Tag Archives: longevity

These African ticks survived for 8 years without food. Females laid eggs years after the last male had died

Argas brumpti. Credit: Jonathan Cohen.

The toughest animals on Earth are often not what you expect. A prime example is the eight-legged tardigrades capable of surviving extreme heat, cold, and even the vacuum of space. But there’s another tough guy you should know about, especially since they often like to take on humans. Meet the East African tick, a blood-sucking arachnid that can go without food for at least 8 years, and with a lifespan of over 27 years. What’s more, females have been able to lay eggs even 4 years after the last male in their group had died.

The remarkable longevity and resilience of the East African (Argas brumpti) tick were just recently revealed by a rare study almost 60 years in the making, which could be a separate story in itself, illustrating the virtues of patience in science.

It all started in 1976, when Julian Shepherd, an associate professor of biological sciences at Binghamton University in New York, was given six adult females, four adult males, and three nymphs of A. brumpti collected from caves near Nairobi, Kenya. He decided to monitor them in his lab in a habitat with stable conditions, where they were fed periodically on mice, rabbits, or drawn rat blood.

For years, the captive ticks enjoyed their regular feast until one day Shepard simply stopped giving them blood when his lab ran out of rabbits and mice to feed on. Little did the biologist realize at the time that, even starving, his original group of ticks would survive until the next century.

East African ticks have soft and leathery skins, unlike the hard shell sported by the common types of ticks that you’ll find in the parks and countryside. And unlike your run-of-the-mill tick, Argas brumpti is not reported to carry any diseases, although its bites can cause substantial, painful lesions with aftereffects sometimes persisting for many months and even years, something that Shepard knows from first-hand experience.

In their natural habitat, the ticks reside in shallow caves, rocky areas, or dust-bath areas used by their favorite prey, such as small to large mammals and lizards, notably in the dust around termite mounds that large mammals rub against. This perennially dry environment with few opportunities to encounter hosts may explain A. brumpti‘s extreme longevity, even within a taxon renowned for sustained survival even without food or water.

“I am always enthralled by the adaptations of organisms to their environment—in this case, a dry environment with virtually no access to water for long periods of time and a lifestyle that must wait for very long intervals of no food between encounters with host animals,” Shepherd said in a statement.

Adaptations to its environment may explain another incredible feat. Four years after the last original tick died, the females continue to live for another four years. These hungry females were eventually fed, and much to Shepherd’s surprise, at least one of the females laid a batch of eggs. This second generation of offspring is still alive and apparently healthy to this day, being 26 years old and counting. The oldest tick from the original batch died after 27 years, during which they were deprived of food for eight years.

One explanation is that the female ticks are capable of parthenogenesis, also known as “virgin births” because embryos can grow and develop without fertilization by sperm. But Shepherd thinks this is extremely unlikely. Instead, the females are probably capable of long-term sperm storage until they have ample food, at which point the sperm moves up the reproductive tract and fertilizes eggs.

In any case, both this longevity and long-term storage are records for any species of tick — and these insights could prove useful beyond the remarkable nature of conducting a 60-year experiment. That’s something for other researchers to learn though, as the ticks have been shipped to South Africa for further study, while Shepherd is now moving onto new research on moths and the physiology of their sperm.

“Research on how organisms master such challenges can inform understanding of how other organisms, including us, might manage similar challenges,” Shepherd said.

The findings appeared in the Journal of Medical Entomology.

Naked mole-rats: the creatures that defy biology

Credit: Smithsonian’s National Zoo/flickr, CC BY-NC-ND.

Although they might not be the prettiest mammals in the world, naked mole-rats (Heterocephalus galbe) are certainly among the most amazing. This burrowing rodent lives 10 times longer than it should, is impervious to pain and largely immune to cancer — among many other mind-boggling facts about these rodents. And beneath their wrinkly pink skin, these bizarre creatures may very well hold the secret to the elixir of life.

They completely lack hair or fur

As their name suggests, naked mole-rats completely lack hair or fur on their bodies. That’s almost unheard of for a mammal. But perhaps that shouldn’t come as a surprise. After all, such a special creature deserves a unique appearance.

Naked mole rats are native to East Africa, where they live underground inside very complex networks of tunnels. Several feet below the surface, the temperature never goes up or down, which is why they don’t really need any hair. All they have are some facial whiskers and a few specialized body hairs that help the mole-rats navigate their surroundings.

They’re the only cold-blooded mammals

In the absence of any environmental pressure to regulate their body temperatures, naked mole-rats evolved to be cold-blooded — it’s the only such mammal on the planet.

Naked mole-rat colonies are akin to bees, with a single breeding queen female

The way mole-rats mate and interact socially is closer to certain insect species than with mammals. Naked mole rats live in colonies that number up to 300 sterile individuals headed by a queen, who is the sole breeding female — yes, just like bees.

This behavior is known as eusociality. But unlike bees, which relay instructions among themselves through pheromones, the naked mole-rat queen uses physical violence and aggression to keep its subjects in line, who are tasked with digging tunnels, foraging, defending tunnel entrances, and even nannying the young. If the queen dies, any other unfertile female can be crowned. The regular working mole-rat is unfertile but can turn on the reproduction function if needed. 

Their teeth have a dedicated part in the brain to manipulate objects

Like any other mole, the naked mole rat’s biggest asset is its teeth. Used for both digging and combat, the creature’s front incisors protrude outside its lips in order to bite through the soil as efficiently as possible while also avoiding a mouthful of earth during each dig. Meanwhile, the lower incisors are more dexterous, allowing the mole rate to manipulate objects. This skill is so important that they have a specialized sensory area in their brains dedicated to their teeth, just like humans have a dedicated space in the brain for processing hand movements.

Cancer resistance

The most amazing things about the naked mole-rat are not visible with the naked eye. One of their greatest gifts is a phenomenal resistance to cancer. There are very few documented cases of cancer in naked mole rats, and scientists hope to one day identify what protects them and transfer it to humans.

Some evidence suggests that the cells of mole rats have a different meshwork of substances providing structural and nutritional support, which doesn’t allow cancer cells to proliferate uncontrollably.

They’re impervious to some types of pain

Some humans can go into shock when they ingest capsaicin (the substance that makes chili peppers hot) but naked mole-rats don’t feel any pain when coming in contact with the substance. What’s more, when they encounter an acid, molecules in the creature’s pain-sensing nerves turn the acid into an anesthetic. So, rather than hurting them, a strong acid actually numbs the naked mole-rats.

Naked mole-rats still feel pain if they’re subjected to intense heat or pressure, just like us, but their abilities to neutralize certain chemicals that should normally cause pain is of great interest to scientists. For instance, there are a lot of people suffering from chronic pain related to acid build-up in their tissue due to various illnesses. A drug based on the mole-rats’ biology might do wonders.

They can survive up to five hours without oxygen

Used to living in packed close quarters with one another, and underground to boot, naked mole-rats have evolved to be highly resilient in low-oxygen conditions. Their oxygen use is so efficient that they can function for up to five hours without any oxygen whatsoever. Instead, when oxygen is low or non-existent, the mammals use fructose to power energy production in their cells.

Up to now, this metabolic pathway was only documented in plants — so finding it in the moles was a big surprise. They’re also seemingly immune to pulmonary edemas — the buildup of fluid which clogs the lungs of mammals in low-oxygen environments, such as climbers at high altitude.

This ability could someday be translated into a novel treatment for patients suffering crises of oxygen deprivation, as in heart attacks and strokes.

They live much longer than they should be able to

Naked mole-rat. Image credits: Buffenstein/Barshop Institute/UTHSCSA.

