Singularity HUBModify

2026-02-18 06:56:48

Gene editing is a numbers game. For any genetic tweaks to have notable impact, a sufficient number of targeted cells need to have the disease-causing gene deleted or replaced.

Despite a growing gene-editing arsenal, the tools share a common shortcoming: They only work once in whatever cells they reach. Viruses, in contrast, readily self-replicate by hijacking their host’s cellular machinery and then, their numbers swelling, drift to infect more cells.

This strategy inspired a team at the University of California, Berkeley and collaborators to modify the gene editor, CRISPR-Cas9, to similarly replicate and spread to surrounding cells.

Led by gene-editing pioneer and Nobel Prize winner, Jennifer Doudna, the scientists added genetic instructions for cells to make a virus-like transporter that can encapsulate the CRISPR machinery. Once manufactured in treated cells, the CRISPR cargo ships to neighboring cells.

The upgraded editor was roughly three times more effective at gene editing lab-grown cells compared to standard CRISPR. It also lowered the amount of a harmful protein in mice with a genetic metabolic disorder, while the original version had little effect at the same dose.

The technology is “a conceptual shift in the delivery of therapeutic cargo,” wrote the team in a bioRxiv preprint.

Recoding Genetics

CRISPR has completely transformed gene therapy. In just a few years, the technology exploded from a research curiosity into a biotechnology toolbox that can tackle previously untreatable inherited diseases. Some CRISPR versions delete or inactivate pathogenic genes. Others swap out single mutated DNA letters to restore health.

The first CRISPR therapies focus on blood disorders and require doctors to remove cells from the body for treatment. The therapies are tailored to each patient but are slow and costly. To bring gene therapy to the masses, scientists are developing gene editors that edit DNA directly inside the body with a single injection.

From reprogramming faulty blood cells and treating multiple blood disorders to lowering dangerous levels of cholesterol and tackling mitochondrial diseases, CRISPR has already proven it has the potential to unleash a new universe of gene therapies at breakneck speed.

Gene editors “promise to revolutionize medicine by overriding or correcting the underlying genetic basis of disease,” wrote the team. But all these tools are throttled by one basic requirement: Enough cells have to be edited that they override their diseased counterparts.

How many depends on the genetic disorder. Treatments need to correct around 20 percent of blood stem cells to keep sickle cell disease at bay. For Duchenne muscular dystrophy, an inherited disease that weakens muscles, over 15 percent of targeted cells need to be edited.

These numbers may seem low, but they’re still challenging for current CRISPR technologies.

“Once delivered to cells, editing machinery is confined to the cells it initially enters,” wrote the team. To compensate, scientists often increase the dosage, but this risks triggering immune attacks and off-target genetic edits.

Work Smarter, Not Harder

Although membrane-bound and seemingly isolated, cells are actually quite chatty.

Some cells package mRNA molecules into bubbles and eject them towards their neighbors, essentially sharing instructions for how to make proteins. Other cells, including neurons, form extensive nanotube networks that shuttle components between cells, such as energy-producing mitochondria.

Inspired by these mechanisms, scientists have transferred small proteins and RNA across cells. So, the team thought, why couldn’t a similar mechanism spread CRISPR too?

The team adapted a carrier developed a few years back from virus proteins. The proteins automatically form a hollow shell that buds off from cells, drifts across to neighboring cells, and fuses with them to release encapsulated cargo.

The system, called NANoparticle-Induced Transfer of Enzyme, or NANITE, combines genetic instructions for the carrier molecules and CRISPR machinery into a single circular piece of DNA. This ensures the Cas9 enzyme is physically linked to the delivery proteins as both are being made inside a cell. It also means the final delivery vehicle encapsulates guide RNA as well, the “bloodhound” that tethers Cas9 to its DNA target.

Like a benevolent virus, NANITE initially “infects” a small number of cells. Once inside, it instructs each cell to make the full CRISPR tool, package it up, and send it along to other cells. Uninfected cells absorb the cargo and are dosed with the gene editor, allowing it to spread beyond treated cells.

Compared to classic CRISPR-Cas9, NANITE was roughly three times more efficient at editing multiple types of cells grown in culture. Adding protein “hooks” helped NANITE locate and latch on to specific populations of cells with a matching “eye” protein, increasing editing specificity. NANITE punched far beyond its weight: Edited cells averaged nearly 300 percent of the initially treated number, suggesting the therapy had spread to untreated neighbors.

