THE OMEGA 3 PHOENIX RISES FROM THE ASHES ONCE AGAIN

Despite many big studies showing it to have no beneficial effects on cancer etc., there still seems to be a compulsion to find that fish oil is good for you. A recent abstract below:

Modulation of prostate cancer genetic risk by omega-3 and omega-6 fatty acids

By Isabelle M. Berquin et al.

Although a causal role of genetic alterations in human cancer is well established, it is still unclear whether dietary fat can modulate cancer risk in a predisposed population. Epidemiological studies suggest that diets rich in omega-3 polyunsaturated fatty acids reduce cancer incidence. To determine the influence of fatty acids on prostate cancer risk in animals with a defined genetic lesion, we used prostate-specific Pten-knockout mice, an immune-competent, orthotopic prostate cancer model, and diets with defined polyunsaturated fatty acid levels. We found that omega-3 fatty acids reduced prostate tumor growth, slowed histopathological progression, and increased survival, whereas omega-6 fatty acids had opposite effects. Introducing an omega-3 desaturase, which converts omega-6 to omega-3 fatty acids, into the Pten-knockout mice reduced tumor growth similarly to the omega-3 diet. Tumors from mice on the omega-3 diet had lower proportions of phosphorylated Bad and higher apoptotic indexes compared with those from mice on omega-6 diet. Knockdown of Bad eliminated omega-3-induced cell death, and introduction of exogenous Bad restored the sensitivity to omega-3 fatty acids. Our data suggest that modulation of prostate cancer development by polyunsaturated fatty acids is mediated in part through Bad-dependent apoptosis. This study highlights the importance of gene-diet interactions in prostate cancer.

J. Clin. Investigations, June 21, 2007. So it works in speciallly prepared mice. Ho Hum!






A jab to halt Alzheimer's could be available within a few years

Vaccine will save patients from worst symptoms of illness



A revolutionary drug that stops Alzheimer's disease in its tracks could be available within a few years. It could prevent people from reaching the devastating final stages of the illness, in which sufferers lose the ability to walk, talk and even swallow, and end up totally dependent on others. The jab, which is now being tested on patients, could be in widespread use in as little as six years. The most common cause of dementia, Alzheimer's affects around 500,000 Britons, with about 500 new cases diagnosed every day as people live longer.

Treatment costs the NHS up to 14billion a year - more than it spends on strokes, heart disease and cancer combined. Existing drugs can delay the progress of the symptoms, but their effect wears off relatively quickly, allowing the disease to take its devastating course. In contrast, the new vaccine may be able to hold the disease at bay indefinitely. Professor Clive Ballard, of the Alzheimer's Society, said: "A successful vaccine would be a groundbreaking treatment advance for the 25million people with Alzheimer's disease worldwide."

Vaccines are typically used to provide immunity to a disease as a preventive measure before it can develop, but this is an example of a therapeutic vaccine, used to treat a disease which has already developed. Known as CAD106, it is the brainchild of scientists at Zurich-based biotechnology firm Cytos, which is also developing anti-smoking, obesity and flu vaccines. Cytos chief executive Dr Wolfgang Renner said: "If it could prevent the progression of Alzheimer's, it would be fantastic."

Early tests showed the vaccine is highly effective at breaking up the sticky protein that clogs the brain in Alzheimer's, destroying vital connections between brain cells. When the jab was given to mice suffering from a disease similar to Alzheimer's, 80 per cent of the patches of amyloid protein were broken up. The vaccine is now being tried out on 60 elderly Swedish patients in the early and middle stages of Alzheimer's. Half of the men and women are being given the vaccine while half are being given dummy jabs. Although the year-long trial is designed to show that the treatment is safe, the researchers will also look at its effect on the patients' symptoms.

While the results are not due until early next year, the initial findings are promising. Dr Renner told a Zurich conference earlier this week: "I am glad to report that the vaccine is very well tolerated." If the trial is successful, larger-scale trials will follow, in which researchers will work out the best dose to give and how often it should be given. The finished product is six to eight years from the market. The vaccine uses a tiny section of the amyloid protein attached to an empty virus shell to trick the immune system into attacking and breaking up deposits of protein clogging the brain.

Scientists at Cytos, who have sold the rights to the vaccine to Swiss pharmaceutical giant Novartis, say the vaccine is likely to be given to those in the early stages of Alzheimer's, to stop the disease from progressing. The development of tests capable of detecting the disease in its earliest stages would allow the jab to be given at the first possible opportunity. It could also be used to keep the disease at bay in those with a strong family history of the illness, and even for the mass vaccination of people in late middle age. However, while the jab may stop the disease in its tracks, it is not expected to repair dead tissue, and so will not be a cure. Nevertheless, preventing the disease's progression would have an enormous impact on sufferers' lives.

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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