Graying hair could be a sign that the body is effectively protecting itself from cancer, a new study suggests.

Cancer-causing triggers, such as ultraviolet (UV) light or certain chemicals, activate a natural defensive pathway that leads to premature graying but also reduces the incidence of cancer, the research found.

The researchers behind the study tracked the fate of the stem cells responsible for producing the pigment that gives hair its color. In mouse experiments, they found that these cells responded to DNA damage either by ceasing to grow and divide — leading to gray hair — or by replicating uncontrollably to ultimately form a tumor.

The findings, reported in October in the journal Nature Cell Biology, underline the importance of these sorts of protective mechanisms that emerge with age as a defense against DNA damage and disease, the study authors say.

Graying hair as cancer defense

Healthy hair growth is dependent on a population of stem cells that constantly renews itself within the hair follicle. A tiny pocket within the follicle contains reserves of melanocyte stem cells — precursors to the cells that produce the melanin pigment that gives hair its color.

"Every hair cycle, these melanocyte stem cells will divide and produce some mature, differentiated cells," said Dot Bennett, a cell biologist at City St George's, University of London who was not involved in the study. "These migrate down to the bottom of the hair follicle and start making pigment to feed into the hair."

Graying occurs when these cells can no longer produce sufficient pigment to thoroughly color each strand.

"It's a sort of exhaustion called cell senescence," Bennett explained. "It's a limit to the total number of divisions that a cell can go through, and it seems to be an anti-cancer mechanism to prevent random genetic errors acquired over time propagating uncontrollably."

When the melanocyte stem cells reach this "stemness checkpoint," they cease to divide, meaning the follicle no longer has a source of pigment to color the hair. Ordinarily, this occurs with old age as the stem cells naturally reach this limit. However, Emi Nishimura, a professor of stem cell age-related medicine, and colleagues at the University of Tokyo were interested in how this same mechanism operates in response to DNA damage — a key trigger for cancer development.

In mouse studies, the team used a combination of techniques to track the progress of individual melanocyte stem cells through the hair cycle after exposing them to different harmful environmental conditions, including ionizing radiation and carcinogenic compounds. Intriguingly, they found that the type of damage influenced how the cell reacted.

Ionizing radiation caused the stem cells to differentiate and mature, and ultimately activated the biochemical pathway responsible for cell senescence. As a result, the melanocyte stem cell reserves were rapidly depleted over the hair cycle, thus halting the production of further mature pigment cells and leading to gray hair.

Meanwhile, by essentially switching off cell division, this senescence pathway prevented the mutated DNA from passing into a new generation of cells, thus lowering the likelihood of those cells forming cancerous tumors.

Exposure to chemical carcinogens — such as 7,12-dimethylbenz[a]anthracene (DMBA), a tumour initiator widely used in cancer research — appeared to bypass this protective mechanism. Instead of switching on senescence, it toggled on a competing cellular pathway.

This alternative chemical sequence blocked cell senescence in the team's mouse studies, enabling the hair follicles to retain their stem cell reserves and the ability to produce pigment, even after DNA damage. That meant that the hair retained its color, but in the long term, the unchecked replication of damaged DNA led to tumor formation and cancer, the team said in a statement.

These findings reveal that the same stem cell population can meet opposite fates depending on the type of stress they're exposed to, lead study author Nishimura said in the statement. "It reframes hair graying and melanoma [skin cancer] not as unrelated events, but as divergent outcomes of stem cell stress responses," Nishimura added.

The next step will be to translate this understanding into human hair follicles, to see whether these observations in mice carry over to people, Bennett said.

This article is for informational purposes only and is not meant to offer medical advice.

Scientists have identified a never-before-seen type of cell that may help to heal brain damage — at least in mice.

The researchers discovered a unique kind of astrocyte, a star-shaped cell that supports communication between brain cells, or neurons, and keeps them healthy by stabilizing the brain's protective barrier and regulating neurons' balances of charged particles and signalling molecules.

In the brain, astrocytes either live in gray matter, which contains the main part of neurons that holds DNA and enables the cells to process information, or white matter — the insulated wires that extend from some neurons. Researchers have long-studied the role of gray-matter astrocytes, but until now, less was known about their white-matter counterparts.

In the new study, published Monday (Feb. 24) in the journal Nature Neuroscience, scientists determined the function of white-matter astrocytes in tissue samples from the brains of mice. They did this by analyzing the activity of the genes these cells expressed, or "switched on."

Related: Super-detailed map of brain cells that keep us awake could improve our understanding of consciousness

The researchers identified two distinct types of white-matter astrocytes. The first performed the role of a "housekeeper," which physically supported nerve fibers and aided neurons in communicating with one another. Meanwhile, the second type performed a function that was previously unheard of for an astrocyte in the white matter — it had a unique ability to proliferate, thus making new astrocytes.

"That is a really important finding because that wasn't known before," study co-author Judith Fischer-Sternjak, the deputy director of the Institute of Stem Cell Research at Helmholtz Munich in Germany, told Live Science.

The researchers also found that some of these special, proliferative astrocytes were able to move from white matter to gray matter regions of the mouse's brain. This finding suggests that these cells may act as a reservoir for new astrocytes.

If similar astrocytes are discovered in the human brain, the research could potentially lead to the development of new therapies to repair the brain after injury or damage, such as that caused by neurodegenerative diseases like multiple sclerosis, the authors suggested. For instance, scientists could theoretically learn to manipulate astrocytes so they're more likely to proliferate and replace defective or lost cells, Fischer-Sternjak said.

In the study, the researchers also looked at human brain tissue samples, which were extracted during the autopsies of 13 organ donors. While the team did identify white-matter astrocytes within these samples, these cells only expressed genes involved in housekeeping functions, rather than proliferation.

It's possible that the human brain samples didn't contain these unique proliferating astrocytes because they were collected exclusively from older patients, and the mouse experiments showed that proliferative astrocytes appear to decline in number with age, Fischer-Sternjak said.

With a wider range of human samples — especially from younger people — it's possible that these cells could still be discovered, Fischer-Sternjak said.

Going forward, the researchers hope to learn more about how white-matter astrocytes contribute to overall brain health in humans. Only then can scientists understand how astrocytes respond to injury and how they might change with disease and aging, Fischer-Sternjak said.

Scientists have identified 13 proteins that may be linked to brain aging and could one day be targeted with anti-aging treatments.

However, experts say that more research is needed to know exactly why these proteins are tied to brain aging, and whether they point to specific solutions for diseases like dementia.

In a new study, scientists analyzed magnetic resonance imaging (MRI) brain scans from nearly 11,000 people ages 45 to 82. They used the scans to estimate each participant's "brain age gap" — essentially how much their "brain age" differs from their chronological age.

The team determined people's brain ages using artificial intelligence to look at specific physiological features, such as brain volume and surface area. This revealed the extent to which their brains were undergoing accelerated aging.

Related: Single molecule reverses signs of aging in muscles and brains, mouse study reveals

The team then assessed the concentration of approximately 3,000 proteins in the blood of nearly 5,000 of the participants. The blood connects the brain to the rest of the body, so changes in the concentration of proteins within the blood should reflect similar alterations in the brain.

Across the board, the researchers identified 13 proteins whose blood concentrations were significantly associated with biological brain age. Proteins that were linked to factors involved in aging — such as cellular stress and inflammation — increased in the blood as biological brain age rose. Meanwhile, levels of proteins that help maintain the brain's function, including those involved in cellular regeneration, decreased as people aged.

Of the proteins that the team identified, one known as brevican showed one of the strongest links with biological brain age — it decreased in concentration as people aged, and those falling numbers showed a strong correlation with conditions such as dementia and stroke.

Brevican is known to help neurons communicate with one another, so this finding supports previous research that suggested the protein could act as a measurable marker for the development of neurodegenerative diseases.

Furthermore, the scientists found that the concentrations of the 13 proteins peaked in the blood at specific chronological ages: 57, 70 and 78. This might reflect "waves" of brain aging that could be used as a reference point to target future anti-aging interventions, the team wrote in a paper published Monday (Dec. 9) in the journal Nature Aging.

However, other experts have voiced concerns about rushing to such conclusions.

