Month-July

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Resveratrol may prevent sedentary lifestyle effects

An article published online on June 29, 2011 in the FASEB Journal reveals yet another benefit for resveratrol, a polyphenol found in red wine and grapes. The current research suggests that resveratrol could help protect against the adverse effects of weightlessness during space flight as well as those caused by a sedentary lifestyle, which has been linked to cardiovascular disease, obesity and other health conditions.

July 18, 2011

Nerves need vitamin C

An article published online on June 29, 2011 in the Journal of Neuroscience reveals that the eye’s nerve cells need vitamin C, which suggests the vitamin may be required by other areas of the nervous system.

Henrique von Gersdorff, PhD of Oregon Health & Science University (OHSU) and his associates studied goldfish retinal cells, which are similar to those found in humans.  They found that the cells’ GABA-type receptors, which assist in the modulation of communication between nerve cells, cease to function properly in the absence of vitamin C.  Because these cells are a type of brain cell, the researchers believe that GABA receptors in other parts of the brain may also need vitamin C, and that the vitamin’s antioxidant property helps preserve the cells and receptors from breakdown due to oxidative stress.

“We found that cells in the retina need to be ‘bathed’ in relatively high doses of vitamin C, inside and out, to function properly,” commented Dr von Gersdorff, who is a senior scientist at OHSU’s Vollum Institute “Because the retina is part of the central nervous system, this suggests there’s likely an important role for vitamin C throughout our brains, to a degree we had not realized before . . . Perhaps the brain is the last place you want to lose vitamin C.”

The findings may have implications for other diseases caused by dysfunction of nerve cells in the retina and brain due to GABA receptor malfunction.   “For example, maybe a vitamin C-rich diet could be neuroprotective for the retina — for people who are especially prone to glaucoma,” Dr von Gersdorff stated. “This is speculative and there is much to learn. But this research provides some important insights and will lead to the generation of new hypotheses and potential treatment strategies.”

July 15, 2011

Shortened telomeres associated with elevated emphysema risk

A report published online on July 15, 2011 in American Journal of Respiratory and Critical Care Medicine reveals the discovery of Johns Hopkins researchers of a connection between shorter telomeres—the DNA structures that protect the ends of the body’s chromosomes–and the risk of emphysema. Telomeres shorten with age, and are recognized as a marker of cellular aging.

Johns Hopkins School of Medicine assistant professor of oncology Mary Armanios, MD and her associates compared the effects of six months of cigarette smoke exposure in normal mice and mice bred to have short telomeres. “With age, short telomeres accumulate and cause cells to stop dividing,” Dr Armanios explained. “Telomeres can be thought of as ‘biological clocks’. We wanted to determine whether telomere length itself was why susceptibility to emphysema increases with age.”

“We found that in mice that have short telomeres, there was a significant increased risk of developing emphysema after exposure to cigarette smoke,” Dr Armanios reported. “Although the mice had no lung disease at baseline, after exposure to cigarette smoke, they surprisingly developed emphysema. In contrast, mice with long telomeres did not develop lung disease during our experiments.”

“We found that cells with damaged DNA stopped dividing, and lung cells with too much damage could no longer be repaired, thus contributing to the emphysema,” she observed. “These results are one of the clearest examples of telomere length, which is an inherited factor, interacting with an environmental insult to cause disease. In fact, our results in mice suggest that short telomeres might contribute to how cigarette smoke accelerates aging in the lung in some individuals.”

“Now that we have examined the question of susceptibility in a rigorous genetic model, we can begin to study how telomere length affects emphysema risk in susceptible populations.”

July 13, 2011

More potassium, less sodium linked with fewer deaths over more than a decade

In the July 11, 2011 issue of the AMA journal Archives of Internal Medicine, a team from the Centers for Disease Control in Atlanta and the Harvard School of Public Health report that having a lower sodium to potassium ratio is associated with a reduced risk of dying from any cause over a 14.8 year median period.

