Eat less, live longer: Scientists find the secret to a long, indulgent life

It is a challenging time of year to be told that eating less is good for you but evidence has for a long time suggested that cutting down on calories extends life.

Now Italian researchers have identified a molecule produced when people diet that could lead to the development of a drug that mimics the effect of restraint, offering a longer life without the need for self-denial.

Experiments have shown that curbing the amount of food rats eat can extend their lives by 25 to 40 per cent. However, anti-ageing benefits are lost when the rats return to a normal diet.

Among humans, the population of the tropical Okinawan islands in Japan’s extreme south-west are home to more than twice the national average of centenarians. As well as having a healthy diet, their longevity is attributed to their cultural habit of calorie control called hara hachi bu – or “eat until you are 80 per cent full”.

Italian scientists from the Catholic University of Sacred Heart in Rome have now come a step closer to understanding how dieting works. It causes the body to activate a molecule called Creb1 which in turn activates another set of molecules linked to longevity called the sirtuins.

While overeating ages the brain and can lead to Alzheimer’s disease, calorie restriction increases the activity of Creb1 which is known to regulate memory and learning. Research in mice has shown that if they lack the molecule, the benefits in terms of improved memory from cutting down calorie intake are not seen.

Giovambattista Pani, who led the study published in Proceedings of the National Academy of Sciences, said: “Our findings identify for the first time an important mediator for the effects of diet on the brain. Our hope is to find a way to activate Creb1, for example through new drugs, to keep the brain young without the need for a strict diet.” Biologists believe that restricting calories causes animals to go into a state normally reserved for near starvation.

Instead of spending their energy reserves on reproduction, they shut down everything but their basic body maintenance, in preparation for a future time when breeding would stand a better chance of success.

Self-preservation: how to stay healthy

* Jeanne Calment, the oldest person in history, who died in 1997 aged 122, attributed her longevity to a diet rich in olive oil, port and “regular smiling”.

* Cleopatra, queen of ancient Egypt, took baths of asses’ milk to preserve the beauty and youth of her skin.

* In 18th-century France, noblemen were obsessed with the quest for longevity. Some believed that if you found a magic formula it should be stored inside a clock, literally to hold back time.

* Seaweed-eating nations often have higher-than-average life expectancies. In Iceland dried seaweed known as sol is credited with helping nationals to live, on average, to 83, thanks to its fat-absorbing qualities.

* Your parents make a difference if you want to live to a grand age – genetic inheritance plays the most important part.

via Another mince pie? Scientists find the secret to a long, indulgent life – News – Food & Drink – The Independent.

Related articles

• Overeating Bad for Your Brain (grantlawrence.blogspot.com)

Tiny Bugs Are Controlling Your Mind!

Image via Wikipedia

 

 

We reported on earlier research on gut bacteria at McMaster University and at Ohio State University. We also mentioned some heady speculations at Texas Tech University Health Sciences Center on a new field of microbial endocrinology, “where microbiology meets neuroscience.”

In the new study, McMaster researchers take a slightly bolder step. They fed mice a broth containing a “benign” bacterium, Lactobacillus rhamnosus. The scientists chose this partly because, well, they had some around, so why not, and also because related Lactobacillus bacteria are a major ingredient of probiotic supplements and very little is known about their potential side effects.

How it works, maybe

They found that mice whose diets were supplemented with L. rhamnosus for 6 weeks exhibited fewer signs of stress and anxiety in standard lab tests, as reported online in the Proceedings of the National Academy of Sciences. For example, the mice spent more time exploring narrow elevated walkways and wide-open spaces, which are scary to rodents. (That might explain the Jackass movies?)

But how does it work? That’s the part that has been puzzling me. First, the McMaster researchers found changes in the activity of genes in the brain that encode portions of the receptor for the neurotransmiter GABA. GABA typically dampens neural activity, and many drugs for treating anxiety disorders target its receptors. (The Texas Tech guys also suggested GABA effects.)

Then they cut the vegas nerve, which runs between the stomach and brain, and lo and behold, the effects stopped. The findings “open up very exciting speculations” about using probiotics to treat mood disorders in people, says Emeran Mayer, a gastroenterologist at the University of California, Los Angeles. But he said he’s skeptical that the findings will translate easily from mice to people.

