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Manore looked at supplements that fell into four categories: products such as chitosan that block absorption of fat or carbohydrates, stimulants such as caffeine or ephedra that increase metabolism, products such as conjugated linoleic acid that claim to change the body composition by decreasing fat, and appetite suppressants such as soluble fibers.

She found that many products had no randomized clinical trials examining their effectiveness, and most of the research studies did not include exercise. Most of the products showed less than a two-pound weight loss benefit compared to the placebo groups.

“I don’t know how you eliminate exercise from the equation,” Manore says. “The data is very strong that exercise is crucial to not only losing weight and preserving muscle mass, but keeping the weight off.”

Manore, professor of nutrition and exercise sciences at OSU, is on the Science Board for the President’s Council on Fitness, Sports and Nutrition. Her research is focused on the interaction of nutrition and exercise on health and performance.

“What people want is to lose weight and maintain or increase lean tissue mass,” Manore says. “There is no evidence that any one supplement does this. And some have side effects ranging from the unpleasant, such as bloating and gas, to very serious issues such as strokes and heart problems.”

As a dietician and researcher, Manore says the key to weight loss is to eat whole grains, fruits, vegetables and lean meats, reduce calorie intake of high-fat foods, and to keep moving. Depending on the individual, increasing protein may be beneficial (especially for those trying to not lose lean tissue), but the only way to lose weight is to make a lifestyle change.

“Adding fiber, calcium, protein and drinking green tea can help,” Manore says. “But none of these will have much effect unless you exercise and eat fruits and vegetables.”

Manore has created general guidelines for a healthy lifestyle. Do not leave the house in the morning without having a plan for dinner. Spontaneous eating often results in poorer food choices. If you do eat out, start your meal with a large salad with low-calorie dressing or a broth-based soup. You will feel much fuller and are less likely to eat your entire entrée. Better yet: split your entrée with a dining companion or just order an appetizer in addition to your soup or salad. Find ways to keep moving, especially if you have a sedentary job. Manore says she tries to put calls on speaker phone so she can walk around while talking. During long meetings, ask if you can stand or pace for periods so you don’t remain seated the entire time. Put vegetables into every meal possible. Shred vegetables into your pasta sauce, add them into meat or just buy lots of bags of fruits/vegetables for on-the-go eating. Increase your fiber. Most Americans don’t get nearly enough fiber. When possible, eat “wet” sources of fiber rather than dry – cooked oatmeal makes you feel fuller than a fiber cracker. Make sure to eat whole fruits and vegetables instead of drinking your calories. Eat an apple rather than drink apple juice. Look at items that seem similar and eat the one that physically takes up more space. For example, eating 100 calories of grapes rather than 100 calories of raisins will make you feel fuller. Eliminate processed foods. Manore says research increasingly shows that foods that are harder to digest (such as high fiber foods) have a greater “thermic effect” – or the way to boost your metabolism.

Source: Oregon State Univ.
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Berries are good for you, that’s no secret. But can strawberries and blueberries actually keep your brain sharp in old age? A new study by researchers at Brigham and Women’s Hospital (BWH) finds that a high intake of flavonoid rich berries, such as strawberries and blueberries, over time, can delay memory decline in older women by 2.5 years. This study is published by Annals of Neurology, a journal of the American Neurological Association and Child Neurology Society, on April 26, 2012.

“What makes our study unique is the amount of data we analyzed over such a long period of time. No other berry study has been conducted on such a large scale,” explained Elizabeth Devore, a researcher in the Channing Laboratory at BWH, who is the lead author on this study. “Among women who consumed 2 or more servings of strawberries and blueberries each week we saw a modest reduction in memory decline. This effect appears to be attainable with relatively simple dietary modifications.”

The research team used data from the Nurses’ Health Study—a cohort of 121,700 female, registered nurses between the ages of 30 and 55—who completed health and lifestyle questionnaires beginning in 1976. Since 1980, participants were surveyed every four years regarding their frequency of food consumption. Between 1995 and 2001, memory was measured in 16,010 subjects over the age of 70 years, at 2-year intervals. Women included in the present study had a mean age of 74 and mean body mass index of 26.

