Tag Archives: telomere

Scientists in Israel found a way to reverse cellular aging with century-old therapy

Telomeres on a chromosome. Credit: Wikimedia Commons.

All living creatures eventually wither and die. There’s no escaping death and taxes, they say. But that doesn’t mean aging can’t be slowed down. In fact, researchers at Tel Aviv University in Israel took it a step further, showing in a new study that weekly hyperbaric oxygen sessions reversed a key process known to be involved in cellular aging.

The caps on your chromosomes

Every day, every hour, every second one of the most important events in life is going on in your body—cells are dividing. Right now as you’re reading this sentence, somewhere cells are dividing, but each replication comes at a cost.

Telomeres cap and protect the ends of chromosomes from degradation, making sure our DNA gets copied properly when cells divide. Due to the way DNA replication is performed in eukaryotic cells (that’s us!), these telomeres shorten with each cellular replication. At some point, the telomeres, which you can envision as the caps of a shoelace, shorten to a critical limit. Just like a shoelace without a cap will detangle and ruin the fabric, so will severely shortened telomeres trigger the malfunction of cellular division, also known as senescence. In time, the accumulation of these senescent cells is believed to be one of the primary causes of aging.

Studies have linked shortened telomeres not only to aging but also to cancer. As such, the processes that regulate telomeres have been targeted by all sorts of experimental therapies meant to slow down aging. Of particular interest is an enzyme called telomerase, which seems to have the ability to regenerate lost sections of the telomere — at least it does so in tissues with a high turnover of new cells, such as the lining of the gut. Some groups look at telomerase gene therapy as being primarily a form of regenerative medicine. However, these therapies haven’t been validated due to the small number of participants so far.

In Israel, researchers led by Shair Efrati, a physician from the Faculty of Medicine and Sagol School of Neuroscience at Tel Aviv University, have taken a different route towards improving telomere health. Their therapy involves breathing pure oxygen in a pressurized chamber with pressure levels 1.5 to 3 times higher than average.

The procedure, known as hyperbaric oxygen therapy (HBOT), is by no means a novelty. For over a century it has been used to treat deep-sea divers suffering from decompression sickness or people who’ve been poisoned with carbon monoxide. 

In a clinical trial, 35 healthy adults aged 64 and older spent 90 minutes in a hyperbaric oxygen chamber, which saturated their blood with oxygen. The participants repeated this experience once a week over the course of three months.

Blood samples were collected before the treatment and during the trial at one-month intervals, as well as two weeks after the trial was over. Strikingly, by the end of the trial, the participants’ telomeres not only showed no shortening, they actually extended by 20%. The participants also experienced a significant drop in the number of senescent T helper cells, showing that the extended telomeres may be reversing some aging, the authors reported in the journal Aging.

As a caveat, the study’s main limitation is its small sample size. Furthermore, the duration of the therapy’s effect has yet to be determined in long-term follow-ups. But all things considered, these are promising results, showing that a relatively straightforward and readily available form of therapy could one day partially reverse aging — and perhaps even extend our lifespans.

Until such therapy is confirmed, the best thing you can do to preserve your telomeres is to have a healthy diet and exercise regularly.

Childbirth can make women’s cells age faster than smoking or obesity

We all know that pregnancy and childbirth change women’s minds and bodies. A new study has found that women who give birth can age very fast, genetically speaking. But how?

Via Pixabay/marvelmozhko

Researchers collected DNA data from 1,505 different women from the US, with ages ranging from twenty to forty-four and discovered that having children significantly altered genetic markers of aging — telomeres, to be exact.

Telomeres are repetitive DNA fragments found at each end of the chromosomes, which protects them from deterioration or from fusion with neighboring chromosomes. At birth, our telomeres are long, but with each cell replication, telomeres grow shorter. Thus, telomere length decreases from birth to death and is considered a marker of aging. Shorter telomeres are correlated with outcomes like cancer, heart disease, and cognitive decline. Another cause of telomere shortening is stress,

Epidemiologist Anna Pollack from George Mason University and her team analyzed data from the National Health and Nutrition Examination Survey (NHANES) – one of the largest cross-sectional studies charting the wellness of people in the US.

Researchers analyzed data collected between the years 1999–2002, a period in which the survey included telomere measurements, and discovered something unsettling.

Once the team had adjusted for things like age, ethnicity, education, and smoking status, they discovered that women who had given birth to at least one child had telomeres that were 4.2 percent shorter on average than those of women who had not borne children.

