Health – The Conversation

Bamboo: superfood or superfad? Here’s what our study actually said

2026-02-04T13:53:32Z

According to the New York Post, our research team has discovered a much-overlooked “superfood”: bamboo shoots. Before you rush out to harvest the ornamental bamboo growing in your garden, there are a few things you should know.

We systematically reviewed all the available evidence on bamboo as a food and its effect on human health. The research base turned out to be surprisingly thin – just 16 studies met our criteria, including four trials in people and four that used cells in a dish. The final eight focused on bamboo characteristics with potential application to nutrition. This is what they showed us.

There is evidence of some positive health effects from eating bamboo. One study showed that eating bamboo shoots in cookies better controlled blood sugar levels, and that more bamboo consumption translated to further lowered levels.

Other studies documented the beneficial effects of the fibre they contain. This isn’t limited to the inevitable bowel movements but also includes the delightfully termed “faecal volume”, both of which were shown to improve.

Also, compared to a fibre-free diet, bamboo shoots lowered overall cholesterol and LDL cholesterol (so-called “bad cholesterol”) that can build up in blood vessels and cause heart disease.

One unusual benefit of bamboo is that it contains flavonoids – plant compounds that can protect against acrylamide, a potentially harmful chemical that forms when starchy foods are cooked at high temperatures. These compounds can increase the risk of some cancers and have been the subject of the Food Standards Agency campaign in 2017 to avoid any burning and “go for gold” when cooking.

Eating bamboo may also help calm inflammation and protect cells from damage. In lab tests, it reduced immune cell activity by 63% and halved the release of substances that trigger inflammation in the body. Bamboo also acts as an antioxidant – lab tests showed it cut by nearly half the production of harmful chemicals like hydrogen peroxide that can damage cells.

Although these findings were in cells in a dish, it gives some insight into the action of bamboo extracts on the human body.

The grass isn’t all green, though

However, if bamboo isn’t properly prepared, it can lead to problems. One study linked it to an increased risk of a condition called goitre. Goitre is an enlargement of the thyroid, a gland in the neck that is important for growth and setting the metabolic rate. It is visible as a swelling in the front of the neck and is most typically associated with low iodine consumption.

Poorly prepared bamboo contains chemicals called cyanogenic glycosides, which the body converts into another chemical called thiocyanate. These block the thyroid from using iodine effectively. People on low-iodine diets, or with existing thyroid issues, are particularly at risk. But the risk of goitre from bamboo shoot consumption may be reduced by properly preparing the shoot to eat, which can be achieved by boiling the shoot in water.

Some of the bamboo samples analysed contained heavy metals, like arsenic, cadmium and lead. These show up in most foods in trace amounts, and have safety levels specified, for example, by the Food Standards Agency.

Some bamboo shoots contained heavy metals. aomas/Shutterstock.com

While most were measured well within permitted limits, lead was found in amounts up to 4.6 times the permitted levels in 21 of the samples assessed. While caution is important, these concentrations were not shown to affect the health of the cells in the lab, which might suggest how easily such chemicals are used by tissues (their so-called “bio-availability”).

There are some other things to bear in mind too. The evidence base in this area isn’t as strong as it could be. The few relevant studies we did find on this topic had some methodological issues and they didn’t offer the most compelling evidence for their findings.

We could only formally assess the four trials on people, which scored in a range indicating “overall satisfactory quality”. As ever, though, they do show the value of research in this area, and the attention our study has garnered shows the public’s clear interest in the topic.

Still, the research shows that bamboo shoots have potential as a sustainable, healthy food. And like the shoots themselves, interest in this area is only likely to grow – rapidly.

The authors do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.

How our lab is helping develop an Alzheimer’s test that can be done at home

2026-02-04T13:53:27Z

These tests could be done at home, making Alzheimer's diagnosis more accessible. nito/ Shutterstock

Imagine diagnosing one of the most challenging neurological diseases with just a quick finger-prick, a few drops of blood and a test sent in the post. This may sound like science fiction, but we are hoping our research could soon help it become a reality.

Our team at the UK Dementia Research Institute’s Biomarker Factory at UCL are part of the global effort working to develop and validate a test for Alzheimer’s disease. We’re currently working to overcome the various technical challenges facing these tests so that this test can one day soon be available to the broader public.

What do finger-prick tests look for?

At their core, these finger-prick tests are designed to detect specific biomarkers.
Biomarkers are biological molecules found in the blood which indicate signs of disease. In the case of Alzheimer’s disease, the brain gradually accumulates abnormal proteins. These proteins form structures such as amyloid plaques and tau tangles which damage the brain’s neural networks. They’re also involved in brain inflammation.

These abnormal proteins can be detected in the brain, cerebrospinal fluid and, importantly, the blood years before symptoms arise.

Recently, research has also shown these biomarkers can be measured in dried blood samples from a simple finger-prick. A study focusing on 337 people showed that these dried blood samples can reliably detect Alzheimer’s-related changes in biomarkers with a diagnostic accuracy of around 86% compared to conventional methods.

Once refined and validated, these tests could aid with early detection, screening at-risk people, tracking disease progression or even evaluating the effectiveness of emerging treatments.

What are the shortcomings of current diagnostic tools?

In addition to cognitive tests (which check for cognitive decline and memory problems), there are currently two robust approaches for diagnosing signs of Alzheimer’s in the brain.

The first is PET imaging. These scans detect disease characteristics using radioactive tracers which light up areas of the brain where tangles and plaques may be present. However, PET scans are expensive, use radioactivity and require specialist facilities.

The second method uses a spinal tap to extract cerebrospinal fluid (the clear, colourless liquid that protects the brain and extracts waste). This looks for the same biomarkers as finger-prick tests. However, this method is invasive and can be painful and stressful to patients. Some people also may not be eligible to have it done.

PET scans are expensive and require specialist facilities. Gorodenkoff/ Shutterstock

Cognitive tests also have shortcomings. As a result, people whose first language isn’t the one in which the test is being administered, or those who have other health conditions that also cause cognitive problems, may be misdiagnosed.

And, while cognitive testing can give an idea about a potential issue, these tests alone can’t tell us what specific condition is causing symptoms. This can also lead to misdiagnosis.

Even traditional blood tests done in a clinic have limitations. These tests require immediate processing (or refrigeration) and careful handling to avoid influencing biomarker levels. This makes traditional blood tests impractical for large-scale, population-level screening – particularly in underserved or rural regions.

By contrast, the finger-prick test we’re developing can be done at home and posted to a lab without refrigeration.

What are we working on in the lab?

Our lab is currently working to improve the sensitivity, reliability and real-world usability of these finger-prick tests.

We’re currently experimenting with different, sensitive biomarker detection methods – using just tiny volumes of blood collected from either the finger or the vein and seeing how these compare.

Alongside tau and amyloid, we’re also testing other proteins associated with Alzheimer’s and various neurodegenerative disorders – such as Parkinson’s disease and multiple sclerosis.

Our hope with these tests is not only to identify Alzheimer’s disease, but to catch it before irreversible brain damage occurs. This would open a window for early intervention.

With novel therapies emerging that may slow the disease, early identification is critical.

What challenges have we encountered?

Designing these tests hasn’t been straightforward. We’ve encountered a few major hurdles along the way.

The first hurdle we encountered had to do with the biomarkers themselves.

Alzheimer’s biomarker levels are often much lower in the blood than they are in cerebrospinal fluid. So the technological methods needed to measure them accurately had to be very sensitive.

Another obstacle we encountered related to sample quality. Without refrigeration, the proteins can degrade – giving inaccurate readings and potentially misdiagnoses. So we’re currently working to develop collection and mailing methods that ensure these dried blood proteins are stable and don’t degrade before testing.

Data interpretation has also been a challenge. Although these tests are accurate for the majority of cases, we still need to figure out how to interpret outliers – such as participants who have high biomarker levels without other signs of the disease, and those who have low biomarker levels with significant signs of the disease. So even when we detect elevated biomarkers, interpreting what that means for a person’s Alzheimer’s risk is complex.

Alzheimer’s biomarkers are also not exclusive to the disease. Similar biomarkers can occur in other neurological conditions such as vascular dementia, multiple sclerosis, and even in otherwise asymptomatic people or even healthy newborns.

We’ve since refined our tests so they’re more sensitive and have sourced and are currently comparing devices that make at-home sample collection easier. These solutions are steadily improving test reliability.

What could our work mean for Alzheimer’s diagnosis?

It’s important to emphasise that these tests are still at least a few years away from routine use. But, if validated, finger-prick tests could revolutionise Alzheimer’s diagnosis in several ways.

It would allow for earlier detection of the disease and broaden access for patients. It would also enable larger, more diverse population studies to be conducted – reducing historical gaps in Alzheimer’s research and improving our understanding of the disease globally.

The idea of diagnosing Alzheimer’s with a quick, finger-prick test marks a profound shift in how we could approach neurodegenerative diseases. Moving beyond invasive, costly procedures toward accessible, patient-friendly diagnostics carries enormous potential — for patients, their families and future research.

Why are scientists calling for urgent action on amoebas?

2026-02-03T18:40:54Z

Naegleria fowleri, the brain-eating amoeba. Kateryna Kon/Shutterstock.com

Scientists are calling for urgent action on free-living amoebas – a little-known group of microbes that could pose a growing global health threat. Here’s what you need to know.

Free-living amoebas are single-celled organisms that don’t need a host to live. They are found in soil and water, from puddles to lakes.

What makes them remarkable is their ability to change shape and move using temporary arm-like extensions called pseudopodia – literally “false feet”. This allows them to thrive in an astonishing range of environments.

What is the ‘brain-eating amoeba’ and how dangerous is it?

The most notorious free-living amoeba is Naegleria fowleri, commonly known as the “brain-eating amoeba”. It lives naturally in warm freshwater, typically between 30°C and 40°C – lakes, rivers and hot springs. But it is rarely found in temperate countries such as the UK, due to the cold weather.

The infection happens when contaminated water enters through the nose, usually while swimming. From there, the amoeba travels along the nasal passages to the brain, where it destroys brain tissue. The outcome is usually devastating, with a mortality rate of 95%-99%.

Occasionally, Naegleria fowleri has been found in tap water, particularly when it’s warm and hasn’t been properly chlorinated. Some people have become infected while using contaminated tap water to rinse their sinuses for religious or health reasons.

Fortunately, you cannot get infected by drinking contaminated water, and the infection doesn’t spread from person to person.

Nasal rinsing with contaminated tap water is risky. Zaruna/Shutterstock.com

Why are these amoebas so difficult to kill?

Brain-eating amoebas can be killed by proper water treatment and chlorination. But eliminating them from water systems isn’t always straightforward.

When they attach to biofilms – communities of microorganisms that form inside pipes – disinfectants like chlorine struggle to reach them, and organic matter can reduce the disinfectants’ effectiveness.

The amoeba can also survive warm temperatures by forming “cysts” – hard protective shells – making it harder to control in water networks, especially during summer or in poorly maintained systems.

