Seeking Longer Lives; Slower Aging; Even Immortality

[ramonmercado]

Calorie Restriction And Increased Longevity Linked To Metabolic Changes
28 Apr 2007

In a study of Labrador retriever dogs, those fed a calorie-restricted diet showed different lifelong patterns relating to energy metabolism and the activities of their gut microbes and lived almost two years longer than similar dogs given a slightly higher-calorie diet. The study, which followed 24 dogs lifelong, is scheduled for the May 4 issue of ACS' Journal of Proteome Research, a monthly publication.

Imperial College London's Jeremy K. Nicholson and colleagues from Nestle and Nestle Purina Research centers in Switzerland and the United States point out that previous studies on a range of animals have established calorie restriction as a proven method for extending the lifespan of animals. Those studies, however, have not explained how calorie restriction works.

The new study aimed at improving knowledge of the metabolic effects of caloric restriction suggests that some of the important beneficial changes may relate to the activities of the symbiotic bacteria that live in the intestinal tract. Those microbes produce a range of biochemicals that may influence disease processes and alter energy metabolism in the host organism. Researchers paired 24 dogs, with one dog in each pair given 25 percent less food than the other. Those with a restricted intake of calories lived, on average, about 1.8 years longer than those with a greater intake. Researchers noted that the study's main goal was to help develop diets that keep pet animals alive and healthy for as long as possible, but that the findings may be relevant to human dietary changes and obesity.

"Metabonomic Investigations of Aging and Calorie Restriction in a Life-Long Dog Study"

CONTACT:
Jeremy K. Nicholson, Ph.D.
Imperial College London
London, UK

###

ACS News Service Weekly PressPac -- April 18, 2007

The American Chemical Society - the world's largest scientific society - is a nonprofit organization chartered by the U.S. Congress and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.

Contact: Michael Woods
American Chemical Society
Article URL:
http://www.medicalnewstoday.com/medical ... wsid=68822

 

[Anonymous]

They say when cells do their stuff and burn energy they produce free radicals which fly off and damage other cells - and thus we age as the number of free radicals increase and our bodies do less to repair or deflect the damage.

So if you get a body to burn more energy by giving it more short term energy like, oh I don't know, a bar of chocolate - would it not produce more free radicals and thus damage more cells leading to shorter life span?

Just a thought.

 

[OldTimeRadio]

Humans first began domesticating the wolf 80,000 - 100,000 years ago, leading eventually to the creation of the dog.

But after all this time even many working dogs have merely a 10 - 12 year lifespan. And even the extremely rare Methusalehs of dogdom rarely make it past 19 or 20.

Why haven't longer-lived dogs been created? Wouldn't it make economic sense to have working farm dogs with the lifespanb of, say, the horse or even the domestic tabby?

Is there some insurmountable "death gene" in canines which prevents this?

Or is it simply that the human race doesn't especially want long-lived dogs?

 

[OldTimeRadio]

Here's a conversation I had with my physician only six days ago:

I mentioned that during my childhood and younger manhood one of the things which most terrified patients was the possibility of going to the doctor and being informed that they had such-and-so cancer and had but six months to live.

But years afterwards, I continued, I read that with modern medicine what used to be that six-months' death sentence has been extended to six YEARS.

"You really are behind the times," said my physician. "It's currently 11 to 20 years. And within the next five or six years it's going to be 30 to 40."

 

[rynner2]

"You really are behind the times," said my physician. "It's currently 11 to 20 years. And within the next five or six years it's going to be 30 to 40."

Just so:

Cancer: The good news
Survival rates soar as cancer treatments improve
By Jeremy Laurance, Health Editor
Published: 16 May 2007

Cancer is no longer the death sentence that it once was. Our most feared disease is turning into a condition that people live with, rather than die from, figures published yesterday show.

In the past 30 years, overall survival rates from cancer have doubled, thanks to better treatments, earlier diagnosis and greater public awareness of the warning symptoms.

Almost half of patients (46.2 per cent) diagnosed in 2000-01 were expected to live 10 years, compared with a quarter (23.6 per cent) of those diagnosed in 1971, according to the charity Cancer Research UK.

Ten-year survival is a benchmark of success in cancer treatment and is regarded as close to a cure.

The breakneck progress, that has accelerated in the past decade, is set to continue, experts predicted. Among 10 goals announced yesterday, Cancer Research UK set a target of 66 per cent overall five-year survival by 2020, up from 50 per cent in 2001.

However, Britain still trails Europe in terms of cancer survival, despite the recent improvement. The last European survey of cancer , Eurocare-3, published in 2003 showed British patients died sooner than in most other European countries.

Professor Michel Coleman, a cancer epidemiologist at the London School of Hygiene and Tropical Medicine, who calculated the latest figures, said cancer was still a "major public health problem" that would affect one in three people during their lifetimes.

"Survival rates for many cancers have been lower in the UK than in many comparable countries. The differences may be less when Eurocare-4 is published later this year - I am hopeful we may have caught up," he said.

Professor Mike Richards, the Government's national cancer director, said: "I await Eurocare-4 with interest. I am optimistic we will see a narrowing of the gap [in survival rates]. We have seen an acceleration in survival in the 90s [in the UK] and I have every hope that will be continued."

A key reason for Britain's past poor performance has been delays in diagnosing patients - hence their cancers were more advanced when treatment started - compared with other countries. But extra investment in the NHS since 2000 has boosted the number of cancer specialists and shortened waits for treatment. About 250,000 patients are treated for cancer in Britain each year and more than 99 per cent are now treated within the Government target of two months.

Professor Richards admitted that uptake of new cancer drugs was slower in Britain than in other countries, as highlighted in a report by the Karolinska Institute, Stockholm, last week. Most of the drugs had been approved for use by the National Institute for Clinical Excellence (Nice) and efforts had been made to speed its assessment process. But he added: "Drugs are only one part of the answer."

Early detection of cancer, greater use of specialist surgery, screening programmes to detect cancer at an earlier stage and advances in chemotherapy and radiotherapy have all helped to increase survival rates.

Cancer is not one disease but many and the chances of survival vary widely with the type of illness. A patient who has pancreatic cancer, the most lethal form of disease, has a 2.5 per cent chance of living five years, compared with testicular cancer which has a 95 per cent survival rate.

There have been big gains in survival rates for some cancers while almost no progress has been made against others. Five-year survival rates for breast cancer have increased from just over 50 per cent to almost 80 per cent over the period. But pancreatic cancer and lung cancer have seen zero improvement with survival rates remaining below 5 per cent.

Harpal Kumar, who was appointed chief executive of Cancer Research UK last month, said there was "a lot to celebrate" in the survival figures but also "a lot further to go".

"Cancer scientists agree we are at the dawn of a new era in cancer research," he said. "New diagnostics and new treatments are on the way and there will be a pay-off in terms of improved survival. Great strides are being made thanks to the basic research done in the past."

Dr Kumar set out 10 goals to be achieved by 2020 against which progress could be measured. They include reducing the number of adult smokers by four million (from 12 to 8 million), reducing the incidence of cancer in under-75s by a quarter, doubling the use of better targeted treatments with fewer side effects and increasing the proportion of patients who are diagnosed at an early stage from the present 45 per cent to 66 per cent.

He said: "Our goals are as broad as they are ambitious. They recognise the importance of furthering our fundamental biological understanding of cancer while, at the same time, taking that knowledge out of the lab and turning it into new treatments."

Jo-Anne Tedd, accounts officer: 'I feel like I have got a new lease of life'

It was a fortnight before her wedding when Jo-Anne Tedd was diagnosed with bowel cancer in 2002. She had consulted her GP for haemorrhoids and he referred her to the local hospital in Warwickshire where she lives.

"It was a shock - it is not what you expect. I got an appointment pretty quickly and the consultant reassured me it could be treated."

Two days after her wedding, Ms Tedd, 44, was in hospital having her bowel removed in a procedure known as an ileostomy. The honeymoon had to wait.

"I had always feared having a colostomy bag. However, since my surgery I have done things I never thought I would." She had suffered for years from ulcerative colitis, a disorder in which the lining of the bowel becomes inflamed. Although unrelated to cancer it had made her feel unwell and restricted what she could do. Removal of her bowel solved that problem overnight.

