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This week 50 years ago
JIM POWELL/IPN/AURORA
This week– THIS WEEK 50 YEARS AGO Fat smokers beware
–Too much of a good thing?
Excess insulin may be bad for the brain COLIN BARRAS
TOO much insulin may be bad for our health, turning the received wisdom about diabetes and Alzheimer’s disease on its head. Mice genetically engineered so that their brains don’t respond to insulin live longer and are less likely than normal mice to develop age-related diseases similar to Alzheimer’s. Insulin plays a key role in encouraging the uptake and storage of glucose by cells. Its effects on the brain are less clear, but previous studies suggested that the hormone may stave off age-related degeneration. “Everybody says insulin is good for you. It keeps cells alive,” says Morris White of the Children’s Hospital in Boston. “But reviews are now starting to suggest that too much insulin can damage the brain and promote Alzheimer’s.” Last week he and his colleagues published research supporting that theory. They genetically 16 | NewScientist | 28 July 2007
engineered mice so that their brains didn’t produce Irs2, a key insulin receptor usually expressed throughout the body. The mice could eat as much food as they wanted and by 2 months of age all had become overweight and glucose intolerant. Like overweight humans, the mice had more insulin in their blood, but remarkably, says White, they did not develop diabetes or the mouse equivalent of Alzheimer’s and lived on average 14 per cent longer than normal mice. “By removing Irs2 from the brain, we protected it from the excess insulin,” says White. This also seemed to lead to healthier brain activity (Science, DOI: 10.1126/science.1142179). White suggests that insulin levels in the rest of the body could be irrelevant to the development of diabetes or Alzheimer’s, provided the brain is protected from excess insulin by removing its Irs2 receptors. “Understanding how insulin is regulated in the brain could
present exciting new treatment opportunities,” says Clive Ballard, director of research at the UK’s Alzheimer’s Society. “A balanced diet and exercise are two suggested ways of keeping insulin levels low in the brain and will also help to reduce the risk of developing dementia.” Others remain sceptical. “It is definitely an exciting result,” says Christian Hölscher of the University of Ulster in Northern Ireland. “But you can’t get insulin desensitisation by simply removing Irs2.” There are other types of insulin receptor in the brain, he says, so the insulin signal will still get through. Hölscher also worries that removing Irs2 could harm health. “If you block insulin receptors in tissue cultures, the cells will die,” he says. White agrees that it is vital that the insulin signal gets through to cells in some way. The key is achieving the right balance, he says. “Removing insulin receptors from the whole body is bad. But regulating Irs2 [in the brain] could be a good thing.” He suggests that controlling insulin activity could benefit people with Alzheimer’s because it drives protein synthesis and the disease is characterised by the build-up of an abnormal protein called beta-amyloid.
It has been common but unproven knowledge for quite some time that people who have given up smoking have found that they put on weight – but how far the two effects are related was always a little in doubt, since the role played by normal middle-age spread was difficult to evaluate. The true position has now been cleared up in an experiment carried out by J. Brozek and A. Keys at the University of Minnesota in the US. They persuaded a group of normal middle-aged men whose weight they had followed for some years to give up smoking. They then matched each abstainer with a smoker who had the same physique and general background. Over the course of two years they discovered that those who smoked put on only a very small amount of weight, while those that had given up increased by more than 9 pounds above their average weight as measured in the two years before they gave up smoking. This seems to provide clear-cut proof that there is a tendency to put on weight after giving up smoking, and the increase persists for at least two years and probably longer. The researchers suggest the reason is that smoking depresses the desire to eat and so counteracts the instincts of the glutton. Smoking is also known to inhibit contraction of the stomach due to hunger. Because obesity is harmful and undoubtedly decreases the expectation of life in middle-aged people, those who give up smoking face an unexpected new hazard. It may well be that the benefit that people secure by reducing their liability to lung cancer is subsequently wiped out by the alternative harm of becoming overweight. So pity the unfortunate tobacco addict. If they happen to be on the stout side, they must steel themselves to not only smoke less but also to diet. It is, it seems, an increasingly hard life. From The New Scientist, 1 August 1957
www.newscientist.com
This week– THIS WEEK 50 YEARS AGO Fat smokers beware
–Too much of a good thing?
