Life Expectancy in the Wild Birds Predicted by Telomere Lengths

seychelles-warblerResearchers at the University of East Anglia have found that biological age and life expectancy can be predicted by measuring an individual’s DNA.

They studied the length of chromosome caps — known as telomeres — in a 320-strong wild population of Seychelles Warblers on a small isolated island.

Published Nov. 20 in Molecular Ecology, their research shows that individuals differ radically in how quickly their telomeres shorten with age, and that having shorter telomeres at any age is associated with an increased risk of death. Telomere length is a better indicator of future life-expectancy than actual age and may, therefore, be an indicator of biological age.

The 20-year research project is the first of its kind to measure telomeres across the entire lifespan of individuals in a wild population.

Telomeres are found at the end of chromosomes. They act as protective caps to stop genes close to the end of the chromosome degenerating — like the hard plastic ends of a boot lace.

Lead researcher Dr David S Richardson said: “Over time these telomeres get broken down and become shorter. When they reach a critical short length they cause the cells they are in to stop functioning. This mechanism has evolved to prevent cells replicating out of control — becoming cancerous. However the flip side is that as these zombie cells build up in our organs it leads to their degeneration — aging — and consequently to health issues and eventually death.

“Telomeres help safeguard us from cancer but result in our aging.”

Researchers studied the warbler population on Cousin Island. Blood samples were collected twice a year and telomere length analysed.

“We wanted to understand what happens over an entire lifetime, so the Seychelles Warbler is an ideal research subject. They are naturally confined to an isolated tropical island, without any predators, so we can follow individuals throughout their lives, right through to old age.

“We investigated whether, at any given age, their telomere lengths could predict imminent death. We found that short and rapidly shortening telomeres were a good indication that the bird would die within a year.

“We also found that individuals with longer telomeres had longer life spans overall.

“It used to be thought that telomere shortening occurred at a constant rate in individuals, and that telomere length could act as an internal clock to measure the chronological age of organisms in the wild.

“However while telomeres do shorten with chronological age, the rate at which this happens differs between individuals of the same age. This is because individuals experience different amounts of biological stress due to the challenges and exertions they face in life. Telomere length can be used as a measure of the amount of damage an individual has accumulated over its life.

“We saw that telomere length is a better indicator of life expectancy than chronological age — so by measuring telomere length we have a way of estimating the biological age of an individual — how much of its life it has used up.”

The research is important because while these ideas have been researched in the lab, they have never been tested in a wild environment.

“It would be virtually impossible to do such a study in humans,” said Dr Richardson. “For one thing it would take a very long time to study a human lifespan. Also in humans we would normally, quite rightly, intervene in cases of disease, so it wouldn’t be a natural study.

“We found that telomeres are linked to body condition and reflect the history of oxidative stress that has occurred within an individual’s lifetime. The healthier you are, or have been, the better telomeres you have. But it’s hard to know whether this is a consequence of being healthy, or a cause.

“Oxidants attack telomeres. So things like smoking, eating foods that are bad for you, and putting your body through extreme physical or mental stress all have a shortening affect on telomeres.

“All these stresses do damage to our bodies. You hear people saying ‘oh they look like they’ve had a hard life’. This is why. A shortened telomere shows an accumulation of damage life has done to you.”

‘Telomere length and dynamics predict mortality in a wild longitudinal study’ is authored by Dr David S Richardson and Emma Barrett from the University of East Anglia (UK), Terry Burke from the University of Sheffield (UK), and Jan Komdeur and Martijn Hammers from the University of Gronigen (Netherlands).

The study was funded by the Natural Environment Research Council (NERC) and carried out in collaboration with conservation group Nature Seychelles.

Eating Egg Yolks Almost as Bad as Smoking?

Egg YolkNewly published research led by Western’s Dr. David Spence shows that eating egg yolks accelerates atherosclerosis in a manner similar to smoking cigarettes.

Surveying more than 1200 patients, Spence found regular consumption of egg yolks is about two-thirds as bad as smoking when it comes to increased build-up of carotid plaque, a risk factor for stroke and heart attack. The research is published online in the journal Atherosclerosis.

Atherosclerosis, also called coronary artery disease, is a disorder of the arteries where plaques, aggravated by cholesterol, form on the inner arterial wall. Plaque rupture is the usual cause of most heart attacks and many strokes.

We suspect that eggs yolks cause increased atherosclerosis because of the way the hens are fed not because there is anything inherently bad about eating the. It is likely a problem similar to the increase in atherosclerosis when people eat beef. The animals are fed large amounts of soy meal and grains which contain much more omega-6 fatty acids than the animals normally eat and close to zero omega-3 fatty acids. As a result the meat and egg yolks are high in arachidonic acid. When consumed by humans that is converted into series 2 prostaglandins which produces inflammation and as a result atherosclerosis and other degenerative diseases.