"I am fitter, stronger, and in better health than before. I do more now than ever. If you have a positive outlook it makes it easier - you deal with it. But you still have your moments," she said.

She has bought a 600cc Suzuki Bandit motorbike to join her husband, Peter, an engineer and keen motorcyclist, on outings to the Cotswolds. She has also learned how to snowboard and does fun runs.

Ms Tedd works as an accounts officer for a large organisation and the couple have four grown-up children from previous marriages. She said: "I was devastated to find out I had cancer. However, I feel like I have got a new lease of life. Of course not everyone is as fortunate as me."

http://news.independent.co.uk/uk/health ... 548751.ece

 

[rynner2]

This is a long article: surprisingly, the aviator Lindbergh got heavily involved in research to prolong life. However, because of his Nazi sympathies, he expected this treatment to be reserved for only the superior types of people: "the weak, the diseased, and the fools" would not benefit.

http://news.bbc.co.uk/1/hi/magazine/7420026.stm

 

[ramonmercado]

Aging Not Slowed By Antioxidants, Study Rejects 50 Year Old Theory
01 Dec 2008

Research led by scientists in the UK has upturned a 50-year old theory that maintains antioxidants stop or slow aging by counteracting the oxidative stress on cells caused by free radicals, a finding that will undermine claims made by beauty and diet products that promote the anti-aging properties of antioxidants.

The research which was funded by the Wellcome Trust, was led by Dr David Gems of the Institute of Healthy Ageing at University College, London, and is published in the 30 November issue of the journal Genes & Development.

Superoxide free radicals are a natural byproduct of metabolism. They are essentially unstable oxygen molecules with too many electrons that go in search of compounds they can bond with that are happy to accept their extra electrons. This process is similar to when iron becomes rusty and turns into iron oxide, except that in the human body, biological mechanisms exist that can stop or reverse it.

In 1956 the biogerontologist Denham Harman proposed that aging was the result of an accumulation of "oxidative stress" such as that inflicted on cells by free radicals. Gems and colleagues now suggest this theory is not correct and that superoxide is not a major cause of aging.

Gems said the free radical theory of aging, which has dominated the field for over 50 years, "just doesn't stand up to the evidence."

For this study, he and his team studied the way genes controlled the removal of superoxide from the bodies of Caenorhabditis elegans, a type of nematode worm often used in aging research. They were able to switch the genes on and off and influence the extent to which the worms' bodies were able to get rid of surplus superoxide and thus reduce the potential damage it could cause through oxidation.

According to the free radical theory, Gems and colleagues expected to see a significant link between the worms' lifespan and the extent to which their bodies were able to mop up excess superoxide, but this is not what they observed. Another study on mice led by researchers at the University of Texas came to similar conclusions, supporting the idea that the 50-year old free radical theory is not correct, said Gems and his team.

If superoxide is involved in the accumulation of molecular damage that characterizes the aging process, it only plays a small part, said Gems.

"Oxidative damage is clearly not a universal, major driver of the ageing process. Other factors, such as chemical reactions involving sugars in our body, clearly play a role," he added.

On the strength of these findings, Gems suggested that anti-aging products that claim to have anti-oxidant effects are unlikely to be as effective as they say. He said that while a healthy and balanced diet reduced the risk of developing diseases of aging such as cancer, diabetes and osteoporosis, there was:

"No clear evidence that dietary antioxidants can slow or prevent ageing. There is even less evidence to support the claims of most anti-ageing products," he said.

Dr Alan Schafer, Head of Molecular and Physiological Sciences at the Wellcome Trust, said this new study should encourage researchers to explore new areas of aging research:

"Research such as this points to how much we have to learn about ageing, and the importance of understanding the mechanisms behind this process," added Schafer.

"Against the oxidative damage theory of aging: superoxide dismutases protect against oxidative stress but have little or no effect on life span in Caenorhabditis elegans.
Doonan, R. et al.
Genes and Development, Published online 30 Nov 2008.

http://genesdev.cshlp.org/


Written by: Catharine Paddock, PhD

--------------------------------------------------------------------------------

Article URL: http://www.medicalnewstoday.com/articles/131363.php

 

[rynner2]

'Immortal' jellyfish swarming across the world
An 'immortal' jellyfish is swarming through the world's oceans, according to scientists.

Last Updated: 11:14PM GMT 28 Jan 2009

The Turritopsis Nutricula is able to revert back to a juvenile form once it mates after becoming sexually mature.

Marine biologists say the jellyfish numbers are rocketing because they need not die.

Dr Maria Miglietta of the Smithsonian Tropical Marine Institute said: "We are looking at a worldwide silent invasion."

The jellyfish are originally from the Caribbean but have spread all over the world.

Turritopsis Nutricula is technically known as a hydrozoan and is the only known animal that is capable of reverting completely to its younger self.

It does this through the cell development process of transdifferentiation.

Scientists believe the cycle can repeat indefinitely, rendering it potentially immortal.

While most members of the jellyfish family usually die after propagating, the Turritopsis nutricula has developed the unique ability to return to a polyp state.

Having stumbled upon the font of eternal youth, this tiny creature which is just 5mm long is the focus of many intricate studies by marine biologists and geneticists to see exactly how it manages to literally reverse its aging process.

http://www.telegraph.co.uk/earth/wildli ... world.html

 

[Mythopoeika]

It's strange how some creatures seem to have evolved with long life built into their genes, like giant turtles or tuataras.

I think it could be that those creatures had natural predators that kept their numbers at a constant level, so they never had to evolve an expiry date into their genes.

Predators like us, however, have to have a time limitation built in - otherwise we'd outgrow the available resources.

 

[ramonmercado]

Yeaaa! Go super size!

Fly Study Suggests Fasting May Not Be Key To Longer Life
14 Jul 2009

Many studies on flies, mice, and more recently monkeys, have suggested that the key to a longer life is to restrict calorie intake, but a new study by US researchers suggests that the old maxim "feed a cold and starve a fever" may have some value, in that they found when it comes to coping with infection, fasting may be risky.

The new study is the work of Dr David Schneider, associate professor of microbiology and immunology at Stanford University School of Medicine and then graduate student Janelle Ayres, who has since attained her PhD and is now doing post-doctoral research at the University of California- Berkeley. They are publishing a paper about their findings this week in the journal PLoS Biology.

Many of the studies that have concluded consuming a calorie-restricted diet extends lifespan have been done under sterile lab conditions and therefore don't properly reflect reality where we are bombarded every day by a vast array of pathogens, some of which seize hold and cause infection.

So Schneider and Ayres decided to investigate this further by measuring the appetites of infected and uninfected fruit flies: in both cases some flies had been reared on a calorie restricted diet while others had not.

Curiously, fruit flies are useful models for studying human reactions to pathogens since much of their immune response parallels ours.

They found that living on a reduced calorie diet altered the flies' response to infection, but in ways that depended on what the flies were infected with: the response was different to different pathogens.

Ayres had already done some work on mutant fruit flies that died faster or more slowly than normal flies after being infected with pathogenic bacteria. She said she had to do so many injections on tiny flies that she couldn't use her hand properly for a while afterwards.

One batch of mutant flies turned out to have a faulty taste receptor that caused them to eat less than other variants. So the researchers decided to use these in the new study. Also, to make sure that the effects were due to calorie restriction and not because of the mutation, they also used normal flies that were fed a calorie restricted diet for some time before being infected. The results were the same for both types of fly.

They used three different types of bacteria to infect the flies, all of which cause death in humans: Enterococcus faecalis, Salmonella typhimurium and Listeria monocytogenes. They then compared the responses of the calorie-restricted flies (including the mutants) to normally fed flies that had also been infected with these bacteria.

In the case of Enterococcus faecalis, the flies that had been on calorie restriction before infection (including the mutant flies) ate no less after infection than uninfected flies, and they survived as long as normal eaters.

In the case of the other two bacteria, the flies that had been on calorie restriction (including the mutant flies) ate less after they were infected compared with uninfected flies, but their survival patterns were different compared to normal flies, depending on which bacteria they were infected with.