In another test, the team tailored NANITE to slash a disease-causing protein called transthyretin in the livers of mice. Mutations to the protein eventually lead to heart and nerve failure and can be deadly. The researchers injected NANITE directly into the rodents’ veins using a high-pressure system. This technique reliably sends circular DNA to the liver, the target organ for the disease, and shows promise in people.

Within a week, NANITE had reduced transthyretin nearly 50 percent while editing only around 11 percent of liver cells. Such results would likely improve and stabilize the disease according to previous clinical trials, although the team did not report symptoms. In contrast, classic CRISPR-Cas9 only edited four percent of cells and had minimal effect on transthyretin production.

The failure could be because the gene editor was confined to a small group of cells, whereas NANITE spread to others, “enabling more efficient tissue-level editing,” wrote the team. Extensive liver and blood tests in mice treated with NANITE detected no toxic side effects.

A three-fold boost in editing is just the beginning. The team is working to increase NANITE efficacy and to potentially convert the system into mRNA, similar to the technology underlying Covid-19 vaccines. Compared to shuttling circular DNA into the body—a long-standing headache—there is a far wider range of established delivery systems for mRNA.

Still, these early results suggest it’s possible to “amplify therapeutic effects by spreading cargo” beyond the initially edited cells. Avoiding the need for relatively large doses, NANITE could increase the safety profile of gene-editing treatments and potentially expand the technology to tissues and organs that are more challenging to genetically alter than the liver.

The technology changes the numbers game. Even if only a fraction of the NANITE therapy reaches its target tissue, its ability to spread could still deliver enough impact to cure currently untouchable genetic diseases. “By lowering effective dose requirements, NANITE could make genome editing more practical and accessible for treating human disease,” wrote the team.

The post Souped-Up CRISPR Gene Editor Replicates and Spreads Like a Virus appeared first on SingularityHub.

2026-02-17 05:56:12

You’re lying on an operating table. A doctor injects a milky white liquid into your veins. Within a minute, your breathing slows, your face relaxes, and you remain limp when asked to squeeze a hand. You’ve been temporarily put to sleep.

We lose consciousness every night with the conviction that a blaring alarm or the whiff of fresh brewed coffee will drag us out of our slumber. Giving up awareness is engrained in the way our brain works. With anesthesia, doctors can artificially induce the process to spare patients from the experience of surgery.

Despite decades of research, however, we’re still in the dark about how the brain lets go of consciousness, either during sleep or after a dose of chemicals that knock you out. Finding the neural correlates of awareness—that is, what changes in the brain—would solve one of the most enigmatic mysteries of our minds. It could also lead to the objective measurement of anesthesia, giving doctors valuable real-time information about whether a patient is completely under—or if they’re beginning to float back into consciousness on the operating table.

This month, Tao Xu at Shanghai Jiao Tong University and colleagues mapped the brain’s inner workings as it descends into the void. By comparing the brain activity of 31 patients before and after anesthesia, they found a unique neural pattern marking when patients slid into unconsciousness. Connections between nine brain regions—some previously implicated in consciousness—rapidly broke down.

The results echo previous findings. But the study stands out for its practicality. Rather than using implants inserted into the brain, the team captured signals with electrodes placed on the volunteers’ scalps. With further validation, this shift in brain activity could be used as a signal for loss of awareness, helping anesthesiologists reliably keep their patients in a dream state—and bring them back.

Never-Ending Quest

Scientists generally agree that consciousness emerges from multiple brain regions working in tandem, but they heatedly debate which ones are involved.

Some researchers believe the seat of consciousness is rooted at the back of the brain. These regions receive and integrate information, giving the brain an overall picture of both inner thoughts and the outer world. Another camp fixates on the front and side areas of the brain. These circuits broadcast signals to the rest of the brain and break down as awareness slips away.

Still more scientists point to connections between the cortex, the outermost part of the brain, and a deeper egg-shaped brain structure called the thalamus, which gives rise to our sense of perception and self.

These latter conclusions come from studies of healthy volunteers looking at flashing images while researchers record their brain signals. Some stimuli are deliberately designed to not reach awareness. Conscious perception seems to rely on wave-like neural activity between multiple areas in the cortex and the thalamus. Without it, participants are oblivious to the images.

