A new diet, appropriately known by the acronym MIND, could significantly lower a person’s risk of developing Alzheimer’s disease, even if the diet is not meticulously followed, according to a paper published online for subscribers in March in the journal Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

Rush nutritional epidemiologist Martha Clare Morris, PhD, and colleagues developed the “Mediterranean-DASH Intervention for Neurodegenerative Delay” (MIND) diet. The study shows that the MIND diet lowered the risk of AD by as much as 53 percent in participants who adhered to the diet rigorously, and by about 35 percent in those who followed it moderately well.

“One of the more exciting things about this is that people who adhered even moderately to the MIND diet had a reduction in their risk for AD,” said Morris, a Rush professor, assistant provost for Community Research, and director of Nutrition and Nutritional Epidemiology. “I think that will motivate people.”

Morris and her colleagues developed the MIND diet based on information that has accrued from years’ worth of past research about what foods and nutrients have good, and bad, effects on the functioning of the brain over time. This is the first study to relate the MIND diet to Alzheimer’s disease.

“I was so very pleased to see the outcome we got from the new diet,” she said.

The MIND diet is a hybrid of the Mediterranean and DASH (Dietary Approaches to Stop Hypertension) diets, both of which have been found to reduce the risk of cardiovascular conditions, like hypertension, heart attack and stroke. Some researchers have found that the two older diets provide protection against dementia as well.

In the latest study, the MIND diet was compared with the two other diets. People with high adherence to the DASH and Mediterranean diets also had reductions in AD — 39 percent with the DASH diet and 54 percent with the Mediterranean diet — but got negligible benefits from moderate adherence to either of the two other diets.

The MIND diet is also easier to follow than, say, the Mediterranean diet, which calls for daily consumption of fish and 3-4 daily servings of each of fruits and vegetables, Morris said.

The MIND diet has 15 dietary components, including 10 “brain-healthy food groups” — green leafy vegetables, other vegetables, nuts, berries, beans, whole grains, fish, poultry, olive oil and wine — and five unhealthy groups that comprise red meats, butter and stick margarine, cheese, pastries and sweets, and fried or fast food.

With the MIND diet, a person who eats at least three servings of whole grains, a salad and one other vegetable every day — along with a glass of wine — snacks most days on nuts, has beans every other day or so, eats poultry and berries at least twice a week and fish at least once a week and benefits. However, he or she must limits intake of the designated unhealthy foods, especially butter (less than 1 tablespoon a day), cheese, and fried or fast food (less than a serving a week for any of the three), to have a real shot at avoiding the devastating effects of AD, according to the study.

Berries are the only fruit specifically to make the MIND diet. “Blueberries are one of the more potent foods in terms of protecting the brain,” Morris said, and strawberries have also performed well in past studies of the effect of food on cognitive function.

The MIND diet was not an intervention in this study, however; researchers looked at what people were already eating. Participants earned points if they ate brain-healthy foods frequently and avoided unhealthy foods. The one exception was that participants got one point if they said olive oil was the primary oil used in their homes.

The study enlisted volunteers already participating in the ongoing Rush Memory and Aging Project (MAP), which began in 1997 among residents of Chicago-area retirement communities and senior public housing complexes. An optional “food frequency questionnaire” was added from 2004 to February 2013, and the MIND diet study looked at results for 923 volunteers. A total of 144 cases of AD developed in this cohort.

AD, which takes a devastating toll on cognitive function, is not unlike heart disease in that there appear to be “many factors that play into who gets the disease,” including behavioral, environmental and genetic components, Dr. Morris said.

“With late-onset AD, with that older group of people, genetic risk factors are a small piece of the picture,” she said. Past studies have yielded evidence that suggests that what we eat may play a significant role in determining who gets AD and who doesn’t, Morris said.

When the researchers in the new study left out of the analyses those participants who changed their diets somewhere along the line — say, on a doctor’s orders after a stroke — they found that “the association became stronger between the MIND diet and [favorable] outcomes” in terms of AD, Morris said. “That probably means that people who eat this diet consistently over the years get the best protection.”

In other words, it looks like the longer a person eats the MIND diet, the less risk that person will have of developing AD, Morris said. As is the case with many health-related habits, including physical exercise, she said, “You’ll be healthier if you’ve been doing the right thing for a long time.”

Morris said, “We devised a diet and it worked in this Chicago study. The results need to be confirmed by other investigators in different populations and also through randomized trials.” That is the best way to establish a cause-and-effect relationship between the MIND diet and reductions in the incidence of Alzheimer’s disease, she said.