The low-cal flies infected with S. typhimurium outlived likewise infected normal eaters: they survived about 15 days after infection compared with 8 days for the normal eaters.

But the low-cal flies infected with L. monocytogenes died faster than likewise infected normal eaters: they lived only 4 days, while the normal eaters lived 6 or 7.

The researchers are still trying to work out what the underlying biological reason might be for these different responses to different types of bacterial infection. But taken as a whole, the results so far suggest that the idea that a calorie-restricted diet is a good regime for life should be viewed with a little skepticism.

Schneider said:

"There's evidence that caloric restriction seems to rev up various individual components of the immune system."

"But in the few studies where diet-restricted animals actually have been infected experimentally, they fared poorly," he added.

Scheider and Ayres concluded that:

"The work reported here should raise a cautionary flag, as it demonstrates that diet restriction can have complex effects on the realized immune response of a diet-restricted animal."

The research was sponsored by the National Institutes of Health, the National Science Foundation, and the Ellison Medical Foundation.

-- PLoS Biology.

Source: Stanford University Medical Center.

Written by: Catharine Paddock, PhD

Article URL: http://www.medicalnewstoday.com/articles/157379.php

 

[ramonmercado]

But then along comes another study! Monkey biz indeed.

Monkey Study Finds Reducing Calories Thwarts Aging, Disease
11 Jul 2009

The bottom-line message from a decades-long study of monkeys on a restricted diet is simple: Consuming fewer calories leads to a longer, healthier life.

Writing in the journal Science, a team of researchers at the University of Wisconsin-Madison, the Wisconsin National Primate Research Center and the William S. Middleton Memorial Veterans Hospital reports that a nutritious but reduced-calorie diet blunts aging and significantly delays the onset of such age-related disorders as cancer, diabetes, cardiovascular disease and brain atrophy.

"We have been able to show that caloric restriction can slow the aging process in a primate species," says Richard Weindruch, a professor of medicine in the UW-Madison School of Medicine and Public Health who leads the National Institute on Aging-funded study. "We observed that caloric restriction reduced the risk of developing an age-related disease by a factor of three and increased survival."

During the 20-year course of the study, half of the animals permitted to eat freely have survived, while 80 percent of the monkeys given the same diet, but with 30 percent fewer calories, are still alive.

Begun in 1989 with a cohort of 30 monkeys to chart the health effects of the reduced-calorie diet, the study expanded in 1994 with the addition of 46 more rhesus macaques. All of the animals in the study were enrolled as adults at ages ranging from 7 to 14 years. Today, 33 animals remain in the study. Of those, 13 are given free rein at the dinner table, and 20 are on a calorie-restricted diet. Rhesus macaques have an average life span of about 27 years in captivity. The oldest animal currently in the study is 29 years.

The new report details the relationship between diet and aging, according to Weindruch and lead study author Ricki Colman, by focusing on the "bottom-line indicators of aging: the occurrence of age-associated disease and death."

In terms of overall animal health, Weindruch notes, the restricted diet leads to longer lifespan and improved quality of life in old age. "There is a major effect of caloric restriction in increasing survival if you look at deaths due to the diseases of aging," he says.

The incidence of cancerous tumors and cardiovascular disease in animals on a restricted diet was less than half that seen in animals permitted to eat freely. Remarkably, while diabetes or impaired glucose regulation is common in monkeys that can eat all they want, it has yet to be observed in any animal on a restricted diet. "So far, we've seen the complete prevention of diabetes," says Weindruch.

In addition, the brain health of animals on a restricted diet is also better, according to Sterling Johnson, a neuroscientist in the UW-Madison School of Medicine and Public Health. "It seems to preserve the volume of the brain in some regions. It's not a global effect, but the findings are helping us understand if this dietary treatment is having any effect on the loss of neurons" in aging.

In particular, the regions of the brain responsible for motor control and executive functions such as working memory and problem solving seem to be better preserved in animals that consume fewer calories.

"Both motor speed and mental speed slow down with aging," Johnson explains. "Those are the areas which we found to be better preserved. We can't yet make the claim that a difference in diet is associated with functional change because those studies are still ongoing. What we know so far is that there are regional differences in brain mass that appear to be related to diet."

Such an observation, however, is novel, according to Weindruch. "The atrophy or loss of brain mass known to occur with aging is significantly attenuated in several regions of the brain. That's a completely new observation."

Since the first studies of caloric restriction in rodents in the1930s, scientists have been intrigued by evidence that reducing calories can effectively extend lifespan. Such studies have been undertaken in a number of different animal species ranging from spiders to humans

The Wisconsin rhesus macaque study, however, is likely to provide the most detailed insight into the phenomenon and its potential application to human health as it has tracked in greatest detail the diets and life histories of an animal that closely resembles humans. Because people are much longer lived than rhesus monkeys, and no similar comprehensive study with human subjects is under way, conclusive evidence of the effects of the diet on human lifespan and disease may never be known.

Source:
Richard Weindruch
University of Wisconsin-Madison
--------------------------------------------------------------------------------

Article URL: http://www.medicalnewstoday.com/articles/157145.php

 

[Yithian]

Marine biologists say the jellyfish numbers are rocketing because they need not die.

I like that turn of phrase: 'they need not die'.

It makes me imagine a cockney jellyfish leaning casually up against a coral whilst bragging to his mates:

"Okay, granted, I could die - in theory, like.

But only if I felt like it, mind you.

Let's get this straight: there ain't nobody forcing me; it's basically all down to me."

 

[ramonmercado]

Fountain Of Youth Found On Easter Island? Compound found on Easter Island shown to make mammals live longer
By Dan Smith

Easter Island Head: Knows the secret of aging

Rapamycin, a compound originally found in Easter Island's soil in the 1970s (right there under the stone heads) has recently been proven to extend the lives of mice.

When tested on mice that had already reached middle age, the subjects treated with rapamycin increased their lifespan by 28-38 percent. Scientists are identifying these studies as the most promising drug-induced technique for increasing longevity, which is generally possible only via genetic manipulation or limiting caloric intake.

Rapamycin has been used for years for its anti-fungal properties to prevent organ transplant rejection, as a stent during angioplasty surgery and is even being tested for its potential as a cancer treatment. However, the newest addition to its resume is life extension by way of mimicking the same effects on the body associated with reduction of calories. Targeting a cell protein called mTOR, rapamycin helps control the metabolism of cells and the response to stress.

The first tests, which showed such positive results, were actually accidentally conducted on mice that were the human equivalent of 60 years old. The trouble was that the researchers had trouble getting the mice to absorb enough of the compound to have an effect. So while they worked on getting more rapamycin into the bloodstream, the mice slowly got older. By the time they figured out the solution, a technique called microencapsulation, the mice were much older than they originally planned. The results, though, were not expected since calorie reduction was shown to not have much of an effect at such an advanced age. This suggests the drug could be more powerful than any previous attempts at longevity.

The study also cross-bred many lines of mice to make a population of subjects that most closely resembled the human population. This showed that not only did it extend life across a wide range of genetically varied mice, but that it also helped prevent some age-related diseases and defects on the cellular level.

Since the pathway the drug responds to has been shown to increase lifespans in yeast, fruit flies, and mice, it could be assumed that the same pathway has been carried on evolutionarily to humans. Unfortunately, since the drug seems to also suppress parts of the immune system, it might be best to be used as a preventative for age-related disease rather than a cocktail to live forever. But the possibilities make you wonder that if only the original inhabitants of Easter Island knew the treasure under their feet, they might still be around to explain those statues to us.

http://www.popsci.com/scitech/article/2 ... ter-island

 

[Mythopoeika]

Yeah, I heard about this on the radio the other day.
I wonder if that is what caused the Easter Island civilisation to finally fall apart - people there lived too long, the island became overcrowded and they used up all the resources available to them?

 

[ramonmercado]

Yeah, I heard about this on the radio the other day.
I wonder if that is what caused the Easter Island civilisation to finally fall apart - people there lived too long, the island became overcrowded and they used up all the resources available to them?

Excellent! Theres probably a novel in that idea.

