Tuesday, 16 November 2010
The Origins of Obesity with Increasing Affluence
I have read the weekly magazine The Economist ever since I began my university studies and each and every issue contains something of interest. the name is misleading, you may think it is only about economics but as you can see in the following article published, interesting and earth shattering news in the field of science gets attention long before the lay press picks it up
Obesity, malnutrition and gestation
Evidence that the problem of obesity starts in the womb
Nov 11th 2010 | Lausanne
Hiding from the future
IN THE late 1980s David Barker, a British doctor, suggested that what a woman eats when she is pregnant shapes her child’s physiology for life. He called the idea fetal programming. Such programming would allow an individual to make optimum use of available nutrients, on the assumption that his own diet will be similar to his mother’s. If it was not similar, though, there could be problems. Dr Barker speculated that fetal programming—in mesalliance with the spread of fatty, sugary foods over recent decades—might explain the epidemic of obesity, heart disease and late-onset diabetes that plagues many rich countries.
It is a neat theory, but hard to prove. On October 29th, though, Sir Peter Gluckman, an endocrinologist and evolutionary biologist at the University of Auckland, in New Zealand, presented evidence to support it at a conference organised in Lausanne by Nestlé, a Swiss food company. Dr Gluckman carried out his study in Jamaica, in collaboration with Terrence Forrester, of the University of the West Indies. He picked Jamaica because malnutrition is endemic there. That allows the theory of fetal programming to be tested by finding out whether those who experienced malnutrition in the womb respond differently to food than those who were properly fed.
Dr Gluckman and Dr Forrester began their study by looking at people who had survived childhood malnutrition. Symptoms normally manifest themselves in one of two ways, known as marasmus and kwashiorkor. Children with marasmus are simply emaciated. The abdomens of those with kwashiorkor, however, distend in a way that is distressingly familiar from televised appeals for famine relief. One significant difference between the two syndromes is that children with marasmus are twice as likely to survive malnutrition as those with kwashiorkor.
Dr Gluckman and Dr Forrester looked at 240 people aged between 25 and 40 who had survived one syndrome or the other as children, and found a systematic difference between them. The marasmus survivors tended to have had low birthweights. The kwashiorkor group had normal birthweights. Low birthweight is an indication of a malnourished mother. Dr Gluckman and Dr Forrester thus hypothesise that the capacity for a marasmus-style response to malnutrition, with its higher survival rate, is programmed into fetuses by maternal malnourishment. Fetuses carried by well-nourished mothers do not, as it were, anticipate the risk of malnutrition, and thus respond to it less well.
That suggests fetal programming is a real phenomenon. But can it help explain obesity, diabetes and so on? To investigate this, the two researchers then offered their volunteers foods that were either high in protein and low in fat, or low in protein and high in fat—but which, crucially, tasted the same, so that they did not know what they were eating.
They found that those who had survived marasmus ate differently from those who had survived kwashiorkor. The bodies of marasmus survivors seemed to demand more protein in their food. When offered a diet low in protein and high in fat, they consumed more of it. That kept their protein intake constant, but meant they were eating 500 calories a day more than a normal maintenance diet (2,000 calories for women and 2,500 for men). Kwashiorkor survivors did not overeat in this way.
This, then, may be the key that unlocks the puzzle. Diets of the past would tend to have been lean (that is, to have favoured protein and complex carbohydrates like starch over fats and sugars). Anticipating scarcity by overeating in times of plenty would be no bad thing if times of scarcity were a real risk. Bodies that expected food to be plentiful, by contrast, should ration themselves to avoid the consequences of chronic overeating. An inability to do that is the price paid for protection from famine by those predisposed to marasmus.
This study thus makes a prediction: as diets become high in sugar and fat in places where malnutrition was once common, those who suffered marasmus as children will become overweight more rapidly than those who suffered kwashiorkor. If that turns out to be the case, it will be evidence that Dr Barker was right. What is not yet clear is whether the children of today’s overfed westerners will experience programming in the opposite direction, and have their appetites restricted.