The study was funded by the National Institute on Aging. All the researchers on this study were from Rush except for Frank M. Sacks MD, professor of Cardiovascular Disease Prevention, Department of Nutrition, at the Harvard School of Public Health. Dr. Sacks chaired the committee that developed the DASH diet.

Author Bryant H. McGill asserts that: ?It is better to have a meaningful life and make a difference than to merely have a long life.? But increasingly one can have both, courtesy of scientific advancement. Extending life and its quality are clearly within our reach.

Life expectancy in industrialized nations has risen from age 47 in 1900 to 80 today, mainly due to breakthroughs in curing childhood illnesses. And while age-related illnesses like heart disease, cancer, stroke and Alzheimer’s are very prevalent, progress in curing ? or effectively managing? them has been remarkable. Eighteen months ago Google launched Calico (California Life Company) to reverse engineer the biology that controls lifespan, while a year ago technology entrepreneurs Craig Venter and Peter Diamindis created Human Longevity with plans to create a database of one million human genome sequences by 2020.

There are a host of treatments and remedies, both natural and pharmacological, nutritional and kinesiologic, that can extend longevity. Unquestionably, one of the greatest scientific breakthroughs in recent times has been in stem cells. Research in this area is clearly revolutionizing health care. Everybody has stem cells in their body.

The main purpose of these cells is to repair and maintain tissue. The concept of stem cell therapy is to harness your body?s own healing potential. Scientists can isolate cells from a patient, enrich them and then direct them to areas of disease. In this case, the stem cells may actually heal tissue or replace damaged cells with functioning cells instead of only masking symptoms. The ability to combat disease without the negative side effects of pharmaceuticals is going to revolutionize medicine.

Adult stem cells are frequently used in medical therapies, with treatment investigations for diabetes, cancer, stroke, Alzheimer?s, and Parkinson?s. But stem cell therapies for heart disease are extremely promising and vitally important, given that heart disease kills 1 of every 4 Americans each year and is the leading cause of death for both men and women.

Florida is one of the fastest growing bioscience regions in the world. With a strong base of biotechnology, medical devices and pharmaceutical companies, world-class research universities and some of the leading non-profit research institutes in the world, Florida has built a resource base to be a top bioscience destination.

With nearly 5,500 bioscience establishments and 40 percent located in Southeast Florida the state is generating over $16 billion in economic output and average compensation two-thirds greater than other industries. Florida?s biotech industry has grown more than 75 percent over the past six years. Florida?s research universities conducts over $12 billion in bioscience related research and development on a yearly basis, with most of the state?s research universities involved directly or indirectly in stem cell research.

llustrative is Bioheart, a Sunrise-based biosciences firm that offers huge promise with its MyoCell therapy, composed of muscle cells that are injected into the scar tissue that has formed in the hearts of patients suffering from heart failure. Clinical trials worldwide have been shown to lead to improved cardiac function and an improved quality of life. With a steady stream of positive clinical outcomes worldwide, Bioheart launched a new facility in South Africa, a stem cell institute, last fall.

What could the state do to build on its existing biosciences infrastructure and enhance its national competitiveness in stem cell research and development?

Clearly, Florida could establish something similar to the grant programs offered by the California Institute for Regenerative Medicine. This could help create new treatments as well as create high tech jobs for the state.

Extending life and improve the quality of one?s existence are clearly within our grasp. Stem cell research and therapies vividly attest to the fact that the future is now. Florida?s bioscience ecosystem has a major role to play in this exciting transformation, not just regionally but nationally, as well. With collaboration between business, academe, scientists, clinical practitioners, and the State (including funding), Florida can surely become an important beacon for medical advancement.

If you’re looking to improve your heart health by changing your diet, when you eat may be just as important as what you eat. Previous research has found that people who tend to eat later in the day and into the night have a higher chance of developing heart disease than people who cut off their food consumption earlier. “So what’s happening when people eat late?” asked a biologist whose research focuses on cardiovascular physiology. “They’re not changing their diet, just the time.”

In a new study published today in Science, researchers at San Diego State University and the Salk Institute for Biological Studies found that by limiting the time span during which fruit flies could eat, they could prevent aging- and diet-related heart problems. The researchers also discovered that genes responsible for the body’s circadian rhythm are integral to this process, but they’re not yet sure how.

Previous research has found that people who tend to eat later in the day and into the night have a higher chance of developing heart disease than people who cut off their food consumption earlier.