 

[ramonmercado]

Nobel Prize Awarded for Contributions to the Quest for Immortality
http://www.popsci.com/scitech/article/2 ... rets-aging
Three U.S. geneticists claim a 2009 Nobel Prize for discovering the genetic code of cell aging
By Jeremy Hsu Posted 10.05.2009 at 5:19 pm 0 Comments


Nobel Winners Three pioneers for the better understanding of aging Gerbil, Licensed by Attribution Share Alike 3.0/Harvard Medical School
Military leaders throughout history have supposedly goaded on their troops with the phrase, "You wanna live forever?" In 2009, the answer for many people is "Yes, please," and the Nobel Committee has today honored three U.S. scientists for discovering the genetic code that regulates aging in cells.

The announcement comes as researchers race to develop anti-aging medicine or technology that can make humans immortal. PopSci recently covered the Singularity Summit 2009 where none other than visionary Ray Kurzweil spoke of a future when a computer could simulate the human brain.

Merging humans with artificial intelligence remains some ways off, but there's also plenty of focus on extending the natural human lifespan. The latest Nobel Prize winners helped illuminate the aging process by discovering the repetitive genetic sequences on the ends of chromosomes known as telomeres. The telomeres serve as protective caps that gradually shorten as genetic material is copied many times over during cell division -- a process that parallels human aging, even if other factors also come into play.

The researchers who will receive this year's Nobel Prize in Physiology or Medicine and share $1.4 million are: Elizabeth Blackburn, a biologist at the University of California in San Francisco; Carol Greider, a molecular biologist at Johns Hopkins University in Baltimore; and Jack Szostak, a geneticist at Massachusetts General Hospital in Boston. This is the first time that the Nobel Prize in medicine has gone to more than one woman in a single year.

Scientific American notes that the prize-winning work has proven invaluable in studies of aging, cancer and stem cells. The researchers also showed the existence of telomerase, the "immortality enzyme" behind the formation of telomeres.


Related Articles
Singularity Summit 2009: Thus Spake Kurzweil
This Pill Will Change Your Life
The Prophet of Immortality

Tags
SciTech, Jeremy Hsu, aging, immortality, medicine, nobel, nobel prize, physiology, telomerase, telomeresScientists have since begun investigating possible anti-aging factors, such as a compound known as resveratrol that's found in red wine. That chemical activates proteins called sirtuins that boost the body's defenses against common diseases of aging, as part of a process that typically helps humans survive famines. The New York Times recently reported that Sirtris Pharmaceuticals has begun developing a drug that can activate sirtuins and hopefully mimic the life extension seen in lab rats, who lived up to 40 percent longer on a famine-style diet.

A different study in the journal Science found how to mimic the famine-style benefits of longer life and better health in mice, when researchers disabled a certain gene in a biochemical signaling pathway. Technology Review explains that the pathway typically helps guide the body's response to food, and may now serve as a target for future drugs.

People may also continue to live longer even without radical new technologies. A study in the medical journal The Lancet suggests that more than half of babies born in wealthy nations will live to 100 years, according to an Agence France-Presse report. That assumes the current rise in life expectancy continues, but still falls short of one controversial theorist's prediction that the average human lifespan could reach 5,000 years within the next century.

 

[ramonmercado]

Science to 'stop age clock at 50'
http://news.bbc.co.uk/2/hi/health/8314442.stm
By Michelle Roberts
Health reporter, BBC News


Professor Eileen Ingham explains the main aims of the project

Centenarians with the bodies of 50-year-olds will one day be a realistic possibility, say scientists.

Half of babies now born in the UK will reach 100, thanks to higher living standards, but our bodies are wearing out at the same rate.

To achieve "50 active years after 50", experts at Leeds University are spending £50m over five years looking at innovative solutions.

They plan to provide pensioners with own-grown tissues and durable implants.

New hips, knees and heart valves are the starting points, but eventually they envisage most of the body parts that flounder with age could be upgraded.


To replace all donor tissue using this technology will take 30 to 50 years
Material scientist Professor Christina Doyle

Send us your comments

The university's Institute of Medical and Biological Engineering has already made a hip transplant that should last for life, rather than the 20 years maximum expected from current artificial hips.

The combination of a durable cobalt-chrome metal alloy socket and a ceramic ball or "head" means the joint should easily withstand the 100 million steps that a 50-year-old can be expected to take by their 100th birthday, says investigator Professor John Fisher.

Meanwhile, colleague Professor Eileen Ingham and her team have developed a unique way to allow the body to enhance itself.

The concept is to make transplantable tissues, and eventually organs, that the body can make its own, getting round the problem of rejection.


BODY PARTS BEING AGE-PROOFED
body showing possible age-proofed body parts
1. Scientists have developed transplantable tissues the body can make its own, tackling rejection. They have made heart valves using the technique
2. A hip has been made from a durable alloy socket and ceramic ball that should last for life, rather than the current 20 years
3. Similar techniques are being developed for artificial knees
4. Eventually scientists hope to make ligaments and tendons to replace old and damaged ones
5. Artificial blood vessels are also being developed
6. The NHS is looking into using the transplantable tissue methods on donor skin for burns patients
7. Researchers also hope to do the same for organs

So far they have managed to make fully functioning heart valves using the technique.

It involves taking a healthy donor heart valve - from a human or a suitable animal, such as a pig - and gently stripping away its cells using a cocktail of enzymes and detergents.

The inert scaffold left can be transplanted into the patient without any fear of rejection - the main reason why normal transplants wear out and fail.

Once the scaffold has been transplanted, the body takes over and repopulates it with cells.

Trials in animals and on 40 patients in Brazil have shown promising results, says Prof Ingham.

They have licensed the technology to the NHS National Blood and Transplant Tissue Services so it can be used on any UK donated human tissue in the future.

The NHS is already looking into using the method on donor skin for burns patients.

Professor Christina Doyle of Xeno Medical, the medical device company that is developing the technologies under Tissue Regenix, said the holy grail was to remove the heavy reliance on donor organs.

"That's where the technology will lead us eventually."

But she said: "To replace all donor tissue using this technology will take 30 to 50 years. Each single product will need to be designed and tested individually."

Prof Doyle said experts elsewhere were also working on similar regenerative therapies, but grown entirely outside of the body, to ensure that people can continue being as active during their second half-century as they were in their first.

 

[ramonmercado]

Hormone fails to fulfil 'fountain of youth' billing
http://www.irishtimes.com/newspaper/hea ... 23_pf.html
DÓNAL O'MATHÚNA

Tue, Dec 15, 2009

DOES IT WORK? DHEA for general health and vitality

ONE OF the steroid hormones produced naturally in the body is DHEA (shorthand for dehydroepiandrosterone). Research has shown that DHEA is involved in producing several compounds that impact many tissues and organs throughout the body.

When it was noted that DHEA levels start to fall off as people approach 30, connections were proposed between DHEA and ageing. In 1994, US regulators changed DHEA from an unapproved drug to a food supplement. It quickly became available in health food shops and on the internet, being promoted as the hormonal fountain of youth. Because it is a steroidal hormone, it remains a prescription-only medication in Ireland.

DHEA is said to relieve depression, give feelings of energy, boost libido, improve memory and generally improve wellbeing. Many of these symptoms accompany chronic illnesses, leading to wide interest in DHEA. Much promotion has been directed at women because their levels are generally lower than men for unknown reasons.

In spite of considerable research in recent years, much remains unknown about the DHEA’s role in the body. DHEA levels are lower during a number of chronic illnesses, including rheumatoid arthritis and major depression, and also during periods of high stress.

One area of considerable interest for DHEA is adrenal insufficiency. This condition is caused by several factors, and leads to the adrenal glands (located beside the kidneys) producing inadequate levels of several hormones.

DHEA is produced by these glands, and people with adrenal insufficiency produce little or no DHEA. Common symptoms include fatigue, muscle weakness, loss of appetite, mood changes, nausea, and dizziness or fainting from low blood pressure.

Conventional treatment involves steroid therapy, but even when this effectively restores steroid levels to normal, people’s quality of life often remains poor. Hence, there has been much interest in using DHEA to improve such patients’ general wellbeing.

