It's easy to feel powerless against cancer, but a new study has identified several ways that we can reduce the odds of it occurring.

According to new analysis from the World Health Organization (WHO), more than a third of all cancer cases globally are preventable.

Lung, stomach, and cervical cancers make up nearly half of those cases.

This means that millions of deadly cancers every year could be prevented through medical intervention, behavior changes, reducing occupational risks, or tackling environmental pollutants.

"Addressing these preventable causes represents one of the most powerful opportunities to reduce the global cancer burden," says Isabelle Soerjomataram, medical epidemiologist at WHO and senior author of the analysis.

The analysis found that in 2022, there were nearly 19 million new cases of cancer. Roughly 38 percent of those diagnoses were related to 30 changeable risk factors.

These included tobacco smoking, alcohol consumption, high body mass index, insufficient physical activity, smokeless tobacco (like chewing tobacco), a traditional stimulant known as areca nut, suboptimal breastfeeding, air pollution, ultraviolet radiation, infectious agents, and over a dozen occupational exposures.

The number one preventable factor associated with cancer? Smoking tobacco. It was linked to 15 percent of all cancer cases that year.

For men, the risk was particularly high. Smoking contributed to 23 percent of all new cancer cases globally in men that year.

But smoking isn't the only cause; air pollution also plays a role, and its impact varies by region. In East Asia, for instance, about 15 percent of all lung cancer cases in women were due to air pollution. In Northern Africa and Western Asia, meanwhile, approximately 20 percent of all lung cancer cases in men were due to air pollution.

After tobacco smoking, the runner-up among changeable lifestyle factors was drinking alcohol. It accounted for 3.2 percent of all new cancer cases (approximately 700,000 cases).

Infections, meanwhile, were linked to roughly 10 percent of new cancer cases. Among women, the largest share of preventable cancers was due to high-risk human papillomavirus (HPV), which can lead to cervical cancer.

Thankfully, we now have a vaccine for HPV that prevents many of these associated diseases, and yet coverage in many parts of the world remains low.

Stomach cancer cases are higher among men and tend to be associated with smoking and infections due to overcrowding, inadequate sanitation, and poor access to clean water.

Related: US Cancer Survival Has Reached a Milestone High of 70%

"By examining patterns across countries and population groups, we can provide governments and individuals with more specific information to help prevent many cancer cases before they start," says André Ilbawi, WHO Team Lead for Cancer Control and co-author of the analysis.

Now it's time to roll up our sleeves.

The study was published in Nature Medicine.

A common bacterium usually found in the respiratory system appears to be linked to cognitive decline and Alzheimer's disease when it's present in the retina.

Chlamydia pneumoniae – often responsible for pneumonia and sinus infections – has previously been spotted in brains affected by Alzheimer's. Now, a new study has detected C. pneumoniae in the vision-generating tissue that lines the back of the eye, at higher levels in people with Alzheimer's.

Led by a team from Cedars-Sinai Medical Center in the US, the research provides fresh insight into the biological processes that may worsen Alzheimer's progression – and could inspire new approaches to slowing the disease.

As well as potentially contributing to the cascade of mechanisms that lead to Alzheimer's, the presence of C. pneumoniae in the retina could also one day be used to detect cognitive decline and dementia – though that possibility wasn't directly tested here.

"The eye is a surrogate for the brain, and this study shows that retinal bacterial infection and chronic inflammation can reflect brain pathology and predict disease status, supporting retinal imaging as a noninvasive way to identify people at risk for Alzheimer's," says neuroscientist Maya Koronyo-Hamaoui, from the Cedars-Sinai Medical Center.

To begin with, the team analyzed eye and brain tissue from 104 people after death. Some had Alzheimer's disease, some had mild cognitive impairment (MCI), and some hadn't reported any cognitive problems.

They found a clear association between the presence of C. pneumoniae in the eye and brain and having a diagnosis of Alzheimer's. Higher levels of the bacterium in tissue were linked to more severe cognitive decline.

