Younger generations may be aging faster than their predecessors, and this may be linked to a rise in early-onset cancers, a new study suggests.

There have been recent increases in the rates of some cancers among adults under 50, including breast, colorectal, kidney and uterine cancers. One 2023 paper suggests that these early-onset cancer diagnoses rose by 25% globally between 1990 and 2019, and scientists are still investigating why.

"The trend of increased cancers at younger ages is very real, and it is not simply because of more efficient diagnosis, or diagnosis at earlier stages," said Dr. Jyoti Nangalia, a hematologist and cancer researcher at the Wellcome Sanger Institute in the U.K. who was not involved in the new study. "It is possible that we are being exposed to new cancer-causing risks or that [our] defences to them are somehow altered," she told Live Science in an email.

The new study, published June 22 in the journal Nature Medicine, suggests that younger generations may have a wider "gap" between their chronological ages and their biological ages — a measurement of how quickly the body's tissues and systems are aging — than older generations do. The greater gap among younger adults seems to be linked with a higher risk of developing cancer early in life.

The new study cannot prove that faster biological aging causes early-onset cancer, but it provides new clues for scientists trying to unpack what might be driving the worrying trend.

"This is really proof-of-concept," study co-author Yin Cao, a molecular and clinical epidemiologist at the Washington University School of Medicine and Siteman Cancer Center, told Live Science.

Concerning trends lurking in dense data

Chronological age is straightforward: It's the number of years that have passed since a person's birth. "Biological age," however, can vary wildly from one person to another. This catch-all term describes a range of metrics, including markers on DNA and in the bloodstream. These are often measured using "aging clocks," which aim to determine if the body is acting much older than its chronological age.

Scientists have increasingly used these summary measures in an attempt to understand why some people are more prone to age-related diseases than others. To check whether there could be a link between biological age and the rise in early cancers, the new study analyzed data from more than 150,000 adults in the UK Biobank, a long-running project that has been tracking the health of about half-a-million U.K. adults since the mid‑2000s.

The participants had provided blood samples, with many already measured for markers used to track biological aging. The study authors plugged these results into PhenoAge, a statistical model that estimates a person's "age gap" at a given chronological age. In essence, this model can compare snapshots of two 40-year-olds — one born in 1950 and the other in 1965 — and see if their blood markers suggest they're the same biological age.

"The traditional approach is really focusing on individual risk factors" for cancer, such as a history of obesity or a high intake of ultraprocessed foods, Cao said. "We are testing whether we can leverage these large biobanks and potentially find some biological imprint as a potential reflection of many exposures that can be linked with cancer risk," she said.

The analysis revealed a concerning pattern: UK Biobank participants born between 1965 and 1974 had a larger age gap than those born between 1950 and 1954 at the same chronological ages. Based on PhenoAge's metrics, the younger cohort had systemic aging levels about 0.23 standard deviations higher than the older cohort — a modest shift toward older-looking biology.

The researchers applied this same approach to about 10,000 participants in the U.S. National Institutes of Health's All of Us Research Program, another large biobank. There, they found a more pronounced pattern: People born between 1990 and 1999 had age gaps about 0.92 standard deviations higher than those born between 1965 and 1969.

Another blood-based aging clock, called the Klemera-Doubal method, showed broadly similar patterns to PhenoAge, albeit slightly weaker ones, the study found.

Real trend or data mirage?

In the UK Biobank cohort, the researchers found that participants with higher age gaps were more likely to develop early-onset solid cancers, meaning cancerous tumors that appear in tissues, rather than "liquid" cancers present in bodily fluids. This link was strongest for lung, gastrointestinal and uterine cancers. This finding was based on the patients' medical records.

When the participants were divided into three groups based on their biological ages, those in the highest group had a roughly 15% higher risk of early-onset solid cancer than those in the lowest group.

To probe deeper, the authors used a different model that estimates biological aging at the level of specific organs and systems, using patterns of proteins in the blood. In almost 20,000 UK Biobank participants, they found that markers suggesting an "older-than-expected" immune system were linked with a higher risk of early-onset lung cancer. Similarly, markers suggesting older-than-expected fat tissue were linked with a higher risk of early-onset colorectal cancer.

Does this mean younger generations are aging faster and that's causing the rise in cancers? Maybe, but maybe not — there are important caveats to the study's findings.

The patterns will need to be confirmed in other datasets and populations, Cao noted. Biological aging tests, including PhenoAge, are also relatively new, and their implications aren't fully understood. While they clearly capture something about health and risk at the population level, at the individual level, different biological age tests can give very different answers for the same person. That raises questions about what any single score really means for individual health.

It may be that the differences PhenoAge uncovered between younger and older people have to do with how the test was originally calibrated, Stephen Burgess, a professor of biostatistics at the University of Cambridge who was not involved in the study, told Live Science in an email. To know if that's the case, one would have to dig deeper into how PhenoAge scores are calculated and see if that might have skewed its assessment of the UK Biobank and All of Us cohorts, he said.

Cao added that, while PhenoAge scores have been tied to mortality risk across a range of adults, the test "requires further validations" when it comes to assessing cancer risk.

As with any observational study using large databases, it is hard to untangle cause and effect, Nangalia added.

"The main issue for this paper is one of correlation versus causality," she said. "Either way, it is useful — with the first, as a potential way of tracking population health and cancer risk, and with the second, as insights into cancer-causing mechanisms."

Cao hopes her team's approach will serve as another useful tool to figure out why more young people are getting cancer. " Hopefully this is just a starting point," Cao said.

Imagine receiving a test result that tells you your body is biologically five years older than your chronological age. You exercise regularly, get good sleep, eat healthy meals and have a happy personal life. What have you been doing wrong? Can this test be trusted?

Dozens of companies are marketing products that promise to reveal a person’s "true" biological age — that is, how well your body is functioning — for a price ranging from around US$30 to over $1,000. These products are based on epigenetic aging clocks, which are research tools that estimate age based on a person's DNA. These clocks are reshaping how scientists study aging and how the public thinks about it.

But while epigenetic clocks are highly effective research tools to study aging at the population level, they aren't designed to make claims about the health of individuals.

We are biobehavioral health scientists who study how early development and environmental factors across the lifespan shape biological aging, influencing health and disease decades later. As researchers who use epigenetic clocks in our work, we have found them to be highly informative tools when studying large numbers of people. But these clocks can provide faulty results at the individual level, and they do not meet the standards required of common medical tests.

What are epigenetic clocks?

Measuring reversible chemical changes to DNA, known as epigenetic marks, can provide information about how your body is aging.

Using DNA obtained from routine blood draws, researchers can measure millions of these epigenetic marks in an individual. Running statistical algorithms on this information can produce a single value that represents that person's epigenetic age, analogous to chronological age.

Epigenetic clocks work because the chemical marks on DNA can shift over time and are influenced by lifestyle, stress and the environment. These changes capture aspects of aging that chronological age alone may not reflect.

In this way, epigenetic clocks help scientists identify the experiences, exposures and behaviors that may accelerate or slow biological aging.

Not for individual health decisions

Why can't epigenetic clocks provide reliable results about biological age for individual people?

First, there are dozens of different types of epigenetic clocks, each designed for a specific purpose. Some are used to predict a person's age, while others are used to predict how fast someone is aging or how many years until they die. These different clocks do not always agree with one another, even when used on the same person.

Second, epigenetic changes are dynamic, making age predictions sensitive to short-term fluctuations in diet, environmental exposures, illness, time of day and other transient factors. As a result, estimated age could vary substantially depending on when someone is tested.

Third, constructing epigenetic clocks is technically challenging, and there is no established gold-standard method for generating clocks across laboratories. For example, testing epigenetic age in saliva versus blood samples can yield substantially different results for the same person. The technologies used to measure epigenetic marks have also evolved over time and will likely continue to improve. As these methods change, the original algorithms designed for specific measurement platforms may not perform the same way.

Fourth, scientists do not universally agree on what aging means, in part because it is a very complex process. Reducing that complexity to a single number, such as an epigenetic age, can be misleading.

Finally, epigenetic clocks are influenced by a person's history of trauma, discrimination and early life adversity. This makes their use at the individual level potentially problematic. On average, marginalized communities tend to show signs of accelerated aging when assessed with epigenetic clocks. If insurance companies began using epigenetic age estimates to set premiums, many people could face higher costs for biological differences shaped by circumstances beyond their control, potentially deepening existing health disparities.

Studying how aging unfolds over time

While epigenetic clocks are not appropriate tools for individual health decisions, this does not mean they lack value.

Researchers have used epigenetic clocks to discover lifestyle habits that can, on average, slow down aging. Some examples include reducing daily calorie intake, exercising regularly, maintaining a healthy diet, getting enough sleep and avoiding smoking.

Epigenetic clocks can also help test new drug therapies aimed at slowing down specific aging processes. For example, researchers have shown that rapamycin, a drug connected to various aging processes, can reduce the epigenetic age of human skin cells. There is also some evidence that a treatment designed to regenerate the thymus may slow or even reverse epigenetic aging after one year of treatment. However, researchers have seen these effects only when looking at groups rather than individuals.

Epigenetic clocks are helping scientists advance scientific research on the aging processes, but they aren't medical tests to measure individual health. In the future, epigenetic measurements may play a useful role in guiding personal health decisions. But for now, epigenetic clocks sold as biological age tests are best used and refined by researchers who are studying populations rather than individual people.

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

Loneliness is something most of us will experience at some point. It is a normal emotion, not a character flaw. But it is also something that can quietly affect how we think and remember, and researchers have long debated whether it might even raise the risk of dementia.

A new study, published in [the journal] Aging and Mental Health, suggests the picture is more complicated than either side of that debate has allowed for.

First, it is worth being clear about what dementia actually is. It is not a single diagnosis but an umbrella term covering a range of conditions — the most familiar being Alzheimer's disease — that cause memory loss, confusion, difficulties with language and a gradual loss of independence.

Cognitive decline, meaning a general slowing or weakening of mental function, is not the same thing. The two terms are often used interchangeably, but they should not be: you can experience cognitive decline without ever developing dementia.

We do not fully understand what causes Alzheimer's. We know that a healthy lifestyle lowers the risk, but it is no guarantee. Plenty of people who have done everything right still develop it. The disease is shaped by genetics, aging and biological factors we are still working to understand.

The new study followed just over 10,000 adults aged between 65 and 94 over six years. All were in good health at the outset, fully independent and free of dementia. Researchers tracked their memory over that period and asked whether loneliness played a role in how it changed.

The answer was nuanced. Loneliness did appear to contribute to memory difficulties — but there was no evidence that it led to dementia itself. That is an important distinction. Memory problems and dementia are not the same thing, and conflating them causes unnecessary alarm. This distinction is crucial, and while the researchers did not conflate the two, this nuance is often lost in interpretation.

Not the whole story

It is also worth noting that loneliness rarely travels alone. Many participants in the study also had diabetes, high blood pressure, depression or low levels of physical activity — all of which affect the brain independently. Diabetes, for instance, can interfere with how the brain processes glucose, the fuel it runs on, which in turn affects memory. Depression has a similar effect. Unpicking loneliness from these other factors is genuinely difficult, and the study does not fully resolve that problem.

One finding that stood out was the high rate of loneliness reported in southern Europe — a region often assumed to have strong social networks. It is a reminder that loneliness is subjective. Feeling lonely is not simply about how many people surround you — it is about how connected you feel to them.

There is also a methodological limitation worth noting. The study treated loneliness as a fixed state, when in reality it shifts — sometimes day to day — across the whole of a life. A single snapshot cannot capture that.

The broader research on loneliness and cognitive decline remains genuinely mixed, and this study does not settle it. What it does suggest, usefully, is that health services might benefit from screening for loneliness alongside routine cognitive testing: treating social connection as part of preventative medicine rather than a soft concern left to one side.

And there is reason for optimism. The brain is resilient. Research suggests that memory difficulties linked to loneliness can improve once that loneliness lifts and that staying socially active may boost cognitive performance more broadly. Loneliness, on its own, is unlikely to be the deciding factor in whether someone develops dementia.

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

Aging may "erase" the epigenetic markers that control gene expression in the brain, and this may snowball to cause unintended consequences, a new mouse study suggests.

Tiny chemical messages attached to our genetic code, called epigenetic markers, change with age in many organs of the human body, leading to the development of ''aging clocks'' that track the loss of these epigenetic tags at specific locations in the genome. However, data from far more locations, particularly the brain, are needed to identify aging processes that could be slowed or reversed.

Now, a new study published March 11 in the journal Cell has mapped these tags across the mouse brain, aggregating data from over 200,000 cells into the most complex epigenetic atlas of aging ever created. The study has revealed how aging affects different areas of the brain and is a stepping stone toward similar studies of the human brain.

Overall, the research paints a picture of genomes that gradually lose grip over their most essential functions over time.

''It shows that aging isn't just wear and tear; it's a loss of control over how genes are regulated,'' said David Sinclair, a geneticist at Harvard University who was not involved in the study.

How do you use your DNA?

Despite the incredible diversity of cell types in the body, every cell, regardless of its role, harbors the same genome.

''The DNA sequence alone is not sufficient to direct how you make a cell,'' said Joseph Ecker, a geneticist at the Salk Institute in San Diego and co-author of the new study. Instead, epigenetic control decides how a cell's genes are expressed. Tight epigenetic control is especially important in the brain, where neurons must last a lifetime and cannot afford to mess up gene expression and alter their physiology.

In the new study, Ecker worked closely with Margarita Behrens, a neuroscientist at the Salk Institute. The researchers examined the brains of mice at three ages: early life (2 months), adulthood (9 months) and old age (18 months). They cut these brains into 18 ultrathin slices. They extracted DNA-packed cellular nuclei from the slices and analyzed key epigenetic signals.

One, called methylation, involves the addition of a small chemical tag called a methyl group to DNA bases. Methylation tends to switch gene expression ''off,'' and Ecker's team saw that their mice's genomes lost their methyl tags with age.

For example, immunity genes were expressed more actively than usual in brain immune cells called microglia in elderly mice because of a drop in methyl groups that silence these genes.

This demethylation happened across the genome and could have had a multiplier effect because it occurred at the sites of transposons, or ''jumping genes.'' These are repetitive DNA sequences that can copy and paste themselves elsewhere in the genome. Repeated gene ''jumping'' can disrupt the expression of many other genes in the process, potentially leading to consequences on brain function. These genetic elements have gone under the radar, according to Sinclair. ''These are genes we've largely overlooked, yet they track remarkably well with aging, suggesting we may be losing control over parts of the genome that are central to brain aging," he said.

The team also analyzed the structure of chromatin, the complex of DNA and protein that organizes our genes into densely packed chromosomes. The team found that increased gene expression in the aging brain altered chromatin structure, adding extra small, tight loops called topologically associated domains (TADs), which are partitions within the genome that organize gene expression. . The team wrote in the study that increased TAD counts could serve as a new signature of aging.

Is epigenetics the key to ''super-aging''?

Genomes' loss of control over their functions could have important consequences for how our bodies work in old age. Ecker and Behrens said the body reacts to increases in jumping genes' activity with brain-cell-killing immune responses that could potentially disrupt delicate neural architecture. They pointed to a recent paper in the journal Nature showing that ''super-agers'' who retain high memory performance in old age have more precursor cells in their brains' memory centers. Ecker and Behrens told Live Science that super-agers may have lower levels of jumping-gene activation, which may, in turn, keep these and other important neurons alive longer.

For these scientists, the current research is a step toward achieving a larger goal: the epigenetic sequencing of the human brain.

Brain quiz: Test your knowledge of the most complex organ in the body

People have long given up on the search for the Fountain of Youth, a mythical spring that could reverse aging. But for some scientists, the hunt has not ended — it's just moved to a different place. These modern-day Ponce de Leóns are investigating whether gut microbes hold the secret to aging well.

The gut microbiome refers to the vast collection of microscopic organisms — bacteria, fungi and viruses — that largely inhabit the colon. These microbes aid in digestion and produce molecules that affect your physiology and psychology. The composition of the microbiome is influenced by a combination of factors, including genetics, diet, the environment, medications and age.

I'm a microbiology professor and author of "Pleased to Meet Me: Genes, Germs and the Curious Forces That Make Us Who We Are," which describes how the gut microbiome contributes to physical and mental health. The discovery that the gut microbiome changes with age has ignited studies to determine whether the Fountain of Youth might be right under your nose, down inside your gut.

You're only as old as your gut microbes

People are most familiar with outward signs of aging, such as wrinkles and graying hair, but there are also microscopic changes taking place deep inside. The gut microbes of older people tend to be less diverse, with more bacteria that promote inflammation and other hallmarks of aging. Changes to the microbiome across age are so consistent that algorithms can reliably predict a person's age based on their microbiome composition.

There are exceptions to this rule. Older adults and supercentenarians who age well have a gut microbiome that looks more like those of younger people. These findings support the idea that maintaining a youthful microbiome fosters healthy aging and longevity.

To confirm that the microbes of youth influence aging, scientists use a technique called fecal microbiota transplantation. This procedure involves obliterating a person's current gut microbiome and replacing it with microbes harvested from a donor's feces. Transplanting microbiota from a young mouse into an elderly mouse reverses age-associated inflammation in the gut, brain and eyes. Conversely, transplanting microbiota from an old mouse into a young one accelerates these aging parameters. Other studies suggest that microbiota from young mice alter metabolism in ways that reduce inflammation that accelerates aging.

The evidence that aging is linked with the microbiome is compelling. However, fecal transplantation is not without risk and is approved only as a last resort to treat severe C. difficile infections. These shortcomings have prompted researchers to search for safer and more refined ways to cultivate an age-friendly microbiome.

Diet and exercise may slow aging

Proper diet and exercise have long been tied to better aging and longevity. One way these lifestyle habits may be beneficial is through their influence on gut microbes.

What people eat — or fail to eat — has a demonstrable effect on their gut microbiomes. The standard American diet, enriched with ultraprocessed foods that are high in sugar, fat and salt and low in nutrients and fiber, depletes microbiome diversity within days. Moving from a non-Western country to the U.S. is also associated with loss of gut microbiome diversity, partly due to dietary changes.

Lack of fiber is a major reason the microbiome adopts a configuration associated with poor aging. Studies in roundworms, mice and rats found that fiber supplements improved overall health and extended lifespan by 20% to 35%. A 2025 study showed that increasing the amount of fiber in your diet is linked to as much as a 37% greater likelihood of healthy aging in women.

Fiber functions as a prebiotic, a nondigestible food component that nourishes the microbiome. Gut bacteria process fiber into compounds such as short-chain fatty acids that promote better aging by improving metabolic, brain and immune function while reducing chronic inflammation. Good sources of prebiotics include most fruits and vegetables, whole grains, legumes, nuts and seeds.

Certain foods, such as yogurt and kefir, or dietary supplements contain probiotics — living microbes that may benefit the gut microbiome. Research on probiotic foods and supplements is mixed, complicated by the variation in bacterial species and dosage in these products. The health benefits that different types of probiotics may confer is still under study.

Physical activity is also linked to a youthful microbiome. Regular exercise can reshape the microbiome of older adults to resemble those seen in younger adults. One study showed that when people ages 50 to 75 underwent 24 weeks of cardiovascular and resistance exercise, their microbiomes became populated by healthier bacteria and their blood had elevated levels of aging-friendly, short-chain fatty acids.

Treatments to manipulate the microbiome

Making healthy lifestyle changes is a noninvasive way to cultivate a youthful microbiome that may slow aging. Scientists are also exploring treatments to tailor the gut microbiome for better health outcomes.

One option may be postbiotics, nonliving but active compounds that probiotic microbes produce. For example, mouse studies have found that short-chain fatty acid supplements can improve age-related heart and lung problems. Similarly, elderly mice given heat-killed bacteria from a human infant saw reduced metabolic dysfunction and inflammation, as well as improved cognitive function.