The study looked at data from 1,231 men and women, with a mean age of 61.5, who were patients attending vascular prevention clinics at London Health Sciences Centre’s University Hospital. Ultrasound was used to establish a measurement of total plaque area and questionnaires were filled out regarding their lifestyle and medications including pack-years of smoking (number of packs per day of cigarettes times the number of years), and the number of egg yolks consumed per week times the number of years consumed (egg yolk-years).

The researchers found carotid plaque area increased linearly with age after age 40, but increased exponentially with pack-years of smoking and egg yolk-years. In other words, compared to age, both tobacco smoking and egg yolk consumption accelerate atherosclerosis. The study also found those eating three or more yolks a week had significantly more plaque area than those who ate two or fewer yolks per week.

“The mantra ‘eggs can be part of a healthy diet for healthy people’ has confused the issue. It has been known for a long time that a high cholesterol intake increases the risk of cardiovascular events, and egg yolks have a very high cholesterol content. In diabetics, an egg a day increases coronary risk by two to five-fold,” said Spence, a professor of Neurology at Western’s Schulich School of Medicine & Dentistry and the director of its Stroke Prevention and Atherosclerosis Research Centre at the Robarts Research Institute.

“What we have shown is that with aging, plaque builds up gradually in the arteries of Canadians, and egg yolks make it build up faster — about two-thirds as much as smoking. In the long haul, egg yolks are not okay for most Canadians.”

Spence added the effect of egg yolk consumption over time on increasing the amount of plaque in the arteries was independent of sex, cholesterol, blood pressure, smoking, body mass index and diabetes. And while he says more research should be done to take in possible confounders such as exercise and waist circumference, he stresses that regular consumption of egg yolk should be avoided by persons at risk of cardiovascular disease.

If Want to Live to be 100 Get Enough Sleep

Woman SleepingYour chances of reaching age 100 could be better than you think ? especially if you get some additional sleep and improve your diet.

New research from United Health Care looks at centenarians and baby boomers, asking the former about the secrets of reaching an advanced age while maintaining good health and then evaluating whether the latter are taking the necessary steps to celebrate a 100th birthday.

The primary findings: Many boomers are embracing lifestyles that could lead to a long and rewarding life ? with two exceptions. More than seven in 10 centenarians ? 71% ? say they get eight hours or more of sleep each night. By contrast, only 38% of boomers say they get the same amount of rest. And when it comes to eating right, more than eight in 10 centenarians say they regularly consume a balanced meal, compared with just over two-thirds (68%) of baby boomers.

The report begins with some startling numbers. As of late 2010, the U.S. had an estimated 72,000 centenarians, according to the Census Bureau. By the year 2050, that number ? with the aging of the baby-boom generation ? is expected to reach more than 600,000. Meanwhile, an estimated 10,000 boomers each and every day ? for the next decade ? will turn 65.

How to reach 100? Centenarians point to social connections, exercise and spiritual activity as some of the keys to successful aging. Among surveyed centenarians, almost nine in 10 ? fully 89% ? say they communicate with a family member or friend every day; about two thirds (67%) pray, meditate or engage in some form of spiritual activity; and just over half (51%) say they exercise almost daily.

In each of these areas, baby boomers, as it turns out, match up fairly well. The same percentage of boomers as centenarians ? 89% ? say they?re in touch with friends or family members on a regular basis. Sixty percent of surveyed baby-boomers say spiritual activity is an important part of their lives, and almost six in 10 boomers (59%) exercise regularly.

Again, sleep and diet are the two areas where baby boomers come up short. Not surprisingly, the one area where boomers are more active is the workplace. Three-quarters (76%) of surveyed baby boomers say they work at a job or hobby almost every day; that compares with 16% of centenarians.

Finally, researchers turned to cultural affairs and asked centenarians and boomers to identify ? from a list of 14 notable people (including President Obama, singer Paul McCartney and actors Tom Hanks and Julia Roberts) ? their preferred dinner guest. The top choice among centenarians and boomers alike: the comedian Betty White.

Life Extension: Protecting prion protein keeps stem cells young

COULD we stem the tide of aging by delaying the deterioration of stem cells? A new compound that appears to do just that could help us find ways to protect our organs from age-related wear and tear, experiments in mice suggest.

As we age, so do our mesenchymal stem cells (MSCs): their numbers in our bone marrow decline, and those that are left lose the ability to differentiate into the distinct cell types – such as bone, cartilage, fat and possibly muscle cells – that help in the healing process.