Findings show that increased consumption of blueberries and strawberries was associated with a slower rate of memory decline in older women. A greater intake of anthocyanidins and total flavonoids was also associated with reduced memory decline. Researchers observed that women who had higher berry intake had delayed memory decline by up to 2.5 years.

“We provide the first epidemiologic evidence that berries appear to slow progression of memory decline in elderly women,” notes Dr. Devore. “Our findings have significant public health implications as increasing berry intake is a fairly simple dietary modification to reduce memory decline in older adults.”

This study was funded by grants from the National Institutes of Health (P01 CA87969) and the California Strawberry Commission. The study was independently controlled by the investigators who performed the data analysis.

Source: Brigham and Women’s Hospital



Source: Federation of American Societies for Experimental Biology

Specific enzyme could slow aging in astronauts, elderly [Have full FASEB paper]

Posted In: Strange But True | R&D Daily | Biology | Biotechnology | Chemistry | Diagnostics | Genomics & Proteomics | Technology | Biology | Chemistry | Biotechnology | Biotechnology | Space

Monday, April 30, 2012


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Scientists discover enzyme that could slow part of the aging process in astronauts...and the elderly

New research published online in the FASEB Journal suggests that a specific enzyme, called 5-lipoxygenase, plays a key role in cell death induced by microgravity environments, and that inhibiting this enzyme will likely help prevent or lessen the severity of immune problems in astronauts caused by spaceflight. Additionally, since space conditions initiate health problems that mimic the aging process on Earth, this discovery may also lead to therapeutics that extend lives by bolstering the immune systems of the elderly.

"The outcomes of this space research might be helpful to improve health in the elderly on Earth," said Mauro Maccarrone, Ph.D., a researcher involved in the work from the Department of Biomedical Sciences at the University of Teramo in Teramo, Italy. "In fact, space conditions [cause problems that] resemble the physiological process of aging and drugs able to reduce microgravity-induced immunodepression might be effective therapeutics against loss of immune performance in aging people. 5-lipoxygenase inhibitors, already used to curb human inflammatory diseases, may be such a group of compounds."

Maccarone and colleagues made this discovery by conducting experiments involving two groups of human lymphocytes that were isolated from the blood of two healthy donors. The first group of lymphocytes was exposed to microgravity onboard the International Space Station (ISS). The second group was put in a centrifuge onboard the ISS, to have the same "space environment" as the other group, but a normal Earth-like force of gravity. When programmed cell death (apoptosis) was measured in both groups, the lymphocytes exposed to microgravity showed an increase above what is considered "normal." The group exposed to the simulated Earth gravity showed no unusual differences. Specifically, the researchers believe that this difference is caused by different levels of the 5-lipoxygenase enzyme.

"It's no surprise that bodies need Earth's gravity to function properly," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal, "because we evolved to survive on this planet. As humanity moves into space and potentially to other planets or asteroids, it's clear that we need know how not only to secure habitable conditions, but also how to secure our health. Fortunately, as we learn how to cope with low gravity environments, we also unlock secrets to longevity back home on Earth."

5-Lipoxygenase-dependent apoptosis of human lymphocytes in the International Space Station: data from the ROALD experiment

Source: Federation of American Societies for Experimental Biology

 

Eating Less Keeps the Brain Young

December 20, 2011

Overeating may cause brain aging while eating less turns on a molecule that helps the brain stay young.

A team of Italian researchers at the Catholic Univ. of Sacred Heart in Rome have discovered that this molecule, called CREB1, is triggered by "caloric restriction" (low caloric diet) in the brain of mice. They found that CREB1 activates many genes linked to longevity and to the proper functioning of the brain.

The work was led by Giovambattista Pani, Faculty of Medicine at the Catholic Univ. of Sacred Heart in Rome, and directed by Prof. Achille Cittadini, in collaboration with Prof. Claudio Grassi of the Institute of Human Physiology. The research appears this week in the Proceedings of the National Academy of Sciences USA (PNAS).