Then he squeaked and ran up the wall.

apibestinclass.com

via Tiny Bugs Are Controlling Your Mind! | Before It’s News.

Related articles

• Mind-Altering Bugs (news.sciencemag.org)
• From guts to brains – eating probiotic bacteria changes behaviour in mice | Not Exactly Rocket Science (blogs.discovermagazine.com)
• How Belly Bugs Control Your Mood (psychologytoday.com)

Chemical in plastic containers makes male mice act like females

By Agence France-Presse
Monday, June 27th, 2011 

WASHINGTON — Male mice who were exposed as babies to BPA, a chemical common in canned foods and plastic containers, act more like females and are seen as less desirable mates, a US study showed Monday.

The findings could have implications for how BPA, or Bisphenol A, may affect human development and behavior, said the study published in the Proceedings of the National Academy of Sciences.

“The BPA-exposed deer mice in our study look normal; there is nothing obviously wrong with them. Yet, they are clearly different,” said lead author Cheryl Rosenfeld at the University of Missouri.

“Females do not want to mate with BPA-exposed male deer mice, and BPA-exposed males perform worse on spatial navigation tasks that assess their ability to find female partners in the wild.”

Mother deer mice were fed a diet with levels of BPA that were proportional to the amount the US government considers safe for pregnant women to ingest.

The lab mice were fed this diet for two weeks prior to breeding and throughout lactation.

After their babies were weaned, the offspring were fed a BPA-free diet and their behaviors were monitored into adulthood.

The male mice who were exposed to BPA showed less ability to navigate a maze safely. This skill — useful in the search for potential mating partners — is well developed only in male mice, since females do not seek out mates.

“The untreated mice quickly learned the most direct approach to finding the correct hole, while the exposed males appeared to employ a random, inefficient trial and error strategy,” said the study.

When scientists observed how fertile females regarded the BPA males compared to the unexposed males, they found females preferred the chemical-free males by a factor of two to one.

“These findings presumably have broad implications to other species, including humans, where there are also innate differences between males and females in cognitive and behavioral patterns,” Rosenfeld said.

“Whether there are comparable health threats to humans remains unclear, but there clearly must be a concern.”

The US Food and Drug Administration has noted “some concern” with BPA, an industrial chemical that has been widely used in packaging since the 1960s, and is studying the risks of exposure, the regulatory agency said in January 2010.

The European Union and Canada have banned the use of BPA in baby bottles. However, there is no scientific consensus on the dangers BPA poses, the study said.

Chemical in plastic containers makes male mice act like females | The Raw Story.

Fastest sea-level rise in 2,000 years linked to increasing global temperatures

ScienceDaily (June 21, 2011) — The rate of sea level rise along the U.S. Atlantic coast is greater now than at any time in the past 2,000 years — and has shown a consistent link between changes in global mean surface temperature and sea level.

The findings are published in the journal Proceedings of the National Academy of Sciences (PNAS).

The research, funded by the National Science Foundation (NSF), was conducted by Andrew Kemp, Yale University; Benjamin Horton, University of Pennsylvania; Jeffrey Donnelly, Woods Hole Oceanographic Institution; Michael Mann, Pennsylvania State University; Martin Vermeer, Aalto University School of Engineering, Finland; and Stefan Rahmstorf, Potsdam Institute for Climate Impact Research, Germany.

“Having a detailed picture of rates of sea level change over the past two millennia provides an important context for understanding current and potential future changes,” says Paul Cutler, program director in NSF’s Division of Earth Sciences.

“It’s especially valuable for anticipating the evolution of coastal systems,” he says, “in which more than half the world’s population now lives.”

Adds Kemp, “Scenarios of future rise are dependent on understanding the response of sea level to climate changes. Accurate estimates of past sea-level variability provide a context for such projections.”

Kemp and colleagues developed the first continuous sea-level reconstruction for the past 2,000 years, and compared variations in global temperature to changes in sea level over that time period.

The team found that sea level was relatively stable from 200 BC to 1,000 AD.

Then in the 11th century, sea level rose by about half a millimeter each year for 400 years, linked with a warm climate period known as the Medieval Climate Anomaly.

Then there was a second period of stable sea level during a cooler period called the Little Ice Age. It persisted until the late 19th century.

Since the late 19th century, sea level has risen by more than 2 millimeters per year on average, the steepest rate for more than 2,100 years.