What is the ‘Trojan-horse effect’ and why does it matter?

Free-living amoebas aren’t just dangerous on their own. They can also act as living shields for other harmful microbes, protecting them from environmental stress and disinfection.

While amoebas normally feed on bacteria, fungi and viruses, some bacteria – like Mycobacterium tuberculosis (which causes TB) and Legionella pneumophila (which causes legionnaires’ disease) – have evolved to survive and multiply inside them. This helps these pathogens survive longer and potentially become more dangerous.

Amoebas also shelter fungi such as Cryptococcus neoformans, which can cause fungal meningitis. It can also shelter viruses, such as human norovirus and adenovirus, which cause respiratory, eye and gastrointestinal infections.

By protecting these pathogens, amoebas help them survive longer in water and soil, and may even help spread antibiotic resistance.

How is climate change making the problem worse?

Climate change is probably making the threat from free-living amoebas worse by creating more favourable conditions for their growth.

Naegleria fowleri thrives in warm freshwater. As global temperatures rise, the habitable zone for these heat-loving amoebas has expanded into regions that were previously too cool. This potentially exposes more people to them through recreational water use.

Several recent outbreaks linked to recreational water exposure have already raised public concern in multiple countries. These climate-driven changes – warmer waters, longer warm seasons, and increased human contact with water – make controlling the risks more difficult than ever before.

Are our water systems adequately checked for these organisms?

Most water systems are not routinely checked for free-living amoebas. The organisms are rare, can hide in biofilms or sediments, and require specialised tests to detect, making routine monitoring expensive and technically challenging.

Instead, water safety relies on proper chlorination, maintaining disinfectant levels, and flushing systems regularly, rather than testing directly for the amoeba. While some guidance exists for high-risk areas, widespread monitoring is not standard practice.

Beyond brain infections, what other health risks do these amoebas pose?

Free-living amoebas aren’t just a threat to the brain. They can cause painful eye infections, particularly in contact lens users, skin lesions in people with weakened immune systems, and rare but serious systemic infections affecting organs such as the lungs, liver and kidneys.

What’s being done to address this threat?

Free-living amoebas such as Naegleria fowleri are rare but can be deadly, so prevention is crucial. These organisms don’t fit neatly into either medical or environmental categories – they span both, requiring a holistic approach that links environmental surveillance, water management, and clinical awareness to reduce risk.

Environmental change, gaps in water treatment and expanding habitats make monitoring – and clear communication of risk – more important than ever.

Keeping water systems properly chlorinated, flushing hot water systems, and following safe recreational water and contact lens hygiene guidelines all help reduce the chance of infection. Meanwhile, researchers continue to improve detection methods and doctors work to recognise cases early.

Should people be worried about their tap water or going swimming?

People cannot get infected with free-living amoebas like Naegleria fowleri by drinking water, even if it contains the organism. Infection occurs only when contaminated water enters the nose, allowing the amoeba to reach the brain. Swallowing the water poses no risk because the amoeba cannot survive or invade through the digestive tract.

The risk from swimming in well-maintained pools or treated water is extremely low. The danger comes from warm, untreated freshwater, particularly during hot weather.

What can people do to protect themselves?

People can protect themselves from free-living amoebas by reducing exposure to warm, stagnant water. Simple steps include avoiding putting your head underwater in lakes or rivers during hot weather, using nose clips when swimming, choosing well-maintained pools, and keeping home water systems properly flushed and heated.

Contact lens users should follow strict hygiene and never rinse lenses with tap water. For nasal rinsing, only use sterile, distilled, or previously boiled water.

Awareness is key. If you develop a severe headache, fever, nausea, or stiff neck after freshwater exposure, seek medical attention immediately – early treatment is critical.

Manal Mohammed does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

What new twins study reveals about genes, environment and longevity

2026-02-03T17:32:02Z

Digital Media Pro/Shutterstock.com

Why do some people live to 100 while their sibling dies decades earlier? Is it luck, lifestyle, or something written into their DNA?

Relative to many other species, humans are particularly long lived, but there is an ongoing argument about how much of our long lifespan is shaped by our genes and how much to our environment. It’s the old “nature versus nurture” debate.

Researchers have repeatedly used large population studies to estimate how much genetics influences longevity. Historically, these studies have found relatively modest effects, typically around 25% to 33%, with some estimates as low as 6-16%.

A recent study published in Science challenged this trend, revising the estimate upward to about 50% by accounting for changes in external causes of death – such as accidents and infectious diseases – and separating the effects of genetics and environment in large historical cohorts of twins.

We know that individual genes affect lifespans in different species. A single mutation in the gene coding for the insulin sensor of worms would cause them to double their lifespan. Since that 1993 discovery, scientists have experimentally extended the lifespans of flies and mice, and even found hints of similar effects in long-lived humans.

However, the effect of this single gene variation seems to be lessened as the species becomes more long lived, so don’t expect a single gene mutation to suddenly cause 200-year human life expectancies. Also, these were gene mutations affecting the sensitivity of insulin and insulin-like growth factor hormones – in other words, the mutations seem to mimic the metabolic effects of a healthy diet and regular exercise.

Perhaps an obvious statement to make, but many of our body’s traits, including longevity, are the sum of all our inherited genes, not just a single gene. But how much is genetics and how much is lifestyle is the open question.

This amount is more than an interesting number. If genetics mostly controls how long we live, then new anti-ageing treatments and lifestyle changes won’t help much. But if genetics plays a smaller role, then what we do and the treatments we use could make a bigger difference in how long we live.

Nature’s perfect experiment

To tackle this question, the authors of the Science paper used data from the Swedish Adoption/Twin Study of Ageing. Because it includes a rare set of twins raised apart, the data makes it easier to tease apart the effects of genes and environment, creating something close to a natural experiment in humans.

By studying monozygotic (“identical”) twins, or people with identical genomes born between 1900 and 1935 and attempting to correct for rapidly changing external influences of health and mortality during this period, the authors conclude that the inherited influence of lifespan is about 50%.

Put another way, about 50% of your potential lifespan is given to you by your parents, and the other 50% is the environment you live in. Things such as exercise, nutrition, sleep, stress, pollution and infectious disease exposure all fall into this external category.

Identical twins, followed over a lifetime, can reveal a lot. JGA/Shutterstock.com

The researchers then validated their models using data from populations in Denmark and the US. However, this also means the study populations were largely white, wealthy and European. Including more diverse populations will be important for determining how well these findings apply to humanity as a whole.

The reason that the authors put forward for their number being so much higher than others is their accounting for the effects of changing external influences on longevity, things such as improving sanitation and medication.

Indeed, if they don’t correct for external causes of death, their model finds numbers in the 20-30% range, or much closer to prior estimates. As the authors note, many health traits seem to be about 50% heritable, so there’s an internal logic of longevity as a trait following this trend.

These estimates could still change. Longevity studies in humans are time consuming, relying on historical records or following populations over roughly 100 years as people live their normal lives. As the authors note: “Heritability is a statistic that applies to a particular population in a particular environment at a particular time.”

This doesn’t mean that your personal actions aren’t helping you – this debate probably isn’t over yet. This is the largest estimate of the effect of genetics on longevity to emerge recently in the scientific literature, but even if genes account for about half our lifespan’s story, the other half is still being written every day.

Bradley Elliott receives funding from the Physiological Society, the British Society for Research on Ageing, the Altitude Centre, and private philanthropic individuals, and has consulted for industry and government on longevity research. He is on the Board of Trustees of the British Society for Research on Ageing.

Why do our joints crack, pop and crunch and should we worry about it?

2026-02-03T12:12:04Z

New Africa/Shutterstock

Many of us have noisy joints. Knees crack on the stairs, necks pop when we stretch, and knuckles seem to crack almost on demand. These sounds can be startling and are often blamed on ageing, damage or the looming threat of arthritis.

As a physiotherapist and researcher of chronic joint pain, I am frequently asked whether joint noises are something to worry about. The reassuring answer is that, in most cases, they are not.

One reason joint sounds cause anxiety is that we tend to treat them as a single phenomenon. Clinically, they are not.

The familiar “crack” from knuckles, backs or necks is usually caused by a process called cavitation. Joints are surrounded by a capsule filled with synovial fluid, a thick lubricant that contains dissolved gases such as oxygen, nitrogen and carbon dioxide. When a joint is stretched beyond its usual range, pressure inside the capsule drops. A gas bubble forms and collapses, producing the popping sound.

This is why you cannot crack the same joint repeatedly. It typically takes around 20 minutes for the gas to dissolve back into the fluid.

Other noises are different. Snapping sounds often come from tendons moving over bony structures. Grinding, crunching or creaking noises, known as crepitus, are particularly common in the knees. These are thought to arise from movement between cartilage and bone surfaces and are often felt as well as heard.

Knees are especially prone to crepitus because of how they work. The kneecap sits in a groove at the front of the thigh bone and is guided by muscles above and below it. If those muscles pull unevenly, because of strength imbalances, tightness or foot and hip mechanics, the kneecap can track slightly off centre. This can increase the crunching or grinding sensation.

Noise on its own is rarely a problem. What matters clinically is whether it comes with other symptoms. Pain, swelling, locking of the joint or a noticeable reduction in function are the things that warrant further assessment.

Does cracking joints cause arthritis?

There is no strong evidence that cracking or popping joints causes osteoarthritis.

Research in this area is challenging, as it requires following people over many years and accurately tracking their habits. The studies that do exist, including retrospective and cross-sectional research, have not found a meaningful link between habitual joint cracking and arthritis.

Some studies have explored other outcomes, such as grip strength or joint laxity, which refers to how loose or flexible a joint is and how much it can move beyond its typical range. Findings have been mixed and inconsistent. Overall, there is no convincing evidence that cracking joints causes damage to joint structures, strength or long-term joint health.

Many people report that joint cracking feels satisfying or relieving. This makes sense. Stretching a joint to the point of cavitation can temporarily increase range of motion and reduce muscle tension. There is also a neurological effect, as nerve endings are stimulated during the movement, sending a reflex signal to the brain which causes local muscle relaxation in the area. The audible pop itself can provide a calming, satisfying sensation which may lead to developing that habitual self-soothing mechanism for tension that annoys your family members and friends.

The key point is that these effects are short lived. Joint cracking does not fix underlying mechanical issues or provide lasting improvements in mobility. If relief only comes from repeated cracking, the underlying cause has not been addressed.

Spinal manipulation

Spinal manipulation, whether performed by physiotherapists, chiropractors or other practitioners, relies on the same cavitation mechanism. There is evidence that it can provide short-term pain relief and reduce muscle tension for some people.

However, it is important to be cautious, particularly with the neck. The cervical spine protects the spinal cord and major blood vessels supplying the brain. Rare but serious complications, including stroke, have been reported following neck manipulation. Anyone considering this type of treatment should ensure it is carried out by a properly trained professional and understand that it targets symptoms rather than underlying causes.

Joint noises do tend to become more common with age. Cartilage changes over time, and muscles and ligaments may lose some of their strength and elasticity. These changes can increase the likelihood of noise during movement.