A systematic review was published in October bringing together all the controlled research in women with adrenal insufficiency. Ten randomised controlled trials were found, with inconsistent results.

When these results were summarised statistically, they found an overall small benefit in quality of life and depression – what the authors rated as “clinically trivial”. The summary scores showed no benefits for anxiety, libido or sexual satisfaction.

Another systematic review of DHEA was published a couple of years ago in the Cochrane Library. This review found no evidence of DHEA benefiting elderly men and women who took it to improve memory and other cognitive functions. The evidence from other DHEA trials in men and women generally does not support a beneficial effect on wellbeing.

People in clinical trials frequently report side effects related to the fact that DHEA is a steroid hormone. Men taking DHEA supplements develop elevated levels of female hormones, while women develop higher levels of male hormones.

These are connected to the common side effects seen in women, including acne, itchy scalp, odorous sweat and, rarely, facial hair. However, some women found some of these effects beneficial, especially those with dry skin and hair who developed additional greasy secretions.

DHEA is a steroid hormone and should be treated with caution. Research demonstrates that DHEA is not a modern fountain of youth. As each new review is published, calls are made in the US to remove DHEA’s status as a food supplement. This recognises that while DHEA may have a legitimate role in the treatment of specific medical conditions, its widespread availability as a supplement is not warranted.

Although serious adverse effects have not been reported, taking any steroid regularly will disturb the complex balance of hormones that exist within the body. Much remains to be learned about why DHEA levels decrease with ageing, but boosting those levels indiscriminately is not warranted.


--------------------------------------------------------------------------------

Dónal OMathúna has a PhD in pharmacy, researching herbal remedies, and an MA in bioethics, and is a senior lecturer in the School of Nursing, Dublin City University. He is author of Alternative Medicine: The Christian Handbook , Updated and Expanded Edition, Zondervan, 2007

 

[ramonmercado]

Great: you live longerand keep your marbles!

Longevity Gene Variant Linked To Lower Risk Of Dementia, Alzheimer's
13 Jan 2010

New research from the US reveals that a variant of the plasma gene CETP that has already been associated with longevity may also be linked to slower age-related memory decline and a lower risk of dementia and Alzheimer disease. The researchers said drugs that mimic the gene's effect and could protect against Alzheimer's are now being developed.

The researchers, from the Department of Neurology, Department of Epidemiology and Population Health and the Institute for Aging Research at the Albert Einstein College of Medicine, Yeshiva University, Bronx, New York, and Departments of Genetics and Genomic Sciences and Neurology at the Mount Sinai School of Medicine, New York, New York, revealed their findings in a paper published in the 13 January issue of JAMA, Journal of the American Medical Association.

The authors explained that CETP helps control the size of cholesterol particles, and the favourable variant increases blood levels of "good" cholesterol (HDL, high-density lipoprotein) while also resulting in larger-than-average sized particles of both HDL and low-density lipoprotein (LDL, or "bad" cholesterol).

They suggest the variant alters the way CETP works so that its associated protein functions less well than usual.

Some of the authors were involved in a study published in 2003, where they identified a variant of CETP, the cholesteryl ester transfer protein, was linked to longevity in a population of Ashkenazi Jews. The gene variant has also been linked to lower cardiovascular disease risk.

But until now, links with memory decline and dementia risk have not been clear, so for this study the researchers specifically evaluated the "longevity" variant of CETP where the amino acid isoleucine is replaced by another amino acid valine, and which is associated with lower CETP protein in the blood and higher activity and levels of HDL.

Senior author Dr Richard B. Lipton, the Lotti and Bernard Benson Faculty Scholar in Alzheimer's Disease and professor and vice chair in the Saul R. Korey Department of Neurology at Einstein, told the media that:

"Most work on the genetics of Alzheimer's disease has focused on factors that increase the danger."

As an example he cited a gene variant of APOE that influences cholesterol metabolism and is known to increase the risk of Alzheimer's among carriers. Lipton said they decided to take the opposite approach, and focus instead on "a genetic factor that protects against age-related illnesses, including both memory decline and Alzheimer's disease".

Lipton and colleagues also wanted to test the idea that the CETP longevity variant might be linked to less cognitive decline as people grow older.

For the study, which was funded by the National Institute on Aging, the researchers searched for links between CETP variants and memory performance and risk for new dementia or Alzheimer's in a community-based sample of 523 healthy adults aged 70 and over.

None of the participants had dementia when the study began, and from blood samples, the researchers were able to determine which CETP variant they carried (the one with isoleucine or the one with valine, the latter being the "longevity" variant).

The participants were taking part in the Einstein Aging Study, an ongoing US federally funded project that has been following an ethnically and racially diverse group of elderly Bronx residents for 25 years, giving this study data covering from 1994 to 2009.

For an average follow up of just over 4 years, the participants underwent annual assessments to test their rates of cognitive decline, and incidence of Alzheimer's disease and other changes. The tests used standardized neuropsychological and neurological measures, and included memory, attention and psychomotor speed tests (the latter assesses the time it takes to process and react to a signal).

The results showed that:

* 40 new cases of dementia occurred during an average follow-up of 4.3 years.

* People with 2 copies of the longevity variant of CETP (the "valine homozygotes") had significantly slower memory decline (relative 51 per cent) and lower risk for developing dementia and Alzheimer disease compared to people who had the non-longevity variant of CETP (the "isoleucine homozygotes").

* The valine homozygotes also had a 72 per cent lower risk of dementia (hazard ratio

---

0.28; 95% confidence interval [CI] ranging from 0.10 to 0.85; P = .02), and a 69 per cent lower risk of Alzheimer disease (HR 0.31; 95%CI 0.10-0.95,P = .04), compared to the isoleucine homozygotes.

The authors concluded that:

"Despite the small number of incident dementia cases and small decline in memory, this preliminary report suggests that CETP valine homozygosity [having two copies of the longevity variant] is associated with slower memory decline and lower risk for incident dementia or AD [Alzheimer Disease]."

They added that this "potentially protective" link is supported by several observations:

"First, some (but not all) prior work has shown that at cross-section valine homozygosity was associated with better mental status. Second, valine homozygosity is associated with a slower rate of memory decline in our entire sample, not just those who developed dementia. Third, the hazard ratios in this analysis suggested a possible gene-dose relationship for the CETP gene."

They argued that a link between CETP status and cognition and dementia makes sense biologically because other genes like APOE that are involved in lipid metabolism are also linked to risk of dementia. They recommended further studies be done to evaluate the "potential protective association of the CETP gene with dementia risk".

Lipton said drugs are now being developed that mimic the longevity CETP variant's effect on its protein, and recommended:

"These agents should be tested for their ability to promote successful aging and prevent Alzheimer's disease."

"Association of a Functional Polymorphism in the Cholesteryl Ester Transfer Protein (CETP) Gene With Memory Decline and Incidence of Dementia."
Amy E. Sanders; Cuiling Wang; Mindy Katz; Carol A. Derby; Nir Barzilai; Laurie Ozelius; Richard B. Lipton.
JAMA, Vol. 303 No. 2, pp150-158, published online 13 January 2010.

Source: JAMA and Archives Journals, Albert Einstein College of Medicine of Yeshiva University.

Written by: Catharine Paddock, PhD

Article URL: http://www.medicalnewstoday.com/articles/175796.php

---

 

[ramonmercado]

Battlefield Camaraderie Yields Long-Term Dividends for Veterans, Study Finds
http://www.sciencedaily.com/releases/20 ... 141825.htm

ScienceDaily (Feb. 19, 2010) — The benefits of wartime camaraderie extend far beyond the battlefield, a new UCLA study of U.S. Civil War veterans suggests.

Veterans who served in military units characterized by a strong esprit de corps were much less likely decades later to die of a stroke or heart condition than veterans from less cohesive companies, two UCLA economists have found.

"On the battlefield, you'd expect your buddy to have your back," said Dora Kosta, the study's lead author and a UCLA professor of economics. "But the fact that camaraderie provides a protective effect that endures long after the war has ended is a new and surprising finding."

