Last week's NY Times notes that exercise creates brown fat in rats ... it is a long jump to claim it would happen in humans, but it is very interesting.
The current issue of Nature reports that exercise also promotes cellular autophagy in rats. A long jump to humans, but the lead researcher said this was enough information enough to get her to get into a regular exercise routine. If it pans out it might explain several benefits of exercise.
Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis
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- Congcong He,
- Michael C. Bassik,
- Viviana Moresi,
- Kai Sun,
- Yongjie Wei,
- Zhongju Zou,
- Zhenyi An,
- Joy Loh,
- Jill Fisher,
- Qihua Sun,
- Stanley Korsmeyer,
- Milton Packer,
- Herman I. May,
- Joseph A. Hill,
- Herbert W. Virgin,
- Christopher Gilpin,
- Guanghua Xiao,
- Rhonda Bassel-Duby,
- Philipp E. Scherer
- &Beth Levine
Nature (2012) doi:10.1038/nature10758
Received 22 September 2010 Accepted 06 December 2011 published online 18 January 2012
Exercise has beneficial effects on human health, including protection against metabolic disorders such as diabetes1. However, the cellular mechanisms underlying these effects are incompletely understood. The lysosomal degradation pathway, autophagy, is an intracellular recycling system that functions during basal conditions in organelle and protein quality control2. During stress, increased levels of autophagy permit cells to adapt to changing nutritional and energy demands through protein catabolism3. Moreover, in animal models, autophagy protects against diseases such as cancer, neurodegenerative disorders, infections, inflammatory diseases, ageing and insulin resistance4, 5, 6. Here we show that acute exercise induces autophagy in skeletal and cardiac muscle of fed mice. To investigate the role of exercise-mediated autophagy in vivo, we generated mutant mice that show normal levels of basal autophagy but are deficient in stimulus (exercise- or starvation)-induced autophagy. These mice (termed BCL2 AAA mice) contain knock-in mutations in BCL2 phosphorylation sites (Thr69Ala, Ser70Ala and Ser84Ala) that prevent stimulus-induced disruption of the BCL2–beclin-1 complex and autophagy activation. BCL2 AAA mice show decreased endurance and altered glucose metabolism during acute exercise, as well as impaired chronic exercise-mediated protection against high-fat-diet-induced glucose intolerance. Thus, exercise induces autophagy, BCL2 is a crucial regulator of exercise- (and starvation)-induced autophagy in vivo, and autophagy induction may contribute to the beneficial metabolic effects of exercise.
pushing drugs on children
What if Ritalin doesn't work for A.D.D. on the long term? (via the NY Times). What if it temporarially gets everyone (but the kids) off the hook for problems that may have other causes?
snip
TO date, no study has found any long-term benefit of attention-deficit medication on academic performance, peer relationships or behavior problems, the very things we would most want to improve. Until recently, most studies of these drugs had not been properly randomized, and some of them had other methodological flaws.
But in 2009, findings were published from a well-controlled study that had been going on for more than a decade, and the results were very clear. The study randomly assigned almost 600 children with attention problems to four treatment conditions. Some received medication alone, some cognitive-behavior therapy alone, some medication plus therapy, and some were in a community-care control group that received no systematic treatment. At first this study suggested that medication, or medication plus therapy, produced the best results. However, after three years, these effects had faded, and by eight years there was no evidence that medication produced any academic or behavioral benefits.
I didn't realize Ritalin is a Schedule II Substance .... pretty serious side effects.
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