Sugar intake from sweet food and beverages, common mental disorder and depression: prospective findings from the Whitehall II study

Intake of sweet food, beverages and added sugars has been linked with depressive symptoms in several populations. Aim of this study was to investigate systematically cross-sectional and prospective associations between sweet food/beverage intake, common mental disorder (CMD) and depression and to examine the role of reverse causation (influence of mood on intake) as potential explanation for the observed linkage. We analysed repeated measures (23,245 person-observations) from the Whitehall II study using random effects regression. Diet was assessed using food frequency questionnaires, mood using validated questionnaires. Cross-sectional analyses showed positive associations. In prospective analyses, men in the highest tertile of sugar intake from sweet food/beverages had a 23% increased odds of incident CMD after 5 years (95% CI: 1.02, 1.48) independent of health behaviours, socio-demographic and diet-related factors, adiposity and other diseases. The odds of recurrent depression were increased in the highest tertile for both sexes, but not statistically significant when diet-related factors were included in the model (OR 1.47; 95% CI: 0.98, 2.22). Neither CMD nor depression predicted intake changes. Our research confirms an adverse effect of sugar intake from sweet food/beverage on long-term psychological health and suggests that lower intake of sugar may be associated with better psychological health

Investigating partner involvement in pregnancy and identifying barriers and facilitators to participating as a couple in a digital healthy eating and physical activity intervention

BACKGROUND: Maternal obesity and excessive gestational weight gain are associated with adverse maternal and foetal health outcomes. Interventions targeting dietary and physical activity behaviours during pregnancy have typically been directed at women only. A digital intervention targeting couples could encourage expectant parents to support each other in improving energy balance (dietary and physical activity) behaviours. AIMS: This study aimed to investigate the role partners play in pregnant women’s energy balance behaviours, and to identify barriers and facilitators to participating as a couple in a digital intervention to encourage healthy eating and physical activity in pregnancy. METHODS: A qualitative design combined online focus groups and telephone interviews. Three focus groups were held with men (n = 15) and one mini focus group (n = 3) and 12 telephone interviews were conducted with women. Participants were either in the last trimester of pregnancy or had a baby under 18 months old. Most were from more deprived population groups where prevalence of maternal obesity is higher. Data were analysed thematically. Barriers and facilitators to participating as a couple in a digital intervention were mapped to the COM-B model and the Theoretical Domains Framework. RESULTS: Four main themes were identified; partner involvement and support; partner understanding of good energy balance behaviours; couple concordance of energy balance behaviours; partner influence on her energy balance behaviours. Most facilitators to participating in a digital intervention as a couple fell within the Reflective Motivation domain of COM-B. Men were motivated by the desire to be supportive partners and good role models. Women were motivated by their belief that partner involvement would improve their success in achieving goals and enhance couple-bonding. Other facilitators included concordance in dietary behaviours (Physical Opportunity), healthcare practitioner recommendation, perceptions of pregnancy as ‘ours’ (Social Opportunity) and feeling supported and involved (Automatic Motivation). Barriers were rarely mentioned but included potential for partner conflict, perceptions of pregnancy as ‘hers’ and economic constraints. CONCLUSIONS: An opportunity exists to harness partner support to improve maternal energy balance behaviours. Barriers and facilitators to participating in a digital intervention as a couple indicate its potential to benefit emotional and relationship wellbeing in addition to physical health

Shared genetic architecture underlying sleep and weight in children.