"We're not sure how it works, but somehow, being armed with close social bonds in the extremely stressful situation of battlefield combat has a protective effect that continues long after the fighting has ended," said Matthew Kahn, the study's co-author and a fellow UCLA economics professor. "Men who went into battle with this emotional armor were much less likely in their late 50s and early 60s to fall victim to stress-related illnesses."

The study, which tracked the veterans for up to 68 years, constitutes the first long-term look at the effect of unit cohesion on soldiers' mortality and health at older ages. It is also one of the longest-running studies of the effect of human social bonds on extreme stress. The findings appear in the latest issue of the peer-reviewed scholarly journal Demography, which is expected to ship Feb. 19 to subscribers.

Drawing on data amassed by the University of Chicago's Center for Population Economics, Costa and Kahn looked at records for more than 35,000 Union veterans who served between 1861 and 1865 in 303 infantry companies. The economists first determined how many men each company lost, reasoning that the companies with the most losses also experienced the most stress.

They also figured out whether the veterans served with men of shared ethnicity, occupation and other commonalities. Previous research has shown that soldiers who fought in companies with men who shared similar characteristics -- a common race, religion, ethnicity, socioeconomic status or hometown -- displayed a higher degree of loyalty to one another than their counterparts in more diverse companies.

The researchers then examined meticulously detailed medical records kept by the Pension Bureau -- the precursor to today's Department of Veterans Affairs -- for the purposes of ascertaining whether the veterans were eligible for age- and disability-related benefits as they aged. In particular, Costa and Kahn looked at whether the men experienced medical conditions with well-documented links to stress, such as arteriosclerosis, heart attacks and strokes.

Finally, they scoured U.S. Census records from 1850 to 1930 for details of the veterans' lives as they unfolded. The researchers were especially interested in the veterans' economic situation and martial status, two variables that have been shown to have a significant effect on an individual's health.

Even after adjusting for these factors, Costa and Kahn found that veterans from companies lacking in cohesion were six times more likely than peers from cohesive companies to suffer from arteriolosclerosis or to have heart attacks or strokes by their late 50s or early 60s.

When translated into total lifespan, the toll was considerable. Of the veterans who died from heart disease or stroke, men who served in an uncohesive company lived one year and four months less than men from a cohesive company.

Costa and Kahn admit they're not sure of the mechanism behind camaraderie's long-term protective influence, but they suspect social bonds somehow moderate stress hormones released either during or after intense battles.

"It may be that you don't have the same release of stress hormones when you go into battle with comrades on whom you feel like you can depend," Costa said.

The study quotes from the journal of a Civil War captain whose personal experiences seem to reinforce this view: "I have always found comforting in battle the companionship of a friend, one in whom you had confidence, one you felt assured would stand by you until the last," Frank Hollinger wrote.

Having a friendly shoulder to cry on at the end of the day also may help dissipate stress hormones, Costa said.

"If you actually see people being killed, your comrade can say, 'No, no. It's all right. It's not your fault.' "

Also unclear is whether veterans from less cohesive units sustained damage that led to stress-related conditions during the war itself or in the years that followed the conflict.

"One theory is that release of hormones in battle may cause systemic inflammation that later in life leads to heart disease and other potentially fatal diseases," Kahn said.

Alternatively, the absence of camaraderie may have made veterans more likely later on to relive battle trauma in the form of post-traumatic stress syndrome.

"Every time a veteran experiences a PTSD reaction, stress hormones are released again," Costa said. "So PTSD leads to repeated exposure to hormones that may over time lead to damaging inflammation."

The latter theory, the researchers admit, is just conjecture. The Pension Bureau did not track PTSD symptoms because the illness was not accepted into diagnostic literature until more than a century later. Neither did the bureau track symptoms that could be ascribed, with the benefit of hindsight, to PTSD. Nonetheless, the researchers view the data as a goldmine.

"Many studies have investigated how social networks combat the effects of stress in people," Costa said. "But they've tended to focus on stress generated in a laboratory setting, where researchers naturally would be prevented from inflicting the high levels experienced on a battlefield. The beauty of the Civil War data is it lets us get as close to a randomized, experimental study of extreme stress and social networks as you can ethically get."

The study also takes advantage of record-keeping quirks unique to the era. To ensure delivery of the country's earliest comprehensive benefits for veterans, the Pension Bureau tracked the veterans to their death. Because neither the Pension Bureau's records nor corresponding U.S. Census data is protected by the kinds of privacy safeguards that U.S. citizens now enjoy, the researchers were able to reconstruct a vivid picture of the types of conditions under which the men served and how they fared as they aged.

Moreover, Civil War soldiers who joined one company stayed with that company for their entire tour of duty. Only in very rare cases did companies add new soldiers as old ones were injured or killed. This distinction facilitated tracking the effects of cohesion. By contrast, soldiers repeatedly cycled in and out of companies during World War II and the Korean and Vietnam wars, infinitely complicating such research.

Even though the findings may date from a 145-year-old conflict, the researchers hope they will shed light on contemporary problems.

"Now that we're in the middle of two long-term wars, it's really important to understand what effect combat has on men's long-term health," Costa said. "If we can find strategies for minimizing the long-term toll of the experience on these brave people, we really need to do so."

The project received funding from the National Institutes of Health.

 

[ramonmercado]

Ageing Gene Influences Lifespan, Immunity And Resilience Say UK Scientists
http://www.medicalnewstoday.com/articles/184260.php
02 Apr 2010

UK researchers have discovered that a gene called DAF-16, that is known to be involved in the process of ageing, strongly influences the rate of ageing and average lifespan in nematode worms, and suggest the finding could open new doors for altering ageing, immunity and stress resilience in humans, since we have the same gene, as do many other animals.

You can read about the study, which was funded by the Biotechnology and Biological Sciences Research Council (BBSRC) and led by Dr Robin May, of the School of Biosciences at the University of Birmingham, in PLoS ONE, where a paper on it has been available online since 1st April.

May said in a statement that all organisms undergo ageing, but at very different rates.

"We know that, even between closely related species, average lifespans can vary enormously," said May, explaining that he and his team wanted to find out how normal ageing is regulated by genes and what other traits might be influenced by the same genes, for instance immunity.

"To do that, we looked at a gene that we already knew to be involved in the ageing process, called DAF-16, to see how it may determine the different rates of ageing in different species," he added.

DAF-16 plays a role in the "dauer" stage of development in nematode worms and affects lifespan and reproduction. It encodes a protein that belongs to a class known as "forkhead transcription factors" that control the expression of other genes. It is active in most cells and is similar to a series of genes in humans known as FOXO1, FOXO3, FOXO4 and FOXO6.

For the study, May and his colleagues compared the longevity of 4 species of nematode worm (Caenorhabditis elegans, Caenorhabditis briggsae, Caenorhabditis remanei and Caenorhabditis brenneri) and how this related to DAF-16 expression.

They found, for example, that DAF-16 expression is 12 times stronger in C. remanei, which also has a longer lifespan, than C. elegans.

When they investigated the worms' resistance to stress and immunity, by exposing them to high temperatures, heavy metals and various bacterial and fungal diseases, they found that in general, the species with the highest DAF-16 expression lived longer, had increased resistance to stress and better immunity against infection.

There was one exception: in the case of infection with Salmonella, they found little difference among the four species.

May said that DAF-16 belongs to a group genes that drivs the biology of ageing, immunity and response to environmental stress.

"The fact that subtle differences in DAF-16 between species seem to have such an impact on ageing and health is very interesting and may explain how differences in lifespan and related traits have arisen during evolution," he added.

May and colleagues are now investigating how DAF-16 controls genes to balance the varying needs of an organism's immune system over time.

Chief Executive of BBSRC Professor Douglas Kell said:

"Research using model organisms that uncovers the biology underpinning ageing gives us the opportunity to understand some of the mechanisms that determine how humans age in a healthy, or at least normal, way."

He said that research like this helps us better understand ageing and develop ways to improve the quality of life for older people, such as coping with illness, daily living tasks and recalling memories.

"Phenotypic Covariance of Longevity, Immunity and Stress Resistance in the Caenorhabditis Nematodes."
Francis R. G. Amrit, Claudia M. L. Boehnisch, Robin C. May.
PLoS ONE, 2010, 5(4): e9978, Published online 01 Apr 2010.
DOI:10.1371/journal.pone.0009978

Source: BBSRC.