In most cases, there’s a direct link between body size and lifespan. Broadly speaking, the larger the body, the longer the lifespan, and this is especially true for mammals. Considering their body size, naked mole-rats might be expected to live 4-6 years. However, they can actually live up to 30 years in captivity.

Interestingly, the colony’s queen and king(s) (up to three males can be fertile in a colony) actually live longer than the sterile workers.

“Our results indicate that when naked mole-rats mature into breeders, it changes their aging rates, meaning that breeders are able to live longer than non-breeders. This is surprising, as evidence from other species suggest that reproduction, which ensures the survival of the species as a whole, reduces the lifespan of the individual. In naked mole-rats reproduction appears to prolong the breeders’ lifespan. This goes against the common expectation that mammals either invest resources in a long life or in reproduction,” said Dr. Martin Bens from the Leibniz Institute on Aging in Germany, who conducted research on naked mole-rat aging.

That’s not all. Rochelle Buffenstein, a comparative biologist who works for Google’s anti-aging company Calico, gathered data from over 3,000 naked mole-rat specimens from her lab and discovered that the Gompertz-Makeham law, a mathematical equation that relates aging to mortality, doesn’t apply to mole-rats.

According to this law, the risk of dying rises exponentially with age; in humans, for example, it doubles roughly every 8 years after the age of 30. This applies to most animals, especially to mammals, but apparently not to our rodent super-heroes. A naked mole-rat’s daily risk of dying is a little more than one in 10,000, even after reaching sexual maturity at 6 months, and stays the same throughout their lives, sometimes even decreasing.

“To me this is the most exciting data I’ve ever gotten,” Buffenstein said in a statement. “It goes against everything we know in terms of mammalian biology.”

What’s even more striking is that the burrowing rodents seem to age without any clear signs of degeneration and age-related health issues. For instance, the mole-rats’ blood vessels retain their elasticity, and the queens do not enter menopause and are still able to breed even at the age of thirty.

“Our research demonstrates that naked mole rats do not age in the same manner as other mammals, and in fact show little to no signs of ageing, and their risk of death does not increase even at 25 times past their time to reproductive maturity,” Buffenstein said.

“These findings reinforce our belief that naked mole rats are exceptional animals to study to further our understanding of the biological mechanisms of longevity.”

These are some of the most amazing facts about naked mole-rats. Many might laugh out loud at their comical appearance, but if there’s anything that we’ve learned today is that these rodents have incredible powers that might one day save many human lives.

Humans live much longer than chimps due to a slower epigenetic ‘clock’

Breakthrough advances in medicine and better nutrition have dramatically improved the longevity of the average human over the past two centuries. But that’s not to say that some couldn’t go on to live a long life even before the advent of modern medicine. As long as they were spared by disease, wars, and other risks that can bring an untimely death, humans could live to see their 70s, 80s, and even reach 100 years old as far back as ancient Rome.

The longevity of humans is somewhat exceptional among primates. Chimpanzees, our closest living relatives, rarely make it past age 50, despite them sharing over 99% of our DNA. In a new study, researchers think they’ve found our secret: chemical changes along our genome that occurred around 7-8 million years ago when our ancestors branched away from the lineage of chimps.

Slower ticker

There are tens of thousands of genes in the human genome, but that doesn’t mean all of them are active. For instance, through the methylation of DNA across certain sites of the genetic sequence, genes are locked in the “off” position. These modifications, known as epigenetic changes (‘epi’ means ‘above’ in Greek), do not alter the DNA sequence itself but, rather, simply regulate the activity of genes.

DNA methylation involves attaching small molecules called methyl groups, each consisting of one carbon atom and three hydrogen atoms, to segments of DNA. When DNA gains or loses a methyl tag, such events mark time. In fact, the changes are so consistent that methylation can be used as an “aging clock”. Previously, scientists were able to estimate a person’s chronological age based on their gene activity within less than four years.

In a new study, researchers at Duke University and George Washington University have analyzed age-related epigenetic changes in chimpanzees. They analyzed over 850,000 methylation sites in blood from 83 chimpanzees aged 1 to 59.

Just like in humans, aging also leaves its epigenetic signature on the genomes of chimps, the authors of the study found. More than 65,000 DNA sites changed in a clock-like fashion across the primates’ lifespan, some gaining methylation and others losing it.

The DNA methylation pattern was so reliable that the researchers could tell a chimp’s age from their genomes with an error within 2.5 years — much more accurate than other methods, such as estimating an animal’s age by measuring the amount of wear on their molars.

When compared to the epigenetic aging clock of humans, the researchers found that a chimp’s clock ticked faster. The authors aren’t sure that these changes actively contribute to aging or merely track the aging process. However, they hope they might eventually learn more about how gene regulation could be involved in physical and cognitive decline that often accompanies aging.

The findings appeared in the Philosophical Transactions of the Royal Society B.

Credit: Pixabay.

Human lifespan is increasing with every generation, new study finds

Credit: Pixabay.

Credit: Pixabay.

People who survive to age 65 living in a developed country can hope to live longer than their parents, according to a new study performed by researchers at Stanford University. These findings seem to push the envelope of human longevity, whose limits are yet to be reached.

“The data shows that we can expect longer lives and there’s no sign of a slowdown in this trend,” Shripad Tuljapurkar, a Stanford biologist and co-author of the new study, said in a statement. “There’s not a limit to life that we can see, so what we can say for sure is that it’s not close enough that we can see the effect.”

No evidence for an impending limit to human lifespan

Tuljapurkar and colleagues analyzed birth and mortality data for individuals aged 65 or older from 1960 to 2010. During this time, the average age of death for people older than 65 increased by three years every 25-year period the equivalent of a generation. This means that people can expect to live six years longer than their grandparents, on average.

This trend seems to have stood the test of time for the entire 50-year period and in all 20 countries where this sort of data was analyzed. Although there were some minor fluctuations due to medical breakthroughs, the rate of lifespan increase was steady for any given decade.

What set this study apart from other longevity research is the fact that the focus was on people over age 65, rather than targeting extreme cases like people who live a long time (i.e. over 100 years). By eliminating outliers, the researchers were better equipped to study longevity trends in an age range with many individuals.

These findings suggest that if there’s such a thing as a limit to human lifespan, we’ve yet to reach it. Otherwise, the distribution of ages when people die should compress as they approach this limit — but this isn’t the case, as the authors reported in the Proceedings of the National Academy of Sciences.

Credit: PNAS.

What was truly surprising was that the shape of the distribution of average age of death did not change. Researchers thought that certain lifestyle factors such as wealth should increase the likelihood of a person living longer. But if that would have been the case, the distribution of data should have widened as the wealthy live past the average age of death. The shape of the data, however, remained consistent over the 50-year period.

In today’s world, it seems, being rich doesn’t help you that much to live longer — at least, not if you’re over 65. By this age, the average person has already overcome the main factors that could shorten life, including violence and early disease.

“But as someone who would like to be a one-percenter but is not, I’m certainly very happy to know that my odds of getting to live longer are just as good as the millionaire down the street,” said Tuljapurkar.


5 Technologies Scientists Are Currently Pursuing to Improve Healthspan


Credit: Pixabay.

During the 20th-century, lifespan in the United States increased by more than 30 years, of which 25 years can be attributed to advances in public health. But while people nowadays are living longer than they ever have in the history of modern civilization, that doesn’t mean that these extra decades are spent in good health.

