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Fat, fate, and disease

By Mark Hanson


We are failing to deal with one of the most important issues of our time – in every country we are getting fatter. Although being fat is not automatically linked to illness, it does increase dramatically the risk of cardiovascular disease, diabetes, and other so-called non-communicable diseases. We are starting to see very high rates of these diseases in some places, sometimes affecting 50% of the population. Even in some of the poorest parts of the developing world, where such disease itself is not yet common, we nonetheless see warning signs of its arrival. There is great concern that it may soon outweigh the burden of communicable disease such as HIV/AIDS. The humanitarian and financial cost of this non-communicable disease in such parts of the world will be unbearable, and made even worse because the risk is passed across generations, so children born today and tomorrow will have a bleak future.

It seems that we don’t know how to tackle this problem, because current attempts are obviously failing and obesity continues to increase. Governments, doctors, and even NGOs seem to have adopted the same strategy – to focus on our sins of “gluttony and sloth” and to transfer the responsibility for slimming down to each of us as individuals. Of course it’s true that we can’t get overweight unless we eat more than we need to, and the wrong types of foods, and get too little physical exercise. Our biology did not evolve to protect us from obesity and its consequences in today’s sedentary world with such easy access to food. But why is it that we find it so hard to lose weight and, if we do shed the kilos, it seems very hard not to put them back on again?

What we are missing is a focus on our early development. We’re just not adopting the right approach to the problem. And it seems that the generals who are leading us in this global war on obesity and disease have adopted the wrong strategy, and they stick resolutely to it as if they were wearing blinkers. They blame us for the failure to win the war, for our greed and laziness; they blame parents for letting their children get fat; they blame the food industry for peddling unhealthy food, and so on. As if we choose to be fat. It’s important to realise just how limited this way of attacking the problem is on a global scale. Does the little girl force-fed before marriage in Mauritania have any choice in her life? Does the 12-year-old child bride in rural India have any choice when she becomes pregnant and drops out of school? Does the little toddler in Detroit have any choice when his mother feeds him French fries? Does the little boy from Tonga whose mother had diabetes in pregnancy have any choice about developing obesity? Does the little girl in Beijing have any choice in being an only child? And yet every one of these scenarios, and many more, sets that little child up to be at greater risk of becoming obese and to have non-communicable disease.

But new research is uncovering many things that will give us new tactics and strategies for the war against obesity and non-communicable disease, and so we’re hopeful. We now know that we will have to give much greater focus to the mother and unborn child. We may well have to give emphasis to the lifestyle of the father as well. And most importantly of all, we’re starting to realise that behaviours such as propensity to exercise, or appetite and taste for certain foods, which we previously thought to be based on individual choice, have a large constitutional component – in part based on inherited genes, in part on epigenetic changes to gene function in response to the developmental environment, and in part through early learning. If we focus on our early development, and in promoting health in parents even before they conceive a child, we can help both them and the next generation to avoid obesity and disease. We don’t have to accept this as our fate.

We now face a world where more people suffer from apparent over-nutrition rather than under-nutrition. But paradoxically both can lead to chronic disease. We may be better to think of unbalanced nutrition, nutrition mismatched to our evolved biology, and affecting much of the world’s population. These issues are growing in the developing world. When combined with climate change, issues of water, food and energy security, changes in longevity, family size and infectious disease, they will make a “perfect storm.” Weathering this storm will require the combined effort not just of health professionals and scientists, but of governments, agencies, foundations, and the private sector.

Prof Mark Hanson is the UK’s leading researcher on developmental pathways to disease. He is current President of the International Society for the Developmental Origins of Health and Disease. He has served on WHO committees and chairs an advisory committee in China focused on the diabetes epidemic. In the UK he directs the Division of Developmental Origins of Health and Disease at the University of Southampton, and overseas he holds visiting appointments in Auckland, Singapore, Dublin and Shanghai. Alongside Prof Sir Peter Gluckman, Mark Hanson co-authored Fat, Fate and Disease: Why excercise and diet are not enough, which published this month in the UK. It publishes in the US in March 2012.

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Recent Comments

  1. Chet

    I don’t think the focus on childhood is the right answer, either. The evidence is that obese children are actually eating less than their healthy-weight peers.

    If the adult’s obesity is determined by the child, but the child’s obesity doesn’t seem to have anything to do with diet, then we reach the point either where we’re supposed to believe that the problem is a nation of sinful, gluttonous infants, or that this obesity crisis is almost entirely the result of genetics.

  2. Beth@WeightMaven

    You write: “Although being fat is not automatically linked to illness, it does increase dramatically the risk of cardiovascular disease, diabetes, and other so-called non-communicable diseases.”

    Is it that “being fat” increases the risk? Or is that what makes us fat — such as an energy dense, nutrient-poor diet — increase the risk? Semantic quibble … and of course, the answer may be “both” as fat is not inert tissue.

    Pottenger and his cats certainly show that there is a way out of this, but there is a considerable challenge to do so!

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