"Our hope is to find a way to activate CREB1, for example through new drugs, so to keep the brain young without the need of a strict diet," Pani says.

Caloric restriction means the animals can only eat up to 70 percent of the food they consume normally, and is a known experimental way to extend life, as seen in many experimental models. Typically, caloric-restricted mice do not become obese and don't develop diabetes; moreover they show greater cognitive performance and memory, are less aggressive. Furthermore they do not develop, if not much later, Alzheimer's disease and with less severe symptoms than in overfed animals.

Many studies suggest that obesity is bad for our brain, slows it down, causes early brain aging, making it susceptible to diseases typical of older people as the Alzheimer's and Parkinson's. In contrast, caloric restriction keeps the brain young. Nevertheless, the precise molecular mechanism behind the positive effects of an hypocaloric diet on the brain remained unknown till now.

The Italian team discovered that CREB1 is the molecule activated by caloric restriction and that it mediates the beneficial effects of the diet on the brain by turning on another group of molecules linked to longevity, the "sirtuins". This finding is consistent with the fact that CREB1 is known to regulate important brain functions as memory, learning and anxiety control, and its activity is reduced or physiologically compromised by aging.

Moreover, Italian researchers have discovered that the action of CREB1 can be dramatically increased by simply reducing caloric intake, and have shown that CREB is absolutely essential to make caloric restriction work on the brain. In fact, if mice lack CREB1 the benefits of caloric restriction on the brain (improving memory, etc.) disappeear. So the animals without CREB1 show the same brain disabilities typical of overfed and/or old animals.

"Thus, our findings identify for the first time an important mediator of the effects of diet on the brain," Dr. Pani says. "This discovery has important implications to develop future therapies to keep our brain young and prevent brain degeneration and the aging process. In addition, our study shed light on the correlation among metabolic diseases as diabetes and obesity and the decline in cognitive activities."

Source: Catholic Univ. of Rome

Scientists Tie DNA Repair to Key Cell Signaling Network [Have full text of paper]

Featured In: Academia News | Genomics

Monday, June 18, 2012

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University of Texas Medical Branch at Galveston researchers have found a surprising connection between a key DNA-repair process and a cellular signaling network linked to aging, heart disease, cancer and other chronic conditions. The discovery promises to open up an important new area of research — one that could ultimately yield novel treatments for a wide variety of diseases.

“This is a totally new concept — it goes against current dogma about the role of DNA repair,” said UTMB professor Istvan Boldogh, senior author of a paper on the work now online in the Journal of Biological Chemistry. “We couldn’t believe it ourselves, but the data convinced us.”

Boldogh and his colleagues came up with the idea of a link between DNA repair and cellular signaling after a close examination of the relationship between DNA damage and cell death produced unexpected results. Conventional DNA-repair dogma holds that a cell’s lifespan is determined by the amount of accumulated DNA damage it suffers — the overall corruption of genetic information stored in sequences of molecules called bases, which form the “rungs” of the DNA double helix. The cells used in Boldogh’s study were especially vulnerable to damage because they lacked a key enzyme that repairs the DNA base guanine. According to dogma, this should have shortened the cells’ lives; instead, they actually lived longer than expected. This made Boldogh wonder if another factor was involved in reducing the lifespan of normal cells.

“We proposed the hypothesis that instead of the accumulation of damaged guanine in DNA causing ill effects, what is significant is the release of a DNA-repair byproduct that somehow activates processes that shorten the lifespan of cells,” Boldogh said.

The researchers knew just where to look to find this hypothetical repair byproduct. The majority of DNA damage is caused by ubiquitous reactive oxygen species, very chemically active molecules created as byproducts of respiration. When DNA meets reactive oxygen species, one of the most common results is the transformation of the DNA base guanine into a molecule called 8-oxoguanine, which can produce mutations in genes.

