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Our bodies are ageing faster than ever. Can we hit the brakes?

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Monday, November 3, 2025

A decade or so ago, I had my biological age measured. I was in my mid 40s at the time and was fit, slim and a disciplined eater. When the results came back, I was gratified to discover that I was, biologically, quite a bit younger than my age. Around six years, if I remember correctly. I dread to think what it is now. In the intervening years, I have gained weight, stopped exercising as much, experienced multiple heatwaves and been through an extremely traumatic event, the suicide of my wife. I definitely feel all of my 55 years, and I wouldn’t be surprised if I’m biologically older. If so, I wouldn’t be alone. In the past few years, scientists have discovered a troubling trend in biological ageing. All over the world, people are getting older faster. Those born after 1965 are ageing, biologically, more rapidly than people born a decade earlier, and diseases that were once considered to be a scourge of the elderly are becoming ever-more common in younger people. People born before 1965 are ageing, biologically, more slowly than those born more recentlySTR/AFP via Getty Images “Cancers are increasing in younger age populations, people under 40 years of age have more heart attacks, more diabetes,” says Paulina Correa-Burrows, a social epidemiologist at the University of Chile in Santiago. “Why? My answer is because we’re ageing faster.” The reasons for this shift are starting to become clear. Some, unfortunately, are unavoidable. Many, thankfully, are modifiable. So, how can we endeavour to keep our biological and chronological ages in step? The best way to measure how rapidly somebody is ageing is by measuring their biological age and then doing so again a few months or even years later. The most accepted tool for this, says Antonello Lorenzini at the University of Bologna in Italy, is epigenetic clocks, tests that analyse modifications to DNA. These aren’t perfect – precise biological ages should be taken with a grain of salt – but they are enough for telling who, out of a group of participants, is ageing faster or slower. “ Some people are 10 years or more younger or older, biologically, than their actual age “ These tests recognise that chronological age – the number of years someone has lived – isn’t always a good indicator of how far along the ageing trajectory they are. In fact, it can be way off. For most people, there is a reasonably good correspondence, but some people are 10 years or more younger or older, biologically, than their actual age. And unlike chronological age, biological age can go down as well as up. The first suggestions that biological ageing is accelerating came from the world of obesity research. In 2016, a team led by Beatriz Gálvez at the National Centre for Cardiovascular Research in Madrid, Spain, noted that the biological effects of obesity overlap substantially with those of ageing. Both are hallmarked by dysfunction of the white adipose (fat) tissue, leading to metabolic conditions, widespread inflammation and damage to multiple organs, including the kidneys, bones and those of the cardiovascular system. Impacts of obesity These effects are usually directly attributed to obesity itself. But Gálvez wondered whether the causality is more indirect: obesity leads to premature ageing, which leads to the early onset of the diseases of old age. She and her colleagues coined the term “adipaging” to capture this relationship, and proposed that “to a great extent, obese adults are prematurely aged individuals”. A couple of years later, Lorenzini and his colleagues took the idea and ran with it. They started from an influential 2013 research paper called “The hallmarks of aging”, which describes nine molecular and cellular causes of age-related diseases. Lorenzini compared these with the consequences of obesity and found strong parallels. Both obesity and ageing lead to imbalanced nutrient sensing, altered intercellular communication, disturbances in protein metabolism, dysfunction of energy-producing mitochondria in cells, and cell senescence, when cells stop dividing but remain alive. “I think that fits very well with accelerating ageing,” says Lorenzini. “For many of the chronic diseases of our time, the major factor is ageing. So, of course, if you accelerate ageing, you will accelerate everything.” That includes death: the life expectancy of people over 40 with obesity is reduced, by about six years in men and seven in women. The biological clocks of people with obesity tick fasterALDOMURILLO/GETTY IMAGES Various attempts have also been made to measure whether the biological clocks of people with obesity really do tick faster. In 2017, for example, a team largely from the University of Tampere in Finland reanalysed archived blood samples from a group of 183 people taken 25 years apart: first during the teenage years or young adulthood, then again in middle age. The participants’ body mass index (BMI) was recorded when the samples were taken, so the researchers knew which of them had become obese. As expected, those who had gained a lot of weight had aged more biologically than they had aged chronologically, some by more than 10 years. Those who had remained lean had less of a mismatch. (The team also wanted to see what had happened to the rate of ageing in people who had lost weight, but there weren’t enough people in this category to do the analysis.) A similar study in women in their 20s, 30s and 40s also found that a higher BMI was associated with an older biological age, with each rise of 1 kilogram of weight per metre of height squared adding about 1.7 months. Another discovered that increased biological age was associated with various measures of obesity – BMI, waist-to-hip ratio and waist circumference – in women aged 35 to 75. Those with a BMI of 35 or more, putting them firmly in the obese category, were on average 3.15 years biologically older than women of the same chronological age who were a healthy weight. Cause and effect None of these studies, however, proved the direction of causality. It is possible that obesity accelerates biological ageing, but also that an increase in biological age somehow leads to obesity. Last year, researchers in Beijing teased these possibilities apart. They reanalysed data on tens of thousands of people who had been enrolled in a previous study and whose BMI, waist circumference and waist-to-hip ratio had been recorded on several occasions, along with five measures of their biological age. Applying a statistical method that can indicate the direction of causality, the researchers showed that obesity causes accelerated ageing compared with people of a healthy weight, to the tune of around three years. These studies all point in the same direction, says Lorenzini. “We are moving from hypothesis to data. The data is piling up.” The latest addition to this pile comes from the lab of Correa-Burrows and her colleagues at the University of Chile. They piggybacked on a research project called the Santiago Longitudinal Study, which started in 1992 and followed around 1000 people from birth up to their late 20s, originally to study the effects of nutrition on health in children and young adults. Correa-Burrows and her team recruited 205 participants who had made it all the way through the study. They were aged between 28 and 31 and comprised three groups: those who had maintained a healthy weight throughout life, those who had been obese since adolescence and those who had been obese since early childhood. There were already masses of data on these people, including their BMI throughout the study, but Correa-Burrows also used epigenetic clocks to measure their biological age. What she found was very clear. Those in the healthy weight group had, on average, biological ages slightly lower than their chronological age. But those in both obese groups were biologically older than their chronological age. This was by an average of 4.2 years in the obese-since-adolescence group and 4.7 in the obese-since-childhood group. A few had biological ages over 40. “We were expecting to find that, but we never expected the magnitude of difference that we saw in some individuals,” says Correa-Burrows. “Some of them had a 50 per cent gap between their biological age and the chronological age, which is huge.” It is now generally accepted in