People who have joint conditions such as knee osteoarthritis and have noisy joints tend to report slightly more pain and reduced function compared to people with osteoarthritis and no crepitus. It may be reassuring to know that there is no difference in tests like walking speed or muscle strength between groups, pointing to a potential psychological impact of noisy knees.

Crucially, noise alone is not a reason to stop being active. Some people reduce their physical activity because they fear they are “wearing out” their joints. In fact, the opposite is true. Movement is essential for joint health. Cartilage relies on regular compression and release to receive nutrients, as it has very limited blood supply.

Exercise is a cornerstone of joint health and is recommended as the first treatment to try in national and international clinical guidelines for conditions such as osteoarthritis. Consistency matters more than the specific type of exercise. The best exercise is the one you will keep doing.

There is no evidence that supplements such as collagen or fish oils reduce joint noise. Large studies show limited effects on pain and function at a population level, although some people report benefits. These supplements are generally safe, but if they do not help, they are unlikely to be worth the cost.

Joint noises are usually harmless. They are worth assessing if they are accompanied by pain, swelling, locking, or reduced function, or if they are limiting your confidence to move. Staying active is one of the best things you can do for your joints, whether they crack, pop, crunch or stay silent.

Strange Health is hosted by Katie Edwards and Dan Baumgardt. The executive producer is Gemma Ware, with video and sound editing for this episode by Sikander Khan. Artwork by Alice Mason.

In this episode, Dan and Katie talk about a social media clip from loryalien via TikTok.

Listen to Strange Health via any of the apps listed above, download it directly via our RSS feed or find out how else to listen here. A transcript is available via the Apple Podcasts or Spotify apps.

Clodagh Toomey receives funding from the Health Research Board Ireland. She is affiliated with the non-profit Good Life with osteoArthritis Denmark (GLA:D).

Is cracking your neck bad? And why can it feel so good to crack your back, knuckles and knees?

2026-02-03T10:09:42Z

Andrey_Popov/Shutterstock

Joint cracking is one of those habits most of us acquire without thinking about it. A knuckle popped mid-sentence. A back twisted as we stand up. A neck gently crunched while the kettle boils. It is common, oddly satisfying and, for anyone sitting nearby, faintly alarming.

It is also surprisingly divisive.

Some people wince at the sound of a knuckle pop or a neck crunch. Others swear by it, twisting, stretching and cracking joints throughout the day in search of relief.

In the third episode of The Conversation’s Strange Health podcast, we turn our attention to one of the body’s most common and least understood noises. Knuckles, backs, knees and necks all feature, along with the enduring warning many of us grew up with: “Stop cracking your joints, you’ll get arthritis.” Is there any truth in it? And why can cracking feel so strangely satisfying?

We turned to this week’s podcast expert guest, Clodagh Toomey, a specialist in musculoskeletal injury and chronic lifestyle-related diseases such as osteoarthritis, to give us the science behind the myths. As she explains in our interview, the familiar popping sound is not bones grinding together. It is caused by a process known as cavitation. Most joints are filled with synovial fluid, which lubricates and cushions movement. When a joint is stretched or twisted, pressure inside it drops suddenly, allowing dissolved gases to form a bubble. The rapid formation or collapse of that bubble creates the cracking noise.

Imaging studies have shown this happening in real time, and decades of research have found no convincing link between habitual knuckle cracking and arthritis. Allergist Donald Unger won the 2009 Ig Nobel Prize in medicine, which recognises quirky research that initially seems trivial or absurd but ends up offering real scientific insight, for his long-running self-experiment. Over decades, he cracked the knuckles on one hand every day and left the other alone, finding no difference between them. Just to prove his mother wrong. You can’t fault his dedication.

So why does it feel good? Part of the answer lies in muscle tension. Stretching a joint stimulates receptors that briefly reduce stiffness and discomfort. Movement also activates sensory nerves that can dampen pain signals, similar to rubbing a sore area after a knock. There may even be a small reward response in the brain, which helps explain why cracking can become habitual.

Neck and back cracking, however, deserves more care. Gentle stretching that produces an occasional crack is usually harmless. Forceful or repeated manipulation, especially by someone untrained, carries more risk. Rare but serious injuries have been linked to damage to blood vessels supplying the brain. These events are uncommon, but they are enough to make aggressive spine cracking a bad idea.

The key message is context. Painless cracking without swelling, locking or loss of movement is usually nothing to worry about. Cracking accompanied by persistent pain, warmth, swelling or a recent injury is a different matter and should be checked out.

Listen to Strange Health to understand why for most people, bone cracking is not a sign of damage or degeneration. It is simply one of the many odd noises the body makes as it moves through the world. Just maybe warn the people sitting next to you first.

Strange Health is hosted by Katie Edwards and Dan Baumgardt. The executive producer is Gemma Ware, with video and sound editing for this episode by Sikander Khan. Artwork by Alice Mason.

In this episode, Dan and Katie talk about a social media clip from loryalien via TikTok.

Katie Edwards is a health and medicine editor at The Conversation in the UK. Clodagh Toomey receives funding from the Health Research Board (Ireland) for research in the area of osteoarthritis. She is affiliated with non-profit initiative GLA:D(r) (Good Life with osteoArthritis Denmark).

Dan Baumgardt does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Trump-style unpredictability isn’t just political theatre – it’s a regulatory problem for your brain

2026-02-02T14:05:28Z

Vitalii Vodolazskyi/Shutterstock.com

Donald Trump can change the temperature of a room with a sentence. One minute he is certain, the next he is backtracking. One day he is threatening, the next he is hinting at a deal. Even before anything concrete happens, people brace for his next turn.

That reaction is not just political. It is what unpredictability does to any system that requires stability. To act at all, you need some working sense of what is happening and what is likely to happen next.

One influential framework in brain science called predictive processing suggests the mind does not wait passively for events. It constantly guesses what will happen, checks those guesses against reality, and adjusts.

A brain that predicts can prepare, even when what it prepares for is uncertainty. The gap between what you expect and what actually happens is known as a prediction error. These gaps are not mistakes but the basis of learning. When they resolve, the brain updates its picture of the world and moves on.

This is not about what anyone intends, but about what unpredictability does to systems that need some stability to work. Trouble starts when mismatches do not resolve because the source keeps changing. People are told one thing, then the opposite, then told the evidence was never real.

The brain may struggle to settle on what to trust, so uncertainty stays high. In this view, attention is how the brain weighs up what counts as best evidence, and turns the volume up on some signals and down on others.

Uncertainty can be worse than bad news

When this keeps happening, it’s hard to get closure. Effort is spent checking and second guessing. That is one reason why uncertainty can feel worse than bad news. Bad news closes the question, uncertainty keeps it open. When expectations will not stabilise, the body stays on standby, prepared for many possible futures at once.

One idea from this theory is that there are two broad ways to deal with persistent mismatch. One is to change your expectations by getting better information and revising your view. The other is to change the situation so that outcomes become more predictable. You either update the model, or you act to make the world easier to deal with.

On the world stage, flattery can be a crude version of the second route, an attempt to make a volatile person briefly easier to predict. Everyday life shows the same pattern, such as unpredictable workplaces. When priorities change without warning, people cannot anticipate what is required. Extra effort may go into reducing uncertainty rather than doing the job.

Research links this kind of unpredictability to higher daily stress and poorer wellbeing.

The same pattern shows up in close relationships. When someone is unpredictable, people scan tone and try to guess whether today brings warmth or conflict. It can look obsessive, but it is often an attempt to avoid the wrong move.

Studies link unpredictable early environments to poorer emotional control and more strained relationships later in life.

The strain does not stay in thought alone. The brain does a lot more than thinking. A big part of its work is regulating the body, such as the heart rate, energy use and the meaning of bodily sensations.

It does this by anticipating what the body will need next. When those anticipations cannot settle, regulation becomes costly.

Words matter here in a literal sense. Language does not just convey information. It shapes expectations, which changes how the body feels.

Trump can do this at a distance. A few words about a situation can raise or lower the stakes for people, whether in Minneapolis or Iran. The point is that signals from powerful, volatile sources force others to revise their models and prepare their bodies for what might come next.

Communication is a form of regulation. Clarity and consistency help other people settle. Volatility and contradiction keep them on edge.

When a single voice can repeatedly unsettle expectations across millions of people, unpredictability stops being a personal stress and becomes a collective regulatory problem.

How to deal with unpredictability

So what helps when unpredictability keeps pulling your attention? Try checking for new information if it changes your next step or plan, otherwise it just keeps the uncertainty alive.

When a source keeps changing, reduce the effort spent trying to decode it. Switch to action. Set a rule that makes the next step predictable. For example, read the news at 8am, then stop and get on with your day.

Learn where not to look. When messages keep reversing, the problem is not a lack of information, it is an unreliable source.

Biological systems survive by limiting wasted predictions. Sometimes that means changing your expectations; sometimes it means changing the situation. And sometimes it means accepting that when Donald Trump is talking, the safest move is to stop trying to predict what comes next.

Robin Bailey does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Your genes matter more for lifespan now than they did a century ago – here’s why

2026-02-02T14:05:26Z

buritora/Shutterstock.com

How much do your genes determine how long you’ll live? It’s a question that fascinates us, and one that’s been debated for decades. For years, the answer seemed settled – genes account for about 20–25% of the variation in human lifespan, with the rest down to lifestyle and environment.

But a new study published in Science has challenged this view, suggesting the genetic contribution might be considerably higher.

The reason, according to the researchers, is that previous estimates failed to account for how the causes of death have changed over time. A century ago, many people died from what scientists call extrinsic causes – accidents, infections and other external threats.

Today, in developed countries at least, most deaths result from intrinsic causes: the gradual wearing out of our bodies through ageing and age-related diseases like dementia and heart disease.

To get a clearer picture, the research team analysed large groups of Scandinavian twins, carefully excluding deaths from external causes. They also studied twins who were raised apart and siblings of centenarians in the US.

When they stripped away deaths from accidents and infections, the estimated genetic contribution jumped dramatically – from the familiar 20–25% to around 50–55%.

The pattern makes sense when you look at individual diseases. Genetics explain much of the variation in dementia risk, have an intermediate effect on heart disease, and play a relatively modest role in cancer. As environments become more favourable, populations age and diseases caused by the ageing process itself become more common, the genetic component naturally appears larger.

Our genes haven’t become more powerful

But here’s where interpretation becomes crucial. A higher estimate doesn’t mean genes have suddenly become more powerful, nor does it mean you can only influence half your chances of reaching old age. What’s changed is the environment, not our DNA.

Consider human height as an example. A hundred years ago, how tall you grew depended heavily on whether you had enough food and whether childhood illnesses stunted your growth.

Today, in wealthy nations, nearly everyone gets adequate nutrition. Because these environmental differences have narrowed, most of the remaining variation in height is now explained by genetic differences – not because nutrition has stopped mattering, but because most people now reach their genetic potential. However, a malnourished child will still fail to grow tall, regardless of their genes.