“So what’s happening when people eat late?” asked Girish Melkani, a biologist at SDSU whose research focuses on cardiovascular physiology. “They’re not changing their diet, just the time.”

Melkani, one of the paper’s senior authors, teamed up with Satchidananda Panda, a circadian rhythms expert at the Salk Institute, to address whether changing the daily eating patterns of fruit flies could affect their heart health. Fruit flies have long been used as model organisms to identify the genetic basis of human disease, including cardiovascular disease.

Shubhroz Gill, a postdoctoral researcher in Panda’s lab and now at the Broad Institute in Boston, was the lead author on this study. Hiep D. Le of the Salk Institute also contributed to the study.

In their experiments, one group of 2-week-old fruit flies was given a standard diet of cornmeal and allowed to feed all day long. Another group was allowed access to the food for only 12 hours a day. Over the course of several weeks, Melkani and Gill recorded how much food the flies were eating and tested a battery of health measures related to their sleep, body weight and heart physiology.

After three weeks, the results were clear: Flies on the 12-hour time-restricted feeding schedule slept better, didn’t gain as much weight and had far healthier hearts than their “eat anytime” counterparts, even though they ate similar amounts of food. The researchers observed the same results after five weeks.

“In very early experiments, when we compared 5-week-old flies that were fed for either 24 hours or 12 hours, the hearts of the latter were in such good shape that we thought perhaps we had mistaken some young 3-week-old fruit flies for the older group,” Gill said. “We had to repeat the experiments several times to become convinced that this improvement was truly due to the time-restricted feeding.”

What’s more, another set of experiments revealed that the benefits of a time-restricted diet weren’t exclusive to young flies. When the researchers introduced these dietary time restrictions to older flies, their hearts became healthier, too. (The average lifespan of a fruit fly is about 60 days.)

“Even if you introduce time-restricted feeding very late, you still have some benefit,” Melkani said.

Some degree of heart protection persisted even for flies that went back to eating whenever they wanted, he added.

Next, the researchers sequenced the RNA of the flies at various points in the experiment to find which of their genes had changed as a result of time-restricted feeding. They identified three genetic pathways that appear to be involved: the TCP-1 ring complex chaperonin, which helps proteins fold; mitochondrial electron transport chain complexes (mETC); and a suite of genes responsible for the body’s circadian rhythm.

Melkani and Gill repeated their experiments using mutant strains of flies with nonfunctional versions of the TCP-1 and circadian rhythm genes. In these flies, time-restricted feeding granted no health benefits, strengthening the case that these genetic pathways play key roles.

Conversely, in mutant flies with altered mETC genes, the flies showed increased protection against cardiac aging.

“If and how these three pathways all work together, we don’t yet know entirely,” Melkani said.

Nix the late-night snacks

The results complement earlier research from Panda’s lab showing benefits of time-restricted feeding for obesity, metabolic diseases and type-2 diabetes in rodents.

“All together, these results reinforce the idea that the daily eating pattern has a profound impact on both the body and the brain,” Panda said.

Gill noted that there are some hurdles to clear before extrapolating this research to humans.

“Humans don’t consume the same food every day,” he said. “And our lifestyle is a major determinant of when we can and cannot eat. But at the very minimum, our studies offer some context in which we should be pursuing such questions in humans.”

Melkani is optimistic that the results could one day translate into cardiac- and obesity-related health benefits for humans. “Time-restricted feeding would not require people to drastically change their lifestyles, just the times of day they eat,” Melkani said. “The take-home message then would be to cut down on the late-night snacks.”

A similar study by Panda published in 2012 involving mice showed that when they were limited to eating only 8 hours out of 24 they had much less obesity even though they consumed the same high fat diet and the same number of calories.

Journal Reference:

Satchidananda Panda et al. Time-restricted feeding attenuates age-related cardiac decline in Drosophila. Science, March 2015 DOI: 10.1126/science.1256682

Hockey legend Gordie Howe?s star power is raising awareness in the United States and Canada about advances in stem-cell therapies as he continues what is being called a ?miraculous? recovery from a massive stroke.

Those closest to him, including his son, Toledo radiologist Dr. Murray Howe, are convinced the former Detroit Red Wings player would have died if he had not traveled to a medical clinic in Tijuana, Mexico, for an experimental stem-cell treatment not yet available in the United States.

After a debilitating stroke on Oct. 26, Mr. Howe, 86, had a few weeks of slight recovery, but then his health ?went downhill? quickly, said Dr. Howe, director of sports medicine imaging for ProMedica Toledo Hospital. The family had started preparing for his funeral. But that all turned around after he had the adult stem-cell treatment on Dec. 8.