“Sea-level rise is a potentially disastrous outcome of climate change,” says Horton, “as rising temperatures melt land-based ice, and warm ocean waters.”

To reconstruct sea level, the scientists used microfossils called foraminifera preserved in sediment cores extracted from coastal salt marshes in North Carolina. The age of the cores was estimated using radiocarbon dating and other techniques.

To test the validity of their approach, the team compared its reconstructions with tide-gauge measurements from North Carolina for the past 80 years, and global tide-gauge records for the past 300 years.

A second reconstruction from Massachusetts confirmed their findings.

The records were corrected for contributions to sea-level rise made by vertical land movements.

The reconstructed changes in sea level over the past millennium are consistent with past global temperatures, the researchers say, and can be determined using a model relating the rate of sea level rise to global temperature.

“Data from the past helped calibrate our model, and will improve sea level rise projections under scenarios of future temperature increases,” says Rahmstorf.

Support for the research also was provided by the National Oceanic and Atmospheric Administration, United States Geological Survey, the Academy of Finland, the European Science Foundation through European Cooperation in Science and Technology and the University of Pennsylvania.

Fastest sea-level rise in 2,000 years linked to increasing global temperatures.

Painkillers cut antidepressants efficacy

Some of the common painkillers such as Aspirin and Ibuprofen may negatively affect the efficacy of the SSRIs, the most widely used antidepressants.

The SSRIs (selective serotonin reuptake inhibitors) such as Prozac and Celexa are a class of antidepressants commonly taken for depression, anxiety and obsessive-compulsive disorder.

Rockefeller University researchers studied the effect of giving non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin to the mice that were already taking Celexa.

The findings showed lower blood levels of Celexa in the mice taking the combination of the antidepressant and a NSAIDs painkiller.

Reportedly, the symptoms of depression decreased by 55 percent in patients taking an antidepressant and NSAID together while only 45 percent of those who were taking an anti-inflammatory alone experienced a significant relief of depressive symptoms.

Compared with those taking antidepressant alone, mice consuming a combination of painkiller and antidepressant also did worse on tests measuring their stress and depression levels, according to the report published in the journal Proceedings of the National Academy of Sciences.

Moreover, the researchers found the same results after analyzing data from a previous study which had followed more than 4,000 people treated with antidepressants for over 7 years.

“It appears there’s a very strong antagonistic relationship between NSAIDs and SSRIs,” said lead author Jennifer Warner-Schmidt. “This may be one reason why the response rate (in patients of SSRIs) is so low.”

Researchers, however, failed to distinguish between individuals who had taken NSAID only once or twice in the past 12 weeks and those who were regularly taking the drug for conditions such as arthritis.

They were also incapable of reporting the main cause contributing to the findings; as a result, further studies are needed to assess the interaction between NSAIDs and SSRIs.

PressTV – Painkillers cut antidepressants efficacy.

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• Aspirin and Antidepressants Can Mix Badly (online.wsj.com)

Drug ‘cuts stroke or heart attack effects by more than half

By Eleanor Harding
19th April 2011

A simple injection could reduce scarring caused by a heart attack by more than 60 per cent, say scientists

The devastating effects of a heart attack or stroke could be reduced by more than half by a simple injection, a study suggests.

British scientists are developing a treatment they say could reduce scarring in the heart and brain by more than 60 per cent.

The drug has been tested on mice and other mammals – but has also on human blood in a laboratory.

Researchers hope to begin human trials of the drug, developed at Leicester University, within two years.

Its key ingredient is an antibody, which could be administered up to 12 hours of the attack to stop damage to cells.

It helps heart attack victims by preventing the body attacking its own oxygen-starved cells.

Professor Wilhelm Schwaeble, an immunologist who carried out the work, said the findings had the potential to be the ‘biggest breakthrough ever’ in treating victims of the two biggest killers in Britain.

It could also be used to stop the body attacking organ transplants.

‘This is potentially the biggest breakthrough in the treatment of heart attacks and strokes ever,’ Prof Wilhelm told a national newspaper.

‘We could not believe what we saw and nor could the cardiologists. What is amazing is that the drug can be given so long after the attack.

‘Even the slowest ambulance journey in the world is going to get you to hospital within nine hours.’

Strokes and heart attacks are caused by a clot or a bleed which blocking the blood flow, causing other parts of the body to be starved of oxygen.