The microbiome can also be modified with drugs, particularly antibiotics. A low-dose oral antibiotic can trigger gut bacteria to release factors that may promote good health and aging by, for example, strengthening the intestinal barrier or reducing inflammation. One such antibiotic, cephaloridine, extends the lifespan of roundworms and mice by triggering gut bacteria to make colanic acid, an anti-aging compound.

Bacteriophages, or phages, offer yet another potential way to manipulate the microbiome for health. Phages are highly selective viruses that infect and kill specific species of bacteria. Phages have been used to treat severe infections from bacteria resistant to antibiotics. Given that phages can alter the gut microbiome of mice, researchers are studying whether they could be used to eliminate gut bacteria associated with unhealthy aging.

Aging is a natural process that can bring many rewards. Cultivating a healthy microbiome could help people enjoy their golden years more fully.

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

For over a century and a half, life expectancy has steadily increased in the wealthiest countries. Spectacular climbs in longevity have been noted in the 20th Century, correlating with the slump in infectious illnesses and advances in cardiovascular medicine.

However, for some years now, experts have been obsessing over one question: when is this slick mechanism going to run out of steam? In several western countries, gains in life expectancy have become so slight, they are practically non-existent.

Some researchers see this as a sign that we are heading toward a "biological human longevity ceiling" while others estimate that there is still room for improvement.

Looking at national figures alone cannot be a decider. Behind a country’s average life expectancy lies very contrasted, region-specific realities. This is what the findings of our study that was recently published in Nature Communications revealed. Analyzing data collected between 1992 and 2019, it focuses on 450 regions in western Europe bringing together almost 400 million inhabitants.

A European study on an unprecedented scale

To complete our research project, we collected mortality and demographic data from offices for national statistics across 13 western European countries including Spain, Denmark, Portugal and Switzerland.

We began by harmonizing the original data, a task that proved crucial because the regions differed in size, and data offered varying amounts of detail according to each country.

Then we recalculated the annual gain in life expectancy at birth for each region between 1992 and 2019, an indicator, which reflects mortality across all ages. Sophisticated statistical methods allowed us to pick out the main underlying trends, regardless of short-term fluctuations caused by the heatwave in 2003, or virulent, seasonal flu outbreaks between 2014-2015, for instance. 2019 is the cut-off date for our analyses because it is still too early to know whether the coronavirus pandemic has a long term effect on these trends or if it was limited to 2020-2022.

The results we obtained provide us with an unprecedented panorama of regional longevity trajectories across Europe over an almost 30-year period, from which we draw three findings.

First finding: Human longevity has not hit its limits

The first message to emerge from the study is that: the limits of human longevity have still not been reached. If we concentrate on regions that are life expectancy champions (indicated in blue on the chart below), we note that there is no indication of progress decelerating.

These regions continue to demonstrate around a two-and-a-half month gain in life expectancy per year for men, and approximately one-and-a-half month gain in life expectancy for women, at an equivalent rate to those observed in previous decades. In 2019, they include regions in Northern Italy, Switzerland and some Spanish provinces.

For France, Paris, and its surrounding Hauts-de-Seine or Yvelines areas (pertaining to both men and women), featured alongside the Anjou region and areas bordering with Switzerland (only applicable to women). In 2019, life expectancy reached 83 for men, and 87 for women.

In other words, despite recurrent concerns nothing presently indicates that lifespan progression has hit a glass ceiling; prolonging life expectancy remains possible. This is a fundamental result which counters sweeping, alarmist statements: there is room for improvement.

Second finding: regional diversity since the mid 2000s

The picture looks bleaker when considering regions with "lagging" life expectancy rates, indicated in red on the chart. In the 1990s and in the early 2000s, these regions saw rapid gains in life expectancy. Progress was much faster here than anywhere else, leading to a convergence in regional life expectancy across Europe.

This golden age, accumulating a fast rise in life expectancy in Europe and a reduction in regional disparities came to an end towards 2005. In the most challenged regions, whether it be East Germany, Wallonia in Belgium or certain parts of the United Kingdom, life expectancy gains significantly dropped, practically reaching a standstill. In women, no regions in France featured among them, but in men, they included some departments in the Hauts-de-France.

Longevity in Europe is ultimately divided into vanguard regions that continue to progress on one side, and on the other side, lagging regions where the dynamic is running out of steam and is even reversed. We are experiencing a regional discrepancy that contrasts with the catch-up momentum in the 1990s.

Third finding: the decisive role of mortality at ages 55-74

Why such a shift? Beyond age-specific life expectancy, we sought to gain a better understanding of this spectacular change by analyzing how mortality rates have evolved for each age bracket.

We can state that regional divergence can neither be explained by the rise in infantile mortality (which remains very slight) nor by the rise in mortality in the over 75 age range (which continues to decelerate everywhere). It mainly stems from mortality around age 65.

In the 1990s this demonstrated a rapid drop, thanks to access to cardiovascular treatments and changes in risk-taking behavior. But since the 2000s, this upturn has slowed. In some regions, in the last few years, the risk of dying between 55 and 74 years old is on the rise, as shown in the maps below.

This is particularly true for women living in France's Mediterranean coastal regions (indicated in pale pink). It's also the case for most of Germany. However, these intermediary ages are crucial for the life expectancy gain dynamic, because a large number of deaths occur here. Stagnation or a leap in mortality between ages 55 and 74 is enough to break the overall trend.

Even though our study does not allow us to pinpoint the precise causes explaining such preoccupying progress, recent documentation provides us with some leads which should be scientifically tested in the future. Among these are risk-taking behavior, particularly smoking, drinking alcohol and poor nutrition, or a lack of physical exercise, which are all factors that manifest at these ages.

Incidentally, the economic crash in 2008 accentuated regional variations across Europe. Some regions suffered durably seeing the health of their populations compromised, while further growth was recorded in other regions with a concentration of highly qualified employment. These factors remind us that longevity isn’t just about advances in medicine; it can also be explained by social and economic factors.

What's next?

Our report offers a dual message. Yes, it's possible to increase life expectancy. Europe's regional champions are proof of this, as they continue to demonstrate steady growth without showing any signs of plateauing. However, this progress does not apply to everyone. For fifteen years, part of Europe has been lagging behind, largely due to a rise in mortality around 65 years.

Even today, the future of human longevity seems to depend less on the existence of a hypothetical biological ceiling than on our collective ability to reduce gaps in life expectancy. Recent trends lead us to believe that Europe could well end up as a two-tier system, setting apart a minority of areas that keep pushing the boundaries of longevity and a majority of areas where gains dwindle.

In actual fact, the question is not only how far can we extend life expectancy, but which parts of Europe are eligible.

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

Around 50% of a person's lifespan is determined by genetics, a new study suggests, more than doubling previous estimates of the heritability of longevity.

The new research, published Jan. 29 in the journal Science, used a carefully designed mathematical model to reach this conclusion. With the model, the team behind the work could account for external causes of death, such as accidents or infections, eliminating these environmental factors from their heritability estimates.

The heritability of different human traits is usually determined using twin studies, which enable scientists to compare individuals who share either nearly 100% or 50% of their DNA. Identical, or "monozygotic," twins share nearly all of their DNA, while fraternal, or "dizygotic," twins share only 50%.

The researchers looked at the correlation of lifespan and genetics in individual sets of twins, and then compared how well those metrics matched across many sets of twins. "If a trait is very genetically determined, then the correlation in the monozygotic twins will be much higher than the correlation in the dizygotic twins," said study co-author Joris Deelen, a geneticist at Leiden University in the Netherlands.

Previous estimates from such studies have placed the heritability of human lifespan between just 6% and 25%, which suggested genetics have a limited influence on how long people live. Those estimates are substantially lower than those for other complex human traits, such as psychiatric disorders, or the heritability of life span observed in other mammals, which are both typically placed at around 50%.

However, observations of long-lived families and the genetic risk associated with age-related diseases, such as heart disease, suggested to Deelen and colleagues that longevity likely has a far larger genetic contribution than scientists once thought.

A different way of looking at lifespan

The difficulty lies in separating drivers of death with strong genetic components — such as the risk of age-related diseases or the speed of physical decline — from external factors, such as accidents and infections. Deelen did note that the divide between these genetic and external factors is not always clear cut; but in the case of infections, for instance, they focused on diseases that are generally very treatable, such as scarlet fever.

"Previously, when we studied lifespan and predictors, we tended to use all-cause mortality, where we're just looking at what age people died and not really considering what the causes are — cause of death is often missing [from those records]," said Luke Pilling, a geneticist at the University of Exeter in the U.K. who wasn't involved in the work.

Deelen's team — which included geneticists, physicians and statisticians — designed a model to mathematically account for these extrinsic contributors, even for cases when the causes of death were not available. The team fed data from twin cohorts in Sweden, Denmark and the U.S. into the model, and each returned an estimated lifespan heritability of around 50%. The datasets collectively included people born between 1870 and 1935.

"They also looked at this study of Swedish twins born between 1900 and 1935, and that allowed them to do a really interesting analysis, stratified by decade," Pilling added. "Because the twins born in 1900 experienced a very different exposure to infection to the twins born in the 1930s, extrinsic mortality was decreasing over that period."

Classical estimates of lifespan heritability would likely show an increase in heritability over that time frame, as genetic factors began to dominate the calculations. That would support the idea that environmental causes of death had influenced previous estimates. In contrast, the new model gives a consistent estimate for heritability, independent of those external factors.

Like all models, though, the new approach has limitations. "The best scenario would be to have a cohort where you know the actual cause of death and can classify it directly as intrinsic or extrinsic so you don't need to model it in," Deelen said. "But that data just doesn't exist."

In addition, the model has so far been tested primarily on people of Northern European descent, owing to a similar lack of data from elsewhere.

"It's a big question," Deelen said. "Is this heritability something specific for Nordic countries, or is it similar in other parts of the world?"

Modern recordkeeping may enable scientists to determine the answer in the future. But for now, what could these results mean for medicine?

Understanding the genetic markers that influence how long people live — and how long they remain healthy during that lifespan — has important consequences for the future of geriatric medicine, Pilling said, particularly as more and more countries deal with aging populations.

"If we understand the biological mechanisms that cause people to live longer and healthier, we can perhaps design interventions to promote those pathways and to promote health span — the period of life spent in good health," Pilling said. "I will certainly be using this in my research."

Crucially, though, the 50% heritability estimate neither guarantees you a long life or dooms you to a short one, Deelen said.

"What it shows is that you have a certain propensity to become long-lived which is in your genes, and the rest is based on what you do and where you live," he clarified. "Environment is still super important, and people should try to optimize their lifestyle as much as they can."

The earliest signs of cognitive decline often appear not in a formal diagnosis, but in the small clues buried in health care providers' notes.

A new study published Jan. 7 in the journal npj Digital Medicine suggests artificial intelligence (AI) can help identify these early signals — such as issues with memory and thinking or changes in behavior — by scanning doctor's notes for patterns of concern. These might include recurring mentions of cognitive changes or confusion from the patient, or worries mentioned by family members attending the appointment with their loved one.

Rather than diagnosing cognitive decline or dementia directly, the system aims to flag patients whose records suggest they may need closer attention.

"The goal is not to replace clinical judgment but to function as a screening aid," study co-author Dr. Lidia Moura, an associate professor of neurology at Massachusetts General Hospital, told Live Science. By highlighting such patients, she said, the system could help clinicians decide which people to follow up with, especially in settings where specialists are in short supply.

Whether that kind of screening actually helps patients depends on how it is used, said Julia Adler-Milstein, a health informatician at the University of California, San Francisco who was not involved in the study. "If the flags are accurate, go to the right person on the care team and are actionable, meaning they lead to a clear next step, then yes, they can be easily integrated into the clinical workflow," she told Live Science in an email.

A team of AI agents, not just one

To build their new AI system, the researchers used what they call an "agentic" approach. This term refers to a coordinated set of AI programs — five, in this case — that each have a specific role and review one another's work. Together, these collaborating agents iteratively refined how the system interpreted clinical notes without human input.

The researchers built the system on Meta's Llama 3.1 and gave it three years of doctors' notes to study, including clinic visits, progress notes and discharge summaries. These came from a hospital registry and had already been reviewed by clinicians who noted whether cognitive concerns were present in a given patient's chart.

The team first showed the AI a balanced set of patient notes, half with documented cognitive concerns and half without, and let it learn from its mistakes as it tried to match how clinicians had labeled those records. By the end of that process, the system agreed with the clinicians about 91% of the time.

The finalized system was then tested on a separate subset of data that it hadn't seen before, but that was pulled from the same three-year dataset. The second dataset was meant to reflect real-world care, so only about one-third of the records were labelled by clinicians as showing cognitive concern.

In that test, the system's sensitivity fell to about 62%, meaning it missed nearly four in ten cases clinicians had marked as positive for signs of cognitive decline.

At first glance, the drop in accuracy looked like failure — until the researchers reexamined the medical records that the AI and human reviewers had classified differently.

Clinical experts reviewed these instances by rereading the medical records themselves, and did so without knowing whether the classification had come from clinicians or the AI. In 44% of cases, these reviewers ultimately sided with the system's assessment rather than the original chart review conducted by a doctor.

"That was one of the more surprising findings," said study co-author Hossein Estiri, an associate professor of neurology at Massachusetts General Hospital.

In many of those cases, he said, the AI applied clinical definitions more conservatively than doctors did, declining to flag concerns when notes didn't directly describe memory problems, confusion or other changes in how the patient was thinking — even if a diagnosis of cognitive decline was listed elsewhere in the record. The AI was trained to prioritize mentions of potential cognitive concerns, essentially, which doctors might not always flag as important in the moment.

The results highlight the limits of manual chart review by doctors, Moura said. "When the signals are obvious, everyone sees them," she said. "When they're subtle, that's where humans and machines can diverge."

Karin Verspoor, a researcher in AI and health technologies at RMIT University who was not involved in the study, said the system was evaluated on a carefully curated, clinician-reviewed set of doctors' notes. But because the data came from a single hospital network, she cautioned that its accuracy may not translate to settings where documentation practices differ.

The system's vision is limited by the quality of the notes it reads, she said, and that constraint that can be addressed only through optimizing the system across diverse clinical settings, she argued.

Estiri explained that, for now, the system is intended to run quietly in the background of routine doctors' visits, surfacing potential concerns alongside an explanation of how it reached them. That said, it is not yet being used in clinical practice.

"The idea is not that doctors are sitting there using AI tools," he said, "but that the system provides insight — what we're seeing, and why — as part of the clinical record itself."

A new mRNA treatment rejuvenates key immune cells in the body, which could help them fight off infections and cancer, a mouse study suggests.

T cells help train other immune cells to fight off disease. But as the body ages, the activity of these T cells declines, and they become less responsive to threats. Additionally, the thymus gland — where T cells mature — begins to shrink with age. These impacts of aging may explain why vaccines and immune-boosting cancer therapies don't work as well in older adults as they do in younger adults, Nature News reported.

In the new study, published Dec. 17 in the journal Nature, scientists tried to counteract these age-driven changes using messenger RNA (mRNA).

Among other roles, mRNA relays instructions from DNA to cells' protein-building organelles, serving as a template from which new proteins are made. The team behind the new study studied T cells in aging mice, pinpointing three proteins that seemed to decline with age, contributing to the aging process. They then generated mRNA for those three proteins, encased them in tiny bubbles of fat, and injected them into middle-aged mice, which were around 16 months old.

These mRNA-filled bubbles traveled through the bloodstream to the liver, where they accumulated. Most T cells are in the bloodstream, and because the liver filters blood, T cells were likely cycled through the liver, where they were exposed to this waiting supply of mRNA.

Mice treated with the mRNA made more T cells than mice that were left untreated. The treated mice's T cells also responded better to vaccination and to cancer immunotherapy, the experiments suggested.

The benefits of the treatment, which was given to the mice twice a week, disappeared quickly when the scientists paused the injections. That's not necessarily surprising, given that mRNA molecules degrade very quickly in the body, whether they were originally made by cells or produced in a lab.

"The transient nature of mRNA delivery necessitates repeated administrations to sustain therapeutic effects," the study authors wrote in the paper. That said, "the long-term consequences of continuous exposure to these factors, especially in aged individuals should be analysed through extensive long-term safety studies."

In short, more research is needed to see if the same approach could work in humans. You can read more about the study in Nature News.

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.

"Zombified" cells in blood vessels may play a key role in the development of metabolic diseases, like diabetes, with age, a new study finds. And slaying these zombie cells could be a promising approach for future treatments.

Cells usually become senescent — a state in which they permanently stop dividing but linger in the body — as a stress response. These senescent cells may have some useful functions; for example, some play a key role in wound healing. But senescent cells are also known to contribute to age-related diseases, as more and more build up in the body over time.

In previous research with mice, scientists found that targeting senescent cells with drugs can alleviate various signs of aging and extend the animals' healthy life span, lead study author Dr. Mayasoshi Suda, an assistant professor at Cedars-Sinai Medical Center in Los Angeles, told Live Science.

In the new study, published Thursday (Nov. 20) in the journal Cell Metabolism, the team focused on endothelial cells, meaning the cells that line blood vessels, and identified a specific case in which senescence can be harmful to the metabolism. The study also hints at a strategy for treating not only age-related metabolic issues but many aspects of aging, an expert told Live Science.

"By finding a unifying target, such as blood vessels, you open up the possibility that you might be able to, at the same time, target very different aspects of aging," said Dr. Christina Aguayo-Mazzucato, an assistant professor of medicine at Harvard Medical School who was not involved in the study.

Identifying harmful senescent cells

Senescent cells are increasingly recognized as contributors to the development of age-related metabolic diseases. But researchers are still trying to identify specific cells in which senescence is harmful, as opposed to beneficial.

In this study, researchers chose to focus on blood vessel cells, which are critical for the function of most organs and have been shown to help control metabolism in many tissues, study co-author Dr. Nicolas Musi, a professor of medicine at Cedars-Sinai Medical Center, told Live Science.

To identify whether these cells were key drivers of metabolic disorders, the researchers fed one set of lab mice a high-fat diet to raise their body weights and induce senescence in their cells; they then removed their senescent endothelial cells for further study. In addition, the team exposed a different set of endothelial cells to radiation to induce senescence and then transplanted those cells into lean lab mice with normal metabolisms.

Removing senescent endothelial cells from the obese mice was associated with reduced fat mass, improved blood sugar levels and an overall reduction of metabolic dysfunction. Conversely, transplanting senescent cells into lean mice was associated with higher blood sugar levels and insulin resistance.

"When these cells go into this dormant state of senescence, they start producing inflammatory substances that are called Senescence-Associated Secretory Phenotype (SASP)," Musi said. This mechanism helps explain why removing senescent cells was associated with an improved metabolic rate. Cells usually take nutrients from the bloodstream, such as fat and glucose, to create the energy they need to function properly. But when they encounter the onslaught of inflammatory molecules from SASP cells, that process gets derailed, he explained.

"Cellular metabolism gets altered, and that translates into abnormal tissue and then abnormal whole-body metabolism," Musi told Live Science.

'Senolytics' are potential treatments

In a second phase of the study, the researchers treated both groups of mice with fisetin, a drug that the team previously found could eliminate senescent cells. This type of drug is known as a senolytic. In both groups, treatment with fisetin was associated with fewer senescent blood-vessel cells and improved glucose tolerance.

The researchers also tested the drug on tissue samples from six adults with obesity who were in their 40s and 50s. They observed a similar decline in senescent blood vessel cells in the treated tissue.

Aguayo-Mazzucato thinks this study could pave the way for new treatments targeting senescent cells in the cardiovascular system. "Metabolic dysfunction is a whole-body problem. You have nutrient utilization alterations in a lot of tissues," she said. Because senescent vascular cells are present throughout the entire body, targeting them in different organs could help doctors address a range of diseases, she added.