Excess insulin may be bad for the brain COLIN BARRAS
TOO much insulin may be bad for our health, turning the received wisdom about diabetes and Alzheimer’s disease on its head. Mice genetically engineered so that their brains don’t respond to insulin live longer and are less likely than normal mice to develop age-related diseases similar to Alzheimer’s. Insulin plays a key role in encouraging the uptake and storage of glucose by cells. Its effects on the brain are less clear, but previous studies suggested that the hormone may stave off age-related degeneration. “Everybody says insulin is good for you. It keeps cells alive,” says Morris White of the Children’s Hospital in Boston. “But reviews are now starting to suggest that too much insulin can damage the brain and promote Alzheimer’s.” Last week he and his colleagues published research supporting that theory. They genetically 16 | NewScientist | 28 July 2007
engineered mice so that their brains didn’t produce Irs2, a key insulin receptor usually expressed throughout the body. The mice could eat as much food as they wanted and by 2 months of age all had become overweight and glucose intolerant. Like overweight humans, the mice had more insulin in their blood, but remarkably, says White, they did not develop diabetes or the mouse equivalent of Alzheimer’s and lived on average 14 per cent longer than normal mice. “By removing Irs2 from the brain, we protected it from the excess insulin,” says White. This also seemed to lead to healthier brain activity (Science, DOI: 10.1126/science.1142179). White suggests that insulin levels in the rest of the body could be irrelevant to the development of diabetes or Alzheimer’s, provided the brain is protected from excess insulin by removing its Irs2 receptors. “Understanding how insulin is regulated in the brain could
present exciting new treatment opportunities,” says Clive Ballard, director of research at the UK’s Alzheimer’s Society. “A balanced diet and exercise are two suggested ways of keeping insulin levels low in the brain and will also help to reduce the risk of developing dementia.” Others remain sceptical. “It is definitely an exciting result,” says Christian Hölscher of the University of Ulster in Northern Ireland. “But you can’t get insulin desensitisation by simply removing Irs2.” There are other types of insulin receptor in the brain, he says, so the insulin signal will still get through. Hölscher also worries that removing Irs2 could harm health. “If you block insulin receptors in tissue cultures, the cells will die,” he says. White agrees that it is vital that the insulin signal gets through to cells in some way. The key is achieving the right balance, he says. “Removing insulin receptors from the whole body is bad. But regulating Irs2 [in the brain] could be a good thing.” He suggests that controlling insulin activity could benefit people with Alzheimer’s because it drives protein synthesis and the disease is characterised by the build-up of an abnormal protein called beta-amyloid.
It has been common but unproven knowledge for quite some time that people who have given up smoking have found that they put on weight – but how far the two effects are related was always a little in doubt, since the role played by normal middle-age spread was difficult to evaluate. The true position has now been cleared up in an experiment carried out by J. Brozek and A. Keys at the University of Minnesota in the US. They persuaded a group of normal middle-aged men whose weight they had followed for some years to give up smoking. They then matched each abstainer with a smoker who had the same physique and general background. Over the course of two years they discovered that those who smoked put on only a very small amount of weight, while those that had given up increased by more than 9 pounds above their average weight as measured in the two years before they gave up smoking. This seems to provide clear-cut proof that there is a tendency to put on weight after giving up smoking, and the increase persists for at least two years and probably longer. The researchers suggest the reason is that smoking depresses the desire to eat and so counteracts the instincts of the glutton. Smoking is also known to inhibit contraction of the stomach due to hunger. Because obesity is harmful and undoubtedly decreases the expectation of life in middle-aged people, those who give up smoking face an unexpected new hazard. It may well be that the benefit that people secure by reducing their liability to lung cancer is subsequently wiped out by the alternative harm of becoming overweight. So pity the unfortunate tobacco addict. If they happen to be on the stout side, they must steel themselves to not only smoke less but also to diet. It is, it seems, an increasingly hard life. From The New Scientist, 1 August 1957
www.newscientist.com