Researchers explain that this percentage translates to around 11 years of rapid cellular aging. Compared to smoking (a cost of 4.6 years of cellular aging) and obesity (8.8 years), motherhood seems to be the champion of accelerated  DNA aging.

The study also revealed that the more children you have, the more your telomeres shrink.

“We found that women who had five or more children had even shorter telomeres compared to those who had none, and relatively shorter relative to those who had one, two, three or four, even,” Pollack told Newsweek.

The authors attributed telomere shortening to the stress accompanying having children, but they are not yet entirely sure of the cause. This study was purely observational, showing only a correlation between the two.

A 2016 study that analyzed telomere size in Mayan communities in Guatemala found that women in the community that had more surviving children had longer telomeres, suggesting that having children could actually protect women from cellular aging. Researchers believe that Mayan communities give more social support to their mothers than the US does — a great deal of stress being involved in the upbringing of the US kids.

“Anecdotally, just chatting with my friends who have children, we all do feel that having kids has aged us,” Pollack said to Newsweek. “But scientifically, this does fit with what we understand pretty well. We know that having kids is associated with a higher risk of heart disease and diabetes. And some large studies have linked telomere length to mortality risk and risks of other major diseases.”

Of course, having a child doesn’t mean you literally age 11 years. The authors write that their dataset lacked information on social factors, stress and fertility status, which may help explain these findings. With only two other previous studies regarding this matter being published, this paper‘s findings should be interpreted with caution, the authors warn.

Closeup of Dolly. Credit: Geographic.

Dolly the cloned sheep did not age prematurely, suggesting cloning hazards have been exagerated

When the world’s first cloned animal died in 2003 at the age of six, many suspected the cloning process put Dolly into an early grave. A new investigation of the cloned sheep’s bones by scientists at the Universities of Glasgow and Nottingham suggests Dolly showed no signs of abnormal aging.

Closeup of Dolly. Credit: Geographic.

Closeup of Dolly. Credit: Geographic.

In 2004, researchers found that Dolly’s telomers — stretches of DNA at the end of our chromosomes which protect our genetic data like shoelace caps, allow cells to divide and hold some secrets to how we age and get cancer — were shorter than they should have been. This has prompted suspicions that the process of cloning itself might reduce lifespan, or that the famous clone’s painful osteoarthritis was the result of some inherent flaws with cloning.

Researchers gained access to the bones of Dolly, now housed at the National Museum of Scotland, but also those of her offspring Bonnie, as well as two other cloned sheep, Megan and Morag (two sheep cloned from non-adult cells who were prototypes for Dolly). All the bones were X-rayed for signs of arthritis. Megan and Bonnie died at the ripe old ages of 13 and nine, respectively, and showed some signs of arthritis, as is normal for their age. Morag died at age four due to the same lung virus that killed Dolly but did not show any signs of arthritis. Ultimately, the researchers concluded that arthritis is no more common among clones than ordinary sheep.

“We found that the prevalence and distribution of radiographic osteoarthritis were similar to that observed in naturally conceived sheep, and our healthy aged cloned sheep,” said Sandra Corr, professor of small animal orthopaedic surgery at Glasgow University.

“As a result we conclude that the original concerns that cloning had caused early-onset osteoarthritis in Dolly were unfounded.”

A researchers prepares a cloned sheep's bones for X-ray. Credit: University of Nottingham.

Researchers prepare a cloned sheep’s bones for X-ray. Credit: University of Nottingham.

Previously, Kevin Sinclair, a developmental biologist at the University of Nottingham and co-author of the new study, studied 13 cloned sheep — including four derived from the same DNA strand as Dolly — and concluded that there didn’t seem to be any evidence that indicates cloning has any long-term health risks. Dolly’s ‘four sisters’ all lived to be at least eight years old, which is the approximate equivalent of 70 in human years, and all lived a healthy life.  “They’re old ladies,” said Kevin Sinclair, a developmental biologist and lead author of the study of the 2016 study published in Nature Communications. “They’re very healthy for their age,” he added.

The Atlantic reports that since Dolly was cloned, a whole menagerie of other animals has been cloned as well: pigs, dogs, cats, monkeys etc. Studies that followed such clones found that their telomeres were shorter, normal or even longer. It all depended on the species and cloning technique.