People with APOE gene variants linked to Alzheimer's risk also had higher levels of the bacterium in their tissues. However, the differences between people without cognitive impairment and those with MCI were much less clear-cut when it came to C. pneumoniae.

Next, the researchers ran tests using lab-grown neurons and animal models to determine what C. pneumoniae might be doing biologically. These experiments showed that infections with the bacterium led to increased inflammation, greater cognitive decline, and more nerve cell death.

The presence of C. pneumoniae was also associated with increased amounts of amyloid-beta protein in the brain, which is known to clump together in dangerous ways in the brains of people with Alzheimer's.

"Seeing Chlamydia pneumoniae consistently across human tissues, cell cultures, and animal models allowed us to identify a previously unrecognized link between bacterial infection, inflammation, and neurodegeneration," says Koronyo-Hamaoui.

There are still unanswered questions, and the findings are only a strong suggestion that C. pneumoniae could contribute to (and be a sign of) Alzheimer's disease – not conclusive proof.

However, if infection by the bacterium is indeed leading to inflammation that extends to the brain and accelerates neurodegenerative processes, then we may have a new target for future treatments.

The researchers describe C. pneumoniae as a potential amplifier rather than a primary trigger, which aligns with growing evidence of just how complex Alzheimer's is. It's likely there are multiple contributing factors that may differ between people.

What's more, the team identified a specific inflammation pathway that C. pneumoniae targets, possibly worsening the damage already being done by Alzheimer's. Further studies will be required to confirm this mechanism, but the signs are there.

Related: A Common Sleeping Pill May Reduce Buildup of Alzheimer's Proteins, Study Reveals

Scientists continue to identify multiple ways the eyes and the brain are linked. In this case, the findings could prove valuable to society's ongoing efforts to combat Alzheimer's and other forms of dementia.

"This discovery raises the possibility of targeting the infection-inflammation axis to treat Alzheimer's," says biomedical scientist Timothy Crother, from the Cedars-Sinai Medical Center.

The research has been published in Nature Communications.

Physical abilities fade as we age, but many of us like to think that won't be an issue until we're well into our golden years.

According to a new study, however, fitness and strength begin to dwindle as early as age 35, regardless of exercise habits. This is followed by a gradual decline that accelerates with age.

While this fate may be unavoidable, that doesn't mean it's out of our hands. Even if physical activity won't help us delay our peak, it can make a difference in how rapidly our abilities deteriorate, the study suggests.

Aging involves a progressive decline in skeletal muscle, which can noticeably manifest for some people in their 60s, sometimes limiting mobility.

Previous research on elite athletes has shown that, despite continuous training, physical performance typically peaks by about age 30. This suggests the mechanics behind age-related muscle loss could already be at work decades before they become clinically significant.

There are advantages to studying physical abilities in athletes, such as data availability and lack of interference by sedentary lifestyles, but there is also the "obvious disadvantage" that elite athletes may not be representative of the general population, the authors note.

For the new paper, researchers conducted a population-based longitudinal study in hopes of measuring the physical capacity of the general population from adolescence to older age.

Research on this subject has typically relied on cross-sectional studies, which analyze data from a population at a specific point in time. Longitudinal studies can therefore provide valuable perspectives on how variables may change over a period.

The researchers used data from the Swedish Physical Activity and Fitness (SPAF) cohort study, a longitudinal study that has been following several hundred participants in Sweden since 1974, when they were 16 years old.

The SPAF includes strength and fitness data from these same people at five intervals in the last five decades (ages 16, 27, 34, 52, and 63), offering a unique opportunity to measure changes in physical abilities over half a century.

Cross-sectional studies seem to have underestimated the age-related decline in physical capacity, the researchers report, but their findings support existing evidence that it affects men and women similarly.

For both sexes, muscular endurance and estimated maximal aerobic capacity peaked between ages 26 and 36 before gradually declining, first by 0.3 percent to 0.6 percent per year, and later by up to 2.5 percent per year, with no sex difference in the rate of decline.

