Eating 100 fewer calories a day could help prevent weight gain in the average individual, say scientists in the US. A wider look at genetics and environment shows that solving weight problems is not quite so easy however.
While 100 fewer calories will not bring about weight loss, it represents a specific, manageable strategy that people can use to stop putting on the 1.8 to 2.0 pounds that the average person gains per year, claims James Hill, a researcher at the University of Colorado Health Sciences Center. This is the most urgent priority in addressing the obesity epidemic, he added.
Hill believes that the first step to fighting the current obesity epidemic is to halt weight gain in populations that are increasing in size each year. "That might not be so overwhelming, since we can break it down into concrete steps," the researcher said.
Hill and his colleagues studied data collected by the National Health and Nutrition Examination Survey (NHANES) and the Coronary Artery Risk Development in Young Adults (CARDIA) study. The NHANES data showed that the prevalence of obesity increased from 23 per cent to 31 per cent between 1988 and 1994 in the United States. And if weight gain continues at the present rate, 39 per cent of the US population will be obese in 2008. (Worldwide, over 300 million are obese, according to the World Health Organisation).
While a long-term approach to curbing obesity would be to mount a social change campaign, like those for stopping smoking, seat belt use, and recycling, said Hill, in the short-term people should be given precise targets.
"We all know you've got to eat less and exercise more, but, well, how much? That's what we've laid out," Hill said.
Using the NHANES and CARDIA data, Hill and his colleagues estimated that individuals are gaining, on average, 14-16 pounds in eight years - an average of 1.8 - 2.0 pounds each year.
Assuming that each pound of body weight gained represents 3500 calories, the researchers calculated that 90 per cent of the population is gaining up to 50 extra calories a day. The body does not store excess energy with 100 per cent efficiency, however. Hill's team estimated that for every 100 extra calories consumed, at least 50 would be stored as fat. The article appears in the 7 February issue of the Science.
"Nobody really ever talks about numbers, but that's what we need. Something around 100 calories a day is do-able," Hill said.
While taking a wider view of the problem, to account for genes as well as environment, other experts agree that a small decrease in weight could have significant benefits for many. In another article in the same journal, Dr Jeffrey M. Friedman stresses the role played by both genes and environment in the onset of obesity.
Friedman writes: "in general, environmental factors account for trends in a population over time, while genetic factors account for most of the differences in weight among individuals in present time."
Friedman, involved in the discovery of the obesity hormone leptin in 1995, argues that increase in weight does not fully account for the increase in the incidence of obesity; the drive to eat is to a large extent hard-wired and differences in weight are genetically determined; and evolution exerts powerful forces that obese people need to fight in order to lose weight.
The researcher reveals that although the incidence of obesity in the United States has increased from 23.3 per cent in 1991 to 30.9 per cent today, the weight of the average American has increased about only seven to 10 pounds, on average. So how does an incremental increase in the average weight have such a significant effect on the incidence of obesity?
We need to look at the definition of obesity, says Friedman. Obesity is diagnosed when BMI passes 30. BMI, or body mass index, measures body fat based on height and weight that applies to both adult men and women. According to Friedman, since obesity is defined as a threshold, an increase in average weight has a disproportionate effect on the increasing incidence of obesity.
This is why a small, achievable decrease in the average weight of the US population could have an enormous benefit to public health, he argues, backing Hill's research.
But going further, Friedman suggests that there could be "a subgroup that is genetically susceptible to obesity and a different subgroup that is relatively resistant."
The interaction of the environment with the biological system that our genes comprise is important. For example, research by Friedman and other scientists has shown that genetic mutations that lead to a full or partial loss of leptin are associated with obesity in some humans. There have also been a number of other hormones and genes identified that play a role in appetite and weight. These hormones orchestrate the unconscious urge to eat, a basic biological drive that is difficult to fight with the conscious desire to eat less.
"The feeling of hunger is intense and, if not as potent as the drive to breathe, is probably no less powerful than the drive to drink when one is thirsty. This is the feeling the obese must resist after they have lost a significant amount of weight.
"The power of this drive is illustrated by the fact that, whatever one's motivation, dieting is generally ineffective for achieving significant weight loss over the long term."
And the role of the environment? According to Friedman, genes that compose the biological system that regulates weight should be expected to vary depending on the environment due to intense selective evolutionary pressure.
So, people who lived when food was sporadically available - for example, hunters-gatherers - benefited from genes that predisposed them to obesity, since "these genes would increase energy stores and provide a survival advantage during times of famine."
For those who lived in areas where the risk of starvation was low because of farming, domestication of animals and the ability to store food - Western civilizations, for example - the same genes that protected people from starvation may have exposed the obese to significant health consequences, such as diabetes and heart disease.
Modern-day humans, according to Friedman, "carry the genetic legacy of both environments. In modern times, obesity and leptin resistance appear to be the residue of genetic variants that were more adaptive in our previous environments. It may be that the obese carry the 'hunter-gatherer' genes and the lean carry the 'Western' genes, protecting them from the consequences of obesity."
Taken together, our genes and our environment collaborate to build a formidable barrier for those who want to lose weight.
"Obesity is not a personal failing," Friedman concludes. "In trying to lose weight, the obese are fighting a difficult battle - a battle against biology, a battle that only the intrepid take on and one in which only a few prevail."