The same principle applies to lifespan. As we’ve improved vaccination, reduced pollution, enhanced diet and adopted healthier lifestyles, we’ve lessened the overall impact of environmental factors.

When environmental variation decreases, the proportion of remaining variation attributed to genetics – what scientists call “heritability” – increases by mathematical necessity. The earlier estimates weren’t wrong; they simply reflected different historical circumstances.

Your genes haven’t changed. The environment has. romakhan3595/Shutterstock.com

This reveals something fundamental: heritability isn’t a fixed biological property but a measure that depends entirely on the population and circumstances you’re looking at. The traditional 20–25% figure described lifespan as it was actually experienced in historical populations, where external threats loomed large.

The new 50–55% estimate describes a different scenario where those threats have been largely removed – essentially describing a different trait.

The headline figure of lifespan being around “50% heritable” risks being misunderstood as meaning genes determine half of a person’s life chances. In reality, the genetic contribution for any given individual can range from very small to very large depending on their circumstances.

There are countless routes to a long life: some people have robust genetic profiles that protect them even in difficult conditions, while others compensate for less favourable genetics through excellent nutrition, exercise and healthcare. Each person represents a unique combination, and many different combinations can result in exceptional longevity.

Which combinations prove most common depends entirely on the population and the conditions in which people live and age. As external causes of death continue to decline in the real world – though they won’t disappear entirely – it will be fascinating to see how these patterns evolve.

The authors of this latest study admit that about half of lifespan variation still depends on environment, lifestyle, healthcare and random biological processes, such as cells dividing out of control in cancer. Their work, they argue, should renew efforts to identify the genetic mechanisms involved in ageing and longevity. Understanding how different genetic factors interact with different environments is probably the key to explaining why some people live much longer than others.

The study offers valuable insights into how different types of mortality have shaped our understanding of lifespan. But its results are best understood as showing how heritability changes across different contexts, rather than establishing a single, universal genetic contribution to how long we live.

In the end, both genes and environment matter. And, perhaps more importantly, they matter together. So whether that feels like good news or bad news, you will probably never get a simple answer to how much of your lifespan is determined by genes alone.

Karin Modig receives funding from Swedish Research Council for Health, Working Life and Welfare and from Karolinska Institutets research funds.

How mental health has changed in baby boomers and gen X across their entire adulthoods

2026-02-02T12:55:43Z

The lifelong mental health impact of socioeconomic inequalities were even larger in women from the Baby Boomer generation. PerfectWave/ Shutterstock

It’s been almost five years since the end of the COVID lockdowns. Yet the world is still continuing to learn about how mental health changed during – and after – this unprecedented time.

My colleagues and I wanted to understand how mental health had changed across the life course of baby boomers and generation X – including during and beyond the pandemic.

We also wanted to understand if (and how) gender and socioeconomic inequalities had changed throughout these periods. Previous research we’d conducted had shown that large, existing gender inequalities in mental ill-health had widened during the pandemic period.

Moreover, the post-lockdown period came with a marked increase in the cost of living – making ends meet harder in a context where there had already been high levels of poverty for decades before.

We found that, on average, mental health bounced back to levels similar to those recorded before the pandemic. However, women and people from socioeconomically disadvantaged backgrounds continued to experience worse mental health across their adult lives, including after the pandemic. And those inequalities could be traced back to their early lives.

To conduct our study, we analysed data from two nationally representative British birth cohorts: the 1958 National Child Development Study and the 1970 British Cohort Study.

These ongoing studies follow the lives of all people born in Britain during one particular week in 1958 and 1970. Information is collected on each participant’s physical and mental health, as well as their social, economic and family circumstances.

These studies gave us the unique opportunity to investigate how different outcomes – including mental health – changed across the life course in baby boomers and generation X.

For our study, we looked at the same 14,182 people over up to four decades: 6,553 of whom were born in 1958 and 7,629 who were born in 1970.

We used the same measure of psychological distress (which encompasses a range of unpleasant mental states, such as feeling depressed, worried or scared) in both cohorts. This allowed us to understand how mental health had changed in the same participants throughout their adult lives – between the ages of 23-64 for baby boomers and 26-52 for generation X.

To ensure our results weren’t due to differences in measurement, we tested this tool to ensure it provided comparable measures across cohorts, genders, socioeconomic backgrounds and ages.

To examine inequalities by gender and socioeconomic background, we used information on sex assigned at birth, parental social class and housing tenure (whether their parents owned or rented their home) when participants were children (aged five-11).

We also examined the intersection of gender and socioeconomic background to understand any dual impact these inequalities may have on mental health throughout adulthood.

What we found

In both cohorts, mental health was generally at its best during a person’s 30s. But, from middle age, average levels of psychological distress began to increase.

During the pandemic, both cohorts experienced a marked increase in psychological distress. Levels reached, and in some cases surpassed, the highest distress levels they’d experienced in any other period of their lives.

In the post-lockdown period, average distress levels declined – largely returning to pre-pandemic levels. While generation X had higher average distress levels across adulthood, post-pandemic improvements were smaller for baby boomers.

Women and people who grew up in socioeconomically disadvantaged households consistently reported higher psychological distress throughout their lives compared to men and people from more advantaged backgrounds. These inequalities, which were already visible in the participants’ 20s, were still present when they were in their 50s or 60s.

Among baby boomers, socioeconomic inequalities were even larger in women – showing a dual effect.

The changing picture of mental health

We were able to track how mental health changed in the same people through different periods in their lives. This also allowed us to identify potential risk factors for poor mental health.

Our study showed further evidence of the life-long impact of gender and socioeconomic disadvantage. These factors are already known to be among the key social determinants of mental health.

Although our study didn’t investigate the specific ways in which these life-long inequalities in mental ill-health came to happen, we believe these inequalities reflect the unfair distribution of opportunities, power and privilege in society. In other words, our findings may reflect the long-term impact of sexism, classism and material deprivation – and the ways these inequalities overlap.

Sexism, classism and material deprivation in childhood had long-term impacts on mental health. CandyRetriever/ Shutterstock

Women and young girls have long been at greater risk of experiencing a number of mental health difficulties. Factors such as sexual violence, safety concerns, labour market discrimination and the unequal distribution of unpaid care work all potentially contribute to this.

Similarly, early-life socioeconomic disadvantage can limit or preclude access to certain resources, such as wealth and knowledge, which can be protective of mental health.

The finding that socioeconomic inequalities were even larger in women from the baby boomer generation may be partly explained by societal changes in the second-half of the 20th century. Changes such as the expansion of women’s education and labour-market participation and small improvements in the gender pay gap may have had a protective effect on mental health for women born in generation X.

In our view, this supports the idea that these inequalities can, indeed, be prevented.

Future of mental health

One one hand, our findings show the remarkable resilience of two British generations when faced with the challenges the pandemic brought.

But on the other hand, our findings also highlight the unfair, life-long factors that can contribute to poor mental health – factors that are largely down to chance.

Around one in three children in the UK currently living in poverty. Global gender equality is stalling – and, in some cases, even going backwards. Finding ways of addressing these inequalities will be key in improving mental health for younger generations.

Darío Moreno-Agostino receives funding from the Wellcome Trust under grant number 304283/Z/23/Z, and has received funding from the Economic and Social Research Council (ESRC) Centre for Society and Mental Health at King's College London under grant number ES/S012567/1. The views expressed here are those of the author and not necessarily those of the Wellcome Trust, ESRC, or King's College London.

The healing power of poisonous plants

2026-02-02T12:55:41Z

Triff/Shutterstock

Some of the best-known medicines come from poisonous plants. The chemotherapy drug taxol comes from the yew tree, morphine from the opium poppy and digoxin from the foxglove. These plants can have lethal toxicity if taken in their raw form. Digoxin is prescribed to treat angina at doses a thousand times more dilute than most prescription medications, highlighting the plant’s extreme potency.

Many people consider herbal medicines a safe alternative to pharmaceuticals. And it’s true that many herbal medicines are fairly mild. However, there is a less well-known group of herbal medicines that are far more potent and controlled under the Medicines Act, where they are restricted to use by medical herbalists and at strictly defined dosages.

Many people think of plants as nice-looking greens. Essential for clean air, yes, but simple organisms. A step change in research is shaking up the way scientists think about plants: they are far more complex and more like us than you might imagine. This blossoming field of science is too delightful to do it justice in one or two stories. This article is part of a series, Plant Curious, exploring scientific studies that challenge the way you view plantlife.

These are known as the schedule 20 herbs in the UK and are prescribed for a variety of health needs. All of these plants are toxic at relatively low doses, mainly due to the presence of chemical compounds called alkaloids, which also have healing properties.

Here are ten examples of these deadly, healing plants.

1. Wild saffron

Known as wild saffron or the autumn crocus, Colchicum autumnale is one of the oldest known medicinal plants. It was first mentioned in the Egyptian medical text, Ebers Papyrus (circa 1550BC), where it was described for the treatment of pain and swelling. It is still used in medicine, chiefly for its anti-inflammatory properties and particularly for the treatment of gouty arthritis.

2. Deadly nightshade

Atropa belladonna is commonly known as deadly nightshade. All parts of the plant are pain relieving, antispasmodic, hallucinogenic, narcotic and sedative. Containing tropane alkaloids (the same group as cocoaine), it is used predominantly for the gastrointestinal tract (colic, gastritis, IBS), but also for asthma and for urinary spasm, Parkinson’s disease and topically for pain relief.

Deadly nightshade has healing properties too. Greens and Blues/Shutterstock

3. Greater celandine

Greater celandine is often seen when walking in the woods. It has a long history of medical use in eastern and central European folk medicine to treat asthma, bronchitis, jaundice, digestive issues and even cancer. However, due to the presence of isoquinoline alkaloids, it has the potential to cause severe liver toxicity when ingested and many experts advise against its use. It can be used relatively safely as a poultice or cream to treat warts and verrucae.

Greater celandine is common in woodland. Zhanna Bohovin/Shutterstock

4. White quebracho

White quebracho is a tropical tree from South America. Rich in indole alkaloids, which are also present in psychoactive drug psilocybin, it has traditionally been used to treat fever, malaria, swellings, stomach upsets, cough, headaches, syphilis, impotence and asthma.

5. Fever tree

Species of chinchona or “fever tree” have been used worldwide to treat malaria. The drug quinine is extracted from its bark. It was introduced into Europe in the 17th century for the treatment of fevers. Although it is commonly used as an appetite stimulant, recent research has suggested that it may have a role to play in weight management and obesity too.

6. Thorn apple

Datura stramonium or thorn apple has traditionally been used for various ailments including respiratory conditions, ulcers, wounds, inflammation, rheumatism and gout, sciatica, bruises and swellings and fever. Modern research has shown that it may also have potential in the treatment of epilepsy.

