IT COULD BE IN YOUR FOOD
Or, your child's food for that matter. In a study commissioned by the UK government, researchers at the Davis Hide Asthma and Allergy Research Centre used 227 children to investigate the effects of food additives on behavior. For two weeks, children were given a juice drink containing various food colorings and preservatives in doses below those permitted by the UK food regulatory ageny. For the following two weeks, they were given a placebo drink that looked exactly the same, but contained none of the additives. The childrens' parents recorded all behavior during the month long experiment. The study was well controlled in that none of the children, parents, nor researchers knew when the children were receiving either drink type. It is interesting to note that even though standard psychological testing was unable to unearth any behavioral changes in the children, fully one-quarter of the parents reported increased disruptive behavior in their children. Some of the disruptive behavior was noted in children who had no prior history of hyperactivity. Read more at
New Scientist.
LONG LIVE THE WORM!!!
Researchers at the University of California, San Francisco have silenced a gene that affects worm lifespan, and in doing so, doubled nematode life-expectancy. The gene is called daf-2, and is present in many lifeforms. However, this gene has been meddled with before. In 1993, Cynthia Kenyon (the author of this current research), knocked the gene out during the hatching phase of development. This resulted in longer living worms, but none could reproduce. This time around, Kenyon has silenced the gene at the onset of adulthood (so, after the worm has completed developing), and the result is reproductively viable long-lived worms. This suggests that the gene is responsible for two distinct pathways in the life-cycle of the worm: reproductive development during the early phases of the cycle, and life-span once the worms reach adulthood. The next question is when will somebody try to shut this gene off in humans???
BELLY FULL OF INSULIN RESISTANCE
Insulin resistance is a precursor to diabetes. Insulin is the molecule responsible for allowing our bodies to absorb glucose. When a person is insulin resistant that means that they can no longer absorb glucose efficiently. This leads to high blood sugar levels, which in turn lead to health problems associated with diabetes. It has long been known that as people age they have a higher likelihood of retaining fat. There are two types of fat in question; visceral fat (fat found internally around abdominal organs) and subcutaneous fat (the fat that forms love-handles). It is also known that as this fat deposition occurs, insulin resistance is likely to become a problem. The questions have been 1)whether visceral or subcutaneous fat is the culprit, 2) whether the culprit causes the resistance, or 3) whether the culprit is a bi-product of insulin resistance. To answer the question, researchers at the Albert Einstein College of Medicine in New York City removed fat from insulin resistant rats. Those from which subcutaneous fat was removed showed no change in insulin resistance, but those which had visceral fat removed suddenly regained their ability to process glucose as well as young rats who had never been through a surgical procedure. This suggests that it our culprit is visceral fat, and that it is the fat that causes insulin resistance. Secondarily, the researchers also found that removing visceral fat altered the molecular signals that subcutaneous fat produced and released into the bloodstream. Overall, fewer insulin blocking molecules were released, and production of the hormone leptin, which alters appetite, was also decreased. This research goes a long way toward proving that calorie restriction and weight control might be important methods for decreasing one's likelihood of acquiring or abolishing age-related insulin resistance.
current science news posted by Kirsten at 10/29/2002 10:37:00 PM
KYOTO PROTOCOL KEY CARBON SINK ISSUE IS FLAWED
Bad news on the environmental front. In a presentation at the CarboEurope conference in Spain last week, evidence showing the harmful effects of forest carbon sinks was presented by researchers from Italy�s University of Tuscia. �Carbon sink� is the term generally used for any aggregate of elements that removes carbon from the atmosphere; forest, the oceans, and certain types of soil bacteria and fungi act as carbon sinks. One of the key issues of the Kyoto accords was that nations could earn �carbon credits� by planting forests. The idea was that such forests would offset projected emissions from any given nation�s industrial carbon output by fixing carbon from the atmosphere. However, the Italian researchers have shown that planting such forests will actually, possibly counter-intuitively, increase the amount of carbon dioxide for at least a decade after planting. The issue arises when vast amounts of soil are tilled in preparation for the planting of young trees. Huge amounts of carbon are released from the soil into the atmosphere during this process, far more than will be re-absorbed by the new forest until at least a decade has passed, in most cases. Related studies from Amsterdam have also shown that moist soils of peat will always release more carbon than their flora absorbs. Furthermore, it has only recently been discovered that older trees pull carbon from the air quicker than young trees, suggesting that it may be wiser to conserve old forests.
current science news posted by ted at 10/29/2002 09:17:00 PM
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