Objectives. We examined the probability of an obese person attaining normal body weight. Methods. We drew a sample of individuals aged 20 years and older from the United Kingdom’s Clinical Practice Research Datalink from 2004 to 2014. We analyzed data for 76 704 obese men and 99 791 obese women. We excluded participants who received bariatric surgery. We estimated the probability of attaining normal weight or 5% reduction in body weight. Results. During a maximum of 9 years’ follow-up, 1283 men and 2245 women attained normal body weight. In simple obesity (body mass index = 30.0–34.9 kg/m²), the annual probability of attaining normal weight was 1 in 210 for men and 1 in 124 for women, increasing to 1 in 1290 for men and 1 in 677 for women with morbid obesity (body mass index = 40.0–44.9 kg/m²). The annual probability of achieving a 5% weight reduction was 1 in 8 for men and 1 in 7 for women with morbid obesity. Conclusions. The probability of attaining normal weight or maintaining weight loss is low. Obesity treatment frameworks grounded in community-based weight management programs may be ineffective.

The Child Eating Behaviour Questionnaire (CEBQ) is a validated parent-report measure of appetitive traits associated with weight in childhood. There is currently no matched measure for use in adults. The aim of this study was to adapt the CEBQ into a self-report Adult Eating Behaviour Questionnaire (AEBQ) to explore whether the associations between appetitive traits and BMI observed in children are present in adults. Two adult samples were recruited one year apart from an online survey panel in 2013 (n = 708) and 2014 (n = 954). Both samples completed the AEBQ and self-reported their weight and height. Principal component analysis (PCA) was used to derive 35 items for the AEBQ in Sample 1 and confirmatory factor analysis (CFA) was used to replicate the factor structure in Sample 2. Reliability of the AEBQ was assessed using Cronbach's α and a two week test-retest in a sub-sample of 93 participants. Correlations between appetitive traits measured by the AEBQ and BMI were calculated. PCA and CFA results showed the AEBQ to be a reliable questionnaire (Cronbach's α > 0.70) measuring 8 appetitive traits similar to the CEBQ [Hunger (H), Food Responsiveness (FR), Emotional Over-Eating (EOE), Enjoyment of Food (EF), Satiety Responsiveness (SR), Emotional Under-eating (EUE), Food Fussiness (FF) and Slowness in Eating (SE)]. Associations with BMI showed FR, EF (p < 0.05) and EOE (p < 0.01) were positively associated and SR, EUE and SE (p < 0.01) were negatively associated. Overall, the AEBQ appears to be a reliable measure of appetitive traits in adults which translates well from the validated child measure. Adults with a higher BMI had higher scores for 'food approach' traits (FR, EOE and EF) and lower scores for 'food avoidance' traits (SR, EUE and SE).

Purpose of Review There is considerable variability in human body weight, despite the ubiquity of the ‘obesogenic’ environment. Human body weight has a strong genetic basis and it has been hypothesised that genetic susceptibility to the environment explains variation in human body weight, with differences in appetite being implicated as the mediating mechanism; so-called ‘behavioural susceptibility theory’ (BST), first described by Professor Jane Wardle. This review summarises the evidence for the role of appetite as a mediator of genetic risk of obesity. Recent Findings Variation in appetitive traits is observable from infancy, drives early weight gain and is highly heritable in infancy and childhood. Obesity-related common genetic variants identified through genome-wide association studies show associations with appetitive traits, and appetite mediates part of the observed association between genetic risk and adiposity. Summary Obesity results from an interaction between genetic susceptibility to overeating and exposure to an ‘obesogenic’ food environment.

Background: Health professionals identify food provision in the home as a key influence on children’s food preferences. In contrast, parents often pe

Background: ‘Food fussiness’ ( FF ) is the tendency to be highly selective about which foods one is willing to eat, and emerges in early childhood; ‘food neophobia’ ( FN ) is a closely related characteristic but specifically refers to rejection of unfamiliar food. These behaviors are associated, but the extent to which their etiological architecture overlaps is unknown. The objective of this study was to quantify the relative contribution of genetic and environmental influences to variation in FF and FN in early childhood; and to establish the extent to which they share common genetic and environmental influences. Method: Participants were 1,921 families with 16‐month‐old twins from the Gemini birth cohort. Parents completed the Child Eating Behaviour Questionnaire which included three FF items and four FN items. Bivariate quantitative genetic modeling was used to quantify: (a) genetic and environmental contributions to variation in FF and FN ; and (b) the extent to which genetic or environmental influences on FF and FN are shared across the traits. Results: Food fussiness and FN were strongly correlated ( r = .72, p < .001). Proportions of variation in FF were equally explained by genetic (.46; 95% CI : 0.41–0.52) and shared environmental influences (.46; 95% CI : 0.41–0.51). Shared environmental effects accounted for a significantly lower proportion of variation in FN (.22; 95% CI : 0.14–0.30), but genetic influences were not significantly different from those on FF (.58, 95% CI : 0.50–0.67). FF and FN largely shared a common etiology, indicated by high genetic (.73; 95% CI : 0.67–0.78) and shared environmental correlations (.78; 95% CI : 0.69–0.86) across the two traits. Conclusions: Food fussiness and FN both show considerable heritability at 16 months but shared environmental factors, for example the home environment, influenced more interindividual differences in the expression of FF than in FN . FF and FN largely share a common etiology.