People have always been looking for a fabled “Fountain of Youth” in some form or the other. No one likes the idea of growing old, which is why It’s no wonder that the global anti-aging market was worth $250 billion in 2016 and is estimated to reach $331.41 billion by 2021. Products in this niche include cosmetic treatments, hormone replacement therapies, implants, prosthetic devices and stem cell treatments. However, the anti-aging industry is rife with advertisements of questionable claims. Many of these treatments are unregulated, clinically unproven, and even potentially harmful, which is ironic seeing how something which was supposed to slow aging may actually accelerate it by making people ill. To date, there is no medicine proven by a clinical trial that can slow down biological aging — but there are some signs that it may be possible.

Recent developments in genetic and cellular research suggest that we may want to focus on how well we live as opposed to how long we live. It’s all about healthspan, not lifespan. Here are some of the most interesting research that scientists are currently pursuing.

Transfusion of young blood

It sounds like the plot of a bad vampire movie but some scientists are truly exploring the rejuvenating effects of transfusing blood from younger individuals. The idea of refreshing old blood with new blood was pioneered by Clive McCay of Cornell University and dates back to the 1950s, when the researcher stitched together the circulatory systems of an old and young mouse. The technique, which is called parabiosis, caused the cartilage of the old mouse to appear much younger than expected.

It wasn’t until much later that researchers were able to find some of the mechanisms responsible for this rejuvenating action. Since McCay’s original research, studies have shown that parabiosis rejuvenates the liver, skeletal stem cells, improves cognition, and reverses heart decline in older mice. A protein called GDF11 found in blood plasma seems to be responsible for some of the rejuvenating effects, as identified by Harvard researchers in 2012. In both mice and humans, GDF11 levels fall with age. We don’t know why this happens yet but there are hints that the decline occurs due to growth control mechanisms.

These fascinating results suggest that a similar rejuvenating effect might be possible in humans, as well. In October 2014, researchers at Stanford transfused young blood to older patients with mild/moderate Alzheimer, but the results have not been published yet, as patients need to be monitored for a long period of time. Meanwhile, a startup called Ambrosia is already offering plasma infusions at $8000 for two liters, to anyone aged over 35. However, be warned that such procedures have not yet been verified by science. Actually, there are even quite a few ‘snake oil’ ploys centered around young-blood transfusion, as reported by Scientific American.

Senolytics that kill old cells

Scientists have been testing the effectiveness of a class of small molecules called senolytics, which kill senescent cells — those that have stopped dividing due to DNA mutations and other damage.

Senescent cells secrete large amounts of some proteins that are harmful to their neighbors, stimulating excessive growth and degrading normal tissue architecture. These cells have also been associated with cancer and release chemicals that cause inflammation.

Senescent cells are still alive, it’s just that they stop functioning properly.

In a study published this year, researchers at the Mayo Clinic in Rochester used a combination of dasatinib and quercetin (D+Q), which killed senescent cells and slowed the deterioration in walking speed, endurance, and grip strength in mice. Previously, when the researchers injected young (four-month-old) mice with senescent cells, the mice began to show impaired physical function, such as maximum walking speed, muscle strength, physical endurance, daily activity, food intake, and body weight.

“This is exciting research,” said Felipe Sierra, Ph.D., director of the National Institute of Aging’s Division of Aging Biology. “This study clearly demonstrates that senolytics can relieve physical dysfunction in mice. Additional research will be necessary to determine if compounds, like the one used in this study, are safe and effective in clinical trials with people.”

NAD+ boosting supplements

Scientists have become increasingly interested in the coenzyme nicotinamide adenine dinucleotide, or NAD+, which plays a very important role in the biological functions that make life possible. NAD+ is crucial to turning nutrients into energy in metabolism, as well as other processes like maintaining healthy DNA and regulating circadian rhythms. A number of studies have demonstrated that increasing NAD+ levels in mice can, for example, restore muscle function and enhance regeneration in the brain. Now scientists are looking to translate this research to humans.

A clinical trial, which involved 60- to 80-year-olds over an eight-week period, found NAD+ levels could be increased by an average of 40 percent at a standard dose of 50 mg of pterostilbene (an antioxidant found in blueberries) and 250 mg of NR, a day. This was the first trial to show it was possible to elevate NAD+ levels sustainably over a period of time.

Although you can already order an NAD+ supplement, more studies will have to be undertaken before any conclusive claims about NAD+ and its rejuvenating properties can be made.

Stem cell therapy

The number of stem cells in our body tends to decrease with age. Stem cells are a class of undifferentiated cells that are able to differentiate into specialized cell types — they’re sort of like the body’s raw materials.

Stem cells are important because they provide new cells for the body as it grows, and replace specialized cells that are damaged or lost. Doctors hope to use stem cells in a guided fashion in order to replace diseased cells and organs.

Mesenchymal stem cells (MSCs) are a particular type of adult stem cell generating a great deal of interest in the world of science. Currently, they’re being used to treat a wide range of diseases from cancer to heart disease, but new research is starting to discover their anti-aging properties as well. A 2017 clinical trial on humans, 15 frail patients with an average age of 76 received a single MSC infusion collected from bone marrow donors aged between 20 and 45 years old. After six months, all patient showed improvements in fitness and an overall improvement in their quality of life.

Researchers at the Albert Einstein College of Medicine in New York found that the hypothalamus — a small portion of the brain that plays a crucial role in many important functions, such as releasing hormones. regulating body temperature —  releases hormones that affect other organs, affecting how mice age. By injecting the hypothalamus with extra stem cells, taken from the brains of newborn mice, the researchers slowed down aging and gave mice an extra two to four months of life — that’s a 20% lifespan increase.

That being said, stem cells therapy for anti-aging or rejuvenating properties is still classed as experimental and people should shy away from “stem-cell-based” topical creams and stem-cell­-injection clinics.

The longevity gene

A study of Amish people found that a subgroup of people with a single mutation in the SERPINE1 gene lived to 85 years, on average — significantly longer than the predicted lifespan of 71 years for the general Amish population. The mutation significantly lowers the production of a protein called PAI-1, and this may explain the tendency to be in better health with advancing age.

A lower PAI-1 protein count in their body seems to make individuals more resilient in the face of disease. According to the researchers, Amish people with the SERPINE1 mutation had no signs of diabetes as opposed to 7 percent of the Amish individuals with the normal SERPINE1 gene. What’s more, those with the mutation also exhibited a better metabolism and lower-than-average levels of fasting insulin, according to the findings published in Science Advances.

Previously, Israeli researchers identified another gene mutation that extends lifespan, also by ten years, but only in men.

Since there aren’t any apparent negative effects related to PAI-I deficiency, it’s possible to use drugs to target this protein. Already, Japanese researchers at Tohoku University are conducting an early phase clinical trial with an orally active PAI-1 blocker. A Japanese company called Renascience holds the patent for the drug which is currently being licensed to Eirion Therapeutics in the United States. There, the drug is marketed as a treatment for baldness since one of the mechanisms by which PAI-1 contributes to aging is by limiting cell mobility, which can be important in hair growth.



Why Getting Married Might Just Save Your Life


Credit: Pixabay.

Most people dream about the day they’ll be married, whether it’s in the near or distant future, but if you haven’t been making it a priority, you might consider it. Research shows that being married is actually good for your health.

“There is fascinating — and compelling — research suggesting that married people enjoy better health than single people,” says Robert H. Shmerling, MD at Harvard Medical School, pointing out some of the many exciting health benefits of being married.

If you’re in a committed relationship, now more than ever, you should be thinking about choosing an incredible vintage engagement ring to seal the deal on lifelong happiness.

Here are a few of the unparalleled health benefits of saying “I do.”

Reduced Stress Levels

Stress is a chronic problem for adults; more than three quarters report feeling stressed on a regular basis, and it can often come with unpleasant side effects like high blood pressure, obesity, and diabetes. There are many treatments for chronic stress, and marriage seems to be one of them, according to studies.

