The Daily Telegraph reported today on a "greedy gene" that causes some children to eat 100 extra calories at every meal. It said scientists had discovered that the gene appears to make...
The Daily Telegraph reported today on a "greedy gene" that causes some children to eat 100 extra calories at every meal. It said scientists had discovered that the gene appears to make the children avoid healthy meal options and eat fatty and sugary foods. The effect could be greater in adults, with those carrying it eating up to 15% more at mealtimes.
This gene variant is very unlikely to be the only explanation for differences in weight between individuals and there may be other genes involved in obesity. The variant is a common one and thought to be present in over half of all people.
This research behind the story does not argue for a single cause to obesity, as the headline might suggest. Instead, it aimed to gain a better understanding of the complex interactions between genes and environment.
Regular exercise and a healthy diet remain the best ways to control and lose weight.
Where did the story come from?
Dr Joanne E Cecil from the Bute Medical School, University of St Andrews and colleagues from Dundee, Brighton and Glasgow, carried out this research. It was funded by the UK Biotechnology and Biological Sciences Research Council and published in the peer-reviewed New England Journal of Medicine.
What kind of scientific study was this?
In this cross-sectional study, 2,726 Scottish children between four and 10 years of age underwent genotyping (scanning their genetic make-up) for a variant of the fat mass and obesity-associated (FTO) gene, rs9939609. Variants are the specific differences on the genetic code within the gene that individual people demonstrate. The children’s height and weight were also measured. A sample of 97 children was then examined for a possible association of the FTO variant with fat mass, energy expenditure and food intake.
The researchers were interested in the FTO gene because it has provided the most robust links with common obesity to date. However, it is unknown how the FTO variants affect energy balance.
The 2,726 children were recruited from the Energy Balance Study, which is an investigation of many different potential genetic and non-genetic associations thought to be involved in the maintenance of energy balance in children. The DNA was isolated from saliva samples with consent from the parents or guardians and with the agreement of the children. The subset of children (97) used in this study were those who had data available for fat mass, energy expenditure, and eating behaviour. They also were more likely to have variants of another gene known as the peroxisome proliferator-activated receptor gene - also studied by obesity researchers.
The researchers took a variety of body measurements such as height, weight, body mass index (BMI), waist circumference and skin fold thickness. They assessed food intake at a test-meal lunch on three separate occasions. The children ingested a drink or a combination of food and drink that varied in energy density. The first was a pre-meal drink with a zero-energy control consisting of 250ml of water (0 kJ). On the second occasion, the children were given a low-energy combination of a 250ml orange drink and 56g muffin (783 kJ). On the third occasion, they had a high-energy combination of a 250ml orange drink and 56g muffin (1628 kJ). The amount of food subsequently consumed at the test meal was assessed by weighing the food items before and after eating.
Energy expenditure, defined as the resting metabolic rate of the children, was tested using a standard process known as indirect calorimetry. The children were placed under a ventilated hood and measurements of their oxygen consumption and carbon dioxide output after approximately four minutes allowed the researchers to calculate the resting energy expenditure.
What were the results of the study?
In the total study group and the subsample, the variant known as the ‘A allele of rs9939609’ was significantly associated with increased weight and BMI. In the subsample of 97 children, the ‘A allele’ was also associated with increased fat mass but not with lean mass.
Seventy-six of the children completed the test meal. When the researchers measured the resting metabolic rates of the children (the energy they used when they sat still and when they moved) they found that the rate increased in the children with the A allele in line with the predicted increases for the age and weight of the child. This suggests that the risky A allele is not acting by simply changing the resting metabolic rate in those who carry the variant.
The researchers also report that the A allele was associated with increased energy intake independently of body weight. In contrast, the weight of food ingested by children who had the allele was similar to that in children who did not have the allele.
What interpretations did the researchers draw from these results?
The researchers say that the FTO variant, the A allele, is linked to obesity but does not appear to be involved in the regulation of energy expenditure. They say that it may have a role in the control of food intake and food choice.
This effect, they suggest, may be due to a tendency for people who have the variant to overeat or to prefer energy-dense foods.
What does the NHS Knowledge Service make of this study?
This reliable study has shown that children carrying the A allele ate more energy-dense foods than the children who were not carrying the A allele, indicating a preference for energy-dense foods. However, as this was a small study, more research is required to confirm these observations.
In addition, the researchers were unable to examine the effect of being homozygous for the A allele (having two copies of the variant) as compared to being heterozygous (having only one) and this will be an important part of future research.
This research does not argue for a single cause for obesity, as the headline might suggest. Instead, its main purpose was to help researchers to understand the complex interactions between people’s genes and their environment.
Similar research might eventually also provide an explanation as to why it is difficult for some individuals to use willpower to change their behaviour.
Sir Muir Gray adds...
The conclusion is simple, all children should take more exercise and have a healthier diet.