Meta-analyses suggest shorter sleep as a risk factor for obesity in children. The prevailing hypothesis is that shorter sleep causes obesity by impacting homeostatic processes. Sleep duration and adiposity are both heritable, and the association may reflect shared genetic aetiology. We examined the association between a body mass index (BMI) genetic risk score (GRS) and objectively-measured total sleep time (TST) in a cohort of Norwegian children (enrolled at age four in 2007-2008) using cross-sectional data at age six. The analytical sample included 452 six-year old children with complete genotype and phenotype data. The outcome was actigraphic total sleep time (TST) measured at age six years. Genetic risk of obesity was inferred using a 32-single nucleotide polymorphism (SNP) weighted GRS of BMI. Covariates were BMI-Standard deviation scores (SDS) (which takes into account age and sex) and, in a sensitivity analysis socioeconomic status. Analyses consisted of Pearson's correlations and linear regressions. In our sample, 54% of participants were male; mean (SD) TST, age and BMI were 9.6 (0.8) hours, 6.0 (0.2) years and 15.3 (1.2) kg/m2, respectively. BMI and TST were not correlated, r = -0.003, p = 0.946. However, the BMI GRS was associated with TST after adjusting for BMI-SDS, standardised β = -0.11; 95% confidence interval (CI) = -0.22, -0.01. To our knowledge, this is the first study to establish a relationship between genetic risk of obesity and objective sleep duration in children. Findings suggest some shared genetic aetiology underlying these traits. Future research could identify the common biological pathways through which common genes predispose to both shorter sleep and increased risk of obesity

The retail food environment and its association with body mass index in Mexico

Background/Objective: Mexico has one of the highest rates of obesity and overweight worldwide, affecting 75% of the population. The country has experienced a dietary and food retail transition involving increased availability of high-calorie-dense foods and beverages. This study aimed to assess the relationship between the retail food environment and body mass index (BMI) in Mexico. Subjects/Methods: Geographical and food outlet data were obtained from official statistics; anthropometric measurements and socioeconomic characteristics of adult participants (N = 22,219) came from the nationally representative 2012 National Health and Nutrition Survey (ENSANUT). Densities (store count/census tract area (CTA)) of convenience stores, restaurants, fast-food restaurants, supermarkets and fruit and vegetable stores were calculated. The association of retail food environment variables, sociodemographic data and BMI was tested using multilevel linear regression models. Results: Convenience store density was high (mean (SD) = 50.0 (36.9)/CTA) compared with other food outlets in Mexico. A unit increase in density of convenience stores was associated with a 0.003 kg/m2 (95% CI: 0.0006, 0.005, p = 0.011) increase in BMI, equivalent to 0.34 kg extra weight for an adult 1.60 m tall for every additional 10% store density increase (number of convenience stores per CTA (km2)). Metropolitan areas showed the highest density of food outlet concentration and the highest associations with BMI (β = 0.01, 95% CI: 0.004–0.01, p < 0.001). A 10% store density increase in these areas would represent a 1 kg increase in weight for an adult 1.60 m tall. Conclusions: Convenience store density was associated with higher mean BMI in Mexican adults. An excessive convenience store availability, that offers unhealthy food options, coupled with low access to healthy food resources or stores retailing healthy food, including fruits and vegetables, may increase the risk of higher BMI. This is the first study to assess the association of the retail food environment and BMI at a national level in Mexico

Behavioural Susceptibility Theory: Professor Jane Wardle and the Role of Appetite in Genetic Risk of Obesity

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

Meal size is a critical driver of weight gain in early childhood

Larger serving sizes and more frequent eating episodes have been implicated in the rising prevalence of obesity at a population level. This study examines the relative contributions of meal size and frequency to weight gain in a large sample of British children. Using 3-day diet diaries from 1939 children aged 21 months from the Gemini twin cohort, we assessed prospective associations between meal size, meal frequency and weight gain from two to five years. Separate longitudinal analyses demonstrated that every 10 kcal increase in meal size was associated with 1.5 g/wk or 4% (p = 0.005) faster growth rate, while meal frequency was not independently associated with growth (β = 0.3 g/wk p = 0.20). Including both meal parameters in the model strengthened associations (meal size: β = 2.6 g/wk, p < 0.001; meal frequency: β = 1.0 g/wk, p = 0.001). Taken together, the implication is that meal size promotes faster growth regardless of frequency, but meal frequency has a significant effect only if meal size is assumed to be held constant. Clearer advice on meal size and frequency, especially advice on appropriate meal size, may help prevent excess weight gain

Appetitive traits and relationships with BMI in adults: Development of the Adult Eating Behaviour Questionnaire

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)

Food fussiness and food neophobia share a common etiology in early childhood

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