"Rather than say we're going to treat cancer or we're going to treat diabetes, Alzheimer's [or] Parkinson's as defined entities, the idea is saying they're all age-related and there are pathways that are common to all age-related diseases," Aguayo-Mazzucato said.

Future research should include clinical studies that investigate whether senescence has the same effects in human blood vessels that were observed in lab mice, Suda said.

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

A new study helps reveal why some vaccines, including those for COVID-19 and influenza, are less effective in older adults than they are in younger people — and it may fundamentally shift our understanding of aging.

Traditionally, scientists have attributed the reduced vaccine response seen in older adults to a decline in the immune system with age. Many have pointed to persistent, low-grade immune activation — a process dubbed "inflammaging" — as one driver of this decline.

But a new study that compared the immune systems of older and younger adults found no consistent increases in biological markers of inflammation with age. Instead, aging appears to reprogram T cells — important immune cells that help train a type of white blood cell, called B cells, to produce antibodies in response to viruses and vaccines.

The findings, published Oct. 29 in the journal Nature, suggest that inflammation may not be as fundamental to the aging process as scientists previously thought.

"We think inflammation is driven by something independent from just the age of a person," Claire Gustafson, an assistant investigator at the Allen Institute for Immunology and one of the lead authors of the study, said in a statement.

Alan Cohen, an associate professor of environmental health sciences at Columbia University who studies aging and inflammation, said the new findings support a more nuanced view of "inflammaging."

The idea that inflammation increases with age "may be true on average in industrialized populations," said Cohen, who was not involved in the work. "But it won't be true for everyone, and it won't be true in every population," he told Live Science.

Cohen cautioned that the participants in the new study were drawn entirely from Palo Alto, California, and Seattle — both highly industrialized areas. Having found significant differences in inflammation between adult populations from Italy, Singapore, Bolivia and Malaysia, he said such findings may not hold up across different environments.

"I certainly wouldn't take this as, 'Oh look, now they've shown definitively there's no change in inflammation with age,'" Cohen said. "I would take it more as, here's an example of a population that doesn't appear to be doing the same things that we have typically expected."

T cell changes are not driven by inflammation

In the interest of improving older adults' responses to vaccines, Gustafson and her colleagues looked at how T cells change with age.

First, they compared younger adults (ages 25 to 35) with an older group (ages 55 to 65, or people at what the researchers call the "cusp of aging.") For two years, the researchers followed 96 healthy volunteers in these age groups, collecting blood samples from each participant eight to 10 times and monitoring their immune systems before and after their annual flu vaccinations. Then, they expanded their research to include a second group of 234 adults ranging in age from 40 to over 90.

To examine the immune system across these groups, the team used single-cell RNA sequencing, which enabled them to look at a type of genetic material called RNA inside each immune cell. RNA reflects which proteins a cell is making at a given moment. The team also used high-dimensional plasma proteomics, which maps the proteins circulating in blood, and spectral flow cytometry,which identifies and counts immune cells by their molecular "fingerprints."

The researchers spotted distinct differences in memory T cells — immune cells that "remember" past infections and help the body respond faster the next time a pathogen shows up.

In older adults, increasing numbers of memory T cells shift into a state that changes how they respond to threats — by changing their interaction with B cells. When memory T cells are not working as they should, B cells become less effective at producing antibodies in response to infections or vaccines, the study found. Meanwhile, the memory T cells of young adults were adept at responding quickly and ramping up the expected antibody response.

These immune changes seem to happen independently of inflammation and of infections with latent viruses, which stay in the body after the initial infection and may go dormant, not causing any overt symptoms. Infections with these viruses, such as cytomegalovirus (CMV), are often blamed for weakening the immune system with age. However, the study found that people under 65 who had experienced a CMV infection at some point in their life did not have signs of faster immune aging or increased levels of inflammatory proteins.

Cohen remains cautious about the study authors' conclusions, noting that the most significant changes in the immune system tend to occur after age 65. "If you don't see a change in inflammation between 25 to 35 versus 55 to 65, is that really because inflammation isn't changing with age, or just because they didn't get old enough to see something?" he questioned.

The researchers said these findings could eventually help scientists design vaccines that compensate for age-related immune changes, thus better protecting older adults. They also think the results could be useful for designing treatments that restore immune function in old age.

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

If you want to know your chronological age, simply count the candles on your next birthday cake. Calculating your biological age, though, is a little more complicated.

Chronological age is the number of years between your birth and now; it's purely time-based. Biological age, on the other hand, describes the progressive breakdown of an individual's physiological and molecular systems over time; it's a measure of how "aged" the body is. The calculation aims to answer the question of how well your systems, organs and cells are working compared to an average, healthy baseline.

"Biological age is notoriously hard to define because it's very much a conceptual notion," said Eric Sun, an assistant professor of biomedical engineering at MIT, where he will launch a new lab starting in 2026. The concept requires you to think less about pure chronology and more about how your body is performing over time, and what your risks and vulnerabilities for various diseases might be in the future, he said.

Scientists have devised a number of "clocks" aimed at determining people's biological ages. Here's how they work and why they might be useful.

Neither Henderson nor Sun thinks modern aging clocks are ready for clinical use. There's still too much noise in the data, too much potential for drawing faulty conclusions about what drives aging and what's just associated with it, Henderson told Live Science. If aging clocks were used to help doctors determine what treatment course a patient needs, false positives could lead to unnecessary medical intervention.

Sun told Live Science he believes future clocks that get adapted for patients will bear similarities to the fourth-generation causal clocks that already exist.

"It won't just be biomarkers for how your entire body or even individual systems are aging," he said, "but multiple biomarkers for different functions within an organ."

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

A new study suggests that human egg cells may be protected against certain age-driven changes seen across the rest of the body.

The work, published Aug. 6 in the journal Science Advances, didn't explore how that protection works, but it did highlight a stark difference between the mitochondria — cellular powerhouses — found in adult women's blood and saliva and those carried in their eggs. Mitochondria carry their own special DNA, and as the body ages, that DNA mutates. But there seems to be an exception to this rule within the mitochondria in human egg cells.

Mutations in mitochondrial DNA (mtDNA) aren't always harmful, but in some cases, they can cause diseases that affect the body's ability to make and use energy. These conditions can be life-threatening. There are no approved cures, and treatments typically focus on easing symptoms rather than on correcting the underlying issue. As such, it's important to understand whether the mitochondria in eggs pick up more mutations as they age, as that could raise the risk of such diseases in children.

This could potentially be a factor to consider in family planning. For instance, if the risk of disease-causing mitochondrial mutations were extremely high in older eggs, it might be an argument for freezing one's eggs at younger ages, study co-author Barbara Arbeithuber, a research group leader at Johannes Kepler University Linz in Austria, told Live Science in an email.

Still, mitochondria are not the only factor to consider in egg quality as it's known that egg cells decline in other ways as they age. And importantly, this new study "does not directly tell us anything on reproductive interventions, as those were not the focus of our work," Arbeithuber said.

"It is premature to apply these findings to clinical practice," said study co-author Kateryna Makova, a professor of biology at Penn State. "Our results should be replicated in a larger number of women and validated in other human populations," Makova told Live Science in an email.

Related: 8-year-old with rare, fatal disease shows dramatic improvement on experimental treatment

Eggs partly "protected" from aging

Studies suggest that, at older ages, egg cells do pick up new mutations in their chromosomes, the DNA found in the cells' nucleus. There's evidence that older oocytes, or egg cells, are less able to repair DNA damage than younger oocytes are. Additionally, pregnancies that occur at maternal ages of 35 and older are associated with a higher rate of chromosomal abnormalities than pregnancies at younger ages. That's partly due to changes in the eggs that make them more likely to have an abnormal number of chromosomes when they reach maturity.

(Notably, advanced paternal age also drives up the rate of genetic abnormalities in offspring, so sperm cells — not just eggs — also contribute to that mutational burden.)

But while the effect of aging on chromosomal DNA in eggs and sperm is fairly well studied, scientists' understanding of what happens to the DNA in an egg's mitochondria as it ages is less clear.

"For human oocytes, previous reports were controversial," Arbeithuber said. The methods used to analyze DNA in those prior studies weren't accurate enough to pin down the true rate of mitochondrial mutations. Arbeithuber and her colleagues instead used an approach called duplex sequencing, which has a much lower error rate.

For the study, they recruited 22 women ages 20 to 42 who were undergoing in vitro fertilization (IVF). For each participant, they analyzed blood and saliva samples, as well as one to five oocytes. In total, they assessed 80 egg cells across the 22 women.

Across all of the blood, spit and egg samples, the eggs' mitochondria had 17- to 24-fold fewer mutations than those in the blood and saliva. And that comparatively low rate of mutations stayed steady. The number of mutations seen in blood increased the most across the age groups, followed by saliva, and there was no statistically significant increase in the number of mutations in the eggs.

When the team zoomed in on the few mutations that did appear in the eggs, they found that they were less likely to impact DNA previously tied to diseases than the mutations seen in blood and saliva.

"The good news is that, unlike what happens in other tissues of the body such as blood or saliva … human oocytes do not accumulate more mutations as women age, at least between 20 and 42," Filippo Zambelli, a lead consultant at the reproductive medicine service TRT Consultancy in Barcelona, Spain, told the Science Media Centre. "This suggests that mtDNA in oocytes is protected against aging and its potential negative impact on cellular function," said Zambelli, who was not involved in the research.

"Overall, this study is reassuring for people trying to conceive children at later ages, because, although chromosomal abnormalities increase with maternal age, at least they should not expect a higher level of mutations in their mtDNA," he said. Notably, though, this study included only 22 people, so the results bear confirmation in larger studies, he added.

Next steps

Prior to the new study, the same researchers had investigated mitochondrial mutations in mice and monkeys. In mice, they observed an increase in mtDNA mutations with age in both egg cells and other body tissues, like muscle. In monkeys, they found that mutations increased in eggs and other tissues until the primates reached about 9 years old — equivalent to roughly 27 years old in human years. At that point, the egg mutation rate plateaued while other body parts accumulated more and more DNA changes.

"It is possible that this is also the case in humans," Arbeithuber suggested, meaning it may be that eggs accumulate some mitochondrial mutations in earlier life and then stop at a certain point.

Their new study was somewhat limited in that they obtained eggs from people undergoing IVF, so "we were restricted by the age of individuals who consult such a clinic," she added. In the future, it could be interesting to analyze eggs from younger age groups and across generations, from mothers to children, she said.

At this point, the researchers don't know how mitochondrial DNA in eggs remains preserved over time while other tissues mutate. "This is an open question," Arbeithuber said. In their paper, the team proposed that there may be a process that helps to eliminate harmful mutations from the oocyte DNA, but more research will be needed to confirm this idea.

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

Aging is the process of getting older. In biology, aging refers to how, over time, the cells in our bodies wear out or get damaged. They no longer work as well as they used to.

Some visible signs of aging include wrinkled skin; gray or white hair; and dark patches, called age spots, on the hands and face. But aging affects every part of the body, including the internal parts we can't see from the outside. Organ and tissue function, physical abilities and mental capacity all change as we age.

Some researchers say that aging starts even before birth, when an embryo's first cells form in the womb. In children and young people, damaged or dying cells are usually replaced pretty quickly. However, as people get older, it takes longer for their bodies to fix or replace those dysfunctional cells. The speed of aging and how it changes the body and brain can vary widely from person to person.

5 fast facts about aging

• As some men age, their eyebrows grow longer and bushier. Older men may also start growing long hairs on their ears and in their noses. This is because certain hormones in men increase with age, and stimulate unusual hair growth.
• Some people are "super-agers," which means their brains age more slowly than average. The brains of super-agers in their 80s resemble those of people who are decades younger.
• The world's oldest-known person was thought to be Jeanne Calment, a French woman who lived to be 122 years, 164 days old. But this is controversial, as some people think Calment's age records were fake.
• People often "shrink" as they get older. Between the ages of 30 and 70, it is normal to lose about 1 to 2 inches of height.
• Scientists still aren't sure how long a human could live under ideal circumstances. Some say 150 years old is the absolute limit, while others think it's likely even higher.

Everything you need to know about aging

Aging pictures

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Scientists can now judge how fast your whole body is aging based on a single snapshot of your brain, researchers claim in a new study.

The scientists, who published their findings July 1 in the journal Nature Aging, have developed a benchmark of biological aging based on brain MRIs. The team says the tool can predict an individual's future risk of cognitive impairment and dementia, chronic conditions like heart disease, physical frailty and early death.

"Our paper presents a new way of measuring how fast a person is aging at any given moment using the information available in a single brain MRI," said first author Ahmad Hariri, a professor of psychology and neuroscience at Duke University. "Faster aging increases our risk for many diseases including diabetes, heart disease, stroke, and dementia," he told Live Science in an email.

Hariri and colleagues used data from the Dunedin Study, which followed 1,037 people from Dunedin, New Zealand, from birth to middle age. These participants, born in 1972 and 1973, periodically received 19 assessments to check the function of their heart, brain, liver, kidneys and more.

To develop their tool, the team analyzed the brain MRIs taken from this cohort at age 45 and ran the data about brain structure — the volume and thickness of various brain regions and the ratio of white to gray matter — through a machine learning algorithm.

They compared the processed brain data to other data collected from the participants at the same time, such as tests of physical and cognitive decline, subjective health statuses, and signs of facial aging, like wrinkles. They asserted that bigger declines in those areas were tied to a faster pace of aging, overall, and then correlated features of the brain data to those metrics. They called their resulting model "Dunedin Pace of Aging Calculated from Neuroimaging," or DunedinPACNI.

Related: Epigenetics linked to the maximum life spans of mammals

Previously, the team created a similar tool called Dunedin Pace of Aging Calculated from the Epigenome (DunedinPACE). That metric looked at methylation — chemical tags that attach to DNA molecules — in blood samples to estimate people's pace of aging. Methylation is a type of "epigenetic change," meaning it alters genes activity without changing DNA's underlying code.

"[DunedinPACE] has been widely adopted by studies with available epigenetic data," Hariri said. "DunedinPACNI now allows studies without epigenetic data but with brain MRI to measure accelerated aging." The researchers directly compared DunedinPACNI to DunedinPACE, finding that they generated similar results.

To see if their new tool could be useful beyond Dunedin, the team used it to estimate the pace of aging using MRIs in other datasets: 42,000 MRIs from the U.K. Biobank; over 1,700 MRIs from the Alzheimer’s Disease Neuroimaging Initiative (ADNI); and 369 from the BrainLat set, which includes data from five South American countries.

"Making sure our findings generalize across datasets and demographic groups is a big priority for brain imaging research," study co-author Ethan Whitman, a doctoral student at Duke, told Live Science in an email.

They found that DunedinPACNI could also estimate the rate of aging in these other cohorts, and that it did so as accurately as other measures used in the past.

The U.K. Biobank and ADNI also include measures of specific health effects of aging, including tests of physical frailty, like grip strength and walking speed, as well as rates of heart attack, stroke, chronic obstructive pulmonary disease (COPD) and death from all causes within the cohorts. Using these additional measures, the team was able to link faster aging rates, as determined with DunedinPACNI, with increased risks of heart attack, stroke, COPD and death.

Hariri believes DunedinPACNI has the potential to be widely adopted because the type of MRIs it uses are routinely collected. Now it's a matter of crunching the data and determining standards of what reflects "healthy" and "poor" aging, he said.

"The fact that it worked well with the BrainLat data is a big win for the investigators because it supports the generalizability of the model,” said Dr. Dan Henderson, a primary care physician at Brigham and Women’s Hospital and instructor of medicine at Harvard Medical School who was not involved with the study. "It would still be worth looking at other data sets where genetic and other factors might be different in important ways," he added.

Henderson said he could see DunedinPACNI eventually being used in place of conventional health measures to fine-tune medical interventions for individual patients. Whitman also sees broad implications for the research. Assuming it's validated for use by doctors, he thinks it could help patients prepare for age-related health issues before they manifest.

"We were really amazed that our tool was able to predict disease risk before symptoms had started," Whitman told Live Science in an email. "We think this is a great example of why it's important to study aging in general, but especially in younger, healthy people. If you only study people after they have gotten sick, you're missing a lot of the story."

Brain quiz: Test your knowledge of the most complex organ in the body

Psilocybin, the main psychoactive ingredient in magic mushrooms, extends the lifespan of human cells, a lab study suggests. Researchers also found that the psychedelic compound slows certain hallmarks of aging in older mice while improving their fur quality.

The findings, published July 8 in the journal npj Aging, provide the first experimental evidence of psilocybin's potential anti-aging properties.

"The study provides a unique look at the potential of psychedelics to promote healthy aging and provides a provocative mechanism to explain how they do it," Scott Thompson, a professor in the University of Colorado Department of Psychiatry who was not involved in the research, told Live Science in an email.

However, "much additional work will be required to take these findings forward in a way that will reveal whether or not the findings are applicable and adaptable for human health," Thompson said.

Recently, studies have explored psilocybin's therapeutic potential for treating various conditions, such as anxiety, depression and neurodegenerative disorders like Alzheimer's disease. Some of this research has led to clinical trials with promising results. But researchers haven't yet pinned down exactly how the psychedelic achieves its benefits.

One theory, dubbed the "psilocybin-telomere hypothesis," proposes that psilocybin preserves the length of telomeres, the protective caps of repetitive DNA sequences located at the ends of chromosomes. Researchers have long understood that telomeres shorten with age, and the rate of that shortening correlates to the rate of aging.

Related: 'Magic mushroom' compound creates a hyper-connected brain to treat depression

So if psilocybin protects telomere length, could it also delay aging?

To find out, study senior author Dr. Louise Hecker, an associate professor at Baylor College of Medicine in Houston, and colleagues administered different doses of psilocin, which psilocybin gets broken down into in the body, to isolated human lung and skin cells. The team found that the psilocin extended the lifespans of the cells by up to 57%, depending on the dose given.

The psilocin also preserved the cells' telomere length and reduced levels of oxidative stress, or the buildup of reactive molecules. Simultaneously, it led to higher levels of Sirt1, a protein associated with longevity.

In short, the psilocin made the cells appear like younger cells, Hecker told Live Science. Hecker's research involves looking at the impacts of aging on the body, and everything she knew to test for "just worked" she said. "I was floored by the data."

The team then went on to study the effects of psilocybin on approximately 19-month-old female mice — which, in human years, would be in their early 60s. The mice received monthly doses of psilocybin for 10 months. At the end of that period, 80% of the treated mice were still alive, compared with only 50% of an untreated group. The treated mice also displayed hair growth where they'd previously had bald spots, and their once-white hair grew back brown.

"It's exciting that we can give this intervention in late life and have such a dramatic impact," Hecker said.

Psychedelics, in general, are known to alter the workings of the immune system and the body's stress resilience, both of which can affect organ health, Thompson said. "What is new in this study is the provocative suggestion that changes in the length of telomeres — important regulators of DNA replication — may be produced by psychedelics."

A major limitation of the study is that the drug doses used in the lab mice are much higher than those typically administered to humans, Thompson said. That said, Hecker argues that this comparison doesn't consider the much faster metabolism of mice and the consequently shortened time the psychedelics are active in the animals.

The findings set the stage for investigating psilocybin as a treatment for aging and age-related diseases, Hecker said. Future research should investigate optimal doses to use in humans, as well as the potential risks, she said.

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

Some chemotherapy drugs cause more damage to healthy cells than other chemo options do, a new study finds.

The researchers have found four new mutational signatures — patterns of DNA damage left by certain classes of drug — linked to chemotherapy. They also pinpointed some medications that can even "artificially age" healthy blood cells via these mutations.