These studies tested perception and awareness in people while they were awake. Another team has compared neural activity in completely or partially comatose patients to alert participants. They found two circuits catastrophically fail in a coma. One of these is at the front of the brain, the other at the back. As results from studies converge on similar patterns, researchers are hopeful we’ll eventually reach a unified theory of consciousness.

But consciousness isn’t all or none. Previous studies capture only a single snapshot in time. To Xu and colleagues, truly understanding awareness means turning that snapshot into a movie.

Slipping Away

The authors of the new study recruited 31 people who were about to undergo surgery with the use of propofol, a popular general anesthetic. Once an anesthesiologist injects the milky liquid into a vein, it rapidly shuts down consciousness. Throughout surgery, the anesthesiologist carefully monitors a patient’s behavior (or lack thereof), heart rate, and other vital signs to adjust dosage in real-time. The goal is to keep the patient fully under without overdosing.

The team gave each person in the study a cap studded with 128 electrodes to capture the brain’s electrical chatter. This brain-recording method is called an electroencephalogram or EEG. It’s popular because the device sits on the scalp and is safe and non-invasive. But because it measures activity through the skull rather than directly from brain tissue, signals can be muffled or noisy.

To increase precision, the team developed a mathematical model to filter signals into five established brain wave types. Like radio waves, electrical activity oscillates across the brain at different frequencies, each of which correlates with a unique brain state. Alpha waves, for example, dominate when you’re relaxed but alert. Delta waves take over in deep sleep.

The team isolated signals from nine areas of the brain previously implicated in consciousness. These included most of the usual suspects: A cortex region in the middle of the brain called the parietal cortex, another cortex region in the back of the skull, and the thalamus and a handful of other deeper structures.

While the patients were alert, their brains hummed with alpha-wave activity between the parietal cortex and thalamus, suggesting the regions were synchronized. Other areas across the cortex were also highly connected, like parts of a well-oiled machine.

But a dose of propofol broke down most of these communications.

Within 20 seconds after patients received the drug, alpha waves disintegrated, and electrical signals between the parietal cortex and thalamus fragmented. Different parts of the cortex also lost connectivity. Although the patients seemed to lose consciousness suddenly, like flipping a light switch, their brain signals showed a steadier decline in synchrony—more like a dimmer that gradually shifted activity from a state of coordination to one of disarray.

The results “emphasize the critical role” alpha waves play in “reflecting the dynamic shifts associated with loss of consciousness,” wrote the team.

Further tests in 46 people undergoing mild sedation showed similar desynchronization in alpha waves. But the breakdown between the parietal cortex and thalamus was smaller. That specific connection seems especially relevant in the transition to unconsciousness, wrote the team.

The results back up other studies suggesting the thalamus is a critical node in consciousness. But they could also fuel further debate about the importance of different cortex regions and their connections. Instead of the front or back of the brain as the root of consciousness, the team thinks the middle parietal cortex is key, at least for patients taking propofol. They’re now exploring whether other anesthetics change brain wave dynamics in different and unique ways.

As the debate over consciousness rages on, the team is focused on practical gains in the clinic. They’re aiming to simplify the brain recording setup so anesthesiologists could routinely use it to measure consciousness in their patients before, during, and after anesthesia.

The post This Brain Pattern Could Signal the Moment Consciousness Slips Away appeared first on SingularityHub.

2026-02-14 23:00:00

The post This Week’s Awesome Tech Stories From Around the Web (Through February 14) appeared first on SingularityHub.

2026-02-14 07:41:11

While we have sent probes billions of kilometers into interstellar space, humans have barely scratched the surface of our own planet, not even making it through the thin crust.

Information about Earth’s deep interior comes mainly from geophysics and is at a premium. We know it consists of a solid crust, a rocky mantle, a liquid outer core and solid inner core. But what precisely goes on in each layer—and between them—is a mystery. Now our research uses our planet’s magnetism to cast light on the most significant interface in the Earth’s interior: its core-mantle boundary.

Roughly 3,000 kilometers beneath our feet, Earth’s outer core, an unfathomably deep ocean of molten iron alloy, endlessly churns to produce a global magnetic field stretching out far into space. Sustaining this “geodynamo,” and the planetary force-field it has produced for the past several billions of years (protecting Earth from harmful radiation), takes a lot of energy.

