Three new obesity genes discovered

Shhhh!

Three new genes that may be involved in obesity have been discovered with a new method for investigating the genetic origins of ill-health

In standard genetic studies, researchers compare the genomes of people with a medical condition and control subjects who are free from it, in search of the DNA markers that are more common in one group or the other. But in the new approach, scientists from the United States looked first at the fat and liver tissue of obese mice. By comparing their gene expression profiles with those of normal mice, they were able to identify three genes, called Lpl, Lactb and Ppml1 that appear to control weight gain.

Using the technique, the US team – led by Eric Schadt, of Rosetta Pharmaceuticals in Seattle – was also able to discover how the genes are switched on and off. The genes were found to promote inflammation in mice which in turn encouraged obesity. If these genes have similar effects in humans, it would add to the number of genes known to affect obesity. Last year a British team discovered the first gene to be reliably associated with obesity, called FTO. The research is published in the journal Nature.

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Hope for blindness prevetion?

A protein found in blood cells could be the key to treating or preventing two of the commonest causes of blindness, scientists in the United States believe. In mice that simulate the processes of age-related macular degeneration (AMD) and diabetic retinopathy, damage was prevented by drugs that activate a protein called Robo4, they report in Nature Medicine. The protein stopped the growth of abnormal blood vessels and stabilised existing ones, according to Professor Dean Li and colleagues from the University of Utah in Salt Lake City.

Abnormal blood vessel growth and leakage are two primary factors in AMD and diabetic retinopathy. “Many diseases are caused by injury or inflammation destabilising blood vessels and causing them to leak fluid into adjacent tissues” Professor Li said. “We found a natural pathway – the Robo4 pathway – that counter-attacks by stabilising blood vessels.”

New treatments are needed for both conditions. AMD is the commonest cause of loss of sight in the elderly and diabetic retinopathy is the commonest cause in people of working age. Treatments for one form of AMD do exist, but the best drugs are extremely expensive and at best slow down the disease. Many patients with AMD have been denied treatment with Lucentis on the NHS, at least until they have lost the sight of one eye.

The implications of the finding may go even farther because there are other diseases, such as severe acute respiratory syndrome, in which blood vessel stability is lost, allowing fluids to leak into the lungs. Tumours hijack blood vessel growth to feed on nutrients. Although this study did not prove Robo4 would treat those diseases, Professor Li believes it merits investigation.

Scientists from the University of Bristol said last week that they were ready to launch clinical trials of a drug to treat AMD and diabetic retinopathy. Professor Dave Bates and Dr Steve Harper have identified a naturally occurring form of vascular endothelial growth factor (VEGF) that inhibits the formation of new blood vessels. Professor Bates said: “We discovered the potential of VEGF165b in 2001 and have spent the last six years proving its efficacy. We plan to demonstrate clinical proof of concept of the drug in diabetic retinopathy and wet AMD patients by mid2009 so this is a very exciting time for us.” The drug technology, which has been developed with the help of the charity Fight for Sight, is being licensed to a biopharmaceutical company, PhiloGene Inc.

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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].

9). And how odd it is that we never hear of the huge American study which showed that women who eat lots of veggies have an INCREASED risk of stomach cancer? So the official recommendation to eat five lots of veggies every day might just be creating lots of cancer for the future! It's as plausible (i.e. not very) as all the other dietary "wisdom" we read about fat etc.

10). And will "this generation of Western children be the first in history to lead shorter lives than their parents did"? This is another anti-fat scare that emanates from a much-cited editorial in a prominent medical journal that said so. Yet this editorial offered no statistical basis for its opinion -- an opinion that flies directly in the face of the available evidence.

Even statistical correlations far stronger than anything found in medical research may disappear if more data is used. A remarkable example from Sociology:

"The modern literature on hate crimes began with a remarkable 1933 book by Arthur Raper titled The Tragedy of Lynching. Raper assembled data on the number of lynchings each year in the South and on the price of an acre's yield of cotton. He calculated the correlation coefficient between the two series at -0.532. In other words, when the economy was doing well, the number of lynchings was lower.... In 2001, Donald Green, Laurence McFalls, and Jennifer Smith published a paper that demolished the alleged connection between economic conditions and lynchings in Raper's data. Raper had the misfortune of stopping his analysis in 1929. After the Great Depression hit, the price of cotton plummeted and economic conditions deteriorated, yet lynchings continued to fall. The correlation disappeared altogether when more years of data were added."

So we must be sure to base our conclusions on ALL the data. But in medical research, data selectivity and the "overlooking" of discordant research findings is epidemic.

"What we should be doing is monitoring children from birth so we can detect any deviations from the norm at an early stage and action can be taken". Who said that? Joe Stalin? Adolf Hitler? Orwell's "Big Brother"? The Spanish Inquisition? Generalissimo Francisco Franco Bahamonde? None of those. It was Dr Colin Waine, chairman of Britain's National Obesity Forum. What a fine fellow!

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