Written by: Catharine Paddock, PhD

 

[ramonmercado]

Ways To Extend Longevity May Affect Memory Differently
19 May 2010

Researchers in the US who explored two ways of extending longevity, dietary restriction and reduced Insulin/IGF-1 signalling, found they had very different effects on memory, and suggest their findings offer scientists a new model, based on the nematode C. elegans, for exploring ways to treat age-related memory decline.

A paper on the study by researchers at Princeton University in New Jersey was published online in the open access journal PLoS Biology on 18 May.

One of the most devastating aspects of aging is memory loss, and while scientists have explored ways to extend life, with many studies using the nematode C. elegans (a type of roundworm) as a model, we know little about how they affect learning and memory.

For this study, the researchers designed new tests ("chemotaxis assays") of learning and memory in C. elegans to identify components of associative learning, associative short-term and associative long-term memory and found that the molecules required for these functions appear to be conserved from this nematode to mammals, implying that the biology of learning and memory is an ancient one.

The researchers also examined how the components declined with age and tested the effect of two longevity treatments, dietary restriction and reduced Insulin/IGF-1 signalling, on them.

They were surprised when they found that:

* Dietary restriction impaired memory in early adulthood, but preserved memory with age,

* Whereas reduced Insulin/IGF-1 signalling improved memory performance in early adulthood but failed to preserve it with age.

They concluded these results suggest that while longevity treatments may help preserve cognitive function with age, they may have distinctly different effects:

"... specific longevity treatments have acute and long-term effects on cognitive functions that decline with age through their regulation of rate-limiting genes required for learning and memory," wrote the researchers.

The researchers were also pleased that this study suggests C. elegans is useful not only for studying longevity but memory as well.

Coleen Murphy, who heads the lab where the experiments took place, told the media that they hope to use the nematode model to find new drugs and treatments for age-related cognitive decline.

"Maybe targeting more than one longevity pathway would be the right approach," she said.

"Insulin Signaling and Dietary Restriction Differentially Influence the Decline of Learning and Memory with Age."
Kauffman AL, Ashraf JM, Corces-Zimmerman MR, Landis JN, Murphy CT
PLoS Biol, 8(5): e1000372; published online 18 May 2010.
DOI:10.1371/journal.pbio.1000372

Sourceublic Library of Science.

Written by: Catharine Paddock, PhD


Article URL: http://www.medicalnewstoday.com/articles/189169.php

 

[rynner2]

Could this man actually live forever? Berlusconi invests in medical company researching long life
By Nick Pisa
Last updated at 8:50 PM on 3rd June 2010

Silvio Berlusconi has thrown his fortune behind a medical company researching long life.
The famously looks-conscious Italian premier has invested £40million in a biotechnology firm researching cancer drugs, becoming its biggest shareholder.

He is also backing the company's second biggest shareholder - a foundation that aims to build a £125million research and treatment centre devoted to warding off the effects of ageing.

Mr Berlusconi, 73, plunged part of his £7billion fortune into the Milan-based Molecular Medicine Spa, which is research two cancer drugs.
Becoming the company's biggest shareholder, he also put his son Luigi, 21, on the board.
Mr Berlusconi - famous for his love of plastic surgery and hair transplants - has already fought off prostate cancer, and once predicted there would be a cure for cancer by 2013.

It is not clear how much the flamboyant billionaire has committed to the company's second biggest shareholder, the San Raffaele del Monte Tabor foundation.
The foundation is planning to build a £125million research centre this year to discover how to ward off the effects of ageing.
It will be called 'Quo Vadis' and will focus on preventing and curing the diseases of old age and studying the beneficial effects of nutrition and exercise.

The premier's doctor Umberto Scapagnini famously once said that Mr Berlusconi was 'immortal' and had the 'mind, body and sexual activity of a 50-year-old'.
The long list of sexual scandals that the infamously flirtatious politician has been embroiled in appear to be testament to the statement.
The doctor has said he hopes to keep the premier alive until he is 120. Mr Berlusconi himself has boasted that he may begin looking for a successor in 100 years.

Business agency Bloomberg revealed the moves made by Mr Berlusconi through his Fininvest holding company.
Molecular Medicine is carrying out tests on two types cancer drugs and describe the trials as being 'in the most advanced stages'.
One of the drugs is aimed at attacking cancerous cells, the other is designed to build up immune systems.

Read more: http://www.dailymail.co.uk/news/worldne ... z0psNujD27

 

[rynner2]

Methodists 'live more than seven years longer than rest of population'
Methodists live more than seven years longer than the rest of the population, according to an academic study.
By Martin Beckford, Religious Affairs Correspondent
Published: 5:47PM BST 25 Jun 2010

Men belonging to the famously clean-living denomination live to the ripe old age of 83.9, research has found, compared with a national average of 77.

For women the difference in longevity was even greater with female Methodists dying at 91.1 on average – nine years longer than the 82 years enjoyed by most British women.

Last week Stanley Lucas died in Cornwall aged 110, having become not just the oldest male member of the Methodist Church but the oldest man in Europe.

Dr Richard Vautrey, vice president of the Methodist Conference, said, “I’m sure there are many different factors at work for Methodists to attain these numbers.

“But I would guess that our emphasis on caring for our spiritual as well as physical health, avoiding excess, engaging with people in our communities and being good neighbours all help.”

Methodism, an evangelical Christian movement that split from the Church of England at the end of the 18th century, is known for its focus on social justice and for many years was at the forefront of the temperance movement that preached “total abstinence” from alcohol.

The increased life expectancy of its followers, who now number 265,000 in Britain, was calculated by researchers working for British Religion in Numbers, based at the University of Manchester.

They studied family announcements placed in the denomination’s newspaper, the Methodist Recorder, which found that the mean age of death for Methodist men and women in 1973 and 2008 was far higher than that of the general population as recorded by the Office for National Statistics.

Study of obituaries for Methodist ministers appeared to confirm the trend, with a mean age of death of 83.4 for men who died in 2009 – again more than six years older than the British average of 77.

The Methodist Conference, currently meeting in Porstmouth, begins each year with a rendition of a hymn called “And are we yet alive?”, written by one of the movement’s founders, Charles Wesley.

http://www.telegraph.co.uk/news/newstop ... ation.html

 

[Kondoru]

So thats why my fathers still young!

He hangs out with the old fogies at the chapel!

I keep on telling him he should play with kids his age, but...

 

[ramonmercado]

The Scientist: NewsBlog:
Longevity's secret code revealed
Posted by Jennifer Welsh
[Entry posted at 1st July 2010 07:01 PM GMT]
View comments(5) | Comment on this news story

Extreme longevity is associated with a select group of genetic markers, according to a new study of centenarians, people living at least 100 years. Using these markers, researchers can predict a person's ability to become a centenarian with 77 percent accuracy.

Researchers say they can predict your
likelihood of becoming a centenarian
with 77 percent accuracy
Image: Flickr,
user Dark_Ghetto28
"Exceptional longevity is not this vacuous entity that no one can figure out," said lead author Thomas Perls, the director of the New England Centenarian Study at Boston Medical Center. "I think we've made quite some inroads here in terms of demonstrating a pretty important genetic component to this wonderful trait."

"This paper is an important breakthrough in the field," agreed Jan Vijg, a gerontological geneticist at the Albert Einstein College of Medicine, who did not participate in the study.

Perls recruited Boston University biostatistician Paola Sebastiani to design the genetic analysis, published on Science Express today (July 1).

The study chose 1000 non-related Caucasian centenarians and super-centenarians (those living 110 years or longer) from the New England Centenarian Study, which has been following people since 1995. The centenarians were compared to younger Caucasians with similar genetic backgrounds.

The researchers compared the frequency of 300,000 single-nucleotide polymorphisms (SNPs) in both groups, then looked for the SNPs that appeared most unique to the centenarians. They sequentially added additional markers down the line, increasing the specificity and sensitivity of the prediction algorithm until the results plateaued. Ultimately, the algorithm contained 150 SNPs that predicted a person's chances of reaching 100 with 77 percent accuracy.