That being said, this doesn’t mean that cloning is 100% safe. Scientists are still learning and more research is needed to investigate the full scope of cloning. For instance, a team from South Korea has recloned the world’s first cloned dog to investigate whether or not cloning shortens or affects lifespan in any way. So far, the nine-month-old pups are healthy and seem normal.


New therapy rejuvenates old cells in the lab, which now behave like young cells

A novel method developed at the University of Exeter rejuvenates old cells cultured in the lab, causing them to behave more like young cells. It took only a couple of hours after the treatment was applied to the old cells for these to start dividing and growing larger telomers. The technique could lead to a new class of therapies meant to help people age not only longer but healthier, too.


Credit: Pixabay.

As we age, the cells in the body quietly but surely enter senescence, meaning they cease to divide. These cells are still alive, it’s just that they stop functioning properly. For instance, a class of genes called splicing factors are progressively switched off as humans age.

Splicing factors are crucial proteins that help gene perform their full range of functions. A single gene can code multiple instructions for the body, such as whether or not to grow new blood vessels, and the splicing factors are the decision makers that choose which message takes priority. Because splicing factors become increasingly inefficient with age, the body ends up losing its ability to respond properly to the many challenges in the environment.

Senescent cells can be found in copious amounts in the organs of the elderly. They’re one of the main reasons why most people over age 85 have experienced some sort of chronic illness. Switched off splicing factors make people more vulnerable to cancer stroke, and heart disease as they age.

Led by Professor Lorna Harries, researchers at the University of Exeter experimented with resveratrol analogs on old cells in the lab. These chemicals are based on a substance naturally found in red wine, dark chocolate, red grapes, and blueberries.

Credit: BMC Cell Biology.

Credit: BMC Cell Biology.

Strikingly, within hours of coming into contact with the compounds, the splicing factors in the cells switched back on. The cells showed signs of rejuvenation as they started dividing, essentially behaving like young cells. What’s more, the cells’ telomeres — the caps on the ends of the chromosomes that shorten as we age —  are now longer, as they are in young cells

“At present, the precise mechanisms behind these observations are unclear, but may involve both the restoration of a more ‘youthful’ pattern of alternative splicing, and also effects of specific splicing factors on telomere maintenance,” the authors conclud in their paper.

“This demonstrates that when you treat old cells with molecules that restore the levels of the splicing factors, the cells regain some features of youth,” Harries said.

The findings published in the journal BMC Cell Biology could potentially lead to therapies that help people age healthier, with less risk of developing chronic disease and by delaying the usual degenerating effects of old age.

“When I saw some of the cells in the culture dish rejuvenating I couldn’t believe it. These old cells were looking like young cells. It was like magic,” said co-author Eva Latorre, Research Associate at the University of Exeter. “I repeated the experiments several times and in each case the cells rejuvenated. I am very excited by the implications and potential for this research.”

Hormone therapy successfully used to stop cells from aging for the first time

Researchers have discovered they can use a male hormone to reverse cell ageing, offering hope for treating a host of conditions caused by cell degradation. Their clinical trial is the first time hormones have been proved to reverse the processes that naturally take place in human cells as they age.

Image via Flickr

US and Brazilian researchers have successfully used danazol, a synthetic male hormone, to stop cells from deteriorating with age. The hormone stimulates the production of telomerase, an enzyme which keeps cells “young” by stopping their genetic material from shrinking. It does this by keeping telomeres — the red caps you see in the picture at the end of chromosomes — intact.

“One of the processes associated with ageing is progressive shortening of telomeres, DNA-protecting structures at the ends of chromosomes, like the plastic tips on shoelaces,” explained one of the researchers, Rodrigo Calado from the University of São Paulo in Brazil.

“Each time a cell divides, its telomeres get shorter,” Calado added. “Eventually, the cell can’t replicate anymore and dies or becomes senescent [biologically aged]. However, telomerase can keep the length of telomeres intact, even after cell division.”

In the study, danazol was prescribed over two years for 27 patients suffering from aplastic anaemia (premature ageing of bone marrow stem cells), caused by telomerase gene mutations. Over this time, a person would typically lose 100 to 120 telomere base pairs per year, but someone with a telomerase deficiency could lose between 200 and 600 base pairs.

Telomerase is naturally produced in cells that constantly divide, such as blood-forming stem cells. Previous research has shown that it has a huge role to play in maintaining these cells in working order, and increasing levels of telomerase helps protect them from wearing out over time. On the other hand, a lack of this enzyme can cause organ damage and increases the risk of cancer.