The "brain waves" findings are not only "unexpected" but "go against pretty much everything that is known about brain aging," during which there is a continuous, gradual decline in brain function and associated changes in cells, Mark Mattson, an adjunct professor of neuroscience at Johns Hopkins School of Medicine who was not involved in the research, told Live Science in an email.

Many questions about the study also remain.

"The correlation between several proteins in blood samples and an MRI image-based indicator of brain aging are interesting," Mattson said. "However, the implications for using measurements of blood levels of those proteins to diagnose brain dysfunction or for developing specific interventions are unclear."

The team acknowledged several limitations of the study in their paper. For instance, they only used data from older people who were mainly of European descent, because their data was drawn from the U.K. Biobank database. More research is needed to see if the proteins fluctuate in the same ways in individuals of different races and ethnicities, as well as how they may change across the entire human life span.

It is also still unknown where in the brain these 13 proteins come from, Mattson added. "Until levels of those proteins in the brain are established, it will be unclear whether they actually play a role in brain aging," he said.

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A test that uses cells from the inside of your cheek may accurately predict the risk of death within the upcoming year, new research hints.

This study, published Oct. 1 in the journal Frontiers in Aging, offers promising support for CheekAge, a new tool that uses cheek — or "buccal" — samples to estimate a person's risk of dying within one year. In a group of adults ages 69 to 101, the test was strongly associated with the risk of death from any cause. A set increase in the study subjects' CheekAge corresponded to a 21% bump in their risk of death within the next 12 months.

CheekAge is a type of epigenetic clock, a tool that measures a person's "biological age" by looking at patterns of chemicals attached to their DNA. In many cases, "biological age is much more telling [about the health of an individual] than the years that they've lived on this planet," said David Furman, an associate professor at the Buck Institute for Research on Aging in Novato, California, who was not involved in the new study.

The long-term hope for tools like CheekAge is to help people slow down or prevent biological aging. But for now, such tools can't tell you how to accomplish that feat, Furman and first study author Maxim Shokhirev, head of computational biology and data science at Tally Health in New York, told Live Science.

Related: Epigenetics linked to the maximum life spans of mammals

What CheekAge does — and what it can't do

In general, epigenetic clocks examine aging of the blood and other tissues to make predictions about a person's chronological age and their risk of death and age-related diseases, like cancer. The most common marker of aging that the clocks look for is DNA methylation, a process by which small molecules called methyl groups attach to DNA over time. These molecules help control gene expression, turning certain genes on and off.

Scientists trained CheekAge using cheek swabs from people ages 18 to 93. They paired patterns of DNA methylation in the cheek cells to an overall score for health, which considered factors such as a person's stress levels, educational and body mass index (BMI). A person's "CheekAge score" was thus tied to their health status and apparent degree of biological aging.

The researchers then determined how accurately CheekAge correlates with one's risk of death. To do so, they looked at volunteers enrolled in the Lothian Birth Cohorts, a long-term research program that tracks aging in participants from childhood through adulthood. In this group of just over 15,000 people, scientists had taken blood samples every three years that could be used to track changes in DNA methylation at roughly 450,000 spots in the genome. Each person's mortality status was taken into account, to tie their epigenetics to their risk of death.

The team then used the epigenetic patterns trained from the cheek on blood data. They found that CheekAge, despite being trained on buccal samples, still showed a strong link to the death risk data drawn from a separate blood dataset that tracked mortality.

"We were surprised to see that CheekAge worked so well in a different tissue," Shokhirev told Live Science in an email. "This may suggest that CheekAge is picking up on health signals that are conserved between different tissue types," he said.

As of yet, CheekAge has been used to look at data retroactively — the researchers knew who lived and died and what their respective epigenetics looked like at the time. Having deduced those patterns, they can now use the tool to estimate living people's risk of death.

"We can't predict if someone will live or die within a year, but we can see an increased or decreased risk of all cause mortality," Shokhirev told Live Science. Further research is needed to determine whether the test can predict other health outcomes, such as the chance of age-related disease.

"One of the primary goals [of making epigenetic clocks] is to identify interventions that can influence or slow down these innate aging mechanisms," Steve Horvath, a professor of human genetics and biostatistics at UCLA who was not involved in the study, told Live Science in an email.

At this point, the tests don't point to any specific treatments, so people should approach them with caution. CheekAge is not available for consumers to purchase, but the same research group has made a similar product, called the TallyAge Test, which is currently on the market. There's a lack of standardization across these commercial epigenetic-clock tests and a risk of misinterpreting the results, said Horvath, who pioneered the first epigenetic clock.

"We understand very little about how to modify an epigenetic landscape," Furman emphasized. He describes epigenetic-clock tests as "moderately useful" to track individuals' behavioral changes, such as in their physical activity or diet, and whether they're tied to epigenetic changes.

"But they [the epigenetic clocks] don't tell you what to do and so there are a lot of limitations on that," Furman said.

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Human life expectancy is increasing at a slower rate than it did in the 20th century, a new study of 10 wealthy countries hints.

During the 20th century, improvements in public health and medicine resulted in "radical life extension": With each passing decade, the average life expectancy at birth in some of the world's longest-lived populations in high-income countries increased by around three years. These increases in life expectancy were initially driven by reductions in the death rates of children, followed by declines in the death rates of middle-aged and older people. For instance, in the U.S. in 1900, the average life expectancy at birth was 47.3; by 2000, it had increased to 76.8.

But now, a new paper suggests that a similar explosion in life expectancy won't occur in the 21st century.

The report, published Monday (Oct. 7) in the journal Nature Aging, predicts that people can only be expected to gain an extra 2.5 years over the next three decades.

Related: COVID pandemic knocked 1.6 years off global life expectancy, study finds

The most likely explanation for this deceleration is that humanity is now approaching the upper limit of its life expectancy, the authors of the study argue. In other words, with more people surviving to older ages, the main risk factors for death are related to biological aging — the gradual accumulation of damage to cells and tissues that inevitably occurs over time. We know how to prevent children from dying of measles, but we can't yet stop the biological clock that keeps ticking once that child reaches age 60, 70 and beyond.

Tackling one age-related disease at a time — for instance, by trying to develop cures for Alzheimer's disease or cancer — is like putting on a "temporary survival Band-Aid," said Jay Olshansky, lead study author and a professor of epidemiology and biostatistics at the University of Illinois Chicago. These efforts to develop better treatments — and, eventually, cures — can enable people to live long enough to experience aging, but they don't tackle the root issue of aging, he told Live Science.

In their new study, Olshansky and colleagues investigated trends in life expectancy between 1990 and 2019. They analyzed national vital statistics data from nine regions with the longest-lived populations — Australia, France, Italy, Japan, South Korea, Spain, Sweden, Switzerland and Hong Kong. They also looked at figures from the U.S., as some scientists made specific predictions about radical life extension in the country, they wrote in the paper. The researchers then used this retroactive analysis to predict future trends in life expectancy that may occur this century.

The team found that overall improvements in life expectancy decelerated across these 10 countries, particularly after 2010. Current birth cohorts have a small likelihood of making it to 100 — females have a 5.1% chance, and males have a 1.8% chance.

Of children born in 2019, those from Hong Kong were most likely to reach 100, with females having a 12.8% chance and males having a 4.4% chance.

These findings suggest that, to continue extending human life expectancy, more research should be channeled into the study of geroscience, which investigates the biology of aging, rather than just the diseases associated with the process, Olshansky said. In this context, it is important to note that life expectancy is different to life span, which defines the maximum age to which any human has ever lived.

Investigating ways to slow or reverse cellular aging could help people remain "younger" for longer, Olshansky suggested. For instance, scientists are developing drugs that may be able to slow aging by extending caps at the end of chromosomes, known as telomeres, which normally dwindle over time.

"Now, we need to focus on manufacturing the most precious commodity on Earth, which is healthy life," he told Live Science.

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From the swimming habits of dead trout to the revelation that some mammals can breathe through their backsides, a group of leading leftfield scientists have been taking their bows at the Massachusetts Institute of Technology for the 34th annual Ig Nobel Prize ceremony. Not to be confused with the actual Nobel prizes, the Ig Nobels recognise scientific discoveries that “make people laugh, then think."