Thorn apple may look fragile but it is a restricted drug. Roman Nerud/Shutterstock

7. Ephedra sinica

Ephedra sinica has been known in traditional Chinese medicine for approximately 5,000 years. The plant contains the alkaloids ephedrine and pseudoephedrine, some of the first drugs to be used in the treatment of respiratory conditions. Side effects can include psychosis, delusions and hallucinations, which is one of the reasons drugs obtained from this plant were restricted in the UK in 2014 for cough and cold remedies for use in young children. The psychoactive properties of ephedra also explain its notoriety as a recreational drug and a number of deaths in the US have been linked to its misuse.

8. Henbane

Plants in the nightshade family, including henbane, are potent medicinal plants. They are purported to have anti-diabetic, antioxidant, anticancer, insecticidal, antiasthmatic, antiallergic, antidiarrhoeal, cardioprotective, anticonvulsant and antidepressant effects but more research is needed. However they also contain psychoactive compounds that can cause delirium and hallucinations.

Henbane is no mild herb. mutie/Shutterstock

9. Pheasant’s eye

Adonis vernalis, (pheasant’s eye) leaves and flowers have long been used in European and east Asian folk medicine to treat cardiovascular conditions. Studies have shown the chemical constituents within this plant also have antimicrobial and anti-inflammatory effects. The cardiovascular effects are largely attributed to the cardiac glycosides (chemicals that slow down heart rate) contained within this plant, which are also responsible for its toxicity, in a similar way to the foxglove.

10. Lily of the valley

A common poisonous plant often found in the garden, lily of the valley, has historically been used to treat cardiovascular conditions such as arrythmias, heart failure and angina. Another plant that contains cardiac glycosides, its common presence in gardens is a particular danger for children and pets.

Other toxic healers

Not all toxic plants are on the schedule 20 list however. Garden herbs comfrey and borage contain pyrrolizidine alkaloids that can be toxic to the liver and comfrey has been banned for medicinal use in many European countries. Comfrey, also known as knitbone, is mainly used topically as an anti-inflammatory and analgesic for acute sprains and strains or more chronic conditions such as osteoarthritis.

Belonging to the same family, borage is not that well known as a medicinal herb in the UK, whereas in Mediterranean countries it has a strong reputation for treating a range of conditions. It is credited with sedative properties, useful for insomnia, and dizziness and melancholy. In gynaecology, it can shift postpartum exhaustion, and helps with the symptoms of menopause. The oil from this plant contains negligible amounts of these alkaloids and supplements are often processed to remove the toxicity.

In the UK there are several professional associations that hold a register of qualified medical herbalists. Learning the right dosage to give a patient was just as important for folk healers. Modern science may help us verify which plants are best for healing but getting the dosage right is an ancient skill.

Anthony Booker is affiliated with The Royal Society of Chemistry, The Register of Chinese Herbal Medicine, The British Pharmacopoeia, The Medicines and Healthcare Products Regulatory Agency, The American Botanical Council, The British Herbal Medicine Association and The European Scientific Cooperative on Phytotherapy..

Preventable deaths in a warming world: how politics shapes who lives and who dies

2026-02-02T12:55:37Z

Floods in Kolkata, West Bengal, India in 2019. ABHISHEK BASAK 90/Shutterstock

In Brownsville, Texas, three members of the Galvan family died after a malfunctioning air conditioner left them exposed to extreme heat. Aged between 60 and 82, all three had chronic health conditions, including diabetes and heart disease. This makes it harder for the body to regulate temperature and increases vulnerability to heat stress.

Nobody arrived to check on them until days after they had died in their apartment in 2024. This isolation also increases risk of heat-related deaths.

Although the immediate trigger appears to have been equipment failure, a pathologist attributed the deaths to extreme heat linked to chronic illness. Deaths like these are classified as “heat-related” when ambient temperatures exceed what bodies can safely tolerate.

Climate change is a contributing factor. As heatwaves become more frequent, intense and prolonged, routine failures in cooling, power or housing infrastructure are more likely to turn existing vulnerability into fatal harm.

Around the world, climate-related deaths follow consistent social patterns. People who are older, already ill, economically disadvantaged, or working outdoors are most affected.

The Intergovernmental Panel on Climate Change (the UN’s climate science advisory group) concludes that roughly 3.3 billion to 3.6 billion people – nearly half of the world’s population – are highly vulnerable to climate risks, with limited capacity to cope. Here, vulnerability is not simply exposure to environmental hazards. Who is protected and who is left at risk depends on social and infrastructural conditions.

Research in climate science, public health and social sciences shows these patterns are clear. My own research spans ecosystem ecology and social science. I examine how climate knowledge is produced, interpreted and acted upon in times of ecological emergency.

The evidence points to an uncomfortable conclusion: much of this suffering is preventable.

The necropolitics of climate change

Cameroonian historian Achille Mbembe introduced the idea of “necropolitics” to explain how some lives come to be treated as more expendable than others. This does not imply intent to kill, but rather the routine political acceptance that some people will be exposed to harm.

From this perspective, the Galvans’ deaths were shaped not only by heat, but by structural inequalities and gaps in policy and infrastructure.

This logic is visible globally. In south Asia and the Middle East, heatwaves claim the lives of elderly people and outdoor workers. In sub-Saharan Africa, floods and droughts disproportionately affect subsistence farmers.

In the UK, air pollution is linked to roughly 30,000 deaths annually. People from ethnic minority and low-income communities are more likely to live in the most polluted areas. These deaths are not random. They follow recognisable social patterns.

Floods hit villages in the Jhenaigati upazila of Sherpur district, Bangladesh on October 6 2024. amdadphoto/Shutterstock

Mbembe’s concept helps describe situations where political, economic or social arrangements leave some populations consistently exposed to harm. That includes climate-vulnerable communities, places where resources are being extracted through mining or areas where people are displaced from their homes. In the US, “Drill, baby, drill!” has re-emerged as shorthand for prioritising fossil fuel extraction over emissions reduction.

These political and economic choices create consistent patterns of vulnerability for environmental risks, from extreme heat to floods and air pollution. Structural neglect, not personal behaviour, underlies the distribution of harm.

Yet, vulnerability is not fate. Heat provides a clear example. With early warning systems, targeted outreach, and timely intervention, many such fatalities can be prevented. As epidemiologist Kristie Ebi notes: “Those deaths are preventable … people don’t need to die in the heat”.

The same is true across climate risks. Even with systemic neglect, deliberate and coordinated action can reduce risk. Connecting social, infrastructural, and institutional responses to climate hazards is a crucial step.

Slow violence as a climate process

Environmental humanist Rob Nixon uses the term “slow violence” to describe harms that accumulate gradually and often invisibly over time. Unlike sudden disasters, the effects of rising temperatures, drought and ecological degradation unfold quietly.

You cannot make a disaster movie out of slow violence. Its harm builds incrementally, striking those already most vulnerable. The deaths of the Galvans exemplify this slow burn, as do the lives lost to prolonged heat exposure, crop failure and environmental degradation worldwide.

People least responsible for emissions, primarily in developing countries, are most exposed to escalating climate harms. Viewed through a necropolitical lens, slow violence shows how neglect becomes lethal through the repeated failure to prevent known and predictable harms.

Feminist theorist Donna Haraway coined the term “Chthulucene”, from the Greek chthonic (“of the earth”), to describe an era defined by entangled relationships between humans, other species and the ecosystems they depend on.

Rather than treating environmental harm as separate from social life, this perspective emphasises how vulnerability emerges through the everyday connections between people, institutions and environments. As Haraway argues harm accumulates through these relationships, revealing how exposure to climate risks, political neglect and ecological stress reinforce one another over time.

This dynamic is visible in Vietnam’s Mekong Delta, one of the world’s most productive rice-growing regions. Here, saltwater intrusion is creeping inland, damaging vast areas of farmland and threatening millions of livelihoods.

Rising sea levels and shifting climate patterns could affect up to 45% of the delta’s farmland by 2030, destabilising both local communities and global food systems. Social and ecological harm cannot be separated.

Politics of life, not death

Political choices amplify any existing environmental threat. Neglect is not a neutral absence: it is a political condition that shapes who lives and who suffers.

Addressing this injustice requires a living politics of care. This means a political system that recognises vulnerability as socially produced and demands solidarity, equity and accountability. Through alliances between affected communities, researchers and advocates who expose neglect, plus decision-makers under pressure to act, care can become politically unavoidable.

Neglect is no longer allowed to remain invisible in some parts of the world. Cities like Ahmedabad, India, are expanding heat mitigation and early-warning systems. Communities in the Mekong Delta are working with Vietnamese and international researchers to experiment with salt-tolerant crops.

Globally, ecocide laws that make large-scale destruction of ecosystems illegal are being introduced. This helps embed responsibility for environmental protection into legal and political systems. Even in the face of political neglect, targeted action and emerging legal frameworks can reduce harm and foster a more caring form of politics.

Don’t have time to read about climate change as much as you’d like?
Get a weekly roundup in your inbox instead. Every Wednesday, The Conversation’s environment editor writes Imagine, a short email that goes a little deeper into just one climate issue. Join the 47,000+ readers who’ve subscribed so far.

Aaron Thierry receives funding from ESRC. He is affiliated with Scientists for Extinction Rebellion.

Routine medical procedures can feel harder for women – here’s why

2026-01-30T16:53:16Z

Oksana Shufrych/Shutterstock.com

Many women recognise the pattern. A routine procedure takes longer than expected. It’s more uncomfortable than promised. The doctor reassures them that this sometimes happens, or suggests anxiety or muscle tension might be playing a role. But often the explanation is simpler – and anatomical.

This mismatch between bodies and procedures isn’t related to rare conditions or specialist care. It reflects a recurring problem in everyday medicine. Many routine procedures were designed around male anatomy, and they don’t always work the same way on female bodies.

Take colonoscopy. It’s one of the most common investigations used to diagnose bowel disease and screen for cancer. Yet women are more likely than men to experience discomfort, require repositioning, or have an incomplete examination on the first attempt.

The reason lies in normal anatomy. On average, women have a longer and more mobile colon, particularly in the sigmoid segment that loops through the pelvis.

The female pelvis itself is broader and shallower, creating sharper angles as the bowel curves downward. These features make the scope more likely to bend and loop inside the bowel, slowing its progress and pulling on surrounding tissue – a major source of pain.

This isn’t abnormal anatomy. It’s normal anatomy that standard techniques don’t always take into account.

Urinary catheterisation is another routine procedure where anatomy matters. Although the urethra performs the same function in men and women, its length, course and anatomical context differ in ways that matter clinically.

In males, the urethra is long – around 18-22cm – and is usually described in three parts: the prostatic urethra, which is wide and fixed as it passes through the prostate; the membranous urethra, the narrowest segment as it crosses the pelvic floor; and the spongy (penile) urethra, which runs in a predictable course to a clearly identifiable external opening at the tip of the penis. Despite its length, the male urethra follows a stable path and ends at a prominent external landmark.

The female urethra is much shorter, usually about 3-4cm long, but lies within a more variable anatomical environment. From the bladder neck, it passes through the bladder wall and pelvic floor, before opening into the vulval vestibule at a meatus (the external opening of the urethra) closely related to the anterior vaginal wall.