?If you saw him now, you wouldn?t know he had a stroke,? Dr. Howe said.

?It?s been wonderful. Every day I would say he?s a little bit better, and there are little hints of improvement. Certainly in the first month, every day his strength, coordination, and balance were better. He has been eating like a horse. He had lost 20 pounds, and now he has gained back 25 pounds, so he is pretty close to his playing weight now,? Dr. Howe said.

In describing his father?s treatment and recovery in the last three months, Dr. Howe does not hesitate to use words such as unbelievable, astonishing, and amazing.

Eight hours after Mr. Howe received what is called a lumbar puncture, where stem cells were injected in the spinal fluid of his lower back by an anesthesiologist, he went from being bedridden and only mumbling short sentences to speaking clearly and walking with assistance, Dr. Howe said.

On the second day at the clinic, he received an IV infusion of a different type of adult stem-cell treatment.

When he returned to his home in Lubbock, Texas, on Dec. 10, Mr. Howe?s recovery from the stroke continued at an rapid rate, his son said.

?His vocabulary had dropped down. If you showed him pictures ? the speech therapists when they were testing him, he could name about one of 10 items. After his stem-cell treatments, he was able to identify 80 percent of the pictures. The speech therapist was just floored,? Dr. Howe said.

?In 28 years of medicine, I have never seen a response, a recovery, from a stroke in such a rapid time frame and such an impressive response to me that is nothing short of miraculous,? he added.

He was doing so well the family accepted an invitation for Mr. Howe to attend a dinner in his honor on Feb. 6 in his hometown of Saskatoon, Sask.

Mr. Howe played 25 seasons with the Red Wings from 1946 to 1971 and played for the Houston Aeros and the New England Whalers of the World Hockey Association from 1973 to 1979. He finished his final season in 1980 at the age of 51 with the Hartford Whalers in the organization?s first season in the NHL.

He won four Stanley Cup championships, six Hart Trophies as the NHL?s most valuable player, and six Art Ross Trophies as the NHL?s leading scorer.

At the event in Canada, Mr. Howe shared the stage with other hockey greats Wayne Gretzky and Bobby Hull. Video of the event, provided by the family, shows Mr. Howe standing under his own power for several seconds as the audience gave him a standing ovation.

?He walked on stage. He goes under his own power, but he is almost 87, and a fall risk, so I just made sure he didn?t trip,? Dr. Howe said.

The lumbar injection Mr. Howe received has not been approved for use in the United States by the Food and Drug Administration partly because the clinical trial process is longer and more cautious in the United States than in some other countries, said Dr. Paula Grisanti, chairman of the National Stem Cell Foundation based in Louisville.

Each new drug or therapy must go through a phase one, phase two, and phase three trial, which can take several years and, depending on the drug, can cost millions of dollars.

Between 4,000 and 5,000 clinical trials dealing with different stem-cell drugs on the FDA website clinicaltrials.gov are in varying stages of completion in the United States and Europe, she said.

?There is a fine line we walk between regulating therapy enough to protect patients but not regulating so much to inhibit innovation,? Dr. Grisanti said.

Stem-cell research is part of a larger field of medicine that is called regenerative medicine. The field has evolved in the last 5 to 10 years and is exploding, she said.

?Every major university in the country has a stem-cell program,? Dr. Grisanti said.

The University of Toledo Medical Center, the former Medical College of Ohio, has multiple researchers looking at various aspects of stem cells but does not have a stem-cell program as such, said Jon Strunk, a university spokesman.

The IV infusion of stem cells that Mr. Howe received on the second day of treatment has been approved for use in the United States, but now patients must wait six months after a stroke to start them, Dr. Howe said.

?They are being conservative and want to see how you recover on your own in the first six months, and after that, we can attribute any improvement you have to the stem cells,? he said.

Dr. Howe does not fault the FDA for being cautious or for having regulations, but he said the result is that U.S. and Canadian doctors are at a disadvantage because other countries such as Russia have been using adult stem cells to treat a variety of illnesses for more than 20 years.

Dr. Gristani estimates it will be at least five years before the stem-cell injection used on Mr. Howe will be through all the clinical trials in the United States. Then insurance companies will have to approve their use before they become widely available, which will likely add several more years to the process.

Because some of the treatments used on Mr. Howe are still in clinical trials here, Dr. Gristani said his recovery is being greeted with skepticism by some in the scientific community.

