Creating an effective childhood obesity strategy
22 August 2016
A complex problem
Health and disease are the product of interactions between our genes and our environment or lifestyle; obesity is a case in point.
How fat we get is undoubtedly due in part to our underlying genetics – our individual variants in multiple genes, mostly those responsible for appetite control, but also to some extent our metabolism and probably also our propensity to undertake physical activity, whether that is formal exercise, enjoying going for a walk or gardening or even just the general restlessness that means some of us wander round to the kitchen for further cups of coffee or down the corridor to stretch our legs. Some people even sit stiller than others.
As so often happens, the poorer people and children suffer most: the food that is cheap and readily available is typically the poorest quality and the most calorie-dense; and children are the most vulnerable
Our body composition is also due to our environment and how we interact with it. This includes the availability of food, both in quality and quantity and the balance of intake with energy expenditure. For the first time in human history, populations (at least in the developed and developing world) are not limited by supply of calories. There is food available on the corner of every street and many of us have supplies about our person, whether a bottled drink, a takeout latte or just snacks, together allowing speedy access to food and drink at a moment’s notice. There has also been a significant culture change whereby the old rules of ‘not eating between meals’ lest it ‘spoil your appetite’ have been supplanted by continuous grazing and instant gratification. As so often happens, the poorer people and children suffer most: the food that is cheap and readily available is typically the poorest quality and the most calorie-dense; and children are the most vulnerable, because their nutrition and the habits they form are strongly controlled and influenced by their parents.
Population and personalised prevention
This week, in their Strategy on Childhood Obesity, it seems the Government has singularly failed to put in place a strategy that will have the desired effect on this obesogenic environment. It has not taken into account much of the evidence and advice from Public Health England (PHE) and others on what works at a population level and although there are some good proposals (eg. a tax on sugary drinks and the gradual reduction in sugar in everyday products) the recommended major public health ‘structural’ changes have been vastly watered down.
PHG Foundation has always advocated that whole population measures and individual ‘personal’ prevention measures to combat major public health problems are two sides of a coin. Ideally, both should be in place and act synergistically, but in this case the weakness of the former makes personal measures even more important – so what can be done? There are two hopeful chinks in the Government report that open the door for more individualised approaches, which just might eventually help to produce a solution. The two penultimate paragraphs talk about ‘harnessing the best new technology’ such as individual digital weight management and the encouragement of health professionals such as health visitors to identify potential weight problems early and develop skills to ‘initiate difficult conversations’ and learn how to influence behaviour change.
What is yet to be acknowledged is that effective diet and weight messages should not be the same for everybody. It is not simply a question of introducing standard content and messages at salient points such as during weaning or alongside childhood immunisation, important though these will be. Rather, it must form general, core content to run alongside very specific advice and strategies tailored to the individual or family – it will only work as part of personalised prevention.
Supporting the individual
In our 2013 report Genomics of Obesity we noted that BMI is a highly heritable trait – it tends to run in families. This can immediately tell us that children whose parents are obese are more likely to become overweight themselves. These children and their families could sensibly be prioritised. We also must not miss those rare genetic causes of very severe obesity in children, some of which, such as the disorders linked to leptin deficiency can now be treated. But, rare traits aside, most obese children (and adults) have simply been dealt a ‘hand’ of susceptibility variants that cause them to put on more weight as children and then carry that effect over, sometimes into morbid obesity as adults. The factors that lead them to some combination of calorie intake and physical activity that results in obesity will undoubtedly be different for everybody and have different solutions, so that each person must engage at an individual level with this health issue.
Rare traits aside, most obese children (and adults) have simply been dealt a ‘hand’ of susceptibility variants that cause them to put on more weight as children and then carry that effect over, sometimes into morbid obesity as adults
Put simply, Public Health England will deem it a great achievement if, by 2020 there has been a reduction in the ‘sales weighted average sugar content per 100 grams of food and drink, reductions in portion size so that these contain less sugar, or a clear sales shift towards lower sugar alternatives’. Indeed, the average BMI may have reduced and the NHS may have seen a small reduction in the number of people with type 2 diabetes or being admitted to hospital for weight related complaints. But the individual is not interested in such small differences. They should and could engage with the questions: how can I prevent myself or my family getting overweight? If I am obese, how can I most effectively lose weight and maximise my healthy life expectancy? A combination of commercially available apps, advances in biomolecular understanding may soon provide some of the tools for this. There will also, no doubt, be an emerging cadre of health coaches who may work alongside the health visitors, school nurses, pharmacists and other health professionals already identified as having a role.
As ever, the most difficult problem to crack will still be those living in relative, or actual, poverty, with little education, few personal resources and poor availability of healthy food. It’s exceptionally hard to diet or eat healthily in such situations; most of us after all recognise the urge to reach out for ‘comfort food’ at the end of a busy day or in stressful situations. Whilst the ‘structural’ aspects of the public policy will help – and it will certainly be good to see better food or exercise programmes in schools, for example - the real emphasis must be on enabling individuals to make sure that they can become active participants in managing their own health. I would put my money into the poorest locations and the poorest schools. Here, the message should be that a child’s BMI is not just the helpless result of national policies, but can be positively affected by engagement with individuals and increased understanding of their own underlying biology, circumstances, preferences and actions.
Obesity is a problem for the state and health providers as a whole and certainly has serious consequences for society. More importantly, it is a catastrophe for individuals who are destined for a life of sub-optimal health, serious long term disease and early death. Our health policies should recognise that only the individual can change these outcomes.