Quanhe Yang PhD and colleagues evaluated data from 12,267 adults enrolled in the Third National Health and Nutrition examination Survey Linked Mortality File, a cohort study of all-cause and cardiovascular and ischemic heart diseases mortality. Over a 14.8 year median follow-up period, 2,270 deaths occurred, which included 825 deaths from cardiovascular disease and 433 from ischemic heart disease.

While having a higher sodium intake was associated with a 20 percent higher adjusted risk of dying over follow up, high potassium intake was associated with a 20 percent lower risk. Those whose sodium to potassium ratio was among the top 25 percent of subjects had a 46 percent greater risk of dying from any cause or from cardiovascular disease, and more than twice the risk of dying of ischemic heart disease compared with those whose ratio was lowest.

“Critical issues are whether dietary or pharmacological potassium supplementation would have the same health benefits as consumption from traditional dietary sources and whether the form of potassium matters,” write Lynn D. Silver, MD, MPH and Thomas A. Farley, MD, MPH in an accompanying commentary. “While potassium supplementation may prove to be of benefit to many persons, a considerable number are at high risk for hyperkalemia. Yet some studies suggest that the greater harm may arise from inadequate intake.“

Dr Yang and colleagues conclude that “Public health recommendations should emphasize simultaneous reduction in sodium intake and increase in potassium intake.”

July 11, 2011

Vitamin D helps rid the brain of Alzheimer’s plaque

A report published online on July 8, 2011 in the journal Fluids and Barriers of the CNS describes experiments conducted by a team from Tohoku University in Japan which found a role for vitamin D in clearing the brain of amyloid beta, a toxic compound that accumulates in the plaques that occur in the brains of Alzheimer’s disease patients.  “It was reported that single nucleotide polymorphisms in the vitamin D receptor (VDR) gene increase the risk of impairment of cognitive function and developing Alzheimer’s disease, suggesting a relation between serum vitamin D levels and risk of Alzheimer’s disease,” the authors write in their introduction to the article.

Professor Tesuya Terasaki and his colleagues at Tohuko University’s Graduate School of Pharmaceutical Sciences injected mice with 1 alpha,25-dihydroxyvitamin D3 (the active form of vitamin D3 in the body), the herbal compound forskolin, or a control substance.  The animals were then examined to determine the rate of amyloid beta clearance and brain levels after 24 hours.

The rate of elimination of amyloid beta across the blood brain barrier was 1.3 times greater in mice that received vitamin D compared to those that received the control substance.  At 24 hours, endogenous amyloid beta levels were significantly lower in the vitamin D-treated group.

Forskolin was also shown to enhanced amyloid beta removal from the animals’ brains and while its action appears to be nongenomic, vitamin D’s actions were determined to be both genomic and nongenomic. “Vitamin D appears increase transport of amyloid β across the blood brain barrier (BBB) by regulating protein expression, via the vitamin D receptor, and also by regulating cell signaling via the MEK pathway,” Professor Terasaki explained. “These results lead the way towards new therapeutic targets in the search for prevention of Alzheimer’s disease.”

July 08, 2011

Calorie restriction in older mice prevents birth defects in offspring

A report published online on July 5, 2011 in the Proceedings of the National Academy of Sciences describes the discovery of researchers at Massachusetts General Hospital of a protective effect for calorie restriction against damage chromosomes that cause infertility in older mothers and birth defects in their offspring.

In earlier research, Jonathan Tilly, PhD and his associates observed that female mice given low calorie diets during adulthood maintain their fertility into advanced ages.  For the current study, three month old female mice were divided to receive unlimited food until they reached one year of age or seven months of a calorie restricted diet followed by free feeding until the study’s conclusion.