Most of the for-profit companies use cells manufactured from fat tissue. They take the cells from liposuction and grow them by the millions in a petri dish and manipulate them to make them more robust. They then inject them into the patient to fix the problem, Dr. Gristani said.

Some scientists, she said, are saying, ?You are harvesting fat cells and injecting them, but you don?t know how long it will last because there is no clinical trial with the requirement for data collection, and how do you know, and are you protecting patients? ?

Dr. Gristani said some private companies are ?leapfrogging? over the U.S. clinical trial process and offering patients treatment in other countries, such as the California-based Stemedica Cell Technologies Inc., which reached out to Mr. Howe?s family and offered him free, no-strings-attached treatment to repair the damage from his stroke.

Dr. Howe said he is aware of the critics who distrust the process. He was skeptical himself when first approached by Stemedica because he wasn?t aware of the treatment.

?Some have said, ?Oh, it?s a placebo effect.? Well, that doesn?t make sense because my dad, because of his short-term memory [problem], he doesn?t remember he had a stroke. He doesn?t remember he had a treatment. He has no idea. All he knows is he is doing great and doing what he likes to do,? Dr. Howe said.

A stem cell treatment for severe cornea damage has been granted conditional approval by the European commission. Holoclar is the first stem cell therapy to be approved in the EU, as well as the first approved treatment for limbal stem cell deficiency.

Holoclar has been developed by Holostem Advanced Therapies, a spin-out from the University of Modena and Reggio Emilia, Italy, in partnership with Chiesi Pharmaceuticals. It uses tissue grown from a biopsy of the patient?s own cells to replace the epithelium in patients whose eyes have been damaged by physical or chemical burns, and lack sufficient limbal stem cells to properly regenerate that tissue.

?The authorization process has been long and complex, but shows that cells can be cultured according to pharmaceutical standards appropriate to guarantee safety and efficacy,? said Michele De Luca, scientific director and co-founder of Holostem.

Cardiac stem cell therapy has been shown to stimulate the growth of new heart cells after a heart attack, but exactly how that happens is unclear.

Some researchers hypothesize that these stem cells are the source of new cardiac muscle cells. They normally divide slowly, but when selectively harvested from a patient, they can be increased in number and then infused back into the recipient’s heart.

“After injection, the new cardiac stem cells proliferate and are the source of new heart muscle cells,” Canty said. “With this approach, only cells from the same patient can be used.”

Led by Dr. John Canty Jr., chief of cardiology in the UB Department of Medicine and a cardiologist with UBMD, a National Institutes of Health award will help determine what types of cardiac stem cell therapy is most effective to treat patients with heart failure.

The new research will study how cardiosphere-derived cells from donors can be as effective; as well as how tissue from heart biopsies can be grown and if they can be used to improve cardiac function.

“Using cardiac stem cells that don’t need to be harvested from the recipient would make this type of therapy more widely available to the increasing number of patients in need of treatments for heart failure,” he said. “Demonstrating the feasibility of using cells from an unrelated donor would also provide an off-the-shelf approach to cardiac stem cell therapy.”

Other researchers on the team include Dr. Gen Suzuki, associate professor in the department of medicine; Munawwar Sajjad, research associate professor in the department of nuclear medicine; and Brian Weil, postdoctoral research fellow in the department of medicine.

Humanity has long been in search of the mythical Fountain of Youth, from Alexander the Great to knights of the Crusades.

But now Silicon Valley scientists believe they are on the cusp of discovering the cause of aging, which will help them achieve the unthinkable: find a cure.

Earlier this year, doctor and investor Joon Yun launched the Palo Alto Longevity Prize, offering $1 million (?650,000) to anyone who could ?hack the code of life? and come up with a way to keep us young.

?It?s always been said that there?s two certainties in life: death and taxation, but death isn?t looking so certain anymore,? says Stuart Kim, one of 50 world-class advisers on the prize board and a professor in Developmental Biology and Genetics at Stanford University.

He believes aging is simply a medical problem for which a solution can be found.

The prize will be awarded to the first team to unlock what many believe to be the secret to aging: homeostatic capacity, or the ability of the body’s systems to stabilise in response to stressors.

As the body ages, being able to recover from diseases, injuries and lifestyle stresses becomes more difficult. In youth, blood pressure and elevated blood sugar levels can return easily to normal levels.

As homeostatic capacity erodes as we get older, the body is no longer able to regulate these changes as effectively, resulting in diseases such as diabetes or hypertension.

Dr Yun, who worked for several years as a radiologist at Stanford Hospital before joining a hedge fund investing in health care, uses the analogy of a “weeble wobble” toy to explain that no matter how far it is pushed, it is able to centre itself again.

