Professor Martin Wiseman is the Medical and Scientific Adviser with World Cancer Research Fund International and a visiting professor at Southampton University.
What is it about nutrition that makes it important for the prevention of so many chronic diseases?
One of the most striking illustrations of the scope for preventing cancer is the huge variation in its occurrence – the different patterns around the globe, and how relatively rapidly they can change. And that variation is a key to understanding the causes of cancer.
Susceptibility
What has become clear is that the main factors that determine patterns of cancer around the world are environmental in origin – or at least not primarily genetic. People’s individual genetic make-up certainly influences their susceptibility to cancer, but it is the wider environment that influences whether that susceptibility ever becomes manifest. And by environment this means the cell’s environment, not just the external world. So people’s metabolic state can be regarded as environmental, if you are looking at it from the perspective of a cell.
It’s often thought that nutrition is simply a passive reflection of dietary intake, but in fact people’s nutritional state results from a complex interaction between their diet and their metabolic requirements, and their physical activity. So nutrition needs to be seen as more than just a dietary issue. It is a reflection of your metabolic and functional state. And it is this nutritionally determined biological environment that cells find themselves in that seems to be most important.
There is no doubt that external carcinogens are important causes of cancer – but fortunately they are not that commonly encountered in more economically developed countries. The best known is tobacco. Of course there are other external carcinogens that are demonstrable causes of cancer in humans – asbestos, some viruses, UV radiation, aflatoxins and so on. But apart from tobacco their impact on the overall burden of cancer pales into insignificance in richer societies compared to the causes of the common cancers related to affluence – breast and colorectal.
Breast and colorectal cancers are linked not so much to specific dietary components but much more to the metabolic and hormonal consequences of obesity – excess oestrogen production, inflammation and disordered glucose and lipid metabolism. These are causal factors that are shared by other chronic diseases such as cardiovascular disease and diabetes. Interestingly diabetes – which is characterised by abnormally elevated blood concentrations of glucose – is an independent risk factor for these cancers. Even more interesting is that even in people without diabetes the level of glycated haemoglobin (a marker of average glucose concentration over about three months) is a predictor of overall cancer risk.
Nutrition in early life
At an even more basic level we are just beginning to understand that susceptibility to cardiovascular disease and diabetes has roots in the nutritional environment of the growing fetus and child – and it is exciting to recognise pointers that this may also be the case for cancer – people who are taller, and born heavier (both markers of early life experience) have higher rates of these cancers.
The fly in the ointment is that these effects are in the opposite direction for diabetes and cardiovascular disease. So it is not easy to say what the best growth trajectory is – is it better to grow fast and big – or not?
We need to understand the mechanisms that link nutrition in early life to chronic disease in later life. How the fetal environment influences the expression of genes through epigenetics will be at the heart of this – and when we know how that works we will be able to develop public health programmes that promote development and maturation that minimises susceptibility to all chronic disease – not one or the other. So that will add to our armoury for promoting long life with good health by dealing with the adult environment of dietary excess and physical inactivity that brings out this acquired susceptibility.