The team is developing a software program for use by other researchers, companies, and individuals to analyze a genetic sequence and determine the likelihood of extreme longevity.

Less than half of the SNPs were located in areas associated with functioning genes. Some linked to the insulin pathway, some to genes associated with Alzheimer's disease (including the ApoE4 gene variant, which is a genetic risk factor for the disease) and dementia. Many of the SNPs point to more basic biological processes, such as chromosomal instability, muscle function and control of the immune system. "Biologically what they show is that many many different processes are involved in achieving these exceptionally old ages," said Sebastiani.

Of course, the researchers could only compare centenarians to younger controls, some of whom may eventually become centenarians themselves. However, given that it is such a rare trait -- only one in six thousand people reaches 100 or older -- the researchers said this potential confounder likely had minimal impact on the findings.

The centenarians were placed into smaller groups based on their SNP profiles. Some of the groups showed special characteristics, like those who survive the longest or those with the most delayed onset of age-related diseases. There was one cluster of centenarians that did not carry many of the SNPs associated with longevity. These could be people who lived really healthy lives, or harbor rare variants linked to longevity, the authors suggested.

Even though the centenarians survived so long, the researchers found that they have similar levels of a large set of disease-associated genetic risk factors as the controls, including risk factors for Alzheimer's, diabetes, and cardiovascular disease. This seems to indicate that long-life indicators also somehow mask disease traits.

"You could conceivably produce a chip that would help predict people's genetic predisposition for exceptional longevity," said Perls, cautioning that such a test would carry serious ramifications.

The study's approach to unraveling the intertwined combination of genetic markers underlying disease could be used to learn more about other complicated genetic diseases like diabetes, Parkinson's, Alzheimer's and cardiovascular diseases, said Sebastiani.

The paper "tells us we should really look closely at aging and longevity if we want to learn more about diseases," said Vijg.

P. Sebastiani, et al. "Genetic signatures of exceptional longevity in humans," Science Express, July 2010

http://www.the-scientist.com/blog/print/57543/

 

[ramonmercado]

Critics cast doubt on recent longevity gene study findings
http://www.physorg.com/news197872790.html
July 9th, 2010 in Medicine & Health / Genetics

(PhysOrg.com) -- A recent study of centenarians (reported in PhysOrg on July 1st) that linked a number of gene variants to longevity has now been questioned by other scientists, who suggest a DNA chip known as 610-Quad, used in the analysis, has a tendency to produce false-positives. The flaw in the chip, along with other concerns, has cast doubts on some of the major findings of the study.

The paper, published in Science, identified 150 genetic variants that may protect the body against disease and increase the chances of reaching 100 years or more. Even some of its critics admit the research was well-designed in almost all respects, and the researchers say they conducted "extensive quality-control procedures and cleaning of the data," and stand by their results.

One of the major components of the work, carried out by researchers at the Boston University School of Medicine, was a genome-wide association study (GWAS), which uses DNA analysis (SNP) chips to analyze DNA from many subjects to identify variants more common in the group of interest, called cases (in this study people over 100) than in controls. The variants seen more often in the cases are then considered to be linked to the trait being studied. The researchers built a model based on their genetic analysis, and found it could predict extreme longevity with 77 percent accuracy.

A single nucleotide polymorphism (SNP) chip is a tool now widely used in genome analysis. The chips are not perfect and are all known to occasionally identify parts of DNA incorrectly, with each type of chip making different errors at different parts of the genome. If only one type of chip is used this can lead to false-positive results, and that is what some scientists, including geneticist David Goldstein of Duke University in Durham, North Carolina, suggest may have happened in the longevity gene study.

Goldstein said it is important to ensure cases and controls are analyzed in exactly the same way using exactly the same chip. If different chips are used for cases and controls the results found may be experimental artifacts rather than real differences. Goldstein added that using the same chip is standard practice for most GWAS research, and the "rigor that seems to be missing from this study is almost always found in others."

In the longevity gene study all the chips were made by the company Illumina, but they were not identical and some of the control and case samples were analyzed in different laboratories. According to the original paper most of the centenarians were analyzed using a 370 chip that looks at 370,000 genetic variations, while around 10 percent were analyzed using the 610-Quad chip that looks at 610,000 genetic variants. Some of the controls were analyzed with the 370 chip, others with the 610, and still others were analyzed using two other chips.

A geneticist from Iceland, Kari Stefansson, who founded deCode Genetics, also suggested a weakness in the research since the 610 chip has a "quirk" related to two of the strongest variants linked by the study to longevity: rs1455311 and rs1036819, in which it tends to always see the minor form (allele) of DNA but does not identify the major allele at those locations in the genome, even though it is usually present.

Stefánsson said when researchers are looking for unusual patterns in their cases, they could mistake these errors for a genetic link that does not really exist. From his knowledge of the 610-Quad quirks he also took the data from the paper and calculated an estimate of centenarians who would have been analyzed with that chip. His result of eight percent is close to the actual figure of 10 percent.

Author of the original paper, biostatistician Paola Sebastiani of Boston University, said the reason was that the 370 chip went off the market during the study and using a different chip was "the best option for us in terms of costs and coverage." She also said the team found the same variants associated with longevity when a third laboratory repeated the analysis of control samples.

The flaw in the chip could be discounted if the analysis was re-run using the same DNA chip for controls and cases, but critics of the study say this should have been done before the paper was published in one of the top science journals. If the analysis were to be repeated it is possible the genetic associations found in the original paper will still hold, but until this is done they say the results found must remain in doubt.

After concerns were raised about the paper’s findings the authors issued a statement acknowledging there had been "a technical error in the laboratory test used on approximately 10% of the centenarian sample that involved the two of the 150 variants." They said their preliminary analysis suggests the error would not affect the overall accuracy of the model, but they are closely re-examining the analysis.

 

[ramonmercado]

Fountain of youth in bile? Longevity molecule identified
http://www.physorg.com/news203763929.html
September 15th, 2010 in Medicine & Health / Research

The human quest for longer life may be one step closer, thanks to research from Concordia University. Published in the journal Aging, a new study is the first to identify the role of a bile acid, called lithocholic acid (LCA), in extending the lifespan of normally aging yeast. The findings may have significant implications for human longevity and health, as yeast share some common elements with people.

"Although we found that LCA greatly extends yeast longevity, yeast do not synthesize this or any other bile acid found in mammals," says senior author Vladimir Titorenko, Concordia University Research Chair in Genomics, Cell Biology and Aging and a professor in the Department of Biology. "It may be that yeast have evolved to sense bile acids as mildly toxic molecules and respond by undergoing life-extending changes. It is conceivable that the life-extending potential of LCA may be relevant to humans as well."

Over 19 000 small molecules screened

Titorenko and colleagues screened more than 19 000 small molecules to test their ability to extend yeast-lifespan. Under both normal and stressed conditions, LCA had a major impact.

"Our findings imply that LCA extends longevity by targeting two different mechanisms," says first author Alexander Goldberg, a Concordia doctoral student. "The first takes place regardless of the number of calories and involves the day-to-day or housekeeping proteins. The second system occurs during calorie-restriction and involves stressor proteins."

"Regardless of their triggers both of these mechanisms work to suppress the pro-aging process," he continues.

Bile acids may be beneficial to health

"Although we have an overall idea how LCA works to extend longevity in yeast, we still need to determine if this is the case for other species," says Titorenko. "We do know from previous studies, however, that bile acids are beneficial to health and longevity. For example, they have shown to accumulate in the serum of long living mice and play a role in improving rodent liver and pancreatic function."

"This leads us to believe that bile acids have potential as pharmaceutical agents for the treatment of diabetes, obesity and various metabolic disorders, all of which are age-related," continues Titorenko. "They may indeed offer hope for a healthy aging life."

More information: http://www.physorg.com/news203763929.html

 

[Zilch5]

5 Reasons Immortality Would be Worse than Death

Read more: http://www.cracked.com/article_18708_5- ... z0zdwGsLOr

 

[Kondoru]

Very funny, but some valid points.

I doubt, somehow, that people would want to live more than a thousand years.