The findings, published Tuesday (July 1) in the journal Nature Genetics, could help doctors select cancer treatments that cause minimal knock-on damage to patients' bodies while still attacking their cancer, the scientists say.

Some cancer chemotherapy medications destroy rapidly dividing cells by damaging their DNA, triggering cell death. While cancer cells fit that description, there are also healthy cells that divide quickly, such as those found in bone marrow and blood. This new study aimed to find out how chemo impacts those healthy cells and to do so in unprecedented detail.

The research team compared the blood of 23 people, ages 3 to 80, who were previously treated with chemotherapy with the blood of nine subjects without histories of cancer or chemo. Collectively, the people in the chemo group had received 21 different therapies, including platinum and alkylating agents, which kill cancer cells by damaging their DNA.

The team isolated blood stem cells and mature blood cells from the groups. They extracted DNA from the cells and put them through whole-genome sequencing. Using mathematical models, they pinpointed a number of mutational signatures in each cell's DNA, four of which had never before been reported to the COSMIC database of mutational signatures and are heavily suspected to be caused by chemo.

Related: Some early-onset cancers are on the rise. Why?

Although some of the signatures were present in samples from both the cancer-free and chemo-treated groups, 11 appeared only in the chemo group. That included the four new signatures.

But interestingly, not all medications within the chemo group caused the same degree of mutational burden. For example, the team found that cyclophosphamide, which is used to treat cancers such as multiple myeloma and breast cancer, causes far fewer mutations than others in its class.

More mutations mean a higher risk of getting another kind of cancer after treatment, called a secondary tumor. "The risk of secondary malignancy with cyclophosphamide is known to be lower" than with other drugs of its class, first study author Dr. Emily Mitchell, a hematologist and researcher at the Wellcome Sanger Institute and a clinician at Cambridge University Hospital, told Live Science in an email. That said, the risk is not zero.

Cancer is caused by mutations that lead to uncontrolled cell growth. But genetic mutations, in general, are also linked to aging.

"Each cell in our body accumulates mutations over time in a constant fashion," said Dr. Francesco Maura, a hematologist and researcher at Memorial Sloan Kettering Cancer Center in New York City who was not involved in the study. When chemo introduces mutations to blood cells, particularly blood stem cells, he said, "it doesn't necessarily mean the stem cell is aged; you just have more mutations." These chemo-induced mutations carry the same risk as age-related mutations, though — that is, their accumulation raises the risk of cancer.

Among the study participants, there was a 3-year-old who had chemo that carried 10 times the number of mutations in his blood than healthy, untreated kids his age. The toddler's blood cells looked older than those of an 80-year-old study participant who had never had chemo. But while mutation buildup makes cells look older, it doesn't always lead to tumor growth — just as not everyone who ages gets cancer.

The study had limitations, such as its small sample size. The researchers conceded that studying blood in test tubes could have skewed the results, because it doesn't fully recreate the human body's environment. Mitchell said her group would like to run similar experiments with a larger cohort and with circulating blood, but there are no plans to do so immediately.

Mitchell pointed to her and her colleagues' work published in 2024 in the journal The Lancet Oncology as an example of where this sort of research could go. They'd demonstrated that an alternative chemo combination for Hodgkin lymphoma worked just as well as the standard option while causing fewer knock-on mutations.

Hodgkin lymphoma has a high cure rate of more than 80%, but for other types of cancers with lower cure rates, applying this approach may be more challenging. Additionally, secondary tumors take years to develop, so people need to survive for some time following their initial treatment to encounter them. Optimizing their initial chemo drugs to minimize mutations wouldn't be helpful if the survival rates for their cancer aren't high.

In Maura's words, "first, you have to cure [that type of] cancer. Then you work toward reducing the toxicity of the treatment."

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

Disease name: Werner syndrome, sometimes called "adult progeria"

Affected populations: Werner syndrome is estimated to affect 1 in 100,000 live births worldwide, though its prevalence varies among countries. In Japan, the syndrome affects an estimated 1 in 40,000 to 1 in 20,000 people, whereas the prevalence in the United States is around 1 in 200,000. This difference between locations is partly attributed to "founder effects" — instances where genetic variation declines after a small group of individuals gets separated from a larger population. This limits the gene pool and can cause disease-causing mutations to become more widespread within a population.

Werner syndrome affects males and females at equal rates.

Causes: Werner syndrome is caused by mutations in the WRN gene, which is needed to make the so-called Werner protein. This crucial enzyme unwinds and separates the two strands of a DNA molecule and also removes bits of damaged DNA. This helps cells to repair their DNA following damage, make copies of their DNA as they multiply and use the genetic instructions to make proteins.

The enzyme may also help maintain telomeres, the protective "caps" at the ends of DNA molecules that prevent them from unraveling like frayed shoelaces. Telomeres get shorter with age, and the rate at which they shorten is tied to the rate of biological aging observed and expected lifespan of an organism.

More than 80 different mutations in the WRN gene have been found in people with Werner syndrome. Most often, such mutations cause cells to make a version of the Werner protein that's too short and doesn't work. The exact consequences of this aren't fully understood, but laboratory studies suggest that cells carrying these mutations can't divide as many times as cells without the mutations can. They also enter senescence — a zombie-like state associated with cellular aging — earlier than healthy cells do. Additionally, mutations in WRN may prevent cells from correcting DNA damage, allowing other, harmful mutations to accumulate.

The syndrome is inherited in an autosomal recessive pattern, meaning it's caused by a person inheriting two broken copies of the WRN gene — one from each parent.

Symptoms: The symptoms of Werner syndrome typically start to emerge in the second decade of life, around adolescence. Children with Werner syndrome are often thin and have a slow growth rate later in childhood, sometimes missing the usual growth spurt seen in adolescence.

People with the syndrome may start growing gray hair before age 20. By 25, they start to lose hair from the scalp, eyebrows and eyelashes, and they may grow only sparse hair elsewhere on the body, including the underarms and chest. This lack of hair is likely related to hypogonadism, in which the ovaries or testes don't work well; hypogonadism also undermines the development of sexual organs and the regularity of menstruation.

Werner syndrome also causes people to lose the layer of fat beneath the skin, along with muscle mass and bone density. Atrophy of the vocal cords causes many people to develop a high-pitched, squeaky or hoarse voice. Their skin develops smooth or hard patches, areas of hyper- or hypopigmentation, and redness due to widened blood vessels. Together, these changes cause people with the syndrome to have a "pinched"-looking face, with prominent eyes and a thin, beaked nose.

In some people, soft tissues such as ligaments and tendons calcify over time, becoming stiffer. Calcium can also build up in the cornea of the eyes. By their 20s or 30s, many people with Werner syndrome develop age-related cataracts, a clouding of the lenses of the eyes that usually does not occur before age 50. In their 30s, people with Werner syndrome can develop type 2 diabetes, hardening of the arteries (atherosclerosis), chest pain (angina), heart attack or heart failure.

People with the syndrome are also prone to certain cancers, such as thyroid cancer, melanoma, osteosarcoma and soft tissue sarcoma. Studies conducted in the 2000s suggested people with the syndrome typically die in their early to mid-50s, but with newer medical treatments, people can now survive a few years longer.

Treatments: There is no cure for the underlying cause of Werner syndrome; treatments are aimed at addressing a patient's specific symptoms. For example, a person may take medications and implement dietary and lifestyle changes to manage type 2 diabetes; undergo surgery and chemotherapy for cancer; and take medicines to counter the hardening of their arteries.

Diagnosing Werner syndrome may involve genetic testing to confirm that a person carries two defective copies of the WRN gene. In addition, the family members of people with Werner syndrome can undergo genetic counseling to see if they're carriers of mutant WRN genes; those who carry only one copy don't develop the syndrome but could pass on the condition to their children if their partner also carries a mutant copy.

Couples who are carriers but still wish to conceive a child can potentially explore preimplantation genetic testing, which is genetic testing performed as part of an in vitro fertilization (IVF) procedure.

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

Taurine — an amino acid found in some foods and also made by the human body — has been shown to slow aging in animals when given as a supplement, raising the idea that it might be a promising anti-aging treatment for people. But now, a new study has raised questions about taurine's relationship to aging.

The study, published Thursday (June 5) in the journal Science, measured taurine in the blood of three groups of people across adulthood, as well as in the blood of adult monkeys and mice. Some previous studies found that circulating taurine declines with age, which could help explain why taurine supplements improve certain signs of aging while extending lifespan — at least in lab animals.

Those previous studies had limitations, though. For example, most were "cross-sectional" — meaning rather than tracking the same organisms through time, they looked at many, different-aged organisms at one point in time. This approach has produced conflicting results, with different papers reporting either a decline, increase or stability in taurine levels with age.

To gain clarity, the new study included both cross-sectional and longitudinal data, the latter of which included blood samples taken at different time points from the same groups of people and lab animals as they aged. Ultimately, what the scientists found is that taurine didn't decline with age; instead, it increased or stayed stable across all of the groups studied.

What's more, the differences in taurine levels seen between individuals "generally is far greater" than the degree of change seen across adulthood, study co-author Maria Emilia Fernandez, a postdoctoral fellow at the National Institute on Aging (NIA), said at a June 3 news conference. Thus, low taurine is "unlikely to serve as a good biomarker of aging," she said.

"The main takeaway is that a decline in taurine is not a universal feature of aging," said Joseph Baur, a professor of physiology at the University of Pennsylvania Perelman School of Medicine who was not involved in the study.

Related: Human aging accelerates dramatically at age 44 and 60

Nevertheless, the amino acid may still be tied to some age-related changes in the body, he told Live Science in an email, adding that, "given that other studies have shown benefits, including lifespan extension in mice, I think the case remains to explore the potential for taurine supplementation to improve health." That said, the new study doesn't make a strong case for or against the therapeutic value of taurine supplements, he clarified.

"There is a discrepancy"

The new study included data from more than 740 participants in the Baltimore Longitudinal Study of Aging who were between 26 and 100 years old. It also included data from over 70 people ages 20 to 85 who participated in the Balearic Islands Study of Aging, conducted in Mallorca, as well as data from about 160 people ages 20 to 68 in the Predictive Medicine Research cohort in Atlanta. The team also analyzed blood from rhesus macaques (Macaca mulatta) ages 3 to 32 and blood from lab mice ages 9 to 27 months old, roughly covering the ages from reproductive maturity to old age and death.

In most of these cohorts, "taurine exhibited an increase with age," Fernandez said. The only exceptions were male mice from one arm of the study and men from the Predictive Medicine Research group, both of which showed stable taurine levels through time. Scientists don't know why those two groups diverged from the overall trend.

The researchers also investigated whether taurine levels showed any association with health metrics that change with age, such as muscle strength. But the connections they found were "inconsistent within and across cohorts," undermining the idea that low taurine levels drive such age-related changes.

This aspect of the study wasn't exhaustive, though. For instance, a 2023 study of taurine found that supplementing taurine in middle-aged mice was linked to better sugar metabolism and less-extensive DNA damage in the animals, but the new study didn't look at these other aspects of aging.

Complicating the picture of what taurine does in health and disease, concentrations of the amino acid are known to differ among people with different medical conditions. For instance, people with obesity show lower taurine concentrations compared with people of lower weights, but when you cross the threshold into severe obesity, you see taurine surge, the study authors noted. In cancer, taurine goes up in leukemia but down in breast cancer, Fernandez added at the news conference.

And at baseline, taurine plays many roles in the healthy body, serving as a key component of bile salts, which are compounds made by the liver that help the body digest fat. It also helps boost the body's supply of antioxidants and build key proteins in mitochondria, the powerhouses of cells.

Taking all this complexity into account, can taurine levels be a proxy for anything?

"The short answer is no — it's not a reliable biomarker of anything yet," study co-author Rafael de Cabo, chief of the Translational Gerontology Branch at NIA, said at the news conference. "I think that we need to be digging into the basic mechanisms … before it can be used reliably as a marker."

Still, given that there are existing studies that suggest taurine plays some part in aging, scientists still see value in studying it further. Vijay Yadav, an associate professor at Rutgers New Jersey Medical School who co-authored the 2023 taurine study, is involved in an ongoing clinical trial to see if daily taurine supplements have any effect on aging in middle-aged humans.

"This trial, we hope, will generate sufficiently rigorous data to show — or not — whether supplementation delays the pace of aging in humans [or] increases health and fitness," he said at the news conference. For now, though, Yadav said there isn't clinical evidence yet to support taking taurine for anti-aging purposes, and the authors of the new study agreed.

Dr. Luigi Ferrucci, a co-author of the new study and scientific director at the NIA, said he thinks further study of the role of taurine in aging could reveal promising new avenues for treatment, even if those don't end up being taurine supplements.

"There is a discrepancy between different studies, and this discrepancy needs to be analyzed more in depth," Ferrucci said at the news conference. "They may reveal some important mechanisms with aging that could be … a target for intervention."

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

Researchers have found that a cocktail of two cancer drugs can increase the lifespan of mice by up to around 30%, according to a new study.

The two drugs, trametinib and rapamycin, were both effective at extending the lives of mice when administered separately, but offered even greater benefits when taken together. They also reduced chronic inflammation and delayed cancer development in the aging mice.

Mice are not humans, however, so the new findings don't necessarily mean that people will live longer by taking these drugs (outside of their current prescribed use). But the study authors noted that the drugs, which are approved by the U.S. Food and Drug Administration (FDA), are good candidates for human trials exploring ways to help older people age better.

The researchers published their study about the potential longevity benefits of the FDA-approved drugs on May 28 in the journal Nature Aging.

"While we do not expect a similar extension to human lifespans as we found in mice, we hope that the drugs we're investigating could help people to stay healthy and disease-free for longer late in life," study co-lead author Linda Partridge, a geneticist at University College London in the U.K. and the Max Planck Institute for Biology of Ageing in Cologne, Germany, said in a statement.

Both drugs work by targeting cell communication pathways in the body, which play a critical role in aging and the development of diseases like cancer. Rapamycin inhibits a protein called mTOR, which regulates the division and death of cells and is associated with cancer and other diseases. Trametinib disrupts a molecular pathway called RAS/Mek/Erk, which also plays a role in cancerous cell proliferation — again, useful if you're trying to stop the growth and spread of cancer cells.

Related: Heat waves may accelerate the aging process

Rapamycin was already known to extend the lifespan of mice, while trametinib has previously been shown to add time to the lifespan of flies. Previous studies have also found that the drugs' separate lifespan-extending effects stack in flies, providing an even greater boost when administered together. However, the new study marks the first time that scientists have combined rapamycin and trametinib to study aging in mammals.

The researchers mixed the drugs into the food of lab mice and found that, individually, rapamycin extended the mouse lifespan by 15% to 20% while trametinib extended it by around 5% to 10%. Just like in flies, the drugs proved stronger together, with a cocktail of the two increasing the mouse lifespan by up to 29%, according to the study.

To explore the biochemical underpinnings of these effects, the team took tissue samples from the mice and analyzed how the activity of their genes was affected by the two drugs. They found that not only did the mice gain separate benefits from the two different drugs but that, when used in combination, the drug cocktail influenced gene activity differently to when either drug was taken alone, according to the statement.

The study highlights that these two drugs could be good candidates for geroprotectors, which are an emerging class of drugs aimed at delaying the onset of diseases and improving the health of older people. However, for now, the researchers plan to optimize the use of trametinib to maximize its benefits while minimizing side effects like weight loss and liver lesions.

"Trametinib, especially in combination with rapamycin, is a good candidate to be tested in clinical trials as a geroprotector," co-lead author Sebastian Grönke, a senior postdoctoral researcher at the Max Planck Institute for Biology of Ageing, said in the statement. "We hope that our results will be taken up by others and tested in humans. Our focus is on optimising the use of trametinib in animal models."

Every day, Kalpana Suryawanshi, 48, looks into the mirror and whispers, "I look older than my age."

Eight years ago, she was diagnosed with Type 2 diabetes. Since then, her health has deteriorated, which she attributes to increased exposure to heat while working in the fields, planting crops, harvesting produce, and carrying heavy loads of cattle fodder. During this time, she frequently experienced dizziness and weakness as temperatures exceeded 40 degrees Celsius (104 F) in her village of Nandani in Maharashtra state, India.

Heat is known to affect cognitive function, cardiovascular health, and kidney function, and a growing body of research suggests that exposure to rising temperatures also accelerates the body's aging process. A 2023 German study published in Environment International was the first to find that higher air temperatures are associated with faster aging at the cellular level. It found that prolonged exposure to elevated temperatures can make the body age faster than its chronological age, a phenomenon known as epigenetic age acceleration. Scientists measure this process using epigenetic clocks, which analyze chemical markers called DNA methylation that turn genes on and off. The study found that in areas where the average annual temperature is 1°C higher, people tend to show signs of accelerated aging at the cellular level.

2024 was the hottest year on record, with 6.8 billion people worldwide experiencing extreme heat for at least 31 days. One unusual effect of this rising heat is observed firsthand by India's community health care workers, who report that more people appear older than their actual age.

How heat could accelerate aging

Scientists are now also finding the biological mechanisms that contribute to premature aging. Wenli Ni, a postdoctoral research fellow at Harvard T.H. Chan School of Public Health and the lead author of the German study, said heat exposure can induce alterations in DNA methylation, which is a biological process that can influence gene expression and cellular function.

She explained that this mechanism can trigger harmful biological processes and accelerate aging. "Heat exposure may also lead to oxidative stress, resulting in DNA damage that could alter DNA methylation patterns and impact aging," she added. Oxidative damage occurs when unstable molecules called free radicals attack cells. They can harm DNA, cell membranes, and proteins, contributing to aging, cancer, and cardiovascular health issues.

These results were repeated in Taiwan, where scientists examined over 2,000 people and found high ambient temperature and heat index exposure were linked to increased aging, with stronger associations in prolonged exposure. The study revealed that a 1°C increase in the 180-day average temperature was linked to a rise of 0.04 to 0.08 years in biological age acceleration, as measured by three different epigenetic aging clocks that estimate biological age.

Related: Human aging accelerates dramatically at age 44 and 60

While this increase in age acceleration might seem small at first, it's important to consider how these effects can build up over time. Even slight increases in biological aging, when sustained year after year, can add up to several years of accelerated aging. This can mean an earlier occurrence of age-related illnesses. Moreover, when these small shifts affect large populations, they can contribute to a tremendous rise in disease burden and health care costs.

A recent study published in Science Advances examined the relationship between heat and aging in more than 3,500 adults aged 56 and above in the U.S. The study found that long-term heat exposure, lasting from one to six years, was associated with epigenetic aging. Persistent exposure to high temperatures can result in frequent sleep disturbances, raising stress and anxiety levels. Over time, this physiological degradation accumulates and may accelerate health decline with age.

Women disproportionately affected

The German study found that women and individuals with obesity or Type 2 diabetes exhibited stronger associations between air temperature and aging. Women generally sweat less and have different body responses to heat, which can make it harder for them to cool down and sometimes cause their body temperature to rise faster, Ni explained.

She also said that studies suggest women have a higher threshold for activating the sweating mechanism at high temperatures, indicating their bodies take longer to start sweating.

Diabetes also makes people more susceptible to high temperatures. People with diabetes often have reduced blood flow to their skin, which can interfere with the body's ability to release heat and stay cool in hot weather.

Additionally, body fat can act as insulation, making it harder for heat to move from the body's core to the skin, reducing its ability to release heat and stay cool.

Epigenetic age acceleration can contribute to cardiovascular diseases, cancer, diabetes, and mortality, putting more pressure on public health care systems.

In 2016, Rajma Jamadar, now 47 years old, from Maharashtra's Haroli village, woke up in the middle of the night with irregular heartbeats. The next day, the doctor said that her blood pressure spiked and prescribed lifelong medication. Within months, her symptoms worsened as her cardiovascular health declined. "Upon further diagnosis, the doctor then told me my heart isn't pumping blood efficiently," she said.

