Do we need yet another weight loss pill?

Smaller waist circumference neededResearchers have recently found a direct connection between the ‘fat’ gene and increased body weight. But how will this improve our health?

The researchers, at Oxford University, have found a direct connection between the ‘fat’ gene (fat mass and obesity-associated gene) and increased weight. The research was published in Nature Genetics.

This gene was found to have multiple variants in 2007 – meaning that its variance in the population could provide an explanation for obesity – so scientists have been searching for its precise connection with obesity since then.

The leaders of the research project have said that the new findings could be used to develop an anti-obesity pill, but any pill resulting from these new findings wouldn’t be available for a long time yet.

The important question is – what would this pill be? Would we take it at birth to make sure we didn’t suffer from obesity? Would it turn into another vaccine we had to line up for at school?

Do we need another magic ‘lose all your ugly fat’ pill?

The diet industry is growing as quickly as obesity levels, which would indicate that something is not quite working.

In 2008, nearly a quarter of adults (over 16 years of age) in England were obese (had a BMI over 30). Just under a third of women, 32%, were overweight (a BMI of 25-30), and 42% of men were overweight.

Amongst children (2-15 years of age), one in six boys and one in seven girls in England were obese in 2008. The number of overweight children was also around one in seven. 

The NHS predicts that the number of overweight and obese people is likely to increase.

The Foresight report, a scientific report used to guide government policy, has predicted that by 2025, nearly half of men and over a third of women will be obese. 

Surely this tells us there should be a greater focus on changing the core reasons for obesity – the decrease in physical activity and increased intake of processed foods. We have to change the focus of our lives from convenience and speed – just look at how well convenience has treated the USA if you need any further evidence.

Most of us spend the majority of our day sitting in front of a computer, then fight to get a seat on the train so we can sit in front of the TV with our dinner. Hands up if you have two or more takeaway dinners a week?

Everything is geared towards us having to expend less and less energy, which is very bad news for our weight and health.

The reason for obesity is clearly much more than a greater susceptibility to the smell of food.

Sorry, we cannot blame our genes for this one.

Scientists identify “fat” gene

London: Scientists have identified an “obesity gene” which predisposes many people to desire fattening foods.

The obesity gene variant is present in 63% of the population, has been
shown to cause people to eat 100 extra calories, on average, at a single

A team at the University of Dundee conducted an eating test with 100
schoolchildren aged between 4 and 10 and found that the children with
the common variant on the `obesity gene’ FTO consumed the extra 100
calories. These children chose to eat food types that contained more
sugar and fats as opposed to more healthy options.

Results of the study are published in this week’s edition of the New England Journal of Medicine.

The research was led by Professor Colin Palmer at the University of Dundee, and included colleagues who are nowbased at the Universities of St Andrews, Brighton and Glasgow Caledonian.

The study measured the metabolism, adiposity (fat distribution),exercise and eating behaviours in the schoolchildren. They were given a test meal at school, which included a mix of options: ham, cheese, crackers, crisps, raisins, grapes, cucumber, carrot, chocolate buttons,water, orange juice and bread rolls. Investigators recorded the foodthat remained on each child’s tray. Importantly, each child wastested with this meal on three occasions to increase the reliability of the results.

Researchers found the gene had no impact on metabolic rates or measures
of physical activity. There was also no evidence that individuals carrying the obesity-related variant had any problem with satiety (knowing when to stop increased calorific intake from a greater consumption of the more fattening foods as opposed to the more healthy options.

“This work demonstrates that this gene does not lead to obesity without overeating and suggests that obesity linked to this gene could be modulated by careful dietary control,” said Professor Palmer, Chair of Pharmacogenomics in the Biomedical Research Institute at theUniversity of Dundee..

“What it effectively shows is that the people with the relevant variants on the gene have a trait which may lead them to eat more unhealthy, fattening foods. I would stress that this is a trait, and not an absolute occurrence.

“The findings do not change the dietary and lifestyle advice to people, which would be to eat relatively healthily and take regular exercise. Doing this will still have a positive effect whether you carry this gene variant or not.

“But these findings do also reinforce the hypothesis that the increase in obesity seen in children over recent years may be largely attributable to the widespread availability of inexpensive and highly energy dense foods, which may be more attractive to the large proportion of the population who carry this genetic variant,” said Professor Palmer.

The results in the newly-published study are also consistent with studies in animals that have shown that feeding or fasting turns the expression of this gene on and off in the regions of the brain that are known to control eating behaviours.

Professor Palmer was part of the large group of scientists from around the UK that discovered the obesity gene, FTO, in 2007. They found that individuals carrying one copy of the variant (49% of the population) have an approximately 30% increased risk of obesity and individuals carrying two copies of the variant (14% of the population) have almost 70% increased risk of obesity. This effect has since been confirmed in many populations around the world.

Work has been continuing to further explore how the gene works.

“What we are doing with this work is debunking the old myths which are still often repeated in relation to obesity: ‘I have big bones’,or ‘I have a slow metabolism’, or indeed ‘it is in my genes’.

While strong genetic effects have been found in extremely rare cases, most obesity is associated with rather weak genetic tendencies that are modifiable by diet and exercise,” said Professor Palmer.

“The genetics of obesity are complicated and it is likely that there are other genes which will have an effect. But we are now clearly seeing the effects of genetic variants like this one in FTO.”