A person only becomes aware of their body’s homeostasis when they start losing it in middle age: often characterised by the loss of ability to tolerate cold or hot weather, or feeling nauseous after a roller-coaster ride where you once felt exhilarated.

“Up until about 45 years old, most people die from external stressors such as trauma or infection, but as we get older we die of what looks like a loss of intrinsic capacities,” he tells The Sunday Telegraph.

Increased homeostatic capacity could allow people to live beyond 120 years ? the theoretical maximum human lifespan.

Scientists could effectively slow down the body’s clock and enable us to remain middle aged for 50 years or more, meaning we can feel 50 when we are really 80. The future could see us not just living longer, but staying healthier for longer.

“This isn’t like plastic surgery where you’re papering over the cracks, this is actually making a person younger from the inside out,” Dr Yun says.

The first half of the prize will be awarded next year to the team that can restore the homeostatic capacity of an aging adult mammal to that of a young one, thereby reversing the effects of aging.

The second half to the team that can then extend the lifespan of their chosen mammal by 50 per cent of published norms.

So far 15 teams have entered, including a handful from Stanford University as well as from further afield at the genetics department at George Washington University in DC and the Albert Einstein College of Medicine, New York.

But they face even fiercer competition outside the prize. Google recently unveiled its own $1.2 billion research centre Calico, or the California Life Company, aiming to achieve the tech giant’s boldest ambition yet ? extend the human lifespan.

While their work, which is led by Arthur Levinson, former CEO of biotech firm Genentech, is shrouded in secrecy, they are said to be focusing on developing drugs for age-related neurodegenerative disorders.

“Our goal is to make progress on a very basic challenge: how to help people stay healthier for longer,” Mr Levinson said of the project.

Meanwhile, Craig Venter, the geneticist who sequenced the first human genome, has set up his own company, Human Longevity Inc., alongside stem cell pioneer Robert Hariri.

They plan to sequence one million human genomes, including those of several supercentenarians, in order to build the world’s largest database of human genetic variation. By looking at the DNA, they hope to discover a common feature among those living longer.

Dr de Grey, a British gerontologist at the SENS Foundation in Silicon Valley, has dedicated his life’s work to solving the perennial problem of death. He believes it should be treated as a disease and can be postponed indefinitely.

“Since the dawn of civilisation, humanity has been enslaved by the knowledge that no lifestyle choice, no medicine, no quirk of fate, can enable anyone to live for more than a few decades without suffering a progressive decline that leads inevitably to death,” the Cambridge University researcher says.

“But scientists have already drawn a road map to defeat biological aging and will one day show there is no such inevitability. This is a when, not an if.”

However, he takes a different approach, looking at fixing the damage caused by metabolism.

The idea of reverse-engineering aging is not a new one. The American Academy of Anti-aging Medicine was set up in 1992, but only recently has the idea gained traction in mainstream medicine.

Dr Yun believes there had not been the support or funding needed to galvanise the field until now. “No one was incentivised to fix the underlying causes of aging as too many of the big players in the medical and insurance industries benefit from the current system,” he says.

There has also not been much of a public appetite, which scientists put down to lack of understanding. A recent survey by Pew Research found that most Americans did not actually want to live beyond the accepted human lifespan.

When asked if they wanted medical treatments that slowed the aging process and allowed the average person to live to at least 120 years, 56 per cent surveyed said no. When asked how long they wanted to live, the median answer was 90.

Even Bill Gates, Microsoft founder and philanthropist, seemed to write off the desire to extend life as Silicon Valley hubris. “It seems pretty egocentric while we still have malaria and TB for rich people to fund things so they can live longer,” he said, however continued “It would be nice to live longer though I admit.”

Along with the reasoning that it felt “fundamentally unnatural”, a number of survey respondents said they would worry about overpopulation and a potential lack of resources.

But Dr Yun says society will adapt to changes in life expectancy. “Just a few generations ago it was common to see people going into the workforce at 13, and dying before they turned 45. Things have changed since then ? people now stay in education for longer, and have children and retire much later.

“Plus if people begin living longer, they will care more about what the world will look like in the future ? impact concerns will shift from being their children’s problem to being their problem.”

Life-extending technology has become a booming industry in Silicon Valley.

Google X and Proteus Digital Health are among a dozen or so companies working on “ingestible tech” that they hope will go some way towards keeping us alive and healthy for longer.

Google’s pill, which is filled with tiny iron-oxide nanoparticles that enter the bloodstream, is able to identify cancer tumour cells, which give off early biochemical signals when they contract the disease.