This was delivered to the core as heat during the Earth’s formation. But it is only released to drive the geodynamo as it conducts outwards to cooler, solid rock floating above in the mantle. Without this massive internal heat transfer from core to mantle and ultimately through the crust to the surface, Earth would be like our nearest neighbors Mars and Venus: magnetically dead.

Enter the Blobs

Maps showing how fast seismic waves (vibrations of acoustic energy) that traverse Earth’s rocky mantle change in its lowermost part, just above the core. Especially notable are two vast regions close to the equator beneath Africa and the Pacific Ocean, where seismic waves travel more slowly than elsewhere.

What makes these “big lower-mantle basal structures,” or “Blobs” for short, special is not clear. They are made of solid rock similar to the surrounding mantle but may be higher in temperature, different in composition, or both.

Strong variations in temperature at the base of the mantle would be expected to affect the underlying liquid core and the magnetic field that is generated there. The solid mantle changes temperature and flows at an exceptionally slow rate (millimeters per year), so any magnetic signature from strong temperature contrasts should persist for millions of years.

From Rocks to Supercomputers

Our study reports new evidence that these Blobs are hotter than the surrounding lower mantle. And this has had a noticeable effect on Earth’s magnetic field over the last few hundreds of millions of years at least.

As igneous rocks, recently solidified from molten magma, cool down at Earth’s surface in the presence of its magnetic field, they acquire a permanent magnetism that is aligned with the direction of this field at that time and place.

It is already well known that this direction changes with latitude. We observed, however, that the magnetic directions recorded by rocks up to 250 million years old also seemed to depend on where the rocks had formed in longitude. The effect was particularly noticeable at low latitudes. We therefore wondered whether the Blobs might be responsible.

The clincher came from comparing these magnetic observations to simulations of the geodynamo run on a supercomputer. One set was run assuming that the rate of heat flowing from core to mantle was the same everywhere. These either showed very little tendency for the magnetic field to vary in longitude or else the field they produced collapsed into a persistently chaotic state, which is also inconsistent with observations.

By contrast, when we placed a pattern on the core’s surface that included strong variations in the amount of heat being sucked into the mantle, the magnetic fields behaved differently. Most tellingly, assuming that the rate of heat flowing into the Blobs was about half as high as into other, cooler, parts of the mantle meant that the magnetic fields produced by the simulations contained longitudinal structures reminiscent of the records from ancient rocks.

A further finding was that these fields were less prone to collapsing. Adding the Blobs therefore enabled us to reproduce the observed stable behavior of Earth’s magnetic field over a wider range.

What seems to be happening is that the two hot Blobs are insulating the liquid metal beneath them, preventing heat loss that would otherwise cause the fluid to thermally contract and sink down into the core. Since it is the flow of core fluid that generates more magnetic field, these stagnant ponds of metal do not participate in the geodynamo process.

Furthermore, in the same way that a mobile phone can lose its signal by being placed within a metal box, these stationary areas of conductive liquid act to “screen” the magnetic field generated by the circulating liquid below. The huge Blobs therefore gave rise to characteristic longitudinally varying patterns in the shape and variability of Earth’s magnetic field. And this mapped on to what was recorded by rocks formed at low latitudes.

Most of the time, the shape of Earth’s magnetic field is quite similar to that which would be produced by a bar magnet aligned with the planet’s rotation axis. This is what makes a magnetic compass point nearly north at most places on Earth’s surface, most of the time.

Collapses into weak, multipolar states have occurred many time over geological history, but they are quite rare, and the field seems to have recovered fairly quickly afterwards. In the simulations at least, Blobs seem to help make this the case.

So, while we still have a lot to learn about what the Blobs are and how they originated, it may be that in helping to keep the magnetic field stable and useful for humanity, we have much to thank them for.

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

The post Vast ‘Blobs’ of Rock Have Stabilized Earth’s Magnetic Field for Hundreds of Millions of Years appeared first on SingularityHub.

2026-02-13 07:13:45

Elon Musk has long said settling Mars is SpaceX’s raison d’être, but the world’s richest man has now pivoted his attention to the moon. The company is targeting an uncrewed lunar landing in March 2027 and has ambitions to create a “self-growing city” on our nearest celestial neighbor.

The news marks a dramatic shift from Musk’s long-standing goal of a permanent human presence on the red planet, which he has framed as a way to hedge humanity’s future against a cataclysmic event on Earth. Only a year ago the billionaire labeled missions to the moon “a distraction.”