To protect the integrity of the genetic code, cells remove 8-oxoguanine from their DNA with a repair enzyme called OGG1. OGG1 does its job by attaching to a damaged base, cutting it free from the DNA molecule, and then releasing it. Boldogh and his collaborators found that their key byproduct was being produced just after this repair process was completed. Analyzing test-tube, cell-culture and mouse experimental data, they realized that immediately after being released by OGG1, 8-oxoguanine reunites with the repair enzyme, attaching at a bonding site different from the one used previously. And the resulting 8-oxoguanine-OGG1 complex, they found, has the ability to activate the powerful Ras signaling pathways, some of the most important biochemical networks in the cell.

“Ras family proteins are involved in almost every cell function: metabolism, activation of genes, growth signals, inflammation signals, apoptosis,” Boldogh said. “Because it activates Ras pathways, the release of 8-oxoguanine in DNA base repair could be a master regulator of many very basic processes.”

According to Boldogh, learning to control this “master regulator,” could result in profound consequences for biomedical science and human health. “The ability to regulate 8-oxoguanine excision may give us the ability to prevent the inflammation that’s key to a number of chronic diseases — arthritis, atherosclerosis, Alzheimer’s and others,” he said. “We believe it may even enable us to extend lifespan, or at least healthy lifespan, which would be a very big achievement. Possibilities like that make us believe that this discovery is going to be very significant.”

Source: University of Texas Medical Branch at Galveston

 

Hidden Vitamin in Milk Yields Remarkable Health Benefits [Have full text of original paper]

Featured In: Academia News

Friday, June 15, 2012

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A novel form of vitamin B3 found in milk in small quantities produces remarkable health benefits in mice when high doses are administered, according to a new study conducted by researchers at Weill Cornell Medical College and the Polytechnic School in Lausanne, Switzerland.

The findings, recently reported in the June 2012 issue of the journal, Cell Metabolism, reveal that high doses of the vitamin precursor, nicotinamide riboside (NR) — a cousin of niacin — prevent obesity in mice that are fed a fatty diet, and also increase muscle performance, improve energy expenditure and prevent diabetes development, all without side effects.

The Swiss researchers, led by Dr. Johan Auwerx, performed the mouse experiments, while the ability to give the animals sufficient doses of NR was made possible by Weill Cornell Medical College researchers, who played key roles in uncovering the biological story of NR.

"This study is very important. It shows that in animals, the use of NR offers the health benefits of a low-calorie diet and exercise — without doing either one," says Dr. Anthony Sauve, associate professor of Pharmacology at Weill Cornell Medical College.

Dr. Sauve is the pharmacologist and organic chemist who has invented a simple method for efficiently synthesizing NR in large scale. He was first to show that NR increases nicotinamide adenine dinucleotide (NAD) levels in mammalian cells. NAD is a central player in energy metabolism. He has pioneered research into the compound, and he is a leader in investigating how NAD can signal adaptation in cells and in physiology.

"The research also suggests that the effects of NR could be even broader," Dr. Sauve says. "The bottom line is that NR improves the function of mitochondria, the cell's energy factories. Mitochondrial decline is the hallmark of many diseases associated with aging, such as cancer and neurodegeneration, and NR supplementation boosts mitochondrial functioning."

The Swiss researchers call NR a "hidden vitamin" that is believed to also be present in many other foods, although levels are low and difficult to measure. Nevertheless, the effects of NR on metabolism "are nothing short of astonishing."

Got nicotinamide riboside?
The study depended on a series of crucial discoveries by Dr. Sauve and his laboratory colleagues.

NR, related to niacin and other common forms of vitamin B3, was first investigated more than 60 years ago by a Stanford researcher and 1959 Nobel Laureate, Arthur Kornberg. But little more was known about its effects in mammals until Dr. Sauve discovered the effect NR had in stimulating levels of NAD in mammalian cells — work he published in 2007.

NAD allows sugars, fats, and proteins to be converted into energy. Dr. Sauve's research provided the first evidence that NR enhances NAD levels in the mitochondria in mammalian cells in culture. These findings are published in the current study. These cell-based observations were key to the demonstration that NR could stimulate tissue NAD levels in animals, and that it could stimulate NAD-dependent sirtuins, which adapt physiology to the low calorie diets that are known to extend the lifespan of many organisms.

