Wednesday, September 09, 2009

On a diet? Then put away those artificial sweeteners... because they may help you GAIN weight

Artificial sweeteners do nothing to help weight loss and could actually cause us to pile on the pounds, scientists say. Our bodies are unable to distinguish between the calorie-free sugar substitutes widely used in the food industry and the real thing, research suggests.

Artificial sweeteners behave in a similar way to sugar, by activating sensors in the gut which are key to the absorption of glucose. As a result, the body processes extra sugar – and all the calories that go with it. For the dieter, it means little or no weight loss. Over time, it could even lead to extra pounds being put on.

Researcher Soraya Shirazi-Beechey said: ‘If someone wants to lose weight, I don’t think artificial sweeteners are going to help. ‘My recommendation is to eat natural foods, but to eat less of them.’

The Liverpool University professor studied the processes in the small intestine by which the sugar or glucose from food is absorbed into the bloodstream. She identified specific cells which detect sugar, releasing hormones essential for its passage through the lining of the gut and into the blood, where it is either burned off or is converted into fat. Crucially, these cells release the hormones when confronted by artificial sweeteners. This primes the gut to absorb real sugar.

Prof Shirazi-Beechey said: ‘Artificial sweetenerscan also activate the glucose sensor and increase the capacity of the intestine to absorb more sugar. ‘You drink diet cola to stay slim but the reverse is true, because the artificial sweeteners can activate the sensor, so you are taking more glucose from your diet.’ Drugs which control the sugar sensor cells, leading to more or less entering the bloodstream, could help treat diseases such as diabetes and obesity.


Vaccine hope after animal leukaemia virus linked to prostate cancer

A rare bit of proper scientific caution in the last sentence below

A virus known to cause leukaemia in animals has been linked to human prostate cancer, suggesting that the disease may have a viral origin. If correct, the finding may lead to more effective screening and vaccination to prevent men from developing the disease.

The main known risk factors for prostate cancer are genetic susceptibility, old age and poor diet. But research suggests that men infected with XMRV, the xenotropic murine leukaemia virus-related virus, may also be more likely to develop the cancer.

Prostate cancer is the most common cancer in British men and the second-most common cause of cancer death after lung cancer. Last year it was diagnosed in about 35,000 men in Britain.

The virus has been shown to cause leukaemia and bone cancer in mice but has never before been detected in humans. It is not known how men come to be infected but one possibility is that it is sexually transmitted.

In the study, details of which were published yesterday in the journal PNAS (Proceedings of the National Academy of Sciences), 200 samples of cancerous prostate tissue and 100 samples of benign tissue were examined. The virus was found in 27 per cent of the prostate cancer samples and was associated with the most aggressive tumours. It was found in 6 per cent of benign samples. Although the study did not explicitly establish a causal link between the virus and the occurrence of cancer, scientists say there are reasons to expect that such a link might exist.

The virus works by inserting a copy of its DNA into the DNA of the cells it infects. Sometimes, as in the case of leukaemia in mice, the virus DNA is inserted next to a gene regulating cell growth. This can disrupt normal cell division,, and lead to a rapid proliferation of the infected cells, eventually leading to a tumour.

The study team are investigating where on the human genome the virus inserts itself and whether it directly affects cell growth. Establishing that the virus is a risk factor would have profound implications for how prostate cancer is screened and treated, according to Professor Greg Towers, an immunologist at University College London. “If this is found to be a cause, I’d expect a big change in policy,” he said. Since viruses are generally easy to detect, testing could pinpoint men at high risk who would then be screened for cancer.

However, developing a vaccine would be a much longer-term project. “If this virus contributes to the development of some prostate cancers, then we could speculate about the possibility of vaccination, similar to the approach used to prevent cervical cancer,” said Chris Parker, a prostate cancer specialist at the Royal Marsden NHS Trust.

Human papillomavirus (HPV), which is sexually transmitted, is present in almost all cases of cervical cancer, although many women carrying it never go on to develop cancer. A vaccine for HPV has been successfully developed and all British girls between 16 and 18 will have been offered vaccination by the end of the year. Scientists are now investigating whether the XMRV virus is also sexually transmitted. A first step will be looking to see if the virus is present in cervical and semen samples.

Helen Rippon, the head of research management at The Prostate Cancer Charity, said: “The findings of this study are intriguing but pose several questions about the role infection has to play in prostate cancer. “The researchers have yet to discover whether the virus is a cause, an effect or simply an innocent bystander in the development of the disease.”


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