But in a surprise announcement posted to X on Super Bowl Sunday, Musk revealed the change in strategy, confirming a Wall Street Journal report earlier in the week that SpaceX was putting off plans for a Mars mission to focus on lunar landings instead.

“For those unaware, SpaceX has already shifted focus to building a self-growing city on the Moon, as we can potentially achieve that in less than 10 years, whereas Mars would take 20+ years,” wrote Musk. “The mission of SpaceX remains the same: extend consciousness and life as we know it to the stars.”

The practical advantages of this shift are clear. As Musk notes, Mars is only accessible when the planets align every 26 months, with each journey taking six months (or longer). Trips to the moon can launch every 10 days and would take just a few days to arrive.

Lunar landings are also a problem SpaceX already needs to solve. The company has a $4 billion contract with NASA to return astronauts to the moon using its Starship rocket. The Artemis III mission will attempt to land a crew on the moon in 2028, though it’s unclear whether SpaceX’s vehicle will be ready in time.

However, the pivot to the moon appears to be about more than just pragmatism. Musk has become increasingly focused on artificial intelligence and, in recent months, has suggested this mission may overlap with his space ventures. In particular, he has floated the idea that space-based data centers may help solve the energy constraints currently holding back AI development.

Last week, Musk put his money where his mouth is by announcing that SpaceX had acquired his AI company xAI in a merger valuing the new entity at a whopping $1.25 trillion. In comments at an all-hands meeting at xAI on Tuesday evening, heard by the The New York Times, Musk unveiled an ambitious vision for how the company could build a factory for AI data centers on the moon’s surface.

The plan includes a giant electromagnetic catapult called a “mass driver” to launch satellites from the lunar surface into space. He also described building “a self-sustaining city on the moon,” which could act as a stepping stone to Mars.

The pivot may also be in response to growing competition from Jeff Bezos, his chief rival in the private space race. The billionaire’s rocket company, Blue Origin, has finally started to deliver with its New Glenn launch vehicle, and sources told Ars Technica that Bezos wants his team to go “all in” on lunar exploration.

Crucially, Blue Origin is developing a crew transportation system that doesn’t require orbital refueling. SpaceX’s Starship, on the other hand, will require around 10 to 12 tanker flights to fill the vehicle with propellant before it sets off on a lunar mission, according to Space.com.

While Starship has a major payload advantage—more than 100 tons to the lunar surface—the relative simplicity of Blue Origin’s technology could allow it to land humans on the moon before its rival.

Despite the refocus on the moon, Musk insisted he hasn’t abandoned Mars. In his Sunday post, he emphasized that SpaceX still has plans to build a city on the red planet and missions to start this process will begin in five to seven years.

Given Musk’s record for overly ambitious timelines, his prognostications on both the moon and Mars should probably be taken with a pinch of salt. Nonetheless, it seems increasingly likely that humanity’s first off-Earth settlement will be a lot closer to home than we thought.

The post Elon Musk Says SpaceX Is Pivoting From Mars to the Moon appeared first on SingularityHub.

2026-02-11 04:23:25

Laura Oliveira fell in love with swimming at 70. She won her first competition three decades later. Longevity runs in her family. Her aunt Geny lived to 110. Her two sisters thrived and were mentally sharp beyond a century. They came from humble backgrounds, didn’t stick to a healthy diet—many loved sweets and fats—and lacked access to preventative screening or medical care. Extreme longevity seems to have been built into their genes.

Scientists have long sought to tease apart the factors that influence a person’s lifespan. The general consensus has been that genetics play a small role; lifestyle and environmental factors are the main determinants.

A new study examining two cohorts of twins is now challenging that view. After removing infections, injuries, and other factors that cut a life short, genetics account for roughly 55 percent of the variation in lifespan, far greater than previous estimates of 10 to 25 percent.

“The genetic contribution to human longevity is greater than previously thought,” wrote Daniela Bakula and Morten Scheibye-Knudsen at the University of Copenhagen, who were not involved in the study.

Dissecting the impact of outside factors versus genetics on lifespan isn’t just academic curiosity. It lends insight into what contributes to a long life, which bolsters the quest for genes related to healthy aging and strategies to combat age-related diseases.

“If we can understand why there are some people who can make it to 110 while smoking and drinking all their life, then maybe, down the road, we can also translate that to interventions or to medicine,” study author Ben Shenhar of the Weizmann Institute of Science told ScienceNews.