We caught up with one of this year’s winners, Saul Justin Newman, a senior research fellow at the University College London Centre for Longitudinal Studies. His research finds that most of the claims about people living over 105 are wrong.

How did you find out about your award?

I picked up the phone after slogging through traffic and rain to a bloke from Cambridge in the UK. He told me about this prize and the first thing I thought of was the lady who collected snot off of whales and the levitating frog. I said, "absolutely I want to be in this club."

What was the ceremony like?

The ceremony was wonderful. It’s a bit of fun in a big fancy hall. It's like you take the most serious ceremony possible and make fun of every aspect of it.

But your work is actually incredibly serious?

I started getting interested in this topic when I debunked a couple of papers in Nature and Science about extreme ageing in the 2010s. In general, the claims about how long people are living mostly don't stack up. I've tracked down 80% of the people aged over 110 in the world (the other 20% are from countries you can't meaningfully analyze). Of those, almost none have a birth certificate. In the US there are over 500 of these people; seven have a birth certificate. Even worse, only about 10% have a death certificate.

The epitome of this is blue zones, which are regions where people supposedly reach age 100 at a remarkable rate. For almost 20 years, they have been marketed to the public. They’re the subject of tons of scientific work, a popular Netflix documentary, tons of cookbooks about things like the Mediterranean diet, and so on.

Related: Does the Mediterranean diet reduce dementia risk? 20-year study hints no

Okinawa in Japan is one of these zones. There was a Japanese government review in 2010, which found that 82% of the people aged over 100 in Japan turned out to be dead. The secret to living to 110 was, don't register your death.

The Japanese government has run one of the largest nutritional surveys in the world, dating back to 1975. From then until now, Okinawa has had the worst health in Japan. They've eaten the least vegetables; they've been extremely heavy drinkers.

What about other places?

The same goes for all the other blue zones. Eurostat keeps track of life expectancy in Sardinia, the Italian blue zone, and Ikaria in Greece. When the agency first started keeping records in 1990, Sardinia had the 51st highest old-age life expectancy in Europe out of 128 regions, and Ikaria was 109th. It's amazing the cognitive dissonance going on. With the Greeks, by my estimates at least 72% of centenarians were dead, missing or essentially pension-fraud cases.

What do you think explains most of the faulty data?

It varies. In Okinawa, the best predictor of where the centenarians are is where the halls of records were bombed by the Americans during the war. That's for two reasons. If the person dies, they stay on the books of some other national registry, which hasn’t confirmed their death. Or if they live, they go to an occupying government that doesn't speak their language, works on a different calendar and screws up their age.

According to the Greek minister that hands out the pensions, over 9,000 people over the age of 100 are dead and collecting a pension at the same time. In Italy, some 30,000 "living" pension recipients were found to be dead in 1997.

Regions where people most often reach 100 to 110 years old are the ones where there's the most pressure to commit pension fraud, and they also have the worst records. For example, the best place to reach 105 in England is Tower Hamlets. It has more 105-year-olds than all of the rich places in England put together. It's closely followed by downtown Manchester, Liverpool and Hull. Yet these places have the lowest frequency of 90-year-olds and are rated by the UK as the worst places to be an old person.

The oldest man in the world, John Tinniswood, supposedly aged 112, is from a very rough part of Liverpool. The easiest explanation is that someone has written down his age wrong at some point.

But most people don’t lose count of their age…

You would be amazed. Looking at the UK Biobank data, even people in mid-life routinely don't remember how old they are, or how old they were when they had their children. There are similar stats from the US.

What does this all mean for human longevity?

The question is so obscured by fraud and error and wishful thinking that we just do not know. The clear way out of this is to involve physicists to develop a measure of human age that doesn't depend on documents. We can then use that to build metrics that help us measure human ages.

Longevity data are used for projections of future lifespans, and those are used to set everyone’s pension rate. You're talking about trillions of dollars of pension money. If the data is junk then so are those projections. It also means we're allocating the wrong amounts of money to plan hospitals to take care of old people in the future. Your insurance premiums are based on this stuff.

What’s your best guess about true human longevity?

Longevity is very likely tied to wealth. Rich people do lots of exercise, have low stress and eat well. I just put out a preprint analysing the last 72 years of UN data on mortality. The places consistently reaching 100 at the highest rates according to the UN are Thailand, Malawi, Western Sahara (which doesn't have a government) and Puerto Rico, where birth certificates were cancelled completely as a legal document in 2010 because they were so full of pension fraud. This data is just rotten from the inside out.

Do you think the Ig Nobel will get your science taken more seriously?

I hope so. But even if not, at least the general public will laugh and think about it, even if the scientific community is still a bit prickly and defensive. If they don't acknowledge their errors in my lifetime, I guess I’ll just get someone to pretend I’m still alive until that changes.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

Maria Branyas Morera, the oldest person in the world, has died. She was 117 years old.

The supercentenarian, who was born in San Francisco on March 4, 1907, died "peacefully in her sleep" in Olot, Spain, her family announced on her X account on Tuesday (Aug. 20). She died on Monday (Aug. 19), a nursing home employee told The New York Times.

Morera had been a resident at the Residencia Santa Maria del Tura nursing home for the last 20 years. Recently, Morera had told her family that she was beginning to feel weak and knew that her time was coming to a close.

In the translated post she stated that "One day I will leave here. I will not try coffee again, nor eat yogurt, nor pet my dog. I will also leave my memories, my reflections and I will cease to exist in this body. One day I don't know, but it's very close, this long journey will be over."

Related: We're nowhere near reaching the maximum human life span, controversial study suggests

In 2023, the Guinness Book of World Records officially announced that Morera was the world's oldest person. She received the title upon the death of Lucile Racon, also known as Sister André, who was 118 years old when she died on Jan. 17, 2023.

Because of her longevity, Morera captured the attention of the medical community. Researchers who studied her genetic and lifestyle habits determined that she not only had low levels of fat and sugar in her blood, but also that her cells aged more slowly than the average person's, The New York Times reported.

Now the world's oldest person is 116-year-old Tomiko Itooka, who was born in Japan on May 23, 1908, according to the U.S. Gerontology Group. 

The human body does not age at a constant rate throughout adulthood — instead, it accelerates dramatically around ages 44 and 60, a new study finds.

The new research, published Aug. 14 in the journal Nature Aging,involved measuring more than 11,000 molecules in the adult body over time, and it revealed that 81% of them undergo dramatic changes at these two ages.

This type of aging research focuses on tracking "biological age," which refers to changes that occur in the body over a lifetime, affecting proteins, metabolites and gene activity. This concept is distinct from the "chronological age" that people celebrate each year on their birthdays.

Finding that biological aging accelerates at two points in midlife could help researchers understand why the risk of certain illnesses increases in fits and starts as chronological age rises. For example, approximately 6.5% of people ages 40 to 59 have coronary artery disease, but the prevalence rises sharply to 19.8% in people ages 60 to 79.

Related: Natural rates of aging are fixed, study suggests

For the study, researchers at Stanford University recruited 108 participants that were of diverse ethnic backgrounds and ranged from 25 to 75 years old. Every three to six months for several years — up to about seven years in total — the scientists collected blood samples from the participants to assess how different factors, such as gene activity and blood sugar levels, varied over time.

Many of the factors that shifted around age 44 and 60 were related to heart health. For example, a protein linked to atherosclerosis, or plaque buildup in arteries, increased in the blood of participants during their 40s and 60s. These age groups also showed declines in the ability to metabolize caffeine, which temporarily raises blood pressure, and alcohol, which initially lowers but then raises blood pressure.

The body's pathway for making unsaturated fatty acids, which lower "bad" cholesterol, also waned at these two ages.

Although the study's multiple links to cardiovascular health were only correlative, they point to potential reasons why heart disease becomes more common with age.

Aside from heart health, blood sugar levels peaked in participants in their 40s and 60s, suggesting a possible link to age-related type 2 diabetes.

Scientists don't yet know why body chemistry changes considerably at these ages, and the study didn’t account for the role lifestyle factors, such as diet or exercise, might play.