Under the new treatment, the study participants’ cell telomere length not only stopped shrinking but increased by 386 base pairs on average. Hemoglobin mass rose too, which meant patients were no longer dependent on blood transfusions.

This study proves that prescription steroids can be used to increase telomerase production on demand. confirming the results previously seen in the lab in live humans. Based on these findings, new treatments for conditions such as aplastic anemia or pulmonary fibrosis (where the lungs become scarred) could be developed, the team said.

But they should be cautious in developing new treatments – sex hormones can come with notable side effects, including mood swings, tiredness, and digestive system problems.

The full paper, titled “Danazol Treatment for Telomere Diseases” have been published in the New England Journal of Medicine.


Mother who birth more children age slower, not faster

The prevailing assumption is that mothers who birth more children live short lives due to accelerated biological aging. Researchers turn this historical thinking upside down after they found having more offspring actually prolongs the life of mothers and slows down cellular degradation.


Image: Pixabay

A team at Simon Fraser University, Canada surveyed mothers from  two neighbouring indigenous rural Guatemalan communities. The researchers measured the telomere lengths pf the participants at two time points 13 years apart, through salivary specimens and buccal swabs.

Telomeres are regions of repetitive nucleotide sequences at each end of a chromatid, which protect the end of the chromosome from deterioration or from fusion with neighboring chromosomes. Think of shoelace caps. Telomeres are also a biomarker of aging, with telomeres shortening with each cellular division or, in other words, as you advance in age. As a cell’s telomeres shorten, it loses its ability to function normally. Basically, shorter telomeres make you more susceptible to a number of diseases, such as cancer or cardiovascular disease – especially in older people.

Credit: PLoS One

Credit: PLoS One

Energy invested in reproduction is not available for tissue maintenance, thus having more offspring is expected to lead to accelerated senescence. Studies made on  non-human specie seem to confirm this thinking, but the Simon Fraser investigation actually revealed the reverse may be true.

According to study lead, professor Pablo Nepomnaschy, women who gave birth to more surviving children exhibited longer telomeres. Essentially, the pace of telomere shortening was slowed down. “Estrogen functions as a potent antioxidant that protects cells against telomere shortening,” Nepomnaschy said, offering a likely explanation. The social environment might also play a role.

“The women we followed over the course of the study were from natural fertility populations where mothers who bear numerous children receive more social support from their relatives and friends,” explains Nepomnaschy. “Greater support leads to an increase in the amount of metabolic energy that can be allocated to tissue maintenance, thereby slowing down the process of aging.”

Findings were published in PLoS One.


Is this the first Proof that Meditation alters Cellular Activity?

There’s an immense body of evidence that proves that meditation has significant beneficial effects for mental health, but it’s only recently that researchers in Canada discovered a link between mindfulness meditation and altered cellular activity in cancer patients.

Biology and meditation: no longer mutually exclusive


Image: Huff Post

“We already know that psychosocial interventions like mindfulness meditation will help you feel better mentally, but now for the first time we have evidence that they can also influence key aspects of your biology,” said Linda E. Carlson, a psychosocial research and the lead investigator at the Tom Baker Cancer Centre, in a press release. She conducted the study alongside scientists from the University of Calgary.

“It was surprising that we could see any difference in telomere length at all over the three-month period studied,” said Carlson. “Further research is needed to better quantify these potential health benefits, but this is an exciting discovery that provides encouraging news.”

Telomeres are protein caps at the end of our chromosomes, sort of like the plastic tips at the end of a shoelace. These are essential for protecting our genetic data, make it possible for cells to divide, and hold some secrets to how we age and get cancer. Each time a cell divides, the telomeres get shorter. When they get too short, the cell can no longer divide; it becomes inactive or “senescent” or it dies. This shortening process is associated with aging, cancer, and a higher risk of death. So telomeres also have been compared with a bomb fuse.

ZME Science previously reported how meditation can be a powerful tool to alter our mood, providing a proxy that later indirectly tackles cognitive dysfunctions like Alzheimer’s or help relieve pain. It’s effects on biological functions have been more or less discusses, and always under debate. We’ve all heard stories – maybe you personally know someone – about people who left to a retreat, relaxed by the beach, surf and meditate, then spontaneously cured from cancer. These stories, heart warming as they may be, are very difficult to test and as such must be regarded under a skeptical lens. But now have the first evidence that suggests mediation directly alters cellular activity, meaning that it might actually be involved in regulating bodily functions and maybe even help cure diseases. Cancer too, why not?

