Prevention is better than cure provided (which is not always the case) that prevention does less harm than the disease it prevents. Since obesity is now of epidemic proportions all over the world, and it is estimated that in just over a decade’s time there will be 500,000,000 people with type II diabetes consequent upon obesity, prevention of obesity is devoutly to be wished – which is not to say that it will be easy or even possible.
An article in a recent edition of the New England Journal of Medicine asks the question of how early in life prevention of obesity should begin, given that once it is established it is refractory to treatment. Although the epidemic may have peaked in the United States, there is no room for complacency because the proportion of fat people is already enormous. A half of American pregnant women are seriously overweight or outright fat, and fat women tend to have fat children. They gain even more weight during pregnancy, and women who gain weight excessively during pregnancy are especially likely to have fat children.
The article is a typical example of what might be called risk factor medicine. A disease or disorder is found to be associated statistically with some independent variable which may or may not be causally related to that disease or disorder, so that doctors hope that by reducing the prevalence of the risk factor in some way they will also reduce the prevalence of the disease or disorder. Since many of the risk factors are behavioral rather than biological, and there is nothing as difficult to change as human behavior, doctors’ hopes are often frustrated.
The article examines several risk factors for the development of childhood obesity: maternal weight gain during pregnancy (and its consequent diabetes), maternal smoking, caesarean section, early weaning from breast-feeding, and reduced periods of sleep by infants. There are physiological explanations as to why some of these factors should be linked to childhood obesity, but that is not the same as demonstrating that, if they were reduced in prevalence, the prevalence of childhood obesity would itself decline. What stands to reason in medicine often turns out not to be the case. In fact it is difficult to demonstrate a cause and effect relationship because there is a long time-lag between the proposed cause and its effect. It is known, for example, that reducing the weight gain of mothers in pregnancy leads to smaller babies, but whether those smaller babies fail in the longer term to become fat children is not known. The situation is even more uncertain with regard to the other factors.
Does a lack of firm evidence mean that no recommendations can honestly be made? The authors of the article suggest that pregnant women are more likely to alter their ways in the direction that doctors wish than other adults because of concern for the welfare of their unborn children, so that (for example) they are more likely than others to give up smoking and change their diet for the better. It should be comparatively easy to reduce the number of births by caesarean section and to encourage women to breast feed for longer, though whether this would have any effect remains unknown.
The authors also consider other possible risk factors for obesity. They write, “Certain modifications in the number and type of microorganisms during infancy are associated with excess weight gain, at least in rodents.” That took me back nearly 40 years, when I attended a lecture by a great expert on rat physiology.
“That’s all very well, Professor X” said one of the doctors in the audience after the lecture was over. “But after all, Man is not a rat.”
“Oh yes he is,” murmured the man sitting next to me.
images courtesy shutterstock / Naeblys