Antioxidants make people more, not less, prone to diabetes

This is further confirmation of the harm that antioxidants can do. Nasty for the food freaks who gobble them up. Another great theory murdered by a brutal gang of facts

We've all heard about the damage that reactive oxygen species (ROS) - aka free radicals - can do to our bodies and the sales pitches for antioxidant vitamins, skin creams or "superfoods" that can stop them. In fact, there is considerable scientific evidence that chronic ROS production within cells can contribute to human diseases, including insulin resistance and type 2 diabetes.

But a new report in the October 7th Cell Metabolism adds to evidence that it might not be as simple as all that. The researchers show that low levels of ROS - and hydrogen peroxide in particular -- might actually protect us from diabetes, by improving our ability to respond to insulin signals. "Our studies indicate that 'physiological' low levels of ROS may promote the insulin response and attenuate insulin resistance early in the progression of type 2 diabetes, prior to overt obesity and hyperglycemia," said Tony Tiganis of Monash University in Australia. "In a way, we think there is a delicate balance and that too much of a good thing - surprise, surprise - might be bad."

Tiganis' team found that mice with a deficiency that prevented them from eliminating physiological ROS didn't become insulin resistant on a high-fat diet as they otherwise would have. They showed that those health benefits could be attributed to insulin-induced signals and the uptake of glucose into their muscles. When those animals were given an antioxidant, those benefits were lost, leaving the mice with more signs of diabetes.

Tiganis said whether antioxidants are ultimately good for people will probably depend on their state of health or disease. "In the case of early type 2 diabetes and the development of insulin resistance, our studies suggest that antioxidants would be bad for you." Under some conditions, treatments designed to selectively increase ROS in muscle - if they can be devised - might even help, he says.

It's not the first time studies have suggested that antioxidants can be a negative, Tiganis adds. Studies in worms have suggested that antioxidants can shorten lifespan, as have some epidemiological studies in humans. Other recent reports indicate that antioxidants may negate the longer-term benefits of exercise training by lowering the activity of certain genes involved in ROS defense.

Tiganis said it will ultimately be important to work out at what stage ROS go from being good to bad. He suspects it probably depends on the levels and/or the source of their generation. (ROS are generated both on the surfaces of cells and within cells by mitochondria, which convert nutrients such as glucose into energy, he explained.)

Although any health implications of the new findings would require further study, the findings lead Tiganis to suspect it is best not to take daily antioxidant vitamins, especially if you are otherwise healthy. "Do exercise," he says, as this is a natural source of ROS that may promote insulin action.

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Will this drug put an end to monthly misery for women?

Let's hope it is not a new thalidomide

For millions of women it's a misery they cannot avoid. But now they might no longer have to soldier on stoically in the face of agonising period pains. Scientists have made a breakthrough by creating a pill which could put an end to the discomfort.

The key to the drug's potential success is that it is designed to tackle the cause of stomach cramps which leave some women bedridden, rather than just the symptoms. Dr Jim Phillips, of Vantia Therapeutics, the Southampton-based company behind the discovery said: 'Dysmenorrhoea [painful menstruation] affects a large number of women and there is currently no targeted therapy to treat the condition. 'I think it would be fair to call it a breakthrough, there is certainly no other treatment like it. 'From our research there is nothing to suggest it won't work.'

The drug, known for now as VA111913, has already been proved safe and has few side effects, and if secondary trials are successful it could be available within four years. It will now be trialled on 128 women aged between 18 and 35 in Britain and the United States. Volunteers who suffer pain severe enough to interfere with normal daily life will receive doses of the drug for a maximum of six days during their menstrual cycle. The drug works by bringing the hormone vasopressin, which controls the muscles that contract in the uterus wall, down to normal levels.

The company's chief medical officer, Hilary McElwaine-John, said: 'We found that what was on the market did not meet the need of those women who can't even get to work or school because of the pain.' Dr Phillips added: 'We believe this could offer an effective alternative to the over-the-counter painkillers.'

Figures show that period pain affects 80 per cent of women at some point in their lives. Many have tried techniques such as relaxing exercises or placing a hot water bottle on the stomach to try to combat it, and the most common treatments offered to sufferers tend to be over-the-counter pills such as ibuprofen or naproxen. There is such a clamour for ways to ease the discomfort that the therapeutic market for period pains is estimated to be worth more than £600million worldwide.

Dr Phillips estimates that if the drug is successful, the revenue it could bring in could run into the multi-millions. He said: 'We won't get any revenue from it for at least five years, but if it is successful we would be looking for commercialisation partnerships that would be worth tens of millions of dollars in the U.S.'

Period pain is caused by contractions in the womb during menstruation. Each one temporarily stops the blood flow, causing the tissue to be starved of oxygen. At the same time chemicals called prostaglandins are released that induce stronger contractions and can cause more pain.

The result of the trial, which will be taking place over the next two months, will be known by the middle of next year.

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