She prepares meals for 175 children at a public school in her village, but rising temperatures make her job increasingly difficult as the heat from cooking takes a toll on her. "Every day, I feel sick," she said.

The risks could start even before birth

Remarkably, climate change may sometimes accelerate epigenetic aging in children even before birth. A study published last year in Nature examined 104 drought-exposed children and 109 same-sex sibling controls in northern Kenya. It found a positive association between in-utero drought exposure and aging, emphasizing that the stressors from drought may decrease overall life expectancy.

According to study author Bilinda Straight, changes can happen through three key pathways in the body. The first is the immune system, the body's first line of defense that protects one from infections and diseases. The second involves metabolic processes that provide the body with energy. The third is responsible for maintaining and repairing cells in response to stress.

"Whether the threat we face is physical or emotional, we still perceive it as a danger to our homeostasis, a health-preserving balance between all our physiological systems," she explained. This suggests that the emotional stress experienced by the women in the study, along with caloric restriction and dehydration, activated systems that help the body manage stress but can harm health if overactivated for extended periods.

Women in the study were seen to be engaged in outdoor labor while they were also experiencing hunger and dehydration. "Those physiological stressors were accompanied by worry about the next meal, for themselves, their children, and loved ones," she added.

Moreover, social factors like gender inequality exposed women to coercion, overwork, and violence. While farmers risk loss from drought, those in livestock agriculture suffer the emotional and financial toll of watching their animals die. Combined with heat stress, dehydration, and hunger, this creates immense hardship. Eventually, this maternal stress during pregnancy contributes to changes in DNA methylation in their children, Straight said.

She suggests adequate nutrition and close monitoring of children's cardiovascular and metabolic health. Researchers advocate for long-term studies to better understand the impacts of the environment on epigenetic age acceleration. "Slowing down epigenetic age acceleration is going to be tied to increasing food security and identifying alternatives to women engaging in high-risk occupational labor," she added. Effective policies are needed to achieve food and livelihood security while reducing social and economic inequalities.

However, for many women, economic insecurity and the lack of social safety nets make it nearly impossible to prioritize health. Suryawanshi's struggle highlights this problem. So far, she has spent over 600,000 Indian rupees ($7,046) on medical treatment. "I can't afford any more expenses, so I've stopped taking some medicines," she said. She visited eight hospitals in two years to search for an effective treatment. "It's a miracle that I survived. Despite being only 48, I have no strength left, but I still have to work."

This article was originally published by Yale Climate Connections.

Menopause can have profound effects on heart health, yet many people are unaware of this important connection.

The hormonal shifts occurring during menopause mark the end of a woman's reproductive years and contribute to an increased risk of cardiovascular disease, the most common cause of death among women globally. As estrogen levels drop, changes in cholesterol, blood pressure, inflammation and fat distribution can lead to plaque buildup in blood vessels, which is a major cause of heart disease.

Hormone therapy has long been prescribed to relieve bothersome menopausal symptoms, but research published in 2002 and 2004 raised concerns about its safety, especially regarding cardiovascular health. Those findings led to years of confusion and debate. Although hormone therapy was also previously prescribed to prevent chronic diseases such as cardiovascular disease, medical guidelines today no longer recommend it for this purpose based on this prior research.

As a cardiologist studying the prevention of heart disease in menopausal women, I investigate how hormone changes affect heart health and how treatments can be improved to lower cardiovascular disease risk. As research continues to shed light on menopause and heart health, it is becoming increasingly clear that hormone therapy used to treat menopausal symptoms in younger, healthy women is not only safe for the heart but may even offer some cardiovascular benefits.

The estrogen-cardiovascular link explained

Menopause, defined as 12 consecutive months without a menstrual period, marks the end of a woman's reproductive years and typically occurs between ages 45 to 55. The transition leading to menopause, known as perimenopause, can last several years and is characterized by fluctuating levels of hormones, including estrogen and progesterone. These hormonal changes often cause symptoms such as hot flashes, night sweats and sleep disturbances.

What's less widely known is that menopause and lack of estrogen also drive changes to the heart and blood vessels. Estrogen has protective effects on the cardiovascular system, and its decline can lead to increased blood vessel stiffness, resulting in high blood pressure, higher cholesterol levels, more inflammation, and shifts in fat deposition, which lead to a greater risk of heart disease.

Related: Women are at higher risk of dying from heart disease. Here's why.

One reason for this is that estrogen helps keep blood vessels flexible and supports the production of nitric oxide, a molecule that allows vessels to relax and maintain healthy blood flow. Estrogen also influences how the body processes cholesterol, helping to make changes to cholesterol to reduce plaque buildup in artery walls. When estrogen levels drop during menopause, these protective factors diminish, making arteries more susceptible to stiffening, plaque buildup and inflammation. These biological processes raise the risk of long-term cardiovascular disease.

Hormone therapy's rocky history

Hormone therapy using estrogen alone or a combination of estrogen and progestin, a synthetic derivative of progesterone, restores estrogen levels and effectively treats menopausal symptoms. It comes with some risks, though, which depend on factors such as a woman's age, time since menopause began and overall health.

The medical community's view on hormone therapy has shifted dramatically over the years. In the 1970s, hormone therapy was widely promoted as a fountain of youth and was prescribed commonly to prevent age-related chronic diseases such as heart attack and stroke.

Then, in the early 2000s, the Women's Health Initiative, one of the largest clinical trials testing oral hormone therapy in women, found an increased risk of stroke and breast cancer in those who used hormone therapy. Doctors abruptly stopped prescribing it, and medical guidelines shifted their recommendations, saying the treatment had more risks than benefits.

However, additional analyses of data from the Women's Health Initiative along with results from further studies pointed researchers to a theory called the timing hypothesis, which suggests that the risks and benefits of hormone therapy depend on when treatment begins.

According to the timing hypothesis, hormone therapy may lower the risk of heart disease in menopausal women who start it before age 60 and within 10 years of menopause onset, and who are otherwise in good health. Women who begin hormone therapy much later — after age 60 or more than 10 years after menopause onset — may instead face increased cardiovascular risks.

A personalized approach to treating menopause

My research supports this idea. In a 2019 study, my colleagues and I analyzed data from 31 clinical trials of women who started hormone therapy at different ages, and we found that women under 60 who used hormone therapy tend to live longer and are less likely to die from heart disease. However, our study did find an increased risk in blood clots and stroke with hormone therapy. This risk was present in menopausal women under 60 years old and continuously increased as women got older.

Additionally, research has shown that different methods of taking hormone therapy may affect its impact on cardiovascular health. For example, using estrogen patches worn on the skin may have a lower risk of blood clots compared with hormone therapy taken as a pill.

This is due to a phenomenon called first pass metabolism. Hormone therapy taken by mouth is processed by the liver before entering the bloodstream. The liver produces clotting factors, which raises the risk of blood clots. In contrast, estrogen patches deliver the medication into the bloodstream, bypassing the liver, and do not increase this risk.

Overall, we found that women who took oral hormone therapy tended to have lower cholesterol levels, and this effect persisted over many years. For healthy younger women who are within 10 years of menopause onset, hormone therapy is safe from a cardiovascular standpoint and may even provide benefit.

However, hormone therapy is still not recommended for women with existing heart disease, history of blood clots, prior stroke, gallbladder disease or certain types of cancers.

Medical experts now recognize that blanket recommendations for or against hormone therapy are not appropriate. Instead, treatment decisions should be individualized, considering factors such as age, time since menopause began and overall health.

If you are considering hormone therapy, discussing risks and benefits with your health care provider is vital.

Here are questions to consider asking your health care provider:

• Am I a good candidate for hormone therapy based on my health history?
• What are the risks and benefits of starting hormone therapy at my age?
• What type of hormone therapy, such as pills, patches or gel, is safest and most effective for me?
• How long should I stay on hormone therapy?

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

The human brain suddenly starts aging much faster around age 44, and that aging reaches a maximum speed at age 67, a new study finds.

The research, published March 3 in the journal PNAS, seems to align with the results of a different study that Live Science recently reported on, which looked at aging using blood samples and found that periods of accelerated aging take place around ages 44 and 60.

The new neuroscience study also found that brain aging was linked to insulin resistance, in which cells need more insulin than usual to keep blood sugar in check. Furthermore, it uncovered early hints that ketone supplements may offer some protection against certain measures of brain aging.

Ketones are compounds in the body that act as an alternative fuel source, standing in for sugars. So if the brain is aging because it's not getting enough sugars, ketones could help fill the gap, the team theorized.

However, much more research is needed to back this idea.

Related: 13 proteins tied to brain aging seem to spike at ages 57, 70 and 78

Early warning signs of brain aging

The researchers used four existing datasets of brain scans that together included scans from 19,300 people ages 18 to 90. To study how different brain regions are linked in networks, the team looked at two types of brain scans: functional magnetic resonance imaging (fMRI), which measures blood flow in the brain, and electroencephalograms (EEGs), which measure electrical firing between neurons in the outermost layer of the brain.

In these scans, the scientists looked for signs that blood flow and electric firing between brain regions either disappeared or became inconsistent, suggesting there was a breakdown in communication between nodes in the network. They had considered this network disintegration a hallmark of aging in previous research wherein they assessed the impact of diet on the brain. Such disruptions are also seen in age-related neurodegenerative diseases, and the degree of disruption typically reflects the person's overall degree of aging.

Through their analysis, the researchers found that the brain starts to age more quickly around age 44 and that the aging accelerates to a maximum rate around age 67. After that, brain aging starts slowing down, until the rate stabilizes around age 90.

"What we did not anticipate was that the effects might be occurring as early as the 40s," study senior author Lilianne Mujica-Parodi, a neuroscientist at Stony Brook University, told Live Science.

Sugars versus ketones

The network disruptions the researchers observed resembled changes previously documented in the brains of people ages 50 to 80 with type 2 diabetes. Mujica-Parodi and her team wondered if the changes arose because neurons were not responding well to insulin, the hormone responsible for shuttling sugar from the blood into cells.

This effect wouldn't affect only people with diabetes. About "88% of North Americans have at least one detectable sign of insulin resistance," said Dr. Luis Adrian Soto-Mota, a metabolism researcher at the Monterrey Institute of Technology in Mexico who was not involved with the study but previously worked with the team.

Looking at all the brain scans, which included scans from people with and without insulin resistance, the team found that people in their 40s with high blood sugar levels experienced faster brain aging than people of the same age with no signs of insulin resistance.

In addition, across all of the scans, certain parts of the brain aged more quickly than others, so the researchers wondered if those brain regions might be more insulin dependent. It's known that a protein named GLUT4 relies on insulin to move sugar into cells. So the team turned to the Allen Brain Atlas, which includes data on the activity of the GLUT4 gene, and found that the fast-aging regions did depend more on GLUT4.

The slow-aging brain regions, on the other hand, had higher levels of a protein that moves ketones into cells, suggesting that those regions use ketones as an alternative energy source.

Related: Biological aging may not be driven by what we thought

Ketone supplements?

That raised the question of whether ketone supplements might be able to slow brain aging. To test this idea, the team recruited 53 men and 48 women, ages 20 to 79, who got fMRI scans after fasting overnight to deprive the brain of sugar.

Half an hour after the scan, the participants received either a ketone-filled drink or a sugary drink with the same number of calories. The researchers then waited 30 minutes for the energy source to reach the participants' brains, before repeating the fMRI scans.

Even over this short time frame, the ketone drink appeared to reduce brain network disruptions tied to aging, while the glucose beverage didn't, the team found.

The ketone drink had the greatest effect on people ages 40 to 59, where its impact was over 80% higher than in younger adults ages 20 to 39. The ketone drink had the smallest effect in the 60-to-79 age group. That might hint that, if ketone supplements prove to be effective for slowing brain aging, early intervention could be necessary.

This part of the study was limited in that the researchers tested the effects of ketone and glucose drinks only at a single time point; they didn't monitor brain aging over time or conduct any cognitive tests. They also considered only specific fMRI data, which may not reflect all aspects of brain aging, so we don't know if ketone supplements would help across the board.

Mujica-Parodi said future studies could track brain aging in people taking these supplements over time and thus provide more insight into its long-term potential. In addition, if the ketone supplements are making up for insulin resistance, the best measure people could take might be to avoid developing insulin resistance in the first place, she suggested, which could be achieved through dietary changes.

Soto-Mota added that when glucose levels are low enough, the body can make more ketones on its own than it can obtain from supplements. That's the goal of the "keto diet," although maintaining the diet for a long time comes with downsides.

Mujica-Parodi said that ketone supplements could be helpful in people with extreme insulin resistance who are incapable of making their own ketones, due to metabolic changes in the body.

Editor's note: Some of the authors on the new paper have patented the ketone supplement tested in the research, and one is the director of a company aimed at developing products based on the science of ketone bodies in human nutrition.

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

Brain quiz: Test your knowledge of the most complex organ in the body

Dormant genes on the X chromosome may reawaken in old age, potentially giving the aging female brain a boost that the male brain doesn't receive.

This phenomenon may help to explain why, on many measures, females show a higher level of cognitive resilience in old age than males do.

The findings come from a new study in lab mice, and the researchers also backed up the results with genetic data from humans. More research is still needed to confirm that the findings in mice translate to people, but overall, the work points to a potential difference in how female and male brains age.

Historically, "we simply haven't looked at the X chrom[osome] very much," said Rachel Buckley, an associate professor of neurology at Harvard Medical School who was not involved in the new study. "And now we're starting to really shine a very, very big spotlight on it, and we're starting to realize things that we had not fully appreciated" — namely, how sex chromosomes might influence how the brain ages.

"There are very important and potentially therapeutic targets that are coming out from these papers" that focus on the X chromosome, Buckley told Live Science.

Related: Is there really a difference between male and female brains? Emerging science is revealing the answer.

The resilience of the female brain

There seem to be fundamental differences in how males and females age. When it comes to the brain, females have lower rates of various forms of dementia than males do, even though females live longer, on average. One exception is that females have higher rates of Alzheimer's disease than males do, although females with Alzheimer's tend to survive longer than males with the condition.

"There's been a lot of documented trends where there's resilience in cognitive aging in female populations, compared to males," said study first author Margaret Gadek, an MD-PhD student at the University of California, San Francisco. "There's a lot of reasons why these trends could be in place, but one thing we wanted to look into was the role of the X chromosome," Gadek told Live Science.

Alongside hormones, the sex chromosomes — X and Y — are one of the starkest biological differences between males and females, and they could help provide biological explanations for why these differences emerge in aging.

Males typically carry one X and one Y in each cell; they inherit the X from their mother and the Y from their father. Females, on the other hand, usually carry two X chromosomes — one from mom and one from dad. But each cell needs only one X to be active, so in females, the second X is "silenced," leaving only the maternal or paternal X switched on.

This is not a seamless process. Some genes on the silenced X chromosome escape that silencing process, and thus remain switched on, while additional genes may get switched back on as a person ages. Gadek and her colleagues wondered how these "reawakened" genes might factor into brain aging, especially given that this silencing is a uniquely female phenomenon.

Related: 'Let's just study males and keep it simple': How excluding female animals from research held neuroscience back, and could do so again

Nearly two dozen "reawakened" genes

In their new study, published March 5 in the journal Science Advances, the researchers crossed two subspecies of lab mice — called Mus musculus and Mus castaneus — so that each of the rodents' offspring would inherit one X from the former subspecies and one from the latter. The team also genetically tweaked the mice such that the X from M. castaneus was always silenced. Normally, the X that happens to be silenced in each cell is random.

This experimental setup made it easier to tell which chromosome an active gene belonged to and, therefore, whether it had "escaped" the silencing process, Gadek explained.

With their modified mice in hand, the team then examined the gene activity in four young mice and four old mice, the latter of which were 20 months old. (That's about 65 in human years.)

They specifically zoomed in on gene activity in cells of the hippocampus, a key memory center in the brain that tends to shrink with normal aging and cognitive decline and is heavily impacted in dementia. They looked at over 40,000 cells in total, including both neurons and various types of glial cells, which help maintain and support neurons in the brain and also make an insulating substance, called myelin.

This analysis revealed that, with age, about 22 genes that were initially silenced got switched back on. Some of the same genes were reawakened across many the mice, while others were more variable, Gadek added.

"I was really shocked to see that we could be thinking about X-related inactivation escapism as a function of age," Buckley said. "So as women get older, there'll be more of it" — meaning X-linked gene activity — "and in fact some of it's quite protective," she added.

Importance of insulation in the brain

Among the 22 reawakened genes, one called PLP1 jumped out as interesting, in part because it was switched on in seven of the nine cell types studied, Gadek said.

PLP1 carries the instructions to make a key component of myelin, the fatty insulation that helps neurons send signals efficiently. It's known that mutations in PLP1 can decrease the amount of myelin in the brain, resulting in intellectual disability. It's also known that myelin can be compromised in aging and that loss of myelin function can contribute to cognitive decline.

To see if the reawakening of PLP1 might boost cognition, the scientists ran some experiments with male and female mice. In one, they confirmed that older female mice had more PLP1 activity in their hippocampi than the older male mice did. In the second experiment, the researchers artificially increased PLP1 using gene editing in both old males and old females, and they found that both sexes performed better on tests of learning and memory after that boost.

To see if any of the findings extended to humans, the team looked at data previously collected for a large study of human brain tissue. Data weren't available for the hippocampus, but the brain tissue immediately surrounding the hippocampus showed more PLP1 activation in older women than in older men. So that hints that the same phenomenon might be unfolding in people.

Gadek said that, in the future, she'd be interested in looking at this reawakened gene in animal models of diseases like dementia, since the current mouse experiments looked at only healthy aging. Buckley added that it would also be interesting to investigate the phenomenon in the context of menopause.

Related: Faster brain aging tied to X chromosome inherited from Mom

In menopause, estrogen levels plummet. The hormone has many functions in the brain, including helping shuttle fuel from the blood into brain cells. Buckley pointed to research led by neuroscientist Roberta Brinton of the University of Arizona, which suggests that, as estrogen levels decline, the brain may break down some of its own myelin for fuel.

In reading the new study, Buckley connected the dots and wondered if the boost in myelin in later life could be a way of recovering from the hit taken earlier, during menopause. "That's something that really made me sit up and take notice," she said, although this idea is speculative for now.

Given the current study was primarily in mice, Buckley did note that more work is needed to see how this phenomenon unfolds in the human brain. And in the long term, it would behoove scientists to study the role of the Y chromosome in brain aging; although it carries far fewer genes than the X, it may still have an impact, she noted.

"One thing that this paper highlights is that studying sex chromosomes isn't a niche woman's health issue," Gadek said. "It provides insights into cognitive aging and certainly other areas of health that could benefit males and females and everyone alike, because we all have an X chromosome."

Maria Branyas Morera was 117 when she died in August 2024 — but aspects of her biology looked much younger, new research finds.

The study could help reveal key factors that help some individuals ward off disease and survive to extremely old ages, scientists say.

Before her death in a nursing home in Catalonia, Spain, Branyas held the record for the world's oldest living person for about a year and a half. Now, a study of urine, blood, stool and saliva samples collected from Branyas in the last year of her life reveals she had a number of factors that potentially protected her against disease. These include genes associated with immune function, fantastic cholesterol levels, and a high level of inflammation-fighting bacteria in her gut.

The study was posted Feb. 25 to the preprint server bioRxiv and has not yet been peer-reviewed.

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

"One of the goals of the study was to see and find an explanation for this separation between extreme longevity and being very old, but at the same time not having the diseases of the old," study lead author Manel Esteller, a cancer epigeneticist at the Josep Carreras Institute in Spain, told Live Science.

Notably, however, not all researchers are convinced that studying supercentenarians — people ages 110 or older — is a fruitful method of understanding longevity. That's partly because the actual ages of these individuals have been called into question.

