Obesity – Who, When and Why?
Pointers from the EarlyBird Study
Terence Wilkin MD and Linda Voss PhD
Peninsula Medical School, UK
There seem to be three questions of key importance – who, when and why? Which children are at risk of obesity, when is the trajectory set, and what are the mechanisms responsible?
The energy equation is incontrovertible, but its application to the prevention of obesity may not be straightforward. It is difficult to influence or even know what school children consume, because they are out of sight for most of the day, and self-report in children is unreliable. Equally, attempts to modify physical activity must first ask what controls it. The ‘environmental’ answer would point to availability of open spaces, access to sports clubs, allocation of time to physical education (PE) at school, etc. The response is intuitive, and satisfies the widely-held, though little tested, assumption that opportunity and activity are linked. Given the same question, the biologist might take a different view. Throughout evolution, maintenance of body mass has been a survival pressure, and the ‘biological’ answer would likely regard central control of energy expenditure as fundamental to the preservation of body mass. Would Nature leave the one modifiable component of energy expenditure to chance?
EarlyBird is a prospective cohort study of healthy children from the age of 5y, which set out 10 years ago to address the three questions. It finds, counter-intuitively, that the average pre-pubertal child is no heavier now than he or she was 20-25 years ago when the children who contributed to the 1990 UK growth standards were measured. The mean BMI of children has risen substantially, but the median very little, suggesting that a sub-group of children has skewed the distribution but not altered its position. Who are these children? New data suggest that the rise in childhood obesity over the past 25y largely involves the daughters of obese mothers and the sons of obese fathers – but not the reverse.2 The daughters of obese mothers have a 10-fold greater risk of obesity, and the sons of obese fathers six-fold, but parental obesity does not influence the BMI of the opposite-sex child. Being non-Mendelian, this gender-assortative pattern of transmission is more likely to be behavioural than genetic. It is well established by the age of 5y, but unaffected by birth weight.
The observation is important, because it may turn the causality of childhood obesity on its head. A large amount of money and effort has been directed at children in the belief that the prevention of childhood obesity would reduce adult obesity. Up to 80% of obese adults, however, were not obese as children, whereas a high proportion of obese children are the offspring of overweight/obese adults. Childhood obesity seems to be a feed-backward effect of obese parents, rather than a feed-forward effect of an obesogenic environment. Maybe the focus of childhood obesity prevention should be on parents-to-be.
When does childhood obesity begin? Trajectories are crucial, because they appear to be set early in life. Thus, >90% of the excess weight gained by girls before puberty (>70% for boys) is gained before 5y. The observation is consistent with the gender-assortative data, suggesting that body weight trajectories are set early in life, before school age. Importantly, the factors popularly associated with childhood obesity – poor school meals, lack of playing fields, insufficient PE at school, too much screen watching – appear to have little impact, at least at primary school age.
Is inactivity the cause of overweight, or does obesity lead to inactivity? An inverse relationship between BMI and physical activity is widely reported, almost always on the basis of cross-sectional data, and interpreted to mean that inactivity leads to obesity. However, cross-sectional association cannot be used to conclude direction of causality, so EarlyBird used time-lagged correlation and the law of temporality to infer direction of causality from longitudinal analysis. We have found no evidence that physical inactivity precedes obesity, but good evidence that obesity precedes inactivity. The implications are clear – strategies aimed at increasing physical activity, even if they achieved the increase, are unlikely to reduce BMI. On the other hand, if children were induced to lose weight, they might tolerate more physical activity.
Can the activity of children be changed? Intervention studies have found it difficult to increase the activity of children sufficient to exert any measurable effect on their BMI, and tend to conclude that the intervention was simply not big enough. EarlyBird examined the impact of a five-fold (highly measurable) difference in PE on the activity that children recorded in and out of school – and repeated the measurements on the same cohort four times throughout the year to control for variation in rainfall, daylight hours etc. While the PE-intense children recorded a whopping 40% more activity during school hours, they recorded correspondingly less out of school, such that the totals over the course of the whole day were the same in all groups, irrespective of opportunity. This compensatory response suggests to us that the physical activity of children is controlled by the brain, rather than the environment, and that the range of activity in children represents a range of set-points rather than a range of environments.
If our conclusions are correct, the body mass of children who meet the Government guidelines for physical activity should be no different from the BMI of those who do no not, while their metabolic health should be better. And this has proved to be the case. The BMI of children who exercise more than 60 minutes per day is no different, but their metabolic risk is substantially less.
Calorie intake is notoriously difficult to measure in free-living children of school age. We have used detailed food choice questionnaires and principal components analysis to demonstrate clear, if modest, differences in food choices which associate with metabolic risk. Large differences are not needed if the effect is cumulative over time.
A picture is emerging from the EarlyBird Study to suggest that weight gain trajectories are set early in life, perhaps very early, by some behavioural sympathy between obese parents and their same-sex offspring. The trajectory appears to be established by 5y and retained – at least until puberty. The most likely cause of such weight gain seems to be over-nutrition, insofar as physical activity is unstructured before 5y, and attempts to structure it thereafter may be unsuccessful because an ‘activitystat’ operates to defend the child’s activity set-point. Physical inactivity does not lead to obesity, but rather obesity to inactivity, suggesting again that the primary cause of childhood obesity is overnutrition, and implying that weight loss might of itself lead to more activity and better metabolic health.
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