However, the worst damage is caused around nine to 12 hours afterwards, when circulation returns to normal but the body’s immune system attacks the oxygen-starved cells.

This causes inflammation and accounts for more than 80 per cent of the permanent damage – often leading to death or serious disability.

Scientists claim the injection stops the body attacking oxygen-starved cells – allowing them to oxygenate normally and therefore reducing permanent damage.

Prof Wilhelm added that the drug could have even more of an effect than the widely-used statins, which lower cholesterol.

The research, published in the Proceedings of the National Academy of Sciences (PNAS), centred around a protein called OMS646.

It was found to knock out MASP-2, enzyme responsible for the immune attack, and is so effective that only two injections would be needed.

Cardiovascular disease, including heart disease and stroke, claims the lives of around 200,000 British people every year.

Drug ‘cuts stroke or heart attack effects by more than half’ | Mail Online.

Scientists find gene linked to alcohol consumption

LONDON – Scientists have identified a gene that appears to play a role in regulating how much alcohol people drink and say their finding could help the search for more effective treatments for alcoholism and binge drinking.

In a study of more than 47,000 people, an international team of scientists found that people who have a rarer version of a gene called AUTS2 drink on average 5 per cent less alcohol than people with the more common version.

The AUTS2 gene, also known as called “autism susceptibility candidate 2″ has previously been linked to autism and attention deficit hyperactivity disorder (ADHD), but its actual function is not clear, the researchers said.

“Of course there are a lot of factors that affect how much alcohol a person drinks, but we know . . . that genes play an important role,” said Paul Elliott of Imperial College London, who was part of the team conducting the study.

“The difference this particular gene makes is only small, but by finding it we’ve opened up a new area of research.”

According to the World Health Organization, harmful use of alcohol results in 2.5 million deaths a year globally.

It is the world’s third largest risk factor for causing diseases such as neuropsychiatric disorders like alcoholism and epilepsy, as well as cardiovascular disease, cirrhosis of the liver and various forms of cancer.

Gunter Schumann from the Institute of Psychiatry at King’s College London said combining genetic studies and behavioural data should help scientists better understand the biological basis of why people drink, some of them to excess.

“This is an important first step towards the development of individually targeted prevention and treatments for alcohol abuse and addiction,” he said.

In their study, published in the Proceedings of the National Academy of Sciences (PNAS) journal, the team analysed DNA samples from over 26,000 volunteers to search for genes that appeared to affect alcohol consumption, and then checked their findings in another 21,000 people. The volunteers answered questionnaires to report how much alcohol they drank.

After identifying AUTS2, the scientists analysed how active the gene was in samples of donated brain tissue. They found that people with the version of the gene linked to lower alcohol consumption had higher activity of the gene.

The researchers also looked at strains of mice that had been selectively bred according to how much alcohol they drink voluntarily, and found there were differences in the AUTS2 gene activity levels among different breeds.

In another part of the study using flies, the researchers found that blocking the effect of a fruit fly version of the same gene made the flies less sensitive to alcohol. This suggests AUTS2 seems to be involved in regulation of alcohol intake in a number of different species, they said.

© Copyright (c) Reuters

Scientists find gene linked to alcohol consumption.

Neuroplasticity: New insight into the brain’s ability to reorganize itself

Image by Mark Cummins via Flickr

ScienceDaily (Mar. 19, 2011)

When Geoffrey Murphy, Ph.D., talks about plastic structures, he’s not talking about the same thing as Mr. McGuire in The Graduate. To Murphy, an associate professor of molecular and integrative physiology at the University of Michigan Medical School, plasticity refers to the brain’s ability to change as we learn.

Murphy’s lab, in collaboration with U-M’s Neurodevelopment and Regeneration Laboratory run by Jack Parent, M.D., recently showed how the plasticity of the brain allowed mice to restore critical functions related to learning and memory after the scientists suppressed the animals’ ability to make certain new brain cells.

The findings, published online this week in the Proceedings of the National Academy of Sciences, bring scientists one step closer to isolating the mechanisms by which the brain compensates for disruptions and reroutes neural functioning — which could ultimately lead to treatments for cognitive impairments in humans caused by disease and aging.