“Although marriage can be pretty stressful, it should make it easier for people to handle other stressors in their lives,” said Dario Maestripieri, Professor in Comparative Human Development at the University of Chicago and lead author of a study on marriage and health. “What we found is that marriage has a dampening effect on cortisol responses to psychological stress and can therefore act as a buffer against stress.”

So, even when you’re dealing with disagreements, you still enjoy less stress when you have a partner by your side.

Safer Sexual Behavior

According to the CDC, 20 million new sexually transmitted diseases and infections occur each year. Unsafe sexual practices are usually the cause of these diseases, and it’s easily preventable.

Those in a committed marriage tend to avoid promiscuous sexual behavior that can cause problems down the road. You’re significantly less likely to contract a sexually-transmitted disease from a lifelong partner.

Lower Risk of Cardiovascular Disease

Heart disease is the number one killer of both men and women, and marriage may be the best medicine, particularly for men. A study in the Journal of Psychosomatic Medicine reveals that married men were almost half as likely as single men to die within ten years of being diagnosed with heart disease.

“There is something in a good relationship that helps people stay on track” says Kathleen King, professor emerita from the School of Nursing at the University of Rochester and lead author on the paper. “Coronary bypass surgery was once seen as a miracle cure for heart disease,” says King. “But now we know that for most patients, grafts are a temporary patch, even more susceptible to clogging and disease than native arteries. So, it’s important to look at the conditions that allow some patients to beat the odds.”

Higher Survival Rates for Health Problems

Severe health problems including stroke, cancer, heart disease, and other serious illnesses often come on suddenly. Many times, they require serious surgeries and other rigorous treatment.

For those undergoing treatment, the survival rates tend to be significantly higher. Sometimes, battling health problems is as much mental as it is physical. Studies have shown that patients who have a spouse are 14 percent more likely to survive serious illnesses than singles.

Fewer Signs of Aging

People often joke about how married men and women tend to “let themselves go” after tying the knot. However, the opposite is usually true; a happy marriage can help you look and feel much younger.

There have been strong links in scientific studies between happy marriages and fewer signs of aging. You’ll have fewer grey hairs and wrinkles and more energy and vitality for life.

Better Mental and Emotional Health

“Our nervous systems are not separate or self-contained; beginning in earliest childhood, the areas of our brain identified as the limbic system (hippocampus, amygdala, anterior thalamic nuclei, and limbic cortex) is affected by those closest to us (limbic resonance) and synchronizes with them (limbic regulation) in a way that has profound implications for personality and lifelong emotional health,” according to the book A General Theory of Love, published by a trio of well-known psychiatric professors. This book goes on to discuss the strong evidence of marriage on the psyche.

Famously, those who are married and stay that way tend to enjoy greater happiness and a reduced risk for debilitating depression and anxiety. Having a committed life partner who cares about your emotional needs is essential in beating the odds of mental illness, according to studies.

Longer Life Expectancy

When added together, these many health benefits obviously point to a longer life expectancy. As you stave off various mental and physical health problems through your happy union, you’ll prolong your life and enjoy that connection for longer.

Credit: Arne Hendriks, Flickr.

We’re still far away from finding a limit to human lifespan

Credit: Arne Hendriks, Flickr.

Pictured here is Jeanne Calment, who lived to be 122. She’s officially the oldest human being that we know of. Credit: Arne Hendriks, Flickr.

If there’s a biological limit to how long humans can live, we haven’t reached it yet. This is the conclusion of a recent study of people aged over 105, finding that their risk of death slows and even plateaus past this age. According to the study, if individuals can live past very perilous ages (their 70s, 80s, and 90s), they can hope to live well into their 110s.

The oldest human being ever hasn’t been born yet

The longest a human has ever lived — that we know of — is 122, a record set by a Frenchwoman called Jeanne Calment. She died 21 years ago, and no one has grown older since.

In 2016, a study performed by researchers at the Albert Einstein College of Medicine in the Bronx analyzed data from the Human Mortality Database, which included data such as when these individuals became deceased, from over 40 countries. The researchers found that since 1900, the survival rate of people 70 years and older had steadily increased with their year of birth. However, this didn’t occur for people aged 100 years and older, suggesting a possible limit to lifespan. Specifically, the authors argued that the biological limit of human beings is 115, simply making Calment an outlier.

This study started a lively debate among scholars, many arguing that the conclusions were based on flawed statistical methods. Although, to be fair, any study attempting to assess the limits of human longevity is challenging by virtue of the nature of its object of inquiry. First of all, there aren’t that many people who are 100 or older, which makes conclusions difficult to draw given the sample size. Secondly, people born in 1900 or around the time often can’t definitely prove their date of birth, as not all countries accurately recorded information about their citizens at the time.

“The statistics aren’t good enough to be able to say you can’t live much longer than that, based on the data we have,” said report author Siegfried Hekimi, chairman of developmental biology at McGill University in Montreal. “It’s simply not good enough to make that claim.”

Kenneth Wachter, a professor of demography and statistics at the University of California, Berkeley, and colleagues came to a totally different conclusion from the 2016 study. They tracked the death trajectories of nearly 4,000 Italian residents who reached age 105 between 2009 and 2015.  Over 87% of these people were women and during the time period, 2,880 deaths had occurred.

The researchers found that the odds of survival decline rapidly as a person enters middle and old age. For instance, Italian women who reached 90 had a 15% chance of dying within the year and could expect to live another six years, on average. If they made it 95, however, the odds of dying within the year increased to 24% and life expectancy dropped to 3.7 years.

This would logically suggest that for every aged year, the odds of dying within the year increase more and more. But that’s not what happened — once they hit 105, the chance of surviving hit a plateau of 50% each year, the researchers reported in the journal Science.

“If mortality rates kept rising at the rates they rise from age 40 to age 90, then there would be a strong barrier to progress at extreme ages—great diminishing returns to behavioral change or to new medical advances,” Wachter said. “The fact these rates ultimately level out gives hope there’s more leeway for those advances.”

“The risk of death is very high at 105 years, but next year it’s not higher,” Hekimi commented about the new study. “Every year you have the same chance of dying, and every year you can be the one who wins the coin toss.”

Wachter says that the plateau is likely due to the influence of genes but also healthy life choices. However, there is no clear-cut genetics that enable people to reach ripe old ages. For instance, genes that seem to be supporting extended lifespan on Okinawa are not the same as ones found in England.

“When you look at a group of older people who are all the same age, some are already quite frail and some are robust. There’s a big difference in the level of frailty,” Wachter said.

“People who go to college 50th reunions, you just look around you and some people are climbing mountains while some people are walking with canes. Now go 15 to 20 years later, the people who were already frail are the ones who are likely to have died,” he said.

The present study suggests that it is possible to extend the survival plateau earlier into the average human lifespan, thus making it likelier for more people to survive into their 100s. Imagine that those people who are 115 today were born in a time when they didn’t have access to modern healthcare and nutritional information. It’s extremely likely that the people who will eventually reach the peak of human lifespan haven’t’ been born yet.

“It gives us a good piece of hope, because there is now lots of opportunity to look at these bad variants as they are in populations today and to try to understand the interaction of those genetic variants with potential medicines and different health challenges,” Wachter said.

“This basic theory could help us inform medical progress and public health progress 10 to 15 years from now as genetic research continues,” he said.

Cutting calories delays ageing, new study shows

A new comprehensive study has shown that reducing caloric intake slows down metabolism. Researchers believe the findings indicate that a low-calorie diet could extend lifespan and prolong health in old age.