Its position varies between individuals and across the life course, influenced by pelvic floor tone and hormonal status. In practice, this can make catheter insertion technically more difficult, increasing the likelihood of repeated attempts and discomfort – particularly in older women or those with atrophic tissue (thin, delicate tissue).

Lumbar puncture and spinal procedures show similar issues. Women tend to have a greater lumbar curve and different pelvic tilt, altering the angle at which a needle must pass between vertebrae. Mild spinal curvature is also more common in women. The procedure itself doesn’t change, but the geometry does, increasing the likelihood of multiple attempts and prolonged discomfort.

Women have a greater lumbar curve. Teeradej/Shutterstock.com

Even airway management, a cornerstone of anaesthesia and emergency medicine, reflects the same mismatch. Female airways are, on average, shorter and narrower. When equipment sizing and technique is based on a “standard” airway, women are more likely to experience sore throat and hoarseness afterward – effects often dismissed as minor, but rooted in anatomy rather than sensitivity.

Even something as commonplace as peripheral venous cannulation, the insertion of a small tube into a vein to deliver fluids, medications, or to take blood, reflects this mismatch. Women’s superficial veins are often smaller, less prominent and more mobile in soft tissue, making standard cannulation techniques more likely to result in repeated attempts, bruising and pain.

Design for variation, not exception

Doctors know bodies vary. In practice, many already adapt – choosing different patient positions, smaller instruments or altered techniques. But these adjustments are informal, inconsistently taught and rarely explained to patients.

Instead, difficulty is often bundled into vague categories: anxiety, tension, low pain tolerance or “one of those things”. The result is that women experience real, anatomy-driven discomfort without being told why, and may internalise it as a personal failing.

This matters. When discomfort is normalised or minimised, patients are less likely to return for screening, more likely to delay care, and more likely to mistrust reassurance that future procedures will be different.

None of this requires radical innovation. It requires naming the issue accurately. When procedures are taught and designed around a single reference body, predictable anatomical variation becomes an obstacle rather than a design feature.

Acknowledging that bodies differ – in length, curvature, mobility and spatial relationships – allows doctors to plan, explain and adapt more effectively.

Crucially, it also shifts the narrative. Instead of “this shouldn’t hurt”, the message becomes: “your anatomy means this procedure can be more challenging, and we’ll adjust it accordingly”.

Michelle Spear does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Allergic to the cold? It’s a real thing and it can even kill

2026-01-30T16:53:06Z

Nicoleta Ionescu/Shutterstock.com

For most people, cold weather is an inconvenience, requiring an extra layer of clothing or the thermostat to be turned up. For others, exposure to cold can trigger an allergic reaction severe enough to cause them to collapse.

Cold urticaria is a rare but potentially dangerous condition in which contact with cold temperatures causes the immune system to misfire. The results can be hives, swelling, pain and in some cases, life-threatening anaphylaxis.

The condition was first described in 1792 by a German physician called Johann Peter Frank. Today, we know it is almost twice as common in women than in men, with the average age of onset in the early twenties, though it can affect people at any age.

There is some good news: between 24% and 50% of people with the condition see improvement – or even full recovery – over the years.

There are two forms of the condition. Primary cold urticaria is the most common, accounting for about 95% of cases and often has no known cause. The remaining 5% are classified as secondary urticaria, which is linked to underlying conditions or infections, such as the Epstein-Barr virus, certain types of lymphoma (blood cancer), HIV and hepatitis C.

Primary cold urticaria typically causes a rash, swelling, bumps or hives, though some people also report fatigue, fever and aching joints. Symptoms usually appear when the skin is exposed to cold, but can also occur as the skin warms up again. Triggers aren’t limited to cold weather – they can include swimming, eating frozen food, drinking cold liquids and handling cold objects.

Aside from a few very rare genetic causes, why some people develop primary cold urticaria remains unknown. What is clear is that mast cells are involved. These sentinel cells act as first responders in the body’s tissues – including the skin – alerting the immune system to danger signals or germs.

What triggers their activation in cold urticaria remains a mystery, though one theory suggests that cold exposure causes the body to produce so-called autoallergens – substances that trigger an immune response against the body’s own tissues. Much more research is needed to understand how this happens.

When mast cells are activated, they release a chemical called histamine. Think of histamine as an alarm that alerts other immune cells to rush to the area. It also makes the blood vessels in that part of your body widen and become “leakier”, which causes the telltale swelling, redness and itchiness.

Normally, this response is helpful – the extra blood flow and leaky blood vessels allow immune cells to squeeze out of the bloodstream and into the surrounding tissue to fight off a genuine threat. But in cold urticaria, it’s a false alarm. Your body is mounting a full-scale immune response when there’s nothing to fight, causing discomfort without any benefit.

Cold foods can trigger the condition. etorres/Shutterstock.com

Doctors test for cold urticaria by placing an ice cube on a patient’s forearm and watching what happens after they remove it. This test typically follows patients noticing they develop welts, hives or rashes on exposure to cold things. This must be done by a medical professional because in about 20% of cases, it can trigger anaphylaxis.

The condition is quite rare, affecting six in every 10,000 people. But it may be underdiagnosed as not all sufferers have severe symptoms and, in some countries, particularly tropical ones, temperatures tend not to drop below 0°C in winter.

Once diagnosed, it’s important to help people with cold urticaria avoid or recognise their trigger temperatures. There are two measures that may be assessed, depending on the availability of measuring devices. One is the cold stimulation time test, which indicates how quickly your skin reacts to cold with a lump or rash (a shorter time suggests a more active response). The other measure is the critical temperature threshold, which is the warmest temperature that can still trigger symptoms.

Antihistamines and beyond

There are treatments that can help manage the symptoms. One approach is taking antihistamines before exposure to cold environments or stimuli.

For many people, though, a standard oral antihistamine dose isn’t enough. Sometimes, up to four times the standard dose may be needed. The trade-off is that some antihistamines can have a sedating effect, so caution is needed.

About 60% of people with cold urticaria respond well to treatment with antihistamines.

During short flare-ups, other drugs, such as corticosteroids, may be beneficial, although longer-term use brings side-effects, such as weight gain, indigestion and mood changes.

Severe cases can be treated with a monoclonal antibody called Omalizumab, which targets immunoglobulin E, a molecule involved in mast cell activation.

Another option is desensitisation: gradually exposing the skin to cooler temperatures over several days (although, sometimes over a few hours) to try to overcome the response and histamine release. There have been some successes with this approach, but most of the studies have been small.

For people with the most severe cases, adrenaline is a lifesaving option in response to anaphylaxis, though it appears to be under-prescribed in patients with cold urticaria.

People with this condition also face increased risk during surgical procedures, where anaesthetic drugs reduce core body temperature and operating theatres are kept deliberately cool. While warming measures are used during surgery, for people with heightened sensitivity to cold, this can present an additional risk.

As winter continues, it’s worth remembering that for some people, the cold isn’t just uncomfortable – it can be genuinely dangerous. Understanding and recognising cold urticaria could make all the difference.

Adam Taylor does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Can pre-workout supplements benefit your workouts?

2026-01-30T13:06:47Z

Pre-workout supplements may modestly boost energy, strength, focus and stamina. Asier Romero/ Shutterstock

Finding the energy to exercise in the morning or after a long day is a common problem. This might explain why pre-workout supplements have become so popular. These supplements can bring you more focus and energy for your training sessions – making it possible to get to the gym, no matter how tired you are.

Pre-workout supplements usually contain multiple ingredients – each of which have different effects on the body.

The primary ingredient in most pre-workouts are stimulants such as caffeine or guarana (a plant which contains caffeine). Stimulants help increase focus and alertness. Caffeine may also make workouts feel easier.

Research shows even a single dose of pre-workout supplement containing caffeine before exercising can lead to small improvements in the number of repetitions a person can do, their power and the amount of weight they can lift during a session.

However, these benefits may solely be due to the caffeine itself. When pre-workout supplements are directly compared against the same dose of caffeine on its own, the supplements generally don’t outperform caffeine. Sometimes, caffeine even works as well or better in improving performance.

Taking between 3-6mg of caffeine per kg (around 225-450 mg for a 75kg person, the equivalent of 2-4 cups of strong coffee) can increase strength by around 7%. It can also enhance endurance by around 15%. This might not sound like much, but over time this can lead to significant training gains.

Alongside caffeine, pre-workout supplements contain other ingredients that reportedly help reduce fatigue and boost fitness gains. For instance, many pre-workouts contain beta-alanine – an amino acid usually found in meat which can counteract muscle tiredness.

One challenge of training is that it results in the metabolic process of acidosis, particularly demanding workouts. This can impact training quality and is often associated with fatigue.

This is where beta-alanine comes in. Beta-alanine increases muscle levels of carnosine, a molecule that buffers against acidosis. This helps delay the fatigue we often experience lifting weights or doing intense training.

However, unlike caffeine, beta‑alanine doesn’t work from a single dose. It must be taken daily for around 2–4 weeks to have any effect.

Creatine is another nutrient added to pre-workout formulas to maximise training gains. Creatine works by restoring short-term energy. This helps us recover faster between sets, making it possible to do more work when training.

Creatine also works better if taken regularly for around four weeks. Taking a single dose of a pre-workout containing creatine probably won’t benefit training quality – though some research does suggest it may help reduce fatigue and boost brain power after a poor night’s sleep.

Alongside creatine, many blends include amino acids such as leucine and taurine. Leucine supports muscle gains, while taurine may help reduce muscle soreness. Both work alongside creatine to support training benefits.

Pre-workout supplements may help improve fitness. Miljan Zivkovic/ Shutterstock

Other amino acids sometimes found in pre-workout formulations include citrulline and arginine. These nutrients increase nitric oxide, a molecule which increases blood flow and oxygen to muscles – helping them function more efficiently.

This effect may improve endurance ability or temporarily make muscles look bigger when doing resistance training, which many people look for. However, not all evidence supports this.

Some pre-workouts formulas also claim to contain ingredients that can help with weight loss or fat burning – such as green tea or carnitine.

These nutrients may enhance the body’s ability to burn fat for energy during and after exercise – although not all studies agree on this. It’s also not clear whether these nutrients actually lead to greater, long-term weight loss as a result.

More recently, supplements have begun including natural nootropics. These plant-based compounds support brain chemicals involved in concentration or energy required by the brain, which is why nootropics may help improve focus, alertness, mood and motivation.

Nootropics such as theanine can improve alertness and athletic performance. Others nootropics, such as ashwagandha or rhodiola rosea, may enhance endurance and the ability to deal with physical and mental stress.

The verdict

Looking at the evidence, pre-workout supplements can modestly boost energy, strength, focus and stamina when used alongside a training program. However, as it may take several weeks for specific ingredients to have an effect, such supplements may need to be taken consistently.

If you’re going to take a pre-workout supplement, it’s best to take it around 30-60 minutes before your workout so it can take effect. Preferably, choose products that are batch‑tested to ensure quality.