The biology of longevity

According to the Guinness Book of World Records, one entity that validates old-age records, Branyas was born in San Francisco in 1907 and lived in Texas and Louisiana before moving to Spain in 1915 with her Spanish-born parents. Other than hearing loss and mobility issues, she remained healthy and cognitively sharp until death.

Esteller and his colleagues investigated Branyas' genes, immune cells, blood levels of lipids, and proteins in her tissues, comparing her results to those of younger individuals who had undergone similar testing. For example, they compared Branyas' genetic results to those of 75 other Iberian women in the 1000 Genomes Project, an effort to map variation in the human genome.

This comparison revealed seven rare genetic variants in Branyas' genome that had never been detected in European populations.

These variants, or distinct versions of genes, were related to cognitive function, immune function, lung function, heart disease, cancer and autoimmune disorders. They may have protected against these diseases and improved organ function, the scientists suggested.

They also found that Branyas had excellent mitochondrial function, meaning the powerhouses that provide cells energy worked better than those of younger women. She also had healthy cholesterol levels and a high production of proteins that are beneficial for immune function.

And based on her stool samples, her gut microbiome was distinct from that of 61- to 91-year olds previously studied. In particular, she showed a high level of actinobacteria, which typically decline in old age. Bacteria of the genus Bifidobacterium, which are known to excrete anti-inflammatory compounds, were especially prevalent. This contrasts the "typical decline of this bacterial genus in older individuals," the study authors noted.

"She had this bacteria in the gut that protected against inflammation and she had this bacteria for two reasons," Esteller theorized. "The genome was very welcoming of the population, but [it was] also due to her food." Branyas reported eating three yogurts a day, he said; fermented foods like yogurt contain probiotics, or living microorganisms that can replenish and maintain the gut microbiome.

A molecular clock

Another intriguing finding was a schism between the molecular markers of aging in Branyas' body and her chronological age.

When people age, structures at the ends of their chromosomes, called telomeres, become progressively shorter. Telomeres help prevent DNA from fraying, which would contribute to cellular aging and cancer.

As expected for someone of an extreme age, Branyas' telomeres were almost nonexistent, Esteller said. She also had a large population of a particular type of immune cell, which is typical in older people.

In these two ways, Branyas' biology looked very old — but another marker of aging on her DNA looked strangely young, the team found.

Related: Worldwide, the life-span gap between the sexes is shrinking

As a person ages, DNA accumulates a bunch of molecular tags on its surface, called methyl groups. The methylation of DNA can act like a "clock," showing how physiologically aged a person is. Branyas' clock looked like that of someone between age 100 and 110, about a decade younger than she was at death.

In that respect, "her cells still feel like they were centenarian cells," Esteller said.

What does the study tell us about aging?

An accumulation of many little genetic benefits and lifestyle choices may enable extreme longevity, Esteller concluded. Given the study's findings, "maybe we can think about interventions now," he said, including potential drugs to increase life span.

But there may be a caveat to this research and other studies like it: the ages of the subjects it focuses on.

The validation of extreme old age is controversial. For example, in 1997, the oldest person to have ever lived, Jeanne Calment of France, died, and her age was validated by longevity organizations and the Guinness Book of World Records at 122 years old. But critics have since cast doubt on the veracity of that claim, suggesting Calment actually died in 1934 at the age 59.

They contend that her daughter, Yvonne, took on her identity to evade taxes — and in doing so, she inadvertently became the purported oldest person ever. (If these critics are right, the woman who died in 1997 was actually only 99.)

Another study, which is currently under peer review, argues that the problems with old-age validation go far beyond Calment. This research, first released as a preprint in 2019, suggests that regions with the highest reported proportions of extremely old residents are disproportionately poor and unhealthy.

"It doesn't make sense that this level of poverty would predict good health at any age," said Saul Newman, a scholar at the Oxford Institution of Population Aging and co-author of that research.

What does predict high numbers of very old people, Newman found, is poor record-keeping. For example, U.S. states established birth certificate systems at different times, and the number of people ages 110 and older drops by an estimated 69% to 82% after that record-keeping improves.

Often, people born before such documentation was de rigueur might not even know their true ages, Newman told Live Science. In poor regions, people might also have been motivated to tack years onto their age or take on the identity of a deceased relative to receive a pension.

In Branyas' case, she was born a little less than two years after statewide birth certificates came to California in July 1905. Esteller and colleagues relied on the work of age-verification organizations to validate Branyas' age and did not have direct access to her documents.

When asked, a representative for the Guinness Book of World records provided Live Science with general information on the organization's methods.

"For age-related record titles, the guidelines include requests for government issued documents and further proof to substantiate the claim," the representative wrote in an email to Live Science. "Exact information on these guidelines is only available to applicants and/ or legal representation of them."

The hazy nature of old-age records makes interpreting research on the oldest of the old difficult, Newman said. That Branyas' epigenetic clock suggests she was between 100 and 110 could indeed suggest that she was a 117-year-old who aged unusually slowly — or it could suggest that her paperwork was wrong, and she was between 100 and 110 when she died, he said.

"How do you distinguish between those two cases?" he said. "That’s the central problem. You don't know."

On the other hand, Branyas did undeniably reach old age in enviable health, even surviving a bout of COVID-19 in 2020. Thus, her biology might still help researchers distinguish between changes associated with healthy aging and changes associated with disease.

"For the first time you have biomarkers that can tell you your age, but other biomarkers that can tell you your pathology," Esteller said. "And these are two different things."

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 often use "epigenetic clocks" to measure biological aging, but what makes these clocks tick is not fully understood. Now, scientists have uncovered a clue: The clocks are synced with random mutations that crop up in DNA as we age.

It's long been known that, over the human lifespan, mutations accumulate in the DNA of cells. This happens when cells replicate or are exposed to insults, such as radiation and infection. Plus, with age, the mechanisms that repair DNA damage don't work as well. As people age and mutations rack up, the odds of immune problems, neurodegeneration and cancer also rise dramatically.

But DNA mutations don't tell the whole story of aging.

There are also molecular changes that take place "on top of" DNA. These alterations, known as "epigenetic" changes, don't directly alter DNA's underlying code. Rather, they switch genes on or off or turn their volume up or down. Research suggests that the pattern of epigenetic markers on DNA changes in predictable ways as we age, and epigenetic clocks work by tracking those patterns and then estimating the "biological age" of a given person or tissue.

The new study, published Jan. 13 in the journal Nature Aging, ties these genetic and epigenetic changes together in a new way.

Related: Pregnancy may speed up 'biological aging,' study suggests

"It's an important study," said Jesse Poganik, an investigator at Brigham and Women's Hospital and instructor in medicine at Harvard Medical School who was not involved in the research.

"People very rightly criticize the so-called black box nature of epigenetic clocks," he told Live Science. There are many questions about what drives the epigenetic changes we see, and whether the changes themselves actually drive aging or are only a reflection of it — like wrinkles are a sign of skin aging, not a cause of it.

"Any further understanding of the basic mechanisms that are at play are going to ultimately help us to advance the field," Poganik said.

A cascade of changes

The new study started with senior study co-author Dr. Steven Cummings, executive director of the San Francisco Coordinating Center at the University of California (UC), San Francisco, who theorized that gene mutations may be directly linked to the changes measured by epigenetic clocks. And ultimately, "that's what we found," said Cummings, who is also a senior research scientist at Sutter Health's California Pacific Medical Center Research Institute.

"The two were very highly correlated," he told Live Science.

To explain the reasoning behind this theory, let's unpack a bit of chemistry.

One common mode of epigenetics, which most epigenetic clocks are based on, is called DNA methylation. It involves molecules called methyl groups latching onto cytosine (C), one of the four letters in DNA's code. This primarily happens at places in DNA molecules where C sits next to guanine (G), known as CpG sites. But if there's a mutation and either the C or G changes, that site is no longer CpG and thus is much less likely to be methylated.

"That's a way in which a mutation could cause a change in methylation — a loss of methylation," said senior study co-author Trey Ideker, a professor at UC San Diego's School of Medicine and Jacobs School of Engineering.

"And it turns out, the opposite could actually be true," Ideker added. Methylation can, in turn, influence where DNA mutations appear. If a methyl group attaches at a particular part of the C, this can spark a chemical reaction that destabilizes the C, making it more likely to mutate later on, Ideker explained.

Given this push and pull between mutations and methylation, the team wondered whether they could tie these interdependent processes back to aging.

To do so, lead study author Zane Koch, a doctoral student in bioinformatics at UC San Diego, looked at two existing databases: the Cancer Genome Atlas and the Pan-Cancer Analysis of Whole Genomes. From these, the team drew mutation and methylation data from more than 9,330 cancer patients. Most of the data came from tumor biopsies, but a subset of the patients also had samples taken from normal, noncancerous tissues. It's difficult to find comparably large datasets with both genetic and epigenetic data, Ideker noted.

Crunching the numbers, the researchers found that mutated CpG sites did bear less methylation than unmutated CpG sites. What's more, the mutations seemed to coincide with a wider ripple effect: Intact CpG sites located near these mutants were "strikingly hypermethylated," by comparison. And these ripple effects could be observed up to 10,000 letters out on each side of the mutation.

"It's like an explosion of methylation change happens around that mutation," Ideker said, but we don't yet know why or how that's happening, or the exact timing of what event happens first. "All we know is that there's this very clear relationship."

Related: New 'biological aging' test predicts your odds of dying within the next 12 months

Seeing this relationship, the team then built clocks based on these patterns of genetic and epigenetic change, respectively. Both clocks made similar predictions of age. In short, the two clocks appear to be synced.

What can this tell us about aging? It may be that the genetic and epigenetic changes are both happening downstream of some other process that is actually the true, underlying driver of aging. However, Cummings favors a different theory: that DNA mutations drive aging and that epigenetics simply reflects this process.

If that's the case, scientists on the quest to reverse or stall aging face a challenge. "They're going to have to figure out how it is you reverse the underlying somatic mutations," Cummings said, rather than only tweaking the epigenetic markers on top of DNA.

More research will need to be done to fully explain the study's findings and their relation to aging. For starters, the current study looked only at tissues from people with cancer, so the findings need to be replicated in individuals without the disease, Poganik said. In addition, the tissue samples from each individual were taken at one point in time, so the team couldn't directly observe changes unfolding with age, he added.

Ideker suggested that, in future laboratory experiments, scientists could trigger mutations in cells and then monitor any epigenetic changes that unfold. Long-term studies of humans, which follow people over time, could also give a sense of which phenomenon happens first, or whether it's really an ongoing interplay between the two, Poganik said.

Together, these future studies would shed new light on what makes epigenetic clocks tick and, more broadly, what makes us age.

"Even the developers and heavy users of the clocks acknowledge that this is a limitation — that we don't understand how they work," Poganik said. "The more we understand about how they work, the more we will understand about the context in which to apply them."

The X chromosome passed from mom to offspring may accelerate brain aging, a new animal study suggests.

The research highlights a potential fundamental difference in how males' and females' brains age. The research was conducted in mice, but if the findings translate to humans, they could point to sex-specific drivers of cognitive decline and, eventually, ways to prevent or treat them.

"Females show resilience in many measures of aging," said senior study author Dr. Dena Dubal, a professor of neurology and the David A. Coulter endowed chair in aging and neurodegenerative disease at the University of California, San Francisco (UCSF). For instance, they tend to live longer than males and have lower rates of various forms of dementia. One exception is Alzheimer's disease, which affects females at higher rates, but even so, some studies suggest that females survive longer with Alzheimer's than males do.

Dubal and colleagues wondered if the sex chromosomes, X and Y, could help explain these differences. There's evidence of genes on the X chromosome that help guard against dementia, while others contribute to the risk of cognitive decline, said Rachel Buckley, an associate professor of neurology at Harvard Medical School who was not involved in the new study.

The new study, published Jan. 22 in the journal Nature, uncovers a potential factor that shapes the X chromosome's influence.

Related: Is there really a difference between male and female brains? Emerging science is revealing the answer.

The origin of the X matters

Typically, females carry two X chromosomes in each cell — one from their mom and one from their dad. But a cell needs only one X to be active, so the other is "silenced." This results in females carrying a mosaic of cells that have silenced either their paternal or maternal X chromosome. Meanwhile, males — who typically carry one X and one Y — only ever inherit their X from their mother, and it's active in every cell.

"That makes us wonder about female resilience and whether that diversity of the X chromosome, having Mom's and Dad's, might contribute to resilience," Dubal said.

To explore this idea, Dubal; Samira Abdulai-Saiku, a postdoctoral fellow at UCSF; and colleagues did experiments with female lab mice of different ages. Some experiments involved using a genetic trick to silence all of the paternal X chromosomes in certain mice, leaving only the mother's X active. These mice were compared with others that had a mix of maternal and paternal X's switched on.

"I actually really liked that approach," Buckley said. Comparing females to males would have introduced additional sex-related factors, like hormonal differences, Buckley told Live Science.

The team also ensured that the X chromosomes from each parent were genetically identical, Dubal noted. So any differences that emerged would be related to which parent passed them along, not to differences in the genes themselves, she explained. This also enabled the team to pinpoint differences in epigenetics — chemical tags that attach to DNA and control which genes can be switched on.

Young "Mom-X" mice were cognitively similar to other young mice, performing about the same in maze-based tests. But at older ages, they showed starker cognitive decline, especially in their spatial memory and working memory. "The assays showed a pretty striking effect," Dubal said.

The team wondered if these declines were related to changes in the hippocampus, a key memory center in the brain. To see, they looked at epigenetic markers on DNA from the hippocampi of young and old mice. Epigenetic tags change across the lifespan, with certain patterns correlating with "higher" biological ages — in other words, a more advanced degree of aging. At older chronological ages, the Mom-X mice showed a greater degree of biological aging in the hippocampus than did mice with both X's.

The scientists then sorted neurons from the hippocampus based on whether the mom's or dad's X was active, so they could look at which genes were switched on.

Three genes were silenced on the maternal X — Sash3, Tlr7 and Cysltr1 — but were very active on the paternal X. Using the gene-editing tool CRISPR, they investigated what would happen if they switched these genes back on in the brains of old mice with only maternal X's. In tests, these mice showed improvements in spatial learning and memory.

What does it mean for humans?

Interestingly, in humans, these three genes are involved in immune protection, but their exact roles in neurons aren't fully understood, Dubal said. Future work could further investigate what the genes do in neurons and in other types of brain cells. It's also unclear how or why the X chromosomes from different parents undergo different epigenetic changes, she added.

The team also wants to investigate what these findings might mean for males, who carry only maternal X chromosomes — and could, in theory, then have greater rates of brain aging. "One can imagine" that, the more active maternal X's a person carries, the more pronounced the impact on brain aging, Dubal speculated. But that remains to be confirmed.

And, of course, because the current study was conducted only in mice, future research should look at human brain tissue to check that the results carry over, Buckley said. "This is such highly unique and novel work … but that is a caveat."

In the long run, this line of research could help scientists understand the influence of sex on dementia risk, differentiating it from other factors, like education, that are more closely tied to gender, Buckley said. By pinpointing those biological drivers of brain aging, researchers could better determine how to intervene and tailor treatments to individual patients.

"Right now, we're doing one size fits all," Buckley said. "And realistically, this is not how we're going to move the needle."

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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Like fine lines on your face or aching joints, gray hair is considered to be one of the many markers of old age. But for those of us not quite ready to embrace the grays, is it possible to reverse this process?

While a small study from 2021 suggests that this may be possible in very specific, short-term scenarios, the resounding answer from experts in dermatology and trichology (specialists who study the hair and scalp) is probably not. At least, not permanently.

"The arrow of time goes in one direction, and hair loses color for a reason that does not seem reversible," Martin Picard, an associate professor of behavioral medicine at the Robert N. Butler Columbia Aging Center in New York City, told Live Science in an email.

Picard was a co-author on the 2021 study published in the journal eLife that explored the role of stress in the advancement — and short-term reversal — of graying hair across a wide range of ages.

In the study, the researchers studied people who had strands of hair with darker pigment at either end but gray hair in the middle, and found that periods of stress reduction correlated with a temporary reversal of the graying process. In the case of one participant, taking a two-week vacation correlated with a repigmentation of hair.

Related: Why does hair turn gray?

However, unlike the infamous story of Marie Antoinette, whose hair supposedly went white overnight before her execution, it's important to remember that one or a handful of stressful days does not determine your hair color. Instead, Dr. Antonella Tosti, a professor of dermatology and cutaneous surgery at the University of Miami in Florida, told Live Science that environmental factors can be more impactful than individual stressful events.

"Oxidative stress, such as smoking or pollution, is something that definitely increases the risk of graying," Tosti said. Whether including antioxidants in your routine, such as antioxidant-rich foods like blueberries or pecans, can effectively combat these risks of gray hair specifically is still being determined, she said. But there is some evidence to support the idea that an antioxidant-rich diet can reduce effects of aging by helping reduce cell and DNA damage caused by unstable molecules called free radicals. Free radicals can occur naturally in the body and they can also be caused by external factors such as smoking, UV exposure and pollution.

Unfortunately, reducing personal and environmental stressors still won't entirely prevent hair from turning gray. More than half of people will begin going gray by the age of 50, and for individuals with a genetic lineage of early gray hair, genetics may play a bigger role than stress management, Dr. Joshua Zeichner, a dermatologist at Mount Sinai Hospital in New York City, told Live Science in an email.

"If you have a family history of early graying then you are likely to go gray early also," Zeichner said. "I have never seen gray hairs go back to normal, which may indicate that there is a permanent change to the hair follicle itself."

While there are no fully effective treatments or solutions to gray hair just yet, this doesn't mean that experts are giving up.

One potential path forward lies in what happens to melanocytes — a melanin-forming cell in the hair responsible for color — in gray hair. Scientists previously believed that melanocytes died off with age. But findings from a rat study published in the journal Nature in 2023 found that melanocytes may simply become concentrated at the follicle root of hair, no longer migrating up the strand to provide pigment.

Through medical treatments, there's a possibility that these melanocytes could be reactivated, Tosti said, to make the hair dark again. However, there's currently no process that can achieve this.

A treatment for oxidative stress may be another avenue, Zeichner said, by boosting free-radical fighting enzymes on the scalp through topical antioxidant application. But as for now, non-medical treatments at a local salon are probably the best bet at reducing grays.

"Right now, the only cure we have for gray hair is a good colorist," Zeichner said.

Many people know the feeling that comes after a few too many drinks: a pounding headache, clammy skin, racing thoughts and an upset stomach. Often, these hangovers seem to get worse with age; older people find that the amount of alcohol they used to drink in their youth with no ill effects now leaves them feeling debilitated.

But do hangovers really get worse with age?

Anecdotally, there are plenty of people who would tell you "yes," from personal experience — but there's no hard scientific evidence that hangovers actually intensify with age. However, there are some plausible reasons why they might do so.

"It isn't clear whether hangovers get worse for everyone as they age or just for some people," Aaron White, leader of the National Institute on Alcohol Abuse and Alcoholism's Epidemiology and Biometry Branch, told Live Science in an email. "There simply hasn't been sufficient research on this topic." But nonetheless, there are some theories.

Related: What happens to your body when you stop drinking alcohol?

Hangovers are caused by myriad changes in the body that occur after overindulging. Alcohol is toxic to cells in that it can damage DNA and impede important cellular processes. As it's broken down, alcohol is briefly transformed into a different toxic substance, called acetaldehyde, before being turned into a less-toxic compound called acetate and, finally, into water and carbon dioxide.

As people age, though, the enzymes in the liver that metabolize alcohol and its toxic byproducts can become less efficient, so those toxic chemicals might stick around in the body longer than they used to. When acetaldehyde hangs around in the liver, it can also cause widespread inflammation in the body. Cytokines, the chemical messengers that prompt inflammation, have been tied to malaise, anxiety, irritability and fatigue — all common hangover symptoms.