Via Pixabay/Divily

Previous studies on animals with short lifespans — such as worms, mice, and flies — have shown that reducing calorie intake might slow down metabolism and prolong life. However, demonstrating this effect on humans and other animals with long lifespans has proven quite difficult.

Researchers studied some of the people who participated in the multi-center trial CALERIE (Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy), sponsored by the US National Institutes of Health. Scientists observed the effects of restricting calories for 2 years on metabolism in over 200 healthy, non-fat adult participants.

“The CALERIE trial has been important in addressing the question of whether the pace of aging can be altered in humans,” says Rozalyn Anderson, who studies aging at the University of Wisconsin–Madison. She leads one of two large, independent studies on calorie restriction in rhesus monkeys. “This new report provides the most robust evidence to date that everything we have learnt in other animals can be applied to ourselves.”

The latest paper, which was published on March 22nd in the journal Cell Metabolism, monitored 53 CALERIE participants recruited at the Pennington Biomedical Research Center in Baton Rouge, Louisiana. Researchers were able to track how the participants used energy with unprecedented precision thanks to state-of-the-art metabolic chambers —  small, hotel-like sealed rooms that measure oxygen and carbon dioxide concentrations every 60 seconds. Researchers calculated the ratio between the two gases and then analyzed occupants’ urinary nitrogen, indicating whether the occupant is burning fat, carbohydrate or protein.

Participants, with ages between 21 and 50, were randomly separated into two groups: the 34 people in the experimental group reduced their calorie consumption by an average of 15%, while the 19 people in the control group ate as usual. Next, researchers tested the participants annually to record overall metabolism and biological markers of aging, including damage associated with oxygen free radicals released during metabolism. At the end of the trial, participants spent 24 hours in the metabolic chamber.

Researchers discovered that the people who had dieted used energy much more efficiently while sleeping than the control group. Their base metabolism had essentially slowed down. In consequence, people in the experimental group lost an average of 9 kilos individually. All other measurements showed a reduced metabolic rate and fewer signs of aging.

“The Rolls-Royce of a human longevity study would carry on for many decades to see if people do actually live longer,” says Pennington physiologist Leanne Redman, the lead author of the latest study.

Low-calorie diets have previously been shown to extend life in different species, such as the short lifespan worm Caenorhabditis elegans, and in the fly Drosophila melanogaster. Following studies also revealed that mice with restricted diets can live up to 65% longer than mice allowed to eat freely. In addition, studies on monkeys suggest longer survival and reduced signs of aging.

Redman wants to repeat the study combining moderate calorie restriction with a diet rich in antioxidants to monitor oxidative stress, or with a drug such as resveratrol, which mimics key aspects of calorie restriction.

If researchers demonstrate the causality between caloric reduction and longer lives in humans, could you stick to such a diet?

Drinking two glasses of wine a day, keeps premature death away

A long-term research, known as The 90+ Study, revealed some interesting statistics about longevity. Scientists were surprised to learn that the risk of premature death is lowered by 18% if you consume alcohol in low quantities (around 2 glasses of beer or wine per day). Meanwhile, exercising 15 to 45 minutes daily reduces the risk of early death by 11%.

Via Pixabay/Goyaines

This data seems a bit odd when looking at other studies which portray alcohol as carcinogenic.

“I have no explanation for it, but I do firmly believe that modest drinking improves longevity,” said neurologist Claudia Kawas from the University of California, that initiated the study in 2003.

Since then, Kawas has been studying a group of over 1,600 people over the age of 90. Scientists paid visits to the participants biannually. They performed various tests, such as cognitive, neuropsychological and physical ones. Researchers also collected data on the participant’s medical history, hobbies, diet, and daily activities.

Another curious discovery was that people who were overweight in their 70s lived longer than normal or underweight people. The team found that 90-year-olds who were a bit overweight, but not obese, had their chances of premature death lowered by 3 percent.

“It’s not bad to be skinny when you’re young but it’s very bad to be skinny when you’re old,” stated Kawas.

Other findings on longevity showed that people who spent about two hours daily on a hobby lowered their risk of premature death by 21 percent. Meanwhile, subjects who drank two cups of coffee each day saw the risk fall by 10 percent.

“These people are inspiring — they drink wine, drink coffee, gain weight, but they exercise and use their brains. Maybe that can tell us something,” Kawas added.

Other major findings discovered by the team are:

  • Over 40% of people aged 90 and older suffer from dementia while almost 80% are disabled. Both are more common in women than men.
  • About half of people with dementia over age 90 do not have sufficient neuropathology in their brain to explain their cognitive loss.
  • People aged 90 and older with an APOE2 gene are less likely to have clinical Alzheimer’s dementia but are much more likely to have Alzheimer’s neuropathology in their brains.

So, who is to tell that we can’t live our lives in a fun way? Perhaps the people who lived to be 90 were more relaxed than the ones who didn’t. Maybe this counts more than imposing restrictions upon ourselves. Maybe we should pay more attention to our desires, engaging more in our hobbies, and relax every night with a glass or two of wine. It doesn’t sound that bad, does it? I, for one, think I will subscribe to these simple ‘rules’ of living. Will you?

Credit: Pixabay.

Gene mutation very common in a Amish community might extend lifespan by 10 years

A tight-knit Amish community in Indiana might hold the secret to longlasting life in their genes. Researchers found that members carrying a key gene mutation lived ten years longer on average than those who lacked the mutation. Some companies are already working on longevity drugs based on the study’s findings.

Credit: Pixabay.

Credit: Pixabay.

Modern health-care and nutrition have vastly improved the human lifespan. Figures published by the Centers for Disease Control and Prevention (CDC) show that babies born in the United States in 1900 had a life expectancy of 50 years. In comparison, Americans born in 2012 have a life expectancy of 78.8 years. In terms of gender, women generally live longer than men, with one in every ten girls born in 2012 expected to live for more than 100 years. All of this is absolutely remarkable progress, but aren’t we nearing a brick wall?

Many scientists researching longevity are now investigating genes with hope that they might find new ways to increase life expectancy at a similar pace to that of the last century. It’s no secret that some people age ‘better’ than others, being less exposed to health risks than their peers despite living in the same environment, eating the same food and so on. It logically follows that the reason must be related to their genes.

One of the main reasons why we biologically age has to do with telomeres — the end of DNA strands which are meant to protect chromosomes from deterioration, functioning like shoelace caps. Every time DNA replicates, the telomeres get a bit shorter leading to what scientists call senescence. As the telomeres get shorter and shorter, cells ramp up production of certain proteins. By measuring the concentration of these proteins, it’s fairly easy to assess the aging process in the body.

One such protein is called plasminogen activator inhibitor-1 or PAI-1 for short. Researchers at Northwestern University’s School of Medicine found that this protein could play a major role in human longevity after they sequenced the genomes of 177 members of the Berne Amish community in Indiana.

Douglas Vaughan, a cardiologist, along with colleagues, determined that 43 of these men and women had a nonfunctional copy of SERPINE1, which is the gene that encodes for PAI-1. The average lifespan of the Berne community is about 75 years — slightly lower than the national average — but those with the SERPINE1 mutation live to a median age of 85.

“This-loss-of-function mutation in SERPINE1 effectively lowers the production of the protein PAI-1 by 50 percent in the individuals that carry one copy of the mutation,” says Vaughan. “This likely has multifactorial effects that reduce the internal signals and factors that drive senescence in cells and tissues, which in turn slows the aging process.”

A lower PAI-1 protein count in their body seems to make individuals more resilient in the face of disease. According to Vaughan and colleagues, Amish with the SERPINE1 mutation had no signs of diabetes as opposed to 7 percent of the Amish individuals with the normal SERPINE1 gene. What’s more, those with the mutation also exhibited a better metabolism and lower-than-average levels of fasting insulin, according to the findings published in Science Advances.