geroscience circles that obesity speeds up the ageing process, she says. Accelerated ageing is also attracting the attention of researchers outside the obesity field. Premature ageing is a well-known phenomenon among adult survivors of childhood cancer, who often become frail and die early as a result of the aftereffects of their illness and treatment. They are also at a higher-than-average risk of developing an unrelated cancer in later life. That may be because they are genetically predisposed to cancer, but this can’t fully explain the elevated risk. The cancer factor Last year, Paige Green at the US National Cancer Institute in Bethesda, Maryland, had a brainwave. Cancer is typically a disease of old age, and the survivors of childhood cancer were ageing prematurely. Maybe they were more vulnerable to cancer because they were biologically older than their chronological age. And not just that: accelerated ageing in the general population might also explain the rise in early-onset cancer, heart failure and strokes. “Cancer used to just be considered a disease of ageing,” says Jennifer Guida, an independent researcher who was formerly Green’s colleague. “Now people are being diagnosed with colon cancer in their 30s, breast cancer in their 30s. Why is that? Perhaps some of the processes of ageing are acting earlier and causing ageing to accelerate, which then causes early-onset cancer.” Green, Guida and their colleague Lisa Gallicchio wrote the idea up in the journal JAMA Oncology as a challenge to others to test it. “We put it out there as a hypothesis,” says Guida. “Maybe somebody will run with it and do the work to show that this is true, or disprove it.” The way to do it would be to measure the biological ages of a large number of people already enrolled in a large-scale study and tally that with early-onset cancers, she says. In fact, a team has already done that. Last year, Ruiyi Tian at Washington University in St. Louis, Missouri, told the American Association for Cancer Research’s annual meeting in San Diego, California, that she and her colleagues had analysed blood samples from nearly 150,000 people stored in the UK Biobank, looking for signs of accelerated ageing. The participants were aged between 37 and 54 when they had their blood taken. Measuring their biological age revealed that those on the younger end of the age spectrum, who had been born after 1965, were 17 per cent more likely to show signs of accelerated ageing than the older ones, born between 1950 and 1954. The researchers also found that accelerated ageing increased the risk of early-onset cancers of the lungs, gastrointestinal tract and uterus. “Accumulating evidence suggests that the younger generations may be ageing more swiftly than anticipated,” Tian told the association’s press office at the time. (The results haven’t been published in a peer-reviewed journal and Tian and her supervisor didn’t respond to requests for further information.) The “obesogenic” environment of many industrialised nations promotes ageing, but there is promise that weight-loss drugs can reverse thisDhiraj Singh/Bloomberg via Getty Images All in all, it seems we have created a world that not only promotes obesity – known as the obesogenic environment – but also ages us. Perhaps we need a new shorthand for it. I suggest the “senesogenic environment”, derived from the Latin verb senescere (“to grow old”). So, if younger people are ageing more rapidly, what is the cause? Obesity is the main one. “We have a huge obesity problem in places that have a Western-type diet,” says Guida. Obesity rates in 5 to 19-year-olds increased 1000 per cent between 1975 and 2022, according to the World Obesity Federation, and children with obesity tend to remain obese as adults. “Obesity’s prevalence has kept rising despite governmental efforts to try to reduce the rates, and by 2030, 1 billion people in the world will be obese,” says Correa-Burrows. What drives accelerated ageing? The mechanism by which obesity leads to accelerated ageing is a bone of contention. It may be that carrying around too much fat is a direct cause, possibly because it promotes long-term inflammation. “When you have chronic inflammation, it triggers these biochemical ageing signatures,” says Correa-Burrows. Alternatively, it could be that flooding the body with excess calories causes both obesity and ageing. Lorenzini favours this hypothesis, noting that many of the pathways associated with the ageing process are involved in nutrient sensing. It is well established that switching these pathways off in animal models – using drugs or caloric restriction – activates repair processes and retards ageing. Maybe people with a high-calorie, morning-noon-and-night diet chronically stimulate the pathways, so their body never has a chance to fix the damage that leads to ageing. Obesity isn’t the only culprit, however. “Anything that increases hormones related to stress, particularly cortisol, is going to have an adverse effect in terms of your biological ageing rate,” says Correa-Burrows. “Pollution has this effect. Early childhood adversity also. Trauma.” Exposure to heatwaves has also been found to speed up biological ageing (see “Heatwaves and premature ageing“), maybe because it activates stress hormones. People are also more sedentary than they used to be, says Guida. “All these things feed into each other to create this perfect storm.” Winding back the biological clock So how can you avoid becoming old before your time? “A lot of it comes down to lifestyle change,” says Guida. “Exercise is probably the biggest thing that you can do to slow your ageing. We know caloric restriction works too, but it’s not always feasible for everybody. Sleep is a great way to promote restoration and repair. And avoiding alcohol and smoking.” Avoiding obesity through healthy eating and exercise is key for slowing down biological ageingAlexander Spatari/Alexander Spatari Down the road, drugs might also help. The type 2 diabetes medicine Ozempic, a GLP-1 receptor agonist, was recently shown to slow the rate of ageing, and another study found that this drug family is also linked to a lower risk of obesity-related cancers. But we don’t yet know enough about the long-term effects to recommend them as an anti-ageing strategy, says Correa-Burrows. The good news, however, is that even if your biological clock has outpaced your chronological clock, lifestyle changes can throw it into reverse. “There are ways to synchronise both clocks or even put your biological clock below your chronological clock,” says Correa-Burrows. “Most of the interventions are based on changes in your lifestyle: exercising and changing your diet.” OK, I get it. Time to lose some weight and get active again. I doubt I can get back to being biologically six years younger than my age. Fifty-five would suit me just fine, though. Need a listening ear? UK Samaritans 116123; US 988 Suicide & Crisis Lifeline 988; hotlines in other countries Heatwaves and premature ageing Accelerated ageing isn’t just caused by obesity, stress and pollution (see main story). Climate change is also making us age faster. Earlier this year, Eun Young Choi and Jennifer Ailshire at the University of Southern California in Los Angeles analysed biological age data from 3686 adults aged 56-plus across the US, and cross-referenced it against climate records going back six years. They found that people who had been exposed to more hot days were ageing more rapidly, with each 10 per cent increase in exposure adding 1.4 months to their biological age. And in August, a team led by Cui Guo at the University of Hong Kong analysed data from nearly 25,000 adults in a medical screening programme in Taiwan. The researchers estimated the participants’ biological age and tallied their exposure to heatwaves – defined as periods of abnormally hot weather lasting for more than 48 hours – in the preceding two years. They found that people with a greater cumulative exposure to heatwaves were ageing faster than those with less exposure. Each four-day increase in total heatwave exposure was associated with a rise in biological age of about nine days. Totted up over a typical lifetime, this adds up to about five months. The mechanism by which heatwaves accelerate ageing isn’t clear, according to Paul Beggs, an environmental health scientist at Macquarie University in Sydney, Australia. But we know that acute heat exposure can damage the brain, heart and kidneys, and disrupt sleep.