While mice that had no restrictions on feeding underwent a decline in the number and quality of eggs released during ovulation, animals that received calorie restricted diets released eggs resembling those of healthy young females.  Eggs from non-restricted animals were shown to have chromosome damage, clumping of mitochondria, and a decline in adenosine triphosphate (ATP), the body’s energy molecule.  “We found that we could completely prevent, in a mouse model, essentially every aspect of the declining egg quality typical of older females,” stated Dr Tilly, who is a professor of Obstetrics, Gynecology & Reproductive Biology at Harvard Medical School. “We also identified a gene that can be manipulated to reproduce the effects of dietary caloric restriction and improve egg quality in aging animals fed a normal diet, which gives us clues that we may be able to alter this highly regulated process with compounds now being developed to mimic the effects of caloric restriction.”

Dr Tilly added that the finding could one day benefit older women who wish to conceive, as well as help to prevent chromosomal disorders in children.

July 06, 2011

High folate intake associated with lower, not higher, colorectal cancer risk

The July, 2011 issue of the journal Gastroenterology reports the conclusion of American Cancer Society (ACS) researchers of a reduced risk of colorectal cancer in association with diets that contain higher amounts of the B vitamin folate.  The finding contradicts recent speculation that consuming additional folate via food fortification or supplements could increase the risk of the disease.

For the current study, Victoria Stevens, PhD and her associates evaluated data from 43,512 men and 56,011 women enrolled in the Cancer Prevention Study II Nutrition Cohort.  One thousand twenty-three participants were diagnosed with colorectal cancer from 1999 to 2007:  a period that followed the mandatory fortification of grain products with folic acid to prevent specific birth defects.

High intake of folate and folic acid was found to be associated with a 19 percent reduction in the risk of colorectal cancer compared to low intake.  Although no effect on risk was found between 1999 to 2001, high folate consumption was associated with a lower risk from 2002 to 2007.

The study is the first to examine the association of colorectal cancer risk with folate during a follow-up period that occurred entirely after the implementation of food fortification with folic acid in the United States.  “While folate fortification has been a public health success in reducing the risk of neural tube defects, the potential for an increase risk of cancer has been legitimate,” stated Dr Stevens, who ACS’ is strategic director of laboratory services. “Our study population included many participants who consumed these very high levels of folate and we found no increased risk of colorectal cancer in these individuals. Nonetheless, one randomized clinical trial failed to show folate supplementation reduced the risk of adenomas, the noncancerous colon polyps that can become cancerous, so we need to continue to investigate the influence of folate on cancer development in high risk populations as well as potential differences in the action of natural and synthetic form of this vitamin.”

July 01, 2011

Resveratrol may prevent sedentary lifestyle effects

An article published online on June 29, 2011 in the FASEB Journal reveals yet another benefit for resveratrol, a polyphenol found in red wine and grapes.  The current research suggests that resveratrol could help protect against the adverse effects of weightlessness during space flight as well as those caused by a sedentary lifestyle, which has been linked to cardiovascular disease, obesity and other health conditions.

“Long-term spaceflight induces hypokinesia and hypodynamia, which, along microgravity per se, result in a number of significant physiological alterations, such as muscle atrophy, force reduction, insulin resistance, substrate use shift from fats to carbohydrates, and bone loss,” Stéphane Blanc of the University of Strasbourg in France and colleagues write. “Each of these adaptations could turn to serious health deterioration during the long-term spaceflight needed for planetary exploration.”

The research team tested the effects of resveratrol in rats undergoing simulated weightlessness.  While animals that did not receive resveratrol experienced a reduction in soleus muscle mass and strength, bone mineral density and resistance to breakage, as well as the development of insulin resistance, treatment with resveratrol protected against these conditions.

“There are overwhelming data showing that the human body needs physical activity, but for some of us, getting that activity isn’t easy,” commented FASEB Journal Editor-in-Chief Gerald Weissmann, MD.  “A low gravity environment makes it nearly impossible for astronauts. For the earthbound, barriers to physical activity are equally challenging, whether they be disease, injury, or a desk job. Resveratrol may not be a substitute for exercise, but it could slow deterioration until someone can get moving again.”

“If resveratrol supplements are not your cup of tea, then there’s good news,” he added. “You can find it naturally in red wine, making it the toast of the Milky Way.”