Genetic Mystery

Eat well, work out, don’t smoke, and drink very moderately or not at all. These longevity tips are so widespread they’ve gone from medical advice to societal wisdom. Focusing on lifestyle factors makes sense. You can readily form healthy habits and potentially alter your genetic destiny, if just by a smidge, and genes hardly seem to influence longevity.

Previous studies in multiple populations estimated the heritability of lifespan was roughly 25 percent at most. More recent work found even less genetic influence. The results poured cold water on efforts to uncover genes related to longevity, with some doubting their impact even if they could be found.

But the small role of genes on human longevity has had researchers scratching their heads. The estimated impact is far lower than in other mammals, such as wild mice, and is an outlier compared to other complex heritable traits in humans—ranging from psychiatric attributes to metabolism and immune system health—which are pegged at an average of roughly 49 percent.

To find out why, the team dug deep into previous lifespan studies and found a potential culprit.

Most studies used data from people born in the 18th and 19th centuries, where accidents, infectious diseases, environmental pollution, and other hazards were often the cause of an early demise. These outside factors likely masked intrinsic, or bodily, influences on longevity—for example, gradual damage to DNA and cellular health—and in turn, heavily underestimated the impact of genes on lifespan.

“Although susceptibility to external hazards can be genetically influenced, mortality in historical human populations was largely dominated by variation in exposure, medical care, and chance,” wrote Bakula and Scheibye-Knudsen.

Twin Effect

The team didn’t set out to examine genetic influences on longevity. They were developing a mathematical model to gauge how aging varies in different populations. But by playing with the model, they realized that removing outside factors could vastly increase lifespan heritability.

To test the theory, they analyzed mortality data from Swedish twins—both identical and fraternal—born between 1900 and 1935. The time period encompassed some environmental extremes, including a deadly flu pandemic, a world war, and economic turmoil but also vast improvements in vaccination, sanitation, and other medical care.

Because identical twins share the same DNA, they’re a valuable resource for teasing apart the impact of nature versus nurture, especially if the twins were raised in different environments. Meanwhile, fraternal twins have roughly 50 percent similar DNA. By comparing lifespan between these two cohorts—with and without external factors added in using a mathematical model—the team teased out the impact of genes on longevity.

To further validate their model, the researchers applied it to another historical database of Danish twins born between 1890 and 1900, a period when deaths were often caused by infectious diseases. After excluding outside factors, results from both cohorts found the influence of genes accounted for roughly 55 percent of variation in lifespan, far higher than previous estimates. They unearthed similar results in a cohort of US siblings of centenarians.

Longevity aside, the analysis also found a curious discrepancy between the chances of inheriting various age-related diseases. Dementia and cardiovascular diseases are far more likely to run in families. Cancer, surprisingly, not so much. This suggests tumors are more driven by random mutations or environmental triggers.

The team emphasizes that the findings don’t mean longevity is completely encoded in your genes. According to their analysis, lifestyle factors could shift life expectancy by roughly five years, a small but not insignificant amount of time to spend with loved ones.

The estimates are hardly cut-and-dried. How genetics influence health and aging is complex. For example, genes that keep chronic inflammation at bay during aging could also increase chances of deadly infection earlier in life.

“Drawing a clear, bright line between intrinsic and extrinsic causes of death is not possible,” Bradley Willcox at the University of Hawaii, who was not involved in the study, told The New York Times. “Many deaths live in a gray zone where biology and environment collide.”

Although some experts remain skeptical, the findings could influence future research. Do genes have a larger impact on extreme longevity compared to average lifespan? If so, which ones and why? How much can lifestyle influence the aging process? According to Boston University’s Thomas Perls, who leads the New England Centenarian Study, the difference in lifespan for someone with only good habits versus no good habits could be more than 10 years.

The team stresses the analysis can’t cover everyone, everywhere, across all time. The current study mainly focused on Scandinavian twin cohorts, who hardly encapsulate the genetic diversity and socioeconomic status of other populations around the globe.

Still, the results suggest that future hunts for longevity-related genes could be made stronger by excluding external factors during analysis, potentially increasing the chances of finding genes that make outsized contributions to living a longer, healthier life.

“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,” said Shenhar in a press release. “By contrast, 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.”

The post Your Genes Determine How Long You’ll Live Far More Than Previously Thought appeared first on SingularityHub.