Does meditation prevent aging?


Image: Terri Paddock

The team studied 88 breast cancer survivors who had completed their treatment at least three months were monitored, aged 55 years on average. All of the participants had to have experienced significant levels of emotional distress. The volunteers were grouped into three segments:

  • Mindfulness-Based Cancer Recovery group: participants attended eight weekly, 90-minute group sessions that provided instruction on mindfulness meditation and gentle Hatha yoga, with the goal of cultivating non-judgmental awareness of the present moment. Participants were also asked to practice meditation and yoga at home for 45 minutes daily.
  • Supportive Expressive Therapy group: participants met for 90 minutes weekly for 12 weeks and were encouraged to talk openly about their concerns and their feelings. The objectives were to build mutual support and to guide women in expressing a wide range of both difficult and positive emotions, rather than suppressing or repressing them.
  • Control group: participants attended one, six-hour stress management seminar.

Before and after the study, each participants had their blood drawn and telemores measured. Lab reports show that both groups that underwent group therapy maintained their telomere length, while for the third group this had shortened.

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Allison McPherson was first diagnosed with breast cancer in 2008. When she joined the study, she was placed in the mindfulness-based cancer recovery group. Today, she says that experience has been life-changing.

“I was skeptical at first and thought it was a bunch of hocus-pocus,” says McPherson, who underwent a full year of chemotherapy and numerous surgeries. “But I now practise mindfulness throughout the day and it’s reminded me to become less reactive and kinder toward myself and others.”

Study participant Deanne David was also placed in the mindfulness group.

“Being part of this made a huge difference to me,” she says. “I think people involved in their own cancer journey would benefit from learning more about mindfulness and connecting with others who are going through the same things.”

Next, the researchers plan on replicating the findings over a much longer period of observation than three months. While the research is definitely exciting on oh so many levels, we advise caution in receiving these findings.

oldest woman in the world

Blood from world’s oldest woman tells us why life reaches its limits

oldest woman in the world

Hendrikje van Andel-Schipper, aged 115. Photo: wikia.com

No matter how much some would like to avoid this prospect, death is inevitable for all living beings (or is it?). Yet, some people at least live longer than others. A great deal of attention has been drawn to longevity for obvious reasons, but any effort to prolong life needs to start with the very root of the problem – death. So, why do people die of old age? What are the underlying processes? Scientists in Netherlands found invaluable clues as to how our bodies steadily succumb to the inevitable, ultimate end after studying blood and tissue collected from who was once the world’s oldest woman.

World’s oldest woman

There aren’t too many people today who can boast they lived in the IXXth century, but  Hendrikje van Andel-Schipper, born in 1890, was one of them. She was the world’s oldest woman, before she unfortunately passed away in 2005, but what’s truly remarkable isn’t the number of days and nights in her life, but how she lived these days – quality vs quantity. Until her very last days, the woman had a crystal clear cognition, according to her doctors and family, and lived a vigorous and independent life. At 115 year, this comes as an astonishing fact.

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Sane as she was at her old age and aware of her privileged status, van Andel-Schipper chose to give her body to science, allowing for any necessary measures to study it that might help scientists understand how she reached her centenarian years. The findings suggest that our lives are limited by  the capacity for stem cells to keep replenishing tissues day in day out. As these stem cell exhaust their ability to replenish cells, we age and eventually die as this replenishing rate reaches its limit.

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For instance, Dutch researchers found after analyzing van Andel-Schipper’s blood that two-thirds of the white blood cells originated from just two stem cells. When a cell replicates, it has a pattern of mutation which also applies to white blood cells. The pattern was so similar in all cells that the researchers could conclude that they all came from one of two closely related “mother” stem cells.

“It’s estimated that we’re born with around 20,000 blood stem cells, and at any one time, around 1000 are simultaneously active to replenish blood,” says Henne Holstege of the VU University Medical Center in Amsterdam, the Netherlands, who headed the research team.

Considering all these white blood cells came from just two stem cells, it’s safe to assume that most of the stem cells she started out with in life faded away, withered and died. Also, besides stem cell count, telomere length is also of key importance.

Life’s too short

Telomeres have been compared with the plastic tips on shoelaces, because they keep chromosome ends from fraying and sticking to each other, which would destroy or scramble an organism’s genetic information. Yet, each time a cell divides, the telomeres get shorter. When they get too short, the cell can no longer divide; it becomes inactive or “senescent” or it dies. This shortening process is associated with aging, cancer, and a higher risk of death. So telomeres also have been compared with a bomb fuse.