All over the world people are ageing more rapidly and succumbing to diseases that typically affected the elderly. But there are ways to turn back the clock on your biological age

A decade or so ago, I had my biological age measured. I was in my mid 40s at the time and was fit, slim and a disciplined eater. When the results came back, I was gratified to discover that I was, biologically, quite a bit younger than my age. Around six years, if I remember correctly.

I dread to think what it is now. In the intervening years, I have gained weight, stopped exercising as much, experienced multiple heatwaves and been through an extremely traumatic event, the suicide of my wife. I definitely feel all of my 55 years, and I wouldn’t be surprised if I’m biologically older.

If so, I wouldn’t be alone. In the past few years, scientists have discovered a troubling trend in biological ageing. All over the world, people are getting older faster. Those born after 1965 are ageing, biologically, more rapidly than people born a decade earlier, and diseases that were once considered to be a scourge of the elderly are becoming ever-more common in younger people.

People born before 1965 are ageing, biologically, more slowly than those born more recently

STR/AFP via Getty Images

“Cancers are increasing in younger age populations, people under 40 years of age have more heart attacks, more diabetes,” says Paulina Correa-Burrows, a social epidemiologist at the University of Chile in Santiago. “Why? My answer is because we’re ageing faster.”

The reasons for this shift are starting to become clear. Some, unfortunately, are unavoidable. Many, thankfully, are modifiable. So, how can we endeavour to keep our biological and chronological ages in step?

The best way to measure how rapidly somebody is ageing is by measuring their biological age and then doing so again a few months or even years later. The most accepted tool for this, says Antonello Lorenzini at the University of Bologna in Italy, is epigenetic clocks, tests that analyse modifications to DNA. These aren’t perfect – precise biological ages should be taken with a grain of salt – but they are enough for telling who, out of a group of participants, is ageing faster or slower.

Some people are 10 years or more younger or older, biologically, than their actual age

These tests recognise that chronological age – the number of years someone has lived – isn’t always a good indicator of how far along the ageing trajectory they are. In fact, it can be way off. For most people, there is a reasonably good correspondence, but some people are 10 years or more younger or older, biologically, than their actual age. And unlike chronological age, biological age can go down as well as up.

The first suggestions that biological ageing is accelerating came from the world of obesity research. In 2016, a team led by Beatriz Gálvez at the National Centre for Cardiovascular Research in Madrid, Spain, noted that the biological effects of obesity overlap substantially with those of ageing. Both are hallmarked by dysfunction of the white adipose (fat) tissue, leading to metabolic conditions, widespread inflammation and damage to multiple organs, including the kidneys, bones and those of the cardiovascular system.

Impacts of obesity

These effects are usually directly attributed to obesity itself. But Gálvez wondered whether the causality is more indirect: obesity leads to premature ageing, which leads to the early onset of the diseases of old age. She and her colleagues coined the term “adipaging” to capture this relationship, and proposed that “to a great extent, obese adults are prematurely aged individuals”.

A couple of years later, Lorenzini and his colleagues took the idea and ran with it. They started from an influential 2013 research paper called “The hallmarks of aging”, which describes nine molecular and cellular causes of age-related diseases.

Lorenzini compared these with the consequences of obesity and found strong parallels. Both obesity and ageing lead to imbalanced nutrient sensing, altered intercellular communication, disturbances in protein metabolism, dysfunction of energy-producing mitochondria in cells, and cell senescence, when cells stop dividing but remain alive.

“I think that fits very well with accelerating ageing,” says Lorenzini. “For many of the chronic diseases of our time, the major factor is ageing. So, of course, if you accelerate ageing, you will accelerate everything.” That includes death: the life expectancy of people over 40 with obesity is reduced, by about six years in men and seven in women.

The biological clocks of people with obesity tick faster

ALDOMURILLO/GETTY IMAGES

Various attempts have also been made to measure whether the biological clocks of people with obesity really do tick faster. In 2017, for example, a team largely from the University of Tampere in Finland reanalysed archived blood samples from a group of 183 people taken 25 years apart: first during the teenage years or young adulthood, then again in middle age. The participants’ body mass index (BMI) was recorded when the samples were taken, so the researchers knew which of them had become obese.

