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Archive - 06 - 2010

Teenage Physical Activity Reduces Risk of Cognitive Impairment in Later Life

Posted by dlife on Wed, Jun 30, 10, 09:33 AM 0 Comment

June 30, 2010 (EurekAlert) - Women who are physically active at any point over the life course (teenage, age 30, age 50, late life) have lower risk of cognitive impairment in late-life compared to those who are inactive, but teenage physical activity appears to be most important. This is the key finding of a study of over nine thousand women published today in the Journal of the American Geriatrics Society.

There is growing evidence to suggest that people who are physically active in mid- and late life have lower chance of dementia and more minor forms of cognitive impairment in old age. However, there is a poorer understanding of the importance of early life physical activity and the relative importance of physical activity at different ages. Researchers led by Laura Middleton, PhD, of Sunnybrook Health Sciences Centre, Canada, compared the physical activity at teenage, age 30, age 50, and late life against cognition of 9,344 women from Maryland, Minnesota, Oregon and Pennsylvania to investigate the effectiveness of activity at different life stages.

Of the participants, 15.5%, 29.7%, 28.1%, and 21.1% reported being physically inactive at teenage, at 30 years, at 50 years, and in late life respectively; the increase in cognitive impairment for those who were inactive was between 50% and 100% at each time point. When physical activity measures for all four ages were entered into a single model and adjusted for variables such as age, education, marital status, diabetes, hypertension, depressive symptoms, smoking, and BMI, only teenage physical activity status remained significantly associated with cognitive performance in old age.

"Our study shows that women who are regularly physically active at any age have lower risk of cognitive impairment than those who are inactive but that being physically active at teenage is most important in preventing cognitive impairment," said Middleton.

The researchers also found that women who were physically inactive at teenage but became physically active at age 30 and age 50 had significantly reduced odds of cognitive impairment relative to those who remained physically inactive. In contrast, being physically active at age 30 and age 50 was not significantly associated with rates of cognitive impairment in those women who were already physically active at teenage.

Middleton added, "As a result, to minimize the risk of dementia, physical activity should be encouraged from early life. Not to be without hope, people who were inactive at teenage can reduce their risk of cognitive impairment by becoming active in later life."

The researchers concluded that the mechanisms by which physical activity across the life course is related to late life cognition are likely to be multi-factorial. There is evidence to suggest that physical activity has a positive effect on brain plasticity and cognition and in addition, physical activity reduces the rates and severity of vascular risk factors, such as hypertension, obesity, and type II diabetes, which are each associated with increased risk of cognitive impairment.

"Low physical activity levels in today's youth may mean increased dementia rates in the future. Dementia prevention programs and other health promotion programs encouraging physical activity should target people starting at very young ages, not just in mid- and late life," said Middleton.

When Food Intake Stops, Enzyme Turns Off Production of Fats, Cholesterol

Posted by dlife on Wed, Jun 30, 10, 09:27 AM 0 Comment

June 30, 2010 (EurekAlert) - Massachusetts General Hospital (MGH) investigators have found that an enzyme with several important roles in energy metabolism also helps to turn off the body's generation of fats and cholesterol under conditions of fasting. The report in Genes & Development describes how SIRT1, one of a group of enzymes called sirtuins, suppresses the activity of a family of proteins called SREBPs, which control the body's synthesis and handling of fats and cholesterol. The findings could lead to new approaches to treating conditions involving elevated cholesterol and lipid levels.

"SIRT1 had previously been shown to act as an energy sensor, promoting the use of stored fat in response to food deprivation; however, its function in shutting down fat and cholesterol synthesis was unknown," says Amy Walker, PhD, of the MGH Cancer Center, the study's lead author. "These findings point to SIRT1 as a master regulator of physiologic energy stability that controls the synthesis and storage of fat, as well as its usage as fuel."

Under normal conditions, the body produces appropriate levels of fats and cholesterol, both of which are essential to life. A high-fat diet can cause abnormal elevations in fat and cholesterol levels in the blood, which may lead to cardiovascular disease, type 2 diabetes, hypertension and other serious disorders. If the body is deprived of food for a short time, it shuts down the production and storage of fat and cholesterol and shifts to using stored fats as the primary source of energy. Fasting also is known to turn off the activity of SREBP proteins, and the research team investigated whether direct suppression of SREBPs by SIRT1 was responsible for the metabolic shift.

A series of experiments in worms, fruitflies and mice showed that the versions of SIRT1 present in those animals suppressed SREBP activity and the associated synthesis and storage of fats. They also showed in mouse and human cells that SIRT1 acts on SREBP by removing a protective molecule, marking the protein for degradation, and that inhibiting SIRT1 activity caused levels of SREBP to rise. Treating genetically obese mice fed a high-fat diet with an agent that increases sirtuin activity suppressed the expression of SREBP-regulated fat synthesis genes and also reduced the amount of fat stored in the animals livers.

"This study is significant because it explains the signals that tell the body to burn fat in response to fasting or dieting," says David Sinclair, PhD, a professor of Pathology at Harvard Medical School (HMS) who helped discover the genes that code for sirtuins but was not involved with this MGH-led study. "This improved understanding could help treat and prevent metabolic diseases such as atherosclerosis and type 2 diabetes."

Sirtuins have also been associated with the increased longevity in response to reduced calorie intake observed in several species of animals. Drugs that stimulate sirtuin activity are currently being investigated for treatment of diabetes and related conditions.

"Sirtuin activators could strengthen SIRT1 functions that may be suppressed in individuals with cardiometabolic disorders," explains Anders Nr, PhD, of the MGH Center for Cancer Research, senior author of the current study. "Our results suggest these agents may be able to 'trick' the body into responding as though it was experiencing fasting, with beneficial metabolic consequences, but that hypothesis needs to be tested in future studies." Nr is an associate professor of Cell Biology and Walker is an instructor in Medicine at HMS.

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