In Andel-Schipper’s case, her white blood cells had drastically worn out telomeres – 17 times shorter than those on brain cells, which hardly replicate at all throughout.

Other important insights came as researchers studied telomeres and stem cells. Invariably, the researchers had to look at cell mutations and this is the first time something like has been performed on a person this old. One reason she grew so old and healthy at the same time, the researchers found, was because of the absence of dangerous mutations. Apparently, van Andel-Schipper had a superior system for repairing or aborting cells with dangerous mutations, and this did wonders for her life.

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So, what can we learn from all of this? Well, first of all the study’s results imply that it may be feasible to inject patients with stem cells collected earlier life, when these are in abundant supply. These stem cells would be substantially free of mutations and have full-length telomeres. “If I took a sample now and gave it back to myself when I’m older, I would have long telomeres again – although it might only be possible with blood, not other tissues,” she says.

In other words, you’d still look just as old, but feel younger and avoid many complications. Still and idea, but my thought is that some researchers will put this into application soon enough. ZME Science is sure to follow any developments.

Findings were reported in the journal Genome Research.


NASA to conduct unprecedented twin experiment: one twin will spend a year circling the Earth, while the other stays grounded

It’s something that puzzled me for years now: consider a pair of identical twins; say, one gets a job as an astronaut and rockets into space. The other is also an astronaut, but he decides to skip this one and stay home. After a while, they reunite, but are they still identical? That’s exactly what NASA wants to find out!

In March of 2015, NASA astronaut Scott Kelly will join cosmonaut Mikhail Kornienko on a one-year mission to the International Space Station. Their lengthy mission is part of a study which will document the effects of long-term space flight on the human body. But here’s the cool part: Scott Kelly also has a twin brother, Mark Kelly – who is also an astronaut, albeit retired. We wrote about his retirement here. While Scott, the test subject, spends one year circling Earth onboard the ISS, his brother Mark will remain home as a control.

“We will be taking samples and making measurements of the twins before, during, and after the one-year mission,” says Craig Kundrot of NASA’s Human Research Program at the Johnson Space Center. “For the first time, we’ll be able two individuals who are genetically identical.”

So what will they be studying? The ISS doesn’t go at high enough speed for an age difference to be noticeable (according to Einstein’s theory, if you travel at fast enough speeds, comparable to that of speed of light, time will slow down for you – so if this were to happen, one twin would be younger than the other). The main focus will be the subjects’ health.

“We already know that the human immune system changes in space. It’s not as strong as it is on the ground,” explains Kundrot. “In one of the experiments, Mark and Scott will be given identical flu vaccines, and we will study how their immune systems react.”

Another experiment will look at telomeres—little molecular “caps” on the ends of human DNA. Telomeres have been linked to aging, and in space, telomere loss could be accelerated by the action of cosmic rays. Researchers will study if space travel accelerates aging. Meanwhile in the gut, says Kundrot:

“There is a whole microbiome essential to human digestion. One of the experiments will study what space travel does to [inner bacteria] which, by the way, outnumber human cells by 10-to-1.”

Another study will focus on how vision changes in outer space, and on “space fog”—a lack of alertness and slowing of mental gears reported by some astronauts in orbit. But these aren’t separate studies – it’s just a big one with many aspects.

“These will not be 10 individual studies,” says Kundrot. “The real power comes in combining them to form an integrated picture of all levels from biomolecular to psychological. We’ll be studying the entire astronaut.”




Biomarker explains why some people catch colds more often than others

Researchers from the Carnegie Mellon University have identified a biological marker in the immune system that (starting from about age 22), predicts the probability of getting a common cold.

telomereThey found that telomeres play a big part in this likelihood. Telomeres are regions of repetitive nucleotide sequences at each end of a chromatid, which protect the end of the chromosome from deterioration or from fusion with neighboring chromosomes. Telomeres are alsoa biomarker of aging, with telomeres shortening as you advance in age. As a cell’s telomeres shorten, it loses its ability to function normally. Basically, shorter telomeres make you more susceptible to a number of diseases, such as cancer or cardiovascular disease – especially in older people. However, as it turns out, it plays a big role in younger adults, and has a tight connection with the common cold as well.