Juan Carlos Verján, who researches aging at the National Institute of Geriatrics in Mexico and was not involved with the study, told Live Science that "the 60-year inflection point, I believe, could be more due to inflammation." For instance, participants over 60 accumulated antioxidant enzymes in their blood. These enzymes neutralize chemical triggers for inflammation and suggests that inflammation could be accumulating in this age group

The aging boost at age 44 also coincides with the time some women start going through perimenopause. However, "we found the same trigger timepoints for women and men," suggesting sex-specific hormonal changes are not responsible for the aging boosts, said study co-author Xiaotao Shen, a computational biologist who's now at Nanyang Technology University in Singapore. Therefore, "there should be another reason to cause the same change in men and women." What that shared factor is remains a mystery.

The study was limited in that the participants ranged from ages 25 to 75, so the researchers could not assess sizable shifts that occur at other key moments in life, such as during puberty or at very advanced ages. The small sample of 108 participants from California was another limitation because the group is unlikely to represent all humans globally.

Generally speaking, "people in California have a lot of years of healthy life," Verján said. He proposed that the researchers could also explore aging in places where people have shorter lifespans, on average.

The team focused on changes to molecules in the blood, but this does not necessarily reflect all the organs in the body. "There are several papers that mention that aging is tissue-related," Verján said, rather than exclusively related to factors in blood. For example, one publication found that, in some people, the heart ages the fastest, whereas for others, it's the kidneys.

Shen's team discovered a number of changes that correlate with the timing of age-linked diseases, but they still need to confirm a causal tie to these factors. In other words, do the changes seen in blood actually drive disease, or are they more of a byproduct of the aging process?

"Animal experiments are a good option for us to study the reasons why there are two peaks for aging," Shen said. Verján speculated that epigenetic changes, which modify the activity of genes without altering their underlying code, might drive these dramatic shifts.

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A nutrient-rich diet with few added sugars may slow rates of biological aging in women, new research suggests.

In a new study, published Monday (July 29) in the journal JAMA Network Open, scientists found that middle-aged women who ate more foods packed with vitamins, minerals and antioxidants had "younger-looking" cells than those who consumed less nutrient-rich diets.

They judged the youthfulness of cells by looking at chemical tags, known as methyl groups, on the surface of DNA molecules. These tags tweak the activity of specific genes without altering the underlying DNA code — a process known as epigenetic modification. The pattern of these methyl groups changes as we age, which is believed to contribute to accelerated cellular aging.

While nutrient-rich diets were tied to slowed aging, added sugars seemed to dampen the effect.

Related: Short-term vegan diet may slow aging, but questions remain

In the study, women who consumed higher amounts of added sugars showed signs of hastened cellular aging compared to others, even if they ate an otherwise healthy diet, the researchers found. "Added sugars" refers to sugars that are added to food during production, such as those in sugar-sweetened drinks and baked goods, as opposed to the naturally occuring sugars found in milk, fruits and vegetables.

The new study is one of the first to demonstrate a link between added sugar consumption and so-called epigenetic aging, the authors said. It is also the first to investigate this association in both Black and white women in midlife, they noted. The participants were 39 years old, on average.

"We knew that high levels of added sugars are linked to worsened metabolic health and early disease, possibly more than any other dietary factor," study co-author Elissa Epel, a professor of psychiatry at the University of California, San Francisco, said in a statement.

"Now we know that accelerated epigenetic aging is underlying this relationship, and this is likely one of many ways that excessive sugar intake limits healthy longevity," she said.

Epel and colleagues analyzed food records cataloged by 342 women over three, non-consecutive days. The team then scored each woman's diet based on how closely it adhered to various established diets. These included the Mediterranean diet, which is rich in plants, whole grains and unsaturated fats and low in red meats, saturated fats and sugars. Another, similar diet, called the Alternative Healthy Eating Index, specifically emphasizes foods and nutrients believed to reduce the risk of chronic disease.

The researchers also devised a new measure of nutrient intake called the "Epigenetic Nutrient Index." This includes nutrients linked to antioxidative and anti-inflammatory processes in the body, as well as to DNA maintenance and repair. For example, it includes vitamins A, C, B12 and E, along with folate and magnesium.

In addition to scoring people's diets, the team assessed how much added sugar the women ate — which ranged between 0.1 and 11 ounces (2.7 and 316 grams) of added sugar a day. The team calculated the participants' epigenetic ages by looking at the DNA methylation of cells within saliva samples.

These data revealed the links between diet and cellular aging, but they only captured a snapshot.

The findings support the idea that eating nutritious foods that are low in added sugars may improve a person's health span, meaning the period of their life in which they are healthy, not just surviving.

However, more research is needed to assess how following these diets might affect epigenetic aging in the long run, the authors wrote in their paper.

This article is for informational purposes only and is not meant to offer medical advice.

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Following a vegan diet for a couple months may slow aging, new research hints.

However, these findings shouldn't be overhyped, experts cautioned, in part due to limitations in how the study was conducted.

In a small clinical trial that included 21 pairs of healthy identical twins, one twin from each pair ate a vegan diet while the other twin followed an omnivorous diet, which included plants, meat, eggs and dairy. The twins followed these diets for eight weeks. The idea behind using identical twins is that, given their shared genetics, the influence of diet can then be isolated and studied more easily.

The twins, who were around 40 years old on average and mainly women, ate meals the researchers prepared for them for the first month of the study. For the second month, the participants cooked for themselves, after receiving nutrition classes.

Related: Extreme longevity: The secret to living longer may be hiding with nuns... and jellyfish

The researchers analyzed the participants' blood before they started their diets, four weeks in, and then again at the end of the study. They looked for changes in the chemical tags on top of DNA within the twins' cells; specifically, they assessed molecules called methyl groups, which latch onto DNA and change the extent to which specific genes are "switched on." They do this without altering the underlying DNA code — a phenomenon known as epigenetic modification.

Changes in methylation patterns are associated with accelerated rates of aging, and scientists have previously studied these changes in order to make "epigenetic clocks" that can be linked to organisms' maximum life spans.

At the eight-week mark, the twins who ate a vegan diet had significantly reduced levels of DNA methylation, compared to before they started the study, the researchers found. Their omnivorous siblings, however, showed no significant changes in DNA methylation during this time.

The team used established tests to see if the methylation changes seen in the vegan group were tied to any specific aging processes. They found they were tied to "younger" scores for organs like the heart and liver, as well as bodily processes including inflammation and metabolism. At least one of the tests that they used is licensed by TruDiagnostics, an epigenetics testing company that also funded the new study.

These findings suggest that going vegan could have anti-aging effects, at least in the short term, the team said. They described their research in a study published Sunday (July 28) in the journal BMC Medicine.

"This trial suggests that a healthy plant-based diet may be superior to a healthy omnivorous diet in changing epigenetic markers that are potentially related to improved healthspan," Dr. Luigi Fontana, a professor of medicine and nutrition at the University of Sydney who was not involved in the research, told Live Science in an email. ("Healthspan" refers to the amount of time a person remains healthy during their life, rather than just alive.)

However, the new findings should be treated with caution, Fontana noted.

Firstly, the study was only two months long, which raises the question of whether these epigenetic changes are temporary, Fontana said. Aging is a lifelong process, so future studies would need to investigate whether these findings can be replicated in the long term, he said.

Another potential caveat of the study is that the twins who followed the vegan diet lost around 4.4 pounds (2 kilograms) more than the omnivores. This is because they were eating substantially fewer calories, lead study author Varun Dwaraka, head of bioinformatics at TruDiagnostics, told Live Science. As such, it could be that these weight changes somehow contributed to the observed changes in DNA methylation.

Notably, calorie restriction has been shown to slow aging in mice and in monkeys, as well as in some early clinical trials in humans.

"What we would hope for in the next analysis is to start to disentangle these aspects," Dwaraka said. Future trials could ensure that the participating twins consume the same amount of calories, regardless of their diet, he said.

Going vegan not only affected measures of biological aging but also changed the types of immune cells circulating in the participants' blood, said Daniel Belsky, an associate professor of epidemiology at Columbia University. Belsky was involved in the development of one of the epigenetic tests used in the study but not in the study itself.

The measures of biological aging were taken from immune cells, so what appears to be an effect of a vegan diet on aging could be an "artifact" of a short-term immune response to this way of eating, Belsky told Live Science in an email.