There was a difference in muscle power, with men and women peaking at ages 27 and 19, respectively. Their muscle power then faded at similar rates, initially decreasing by 0.2 percent to 0.5 percent per year, and later escalating to an annual decline of 2 percent or more. By age 63, participants' overall drop from their peak physical capacity ranged from 30 percent to 48 percent.

There is good news. While we may be unable to dodge or delay our physical decline, we can reduce its speed with regular exercise, the authors report.

"Individuals who were physically active in their leisure time at age 16 maintained higher aerobic capacity, muscular endurance, and muscle power throughout the observation period," they write.

This highlights the importance of promoting physical activity to teenagers and young adults, but that message is helpful no matter how old you are. Participants who became more active in adulthood still managed to improve their physical capacity by around 10 percent, the study found.

Related: Study Reveals The Surprising Age at Which Your Brain Reaches Its Peak

"It is never too late to start moving. Our study shows that physical activity can slow the decline in performance, even if it cannot completely stop it," says lead author Maria Westerståhl, lecturer in the Department of Laboratory Medicine at the Karolinska Institute.

"Now we will look for the mechanisms behind why everyone reaches their peak performance at age 35, and why physical activity can slow performance loss but not completely halt it," Westerståhl says.

The study was published in the Journal of Cachexia, Sarcopenia and Muscle.

Yawning has an unusual and unexpected effect on the flow of fluid protecting the brain, a recent study reveals, though it's not yet clear what the impact of this shift might be.

According to researchers from the University of New South Wales in Australia, the findings could provide a crucial clue in understanding why humans (and many other species) evolved the capacity to yawn.

The research team used MRI to scan the heads and necks of 22 healthy participants while they were told to yawn, take deep breaths, stifle yawns, and breathe normally.

Given that yawning and deep breathing share similar mechanisms, the researchers expected them to look similar on the scans. Surprisingly, the images revealed a key difference: unlike deep breaths, yawns sent cerebrospinal fluid (CSF) away from the brain.

"The yawn was triggering a movement of the CSF in the opposite direction than during a deep breath," neuroscientist Adam Martinac told James Woodford at New Scientist.

"And we're just sitting there like, whoa, we definitely didn't expect that."

This wasn't observed in every case, and occurred less often in men, though the researchers caution that this may be due to interference from the scanner itself.

The analysis also revealed that both deep breaths and yawns increased the flow of blood leaving the brain, making more room for fresh blood to be pumped in.

Blood flow didn't change direction with yawns. Yet during its initial stages, carotid arterial blood flow into the brain surges by around a third, providing potential evidence for multiple reasons for the behavior.

In addition, the participants all had unique yawning patterns that were closely followed each time they yawned. It's a sign that we all have our own central pattern generator determining how we yawn.

"This flexibility might account for the variations in inter-participant yawning patterns while still maintaining a recognizable, individual-specific pattern; and implies that the patterns of yawning are not learned but are an innate aspect of neurological programming," write the researchers in their paper.

The next big question is what all of this means, and why yawns should differ from deep breaths so substantially when it comes to CSF, a fluid that keeps the central nervous system running smoothly, delivering nutrients and removing waste.

One possibility raised by the researchers is that yawning has a specific role in cleaning out the brain. Another idea is that it's some kind of brain cooling function in operation.

Yawns do appear to be closely connected to the brain and the central nervous system – bigger brains typically lead to longer yawns, for example, perhaps a nugget of trivia you can share with friends and family the next time you yawn for an extended period of time.

Related: This Article on The Science of Yawning Will Probably Make You Yawn

Yawning continues to be a rather baffling phenomenon with a largely unclear purpose, despite being a behavior seen in many different species, and which tends to be contagious among people and animals.

"Yawning appears to be a highly adaptive behavior and further research into its physiological significance may prove fruitful for understanding central nervous system homeostasis," write the researchers.

The research has yet to be peer-reviewed, but is available on bioRxiv.

For more than a century, the Green River's course through the Uinta Mountains in Utah's northeast has been a geological mystery, seemingly defying physics.