As expected, those who had gained a lot of weight had aged more biologically than they had aged chronologically, some by more than 10 years. Those who had remained lean had less of a mismatch. (The team also wanted to see what had happened to the rate of ageing in people who had lost weight, but there weren’t enough people in this category to do the analysis.)

A similar study in women in their 20s, 30s and 40s also found that a higher BMI was associated with an older biological age, with each rise of 1 kilogram of weight per metre of height squared adding about 1.7 months. Another discovered that increased biological age was associated with various measures of obesity – BMI, waist-to-hip ratio and waist circumference – in women aged 35 to 75. Those with a BMI of 35 or more, putting them firmly in the obese category, were on average 3.15 years biologically older than women of the same chronological age who were a healthy weight.

Cause and effect

None of these studies, however, proved the direction of causality. It is possible that obesity accelerates biological ageing, but also that an increase in biological age somehow leads to obesity.

Last year, researchers in Beijing teased these possibilities apart. They reanalysed data on tens of thousands of people who had been enrolled in a previous study and whose BMI, waist circumference and waist-to-hip ratio had been recorded on several occasions, along with five measures of their biological age. Applying a statistical method that can indicate the direction of causality, the researchers showed that obesity causes accelerated ageing compared with people of a healthy weight, to the tune of around three years.

These studies all point in the same direction, says Lorenzini. “We are moving from hypothesis to data. The data is piling up.”

The latest addition to this pile comes from the lab of Correa-Burrows and her colleagues at the University of Chile. They piggybacked on a research project called the Santiago Longitudinal Study, which started in 1992 and followed around 1000 people from birth up to their late 20s, originally to study the effects of nutrition on health in children and young adults.

Correa-Burrows and her team recruited 205 participants who had made it all the way through the study. They were aged between 28 and 31 and comprised three groups: those who had maintained a healthy weight throughout life, those who had been obese since adolescence and those who had been obese since early childhood. There were already masses of data on these people, including their BMI throughout the study, but Correa-Burrows also used epigenetic clocks to measure their biological age.

What she found was very clear. Those in the healthy weight group had, on average, biological ages slightly lower than their chronological age. But those in both obese groups were biologically older than their chronological age. This was by an average of 4.2 years in the obese-since-adolescence group and 4.7 in the obese-since-childhood group. A few had biological ages over 40.

“We were expecting to find that, but we never expected the magnitude of difference that we saw in some individuals,” says Correa-Burrows. “Some of them had a 50 per cent gap between their biological age and the chronological age, which is huge.” It is now generally accepted in geroscience circles that obesity speeds up the ageing process, she says.

Accelerated ageing is also attracting the attention of researchers outside the obesity field. Premature ageing is a well-known phenomenon among adult survivors of childhood cancer, who often become frail and die early as a result of the aftereffects of their illness and treatment. They are also at a higher-than-average risk of developing an unrelated cancer in later life. That may be because they are genetically predisposed to cancer, but this can’t fully explain the elevated risk.

The cancer factor

Last year, Paige Green at the US National Cancer Institute in Bethesda, Maryland, had a brainwave. Cancer is typically a disease of old age, and the survivors of childhood cancer were ageing prematurely. Maybe they were more vulnerable to cancer because they were biologically older than their chronological age. And not just that: accelerated ageing in the general population might also explain the rise in early-onset cancer, heart failure and strokes.

“Cancer used to just be considered a disease of ageing,” says Jennifer Guida, an independent researcher who was formerly Green’s colleague. “Now people are being diagnosed with colon cancer in their 30s, breast cancer in their 30s. Why is that? Perhaps some of the processes of ageing are acting earlier and causing ageing to accelerate, which then causes early-onset cancer.”

Green, Guida and their colleague Lisa Gallicchio wrote the idea up in the journal JAMA Oncology as a challenge to others to test it. “We put it out there as a hypothesis,” says Guida. “Maybe somebody will run with it and do the work to show that this is true, or disprove it.” The way to do it would be to measure the biological ages of a large number of people already enrolled in a large-scale study and tally that with early-onset cancers, she says.

In fact, a team has already done that. Last year, Ruiyi Tian at Washington University in St. Louis, Missouri, told the American Association for Cancer Research’s annual meeting in San Diego, California, that she and her colleagues had analysed blood samples from nearly 150,000 people stored in the UK Biobank, looking for signs of accelerated ageing. The participants were aged between 37 and 54 when they had their blood taken. Measuring their biological age revealed that those on the younger end of the age spectrum, who had been born after 1965, were 17 per cent more likely to show signs of accelerated ageing than the older ones, born between 1950 and 1954. The researchers also found that accelerated ageing increased the risk of early-onset cancers of the lungs, gastrointestinal tract and uterus.

“Accumulating evidence suggests that the younger generations may be ageing more swiftly than anticipated,” Tian told the association’s press office at the time. (The results haven’t been published in a peer-reviewed journal and Tian and her supervisor didn’t respond to requests for further information.)

The “obesogenic” environment of many industrialised nations promotes ageing, but there is promise that weight-loss drugs can reverse this

Dhiraj Singh/Bloomberg via Getty Images

All in all, it seems we have created a world that not only promotes obesity – known as the obesogenic environment – but also ages us. Perhaps we need a new shorthand for it. I suggest the “senesogenic environment”, derived from the Latin verb senescere (“to grow old”).

So, if younger people are ageing more rapidly, what is the cause? Obesity is the main one. “We have a huge obesity problem in places that have a Western-type diet,” says Guida. Obesity rates in 5 to 19-year-olds increased 1000 per cent between 1975 and 2022, according to the World Obesity Federation, and children with obesity tend to remain obese as adults. “Obesity’s prevalence has kept rising despite governmental efforts to try to reduce the rates, and by 2030, 1 billion people in the world will be obese,” says Correa-Burrows.