Dr. Sauve invented a relatively simple method for efficiently synthesizing NR in large scale so that its health benefits can be studied. This methodology, which makes it possible to make NR commercially available, was patented by Cornell's Center for Technology Enterprise and Commercialization and subsequently licensed to ChromaDex Corporation.

The development of a means to synthesize NR in adequate quantities was crucial to the current research, and the Sauve lab provided methods and NR to make the study possible. In addition, the biological observations on the effects of NR on NAD levels in cells and on mitochondria were key to the study. Finally, the Sauve laboratory has developed state of the art analytical methods to determine NAD levels in cells, tissues and organelles, and the laboratory provided several key metabolic measurements highlighted in the study.

"Our published scientific work has verified that NR is perhaps the most potent NAD enhancing agent ever identified," he says. His laboratory is also widely recognized for developing an expertise in the measurement of NAD metabolism in cell tissues.

With this compound, the Swiss researchers found that mice on a high-fat diet supplemented with NR gained significantly less weight (60 percent) than mice fed the same diet without NR, even though the mice supplemented with NR ate the same amount of food as mice on the high fat diet not treated with NR. They had improved energy. They were in better shape than the untreated mice, with significantly better endurance and stronger muscles. Additionally, none of the treated mice developed diabetes, as seen in the untreated mice on the high fat diet. And when fed a normal diet, NR treated mice had improved sensitivity to insulin. The NR treated mice also showed lower cholesterol levels. All of these benefits came without toxicity.

While the new study demonstrates that high doses of NR can largely prevent the negative health consequences of a poor diet in mice, Dr. Sauve stresses that the effects of high doses of the vitamin in humans have not been evaluated. "It is important to keep in mind that the amount of NR in milk and other foods appears to be small. We don't know what effects NR would have in humans at relatively high doses," he says.

"Still, we have very encouraging evidence of benefits of NR and NAD augmentation in general from this animal study — and much more work to do," he says.

Source: Weill Cornell Medical College

 

Study Unmasks Regulator of Healthy Life Span
Tue, 2012-12-18 09:43

A new series of studies in mouse models by Mayo Clinic researchers uncovered that the aging process is characterized by high rates of whole-chromosome losses and gains in various organs, including heart, muscle, kidney and eye, and demonstrate that reducing these rates slows age-related tissue deterioration and promotes a healthier life span. The findings appear in Nature Cell Biology.

"We've known for some time that reduced levels of BubR1 are a hallmark of aging and correspond to age-related conditions, including muscle weakness, cataract formation and tumor growth," says co-author Jan van Deursen, Ph.D., of Mayo Clinic. "Here we've shown that a high abundance of BubR1, a regulator of chromosome segregation during mitosis, preserves genomic integrity and reduces tumors, even in the face of some genetic alterations that promote inaccurate cell division. Our findings suggest that controlling levels of this regulator provides a unique opportunity to extend healthy life span."

Researchers studied two lines of transgenic mice, one with moderate expression of BubR1 and the other with high expression. Outcomes of a series of experiments showed that mice with high expression of the gene were dramatically effective in preventing or limiting age-related disease compared to those with moderate expression and especially to wild type mice.

The findings were significant. Only 33 percent of these high expressing mice developed lung and skin tumors compared to 100 percent of the control group. BubR1 overexpression markedly reduced aneuploidy (a state of having an abnormal number of chromosomes), which causes birth defects. Other results showed these mice were protected from muscle fiber deterioration, that they were better performers in treadmill tests, that they had much reduced levels of renal sclerosis, intestinal fibrosis and tubular atrophy — all signs of aging. They also showed higher cardiac-stress tolerance and resistance to age-related retinal atrophy.

Co-author Darren Baker, Ph.D., of Mayo Clinic, says the findings show BubR1 and its associated regulators are "promising targets for a broad spectrum of aneuploid human cancers and key age-related disorders that dictate human health."

The research was supported by the National Institutes of Health grant CA96985, the Ellison Medical Foundation, the Noaber Foundation and the Robert and Arlene Kogod Center on Aging.

Source: Mayo Clinic