Rivers carve their paths by flowing downhill across many years, which means they usually follow the slopes and furrows of any mountain ranges they encounter.

And yet the Green River, which has been following this course for just 8 million years, cuts right across the 50-million-year-old mountains to meet with the Colorado River, etching out the 700-meter (roughly 2,300-foot) deep Canyon of Lodor that runs perpendicular to the range (and all logic).

Geologist Adam Smith from the University of Glasgow in Scotland led a team to interrogate this long-held mystery. It turns out, the Green River did not have to flow uphill at all: instead, the mountain range was conveniently lowered, in a phenomenon known as lithospheric drip.

"Other rivers in the Uinta Mountains provide evidence that the height of the Uinta Mountains changed in the last few million years," Smith and team write.

Their data suggests the root of the Uinta Mountains, a dense mineral chunk at the base of the lithosphere, became so heavy that it 'dripped' into Earth's liquid mantle. This would have temporarily pulled the mountain range down, allowing the Green River to chart its unlikely course.

Later, the Uinta mountains grew by 400 meters up around the river, forming the canyon we have today.

Seismic imaging involves reading the scatter of earthquake vibrations as they pass through Earth to create a picture of what's going on down there. At the Uinta Mountains, seismic images revealed a cold, round chunk about 200 kilometers below the surface: probably the drip in question.

What's more, the crust below these mountains is much thinner than you'd usually expect: more evidence that the drip had torn away the lower layers.

Related: Earth's Crust Is Dripping Under Midwest US, Scientists Discover

Once this drip broke free from the lithosphere about 2-5 million years ago, the mountain range was able to rebound. By then, the Green River had settled in for good: The Canyon of Lodor was there to stay, and the Green River became a tributary of the Colorado River.

"The merging of the Green and Colorado Rivers millions of years ago altered the continental divide of North America," Smith explains.

"It created the line that separates the rivers that flow into the Pacific from those that flow into the Atlantic, and created new habitat boundaries for wildlife that influenced their evolution."

The research is published in the Journal of Geophysical Research: Earth Surface.

For the first time, scientists have discovered evidence of bacteria hiding in 'noninfectious' kidney stones.

These hardened clumps of small crystals are made from chemicals in urine and are thought to form due to a lack of fluid or a high concentration of minerals and chemicals.

Most kidney stones are considered noninfectious after they are passed. But that may not be true after all.

A study led by researchers at the University of California Los Angeles (UCLA) has now found that calcium oxalate kidney stones, the most common type, are enriched with bacteria.

In fact, these stones contain sheets of bacteria as part of their intrinsic internal structure.

"This breakthrough challenges the long-held assumption that these stones develop solely through chemical and physical processes, and instead shows that bacteria can reside inside stones and may actively contribute to their formation," explains urologist Kymora Scotland from UCLA.

"By uncovering this novel mechanism, the study opens the door to new therapeutic strategies that target the microbial environment of kidney stones."

The findings suggest that in some cases where kidney stones keep coming back, there may be a bacterial infection in the kidney, ureter, or bladder contributing to recurrence.

If this infection is treated, then perhaps there may be fewer kidney stones going forward.

Using electron and fluorescence microscopy, the researchers found structural and chemical evidence of bacteria in calcium oxalate stones taken from human patients.

This was true even among participants without underlying urinary tract infections.

"We found a new mechanism of stone formation that may help to explain why these stones are so common," says Scotland.

"These results may also help to explain the connections between recurrent urinary tract infections and recurrent kidney stone formation, and provide insights on potential future treatment for these conditions."

Related: These 7 Common Daily Habits Could Be Damaging Your Kidneys

As many as one in 11 people will suffer from kidney stones in a lifetime, and more than 70 percent of cases are attributed to calcium oxalate stones.

If bacteria play a significant role in their formation, then treatments and guidance for kidney stones may need to be updated.

The study was published in PNAS.

Could humanity nuke an incoming asteroid to deflect it and save the Earth, disaster-movie style? A unique new impact simulation suggests that a nuclear option could be a viable last resort to avert an apocalypse.