What drives accelerated ageing?

The mechanism by which obesity leads to accelerated ageing is a bone of contention. It may be that carrying around too much fat is a direct cause, possibly because it promotes long-term inflammation. “When you have chronic inflammation, it triggers these biochemical ageing signatures,” says Correa-Burrows.

Alternatively, it could be that flooding the body with excess calories causes both obesity and ageing. Lorenzini favours this hypothesis, noting that many of the pathways associated with the ageing process are involved in nutrient sensing. It is well established that switching these pathways off in animal models – using drugs or caloric restriction – activates repair processes and retards ageing. Maybe people with a high-calorie, morning-noon-and-night diet chronically stimulate the pathways, so their body never has a chance to fix the damage that leads to ageing.

Obesity isn’t the only culprit, however. “Anything that increases hormones related to stress, particularly cortisol, is going to have an adverse effect in terms of your biological ageing rate,” says Correa-Burrows. “Pollution has this effect. Early childhood adversity also. Trauma.” Exposure to heatwaves has also been found to speed up biological ageing (see “Heatwaves and premature ageing“), maybe because it activates stress hormones.

People are also more sedentary than they used to be, says Guida. “All these things feed into each other to create this perfect storm.”

Winding back the biological clock

So how can you avoid becoming old before your time? “A lot of it comes down to lifestyle change,” says Guida. “Exercise is probably the biggest thing that you can do to slow your ageing. We know caloric restriction works too, but it’s not always feasible for everybody. Sleep is a great way to promote restoration and repair. And avoiding alcohol and smoking.”

Avoiding obesity through healthy eating and exercise is key for slowing down biological ageing

Alexander Spatari/Alexander Spatari

Down the road, drugs might also help. The type 2 diabetes medicine Ozempic, a GLP-1 receptor agonist, was recently shown to slow the rate of ageing, and another study found that this drug family is also linked to a lower risk of obesity-related cancers. But we don’t yet know enough about the long-term effects to recommend them as an anti-ageing strategy, says Correa-Burrows.

The good news, however, is that even if your biological clock has outpaced your chronological clock, lifestyle changes can throw it into reverse. “There are ways to synchronise both clocks or even put your biological clock below your chronological clock,” says Correa-Burrows. “Most of the interventions are based on changes in your lifestyle: exercising and changing your diet.” OK, I get it. Time to lose some weight and get active again. I doubt I can get back to being biologically six years younger than my age. Fifty-five would suit me just fine, though.

Need a listening ear? UK Samaritans 116123; US 988 Suicide & Crisis Lifeline 988; hotlines in other countries

Heatwaves and premature ageing

Accelerated ageing isn’t just caused by obesity, stress and pollution (see main story). Climate change is also making us age faster.

Earlier this year, Eun Young Choi and Jennifer Ailshire at the University of Southern California in Los Angeles analysed biological age data from 3686 adults aged 56-plus across the US, and cross-referenced it against climate records going back six years. They found that people who had been exposed to more hot days were ageing more rapidly, with each 10 per cent increase in exposure adding 1.4 months to their biological age.

And in August, a team led by Cui Guo at the University of Hong Kong analysed data from nearly 25,000 adults in a medical screening programme in Taiwan. The researchers estimated the participants’ biological age and tallied their exposure to heatwaves – defined as periods of abnormally hot weather lasting for more than 48 hours – in the preceding two years. They found that people with a greater cumulative exposure to heatwaves were ageing faster than those with less exposure. Each four-day increase in total heatwave exposure was associated with a rise in biological age of about nine days. Totted up over a typical lifetime, this adds up to about five months.

The mechanism by which heatwaves accelerate ageing isn’t clear, according to Paul Beggs, an environmental health scientist at Macquarie University in Sydney, Australia. But we know that acute heat exposure can damage the brain, heart and kidneys, and disrupt sleep.

Read the full story here.
Photos courtesy of

Contributor: 'Save the whales' worked for decades, but now gray whales are starving

The once-booming population that passed California twice a year has cratered because of retreating sea ice. A new kind of intervention is needed.