Nevertheless, the new study suggests that epigenetic tests can help estimate how different diets affect the aging process, Dwaraka said. Going forward, the team plans to investigate whether following other diets — such as keto or paleo diets, for instance — could produce similar anti-aging benefits.

This article is for informational purposes only and is not meant to offer medical advice.

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By blocking the action of a single protein, scientists have extended the average life span of the mice in their experiment by around 25%. This recent finding has raised the question of whether such a treatment could ever work for people, and so far, there are some promising early hints that it might.

In the new study, scientists injected middle-aged mice with an antibody that blocks the action of interleukin-11, a protein that spurs inflammation and has been tied to aging processes in human cells.

At the beginning of the experiment, these mice were about 17 months old, which is roughly equivalent to being 55 in human years. The mice received injections every three weeks until they died, while a comparison group of mice was left untreated.

The treated mice lived around 25% longer than their untreated counterparts, the researchers found.

Related: Single molecule reverses signs of aging in muscles and brains, mouse study reveals

The treated rodents also maintained better health into old age. For instance, they were slimmer and stronger than the untreated mice, and they showed better liver function and metabolism. Furthermore, only 16% of the treated mice developed cancer, compared with 61% of the rodents that didn't receive antibody injections.

These findings suggest that targeting IL-11 could be a promising approach to combating the negative health impacts of aging, according to the team behind the new study, which was published Wednesday (July 17) in the journal Nature.

This is "very impressive work," said Joao Pedro de Magalhaes, a professor of molecular biogerontology at the University of Birmingham in the U.K. who was not involved in the research.

"While the role of the immune system in aging and its potential target to retard aging is well-established, IL-11 is a new important player for understanding the impact of the immune system and inflammation in aging," de Magalhaes told Live Science in an email.

Despite these encouraging results, though, much more research will be needed to determine if this kind of therapy would produce similar effects in humans. Scientists need to determine how blocking the action of IL-11 actually increases mice's lifespan. For now, that's unclear, de Magalhaes said. It's possible that the mice's longevity could stem mostly from the antibody preventing the onset of cancer in some way, as shown in the new study, he suggested. As in humans, cancer is a common cause of death in older mice.

The researchers behind the work hope to carry it into clinical trials, Anissa Widjaja, lead study author and an assistant professor at the Duke-NUS Medical School in Singapore, told Live Science.

Some treatments that target IL-11 are already in early-stage trials; these are being tested for age-related diseases, such as fibrotic lung disease, which involves excessive scarring of the lungs. Prior to these trials, past research had shown that IL-11 can induce fibrosis, so it's thought that blocking the protein might prevent this effect.

Such trials will help determine the efficacy and safety of any new therapies targeting IL-11. One potential concern with these treatments is that inflammation is an "important and necessary" component of the immune system, said Jason Kim, a professor of molecular medicine at the University of Massachusetts Chan Medical School who was not involved in the research. As such, blocking IL-11 with a drug could potentially have side effects that outweigh the proteins' positive effects on aging, Kim told Live Science in an email.

Related: 'If you don't have inflammation, then you'll die': How scientists are reprogramming the body's natural superpower

For instance, anti-IL-11 treatments could theoretically make people more susceptible to other illnesses, including infections. This potential side effect wouldn't likely be obvious in lab mice, as they are kept in clean environments free of pathogens, de Magalhaes noted.

Nevertheless, the possibilities for this research are exciting, Widjaja said. She and her team are now investigating whether short-term treatment with the IL-11-targeting antibodies might also have anti-aging benefits in mice.

"People are already living longer now, so the question is whether they can stay healthy for longer," she said. "It is very hopeful that our research has shown that anti-IL-11 therapy can help us achieve that."

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People around the world are, on the whole, living longer. At the same time, the gap between how long men and women live is decreasing, new research shows.

The study of more than 190 countries identified these trends around the world. Zooming in on the cluster of countries with the best outcomes — including North America, Europe, Japan, Australia and New Zealand — females had an average life expectancy of 77.17 years old in 1990, while males had a life expectancy of 72.23. In 2010, those life expectancies rose to 83.10 in females and 78.37 in males. So the life-span gap slightly narrowed, by about 0.2 years.

The life span gap between the sexes has narrowed because male life spans are now lengthening at a faster rate than female life spans are, said study first author David Atance, a professor of economics and business management at the University of Alcalá in Spain. "The pace of mortality declines — or, in other words, the pace of increase in longevity — among women has been slowed," he told Live Science in an email.

The researchers predict that, worldwide, the average life expectancy in 2030 will be 86.54 years old for females and 83.13 years old for males.

"This study is consistent with epidemiologic trends that would suggest a rise in global life expectancy and a narrowing of the gender gap over time," Dr. Brandon Yan, a physician at  the University of California, San Francisco School of Medicine who wasn't involved in the work, told Live Science via email.

Related: We're nowhere near reaching the maximum human life span, controversial study suggests

Past research suggests that, between 2000 and 2019, life expectancy worldwide went up from 66.8 years old in 2000 to 73.4 years old in 2019, according to the World Health Organization. And a 2022 study found that, between 1998 and 2016, the gap in life expectancy between females and males narrowed in 10 countries. So at a global level, these same trends appear to persist.

However, Yan published a report on the sex-related life-span gap in the United States last year, and contrary to global data, the gap appears to be widening within the country. The difference between how long American men and women live went from 4.8 years in 2010 to 5.8 years in 2021.

For the new global study, published Wednesday (Jan. 17) in the journal PLOS One, researchers tracked trends in death rates in different countries and determined which places showed the same tendencies over time, Atance told Live Science. 

The data came from the United Nations Population Division, which includes life expectancy and mortality data for people at different ages and from different countries. The team examined data from 1990 to 2020, grouping 194 countries around the world into clusters based on their similarities on nine mortality-related indicators.

These indicators included citizens' average life expectancy at birth and at age 65, as well as the modal age at death, or the overall number of deaths that occur among people at specific ages. These data lumped the countries into five clusters, or "convergence clubs," which largely correlated with five continents.

"The countries within each convergence group are becoming more and more similar  because they present more similar mortality longevity indicators," Atance said. And based on the team's analyses, there are fewer differences among countries in each cluster as time goes on, he added.

Notably, of the convergence clubs, the one that primarily included Africa had the most significant improvements in mortality indicators. This likely reflects improvements in addressing the HIV crisis and the conclusion of various conflicts on the continent, the authors wrote in their report.

Since the 2000s, data has suggested that the male-female longevity gap is narrowing — the new study confirms this and also suggests the gap will continue to narrow, Atance said. The team was able to conclude this by leveraging the existing data to make predictions about patterns in the future. They predicted that the decreases in the life-span gap and the overall increase in life expectancy would continue in 2030.

Despite these trends, women still have longer life expectancies than men, on average. "And, as the projections show, it is possible that this difference, even if it shortens, will be maintained in the future," Atance said.

This is partly because, with age, many males lose the Y chromosomes in a portion of their cells. This chromosome loss is linked to age-related disease and death, and it was cited by the researchers as one possible reason men tend to die younger than women, Atance noted.

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Wrinkles are a telltale sign of aging, but not everyone develops them at the same rate. Some people get their first wrinkles in their early 20s, while others may boast a smooth-faced, youthful look well into old age.

So why do wrinkles form, exactly?

There is no single answer to this question, because human skin is a complex organ and many factors can affect its appearance, Dr. Debra Jaliman, a board-certified dermatologist based in New York and a member of the American Academy of Dermatology, told Live Science.

The skin is composed of multiple sheets of tissue divided into three layers: the epidermis on top, the dermis in the middle, and the hypodermis at the bottom. The dermis is much thicker than the epidermis and the hypodermis, as it contains nerves, blood vessels, sweat glands, hair follicles and proteins that support the skin's overall structure. Specifically, it's mostly made up of the fibrous proteins collagen and elastin, which are suspended in a gooey matrix.

Related: Why does hair turn gray?

Wrinkles start to appear as these structural components of the dermis start to degrade, a process broadly known as skin aging. However, exactly when the age-related creases develop depends on a combination of factors, including a person's genetics and lifestyle, Jaliman said.