Researchers have recently found that space rocks can withstand much more stress than previously inferred from experiments and observations. Counter-intuitively, asteroids actually grow stronger when subjected to an intense impact.

It may sound discouraging, but this discovery can improve planetary defense strategies because it suggests that a nuked asteroid will remain intact, rather than fragmenting into many space rocks that would rain down across our planet.

As detailed in a recently released paper, a team of researchers, including physicists from the University of Oxford, partnered with the Outer Solar System Company (OuSoCo), a nuclear deflection startup, to analyze what happens to an iron space rock under different levels of stress.

"These analyses are intended to examine changes in the meteorite's internal structure caused by the irradiation and to confirm, at a microscopic level, the increase in material strength by a factor of 2.5 indicated by the experimental results," explains Melanie Bochmann, co-founder of OuSoCo and co-leader of the research team.

Like the DART mission displayed in 2022, one promising way to avert an asteroid-induced apocalypse is to deflect the incoming threat with a kinetic impactor, a human-made cosmic battering ram sent to smash into a looming asteroid at many times the speed of a bullet.

It's conceptually simple, but the reality is fraught with perilous uncertainties; a hit in the wrong spot may only delay an asteroid's doomsday approach toward Earth. Furthermore, the impactor's energy and the asteroid's material response can lead to unexpected consequences like fragmentation or a surprising shift in momentum.

So, to decide between an impactor like DART or an as-yet untried nuclear approach, planetary defenders must ascertain the mechanical behavior of different asteroid materials. This knowledge is essential to transfer energy to said asteroid and redirect its trajectory away from Earth.

Yet such data is scarce, especially data that shows how materials react in real-time. For example, different models yield different values for yield strength, a measure of how easily a body breaks under stress.

These models may differ by up to a factor of seven, depending on whether they test for local (microscopic) or bulk (macroscopic). Additionally, the destructive nature of previous tests precluded direct measurement of material responses as they occurred.

"This is the first time we have been able to observe – non-destructively and in real time – how an actual meteorite sample deforms, strengthens, and adapts under extreme conditions," says Gianluca Gregori, a physicist at the University of Oxford and one of the study's co-authors.

Researchers employed a unique technique to ensure they didn't destroy the evidence. They used the Super Proton Synchrotron particle accelerator at CERN's High Radiation to Materials (HiRadMat) facility to irradiate a sample from a Campo del Cielo iron meteorite, blasting it with high-energy, short-duration proton beam pulses at lower and higher intensities.

As a result, temperature sensors and laser Doppler vibrometry (a technique to analyze surface vibrations) revealed that the meteorite sample softened, flexed, then surprisingly re-strengthened. It also displayed a quality called strain-rate dependent damping, which means that the harder it's hit, the more effectively it dissipates energy.

This study method provides invaluable data that explain why discrepancies in yield strength observed in previous laboratory experiments differ from evidence of meteor fragmentation in Earth's atmosphere, and that these discrepancies are due to factors such as internal stress redistribution.

It also highlights that these mechanical properties evolve in real time and should not be assumed to be fixed, as may often be the case in existing asteroid deflection models. Further research will involve other types of asteroid compositions.

Here, researchers chose an iron-rich sample for its relative homogeneity, but more heterogeneous space rocks will exhibit different stress-dissipation capabilities based on the spatial distribution of their constituent materials.

The ultimate scope of this research will hopefully remain theoretical:

"The world must be able to execute a nuclear deflection mission with high confidence, yet cannot conduct a real-world test in advance. This places extraordinary demands on material and physics data," says Karl-Georg Schlesinger, co-founder of OuSoCo and co-leader of the research team.

Related: NASA: Nuclear Explosion Could Save Moon From Asteroid Strike in 2032

However, should a nuclear option ever be necessary, it likely won't mirror the movies – no drilling necessary. Instead of loading an asteroid with explosives, some physicists propose a standoff nuclear detonation near an asteroid to vaporize part of its bulk and deflect its orbital path.

This research is published in Nature Communications.