“Our work suggests the possibility that telomere length is a relatively consistent marker across the life span and that it can start predicting disease susceptibility in young adulthood,” said Sheldon Cohen who conducted the study, the Robert E. Doherty Professor of Psychology in CMU’s Dietrich College of Humanities and Social Sciences. “We knew that people in their late 50s and older with shorter telomeres are at a greater risk for illness and mortality. We also knew that factors other than aging, such as chronic stress and poor health behaviors, are associated with shorter telomeres in older people. Consequently, we expected that younger people would vary in their telomere length as well and wanted to see what this would mean for their health.”

He and his team measured the telomere length of white blood cells from 152 healthy volunteers aged 18-55 – inviduals who had been previously exposed to a rhinovirus, which causes a common cold, and quarantined for five days to see if they developed the cold.

The results clearly showed that that particpiants with shorter telomeres were much more likely to become infected with the virus. There was no connection to telomere length and this occurence in people 21 or younger, but after 22 years, telomere length started to predict whether individuals would develop an infection. As participant age increased, telomere length became an even stronger predictor; one telomere especially, of a specific white blood cell (a CD8CD28- T-cytolytic cell) was a superior predictor of infection and cold symptoms than other white blood cell types.

sheldon cohen“These cells are important in eliminating infected cells and those with shorter telomeres in the CD8CD28- cell population may be at greater risk for infection because they have fewer functional cells available to respond to the [cold] virus,” Cohen said. “The superior ability of CD8CD28- T-cytolytic cells to predict infection gives us an idea of which cells to focus on in future work on how telomere length influences the immune system’s response to infection and other immune-related challenges.”

Cohen then added:

“The increased importance of telomere length with age is likely because the younger participants had fewer very short telomeres, or that their young immune systems were able to compensate for the loss of effective cells.”

It has to be emphasized however that these are just the preliminary results, and much more research has to be conducted to clarify the implications of such an association.

The research was published in the Journal of the American Medical Association (JAMA)


Genetics might predict how long you’ll live. Trauma might shorten life span

Researchers at Duke University studied the telomeres – the tip of chromosomes that protect them  – in a group of children and found that those who had experienced trauma had their telomeres shorter than those that hadn’t. These chromosome tips, which can be viewed akin to shoelace tips, have been linked by scientists with aging and have been the subject of research for many scientists studying longevity.

TelomeresDo you remember those stupid internet quizzes where you would input your date of birth and some random facts about you , and then a tombstone with your name and expected decease date popped out? We’ve all had our laughs with it, and even shrieked at the sight of some friends which took them too serious, but could science predict how long an individual is supposed to live? A lot of factors are at play, of course. An instance of myself that smokes and doesn’t exercise will most likely have a shorter life span than an instance that eats healthy, exercises and doesn’t come in contact with stress. But is there a sort of default life span hard coded in our very genes?

This hidden secret might lie in telomeres, located the ends of chromosomes which make up our genes. Scientists have found for a while that there’s a link between aging and telomeres, which become shorter and shorter with each cell division. Some people shorten their telemores more than others, but an undisputed fact is that these go only way with age – down.

Scientists at Duke University may have come across a new fact that’s startling and surprising at the same time, namely that trauma might accelerate telomere shortening. For their research, the scientists sampled genes from 5-year olds and then again when they turned ten. Some of this children, unfortunately, were subjected to physical abuse or bullying, or had witnessed adults engage in domestic violence.

“We found that children who experience multiple forms of violence had the fastest erosion of their telomeres, compared with children who experienced just one type of violence or did not experience violence at all,” says Idan Shalev, the study’s lead author.

Now, their study group might not be spread enough to deliberate a sound conclusion, but coupled with a separate study their findings don’t seem that far off.  A study was conducted at Brigham and Women’s Hospital in Boston looked at a huge sample of 5,243 nurses nationwide and found that those suffering from phobias had significantly shorter telomeres than those who didn’t.

“The telomeres are essential for protecting chromosome ends,” says Carol Greider, a molecular biologist at the Johns Hopkins University and a pioneer telomere researcher awarded a share of the 2009 Nobel Prize in Physiology or Medicine. “When the telomere gets to be very, very short, there are consequences,” she says, noting the increased risk of age-related ailments.

