'Fat' gene found by scientists

A GENE that contributes to obesity has been identified for the first time, promising to explain why some people easily put on weight while others with similar lifestyles stay slim. People who inherit one version of the gene rather than another are 70 per cent more likely to be obese, British scientists have discovered. One in six people has the most vulnerable genetic make-up and weighs an average 3kg more than those with the lowest risk. They also have 15 per cent more body fat.

The findings provide the first robust link between a common gene and obesity, and could eventually lead to new ways of tackling one of the most significant causes of ill health in the developed world. Obesity is a main cause of heart disease, cancer and type 2 diabetes. [Rubbish!]

If the biological function of the gene, known as FTO, can now be understood, it could become possible to design drugs that manipulate it to help people to control their weight. "Even though we have yet to fully understand the role played by the FTO gene in obesity, our findings are a source of great excitement," Mark McCarthy, of Britain's University of Oxford, who led the research, said. "By identifying this genetic link it should be possible to improve our understanding of why some people are more obese, with all the associated implications such as increased risk of diabetes and heart disease. New insights will hopefully pave the way for us to explore novel ways of treating this condition."

While it has long been understood from family studies that obesity is heavily influenced by genetics, scientists have struggled to pin down individual genes that are involved. A handful of serious genetic mutations that cause rare obesity disorders such as Prader-Willi Syndrome have been found, but the search for common genes that affect an ordinary person's risk of becoming obese or overweight has remained elusive.

The effect of FTO emerged from a key study of the genetic origins of disease funded by the Wellcome Trust known as the Case Control Consortium, in which 2,000 people with type 2 diabetes had their genomes compared to 3,000 healthy controls. Scientists from Oxford and the University of Exeter first found that certain versions of the FTO gene were more common among people with type 2 diabetes, but that the effect disappeared when the data were adjusted for obesity. This led them to wonder whether FTO really influenced obesity instead, and they followed up their theory in a further 37,000 people.

FTO comes in two varieties, and everyone inherits two copies of the gene. The team found that those who inherit two copies of one variant - 16 per cent of white Europeans - were 70 per cent more likely to be obese than those who inherited two copies of the other variant. The 50 per cent of subjects who inherited one copy of each FTO variant had a 30 per cent higher risk of obesity. Those in the highest risk group weighed an average of 3kg more and those at medium risk were an average of 1.2kg heavier. In each case the extra weight was entirely accounted for by more body fat, not greater muscle or extra height. The results, published in the journal Science, apply to men and women, and to children as young as 7.

FTO will not be the only gene that influences obesity, and inheriting a particular variant will not necessarily make anyone fat. "This is not a gene for obesity, it is a gene that contributes to risk," Professor McCarthy said. The research involved too many people to control for exercise and diet, so it is not yet known whether FTO affects how much people eat or how active they are. But it may explain how people with apparently similar lifestyles differ in propensity to put on weight. Independent experts called the discovery highly significant. Susan Jebb, of the MRC Human Nutrition Unit, said: "This research provides clear evidence of a biological mechanism which makes some people more susceptible to gaining weight in a world where food is plentiful and sedentary lifestyles the norm."

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Gonorrhoea joins 'superbugs' list

US health officials are recommending wider use of a new drug to treat gonorrhoea because the sexually transmitted disease is steadily becoming resistant to the longtime standard antibiotic. Fluoroquinolones, a class of antibiotics that includes Cipro, have been the most common way to treat the bacterial disease since the early 1990s. Since then, gonorrhoea has grown increasingly resistant to those drugs. The Federal Centres for Disease Control and Prevention has recommended that a different class of antibiotics, cephalosporins, be used instead.

"Gonorrhoea has now joined the list of other superbugs for which treatment options have become dangerously few," said Dr Henry Masur, president of the Infectious Disease Society of America. "To make a bad problem even worse, we're also seeing a decline in the development of new antibiotics to treat these infections."

The CDC made the new recommendation after discovering that nearly seven per cent of gonorrhoea cases among heterosexual men in a survey of 26 US cities last year had drug-resistant strains of the disease. In 2001, only about 0.6 per cent of gonorrhoea cases among heterosexual men were drug-resistant. "That leaves us with a single class of highly effective antibiotics," said Dr John Douglas Jr, director of the CDC's division of STD prevention. Other experts called the situation perilous. It's the first time cephalosporins have been recommended to treat gonorrhoea for the entire US population, although the CDC recommended the antibiotics to treat against drug-resistant gonorrhoea in California and Hawaii in 2002. Two years later, the CDC made the same recommendation to treat the bacterial infection among American men who have sex with men.

The newly recommended class of antibiotics includes the generic drug ceftriaxone, also known under the brand name Rocephin, which must be injected and "works very well" although the drug is not commonly stocked in doctor's offices, Douglas said. In contrast, Cipro and other fluoroquinolones were more commonly available and easy to use because they could be taken orally in a single dose. Ceftriaxone must be given as a shot and costs about $US20 ($A24).

The CDC estimates that more than 700,000 people in the US acquire gonorrhoea each year through sexual contact. It is the second most commonly reported infectious disease in the United States, the infectious disease society says. The highest rates of infection are among sexually active teens, young adults and African-Americans. Because many people don't have obvious symptoms, they can unknowingly spread it to others. Though treatable, gonorrhoea puts people at greater risk of catching the AIDS virus. In women, gonorrhoea can cause pelvic inflammatory disease. In men, it can cause epididymitis, a painful condition of the testicles that can lead to infertility if untreated, the CDC said.

In the survey of 26 cities last year, Philadelphia had the highest percentage of drug-resistant cases with almost 27 per cent, followed by areas in California and Hawaii where health officials long have known about gonorrhoea drug resistance. A quarter of gonorrhoea cases among heterosexual men in Honolulu, San Diego and Orange County, California, were drug-resistant, followed by 22.5 per cent of cases in San Francisco and 22 per cent in Long Beach, California. More than 15 per cent of cases in Miami were drug-resistant to the bacteria, the CDC said.

Source

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Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

Trans fats:

For one summary of the weak science behind the "trans-fat" hysteria, see here. Trans fats have only a temporary effect on blood chemistry and the evidence of lasting harm from them is dubious. By taking extreme groups in trans fats intake, some weak association with coronary heart disease has at times been shown in some sub-populations but extreme group studies are inherently at risk of confounding with other factors and are intrinsically of little interest to the average person.

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