Supplementing the guts of older mice with poop from younger ones has revealed the key role microbes play in intestinal stem cell function.

After receiving a fecal microbiota transplant from younger mice, one aspect of age-related decline in the guts of older mice was reversed, driven by increased intestinal stem cell activity that maintains the intestinal walls.

The findings suggest that such transplants could someday be a treatment pathway for age-related intestinal conditions, such as inflammation and obesity.

"As we age, the constant replacement of intestinal tissue slows down, making us more susceptible to gut-related conditions," says molecular biologist Hartmut Geiger of Ulm University in Germany. "Our findings show that younger microbiota can prompt older intestine to heal faster and function more like younger intestine."

Intestinal stem cells are crucial for maintaining a stable, healthy gut. They're the mechanism by which the gut lining – the epithelium – constantly replenishes and renews itself, ensuring consistent gut function.

However, as we age, the rate of this renewal slows, increasing vulnerability to age-related gut dysfunction.

In previous research, Geiger and his colleagues, cell biologists Yi Zheng and Kodandaramireddy Nalapareddy of Cincinnati Children's Hospital Medical Center, determined that this slowed regeneration is directly linked to reduced function of intestinal stem cells.

We also know that the microbial communities that live in our guts change with age, with such changes linked to conditions like Parkinson's disease, Alzheimer's disease, and even vision loss. The researchers wanted to know if the gut microbiome affects stem cell activity, too.

So, they recruited more team members and designed a simple experiment to test it: transplanting fecal samples between and within groups of old mice and young mice.

After the series of transplants was complete, the researchers studied the intestines to see what changes, if any, resulted from the transfer.

In the older mice, the change was dramatic. Stem cell activity had increased, as well as the Wnt signalling that these cells need in order to function. The regeneration of the epithelium picked up pace – and, critically, the gut healed more quickly after radiation damage.

"This reduced signaling causes a decline in the regenerative potential of aged ISCs," Zheng says. "However, when older microbiota were replaced with younger microbiota, the stem cells resumed producing new intestine tissue as if the cells were younger. This further demonstrates how human health can be affected by the other life forms living inside us."

In the younger mice, the change was less dramatic. There was only a slight drop in stem cell activity, Wnt signalling, and regeneration; the intestines continued to function reasonably well. This suggests that the aging gut is far more sensitive to microbiome changes than younger ones.

Another really interesting finding was that one of the perpetrators of stem cell curtailment in the aging gut is Akkermansia, a bacterium that is generally considered beneficial in several ways, with signs that it can help reduce diet-induced obesity and depression-like behavior in mice.

In aging mice, elevated levels of Akkermansia actually contribute to the suppression of Wnt signalling – a finding that implies that gut bacteria are not necessarily good or bad, but that their contribution may depend on context.

This isn't a slam-dunk for human health; our bodies (and intestines) are more complex than those of mice, and we'd need to perform separate studies to see if this phenomenon occurs in our own species.

Related: Most People Develop Diverticulosis in Their Gut by Age 80… So What Is It?

However, the research does illuminate a promising avenue for future study.

It also suggests that age-related stem cell decline may not be irreversible. By harnessing the ability of gut microbes to shape how intestinal tissue renews itself, scientists could one day develop ways to help preserve intestinal health as we age.

The research has been published in Stem Cell Reports.

'Zombie' coronavirus fragments not only help drive inflammation in long-COVID, but also destroy our immune cells.

A recent study by an international team of more than 30 authors reveals how the destruction of the virus within our body leaves dangerous protein fragments that target specific immune cells, which may explain some of the debilitating consequences millions of people with long-COVID now face.

"These fragments target a specific kind of curvature on the membranes of cells," explains bioengineer Gerard Wong from the University of California, Los Angeles. "Cells that are spiky, that are star-shaped, or that have lots of tentacles end up getting preferentially suppressed."

These "spiky" cells include early-warning dendritic cells that detect and alert the rest of the body to viruses, as well as CD8+ and CD4+ T cells that help destroy already infected cells.