Since the main ingredient in pre-workouts tends to be caffeine, those who train later in the day might want to use formulas with a lower caffeine content (or none at all) to avoid sleep issues and anxiety.

Excessive caffeine intake can also lead to gut issues for some, so always check the label to see what the doses are.

Most pre-workout formulas are generally considered safe for most people to use over a period of a few weeks.

However, those with heart issues should avoid formulas containing high levels of stimulants – particularly products containing p‑synephrine (bitter orange). This plant derivative has been linked with heart issues – especially when combined with caffeine.

Researchers also currently don’t know the effects of pre-workout supplements during pregnancy, so it might be best to avoid them – particularly if the caffeine content is high.

Some people may also experience side-effects from taking pre-workout supplements – most commonly tingling or itchiness which occurs around 30 minutes of taking a pre-workout. This is usually caused by higher intake of beta-alanine which affects sensory receptors in the skin.

These effects are harmless, and usually subside within an hour. Taking a smaller dose or using a timed-release formulation can minimise effects.

Overall, although the benefits of pre-workouts may be small, if the supplement helps you train more consistently, this will ultimately benefit your training results.

Correction: This article was updated on 4 February 2026 to clarify that it is the metabolic process of acidosis that results in reduced training quality and muscle fatigue after an intense workout. An earlier version of the article incorrectly suggested that the body produced lactic acid after intense exercise – and that the lactic acid was responsible for this fatigue.

Professor Justin Roberts is employed by Anglia Ruskin University, Cambridge and Danone Research & Innovation, and has previously received external research funding unrelated to this article.

Fernando Naclerio is employed by the University of Greenwich (UK) and is a consultant for Crown Sport Nutrition, Spain.

Joseph Lillis does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Small improvements in sleep, physical activity and diet are linked with a longer life

2026-01-29T17:34:36Z

CandyRetriever/Shutterstock

We may not need to completely overhaul our lives to live healthier for longer, according to a large UK-based study. This is welcome news, particularly as many people will already have abandoned their New Year’s resolutions.

The recent study followed around 590,000 people in the UK, with an average age of 64, over an eight-year period. The researchers confirmed earlier findings that healthier lifestyles are associated with lower risk of disease, including dementia, and with living longer in good health and independence.

The authors reported that even very small changes were associated with such benefits. These included around five additional minutes of sleep per night, two extra minutes per day of moderate to vigorous physical activity, and modest improvements in diet. Together, these changes were associated with roughly one additional year of healthy life. “Healthy life” here refers to years lived without major illness or disability that limits daily functioning.

More substantial changes were linked to larger gains. Almost half an hour of extra sleep per night, combined with four additional minutes of exercise per day, which adds up to nearly half an hour of extra activity per week, along with further dietary improvements, was associated with up to four additional healthy years of life.

This matters because, although women live longer on average than men, those extra years are often spent in poorer health, with significant personal and economic costs. Women face a higher risk of dementia, stroke and heart disease at older ages, as well as conditions that lead to vision loss and bone fractures. These illnesses can reduce quality of life and threaten independence.

Lifestyle change may also reduce the risk of early death. The same lifestyle factors examined in this cohort were analysed last year in a separate study, which focused on mortality (the risk of dying).

In that analysis, people who followed healthier lifestyle patterns over an eight-year period had a 10% lower risk of death in that period. The combination of 15 extra minutes of sleep per night, two additional minutes of moderate to vigorous physical activity per day and a healthy diet was linked to a modest reduction in the risk of dying. A much larger reduction of 64% was seen among people who slept between seven and eight hours per night, ate a healthy diet and engaged in between 42 and 103 additional minutes of moderate to vigorous physical activity per week. Importantly, this benefit was only seen when these behaviours occurred together. Diet alone had no measurable effect, for instance.

Strengths and limitations

One of the key strengths of these studies is that they show health benefits at very low thresholds of behaviour change. This reduces the likelihood that the results are driven only by people who are already healthier or more motivated, and makes the findings more applicable to older adults and those with limited capacity to change their routines.

Another strength is the use of objective measurements rather than self-reported data. Physical activity and sleep were measured using wearable devices, rather than relying on participants to estimate their own behaviour. Self-reporting can be unreliable, particularly for people with memory problems, such as those in the early stages of dementia.

However, there are important limitations. The objective measurements were only collected for three to seven days, which may not reflect people’s long-term habits. From personal experience, wearing activity trackers can lead people to exercise more while they are being monitored, but these changes are often short-lived.

In addition, wrist-worn accelerometers estimate sleep and activity based on movement. During deep sleep, people move very little, but lack of movement does not always mean someone is asleep. These devices may therefore not fully capture true sleep patterns or physical activity levels. Other methods, such as thigh-mounted sensors or mattress-based sensors that detect movement during sleep, may provide more accurate assessments.

Despite these issues, objective measurements are generally more reliable than self-report. Still, because behaviour was only measured once, it is unclear whether actual changes in behaviour over time influenced health outcomes. It is also not clear whether the recorded activity reflected leisure-time exercise or physical activity at work, which can have different effects on health.

Dietary information presents another challenge. Diet was self-reported and collected three to nine years before collection of sleep and activity data. Diets often change over time, particularly after diagnoses such as cardiovascular disease, where people may be advised to reduce their cholesterol intake, or in conditions such as dementia, where people may forget to eat. As a result, it is difficult to know whether diet influenced disease risk, or whether emerging disease altered diet, eventually contributing to poor health and earlier death.

There are also broader social factors to consider. Healthy behaviours tend to cluster together and are strongly linked to education and financial security. For example, smoking and having overweight and obesity are closely associated with deprivation and poverty.

Participants in the UK Biobank, a large long-term health research project that collects genetic, lifestyle and health data from hundreds of thousands of UK adults, are generally healthier than the average UK population.

Health research often attracts people who are healthier, better educated and more financially secure. This may reflect both interest in research and having the time and resources to take part in such studies.

Wealth also shapes exposure to risk. People with higher incomes are less likely to live in areas with high levels of pollution and are more likely to have control over their working conditions and finances. Financial stress can affect sleep quality, leading to fatigue and reducing the likelihood of exercising, shopping for fresh food, or preparing healthy meals. Over a lifetime, these factors contribute to poorer health and earlier death.

Although researchers attempted to account for these influences using statistical methods, these are deeply interconnected and difficult to separate. The widening health-wealth gap, with many people now living in severe poverty, highlights the limits of personal responsibility. These structural issues require action from policymakers, rather than placing the burden solely on people who may have very little control over the conditions that shape their health.

Eef Hogervorst has received funding from several governmental and charity foundations for her research into lifestyle and health including currently the ISPF and Alzheimer's Research UK. She is affiliated with Loughborough university and has recently acted as dementia expert for NICE and the BBC. In the past she has acted as consultant on diet and dementia risk for Proctor

Finding stillness in motion: how riding a motorcycle can teach us mindfulness

2026-01-29T12:36:45Z

Speeding along an open road on my motorcycle, flanked by the great outdoors, the engine hums and the noise in my mind disappears. Riding a motorcycle demands total presence. Focus isn’t optional. It’s a matter of survival. After all, a wandering mind could lead to disaster.

But it’s not fear or panic that sharpens my attention. It is something else entirely. As a clinical psychologist, I understand fear well. I know how danger activates the fight-or-flight response. And yet, paradoxically, it is on my motorcycle that I feel most calm. This is where I experience the greatest joy. It is where I find what I would describe as a state of mindfulness.

Mindfulness is the practice of paying attention to the present moment, on purpose and without judgment. In psychological therapy, it is usually cultivated through meditation. People are encouraged to sit quietly, focus on the breath and observe thoughts and sensations as they arise.

Mindfulness is not an “in the moment” technique to reduce immediate distress. It is a skill developed through regular practice. Research shows that it activates brain areas involved in emotional regulation and focused attention. Studies also suggest mindfulness can improve emotional health, reduce symptoms of depression, anxiety and stress, and help people respond to difficult situations more thoughtfully rather than reacting on impulse.

Mindfulness can be practised in many ways. Some approaches rely on stillness, such as body scans and breathing exercises. Others involve movement, including yoga, tai chi and walking meditation. What unites them is deliberate attention to the here and now.

Because mindfulness is accessible, cheap and relatively easy to learn, it has spread far beyond therapy rooms. It now appears everywhere, from healthcare settings to social media reels and YouTube tutorials promising calm in minutes. This popularity is not necessarily a problem. But mindfulness is not without its limits.

Mindfulness is not a cure for serious mental illness. It cannot resolve structural problems such as poverty, trauma or unsafe environments. For some people, particularly those with a history of trauma or certain mental health conditions, sitting still with their thoughts can be distressing. Mindfulness practices can sometimes intensify intrusive or triggering thoughts rather than soothe them.

As with all types of psychological therapy, there is no one-size-fits-all approach. That is why it is worth broadening how we think about attention, emotional regulation and mental wellbeing.

Attention under pressure

Motorcycling offers one such alternative. It’s a mentally and physically demanding activity. The bike itself is heavy and a rider needs strength and balance, particularly when riding at slow speeds and when stopping. Core muscles are engaged when manoeuvring and all limbs are engaged in braking, clutch control and gear changes.

Mentally, the demands are even greater. Riders must remain continuously alert to road conditions, traffic, weather and the unpredictable actions of other road users. Decisions often need to be made in seconds, like when to brake, when to accelerate, how to navigate a bend, how to respond to an unexpected hazard. All of this takes place knowing that the rider’s protection is limited to their clothing.

These demands may explain why riding a motorbike can feel so absorbing. Research supports this. A study exploring the mental and physical effects of motorcycling showed improvements in focused attention, sensory awareness and the ability to ignore distractions.

Riders become better at scanning their environment and predicting what might happen next. This is a skill known as “situational awareness”. Many riders also report these benefits in their own accounts of riding motorbikes.

Perhaps most strikingly, despite motorcycling being a high-risk activity, research found reductions in stress hormones while riding. The proposed explanation is that the intense concentration required leaves little room for ruminating on everyday worries. Attention is fully captured by the task at hand.

Finding stillness in motion. O_Zinchenko/Shutterstock

Rethinking mindfulness

Unlike traditional mindfulness practice, motorcycling does not require deliberate non-judgment of thoughts or sensations. There is no effort to observe the mind. The activity itself does the work. Similar effects have been observed in other high-demand pursuits, such as rock climbing and athletic performance.

Clinically, this matters. While traditional mindfulness practices may not be suitable or achievable for everyone, there are alternatives. Activities which demand full engagement – mentally and physically – may offer similar psychological benefits. Purposeful, absorbing activities can help regulate emotions, sharpen attention and reduce stress over time.

For some people, stillness is not the route to being present. Sometimes, mindfulness is found not by slowing down, but by moving – fully, deliberately and with purpose.

Judith Roberts does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

People who survive cancers are less likely to develop Alzheimer’s – this might be why

2026-01-29T12:36:35Z

Dragon Images/Shutterstock.com

Cancer and Alzheimer’s disease are two of the most feared diagnoses in medicine, but they rarely strike the same person. For years, epidemiologists have noticed that people with cancer seem less likely to develop Alzheimer’s, and those with Alzheimer’s are less likely to get cancer, but nobody could explain why.