Recently, while sailing with friends on San Francisco Bay, I enjoyed the sight of harbor porpoises, cormorants, pelicans, seals and sea lions — and then the spouting plume and glistening back of a gray whale that gave me pause. Too many have been seen inside the bay recently.California’s gray whales have been considered an environmental success story since the passage of the 1972 Marine Mammal Protection Act and 1986’s global ban on commercial whaling. They’re also a major tourist attraction during their annual 12,000-mile round-trip migration between the Arctic and their breeding lagoons in Baja California. In late winter and early spring — when they head back north and are closest to the shoreline, with the moms protecting the calves — they can be viewed not only from whale-watching boats but also from promontories along the California coast including Point Loma in San Diego, Point Lobos in Monterey and Bodega Head and Shelter Cove in Northern California.In 1972, there were some 10,000 gray whales in the population on the eastern side of the Pacific. Generations of whaling all but eliminated the western population — leaving only about 150 alive today off of East Asia and Russia. Over the four decades following passage of the Marine Mammal Protection Act, the eastern whale numbers grew steadily to 27,000 by 2016, a hopeful story of protection leading to restoration. Then, unexpectedly over the last nine years, the eastern gray whale population has crashed, plummeting by more than half to 12,950, according to a recent report by the National Oceanic and Atmospheric Administration, the lowest numbers since the 1970s.Today’s changing ocean and Arctic ice conditions linked to fossil-fuel-fired climate change are putting this species again at risk of extinction.While there has been some historical variation in their population, gray whales — magnificent animals that can grow up to 50 feet long and weigh as much as 80,000 pounds — are now regularly starving to death as their main food sources disappear. This includes tiny shrimp-like amphipods in the whales’ summer feeding grounds in the Arctic. It’s there that the baleen filter feeders spend the summer gorging on tiny crustaceans from the muddy bottom of the Bering, Chuckchi and Beaufort seas, creating shallow pits or potholes in the process. But, with retreating sea ice, there is less under-ice algae to feed the amphipods that in turn feed the whales. Malnourished and starving whales are also producing fewer offspring.As a result of more whales washing up dead, NOAA declared an “unusual mortality event” in California in 2019. Between 2019 and 2025, at least 1,235 gray whales were stranded dead along the West Coast. That’s eight times greater than any previous 10-year average.While there seemed to be some recovery in 2024, 2025 brought back the high casualty rates. The hungry whales now come into crowded estuaries like San Francisco Bay to feed, making them vulnerable to ship traffic. Nine in the bay were killed by ship strikes last year while another 12 appear to have died of starvation.Michael Stocker, executive director of the acoustics group Ocean Conservation Research, has been leading whale-viewing trips to the gray whales’ breeding ground at San Ignacio Lagoon in Baja California since 2006. “When we started going, there would be 400 adult whales in the lagoon, including 100 moms and their babies,” he told me. “This year we saw about 100 adult whales, only five of which were in momma-baby pairs.” Where once the predators would not have dared to hunt, he said that more recently, “orcas came into the lagoon and ate a couple of the babies because there were not enough adult whales to fend them off.”Southern California’s Gray Whale Census & Behavior Project reported record-low calf counts last year.The loss of Arctic sea ice and refusal of the world’s nations recently gathered at the COP30 Climate Summit in Brazil to meet previous commitments to reduce greenhouse gas emissions suggest that the prospects for gray whales and other wildlife in our warming seas, including key food species for humans such as salmon, cod and herring, look grim.California shut down the nation’s last whaling station in 1971. And yet now whales that were once hunted for their oil are falling victim to the effects of the petroleum or “rock oil” that replaced their melted blubber as a source of light and lubrication. That’s because the burning of oil, coal and gas are now overheating our blue planet. While humans have gone from hunting to admiring whales as sentient beings in recent decades, our own intelligence comes into question when we fail to meet commitments to a clean carbon-free energy future. That could be the gray whales’ last best hope, if there is any.David Helvarg is the executive director of Blue Frontier, an ocean policy group, and co-host of “Rising Tide: The Ocean Podcast.” He is the author of the forthcoming “Forest of the Sea: The Remarkable Life and Imperiled Future of Kelp.”

Pills that communicate from the stomach could improve medication adherence

MIT engineers designed capsules with biodegradable radio frequency antennas that can reveal when the pill has been swallowed.

In an advance that could help ensure people are taking their medication on schedule, MIT engineers have designed a pill that can report when it has been swallowed.The new reporting system, which can be incorporated into existing pill capsules, contains a biodegradable radio frequency antenna. After it sends out the signal that the pill has been consumed, most components break down in the stomach while a tiny RF chip passes out of the body through the digestive tract.This type of system could be useful for monitoring transplant patients who need to take immunosuppressive drugs, or people with infections such as HIV or TB, who need treatment for an extended period of time, the researchers say.“The goal is to make sure that this helps people receive the therapy they need to help maximize their health,” says Giovanni Traverso, an associate professor of mechanical engineering at MIT, a gastroenterologist at Brigham and Women’s Hospital, and an associate member of the Broad Institute of MIT and Harvard.Traverso is the senior author of the new study, which appears today in Nature Communications. Mehmet Girayhan Say, an MIT research scientist, and Sean You, a former MIT postdoc, are the lead authors of the paper.A pill that communicatesPatients’ failure to take their medicine as prescribed is a major challenge that contributes to hundreds of thousands of preventable deaths and billions of dollars in health care costs annually.To make it easier for people to take their medication, Traverso’s lab has worked on delivery capsules that can remain in the digestive tract for days or weeks, releasing doses at predetermined times. However, this approach may not be compatible with all drugs.“We’ve developed systems that can stay in the body for a long time, and we know that those systems can improve adherence, but we also recognize that for certain medications, we can’t change the pill,” Traverso says. “The question becomes: What else can we do to help the person and help their health care providers ensure that they’re receiving the medication?”In their new study, the researchers focused on a strategy that would allow doctors to more closely monitor whether patients are taking their medication. Using radio frequency — a type of signal that can be easily detected from outside the body and is safe for humans — they designed a capsule that can communicate after the patient has swallowed it.There have been previous efforts to develop RF-based signaling devices for medication capsules, but those were all made from components that don’t break down easily in the body and would need to travel through the digestive system.To minimize the potential risk of any blockage of the GI tract, the MIT team decided to create an RF-based system that would be bioresorbable, meaning that it can be broken down and absorbed by the body. The antenna that sends out the RF signal is made from zinc, and it is embedded into a cellulose particle.“We chose these materials recognizing their very favorable safety profiles and also environmental compatibility,” Traverso says.The zinc-cellulose antenna is rolled up and placed inside a capsule along with the drug to be delivered. The outer layer of the capsule is made from gelatin coated with a layer of cellulose and either molybdenum or tungsten, which blocks any RF signal from being emitted.Once the capsule is swallowed, the coating breaks down, releasing the drug along with the RF antenna. The antenna can then pick up an RF signal sent from an external receiver and, working with a small RF chip, sends back a signal to confirm that the capsule was swallowed. This communication happens within 10 minutes of the pill being swallowed.The RF chip, which is about 400 by 400 micrometers, is an off-the-shelf chip that is not biodegradable and would need to be excreted through the digestive tract. All of the other components would break down in the stomach within a week.“The components are designed to break down over days using materials with well-established safety profiles, such as zinc and cellulose, which are already widely used in medicine,” Say says. “Our goal is to avoid long-term accumulation while enabling reliable confirmation that a pill was taken, and longer-term safety will continue to be evaluated as the technology moves toward clinical use.”Promoting adherenceTests in an animal model showed that the RF signal was successfully transmitted from inside the stomach and could be read by an external receiver at a distance up to 2 feet away. If developed for use in humans, the researchers envision designing a wearable device that could receive the signal and then transmit it to the patient’s health care team.The researchers now plan to do further preclinical studies and hope to soon test the system in humans. One patient population that could benefit greatly from this type of monitoring is people who have recently had organ transplants and need to take immunosuppressant drugs to make sure their body doesn’t reject the new organ.“We want to prioritize medications that, when non-adherence is present, could have a really detrimental effect for the individual,” Traverso says.Other populations that could benefit include people who have recently had a stent inserted and need to take medication to help prevent blockage of the stent, people with chronic infectious diseases such as tuberculosis, and people with neuropsychiatric disorders whose conditions may impair their ability to take their medication.The research was funded by Novo Nordisk, MIT’s Department of Mechanical Engineering, the Division of Gastroenterology at Brigham and Women’s Hospital, and the U.S. Advanced Research Projects Agency for Health (ARPA-H), which notes that the views and conclusions contained in this article are those of the authors and should not be interpreted as representing the official policies, either expressed or implied, of the United States Government.

