Variation in the fat mass and obesity–associated (FTO) gene has provided the most robust associations with common obesity to date. However, the role of FTO variants in modulating specific components of energy balance is unknown.

University represents a key transition into adulthood for many adolescents but there are associated concerns about health and behaviours. One important aspect relates to diet and there is emerging evidence that university students may consume poor quality diets, with potential implications for body weight and long-term health. This research aimed to characterise dietary patterns of university students in the UK and their sociodemographic and lifestyle antecedents. An online, cross-sectional survey was undertaken with a convenience sample of 1448 university students from five UK universities (King’s College London, Universities of St Andrews, Southampton and Sheffield, and Ulster University). The survey comprised a validated food frequency questionnaire alongside lifestyle and sociodemographic questions. Dietary patterns were generated from food frequency intake data using principal components analysis. Nutrient intakes were estimated to characterise the nutrient profile of each dietary pattern. Associations with sociodemographic variables were assessed through general linear modelling. Dietary analyses revealed four major dietary patterns: ‘vegetarian’; ‘snacking’; ‘health-conscious’; and ‘convenience, red meat & alcohol’. The ‘health-conscious’ pattern had the most favourable micronutrient profile. Students’ gender, age, year of study, geographical location and cooking ability were associated with differences in pattern behaviour. Female students favoured the ‘vegetarian’ pattern, whilst male students preferred the ‘convenience, red meat & alcohol’ pattern. Less healthful dietary patterns were positively associated with lifestyle risk factors such as smoking, low physical activity and take-away consumption. The health-conscious pattern had greatest nutrient density. The ‘convenience, red meat & alcohol’ pattern was associated with higher weekly food spending; this pattern was also identified most consistently across universities. Students reporting greater cooking ability tended towards the ‘vegetarian’ and ‘health-conscious’ patterns. Food intake varied amongst university students. A substantial proportion of students followed health-promoting diets, which had good nutrient profiles obviating a need for dietary intervention. However, some students consumed poor diets, incurred greater food costs and practised unfavourable lifestyle behaviours, which may have long-term health effects. University policy to improve students’ diets should incorporate efforts to promote student engagement in cooking and food preparation, and increased availability of low cost healthier food items.

An age-dependent association between variation at the FTO locus and BMI in children has been suggested. We meta-analyzed associations between the FTO locus (rs9939609) and BMI in samples, aged from early infancy to 13 years, from 8 cohorts of European ancestry. We found a positive association between additional minor (A) alleles and BMI from 5.5 years onwards, but an inverse association below age 2.5 years. Modelling median BMI curves for each genotype using the LMS method, we found that carriers of minor alleles showed lower BMI in infancy, earlier adiposity rebound (AR), and higher BMI later in childhood. Differences by allele were consistent with two independent processes: earlier AR equivalent to accelerating developmental age by 2.37% (95% CI 1.87, 2.87, p = 10⁻²⁰) per A allele and a positive age by genotype interaction such that BMI increased faster with age (p = 10⁻²³). We also fitted a linear mixed effects model to relate genotype to the BMI curve inflection points adiposity peak (AP) in infancy and AR. Carriage of two minor alleles at rs9939609 was associated with lower BMI at AP (−0.40% (95% CI: −0.74, −0.06), p = 0.02), higher BMI at AR (0.93% (95% CI: 0.22, 1.64), p = 0.01), and earlier AR (−4.72% (−5.81, −3.63), p = 10⁻¹⁷), supporting cross-sectional results. Overall, we confirm the expected association between variation at rs9939609 and BMI in childhood, but only after an inverse association between the same variant and BMI in infancy. Patterns are consistent with a shift on the developmental scale, which is reflected in association with the timing of AR rather than just a global increase in BMI. Results provide important information about longitudinal gene effects and about the role of FTO in adiposity. The associated shifts in developmental timing have clinical importance with respect to known relationships between AR and both later-life BMI and metabolic disease risk. Variation at the FTO locus is reliably associated with BMI and adiposity-related traits, but little is still known about the effects of variation at this gene, particularly in children. We have examined a large collection of samples for which both genotypes at rs9939609 and multiple measurements of BMI are available. We observe a positive association between the minor allele (A) at rs9939609 and BMI emerging in childhood that has the characteristics of a shift in the age scale leading simultaneously to lower BMI during infancy and higher BMI in childhood. Assessed in cross section and longitudinally, we find evidence of variation at rs9939609 being associated with the timing of AR and the concert of events expected with such a change to the BMI curve. Importantly, the apparently negative association between the minor allele (A) and BMI in early life, which is then followed by an earlier AR and greater BMI in childhood, is a pattern known to be associated with both the risk of adult BMI and metabolic disorders such as type 2 diabetes (T2D). These findings are important in our understanding of the contribution of FTO to adiposity, but also in light of efforts to appreciate genetic effects in a lifecourse context.

Obesity is a global and growing problem. The detrimental health consequences of obesity are significant and include co-morbidities such as diabetes, cancer and coronary heart disease. The marked rise in obesity observed over the last three decades suggests that behavioural and environmental factors underpin the chronic mismatch between energy intake and energy expenditure. However, not all individuals become obese, suggesting that there is considerable variation in responsiveness to 'obesogenic' environments. Some individuals defend easily against a propensity to accumulate fat mass and become overweight whilst others are predisposed to gain weight, possibly as a function of genotype. The genetic contribution to obesity is well established. Common obesity is polygenic, involving complex gene-gene and gene-environment interactions, and it is these interactions that produce the multi-factorial obese phenotypes. Candidate gene variants for polygenic obesity appear to disrupt pathways involved in the regulation of energy intake and expenditure and include adrenergic receptors, uncoupling proteins, PPARG, POMC, MC4R and a set of single nucleotide polymorphisms in the FTO locus. Notably, the FTO gene is the most robust gene for common obesity characterised to date, and recent data shows that the FTO locus seems to confer risk of obesity through increasing energy intake and reduced satiety. Gene variants involved in pathways regulating addiction and reward behaviours may also play a role in predisposition to obesity. Understanding the routes through which the genotype is expressed will ultimately provide opportunities for developing strategies to intervene, as the interaction between genotype and environment is potentially modifiable through behaviour change.