In general, as we get older, the number of cells in the skin that produce collagen and elastin, known as fibroblasts, begins to decrease and the remaining fibroblasts become less productive, Dr. Ginni Mansberg, a Sydney-based primary care physician and the medical director of Evidence Skincare, told Live Science by email.

In addition, with age, existing structural proteins in the skin are broken down by enzymes at a higher rate than they were in the past. Aging also causes the top layer of the skin's epidermis, called the stratum corneum, to become thinner. This structural shift makes it more difficult for the skin to retain moisture, and dry skin makes any wrinkles more visible, Mansberg said.

Another aspect of aging that may drive wrinkle formation is cellular senescence — a zombie-like state damaged cells enter when they don't die off when they normally would. Instead of being removed or repaired, more of these zombie cells accumulate in the skin with age, releasing chemicals that can fuel the degradation of skin's structural components.

The overall number of senescent cells in the body increases with age, but that's not the only factor that can lead to this shift. Senescence can be triggered by inflammation and DNA damage, for example, according to a 2021 review published in the journal Ageing Research Reviews.

The rate at which aging drives wrinkle formation depends on additional factors, such as our genetic makeup.

"For example, people with lighter skin tones will find that their skin ages faster than people with darker skin," Jaliman said. That's because the same genes involved in skin color can also influence the skin aging process. This is partly due to genes related to the protective skin pigment melanin, but also genes that contribute to wrinkles through melanin-independent pathways that are not yet fully understood, according to a 2022 review in the journal Scientific Reports.

Unlike genetics, some factors that contribute to wrinkle formation are within our control. For example, excessive sun exposure can accelerate skin aging, because the sun's ultraviolet rays cause inflammation and DNA damage in skin cells, Mansberg said. This can drive not only wrinkle formation but also skin cancer, which is why sunscreen is so important.

Being exposed to air pollution and smoking cigarettes can also fuel the formation of wrinkles by inducing oxidative stress, a state of imbalance between cells' production and elimination of harmful molecules called free radicals, Jaliman noted.

Free radicals are byproducts of the breakdown of oxygen in the body. If they are not counteracted by antioxidants, either produced in the body or ingested, these highly reactive particles can damage the skin's structural components. Therefore, a diet rich in foods that contain high levels of antioxidants, such as fruit and vegetables, may somewhat help to slow the formation of wrinkles, Jaliman said.

However, you are bound to get wrinkles eventually, regardless of what you eat or what cosmetics you use to slow down the aging process.

This article is for informational purposes only and is not meant to offer medical advice.

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When we look at old pictures of our grandparents, we often notice how drastically their facial features changed throughout the years. But it's not just that they gained new wrinkles and their cheeks sag a bit — it's that their noses and ears appear to have gotten visibly bigger over time.

But why do ears and noses seem to grow with age?

These facial features do truly increase in size across the life span, but it's not due to their tissues actually growing, as they would in childhood, for instance. Your ears and nose are fully developed by your 20s, Dr. Alan Matarasso, a clinical professor of surgery at the Zucker School of Medicine in Hempstead, New York, and a former president of the American Society of Plastic Surgeons, told Live Science.

After adolescence, most changes to their shape and size can be attributed to the aging process, he said.

Related: Natural rates of aging are fixed, study suggests

The underlying structures of both the ears and nose are made of cartilage, a strong-yet-flexible connective tissue that also cushions your bones and joints. Cartilage is composed of specialized cells called chondrocytes, which are suspended in a gooey matrix and stabilized by a network of structural proteins called collagen and elastin. As we get older, our bodies become less efficient at producing new collagen and elastin fibers, which leads to the weakening and loosening of the entire cartilage structure, Matarasso said.

Moreover, age affects the structure of tissues that surround the cartilage. For example, once-taut facial tissues begin to relax with age, and combined with the effects of gravity, this causes the earlobes to sag and the tip of the nose to droop. This can contribute to the perception of increased nose and ear size, Matarasso said.   

In addition, the skin on the nose can get heavier due to higher activity of sebum glands, and this additional weight of the skin can pull the nose further forward, Matarasso explained.

The cartilage scaffolding of the ears and nose may also get looser if the bones they're anchored to lose some of their density. This may be caused by osteoporosis or osteopenia, and the risk of these two degenerative bone diseases rises substantially with age. A decrease in muscle tone in and around the ears and nose that support those cartilage structures also change with age, he said.

However, exactly how much one's nose and ear size will change over the years depends on a number of genetic and environmental factors, Matarasso said.

Facial features are generally a highly heritable trait, and the shape of the nose, in particular, appears to be linked to one's genetic makeup, according to a 2018 review published in the journal Frontiers in Genetics. Additionally, age-related nasal changes seem to be far more common in males than in females, but the reason for this is unclear, according to a 2021 study published in the National Journal of Maxillofacial Surgery.

In terms of environmental factors, there's evidence to suggest that exposure to pollution and the sun can accelerate aging processes in the cartilage, Matarasso told Live Science.

The takeaway? Although our noses and ears seem to swell with age, it's nothing to be concerned about.

This article is for informational purposes only and is not meant to offer medical advice.

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Gray hair is an inevitable part of growing older. The chances of hair graying increase 10% to 20% every decade after age 30, the Library of Congress notes. By age 61 to 65, 91% of people will display some level of hair graying, according to Melissa Harris, an associate professor of biology at the University of Alabama at Birmingham.

But why does hair turn gray?

The color in hair, skin and eyes is largely the result of pigments known as melanins. There are two kinds of melanin in hair: eumelanin, which is found in black, brown and blond hair, and pheomelanin, which is in red hair, according to the National Library of Medicine.

Melanin in hair is produced by cells known as melanocytes, which inject the pigment into the shaft of each hair as it grows, according to the University of Alabama at Birmingham. These cells reside at the bases of hair follicles, the structures within the skin that grow hair.

With age, melanocytes decrease in number. Less melanin results in gray hair, while no melanin leads to white hair, according to the Library of Congress.

Related: Why do men have facial hair but women don't?

Melanocytes are generated by a small number of melanocyte stem cells within a niche in the hair follicle. Scientists had thought a long-term group of these cells multiplied continually to produce more of themselves, with some of these cells occasionally migrating down the hair follicle to mature into melanocytes, according to New York University Grossman School of Medicine and NYU Langone Health.

After researchers had monitored melanocyte stem cells in mice for two years, a 2023 study in the journal Nature unexpectedly found that these cells actually migrate up and down the hair follicle over time. As these cells age, they stop these migrations, resulting in fewer melanocytes and graying hair.

Specifically, the Nature study found that during the active phase of hair growth in mice, melanocyte stem cells moved toward the base of the hair follicle to mature into melanocytes. Surprisingly, later during hair growth, melanocytes migrated back up to their original niche in the hair follicle, where they reversed their maturation to become stem cells again. In mice, these cells could perform this yo-yo cycle of migration for at least two years, about the adult lifetime of the rodents.

However, as hair ages, increasing numbers of the cells do not migrate back to their niche. Instead, they get stuck within the hair follicle, incapable of either maturing into melanocytes or continuously proliferating as stem cells, the Nature study found.

Previously, scientists thought gray hairs resulted from melanocyte stem cells depleting in number over time. "The fact that our hairs may contain inactive melanocyte stem cells suggests a target for reactivation for the purposes of repigmentation," Harris told Live Science. "That would be cool."

No other stem cells are currently known to migrate back and forth and switch maturity in this manner. Discovering a way to target this flexible behavior could help treat melanoma, a dangerous form of cancer that may result from melanocyte stem cells, William Lowry, a professor of molecular, cell and developmental biology at the University of California, Los Angeles, told Live Science.

"Zombie cells" that lurk in the body and contribute to age-related diseases make small, strange molecules not seen in normal cells. The exact function of these "cryptic" molecules remains a mystery, but now, scientists think they may know why zombies build them in the first place, The Scientist reported.

Scientifically known as "senescent" cells, zombie cells don't die but stop dividing due to damage or stress. These undead cells secrete molecules that rally the immune system and spark inflammation. Senescent cells aren't all bad — some studies suggest that they help repair damaged tissues — but as the body ages, these zombies start to accumulate and drive inflammation that contributes to age-related diseases like cancer, Alzheimer's and osteoarthritis.