“It’s amazing how the brain is capable of reorganizing itself in this manner,” says Murphy, co-senior author of the study and researcher at U-M’s Molecular and Behavioral Neuroscience Institute. “Right now, we’re still figuring out exactly how the brain accomplishes all this at the molecular level, but it’s sort of comforting to know that our brains are keeping track of all of this for us.”

In previous research, the scientists had found that restricting cell division in the hippocampuses of mice using radiation or genetic manipulation resulted in reduced functioning in a cellular mechanism important to memory formation known as long-term potentiation.

But in this study, the researchers demonstrated that the disruption is only temporary and within six weeks, the mouse brains were able to compensate for the disruption and restore plasticity, says Parent, the study’s other senior author, a researcher with the VA Ann Arbor Healthcare System and associate professor of neurology at the U-M Medical School.

After halting the ongoing growth of key brain cells in adult mice, the researchers found the brain circuitry compensated for the disruption by enabling existing neurons to be more active. The existing neurons also had longer life spans than when new cells were continuously being made.

“The results suggest that the birth of brain cells in the adult, which was experimentally disrupted, must be really important — important enough for the whole system to reorganize in response to its loss,” Parent says.

Additional Authors: Benjamin H. Singer, Ph.D., Amy E. Gamelli, Ph.D., Cynthia L. Fuller, Ph.D., Stephanie J. Temme, all of U-M

The research was supported by grants from the National Institutes of Health, National Institute on Aging, National Institute of Neurological Disorders and Stroke. Temme is a National Science Foundation Graduate Research Fellow and was also supported by a U-M Rackham Merit Fellowship.

---

Journal Reference:

1. B. H. Singer, A. E. Gamelli, C. L. Fuller, S. J. Temme, J. M. Parent, G. G. Murphy. Compensatory network changes in the dentate gyrus restore long-term potentiation following ablation of neurogenesis in young-adult mice. Proceedings of the National Academy of Sciences, 2011; DOI: 10.1073/pnas.1015425108

New insight into the brain’s ability to reorganize itself.

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It’s never too late to grow your brain

Image via Wikipedia

It’s never too late to start exercising, especially when it comes to brain fitness.

Neurologists have long known that our brains get slightly smaller as we grow older and that this shrinkage is associated with a gradual decline in certain mental functions. Previous research has demonstrated that regular exercise can slow the pace of shrinkage and help protect memories and preserve the ability to learn new things.Now, a new study suggests that even starting an exercise program later in life can undo some of the brain shrinkage in seniors who’ve spent years as couch potatoes.

• How to grow your brain

“Our results show we can reverse the atrophy that was already taking place,” said the lead researcher, Kirk Erickson of the University of Pittsburgh.

For the study, they recruited 120 healthy but sedentary volunteers, ranging in age from 60 to 80. (None had been diagnosed with dementia or were suspected of having Alzheimer’s disease.)

Half of the seniors were given an aerobic exercise regimen of walking around a track for 40 minutes a day, three days a week. Aerobic exercise is designed to increase the heart rate for an extended period.

The other half served as a control group. They were told to do stretching and toning exercises – activities that would barely budge their heart rates.

Each participant underwent a series of MRI scans to measure changes in the size of the hippocampus, the brain structure involved in all forms of memory formation.

The findings, published in the Proceedings of the National Academy of Sciences, revealed a dramatic difference in the two groups after one year. The walkers experienced increases in volume of the left and right hippocampus by 2.12 and 1.97 per cent respectively. The same regions of the brain in those who did stretching decreased by 1.40 and 1.43 per cent, respectively, which amounts to the normal expected shrinkage.

“You can think of the increase in volume of the hippocampus as turning back the clock by about two years,” explained the senior author of the study, Art Kramer of the University of Illinois.

Furthermore, the bigger brains seemed to work better. Tests conducted over the course of the study showed that those in the aerobic exercise group demonstrated improved memory function, compared with their performance measured at the beginning of the trial.

The researchers are continuing to observe the volunteers. Dr. Erickson expects that hippocampus expansion of the walkers “will eventually slow down and stop” because the brain generally shrinks with age. But when atrophy does becomes apparent once more, the rate of shrinkage will likely be slowed if they keep exercising regularly.

Dr. Kramer stressed that it doesn’t take a complex or particularly strenuous exercise program to produce meaningful results. “All you need is a pair of walking shoes and a place to walk,” he added.

It’s never too late to get your brain off the couch, study finds – The Globe and Mail.