Proteus, having already gained FDA approval, is now in talks with Britain’s National Health Service about the possible use of its sensor pill, which sends biological information it retrieves from the body to a smartphone.

At the same time, the XPrize Foundation, a charity that runs technology competitions, is working on developing a hand-held all-in-one diagnostic device. With one drop of blood, the “tricorder” will be able to accurately detect conditions such as diabetes and tuberculosis as well as measuring blood pressure and temperature ? all from the comfort of your home.

Grant Campany, director of the XPrize, told The Sunday Telegraph: “It will all but eradicate the need to see a doctor for check-ups. The device will help people take their health back into their own hands.”

The Longevity Prize’s Dr Kim, who has spent the last 10 years looking into the causes of aging, believes we cannot afford not to come up with a solution. “We shouldn’t just be thinking of how to treat diseases like cancer, we should be looking at how to prevent them by figuring out why old people are much more likely to get them,” he says. “If you could take 80-year-olds and make them biologically more like 60-year-olds, that’s a 15-fold decrease in the rate of cancer right there.

“If we solve this, we all win.”

HONG KONG: Scientists mapping the genome for the world?s longest-lived mammal, the bowhead whale, have found the longevity genes that give it a 200-year-plus lifespan ? and say the discoveries might be used to extend human life.

The genome mapping is a result of two separate studies carried out in the US and UK allowing scientists to identify a small number of genes linked to cancer resistance, DNA damage repair and increased longevity.

Joao Pedro de Magalhaes, the lead researcher of the UK-based study at Liverpool University, said the discovery could lead to those genes being used to help humans enjoy a longer life.

The work, conducted in the Liverpool Centre for Genomics Research was done in collaboration with scientists in Alaska, Denmark, Ireland, Spain and South Korea, and compared the bowhead?s genes with a minke whale, which typically lives for only 30-50 years.

Using this method, the researchers found that the bowhead had unique mutations in two genes linked to lifespan in animals.

These are the ERCC1 gene, which is believed to repair DNA, increase cancer resistance and slow ageing, and the PCNA gene, which is also linked to DNA repair.

Magalhaes is now seeking funding for a project that will insert the whales? genes into mice to see if that improves their resistance to disease, ?The Sunday Times? reported.

If that is successful, the scientist hopes to test its effects on humans either by using drugs that activate the genes already inside the body or by incorporating the bowhead?s genes into human cells and inserting them back into people.

Magalhaes? work follows a study published in October by Harvard Medical School researchers which also analysed the bowhead?s genes and made similar findings.

They proposed that similar genetic patterns also existed in other remarkably long-lived animals such as the naked mole rat and the Brandt?s bat.

In a research area that will generate blockbuster profits if/when it pans out, a science team reported creating new hair cells from pluripotent stem cells in a recent issue of PLOS (Proceedings of the Library of Science) One.

The team, led by the Sanford Burnham Medical Research Institute, got their results using two different kinds of cells: embryonic stem (ES) cells and induced pluripotent stem (iPS) cells. ES cells can form all body cells. IPS cells can, as well. The difference is iPS cells are derived from adult cells, not in vitro fertilization (IVF) clinic embryos. The clock is turned back on the adult cells, until they reach a pluripotent state like that of ES cells.

?The relative simplicity of the procedure to derive [dermal-papilla]-like cells was a pleasant surprise,? Sanford Burnham developmental biologist Alexey Terskikh told Drug Discovery & Development. Terskikh is senior author on the paper. ?To the best of my knowledge, we are the first team to report the generation of hair inducing cells? from embryonic stem cells. ?The most critical next step is to investigate whether this approach works in humans.?

The new approach

Terskikh?s group believes their creation of neural crest cells from ES cells, which then formed dermal papilla cells, was a key step. Dermal papilla cells regulate hair-follicle formation and growth cycle. Limited adult dermal papilla (DP) cells do not work as hair transplants as they generally can?t be obtained in the large amounts, and can quickly lose hair-follicle forming ability in culture.

But neural crest cells transiently arise from the dorsal neural tube during development, and give rise to many tissues at that time, including hair follicle cells. So Terskikh?s group first worked on persuading their pluripotent cells to become neural crest cells. Human ES cells ?have been directed to various cell fates including hair follicle epidermal cells?keratinocytes; however, the derivation of DP cells have not been reported? from ES cells, the team wrote. ?Here we describe for the first time the derivation of functional DP-like cells human embryonic stem cells.?