In addition to spewing inflammatory molecules, senescent cells undergo a process called "cryptic transcription," according to The Scientist. This process describes when cells erroneously use supershort snippets of DNA — mere fragments of genes — to build tiny molecules of RNA, DNA's molecular cousin. Normally, cells use RNA as blueprints to build proteins, among other things.

And usually, cells read genes starting at specific locations on the DNA molecule. Think of how a capital letter marks the start of a sentence and a period marks the end — genes have similar start and end points. However, in cryptic transcription, cells may start reading in the middle of a DNA "sentence," and this results in the cell making an unusually short RNA molecule. 

Related: The secrets to extreme longevity may be hiding with nuns... and jellyfish 

The exact function of these cryptic RNAs remains unknown. However, Payel Sen, a molecular biologist at the National Institute on Aging within the National Institutes of Health (NIH), told The Scientist that she suspects that the production of these small molecules may sap the cell's resources, causing it to grow less and less efficient with age. Furthermore, the cell may use the instructions within the RNA to build tiny proteins that somehow interfere with the cell's normal functions.

Learning why zombie cells undergo cryptic transcription and how this impacts aging could be key to scientists' overall understanding of the aging process, as well as their attempts to prolong life span and prevent age-related disease. In a new study, published March 31 in the journal Nature Aging, Sen and her colleagues started to unravel the "why" behind this phenomenon.  

The team identified more than 350 "cryptic sites" in human senescent cells, meaning they identified gene fragments from which the weird RNAs are made. They also identified "epigenetic" changes at these sites that weren't present in young, healthy cells and may explain why cryptic transcription happens. 

Epigenetics literally means "on top of genetics" and refers to molecules that latch onto DNA and affect which genes can be used to make proteins. The epigenetic changes observed in the zombie cells were specifically seen in histones — spool-like proteins in chromosomes that DNA is wound around — and the changes seemed tied to the cells' ages. In the zombie cells, these epigenetic changes exposed parts of the genome to cells' RNA-making machinery, whereas in young cells, the same gene fragments were "hidden" and therefore unexpressed. 

This finding supports the idea that zombie cells undergo cryptic transcription because their ability to control gene expression withers over time, as such epigenetic changes accumulate atop their DNA. Read more in The Scientist.

An American biotech company has launched clinical trials in Colombia to test a new therapy designed to reverse the aging process, and in turn, treat age-related diseases, according to news reports. 

But to steal a sip from this purported fountain of youth, participants in the trial must first fork over $1 million — a fee that seems even more astronomical when you consider that most clinical trials are either free or provide participants with financial compensation, according to a report by OneZero, a Medium publication about tech and science. 

The pricey trial is being run by Libella Gene Therapeutics, a Kansas-based company whose website proclaims that "the future is here." The company announced its intention to test its anti-aging remedies in Cartagena, Colombia, in 2018, and began recruiting for the trials in October of this year. Using a single-gene therapy, Libella aims to "prevent, delay, or even reverse" the general effects of aging, as well as treat diseases that emerge in old age, such as Alzheimer's, according to ClinicalTrials.gov.

In fact, in its own press release, the company boasted, without evidence, that its gene therapy "may be the world's first cure for Alzheimer's disease." The bold claim raises an obvious question: Will the treatment actually work?  

Short answer: No one really knows, but the fact that Libella shipped its operation beyond the reach of the U.S. Food and Drug Administration (FDA) doesn't inspire confidence, experts told OneZero. 

Related: 5 Reasons Not to Fear Getting Older

A cure for aging?  

Unlike anti-aging face creams that soften the superficial signs of aging, the Libella therapy aims to reverse aging from the ground up, so to speak, starting at the level of our genes. Specifically, the gene therapy is intended to lengthen patients' telomeres — structures that cap the tips of chromosomes and prevent the genetic material inside from fraying. Telomeres grow shorter each time a cell divides, and when the structures reach a critical length, cells either stop dividing or perish, according to Stanford Medicine.

The theory goes, if you rebuild the body's shortened telomeres, the process of aging might be thrown in reverse. This is not a new idea. Several studies in mice suggest that using gene therapy to lengthen telomeres can reverse certain signs of aging in the animals. A 2015 study from Stanford prompted similar effects in isolated human cells; the treatment lengthened cells' telomeres by fiddling with a close cousin of DNA, called RNA, which helps cells build proteins. 

The Libella therapy aims to help cells rebuild telomeres by activating a gene in their DNA that would normally be switched "off." The gene, called TERT, contains instructions to build a protein called "telomerase," an enzyme that adds molecules to the end of telomeres and prevents the structures from shortening during cell replication, according to a 2010 report in the journal Biochemistry.     

Libella's lead scientific officer, molecular biologist William Andrews, originally helped identify the human telomerase enzyme at the biotech firm Geron. Later, he licensed a gene therapy based on the finding to Libella, according to OneZero. "I can't say [telomere shortening is] the only cause of aging, but it plays a role in humans," Andrews told the publication.   

Related: 8 Tips for Healthy Aging

Andrews' therapies will soon be put to the test in Colombia, where one 79-year-old will receive the anti-aging treatment in next month, according to OneZero. The anti-aging trial will include four more participants over age 45 and focus on verifying that the treatment is "safe and tolerable," meaning it does not harm patients or cause unacceptable side effects. 

Two more trials will use the same therapy but aim to "prevent, delay, or even reverse the development" of Alzheimer's disease and critical limb ischemia, an age-related condition in which a person's arteries become severely obstructed. Participants in these trials must already be diagnosed with the disorders. 

After treatment, participants in all three trials will remain in the clinic for 10 days for further monitoring, and then return at regular intervals for checkups over the following year.   

Experts are concerned

Libella's gene therapy involves a one-time injection delivered through an IV; the Alzheimer's therapy uses the same formula but doctors inject the product into the patient's spinal fluid. Within the product, a modified virus carries the TERT gene into cells and injects the genetic material into their DNA. The modified viruses cannot transmit diseases to people, but in high enough doses, the germs could provoke a harmful immune response in the patient, according to a 2018 animal study. Libella representatives declined to say how high a dose their clinical trial participants will receive.

"All I can say is, it's a lot," Andrews told OneZero.

Potential side effects aside, the fact that the Libella treatment will be administered beyond the purview of the FDA is telling, according to one expert. Leigh Turner, a bioethicist at the University of Minnesota, told OneZero that "even though the company is based in the United States, they've managed to find a way to evade U.S. federal law by going to a jurisdiction where it's easier to engage in this activity."

The $1 million entry fee is also alarming, Turner said, given that most clinical trials don't charge patients anything to enter. Andrews told OneZero that the fee is justified because it costs the company hundreds of thousands of dollars to make enough product to treat just one person.

The appearance of the trials on ClinicalTrials.gov, an official registry maintained by the National Institutes of Health, does not boost their credibility, she added. The automated database can be easily manipulated and "can basically be used as a marketing platform," she said.

Other stakeholders in the telomere-lengthening business are concerned, too. Michael Fossel, founder and president of the biotech startup Telocyte, told OneZero that his company's own therapy is similar to the Libella treatment — the difference is that Telocyte is seeking approval through the FDA. "We're afraid that something will go wrong [with the Libella trials], whether it's from a safety or efficacy standpoint," he said.

Related: Extending Life: 7 Ways to Live Past 100 

But even in a best case scenario, wherein no patients come to harm, the Libella therapy still might not deliver any notable health benefits. Some research suggests that no link exists between telomere length and aging.

For instance, a study published this year examined more than 261,000 people between age 60 and 70, and found no correlation between participants' telomere lengths and their age-related health outcomes, including their overall cognitive function, muscular integrity and the age of their parents. Long telomeres were associated with a lowered risk of coronary heart disease as compared with short telomeres, but longer telomere length was also linked to a heightened risk of cancer.

"Telomere lengthening may offer little gain in later‐life health status" and lead to an increased risk of cancer, the authors noted.

It remains to be seen whether Libella has truly tapped the fountain of youth, but given the dubious nature of their clinical trials, potential participants may want to exercise caution before relocating to Colombia and shelling out $1 million for a chance to live longer.