Previously, Israeli researchers identified another gene mutation that extends lifespan, also by ten years, but only in men.

“The findings astonished us because of the consistency of the anti-aging benefits across multiple body systems,” Vaughan said in a statement. “That played out in them having a longer lifespan. Not only do they live longer, they live healthier. It’s a desirable form of longevity. It’s their ‘health span.’”

Since Amish communities are so isolated, it’s fairly easy for unique genes and mutation to become widespread among the population within just a few generations. Amazingly, almost every living Amish can trace their roots to one of 200 German-Swiss immigrants that came to American during the 18th and 19th centuries. The big downside is that the little genetic variance makes the Amish population particularly susceptible to high rates of genetic disorders like dwarfism or development delays. In the general population, however, the SERPINE1 mutation is very rare.

The good news is that some scientists think that you don’t have to be born with such a mutation to reap the longevity benefits. Since there aren’t any apparent negative effects related to PAI-I deficiency, it’s possible to use drugs to target this protein. Already, Japanese researchers Tohoku University are conducting an early phase clinical trial with an orally active PAI-1 blocker. A Japanese company called Renascience holds the patent for the drug which is currently being licensed to Eirion Therapeutics in the United States. There, the drug is marketed as a treatment for baldness since one of the mechanisms by which PAI-1 contributes to aging is by limiting cell mobility, which can be important in hair growth. Besides preventing baldness, the drug might also prolong our lifespan — but that’s something which we won’t discover until the last clinical trials are reported.

Jeanne Louise Calment on her 121st birthday, shortly before she died. Calment is still the oldest person that we know of that has ever lived. Credit: Wikimedia Commons

Human lifespan might have hit the ceiling at 115 years of age — can we live longer than this?

Jeanne Louise Calment on her 121st birthday, shortly before she died. Calment is still the oldest person that we know of that has ever lived. Credit: Wikimedia Commons

Jeanne Louise Calment on her 121st birthday, shortly before she died. Calment is still the oldest person that we know of that has ever lived. Credit: Wikimedia Commons

When Jeanne Louise Calment died in 1997 she did so at the venerable age of 122 years. Her family grieved but the rest of the world looked to the future with hopeful eyes since Calment, the oldest person at the time ever at the time of her death, was a symbol for rising human longevity. People started to say at the time “Well if a person ca live to 122 then a couple decades from now we can expect people to live 130 maybe 150 years.” But almost 20 years later, Calment is still the oldest human. The second oldest people died at 119 and 117, respectively, and right now the oldest living person is 116. Despite considerable advances in medicine and living standards, we seem to have reached a longevity ceiling and a new study has the data to back this claim.

Don’t make plans past 115

Researchers at the Albert Einstein College of Medicine, New York, systematically scoured all the demographic data they could find from the last century. Their research suggests there’s a biological limit to how long people can live and estimates suggests this ceiling sits at around 115 years of age. Calment or Emma Morano, the current oldest person in the world, are exceptions to the rule.

The team specifically looked at demographics from the United States, France, Japan and the United Kingdom since these four countries have the most supercentenarians — people over 100 years of age.

According to the researchers, in the 1970s the maximum age was 110. Then in the 1990s it was 115 but 20 years later there wasn’t any meaningful improvement in longevity. In other words, we seem to have reached a plateau.

[ALSO READ] How immortal worms regenerate indefinitely

From a statistical point of view, the odds of at least one person in the world living past his 125th birthday is less than 1 in 10,000, as reported in the journal Nature. That’s pretty slim and explains why there are some deviations from the rule, like Calment.

The 115 ceiling is probably rooted in our biology and can be explained from an evolutionary standpoint. The primary reason why we age and what ultimately causes death from natural causes is DNA damage. Every time a cell divides, telomeres — structures that keep chromosome ends from fraying and sticking to each other sort of like shoelace tips — 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.

That’s why around age 80 or 90, many develop diseases like cancer or Alzheimer’s. But there’s a weird quirk. If you make it past 90, the odds of developing such diseases actually goes down, not up. We don’t know why for sure yet but some speculate that rare genetic makeup helps the venerable old advance in age towards supercentenarian status.

Then there’s the problem that evolution favors the young, who can reproduce and carry their genes, not the old. As such, genetic changes that threaten our existence are rarer at a young age and more common at old age, simply because the old are more expendable. It sounds ruthless but that’s how life works. The old must make room for new blood.

Things like antibiotics, vaccines, cancer therapies have not only raised the survival rate of the young but extended our lifespan as well. The average lifespan has increased by twenty years since the dawn of the last century, and in some parts of the world by thirty. But there seems to be a ceiling. Then again, the world’s oldest people today were born around 1900 — a time when most of the medical procedures we take for granted today didn’t even exist. We also have, arguably speaking, better diets than 100 years ago. So some speculate that those that will reach 150 years of age were born yesterday, in a manner of speaking.

So far, the data says otherwise, and we might have to wait a long time to know for sure. If there’s truly a biological limit to how long we can live, then our only chance to augment longevity is through some sort of gene therapy. The future’s double centenarians might be designer babies, for instance.


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.

Strict diet doubles lifespan of worms

Taking food away from C. elegans in larval stages suspends their development; while they still wiggle around and look for food, they are in a state of arrested development. However, when food becomes plentiful again, they start to develop normally – but live twice as long.

This shows the nematode worm C. elegans with muscle cells fluorescently labeled in green and germ cells fluorescently labeled in red. These cells and others pause at a checkpoint in development and slow their aging when worms encounter a period of starvation. Credit: David Sherwood Lab, Duke University

This remarkably simple way of achieving longevity is not entirely surprising. It has been known for quite a while that a low intake of nutrients and reduced cellular activity are generally linked with longevity – but doubling the lifespan only through a strict but temporary diet, that’s something quite surprising.

“It is possible that low-nutrient diets set off the same pathways in us to put our cells in a quiescent state,” said David R. Sherwood, an associate professor of biology at Duke University. “The trick is to find a way to pharmacologically manipulate this process so that we can get the anti-aging benefits without the pain of diet restriction.”

Sherwood and his colleagues from Duke University took a myriad of creatures and deprived them of food, in order to study the effects on longevity. They studied rats, mice, yeast, flies, spiders, fish, monkeys and worms; the effects on longevity varied between 30 percent to 200 percent, but in all cases, the lifespan was increased. Caenorhabditis elegans, a non-parasitic worm showed the most promise.

In nature, C. elegans often suffers from hunger, and its bodily development heavily depends on the available nutrients. But what researchers observed was that during the later stages of the larval development (known as L3 and L4), if they don’t have enough nutrients, they just stop developing. It’s as if they simply pause or slow down their development until they have sufficient nutrients around.

“Development isn’t a continuous nonstop process,” said Schindler, who is lead author of the study. “Organisms have to monitor their environment and decide whether or not it is amenable to their development. If it isn’t, they stop, if it is, they go. Those checkpoints seem to exist to allow the animal to make that decision. And the decision has implications, because the resources either go to development or to survival.”

Researchers starved the larvae for two weeks, and then fed them nutrients they would stumble upon in nature. What they observed was that the worms would develop normally after that – with their lifespans drastically increased.

“This study has implications not only for aging, but also for cancer,” said Sherwood. “One of the biggest mysteries in cancer is how cancer cells metastasize early and then lie dormant for years before reawakening. My guess is that the pathways in worms that are arresting these cells and waking them up again are going to be the same pathways that are in human cancer metastases.”


