Sunday, December 14, 2008

The junk food gene: DNA flaw means two-thirds of us can't stop eating

Genetics again

Slimmer souls have always maintained that a sweet tooth can be banished with a big helping of will-power. But perhaps those who always succumb to the lure of the biscuit tin and the creamcake shop shouldn't feel so guilty about their weakness. The ability to resist or otherwise, it seems, may be built into your DNA.

Researchers say that almost two-thirds of us carry 'junk food genes' making us crave fatty and sugary foods. Those with this genetic flaw eat 100 calories more per meal - the equivalent of a small Kit Kat or a bag of Wotsits. It may not sound much, but over a week, this amounts to an extra 2,100 calories - an entire day's food. The research helps explain why some men and women find it hard to resist fast food, and why some diets are doomed to fail. But it may also lead to ways of treating obesity, which blights the lives of almost a quarter of us.

The scientists, from Dundee University, pinned down the effect of a rogue version of a gene called FTO, they explained in the respected New England Journal of Medicine. The flaw, carried by almost twothirds of Britons, was first linked to obesity last year. Up to 14 per cent of Britons carry two rogue copies of the gene, increasing their risk of obesity by 70 per cent and diabetes by 50 per cent. These people are on average almost half a stone heavier. The 49 per cent who have inherited just one flawed FTO gene are 30 per cent more likely to be obese than those with two normal copies of the gene and 25 per cent more likely to develop diabetes.

It wasn't clear if the flaw led to weight gain by increasing appetite, slowing down metabolism, cutting exercise levels or by making men and women take longer to feel full. But the latest research shows that it drives us to eat calorie-laden foods. Scientists tested the DNA of 100 primary pupils and looked at what they ate for lunch. Although those with the rogue gene didn't eat more, they were drawn to fatty and sugary foods, so took in 100 calories more per meal. The gene did not affect their metabolic rate, exercise levels or how full they felt.

Researcher Professor Colin Palmer said: 'The increase in obesity-seen in children may be largely attributable to the widespread availability of inexpensive and energy-dense foods.' These may be more attractive to those with the genetic variant, he explained. 'One hundred calories in a single sitting is half a Mars Bar. It doesn't seem like a lot but in terms of an increased risk of obesity, it is enough.'

But the effects of the gene are not overpowering, he added. So the 63 per cent of us with the 'junk food gene' should not feel that losing weight is out of our control. 'The advice is the same - you will not become overweight if you do not overeat.'

In an accompanying editorial, Dr Rudolph Leibel, of Columbia University in New York, predicted the advent of genetic tests to give early warning of those at risk of putting on weight.


Found: The hormone that makes teens unbearable

A `Kevin and Perry' hormone that turns angelic children into foul-tempered teenagers has been pinpointed by scientists. Neurokinin B switches on puberty causing the hormonal surge behind the angst and anger of adolescence, the Cambridge University study found.

A better understanding of the hormone could lead to new contraceptives, as well as treatments for sex hormone-fuelled diseases such as prostate cancer. Researcher Professor Steve O'Rahilly said: `This unexpected finding puts one more important piece in the unfinished jigsaw puzzle that is our understanding of puberty. It could also open up new ways of treating certain sex hormone related diseases.'

Analysis of the DNA of Turkish families with members who did not go through puberty, published in the journal Nature Genetics, flagged up neurokinin B's key role in the process. Neurokinin B has been linked to puberty in a handful of animal studies but it had been assumed its main role lay elsewhere. Now it appears it is key to the awkwardness of adolescence epitomised by the Harry Enfield characters Kevin and Perry.

Researcher Dr Robert Semple said: `I am excited by this discovery as it helps to understand the problem in rare patients with inherited defects in sexual maturation and suggests a potential target for their treatment. `However, identifying single genetic defects in patients with rare disorders also has implications for understanding normal regulation of key bodily functions.' He added that a better understanding of neurokinin B's role in puberty could lead to the development of new drugs.

Other research has shown that the teenage brain works differently to its adult counterpart. The result is they do not have the ability to consider how their actions will affect others - leading to them being perceived as sullen, selfish and thoughtless. They also find it harder to put themselves in someone else's shoes and imagine how they might feel in a given situation. The moodiness of adolescence might also be partly explained by differences in teenagers' biological clocks which leave them in a permanent state of `jetlag'.


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