Plus, compared with young people, older people are more likely to suffer from chronic pain and conditions that cause knock-on inflammation, such as diabetes and arthritis. Thus, drinking too much could result in a double whammy of inflammation on top of an already-high baseline. White said this could "worsen existing physical discomfort" and ultimately result in a more severe hangover.

Both drinking alcohol and experiencing normal aging can make it difficult to stay hydrated, so the combination of the two could be a recipe for a rough morning.

Alcohol is a diuretic, meaning it expels water from the body. Scientists are still debating exactly how much of a role dehydration plays in hangovers, White said, but it's well known that being dehydrated can cause headaches and fatigue, both common hangover symptoms. And after age 60, the overall amount of water in the body starts to decline due to tissue loss. This dehydration not only tees you up for a hangover but could also boost the concentration of alcohol in your blood after you drink, White said.

"It is possible that each drink packs more of a punch as we get older," he said, "which could mean more misery the next day."

Both alcohol and age disrupt sleep, too. Downing a few drinks can speed up the initial process of falling asleep, but it can also undermine sleep quality and cause people to wake up earlier, resulting in a worse night's sleep overall. White said sleep quality tends to decrease with age anyway, so "we might feel the impact of alcohol on next-day fatigue more than when we are younger."

Though there are many potential reasons alcohol could hit harder with age, bad hangovers aren't a guaranteed part of getting older. One survey of more than 50,000 people ages 18 to 94 found that older people actually reported a lower incidence of hangovers after binge drinking, compared with their younger counterparts. The researchers couldn't explain this pattern even when accounting for each age group's usual alcohol consumption or frequency of binge drinking.

These results were echoed in a smaller, self-reported survey that found hangover severity decreased with age. Although younger participants reported drinking more, when the researchers corrected their results for the amount of alcohol consumed, they found that older participants reported less severe and less frequent hangovers than younger people. The researchers theorized that this may be the case because older people become less sensitive to pain over their lives.

While there's still some debate on exactly how aging affects hangovers, White said one thing is clear: The only guaranteed way to avoid a hangover is to avoid drinking too much in the first place.

"Time is the only universal cure for hangover symptoms," White said. "And not overindulging is the best strategy for preventing them."

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

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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.

Aging egg cells can be rejuvenated when placed inside young follicles, a new study of mouse cells suggests.

The study could serve as proof-of-concept for future fertility treatments aimed at reversing aging in human egg cells — but much more research is needed to translate these findings to people.

As immature egg cells, called oocytes get older, they begin having problems with cell division. This can result in aneuploidy, in which the chromosomes in the early oocyte don't separate correctly, resulting in extra or missing chromosomes. This causes higher rates of miscarriage.

People can now freeze their oocytes to help preserve their ability to have children. However, there is currently no method of reversing the effects of aging on older oocytes.

Related: Human aging accelerates dramatically at age 44 and 60

In a paper published Monday (Sept. 7) in the journal Nature Aging, scientists at the National University of Singapore demonstrated a new way to model the maturing oocyte in the lab. Through that work, they found that oocytes from older mice that were grown with young mouse cells became rejuvenated, and this improved the rates of live births when the eggs were implanted back into mice.

Senior study author Rong Li, director of the Mechanobiology Institute at the University of Singapore, and her team have been interested in cellular aging for a long time. They started studying the oocyte when they realized that the ovary is the fastest aging organ in the body.

"So when someone is only 40 years of age, everything else is very young and healthy, but the ovary is very old, [limiting] reproductive ability," Li told Live Science. This also makes ovaries a great model for the study of aging, in general.

As an oocyte matures, it undergoes multiple rounds of cell division before it's eventually released from the ovary during ovulation. This complex and energetic process is made possible by a follicle that surrounds the maturing oocyte and provides the energy and nutrients needed through thin filaments called tranzonal projections, or TZPs. Without these lifelines to the follicle, an oocyte cannot mature properly.

Earlier work on oocyte aging focused on later stages of development, but Li and her team wanted to look earlier when the oocyte is going through the most extreme stages of maturation and cell division that show the most TZP connections.

First author Haiyang Wang, a senior research fellow in the Li lab, designed a 3D system that enables scientists to implant oocytes from one mouse into the empty follicle of another. Wang first removes the oocyte and follicle — which are slightly larger than the width of a human hair — from the mouse ovary by hand using a microscope and tiny tools. When the oocyte is separated from its follicle and then joined to a new one, the TZPs reform and the connections between the follicle and oocyte are reestablished.

Related: Should we rethink our legal definition of a human embryo?

"This is an innovative technology, it's very useful, and it can test the [effect of] environmental factors on oocyte aging," Wang told Live Science.

But Li and her team wanted to go a step further. "If we put an old oocyte into a young [follicle], can it actually become younger?" Li said "Which is also asking another question: is aging reversible?"

The researchers tried implanting oocytes from aging mice into young mouse follicles, finding that the older oocytes showed an uptick in TZP connections, comparable to much younger young egg cells. The eggs also showed improved rates of maturation and about half the rate of chromosomal abnormalities seen in unmodified cells. They also showed quadruple the rate of live births compared to baseline when they were fertilized and reimplanted into mice.

This is the first study to show that oocyte aging can be reversed, and it suggests that it's this connection with younger follicle cells that turns back the clock.

"This impressive study highlights the critical role of the follicular environment in oocyte quality," said Farners Amargant i Riera, a professor of obstetrics and gynecology at Washington University in St. Louis who was not involved in the study. "In addition, it shows that methods to rejuvenate this environment are critical to improve oocyte quality and extend fertility," she told Live Science in an email.

How could these results translate to the problem of age-related fertility? The team would first need to validate the same model and experiments in human cells. But eventually, Li and her colleagues think it would be possible to make a commercial cell line for follicle-forming cells that can be cultured alongside aging oocytes. This, in theory, could be a viable treatment to rejuvenate the old eggs and thus reduce the chance of miscarriage, they propose. Such a treatment would likely be used in the context of IVF.

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Have you noticed someone getting shorter as the years slip by? Some people may start hunching over and even get a few inches shorter. So what makes us shrink as we age? 

It turns out that it's a combination of our bones "eating" themselves, our cartilage thinning and our muscles being whittled away. But the rates at which these processes happen vary depending on genes, physical nutrition and activity levels across a person's lifespan.

"We all age differently biologically," Marian Hannan, an epidemiologist at Harvard Medical School who researches aging, told Live Science. 

Nonetheless, people invariably get shorter as they age. A National Institute of Aging study that followed 2,084 men and women for 35 years found that they started losing height around age 30 and that the shrinking accelerated over time. 

The study, which included people ages 17 to 94, found that the men, on average, lost 1.2 inches (3 centimeters), and the women lost 2 inches (5 cm), between age 30 and 70. By age 80, men had lost 2 inches (5 cm), and women had lost 3 inches (8 cm). Largely, that's because our bones begin breaking down as we age. Bones start forming around the eighth week of pregnancy. They continue to grow until people reach their mid-20s. Bones also become denser when they have to support higher muscle mass. As muscle grows, it produces collagen fibers that stretch and increase local blood flow, which in turn stimulates bone growth. 

Bone growth plateaus by about ages 25 to 30. And around age 40 to 50, we begin to gradually lose bone mass, as our bones start breaking down old bone faster than the body can make new bone. 

Related: Scientists discover 4 distinct patterns of aging

Bones are "like a matrix that are all connected to each other," Hannan said. The bone matrix is made mainly of collagen protein and hydroxyapatite minerals. When people lose bone mass, "those bridge-like structures become weakened, and little, tiny loads that are added to them can cause microfractures, breaking down those little, tiny bone bridges."

Accumulation of small-scale bone damage can cause osteoporosis, which makes bones thin, brittle and weak.

Osteoporosis can, in turn, cause larger bone fractures, which are common in the spine, hips and arms. It can also lead to height loss. In 2021, Hannan and her colleagues encountered a study participant who had lost 8 inches (20 cm) of height. 

"This person had probably seven or eight vertebral fractures in their spine, which is unusual — it's a lot of fractures," Hannan said.

Height loss can also be caused by poor posture. Slouching or severe forward curving of the spine, also known as hyperkyphosis, could lead to permanent rounding of the upper back that shaves off a few inches of height. 

Another reason we lose height is that the cartilage disks between vertebrae are damaged or become thin due to injuries or drying over time, Hannan said.

Our muscles may also play an important role in age-related shrinking. In older people, muscles can waste away, a condition known as sarcopenia. And sarcopenia is associated with poorer bone structure and a higher likelihood of bone loss.  Lack of muscle support around the torso will impair someone's ability to stand upright. 

"We know that people, and basically all creatures, slow down as they age," said Peggy Cawthon, the scientific director and an epidemiologist at the California Pacific Medical Center, told Live Science. 

But whether this slowdown causes people to move less, leading to muscle loss, or if people lose muscles first and then become slower is not entirely clear. 

Unlike osteoporosis, which can be treated with medications such as alendronate, there's no "magic pill" for sarcopenia, Cawthon said. 

But physical exercises and a better diet do help. "Even very old people can exercise and greatly improve their strength," Cawthon said.

Height loss may have serious health consequences. While the reason is still unclear, multiple studies have shown links between height loss and serious health conditions, such as respiratory issues and cardiovascular disease.

"You can think of [height loss] as a canary in a coal mine or an early warning," Hannan said. "If people notice they have a height loss, they should talk to their doctor or their health care provider about it," Hannan said.

An Atlantic comb jelly known as the "sea walnut" has the ability to reverse its own aging process, a new study suggests.

When food is scarce or the sea creature is injured, the gelatinous invertebrate can develop backward into its larval form, which has two tentacles to catch food. The adult form, which looks like a small pair of transparent lungs, lacks these tentacles.

The sea walnut (Mnemiopsis leidyi) is the third-known animal species, and the first-known comb jelly (Ctenophora), that can revert to an earlier life stage after already reaching adulthood, according to the study, which was published Aug. 10 on the preprint database BioRxiv. (It has not yet been peer-reviewed).

Scientists previously showed that a handful of cnidarians — a group that includes jellyfish, sea anemones and corals — can develop backward, but only before reaching sexual maturity. The two other documented species that can develop backward as adults are the so-called immortal jellyfish (Turritopsis dohrnii) and the dog tapeworm (Echinococcus granulosus).

Age reversal in comb jellies "confirms that reversal development might be more widespread than previously thought," researchers wrote in the study, which builds on previous work investigating the sea walnut's hardiness.

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

The sea walnut is native to the western Atlantic Ocean, but the species has spread to become an invasive nuisance in Europe and Asia. M. leidyi can survive in the ballast water of ships for weeks despite the lack of food, which is how researchers think the comb jellies made it across the Atlantic. The species is now found in the Black and Caspian seas, where it has contributed to the collapse of fisheries by competing with native creatures for food, as well as in the Mediterranean, Baltic and North seas.

To shed light on the sea walnut's survival tactics, the researchers carried out experiments in which they starved one group of comb jellies and physically injured another by removing tissue from their lobes. (Like other ctenophores, sea walnuts can regenerate entirely from even a small chunk of flesh. The same researchers previously found that the sea walnut's nervous system is fused, which may confer some advantage for tissue repair and healing.)

Starved and amputated sea walnuts shrunk into tiny blobs, but they didn't die. When the researchers fed both groups again, they observed that 13 out of the 65 comb jellies tested had grown tentacles, a sign they had regressed to the larval stage.

Co-author Joan J. Soto-Angel, a marine biologist and postdoctoral fellow at the University of Bergen in Norway, told Science that the jellies used their tentacles to capture food to which they would not have had access as adults, tapping into a new ecological niche. With enough food, the comb jellies eventually reached their original size again and regrew their lobes. The creatures even regained their ability to reproduce, according to the study.

Finding a third animal capable of aging in reverse "was quite a surprise," Soto-Angel said. The process by which M. leidyi regresses to its larval form is different from how the immortal jellyfish does it, he said, but both animals could help researchers understand aging better.

Comb jellies are also one of the oldest extant animal lineages and possibly the sister group to all animals, making them a unique model to study evolution.

It remains unclear whether the comb jellies really turned back the clock on their age, or whether they simply shrunk, Yoshinori Hasegawa, a zoologist at the Kazusa DNA Research Institute in Japan who was not involved in the research, told Science. “It looks like an imperfect rejuvenation,” Hasegawa said.

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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Nearly half of all dementia cases could be delayed or prevented altogether by addressing 14 possible risk factors, including vision loss and high cholesterol.

That is the key finding of a new study that we and our colleagues published in the journal The Lancet.

Dementia, a rapidly increasing global challenge, affects an estimated 57 million worldwide, and this number is expected to increase to 153 million by 2050 worldwide. Although the prevalence of dementia is on the decline in high-income countries, it continues to increase in low- and middle-income countries.

This third updated report of the Lancet Commission on Dementia offers good news and a strong message: Policymakers, clinicians, individuals and families can be ambitious about prevention and reduce dementia risk; and for those living with dementia and their caregivers, support their quality of life using evidence-based approaches.

The new report confirms 12 previously identified potentially modifiable risk factors from two previous reports, published in 2017 and 2020. It also offers new evidence supporting two additional modifiable risk factors: vision loss and high levels of low-density lipoprotein (LDL) cholesterol, often called “bad” cholesterol.

Our study of published evidence found that collectively, addressing 14 modifiable risk factors could potentially reduce the prevalence of dementia by 45% worldwide. Even greater risk reductions could be possible in low- and middle-income countries and for people with low income in higher-income countries given the higher prevalence of dementia, health disparities and risk factors in these populations.

The report further indicates that reducing these 14 risks can increase the number of healthy years of life and reduce the length of time with poor health in people with dementia.

RELATED: Gene variant carried by 1 in 5 people may guard against Alzheimer's and Parkinson's, massive study finds

Additionally, the report cites clinical trials showing that nonpharmacological approaches, such as using activities tailored to interests and abilities, can reduce dementia-related symptoms and improve quality of life.

We are a general internist and an applied sociologist and intervention scientist, and our work focuses on memory and wellness in older adults. Together with 25 other internationally recognized dementia experts under the leadership of psychiatry professor Dr. Gill Livingston, we carefully reviewed the evidence to derive recommendations for prevention, intervention and care.

Why it matters

The rapid growth of aging populations worldwide is a triumph of better public and personal health throughout the entire life span. Yet, given the lack of a dementia cure, this report highlights the importance of prevention as well as supporting quality of life for those with a dementia diagnosis.

In the new report, our team proposed an ambitious program for preventing dementia that could be implemented at the individual, community and policy levels and across the life span from early life through mid and late life. The key points include:

• In early life, improving general education.
• In midlife, addressing hearing loss, high LDL cholesterol, depression, traumatic brain injury, physical inactivity, diabetes, smoking, hypertension, obesity and excessive alcohol.
• In later life, reducing social isolation, air pollution and vision loss.

Together, these add up to the Lancet Commission on Dementia’s estimate that 45% of dementia risk can be reduced. And an abundance of new research shows that when risk factors are addressed, such as exposure to air pollution, they are linked with improved cognition and likely reduction of dementia risk.

New evidence supports the notion that in high-income countries, reducing dementia risk can translate to more healthy years, years free of dementia and a shorter duration of ill health for people who develop dementia.

What still isn’t known

The 45% reduction in dementia risk across the world’s population is based on a calculation that assumes that risk factors are causal and can be eliminated. It shows how dementia prevention is critical and the impact it would have on individuals and families.

The commission emphasized the need for more research to identify additional risk factors, test risk factor changes in clinical trials, provide guidance for public health efforts, and identify and evaluate strategies for implementing and scaling evidence-based programs that support people with dementia and caregivers.

The updated report has worldwide public health and research impact and is being widely disseminated. It serves as a guideline to clinicians and policymakers and outlines new research directions.

The Research Brief is a short take on interesting academic work.

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

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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As males reach their 40s and 50s, they may start to experience erectile dysfunction and declines in their sex drive, all while they produce less and less testosterone. These changes may sound akin to those that arise during perimenopause and menopause, the time windows that lead up to and then follow a female's last menstrual period.

Given these similarities, could this mean there's a "male menopause"? 

Not really, an expert told Live Science — although the changes that aging males experience can still affect their quality of life.

Although middle-aged males describe symptoms similar to those that females experience during menopause, including hot flashes, calling these experiences "male menopause" would not be accurate.

Related: Why do women tend to outlive men?

The hormone-making functions of a male's testes and a female's ovaries decline with age, but in the case of females, this happens abruptly — over the course of a couple of years. In males, this age-related decline is more gradual, taking several decades. The key hormone made by the testes is testosterone, the primary male sex hormone that's responsible for supporting sexual development and function.  

"Andropause" is a nonmedical term that's often used to describe the declining testosterone levels seen in aging men, Dr. Jesse Mills, director of the Men's Clinic at UCLA Health, told Live Science in an email.

"But it's not the same as menopause," Mills said, since men can maintain testosterone levels in the "normal" range into their 80s and beyond.

In comparison, females usually enter perimenopause, or the transition toward menopause, around the ages of 45 to 55. During this time, the ovaries make much less estradiol, the main form of estrogen in the body before menopause. At its peak, estradiol can reach levels up to 400 picograms per milliliter (pg/mL) of blood, and  these levels can fall to less than 0.3 pg/mL after menopause.

The body continues making another, weaker form of estrogen — called estrone — but it can't make up for the lost estradiol. This leads to the loss of periods, changes in vulvar tissue, hot flashes and diminished vaginal lubrication associated with menopause.  

While males do see declining testosterone levels as they age, according to Mills, their symptoms are not nearly as dramatic as what females go through. Testosterone levels fall at an average of 1.6% a year in males, starting around age 30. The testes would only completely stop making testosterone in the event a person lost testicular function due to disease, an accident or castration, which might be used to treat prostate cancer, for instance. 

Related: Move over, Viagra — this spider's boner-inducing venom could treat people let down by the blue pill 

The exact reason for age-related declines in testosterone is not fully understood. Some evidence suggests that the cells that make testosterone grow less responsive and decline in number with age. Signals from the brain would normally direct these cells, and that signaling also changes with age.

"Low testosterone is associated with many things that get worse as we age," Mills noted. "Diabetes, high blood pressure, high cholesterol, poor sleep and lower activity are common examples." There's a known link between low T and these conditions, but at this point, it's not clear if one leads to the other, or vice versa.

Mills recommends adopting healthy lifestyle practices to help maintain testosterone levels into old age, as there's some evidence that such interventions can help. For instance, he recommends intensive exercising 20 minutes a day, getting at least seven hours of deep sleep each night, staying hydrated and consuming a diet rich in lean proteins and green vegetables.

When asked whether aging men should take testosterone supplements, Mills said that individuals should do so only if they need it. 

International guidelines suggest men with testosterone levels lower than 350 nanograms per deciliter (ng/dL) of blood who are experiencing symptoms may benefit from such supplements, he said. In particular, older men with levels under 200 ng/dL are at higher risk for brittle bones, heart disease and weight gain, as well as sexual symptoms such as erectile dysfunction and low libido, Mills said.

Many direct-to-consumer companies make supplements available to people with normal testosterone levels, Mills noted. The supplements don't necessarily pose a danger, but they may not be very beneficial to those without a testosterone deficiency, he said. 

It's important to emphasize that the effects of testosterone on health and life span aren't yet fully understood, so future studies may provide better guidance.

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

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A single, small molecule can restore muscle strength, fuel brain cell growth and reduce inflammation in old mice, new research shows.

So far, the anti-aging molecule has only been tested in rodents and in human cells in lab dishes. But the researchers say the results are compelling enough to move the compound toward human trials, potentially within a few years. 