Costa Rica Rescues Orphaned Manatee Calf in Tortuguero

A young female manatee washed up alone on a beach in Tortuguero National Park early on January 5, sparking a coordinated effort by local authorities to save the animal. The calf, identified as a Caribbean manatee, appeared separated from its mother, with no immediate signs of her in the area. Park rangers received the first […] The post Costa Rica Rescues Orphaned Manatee Calf in Tortuguero appeared first on The Tico Times | Costa Rica News | Travel | Real Estate.

A young female manatee washed up alone on a beach in Tortuguero National Park early on January 5, sparking a coordinated effort by local authorities to save the animal. The calf, identified as a Caribbean manatee, appeared separated from its mother, with no immediate signs of her in the area. Park rangers received the first alert around 8 a.m. from visitors who spotted the stranded calf. Staff from the National System of Conservation Areas (SINAC) quickly arrived on site. They secured the animal to prevent further harm and began searching nearby waters and canals for the mother. Despite hours of monitoring, officials found no evidence of her presence. “The calf showed no visible injuries but needed prompt attention due to its age and vulnerability,” said a SINAC official involved in the operation. Without a parent nearby, the young manatee faced risks from dehydration and predators in the open beach environment. As the day progressed, the Ministry of Environment and Energy (MINAE) joined the response. They decided to relocate the calf for specialized care. In a first for such rescues in the region, teams arranged an aerial transport to move the animal safely to a rehabilitation facility. This step aimed to give the manatee the best chance at survival while experts assess its health. Once at the center, the calf received immediate feeding and medical checks. During one session, it dozed off mid-meal, a sign that it felt secure in the hands of caretakers. Biologists now monitor the animal closely, hoping to release it back into the wild if conditions allow. Manatees, known locally as manatíes, inhabit the coastal waters and rivers of Costa Rica’s Caribbean side. They often face threats from boat strikes, habitat loss, and pollution. Tortuguero, with its network of canals and protected areas, serves as a key habitat for the species. Recent laws have strengthened protections, naming the manatee a national marine symbol to raise awareness. This incident highlights the ongoing challenges for wildlife in the area. Local communities and tourists play a key role in reporting sightings, which can lead to timely interventions. Authorities encourage anyone spotting distressed animals to contact SINAC without delay. The rescue team expressed gratitude to those who reported the stranding. Their quick action likely saved the calf’s life. As investigations continue, officials will determine if environmental factors contributed to the separation. For now, the young manatee rests under professional care, a small win for conservation efforts in Limón. The post Costa Rica Rescues Orphaned Manatee Calf in Tortuguero appeared first on The Tico Times | Costa Rica News | Travel | Real Estate.

New Records Reveal the Mess RFK Jr. Left When He Dumped a Dead Bear in Central Park

Robert F. Kennedy Jr. says he left a bear cub's corpse in Central Park in 2014 to "be fun." Records newly obtained by WIRED show what he left New York civil servants to clean up.

This story contains graphic imagery.On August 4, 2024, when now-US health secretary Robert F. Kennedy Jr. was still a presidential candidate, he posted a video on X in which he admitted to dumping a dead bear cub near an old bicycle in Central Park 10 years prior, in a mystifying attempt to make the young bear’s premature death look like a cyclist’s hit and run.WIRED's Guide to How the Universe WorksYour weekly roundup of the best stories on health care, the climate crisis, new scientific discoveries, and more. At the time, Kennedy said he was trying to get ahead of a story The New Yorker was about to publish that mentioned the incident. But in coming clean, Kennedy solved a decade-old New York City mystery: How and why had a young black bear—a wild animal native to the state, but not to modern-era Manhattan—been found dead under a bush near West 69th Street in Central Park?WIRED has obtained documents that shed new light on the incident from the New York City Department of Parks and Recreation via a public records request. The documents—which include previously unseen photos of the bear cub—resurface questions about the bizarre choices Kennedy says he made, which left city employees dealing with the aftermath and lamenting the cub’s short life and grim fate.A representative for Kennedy did not respond for comment. The New York Police Department (NYPD) and the Parks Department referred WIRED to the New York Department of Environmental Conservation (NYDEC). NYDEC spokesperson Jeff Wernick tells WIRED that its investigation into the death of the bear cub was closed in late 2014 “due to a lack of sufficient evidence” to determine if state law was violated. They added that New York’s environmental conservation law forbids “illegal possession of a bear without a tag or permit and illegal disposal of a bear,” and that “the statute of limitations for these offenses is one year.”The first of a number of emails between local officials coordinating the handling of the baby bear’s remains was sent at 10:16 a.m. on October 6, 2014. Bonnie McGuire, then-deputy director at Urban Park Rangers (UPR), told two colleagues that UPR sergeant Eric Handy had recently called her about a “dead black bear” found in Central Park.“NYPD told him they will treat it like a crime scene so he can’t get too close,” McGuire wrote. “I’ve asked him to take pictures and send them over and to keep us posted.”“Poor little guy!” McGuire wrote in a separate email later that morning.According to emails obtained by WIRED, Handy updated several colleagues throughout the day, noting that the NYDEC had arrived on scene, and that the agency was planning to coordinate with the NYPD to transfer the body to the Bronx Zoo, where it would be inspected by the NYPD’s animal cruelty unit and the ASPCA. (This didn’t end up happening, as the NYDEC took the bear to a state lab near Albany.)Imagery of the bear has been public before—local news footage from October 2014 appears to show it from a distance. However, the documents WIRED obtained show previously unpublished images that investigators took of the bear on the scene, which Handy sent as attachments in emails to McGuire. The bear is seen laying on its side in an unnatural position. Its head protrudes from under a bush and rests next to a small patch of grass. Bits of flesh are visible through the bear’s black fur, which was covered in a few brown leaves.Courtesy of NYC Parks