Scientists have yet to come up with a pertinent explanation of how positive or negative experiences might influence telomere length, nevertheless a beckoning question arises – does destiny shape us or do we shape destiny?


via Smithsonian



Scientists prove ‘immortal worms’ can regenerate indefinitely and stay forever young


University of Nottingham scientists spurred a slew of debate in 2008 when they claimed their object of study, the planaria or “flatworm”, might actually be immortal, possessing an indefinite ability to regenerate its cells and thus practically never grow old. In fact, an important distinction must be made, it’s not that the flatworm never grows old that’s interesting, it’s the fact that it stays forever young!

As you can imagine a discovery of such interest didn’t go unnoticed, and it wasn’t long before the essential question was put – how do you really know that they’re immortal? A simple question, with an extremely complicated answer. To answer this question, you must first define what makes an animal immortal in the first place. Simply standing by an allegedly immortal animal waiting for it to die is far from being practical at all, in scientific terms. The researchers identified a number of genetic criteria which need to be filled in order for an animal to be considered immortal. First of all, it needs to retain the ability of replacing old cells with new cells indefinitely, and this is what stem cells are for.

Most animal in the world gradually tend to lose this ability as they age, thus causing them to get older, function improperly and eventually die. The flatworm not only is able to regenerate its old, dead cells, but it can literary grow a new brain, gut or tail when severed in two. Both cut ends grow into a new individual. Over the course of their several year long research, Notthingham University scientists have cloned a few thousand individuals starting from one single flatworm that was cut in two, which were also at their own term cut in two, and so on so forth. Biologist Dr. Aziz Aboobaker, who heads the project explains:

“We’ve been studying two types of planarian worms; those that reproduce sexually, like us, and those that reproduce asexually, simply dividing in two,” said Dr. Aziz Aboobaker from the University’s School of Biology.

“Both appear to regenerate indefinitely by growing new muscles, skin, guts and even entire brains over and over again.

“Usually when stem cells divide — to heal wounds, or during reproduction or for growth — they start to show signs of aging. This means that the stem cells are no longer able to divide and so become less able to replace exhausted specialized cells in the tissues of our bodies.

“Our aging skin is perhaps the most visible example of this effect. Planarian worms and their stem cells are somehow able to avoid the aging process and to keep their cells dividing.”

The key lies in DNA

Each time a cell divides, the tip of its DNA, called the telomere, gets shorter. An enzyme called telomerase regenerates the telomores, however in most sexually reproductive organisms it is only active during the organism’s development. Once it reaches maturity, the enzyme stops functioning, and the telomeres become shorter and shorter until cell replication is made impossible, otherwise the DNA would become too severely damaged. An immortal animal is able to maintain telomere length indefinitely so that they can continue to replicate, and Dr. Aboobaker and colleagues were able to demonstrate that the flatworms actively maintain the ends of their chromosomes in adult stem cells, leading to theoretical immortality.

Doctoral student Thomas Tan performed a series of crucial experiments, as part of the project, in order to scientifically explain the worm’s fascinating, yet theoretical, immortality. A possible planarian version of the gene coding for the telomerase enzyme was identified, and had its activity turned off. Since the telomere shrank in size, it was thus confirmed to be the right gene. Armed with this new found knowledge, the scientists monitored and measured the gene and observed that asexual worms dramatically increase the activity of this gene when they regenerate, allowing stem cells to maintain their telomeres as they divide to replace missing tissues.

“It was serendipitous to be sandwiched between Professor Edward Louis’s yeast genetics lab and the Children’s Brain Tumour Research Centre, both University of Nottingham research centres with expertise in telomere biology. Aziz and Ed kept demanding clearer proof and I feel we have been able to give a very satisfying answer,” Dr. Tan stated.

From immortal worms to immortal humans

The same didn’t apply to sexual flatworms, though, which still, however, display the same apparently indefinite ability to regenerate. The researchers explain that either these flatworms will eventually shorten their telomeres, albeit very gradually, or they found a different way to maintain indefinite cell replication that doesn’t involve the telomerase  enzyme.

The researchers claim that the next natural step is to study how this might apply to more complex organisms, like humans.

“The next goals for us are to understand the mechanisms in more detail and to understand more about how you evolve an immortal animal,” said Aboobaker.

“The worms are a model system in which we can ask questions, like is it possible for a multicellular animals to be immortal and avoid the effects of aging?”

“If so, how does this animal do this in comparison to animals that don’t? Of course we hope that this impacts humans, that’s why we do it. But we aren’t planning on making any drugs or medicines… other people are, I’m sure.”

The findings were published in the journal PNAS. University of Nottingham PR