Previous research already noted this T cell depletion, which has since been recognized as a plausible diagnostic tool.

"Viruses do so many things that we don't understand," says Wong. "We want to understand what all the leftover viral matter does to us, both during COVID and after. With these viral fragments, all of a sudden there's a whole new range of possibilities to consider."

The fact that multiple types of these viral fragments can attack immune cells may explain why those with preexisting immune conditions are more susceptible to these impacts, even when they are otherwise healthy.

In further verification, the Omicron strain of COVID-19, infamous for being highly infectious but less dangerous, breaks down into a greater variety of protein fragments in our bodies than previous strains.

"No one could really explain why it replicated as fast as the original strain but generally did not cause infections that were as serious," explains Yue Zhang, a bioengineer at China's Westlake University.

"We found that pieces of the Omicron spike were much less able to kill these important immune cells – suggesting that a patient's immune system is not going to be as depleted."

Despite the rhetoric of the pandemic being a thing of the past, COVID-19 continues to kill about 100,000 people in the US annually and disable many more. Up to 17 million people in the US had long COVID in 2024.

Related: Strange Structures Found Lurking in The Blood of People With Long COVID

Amid this backdrop, many have been left struggling without adequate support for the ongoing consequences of long COVID, which are very real and debilitating. What's more, recent studies found that the risk of long COVID can increase with subsequent infections in children and adults.

"One of the strongest reasons I give patients, families, and physicians about getting vaccinated: More vaccines should lead to fewer infections, which should lead to less long COVID," urged pediatrician Ravi Jhaveri of Lurie Children's Hospital in Chicago last September.

This research was published by PNAS.

Putting aside the risk of an early grave by accident or injury, your genes may have a much greater impact on your lifespan than previously thought, according to an unparalleled study of twin data.

The recent analysis, led by researchers from the Weizmann Institute of Science in Israel, suggests that around 55 percent of the variation in human lifespans is influenced by genes.

That's much higher than previous estimates of around 20-25 percent, with measures falling as low as just 6 percent in some studies.

The findings have implications for our understanding of genetic aging and the search for genes specifically associated with longevity, according to the researchers.

"For many years, human lifespan was thought to be shaped almost entirely by non-genetic factors, which led to considerable skepticism about the role of genetics in aging and about the feasibility of identifying genetic determinants of longevity," says molecular biologist Ben Shenhar, from the Weizmann Institute of Science.

All the myriad ways in which human life can come to an end can be put into two categories: intrinsic and extrinsic. Intrinsic deaths are driven by internal factors like aging and genetics, while extrinsic deaths cover accidents, infections, and other outside causes.

In much of the historical data used in earlier studies, causes of death weren't captured in sufficient detail, making it hard to distinguish the different factors.

Here, the team analyzed data on thousands of twins, including data on siblings raised apart, which had not been considered in lifespan heritability studies before.

Twin data is crucial for genetic studies, separating the effects of genes on an individual from everything that comes after birth such as lifestyle choices, diet, and education.

Extrinsic causes of death were sifted out using mathematical models of mortality that suggest deaths are more likely to be intrinsic the older we get.

Not only did the results closely match real-world data, but the new estimate of 55 percent is also closer to existing estimates on genes accounting for variations in other aspects of our physiology, such as height.

"Such high heritability is similar to that of most other complex human traits and to life-span heritability in other species," write the researchers in their published paper.

While the new research doesn't necessarily counter earlier studies, it does suggest that the data we've used previously haven't told the full story when it comes to the balance of life and death.

Related: Something About Brazil's Oldest People May Reveal Missing Clues on Longevity

The researchers are now seeking to test their conclusions against modern datasets that do a better job of separating different causes of death. Learning that genetics has such significance in determining lifespan raises questions on which genes have the most effect and how they work – two possible areas for future research.

"If heritability is high, as we have shown, this creates an incentive to search for gene variants that extend lifespan, in order to understand the biology of aging and, potentially, to address it therapeutically," says Shenhar.

The research has been published in Science.