment in girls.
| S-EPMC5679065 | biostudies-literature
Project description:ObjectiveProspective studies on relationships between hedonic hunger and BMI (Body Mass Index) during weight management are lacking. This study examined if hedonic hunger reduced during a behavioural weight management programme, and if hedonic hunger predicted future BMI.MethodsParticipants were 594 community-dwelling, UK-based adults(396 female; age 56.43 years, s.d. = 12.50, range 20-83 years); 490 participants (82.5%) had obesity. Participants were randomised to a 12- or 52-week behavioural weight management intervention (WW12 or WW52, respectively) or a brief self-help intervention (BI). Relationships between hedonic hunger and BMI over 24 months (baseline, 3, 12, 24 months) were analysed using an autoregressive cross-lagged model.ResultsHedonic hunger scores decreased from 2.71 (s.d. = .91) at baseline to 2.41 (s.d. = .88) at 3 months (p < .001, CI .22 to .38), remained reduced to 24 months, and were not affected by intervention arm at any time point (p's>.05). Baseline hedonic hunger scores predicted 3-month scores (B = .76, SE = .03, p < .001, CI .71 to .82), 3-month scores predicted 12-month scores (B = .76, SE = .03, p < .001 CI .72 to .80), and 12-month scores predicted 24-month scores (B = .72, SE = .03, p < .001, CI .64 to .77). Higher hedonic hunger at 3 months predicted higher BMI at 12 months (B = .04, SE = .02, p = .03, CI .01 to .07) but not at 24 months (p>.05). BMI at 12 months was lower in WW52 30.87kg/m2, s.d. = 5.02) than WW12 (32.12 kg/m2, s.d. = 5.58, p = .02, CI .16 to 2.34) and BI (32.74 kg/m2, s.d. = 4.15, p = .01, CI .30 to 3.45). BMI was not affected by intervention at any other time point (p's>.05).ConclusionHedonic hunger reduced during weight management irrespective of intervention. Early reductions in hedonic hunger appear to be associated with lower BMI in the medium-term. Identifying ways to reduce hedonic hunger during weight loss could aid weight management for some people.
| S-EPMC8189467 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-12-06 | GSE190168 | GEO
Project description:The present study examined the role of cardiovascular regulation in predicting pediatric obesity. Participants for this study included 268 children (141 girls) obtained from a larger ongoing longitudinal study. To assess cardiac vagal regulation, resting measures of respiratory sinus arrhythmia (RSA) and RSA change (vagal withdrawal) to three cognitively challenging tasks were derived when children were 5.5 years of age. Heart period (HP) and HP change (heart rate (HR) acceleration) were also examined. Height and weight measures were collected when children were 5.5, 7.5, and 10.5 years of age. Results indicated that physiological regulation at age 5.5 was predictive of both normal variations in BMI development and pediatric obesity at age 10.5. Specifically, children with a cardiovascular regulation profile characterized by lower levels of RSA suppression and HP change experienced significantly greater levels of BMI growth and were more likely to be classified as overweight/at-risk for overweight at age 10.5 compared to children with a cardiovascular regulation profile characterized by high levels of RSA suppression and HP change. However, a significant interaction with racial status was found suggesting that the association between cardiovascular regulation profile and BMI growth and pediatric obesity was only significant for African-American children. An autonomic cardiovascular regulation profile consisting of low parasympathetic activity represents a significant individual risk factor for the development of pediatric obesity, but only for African-American children. Mechanisms by which early physiological regulation difficulties may contribute to the development of pediatric obesity are discussed.
| S-EPMC3293254 | biostudies-literature