Bowel cancer: Genetic finding brings screening closer

RESEARCHERS have identified for the first time a gene that triggers bowel cancer, a move that could bring closer a genetic screening test for the disease. The gene, carried by about half the population, appears to increase the risk of developing bowel cancer by 20per cent. Bowel cancer is the second most commonly diagnosed cancer in Australia, accounting for about 13,000 new cases a year. So far, faulty genes have only been implicated in about 5 per cent of all cancers, and 5 per cent of bowel cancers.

In the case of bowel cancers, the genetic defects so far associated with the disease are all thought to be associated with faulty cellular repair mechanisms, meaning that the body loses the ability to kill off cells that start to divide abnormally.

The latest findings, published in international journal Nature Genetics, suggest a faulty gene found on chromosome 8 may trigger bowel cancer, and account for 10per cent of all cases of the disease. Ian Olver, head of Cancer Council Australia, said the implications of the discovery were "several-fold", including the fact that people carrying the gene were 20 per cent more likely to develop bowel cancer. "Now that we have a gene associated with a bigger percentage of bowel cancer cases, we are closer to developing a screening test for bowel cancer," Professor Olver said.

Although the new gene was only responsible for 10 per cent of cases by itself, by adding various other genes associated with an increased risk for the disease researchers could build up "a genetic profile for people likely to develop bowel cancer", Professor Olver said. "It really is a step forward - we have done a lot better at discovering the genes responsible for breast cancer. "Bowel cancer was lagging behind and this has taken it a major step forward."

Up to about 30 per cent of bowel cancers are thought to have a hereditary element, suggesting that even with the new discovery there is much scientists have yet to discover about which genes are involved and how bowel cancers start. The bowel cancer gene identified in the new research is found on the same chromosome as genes already linked to prostate cancer.

Source





Anti-smoking drug may curb drinking

Given that 85 percent of alcoholics also smoke, a drug recently approved as a stop-smoking aid may turn out to be a pharmaceutical two-for-one deal. Varenicline, marketed by Pfizer as Chantix to help people stop smoking, helped rats kick their drinking habit, according to a study published today in the Proceedings of the National Academy of Sciences. This paves the way for clinical studies using this drug to treat alcoholism. "Varenicline is the first drug on the market for nicotine cessation that's not nicotine itself. It's safe," said Selena Bartlett, senior author on the study. "We were surprised to find that this drug also serves to reduce alcohol drinking in animals."

Bartlett directs preclinical development at the Ernest Gallo Research Center at the University of California, San Francisco. For the study, researchers trained rats to drink in order to test the drug's effect on alcohol consumption. Although visions of rats stumbling in a drunken stupor are off the mark, Bartlett's lab got rats to be "social," "chronic" or "heavy" drinkers. When the drug was given at the dose that stems nicotine craving in animals, the amount of alcohol consumed decreased by about half. If given over six days, alcohol intake was reduced over the whole period.

Since "withdrawal" from a drug could lead to an even greater desire for alcohol, Bartlett's team monitored drinking after the last dose of varenicline was given. Coming off the drug did not result in a bad rebound -- alcohol intake was not more than it had been before taking the drug.

Why would a stop-smoking drug curb alcohol craving? Nicotine and alcohol both trigger the brain's reward system. While food, sex and exercise tickle the system, drugs hijack the system and send it into overdrive. The reward comes when nicotine binds to a protein that triggers a "feel-good" chemical called dopamine. A craving comes when the amount of dopamine drops. Varenicline works by binding to the same protein and blocking nicotine. It results in a lower, but constant, level of dopamine, reducing the craving that leads to relapse. Since alcohol indirectly activates the same protein as nicotine, varenicline likely curbs alcohol craving in the same way that it helps with nicotine.

Approval of the drug in humans for alcoholism may be faster than for a drug that has never been tested in humans. In addition to medication, behavioral treatments such as Alcoholic Anonymous are available. The group is neutral on using drugs to curb craving, said Ivo V., an AA member and chair of public information for the Sacramento chapter. (The group does not give out full names of its members.)

Scientists look at alcoholism as a disease. The chronic nature, relapses, genetic links and changes in the brain associated with alcoholism make it a disease, explained Dr. Charles O'Brien, professor of psychiatry at the University of Pennsylvania medical school. Alcoholism is where schizophrenia was in the 1960s because of its public stigma and a lack of attention from drug companies, Bartlett said. "It's really exciting to see that you can help people," Bartlett said, "especially in areas where there is very little help right now."

Source

****************

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.

*********************