• 5 Reasons Aging Is Awesome 
• 7 Ways the Mind and Body Change With Age 
• Genetics by the Numbers: 10 Tantalizing Tales 

Originally published on Live Science. 

Scientists know that our brains shrink with aging, but does less gray matter really matter?

Apparently not, according to a new study of 446 people in Australia.

"We found that, on average, men aged 64 years have smaller brains than men aged 60," said Helen Christensen of the Australian National University. "However, despite this shrinkage, cognitive functions -- like memory, attention and speed of processing -- are unaffected."

The conclusion was based on questionnaires and brain scans.

The study, announced Friday, yielded another surprise. Previous studies had indicated that higher levels of education or continuing intellectual activity could serve as a sort of Pilates for the brain, keeping an aging mind fit.

"Our findings do not support these beliefs," Christensen said. "In the present study, we found no relationship between brain shrinkage and education level."

Older minds do sometimes fail, of course, owing to conditions such as Alzheimer's that scientists are only beginning to understand. Little is known about brain shrinkage, too.

"It is known that the brain shrinks over the course of a person's life, although the exact trajectory is not well understood, and there are huge individual differences," Christensen said.

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Maybe you can't put a price on death, but life certainly has its monetary rewards. And for scientists who can put mice on the road to immortality, the purse just reached $1 million.

The growing prize, offered by the Methuselah Foundation, is designed to stimulate anti-aging research with the ultimate goal of making us all live forever.

A cure for human aging, foundation members figure, will only come if more work is done on rodents.

Contributions rise

The Methuselah Mouse Prize, or M Prize as it is popularly known, offers awards to researchers who make significant advances in extending the lives of lab mice -- on the assumption that the work will lead eventually to extended human life. The organization offers two prizes. The Longevity Prize is for extending the life of a single mouse; the Rejuvenation Prize is for slowing aging in middle-aged mice.

Funds for the M Prize are solicited from individuals, including a growing group that have pledged to contribute $1,000 a year for the next 25 years. The latest contributor is William Haseltine, biotech pioneer of Human Genome Sciences, M Prize officials announced Tuesday.

The fund now stands at $1,006,187. Only $129,329 of that is in the organizations coffers, however, while the rest is in the "committed" column.

"There's nothing to compare with this effort, and it has already contributed significantly to the awareness that regenerative medicine is a near term reality, not an if," Haseltine said in a statement.

The M Prize is modeled loosely after the popular Ansari X Prize that was awarded last year to the first private spacecraft to achieve suborbital flight. But there are significant differences.

A Longevity Prize will awarded whenever the record for the world's oldest mouse is beaten, with the cash doled out being related to the size of the fund at the time. Winning the Rejuvenation Prize requires advancements involving groups of mice.

The first Rejuvination Prize was awarded in December.

Eccentric origins

The non-profit Methuselah Foundation is the brainchild of eccentric researcher Aubrey de Grey, the organization's chairman. De Grey has never done laboratory research in biology. He's a computer scientist at the University of Cambridge who works with a team of geneticists. But a life-long interest in why people grow old has led him to a new specialty: biogerontology, the science of aging.

"If we are to bring about real regenerative therapies that will benefit not just future generations, but those of us who are alive today, we must encourage scientists to work on the problem of aging," de Grey said Tuesday.

De Grey believes there are exactly seven root causes of aging, all of which are reversible. Among the seven deadly, well, things, are cell atrophy, cell death, and unwanted mutations.

Methuselah was a patriarch in the Bible said to reach 969 years of age.

"It's not just better medical care, it's advances [in research] that will allow us to really slow down aging ... People have wanted it forever, and now here it is. Now that we have all these research tools, we can work on it seriously."

-- Steve Austad, Methuselah Foundation science advisor

Old and tired muscles might repair themselves just fine if it weren't for the old blood running through the aging human body, a new study shows.

It's not quite a recipe for the fountain of youth, but the work could lead to methods for healing wounds in the elderly and tackling some diseases.

Stanford neurologist Thomas Rando knew from previous work that aging muscles seemed to have all the ingredients to repair themselves but for some reason did not. In the new work, his team focused on specialized stem cells in muscle tissue.

Stem cells of various kinds are able to make new tissue, so they are key to the body's ability to replenish damaged skin, bone, muscle and more. Satellite muscle stem cells lay dormant when not needed. In young bodies, both of humans and rodents, these cells come alive when muscle is damaged.

In older mice, the study found, satellite stem cells appear normal but don't do their job.

In a test not for the squeamish, Rando and his colleagues fused the blood supplies of younger and older mice. Then they damaged the muscles in the older rodents by zapping spots with dry ice. The muscles healed, thanks to the young blood coursing through their bodies.

In a similar test, the livers of older mice responded better to the infusion of young blood, too. The researchers suspect a similar process might occur with other body cells.

The key to the process appears to involve a protein called delta. When muscles are damaged, satellite muscle cells produce more delta. But in older cells, the delta production doesn't rise. In old mice with young blood, delta again rises in response to injury.

The research demonstrates that "the decline of tissue regenerative potential with age can be reversed through the modulation of systemic factors," the scientists write in the Feb. 17 issue of the journal Nature.

It might seem like the fabled fountain of youth is a sanguine river running through you. But staying forever young is not so simple.

"Basically, the main implications of our findings are not longer life, not a reversal of aging per se, and not really even a delay of the aging process," Rando told LiveScience. "Our findings really speak more the issue of tissue repair, for example in the setting of an acute injury."

Eventually, the research could lead to techniques that would help an older person with a broken bone, a skin wound, or a muscle injury.

"Tissue repair in older people could be enhanced so that it approaches that of younger people," Rando said. The idea is to restore function "not so much to a 'youthful' level but rather back to the point that the person was before the injury."

But there is much work to be done before even that is possible. It's not known what triggers the extra delta production in the muscle. It could be any of the thousands of proteins, lipids, sugars or other molecules in the blood, the researchers caution.

And for now, there's no evidence that the same trigger works for repairing different types of tissues.

"It's as big a fishing expedition as you can possibly imagine," Rando said.

One of the more frustrating things about getting old is growing slower. But a new study finds old people are quicker at one important task: Seeing the big picture.

Subjects looked at bars on a computer screen that appeared and moved either left or right. When the bars were small or varying shades of gray, young people processed the scene more quickly. But when the bars were large and had high contrast -- black and white -- older people consistently outperformed the younger ones by about 30 percent.

The results partly involve differences in vision. But scientists see a deeper meaning.

Young brains are able to find things amid clutter by tuning out noise, the researchers contend. As our brains age, they lose the ability to inhibit information processing in this way, so they can't tune things out so easily. The young brain, when presented with a simple, high-contrast picture, is still in tune-things-out mode and, because there is no hidden object to find, is slower at seeing the big picture.

Here's how the difference might play out when watching a soccer game:

"It might be more difficult for older observers to follow the movements of an individual, but they might be able to better see where the team as a whole is going," explained study co-leader Allison Sekuler of McMaster University in Canada.

"In general older people are not better on most tasks," Sekuler told LiveScience. "But they're better at grasping the big picture instead of focusing in on details."

The study, detailed in the Feb. 3 issue of the journal Neuron, provides insight into how the brain changes with age. Specifically, it reveals something about chemical messengers called neurotransmitters, which are like old-fashioned operators at the phone company, in this case directing communications between brain cells.

"As we get older, it becomes harder to concentrate on one thing and ignore everything else," says McMaster researcher Patrick Bennett, the other study leader. "It takes more effort to tune out distractions. We've seen it in cognition and speech studies, and now we see it in vision. Although we don't know if those are all linked, we think the visual effect is due to changes in the effectiveness of inhibitory neurotransmitters in the brain."

The initial study involved eight young people and eight old people. A follow-up test was done with 54 people to verify the results.

In a separate paper analyzing the study, vision specialists Duje Tadin and Randolph Blake from Vanderbilt University caution that "a large number of outstanding questions" must still be answered to figure out exactly why older people did well at this task. But the results are encouraging, they say.

"We can all hope that this line of research will eventually yield treatment options for some of the problems that await us in old age," Tadin and Blake write.

Sekuler said follow-up studies are being designed to find out how drugs might affect the neurotransmitters. The question, she said: "Can we turn old brains into young ones and young brains into old ones?"