U.S. Military Ends Practice of Shooting Live Animals to Train Medics to Treat Battlefield Wounds

The 2026 National Defense Authorization Act bans the use of live animals in live fire training exercises and prohibits "painful" research on domestic cats and dogs

U.S. Military Ends Practice of Shooting Live Animals to Train Medics to Treat Battlefield Wounds The 2026 National Defense Authorization Act bans the use of live animals in live fire training exercises and prohibits “painful” research on domestic cats and dogs Sarah Kuta - Daily Correspondent January 5, 2026 12:00 p.m. The U.S. military will no longer shoot live goats and pigs to help combat medics learn to treat battlefield injuries. Pexels The United States military is no longer shooting live animals as part of its trauma training exercises for combat medics. The 2026 National Defense Authorization Act, which was enacted on December 18, bans the use of live animals—including dogs, cats, nonhuman primates and marine mammals—in any live fire trauma training conducted by the Department of Defense. It directs military leaders to instead use advanced simulators, mannequins, cadavers or actors. According to the Associated Press’ Ben Finley, the bill ends the military’s practice of shooting live goats and pigs to help combat medics learn to treat battlefield injuries. However, the military is allowed to continue other practices involving animals, including stabbing, burning and testing weapons on them. In those scenarios, the animals are supposed to be anesthetized, per the AP. “With today’s advanced simulation technology, we can prepare our medics for the battlefield while reducing harm to animals,” says Florida Representative Vern Buchanan, who advocated for the change, in a statement shared with the AP. He described the military’s practices as “outdated and inhumane” and called the move a “major step forward in reducing unnecessary suffering.” Quick fact: What is the National Defense Authorization Act? The National Defense Authorization Act, or NDAA, is a law passed each year that authorizes the Department of Defense’s appropriated funds, greenlights the Department of Energy’s nuclear weapons programs and sets defense policies and restrictions, among other activities, for the upcoming fiscal year. Organizations have opposed the military’s use of live animals in trauma training, too, including the Physicians Committee for Responsible Medicine and the People for the Ethical Treatment of Animals. PETA, a nonprofit animal advocacy group, described the legislation as a “major victory for animals” that will “save countless animals from heinous cruelty” in a statement. The legislation also prohibits “painful research” on domestic cats and dogs, though exceptions can be made under certain circumstances, such as interests of national security. “Painful” research includes any training, experiments or tests that fall into specific pain categories outlined by the U.S. Department of Agriculture. For example, military cats and dogs can no longer be exposed to extreme environmental conditions or noxious stimuli they cannot escape, nor can they be forced to exercise to the point of distress or exhaustion. The bill comes amid a broader push to end the use of live animals in federal tests, studies and training, reports Linda F. Hersey for Stars and Stripes. After temporarily suspending live tissue training with animals in 2017, the U.S. Coast Guard made the ban permanent in 2018. In 2024, U.S. lawmakers directed the Department of Veterans Affairs to end its experiments on cats, dogs and primates. And in May 2025, the U.S. Navy announced it would no longer conduct research testing on cats and dogs. As the Washington Post’s Ernesto Londoño reported in 2013, the U.S. military has used animals for medical training since at least the Vietnam War. However, the practice largely went unnoticed until 1983, when the U.S. Army planned to anesthetize dogs, hang them from nylon mesh slings and shoot them at an indoor firing range in Maryland. When activists and lawmakers learned of the proposal, they decried the practice and convinced then-Defense Secretary Caspar Weinberger to ban the shooting of dogs. However, in 1984, the AP reported the U.S. military would continue shooting live goats and pigs for wound treatment training, with a military medical study group arguing “there is no substitute for the live animals as a study object for hands-on training.” In the modern era, it’s not clear how often and to what extent the military uses animals, per the AP. And despite the Department of Defense’s past efforts to minimize the use of animals for trauma training, a 2022 report from the Government Accountability Office, the watchdog agency charged with providing fact-based, nonpartisan information to Congress, determined that the agency was “unable to fully demonstrate the extent to which it has made progress.” The Defense Health Agency, the U.S. government entity responsible for the military’s medical training, says in a statement shared with the AP that it “remains committed to replacement of animal models without compromising the quality of medical training,” including the use of “realistic training scenarios to ensure medical providers are well-prepared to care for the combat-wounded.” Animal activists say technology has come a long way in recent decades so, beyond the animal welfare concerns, the military simply no longer needs to use live animals for training. Instead, military medics can simulate treating battlefield injuries using “cut suits,” or realistic suits with skin, blood and organs that are worn by a live person to mimic traumatic injuries. However, not everyone agrees. Michael Bailey, an Army combat medic who served two tours in Iraq, told the Washington Post in 2013 that his training with a sedated goat was invaluable. “You don’t get that [sense of urgency] from a mannequin,” he told the publication. “You don’t get that feeling of this mannequin is going to die. When you’re talking about keeping someone alive when physics and the enemy have done their best to do the opposite, it’s the kind of training that you want to have in your back pocket.” Get the latest stories in your inbox every weekday.

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