Alexey Terskikh, Ph.D, the Sanford Burnham Medical Research Institute developmental biologist behind a recent effort to create hair cells from stem cells Alexey Terskikh, Ph.D, the Sanford Burnham Medical Research Institute developmental biologist behind a recent effort to create hair cells from stem cells The group reported their human ES-cell derived neural crest cells, cultured in serum, progressively acquired the markers of DP cells, and gave rise to cell populations with ?robust? hair-inducing potential in mice. They speculated the superior hair-creation capacity of their pluripotent cell derived DPs to most reported adult DPs may have to do with the resemblance of their cells to embryonic or neonatal DP precursor cells.

The group also reported their cells are heterogeneous, a ?mixed population? of neural-crest-derived cells that ?contain DP-like cells with hair-inducing properties, but also might contain melanocyte- and keratinocyte-forming cells.? Therefore, ?further analysis?is needed to address this question.?

The group also noted they had more success with human ES cells than with human IPS cells. They only achieved hair cells with one of three iPS cell lines. However, if many lines are used, hair cells should ultimately result, they wrote.

Overall, the group reported, ?our results suggest that the intermediate step of hESC differentiation into the NC [neural crest] lineage seems critical, skipping the NC induction results in a complete loss of hair-inducing activity.? The group believes that directing human ES cells to neural crest cells ?might limit the variety of mesenchymal cell types to the subset that is developmentally specified downstream from NC cells in skin (e.g. cephalic DP during development, melanocytes, cephalic bulge).? Resulting cultures become ?enriched in hair-inducing DP-like cells using relatively common mesenchymal-enriching conditions, such as differentiation in serum containing medium and selection for the adherent cell types.?

The group said adult skin-derived precursors have been found in the past to be ?highly potent in hair induction, but progressive loss? of those cells during aging ?might hamper the process of isolation? of those cells.

In 2013, a Columbia University and Durham University team reported pairing up to generatesignificant hair growth, for the first time, from adult DP cells using unique 3-D cultures. Results varied between donor cells, but those groups reported they were perfecting that approach.

It?s been known for decades that some metals, including iron, accumulate in human tissues during aging and that toxic levels of iron have been linked to neurologic diseases. Common belief has held that iron accumulation happens as a result of the aging process. But research in the nematode C. elegans in the Lithgow lab at the Buck Institute shows that iron accumulation itself may also be a significant contributor to the aging process, causing dysfunction and malfolding of proteins already implicated in the aging process. The research is online in Aging

Similar to what happens in humans and other mammals, researchers found that levels of calcium, copper, iron and manganese increased as the worms aged. But iron accumulated much more than the others, said Buck faculty Gordon Lithgow, PhD, senior scientist on the project. ?We were drawn to iron because there is all this literature that links excess iron to Alzheimer?s and Parkinson?s.?

Researchers began manipulating the nematode?s diet. ?We fed iron to four day-old worms, and within a couple of days they looked like 15 day-old worms,? said Lithgow. ?Excess iron accelerated the aging process.? Lithgow says excess iron is known to generate oxidative stress and researchers expected to see changes in the worm based on that toxicity. ?Instead, what we saw looked much more like normal aging,? said Lithgow. ?The iron was causing dysfunction and aggregation in proteins that have already been associated with the aging process. Now we?re wondering if excess iron also drives aging. ?

Researchers, led by graduate student Ida Klang, also treated normal nematodes with the FDA-approved metal chelator CaEDTA ? a drug that?s used in humans at risk for lead poisoning. The drug slowed age-related accumulation of iron and extended the healthspan and lifespan of the nematodes. Klang also gave the drug to worms genetically bred to develop specific protein aggregations implicated in human disease. The chelator was also protective in those animals.

Lithgow says the work has implications for the aging research field. ?Maintaining the proper balance of metals is key to good health throughout the lifespan, and it?s pretty obvious that this delicate balance can go off-kilter with age,? he said. ?This is a phenomena that has not been extensively studied by aging researchers and it?s an area that has potential for positive exploitation.? As far as the general public is concerned, Lithgow was quick to warn people away from taking CaEDTA and other available metal chelators as anti-aging medication. ?CaEDTA has a very blunt mechanism of action and is associated with dangerous side effects in humans and the track record for other chelators is not well established,? said Lithgow, who urged people to talk to their physicians about the use of iron supplementation, especially for postmenopausal women.

Lithgow said his lab wants to find new chelators that act more like drugs and then move those drugs into testing in mice.

Reference: Iron promotes protein insolubility and aging in C. elegans