“We think this ageing of stem cells may be linked to the onset of some age-related disorders, such as osteoporosis,” says Ilaria Bellantuono at the University of Sheffield in the UK.

Earlier research in mice had suggested that the prion protein expressed by MSCs might play a role in holding back stem cell ageing. Mice lacking the prion protein were less able to regenerate blood cells. The study provided more evidence that correctly folded prions serve a useful purpose in the body, despite the role that misfolded prions play in BSE and vCJD.

Bellantuono and her colleagues have now found that the prion protein performs a similar function in humans – older MSCs from human bone marrow expressed less of the protein than younger ones.

In a bid to find a compound that might slow MSC ageing, the team tested numerous molecules known to target prion proteins on dishes of human stem cells. One molecule emerged as a potential candidate – stem cells treated with it produced 300 times the number of cells over 250 days than untreated stem cells. The treated cells kept on dividing for longer.

The team then injected treated cells into the thigh bones of mice, and three days later found that they had produced three times as many new cells as they would normally produce. After five weeks, there were 10 times as many cells.

The new cells appeared to be of higher quality, too, and readily differentiated into bone and fat cells, as well as those that support the tissue and blood vessels.
Bellantuono’s team think the molecule works by helping the prions protect the stem cells from the DNA damage associated with normal ageing. When they exposed both treated and untreated cells to hydrogen peroxide – a compound known to cause DNA damage – they found that the treated cells were protected from damage (Stem Cells, DOI: 10.1002/stem.1065).

“You can delay the loss of stem cells’ function by manipulating the prion protein,” says Bellantuono, who presented the findings at the Aging Online Symposium last month. “In the long term, you may go a long way to maintaining tissue health in [old] age.”

It may be some time before the compound can be used to fight ageing, but similar molecules might have a more immediate benefit in stem cell therapies.

“A big problem with using MSCs for therapy is that you need to inject millions of cells, but it’s difficult to get millions in a dish,” says James Adjaye of the Max Planck Institute for Molecular Genetics in Berlin, Germany. “This molecule lets the cells grow for longer – it’s very interesting in that respect.”

Does longevity have a biological limit?

“Medicine is about transcending biology.”
July 5, 2012 by Aubrey de Grey

Gerontologists and demographers have argued about this for a long time, with the balance of opinion heavily influenced by the changes seen in the wealthiest nations? ?survival curves? ? graphs showing, broadly speaking, the proportion of an initial population that survived to a given age.

Until a couple of centuries ago, these curves looked very much like radioactive decay curves, because one?s chance of dying at any given age was pretty much the same. As medicine emerged and we became protected from most infectious diseases, the curve became more rectangular, implying a biological limit that most people were getting fairly close to.

Then, since about 1960, the pseudo-rectangle has just got longer, without becoming more rectangular, suggesting no limit (or at least no close one). Very recently, however, the tip of the curve (repreenting those reaching the oldest ages, over 110) has become more rectangular again, swinging the pendulum back in favor of the existence of a limit.

From a biological perspective, this demographic analysis is all a bit curious: in a sense it is obvious that such a limit must exist. This is because so much of aging is independent of lifestyle, diet, stress level or anything else that might distinguish some people from others ? in particular, a great deal of the rate of aging is determined by the chemistry associated with oxygen consumption.

In a nutshell, breathing is bad for you ? but it?s rather non-negotiable.

Belief in a medical limit

So, why am I exercised about this? Simply because the belief in a biological limit to longevity is very often elided into a belief in a medical limit. And unfortunately, this inference is being taken seriously by influential observers and commentators, with all that that entails for public policy going forward.

I spend a painful amount of my time disentangling innumerable misconceptions about aging harbored by various groups, but this particular one ranks very high on my list of bugbears, on account of its rare combination of seductiveness and idiocy.

How do we keep 50-year-old VW Beetles on the road? How did Jenner or Pasteur save so many lives, despite knowing hardly the first thing about the immune system?

Technology is about transcending what nature has created. To say that the biological limits to longevity are any kind of evidence of what we can do with medicine is a mixing of apples with oranges of the most egregious nature. And the reason it matters, of course, is that those who have not the time or intellect to see through it have the power to dissipate society?s enthusiasm for attacking aging, by reinforcing the age-old belief that it is as immutable as the heat death of the universe.

The result is a delay in the defeat of aging with medicine, the unnecessary loss of life and the unnecessary perpetuation of the untold suffering caused by aging. This cannot be allowed.

We must clarify, loud and clear, that medicine is about transcending biology.

Dr. Aubrey de Grey is a biomedical gerontologist based in Cambridge, UK, and is the Chief Science Officer of SENS Foundation, a California-based 501(c)(3) charity dedicated to combating the aging process. He is also Editor-in-Chief of Rejuvenation Research, the world?s highest-impact peer-reviewed journal focused on intervention in aging.