"Given the strength of the preclinical data, it is my view that there's justification for moving this forward," said senior study author Dr. Ronald DePinho, a professor and former president at The University of Texas MD Anderson Cancer Center.

"We have confidence that this mechanism would have beneficial effects with respect to things that impact health span," enabling people to live healthier lives into old age, DePinho told Live Science. 

Related: 'Biological aging' speeds up in times of great stress, but it can be reversed during recovery 

Reversing aging with one molecule

In  the new study, published June 21 in the journal Cell, researchers looked to increase the amount of a protein that normally dwindles with age: telomerase reverse transcriptase (TERT).

TERT is a key cog in a cellular machine that extends the length of telomeres — protective caps that prevent fraying at the ends of chromosomes. The shortening of telomeres has been tied to aging and age-related diseases, such as cancer. This shortening happens partly because, with age, chemical tags build up on our chromosomes, causing what's known as "epigenetic" changes. Some of these changes switch off the gene for TERT, causing cells to make less of the protein. 

This threatens the integrity of telomeres and has wide-ranging effects on how much other genes are expressed. That's because TERT seems to be a master controller that helps regulate a suite of genes tied to aging, including genes involved in brain cell growth and senescence, a zombie-like state that more and more cells enter as the body ages. As these zombies grow in number, they trigger damaging inflammation in the body.  

"Our lab was the first to show that aging is a reversible process," and that TERT can mediate that shift into reverse, DePinho said. In 2010, DePinho and colleagues reported that, when they switched off the TERT gene in mice using experimental methods, the animals aged prematurely.

"When we flipped it back on, we were expecting just an arrest of the aging process," DePinho said. "But instead we saw rejuvenation." 

This rejuvenation showed up in cells across the body. Subsequent work by the team showed that restoring "youthful" levels of TERT in a mouse model of Alzheimer's disease reversed signs of the illness, including the accumulation of abnormal proteins in the brain.  

Given these results, in the new study the researchers wanted to uncover drug-like substances that could boost TERT to levels seen in healthy, young cells. They developed a screen using mouse cells tweaked to carry the human version of the TERT gene. They screened 653,000 compounds in total, landing on one that appeared most potent, which they dubbed TERT-activating compound (TAC).

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

In lab dishes, the molecule increased the amount of TERT in healthy human cells and in cells derived from people with Werner syndrome, a rare condition that causes rapid, premature aging. These latter cells notably lengthened their telomeres when exposed to the molecule. 

In mice injected with TAC, the molecule boosted TERT in tissues throughout the body, including the brain. This suggests the drug passes easily into the brain, DePinho said, which many molecules cannot.

In aged mice, the researchers looked at short-term treatments with TAC, lasting around one week, and chronic treatment lasting six months. The short-term treatment reversed signs of aging in blood cells; reduced a known driver of senescence in many tissues; and boosted a key molecule for brain cell growth. Long-term treatment increased brain cell growth in the hippocampus, a key memory center in the brain, and also seemed to improve the rodents' performance in memory tests. Additional tests showed it improved the mice's coordination and muscle strength, too.

TAC works by jump-starting a chain of events in cells that switches on a master gene regulator and ultimately unmutes the TERT gene. These effects are temporary, peaking within about eight hours and wearing off after 24 hours of injection, DePinho said.

Within that time window, the drug "restores physiological, youthful levels of TERT," he said. 

More work will be needed to bring TAC to human patients. The next steps will be to modify the drug to improve its potency as well as identify and weed out any harmful effects. (None were observed in these initial experiments.) The drug, or a derivative of it, will need to be tested further in animals before moving into trials with healthy human volunteers and then people with various age-related diseases, DePinho said.

In theory, the drug could be explored as a way to prevent age-related disease before it even sets in, but it would likely be approved for a specific disease, like Alzheimer's, first, DePinho said.

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"Zombie cells" lurking in the placenta may underpin a type of heart failure that strikes in late pregnancy or shortly after birth, a new study finds.

These undead cells point to potential ways to treat the poorly understood condition, known as postpartum cardiomyopathy (PPCM), which weakens the heart so it can't pump blood as efficiently. Symptoms of this type of heart failure range from mild to deadly, and it affects an estimated 1 in 1,000 live births in the U.S. and closer to 1 in 100 live births in Nigeria.

The new study, published Wednesday (April 17) in the journal Science Translational Medicine, may also shed light on biological aging — a process that appears to speed up during pregnancy, at least by some measures. 

"We do believe that there may be a link here," first study author Dr. Jason Roh, an assistant professor of medicine at Harvard Medical School and a cardiologist at Massachusetts General Hospital, told Live Science in an email.

Studies of biological aging in pregnancy have looked mostly at epigenetics — chemical tags found on top of DNA — but the new study looked at proteins made by cells in the placenta. There isn't yet direct evidence linking these two processes, but that could potentially be revealed in later research.

Related: 'Mini placentas' may reveal roots of pregnancy disorders like preeclampsia

Biological aging in the placenta

The exact cause of PPCM is a mystery, but the condition has been tied to preeclampsia, a condition involving persistent high blood pressure that emerges between midpregnancy and the postpartum period. It's well established that preeclampsia is a risk factor for this type of heart failure, but in recent years, emerging evidence has suggested that the two conditions may actually share underlying causes.

This overlap seems related to substances that increase in the blood during pregnancy.

The idea is that, in mothers with a genetic risk, these conditions are "unmasked by certain factors released into the blood during late pregnancy," said senior study author Dr. Anthony Rosenzweig, a professor of medicine at the University of Michigan and the director of the Stanley and Judith Frankel Institute for Heart and Brain Health. "These circulating factors are thought to have direct effects on the function of the mom's heart," Rosenzweig told Live Science in an email.

To identify what these factors might be, the team screened for more than 1,000 proteins in the blood of patients with PPCM or preeclampsia. They compared these patients to people with uncomplicated pregnancies; people with heart muscle problems unrelated to pregnancy; and people with gestational diabetes.

They found that, as shown in previous studies, people with PPCM or preeclampsia carried more proteins related to inflammation in their blood than the comparison groups did. But they also showed a distinct signature of biological aging, despite all of the study participants being in their 20s and 30s.

This signature has historically been tied to "senescence," a state that cells can enter following damage or stress. Senescent cells stop multiplying but start spewing molecules that alter the tissue around them, sparking inflammation, for example. The immune system then clears these cells away, but as the body ages, this cleanup becomes less efficient and the senescent cells accumulate. This buildup has been tied to age-related diseases such as cancer.

Because the placenta is a temporary organ that's not needed after pregnancy, it's known to show extensive signs of senescence toward the end of pregnancy. That part is normal. But the researchers speculated that maybe, in PPCM and preeclampsia, this aging process happens faster than usual.

"After picking up this signal in the blood, we knew we were on to something," Roh said. They found that 28 senescence-related proteins were boosted in the blood of people with the conditions, and the same proteins showed up in placental tissue from people with preeclampsia.

The most dramatically boosted protein was Activin-A, which has previously been tied to heart failure and cardiac complications of COVID-19 in older adults, Rosenzweig noted. To confirm the protein's relevance in this new context, the team looked at blood samples and medical records of two independent groups of women with preeclampsia or PPCM. In both, Activin-A levels were not only high but were also correlated with poor cardiac function and heart failure.

What's more, the team found that blocking Activin-A dramatically reduced the incidence of heart failure — at least in pregnant mice prone to PPCM. They tested two different methods of blocking the protein; one was tested in early pregnancy and one in late pregnancy.

"While these experiments [provide] exciting proof-of-concept validation for the role of these pathways," Rosenzweig said, "the safety and efficacy of this approach needs to be rigorously assessed in clinical studies." So while the mouse experiments hint at future treatments for people, much more work needs to be done.

"We still don't fully understand why placental senescence becomes so perturbed in these conditions," Roh said. "If we are to intervene on this process, it is absolutely critical that we first rigorously determine the best approaches to safely and effectively target it to optimize both the mom's and baby's health."

There's also a lingering question as to whether placental senescence could be partly responsible for the health effects of sped-up biological aging seen later in life, he added. In this particular study, though, the subjects weren't followed over time, so that's a question for future research.

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The science of why we age is a hot topic, with studies pointing to changes in our chromosomes, cellular stress and epigenetics as culprits. These changes are difficult to reverse with treatments — but what if there were a molecular cause of aging that we could change more easily?

In a study published Friday (April 12) in the journal Nature Aging, researchers may have identified a particular kind of fat molecule, or lipid, that plays a major role in the aging process. This lipid, called bis(monoacylglycero)phosphate (BMP), was found at consistently higher levels in the muscles of older people than in those of younger people. And notably, those high levels fell with short periods of exercise. The researchers also studied this effect in more detail in mice.

Aging research lacks detailed studies of fat molecules, "so it was great to see this study doing such a comprehensive analysis of the changes in many different tissues in mice and humans," Dr. Alexandra Stolzing, a professor of biogerontological engineering at Loughborough University who was not involved in the study, told Live Science in an email.

Related: 'Biological aging' speeds up in times of great stress, but it can be reversed during recovery

Creating a map of fat

Scientists generally understand how simple fats, such as cholesterol, contribute to aging and diseases like coronary artery disease. However, "little is known on how 'complex' lipids contribute," said Dr. George Janssens, an assistant professor of genetic metabolic disease at Amsterdam UMC and first author of the study.

The researchers started exploring this relationship by analyzing the fats of young and old mice. Using "lipidomics" — a technology that quantifies the many different fats in the same tissue simultaneously — they looked at 10 different tissues and identified more than 1,200 unique types of lipids.

What jumped out at them was the consistent increase of BMP in old mice, which they saw across most of the tissues analyzed.

The researchers then analyzed muscle tissue biopsied from human volunteers of different ages; younger participants were 20 to 30 years old while older participants were ages 65 to 80. Again, they found that BMP accumulated in the aging tissue.

"The nearly tissue-wide accumulation of one lipid in mice, and the same change conserved in human muscle … was astonishing," Janssens told Live Science in an email. The results suggest that BMP lipids may be a driving force in the aging process — however, more research is needed to determine whether they actually drive aging or rather increase as a result of it.

An hour a day keeps the lipids away

Evidence suggests that even short bouts of daily exercise reduce people's risk of early death. And in general, exercise has been closely linked with improvements in longevity, with one explanation being that it tends to change how the body breaks down lipids.

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

In a second phase of their study, the researchers analyzed the lipid content in people's muscles once before and once after they exercised one hour a day for four days. They compared these numbers with those of people who remained seated for most of that time period.

Surprisingly, even within such a short time frame, BMP levels were significantly reduced in those who exercised versus those who were sedentary. This suggests this lipid could be a key player in the benefits of exercise on longevity.

"This study is intriguing" because the researchers discovered that this fat increases with age in both mice and humans, said Adiv Johnson, director of research and innovation at the longevity company Tally Health, who was not involved in the study. But the findings also show that exercise — "a powerful pro-longevity intervention" — can deplete this age-related fat in humans, he told Live Science in an email.

"The idea that we could reverse aging is something that was long considered science fiction," senior study author Riekelt Houtkooper, a professor of genetic metabolic diseases at Amsterdam UMC, said in a statement. "But these findings do allow us to understand a lot more about the aging process."

The scientists plan to conduct further studies to learn why BMP accumulates in the first place and whether methods other than exercising could deplete BMP. 

Until then, the study provides one hint as to why going for a walk or run around the neighborhood might help us live just a little longer. For those who are physically unable to exercise, there could be other solutions on the horizon, as some scientists are working on drugs to mimic the helpful effects of physical activity. 

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

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Women in their early 20s who have been pregnant are "biologically older" than those who have never been pregnant, and by some measures, this age gap seems to widen in people who have had multiple pregnancies, a new study suggests.

The research, conducted in the Philippines, used various tools to look at people's epigenetics, meaning the chemical tags attached to their DNA. These tags don't change the DNA's underlying code but rather help control which genes are activated and to what degree. The new study specifically looked at methyl groups, a type of molecule long linked to different aspects of the aging process.

By studying patterns of methylation seen throughout the human life span, scientists have created a number of "epigenetic clocks" that can be used to assess a person's biological age. While chronological age simply reflects how long someone's been alive, biological age reflects their physiological state and chances of age-related diseases and death.

"What epigenetic clocks are doing is they're serving a predictive function rather than a sort of causal explanation," said first study author Calen Ryan, an associate research scientist in the Columbia Aging Center. "They're trained to predict things that we think of as representing aspects of aging." So one clock may be designed to predict a person's chronological age, while others predict a person's likelihood of death and still others estimate the length of their telomeres, the protective caps at the end of DNA that keep it from fraying.

Related: 'Biological aging' speeds up in times of great stress, but it can be reversed during recovery

The research, published Monday (April 8) in the journal PNAS, used six different epigenetic clocks to make predictions about 1,735 young women and men in the Philippines. The full group had blood samples taken in 2005, between the ages of 20 and 22. A subset of the women — around 330 — who became pregnant in the years following their first blood sample also had a second sample taken about four to nine years afterward.

Across all of the clocks used, women who'd had at least one pregnancy showed accelerated aging compared with women with no pregnancy history, the analysis revealed; the pregnancies included those that resulted in miscarriages, stillbirths and live births. The pattern still showed up when the scientists controlled for other factors that also affect a person's rate of biological aging, such as socioeconomic status, smoking history and some genetic risk factors.

The researchers also found that women who'd had more pregnancies showed faster aging than those with fewer pregnancies "for all six of the clocks," Ryan told Live Science. "We do not find that relationship among the men we looked at cross-sectionally." In other words, the number of pregnancies a man fathered didn't seem to affect the speed at which his epigenetic clock ticked.

(Notably, the men looked biologically older than the women overall, regardless of pregnancy status; it's just that impregnanting people didn't increase the men's biological ages even higher. This pattern of biological aging in men is consistently seen across epigenetic-clock studies and may be connected to men generally dying at younger ages than women, Ryan said.)

The team then looked at the 330 women they followed over time, to see if there were differences between the women's first and second blood samples. In that analysis, experiencing more pregnancies also was associated with faster aging compared with fewer pregnancies. However, this pattern showed up for only two of the six clocks — specifically the two designed to predict chronological age.

Based on all of these data, the team estimates that each pregnancy was tied to about 4 to 4.5 months of biological aging among the women in the study.

Related: Epigenetics linked to the maximum life spans of mammals

The study's findings may have been affected by where it was conducted. For instance, people's access to adequate nutrition, health care and social support during pregnancy vary throughout the Philippines, and these factors may influence the extent to which pregnancy influences aging. It's also relevant that most epigenetic clocks have been confirmed to work well at tracking aging in white people in developed countries, but many clocks still need to be fully validated in people of other demographics elsewhere in the world, Ryan noted.

"They're still basically our best measures yet," but they could likely be improved for different populations, he said. More work is also needed to tease out the effects of parenting on aging from those tied to being pregnant and giving birth, the authors noted in their report.

In addition, "these women are quite young at the time of the sample," Ryan said of the study participants. So it's not clear if women who are older at the time of their first pregnancy would show the same patterns. That said, it was helpful for the team to study young women because the researchers were trying to see if biological aging tied to pregnancy could be seen early, before the health outcomes of accelerated age show up.

If you can catch this accelerated aging early, that could theoretically inform future treatments to help prevent or reverse the process, Ryan said — although at this early stage of research, it's unclear what such treatments would entail.

Similar upticks in biological aging have been seen in some other contexts, but not all. For example, they've been observed among Filipino women in the U.S. but not in women in Finland. A recent Yale study also found that epigenetic clocks accelerate during pregnancy but that much of that effect disappears after the child's birth, especially in people who breastfeed.

So "we do have decent evidence of biological aging being sped up from pregnancy, but maybe not in all contexts," Ryan said.

For now, this new study is helping scientists start to unpack the impact of pregnancy on the aging process. Someday, though, it could pave the way for medical interventions.

"My hope is that we can start to maybe use tools like this [epigenetic clocks] to identify at-risk individuals," meaning people who may age more with each pregnancy, Ryan said. If they can identify factors that help buffer against biological aging, scientists could potentially design interventions that mimic those factors in people more susceptible to it.

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For science, volunteers sniffed out odorous chemicals in the armpit sweat of babies and teenagers. Perhaps unsurprisingly, they found that young children smelled like flowers and teens smelled like goats — but now, we know which chemicals are responsible for each of these odors.

Many of us are familiar with babies' sweet scent, but we may wince while catching a whiff of a teen who's skipped out on that day's deodorant. Previous studies have also found that parents prefer the odors of babies to those of teenagers, which may somewhat influence their affection toward their children. Intrigued by the role scent plays in relationships, lead study author Helene Loos, an aroma researcher at Friedrich Alexander University in Germany, aimed to explore how BO changes throughout life.

In the research, published March 21 in the journal Communications Chemistry, Loos and her colleagues provided 18 young children, ages 0 to 3, and 18 teenagers, ages 14 to 18, with T-shirts with cotton pads sewn into the armpits. After the participants wore the tees for one night's sleep, the researchers sampled smelly substances that had soaked into the pads.

Using gas chromatography, a technique that splits up chemicals with different properties, the researchers separated and detected the individual odorants in each BO sample. Then, they asked volunteers to smell and describe each chemical's scent.

Related: Super sensitive to BO? Maybe blame your genes

Forty-two odorants were detected, with both age groups producing most of them, Loos told Live Science. Note that a single odorant can set off many smell sensors in the nose, and combinations of odorants can trigger unique and complex patterns of activity that differ from what one odorant does alone. Nonetheless, the component scents in a given bouquet influence whether it smells bad or good to the sniffer.

"We were not surprised by the overall findings, but it was very interesting to see the rich variety of compounds," Loos said of the odorants detected. Among these, a group of chemicals called aldehydes was the most diverse, giving off "cardboard-like," "deep-fried" and "nutty" aromas, for example.

BO from both age groups also contained carboxylic acids, a class of organic compounds. Some were pleasant, giving off "fruity" or "dried plum-like" notes. Others were less so, smelling "cheesy," "musty" or like "goat." The team diluted each carboxylic acid several times to assess how intensely each one contributed to BO in both groups. The carboxylic acids from teens' armpits retained their scents after more dilutions than did those from young children, suggesting the chemicals might be secreted in higher concentrations after puberty.

The teen BO also harbored two steroids that were absent from the young kids' samples. One smelled like sandalwood, a common fragrance in perfumes. The other smelled like sweat and urinals — parfum de locker room, if you will.

Changes in people's BO between infancy and puberty may be linked to alterations in their skin, including hormonal changes; a shift in its lipid, or fat, makeup; differences in the skin microbiome; or the activation of sweat glands and sebum glands, which exude an oily substance. However, it's still unclear which of these anatomical changes may explain the differences in this study.

Related: Humans can 'smell' each other's emotions — but we don't know how

In studying the participants' self-made body odorants, "we were very careful in considering all kinds of potential contamination," Loos said. They asked the infants' parents and the teens to avoid smelly foods containing spices, onions or garlic, and they provided perfume-free shower gels and unscented detergents. Nonetheless, many odorants picked up in BO samples were also detected in these provided supplies, so it's unclear how much they influenced the findings.

Conscious that odorants in the air might absorb into the cotton pads, the researchers also provided each participant with a second T-shirt to leave in the room, unworn. Most of the 42 odorants were also found in these unworn tees, but it's unclear whether they emanated off the participants or came from another source.

Some chemicals previously linked to BO went undetected in this study, including acetic acid, which gives vinegar its signature scent. This may be explained by the team studying a small, non-diverse cohort, or the fact that techniques differ in their ability to detect different substances.

Loos and colleagues plan to employ other approaches to capture a wider variety of odorants, as well as to explore how BO changes in other age groups, including older people. They also want to study more-intense BO, following exercise or multiple nights of sleep, for instance.

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