Journal Reference: Adam J. Schindler, L. Ryan Baugh, David R. Sherwood. Identification of Late Larval Stage Developmental Checkpoints in Caenorhabditis elegans Regulated by Insulin/IGF and Steroid Hormone Signaling Pathways. PLoS Genetics, 2014; 10 (6): e1004426 DOI: 10.1371/journal.pgen.1004426

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.

[RELATED] Better muscle mass, not BMI, prolongs life

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.

[RELATED] The secret to a long life: consciousness 

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.

[NOW READ] Sirtuin supplement prolongs life in mice

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.


mouse age reversal

Old organ regenerated to youthful state in elderly mice using gene manipulation

mouse age reversal

Photo: guardian

The popular myth of the fountain of youth tells the story of a magical spring that restores youth to anyone who drinks from it. Scientists working with longevity research have made important strides forward in recent years, however all of these efforts concentrate on prolonging life and slowing the effects old age has on the body, not reversing them. A breakthrough by researchers at University of Edinburgh may cause a paradigm shift in regenerative medicine after an old organ in elderly mice was regenerated into a youthful state, simply by manipulating a single gene.

The thymus is a specialized organ in the immune system. The functions of the thymus are the “schooling” of T-lymphocytes (T cells), which are critical cells of the adaptive immune system, and the production and secretion of thymosins, hormones which control T-lymphocyte activities and various other aspects of the immune system.

With old age, however, the thymus becomes progressively smaller making the body more vulnerable to infections and diseases. In fact, by the age of 70 the thymus is just a tenth of the size in adolescence. So, the team at the MRC Centre for Regenerative Medicine at the University of Edinburgh thought of a way to regenerate the thymus.

Rejuvenating elderly mice

Previous research showed that a gene, called Foxn1, naturally gets shut down as the thymus ages, so the Edinburgh researchers concentrated on boosting the gene back to youthful levels. A drug that targets this protein and instructs stem cell-like cells to rebuild the organ was made and given to elderly mice. The results were striking: just by manipulating this single gene, the thymus in elderly mice increased in size and made more T-cells. It almost completely regenerated.

“Our results suggest that targeting the same pathway in humans may improve thymus function and therefore boost immunity in elderly patients, or those with a suppressed immune system. However, before we test this in humans we need to carry out more work to make sure the process can be tightly controlled,” said Clare Blackburn, Professor of Tissue Stem Cell Biology, MRC Centre for Regenerative Medicine.

It’s not clear why the thymus shrinks with age, but one theory says it’s because more energy is diverted towards reproduction once entering adolescence. As such, if human trials are to begin, there needs to be a tightly controlled setting to ensure no negative side-effects are encountered. The discovery could also offer hope to patients with DiGeorge syndrome, a genetic condition that causes the thymus to not develop properly.

“One of the key goals in regenerative medicine is harnessing the body’s own repair mechanisms and manipulating these in a controlled way to treat disease. This interesting study suggests that organ regeneration in a mammal can be directed by manipulation of a single protein, which is likely to have broad implications for other areas of regenerative biology,” said Dr Rob Buckle, Head of Regenerative Medicine, Medical Research Council.

But what about other organs? The heart, lungs, liver, maybe there’s a way to regenerate these by gene manipulation as easily as it was for the thymus. The full paper can be read here.

Also worth noting is a different path that leads to the same destination – reactivating the enzyme telomerase, which repairs damaged tissue and reverses signs of aging, as shown by studies on mice at the Dana-Farber Cancer Institute, Harvard Medical School. A synergy between the two methods may propel medicine into a new age.

Representative photographs from blinded histopathological analysis of kidney, liver, and lung panels for mice on standard diet (SD) and SRT1720 supplementation (credit: Sarah J. Mitchell et al./Cell Reports)

Sirtuin supplement diet prolongs life in mice

A wonder pill that prolongs life and cuts the risks of developing deadly diseases. Scientists have been looking for such a drug for a long time. Research in this direction shows that enhancing the expression of a certain gene called SIRT1 (sirtuin 1) may fare good results in this respect. Recently, researchers at the National Institute on Aging at the National Institutes of Health  report that after feeding mice with sirtuin supplements their lives were significantly prolonged and showed better health than the control group of mice.

Sirtuin 1, or SIRT1, is known to play an important role in maintaining metabolic balance in multiple tissues, and studies in various organisms have shown that activating the protein can lead to many health benefits. Additionally, the NIANIH scientists report in the Cell Press journal that expression of SIRT1 is also associated with  the delay of age-associated diseases in several animal models.

Representative photographs from blinded histopathological analysis of kidney, liver, and lung panels for mice on standard diet (SD) and SRT1720 supplementation (credit: Sarah J. Mitchell et al./Cell Reports)

Representative photographs from blinded histopathological analysis of kidney, liver, and lung panels for mice on standard diet (SD) and SRT1720 supplementation (credit: Sarah J. Mitchell et al./Cell Reports)

Dr. Rafael de Cabo  along with colleagues fed mice beginning at 6 months of age with a diet containing  a small molecule that activates SIRT1, called SIRT1720,  for the remainder of their lives. It was found that SIRT1720 significantly extended the average lifespan of mice by 8.8%. In addition, the  100 mg/kg SRT1720 diet also reduced body weight and body fat percentage, and it improved muscle function and motor coordination throughout the animals’ lives.

Besides the beneficial metabolic effects,  SRT1720 supplementation led to decreases in total cholesterol and LDL-cholesterol levels, which might help protect against heart disease, and improvements in insulin sensitivity, which could help prevent diabetes.  The supplement was also found to be effective against tissue inflammation, yet again backing it longevity properties since low-grade chronic inflammation is thought to contribute to aging and age-related diseases.

“Here, we show for the first time that a synthetic SIRT1 activator extends lifespan and improves healthspan of mice fed a standard diet,” says Dr. de Cabo. “It illustrates that we can develop molecules that ameliorate the burden of metabolic and chronic diseases associated with aging.”

Like I said before, though, sirtuin is no new player in the longevity game. Two years ago, I wrote about the developments at the time concerning sirtuin research. No particular connection to enhanced  lifespan from SIRT1 in fruit flies or nematodes was discovered, but tests on mammals hadn’t been made yet.

What’s more interesting maybe is that researchers at Bar-Ilan University in Ramat-Gan, Israel chose to take an alternate route, yet still in the sirtuin family – SIRT6. Instead of feeding them supplements, the Israeli researchers engineered mice that overexpressed SIRT6 and found male mice median lifespan  rose by 14.5% in one line of their transgenic mice and 9.9% in another. When maximum life span is concerned, the metric rose by 15.8% in the first line of mice, and 13.1% in the second. Curiously enough, there weren’t any signaled differences in lifespan for female mice.


Women may live longer than men due to stronger immune system


The life expectancy gap between men and women is a rather attested fact, and while in the past a laborious, physically tense lifestyle for men was used to serve as an explanation, in our day and age of gender equality this doesn’t quite cut it anymore. Researchers in Japan might have stumbled across a clue that explains why women life longer then men, after they found that at old age women’s immune system is stronger than men’s.

In the United States, based on a 2005 census, the life expectancy gap between men and women is 5.3 years, with women expected to live on average up to 80.1 years. In Japan, a country which holds the record for life expectancy among the world’s populations, the gap is even wider with women being expected to live on average six years longer than men.

Many theories have been proposed in attempt to explain this gap. In fact, it turns out the females of most species live longer than males, which might mean that the life expectancy gap might be deeply rooted in our biology. A theory says women live longer men because they’re less ‘disposable’. Bear with me. The idea is that men’s reproductive role is less dependent on health than that of women, and as such the biological repairing mechanisms (DNA and cell division to replace old and dead cells) might be more refined in women. Other ideas state that male testosterone is actually harmful in the long run and may reduce life expectancy, although tangible evidence is insufficient to back this up.