References:

Aubrey D.N.J. de Grey. Biological Versus Medical Limits on Aging: A Distinction We Must Not Elide. Rejuvenation Research. June 2012, 15(3): 255-256. doi:10.1089/rej.2012.1354

Young Stem Cell Injections Makes Rapidly Aging Mice Live 2 to 3 Times Longer

ScienceDaily (Jan. 3, 2012) – Mice bred to age quickly seemed to have found the fountain of youth after scientists injected them with stem cells from the muscle of young, healthy animals. Instead of becoming infirm and dying early like the untreated mice, those that got the stem cells/progenitor cells showed better health and lived 2 to 3 times longer than expected, according to the study published in the January 3, 2012 edition of Nature Communications. The study was conducted by scientists at the University of Pittsburgh School of Medicine.

More detailed information about the study results can be found on ScienceDaily.com at https://www.sciencedaily.com/releases/2012/01/120103135131.htm

The Tithonus Error

The Tithonus Error is the belief that extending life means making people older for longer. Most people have an entirely justified horror of the later stages of degenerative aging, and so the idea of more of that just isn’t on the table. The rejection of more life under those terms is instinctive and visceral.

The goal of longevity science, is to enable people to be younger for longer, not older for longer. The medical control of aging and the defeat of all disease is an opportunity to be seized rather than a certainty already in the bag for those people in middle age today. Let’s stop confusing people with a term “life extension” and replace it with “youth extension” or “health extension” (with the former being far more descriptive, inspiring and marketable). People will be less likely to commit Tithonus Error if they are presented with terms that actually correctly label their intended meaning. I don’t think there would be many people who would reject “youth extension”.

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Bioelectric Signals Utilized to Trigger Formation of New Organs

ScienceDaily (December 7, 2011) ? Using genetic manipulation of membrane voltage in Xenopus (frog) embryos, biologists at Tufts University’s School of Arts and Sciences were able to cause tadpoles to grow eyes outside of the head area. The researchers achieved most surprising results when they manipulated membrane voltage of cells in the tadpole’s back and tail, well outside of where the eyes could normally form. “The hypothesis is that for every structure in the body there is a specific membrane voltage range that drives organogenesis,” said Pai. “These were cells in regions that were never thought to be able to form eyes. This suggests that cells from anywhere in the body can be driven to form an eye.”

These findings break new ground in the field of biomedicine because they identify an entirely new control mechanism that can be capitalized upon to induce the formation of complex organs for transplantation or regenerative medicine applications, according to Michael Levin, Ph.D., professor of biology and director of the Center for Regenerative and Developmental Biology at Tufts University’s School of Arts and Sciences.

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This study is interesting because it could lead to the ability to regrow lost limbs or damaged organs. The problem is it does not get around Hayflick’s limit / telomere loss so would likely not be entirely effective in adults, especially if they are older. So a large supply of young adult stem cells is needed.

Scientists Regenerate Muscle Tissue in Mice

ScienceDaily (Nov. 29, 2011) ? A team of scientists from Worcester Polytechnic Institute (WPI) and CellThera, a private company located in WPI’s Life Sciences and Bioengineering Center, have regenerated functional muscle tissue in mice, opening the door for a new clinical therapy to treat people who suffer major muscle trauma.

The team used a novel protocol to coax mature human muscle cells into a stem cell-like state and grew those reprogrammed cells on biopolymer microthreads. The threads were placed in a wound created by surgically removing a large section of leg muscle from a mouse. Over time, the threads and cells restored near-normal function to the muscle, as reported in the paper “Restoration of Skeletal Muscle Defects with Adult Human Cells Delivered on Fibrin Microthreads,” published in the current issue of the journal Tissue Engineering Part A. Surprisingly, the microthreads, which were used simply as a scaffold to support the reprogrammed human cells, actually seemed to accelerate the regeneration process by recruiting progenitor mouse muscle cells, suggesting that they alone could become a therapeutic tool for treating major muscle trauma.

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Scientists Turn On Fountain of Youth in Yeast

ScienceDaily (Nov. 23, 2011) – Scientists have successfully manipulated the life span of common, single-celled yeast organisms by figuring out how to remove and restore protein functions related to yeast aging.

A chemical variation of a “fuel-gauge” enzyme that senses energy in yeast acts like a life span clock: It is present in young organisms and progressively diminished as yeast cells age.

In a report in the September 16 edition of Cell, the scientists describe their identification of a new level of regulation of this age-related protein variant, showing that when they remove it, the organism’s life span is cut short and when they restore it, life span is dramatically extended.

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