Is our fatty future in our genes

The average male population is heading for obesity – do we know why, and can we do anything to stop it?

Several new studies have found that not only do humans face a fatter future but also four genetic mutations that could explain this increase in obesity - now, say scientists, the challenge is to find out what we can do about it.
Research looking at the differences in height and body mass index between people born in 1946 and 1958 has found that health gains in post-war generations have been overshadowed by increasing obesity. The 1958 cohort gained weight at a faster rate from early adulthood and continued to do so throughout adult life.

Dr Leah Li, lead researcher on the project, explained: “Using the results of our study, we can estimate that the average BMI of those born in 1958 will reach 30kg/m2 for men and 29kg/m2 for women by age 53 years, and thus the average male population will be obese. With the relatively low level of childhood obesity in these two early cohorts compared with today’s children, if the obesity epidemic continues at its current pace, the level of obesity will increase substantially in the future adult population.”

With such worrying evidence - combined with the Department of Health’s National Child Measurement Programme which states that already in the UK, one in ten children under the age of six is obese - the next question is why? Two separate studies published last month suggest genetic mutations play a strong role in this increasing obesity risk.

The first - published in Nature Genetics - has identified three previously unknown genetic variations that together can increase a young child’s risk of becoming severely obese by 50%. In the ten-year study, scientists looked at the genetic makeup of obese children under six and morbidly obese adults and compared this with people of normal weight at the same age.

The gene variant most strongly associated with childhood obesity and adult morbid obesity in the study is located near the PTER gene, the function of which is not known. This variant is estimated to account for up to a third of all childhood obesity, and a fifth of all cases of adult obesity. The second variant associated with obesity is found in the NPC1 gene - thought to be an appetite controlling gene - and is thought to account for around 10% of all childhood obesity and about 14% of adult morbid obesity cases. The final variant is found near the MAF gene, which controls the production of the hormones insulin and glucagon, as well as chains of amino acids called glucagon-like peptides. This variant accounts for about 6%of early-onset obesity in children, and 16% of adult morbid obesity.

The second study - published in the International Journal of Obesity - also suggests the tendency to overeat could be genetic.  They found the children who ate more were more likely to have one or two of the 'higher' risk versions of the FTO gene - thought to play a role in appetite.

With the evidence strongly suggesting obesity is on the increase and that this, at least in part, is driven by genetic factors are we in a position to alter the march to a fatter future?
 
Professor Philippe Froguel, one of the authors of the Nature Genetics study points out that simply uncovering the genetic influences in obesity is only the beginning: “Understanding the genetic basis of obesity is the first step towards helping these children. Once we identify the genes responsible, we can develop ways to screen children to find out who is most at risk of becoming obese.”