Scientists at Tokyo Medical & Dental University have a different explanation, and their research has provided evidence to that shows women’s immune system at old age is stronger than in men. The findings were made after the researchers examined the blood of 356 men and women aged between 20 and 90 years old, looking to study key immune system signals – the levels of white blood cells and cytokines, which help to carry messages in the immune system.

As expected, in both sexes the number of white blood cells decreased with age, but two key elements – known as the T-cell and B-cell lymphocytes, declined faster in men. They also found that another type of cell that tackles viruses and tumours increased with age, with women having a higher rate of increase than men. Moreover,  two types of cytokines that help to keep the immune system under control and prevent inflammation from damaging surrounding tissue showed a decline only in men.

“It is well known that ageing is associated with a decline in the normal function of the immune system, leading to increased susceptibility to various diseases and shortened longevity,” said Professor Katsuiku Hirokawa.

“However, specific dysfunctions in the immune system directly responsible for this have yet to be identified.

“Among the important factors, T cells are central to the immune response, and their function is significantly altered with increasing age.”

Besides trying to explain the life expectancy gap, the findings also could serve a better indicator for calculating biological age, based on the state of one’s immune system.

 “Because people age at different rates, a person’s immunological parameters could be used to provide an indication of their true biological age,” Hirokawa said.

The findings were reported in the journal  Immunity and Ageing


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



Longevity gene that makes the Hydra immortal identified

HydraThe Hydra is a tiny animal that can be found in just about any freshwater pond, just a few millimeters long, that has attracted the attention of scientists for years now due to its extraordinary regenerative abilities. The Hydra is consider to be biological immortal – it does not die from old age – although a scientific consensus has yet to be reached. Scientists studying the polyp Hydra claim they now know how the creature escapes senescence after they found a key gene. This gene is also believed to be linked with aging in humans.

The animal’s potential immortality is made possible by its reproductive system. The Hydra is an asexual being and doesn’t mate, instead it reproduces by producing buds in the body wall, which grow to be miniature adults and simply break away when they are mature. Popular scientific consensus has found that animals that reproduce later on and less frequently tend to live longer. The Hydra, however, begins to reproduce almost immediately.

The forever young Hydra

Biology Professor Daniel Martínez at first was extremely skeptical of the claim that Hydras were biological immortal. He set out to disprove this assumptions and cultured tens of specimens, which he kept in isolation waiting for them to die. It’s already been four years and no specimen has yet succumbed from natural causes. For an animal of this size, nature dictates that it should have died long before.

Returning to the Hydra’s reproductive system. For this vegetative-only reproduction to work,  each polyp contains stem cells capable of continuous proliferation. “Hydra is a bag of stem cells,” Martinez says. “It is an adult that is produced by embryonic cells, so it is really a perennial embryo. The genes that regulate development are constantly on, so they are constantly rejuvenating the body.”

The gene that makes it all happen

As humans age, as well as many other complex biological lifeforms, stem cells lose the ability to proliferate and thus to form new cells. This causes tissue decline, which is why muscles get weakened with old age for instance. Influencing the processes that go with aging has been a goal for scientists science the advent of modern science. The Hydra might potentially have the ability to open new doors, especially after the latest research from scientists at the University Medical Center Schleswig-Holstein (UKSH) who recently found the gene that causes Hydra to be immortal – the FoxO gene.

Now, the gene itself isn’t something new. It’s been known by scientists for years and is present in all animals, and humans as well. However, until now it was not known why human stem cells become fewer and inactive with increasing age, which biochemical mechanisms are involved and if FoxO played a role in aging.

The German researchers genetically modified a batch of polyps such that they obtained Hydras with: no FoxO gene, deactivated FoxO gene and enhanced FoxO gene. Their  findings show that the animals with no FoxO gene have significantly fewer stem cells. Interestingly, the immune system in animals with inactive FoxO also changes drastically.

“Drastic changes of the immune system similar to those observed in Hydra are also known from elderly humans,” explains Philip Rosenstiel of the Institute of Clinical Molecular Biology at UKSH, whose research group contributed to the study.

The researchers go on to note that there’s a link between FoxO and aging in humans.

“Our research group demonstrated for the first time that there is a direct link between the FoxO gene and aging,” says Thomas Bosch from the Zoological Institute of Kiel University, who led the Hydra study. Bosch continues: “FoxO has been found to be particularly active in centenarians — people older than one hundred years — which is why we believe that FoxO plays a key role in aging — not only in Hydra but also in humans.”

Fighting aging in humans

That’s to say that FoxO has been proven to be linked with aging in humans, since testing such a hypothesis would require genetic modification of actual people. Remember, that the Hydra is an extremely primitive organism – immortal as it may be. Imagine that if you  take a hundred hydra, make a cell suspension, dissociate all the tissue, put it in a centrifuge, make it into a bowl, you’ll soon see how from those cells, somehow they bind together and you’ll get a couple of new hydras!

It’s been tested with mice, however, and apparently though they didn’t make them immortal, the enhanced gene therapy did in fact prolonged their lives considerably.

Here’s the take away: FoxO gene plays a decisive role in the maintenance of stem cells, according to these findings. I may be overstating this, so someone please correct me if so, but it also means that the FoxO gene determines life span in all animals, from simple being to the top of the food chain humans. So what’s the key to longevity? The maintenance of stem cells and the maintenance of a functioning immune system. If you you’ve got these two in cue, you’ve got nothing to worry about – except freak accidents!

I recommend you also read one of my earlier pieces which also discusses another immortal animal – that’s right, you’re own backyard flatworm. This little puppy can regenerate its cells indefinitely thanks to the telomerase enzyme, which keeps DNA telomeres from shrinking and thus also keeps cell regeneration indefinite.

The findings of the German scientists were documented in the journal Proceedings of the National Academy of Sciences(PNAS).

How exercise prolongs your life

“We found that adding low amounts of physical activity to one’s daily routine, such as 75 minutes of brisk walking per week, was associated with increased longevity: a gain of 1.8 years of life expectancy after age 40, compared with doing no such activity,” explained Harvard Medical School Professor of Medicine I-Min Lee.

75 minutes of walking per week is about 10 minutes per day, just think about it for a second. Just ten minutes per day increases your life expectancy, increases your health, and makes you feel better – talk about a great investment return.

While previous studies have shown the link between physical activity and a lower risk of premature mortality, the exact number of years added to the life expectancy was a mystery – until now. In a new study from Harvard-affiliated Brigham and Women’s Hospital (BWH), in collaboration with the National Cancer Institute, researchers have managed to quantify just how much life expectancy different levels of exercise can give you.

“Physical activity above this minimal level [10 minutes of walking daily] was associated with additional gains in longevity. For example, walking briskly for at least 450 minutes a week was associated with a gain of 4.5 years. Further, physical activity was associated with greater longevity among persons in all BMI groups: those normal weight, overweight, and obese.”

Researchers analyzed associations of leisure-time physical activity of a moderate to vigorous intensity for more than 650.000 subjects, following them for 10 years. The findings show a direct correlation between physical activity and longevity. Just by participating in low level of leisure time physical activity, you get a 19 percent reduced risk of mortality compared with no such activity.

“Our findings reinforce prevailing public health messages promoting both a physically active lifestyle and a normal body weight,” explained Steven C. Moore, research fellow at the National Cancer Institute and lead author of this study.

There you have it people; want to live a longer,healthier, life? Get out of the house and start doing something with your body – it really is as simple as that. Besides, you too can look as fine and be as photogenic as this guy.