A new study in mice suggests a surprising possibility: certain cancers may actually send a protective signal to the brain that helps clear away the toxic protein clumps linked to Alzheimer’s disease.

Alzheimer’s is characterised by sticky deposits of a protein called amyloid beta that build up between nerve cells in the brain. These clumps, or plaques, interfere with communication between nerve cells and trigger inflammation and damage that slowly erodes memory and thinking.

In the new study, scientists implanted human lung, prostate and colon tumours under the skin of mice bred to develop Alzheimer‑like amyloid plaques. Left alone, these animals reliably develop dense clumps of amyloid beta in their brains as they age, mirroring a key feature of the human disease.

But when the mice carried tumours, their brains stopped accumulating the usual plaques. In some experiments, the animals’ memory also improved compared with Alzheimer‑model mice without tumours, suggesting that the change was not just visible under the microscope.

The team traced this effect to a protein called cystatin‑C that was being pumped out by the tumours into the bloodstream. The new study suggests that, at least in mice, cystatin‑C released by tumours can cross the blood–brain barrier – the usually tight border that shields the brain from many substances in the circulation.

Once inside the brain, cystatin‑C appears to latch on to small clusters of amyloid beta and mark them for destruction by the brain’s resident immune cells, called microglia. These cells act as the brain’s clean‑up crew, constantly patrolling for debris and misfolded proteins.

In Alzheimer’s, microglia seem to fall behind, allowing amyloid beta to accumulate and harden into plaques. In the tumour‑bearing mice, cystatin‑C activated a sensor on microglia known as Trem2, effectively switching them into a more aggressive, plaque‑clearing state.

Surprising trade-offs

At first glance, the idea that a cancer could “help” protect the brain from dementia sounds almost perverse. Yet biology often works through trade-offs, where a process that is harmful in one context can be beneficial in another.

In this case, the tumour’s secretion of cystatin‑C may be a side‑effect of its own biology that happens to have a useful consequence for the brain’s ability to handle misfolded proteins. It does not mean that having cancer is good, but it does reveal a pathway that scientists might be able to harness more safely.

The study slots into a growing body of research suggesting that the relationship between cancer and neurodegenerative diseases is more than a statistical quirk. Large population studies have reported that people with Alzheimer’s are significantly less likely to be diagnosed with cancer, and vice versa, even after accounting for age and other health factors.

People with Alzheimer’s are significantly less likely to get cancer, and vice versa. Halfpoint/Shutterstock.com

This has led to the idea of a biological seesaw, where mechanisms that drive cells towards survival and growth, as in cancer, may push them away from the pathways that lead to brain degeneration. The cystatin‑C story adds a physical mechanism to that picture.

However, the research is in mice, not humans, and that distinction matters. Mouse models of Alzheimer’s capture some features of the disease, particularly amyloid plaques, but they do not fully reproduce the complexity of human dementia.

We also do not yet know whether human cancers in real patients produce enough cystatin‑C, or send it to the brain in the same way, to have meaningful effects on Alzheimer’s disease risk. Still, the discovery opens intriguing possibilities for future treatment strategies.

One idea is to develop drugs or therapies that mimic the beneficial actions of cystatin‑C without involving a tumour at all. That could mean engineered versions of the protein designed to bind amyloid beta more effectively, or molecules that activate the same pathway in microglia to boost their clean‑up capacity.

The research also highlights how interconnected diseases can be, even when they affect very different organs. A tumour growing in the lung or colon might seem far removed from the slow build up of protein deposits in the brain, yet molecules released by that tumour can travel through the bloodstream, cross protective barriers and change the behaviour of brain cells.

For people living with cancer or caring for someone with Alzheimer’s today, this work will not change treatment immediately. But the study does offer a more hopeful message: by studying even grim diseases like cancer in depth, scientists can stumble on unexpected insights that point towards new ways to keep the brain healthy in later life.

Perhaps the most striking lesson is that the body’s defences and failures are rarely simple. A protein that contributes to disease in one organ may be used as a clean‑up tool in another, and by understanding these tricks, researchers may be able to use them safely to help protect the ageing human brain.

Justin Stebbing does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Scabies outbreak in UK and Europe – what you need to know

2026-01-28T13:51:35Z

3dMediSphere/Shutterstock.com

Scabies cases are surging across the UK and Europe. The tiny mites that cause it spread easily through skin contact, making children, young adults and elderly people particularly vulnerable. Effective treatments are available, but myths and stigma are getting in the way of proper control.

What is scabies and how do people catch it?

Scabies is a skin infestation with tiny mites called Sarcoptes scabiei. The mites transfer from person to person through skin-to-skin contact – when parents cuddle children, care workers help residents, people share beds, or during sex. Occasionally, contaminated clothing or bedding can spread them too.

Are scabies cases rising in the UK, and if so why?

In institutions across England and Wales, such as care homes and schools, our team found 241 outbreaks in just one year.

In the wider population, the picture is less clear because scabies does not have to be officially reported to health authorities, and many people treat it themselves using over-the-counter medicines. However, reports from GP surgeries and sexual health clinics suggest cases have risen sharply over the last few years.

We don’t yet know all the reasons for this rise. However, one of the main culprits is that in 2023 and 2024 supply chain problems left pharmacy wholesalers struggling to stock imported scabies creams. With treatments delayed, more people became infested.

Who is most at risk of catching scabies?

Anyone can catch it, but three groups face the highest risk: children, sexually active young people and the elderly. This is mainly because these three groups tend to have more physical contact and are congregated in institutions like nurseries, universities and care homes. People in other crowded settings, such as migrant centres or prisons, are also at risk.

Is scabies caused by poor personal hygiene?

Absolutely not. Bathing habits make no difference to scabies rates. Unlike many bacteria and viruses, these mites tolerate soap and alcohol handwash just fine.

What are the symptoms?

Scabies usually causes an intense itch, particularly at night. However, these symptoms usually take around four to six weeks to arise if it is the first time someone is exposed.

Sometimes you can spot S-shaped burrows on the skin, particularly between fingers or on genital areas. In elderly patients, we’ve found scabies can look quite different – they may not even complain of itching.

Scabies can cause intense itching. Zay Nyi Nyi/Shutterstock.com

How contagious is scabies and how long can mites survive off the body?

Scabies is highly contagious. Even a few minutes of skin-to-skin contact – such as holding hands – can be enough for a mite to crawl from one person to another. This is how most people become infested. Depending on room temperature and humidity, the mites can survive off the body for up to a week, but human skin is their natural habitat.

Why does scabies treatment sometimes fail or seem not to work?

Traditional cream treatments work well in ideal circumstances, but using them correctly can be difficult. The creams need to be put over the entire body and left on for hours. At the same time, clothing and bedding need to be washed, and close contacts, such as family members, need to be treated even if they have no symptoms.

This whole process then needs to be repeated seven days later. This is because the creams work excellently at killing the adult mites, but less well at penetrating egg-cases. The second treatment will kill the newly hatched mites before they have a chance to mate. Not carrying out any of these steps risks failing to eradicate the mites.

Even successful treatment can leave itching that persists for weeks, wrongly leading people to assume they’re still infested.

Why was an oral medication recently introduced?

In many countries, an oral medication called ivermectin has been available for treating scabies for many years – making treatment far easier. To tackle the surge in cases, my colleagues and I in the NIHR Applied Research Collaboration Kent, Surrey, Sussex were involved in getting the drug licensed and available on prescription in the UK. But like the creams, it usually needs repeating after seven days to be fully effective.

Ivermectin is an effective treatment for scabies. Carl DMaster/Shutterstock.com

Is scabies becoming resistant to medicated cream?

There is evidence scabies mites in other countries have developed some resistance to permethrin, the medicated cream used to eradicate them. However, most treatment failures in the UK probably stem from the practical difficulties of using treatments correctly rather than the medication itself not working.

What are the emotional and mental health effects of scabies on patients and families?

The visible signs on skin, combined with the persistent myth about poor hygiene, create real problems. When we’ve spoken to patients and their families, they describe feeling ashamed, being judged by others, and withdrawing socially. Add in disrupted sleep from the itching, and the mental health impact can be serious.

Why do shame and embarrassment make scabies harder to control?

Early diagnosis and treatment reduce how many people catch it from an infected person. But shame causes delays – people put off seeking help for themselves, their family members, or even residents in their care. This gives the mites more time to spread.

What should people do if they think they have scabies?

If you are concerned about scabies, you should see your GP. They can examine your skin to determine if it is indeed scabies and put a treatment plan in place, if necessary.

Dr Jo Middleton receives funding from the National Institute for Health and Care Research (NIHR) through its Applied Research Collaboration Kent, Surrey, Sussex (NIHR200179). The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health and Social Care.

How to use cleanser properly – by an expert in skin science

2026-01-28T13:51:32Z

Cleansing is an important part of any skincare routine. leungchopan/ Shutterstock

Cleansing has long been an important part of hygiene rituals across cultures. Nowadays, cleansing remains an essential part of daily skincare routines, helping to remove sweat, makeup and old skin cells.

But with skincare routines becoming more and more extensive (and expensive), it can be difficult to know which cleanser to use – and how to use it. The right product can benefit skin health and overall wellbeing, while the wrong product could potentially damage the skin.

What does cleanser do?

Cleansers are designed to clean the surface of the skin. They remove excess oils, dirt and other products – such as makeup or sun cream.

Cleansers can be divided into four base ingredients: soap, detergent, surfactants and emulsifiers. These are all compounds with properties that allow them to solubilise particles – a process which allows particles (such as makeup or dirt) to be dissolved in water. This process separates these particles from the surface of the skin so they can be washed away – leaving the surface of the skin clean.

The first cleansers were soaps. These are relatively harsh on the skin as they strip away the skin’s natural oils, causing dryness or even irritation.

Most modern cleansers contain synthetic detergents, which are less irritating to the skin. Some cleansers also contain a higher proportion of lipids (fats). This prevents the skin from becoming dry by replacing the oils that are removed by cleansing.

When should we cleanse?

How often you should cleanse is a personal matter, depending on factors such as lifestyle, skin type and genetics.

For instance, if you have dry skin, cleansing less frequently or with milder products may suit your skin better. But if you’re someone with oily skin you may want to cleanse more often.

How do you pick the right cleanser?

The type of cleanser that works best for a specific person will vary depending on a whole host of factors such as skin type, age and lifestyle. So what works for one person doesn’t guarantee it will work well for the next.

Cleansers are typically made with a specific base ingredient – such as water or oil. Water-based cleansers remove water-soluble particles, such as dirt and sweat, while oil-based cleansers can remove oil-soluble particles, such as makeup and sun cream. Additional ingredients are also often added to cleansers to help provide specific results.

Some cleanser ingredients can help control acne and blemishes. New Africa/ Shutterstock

For example, salicylic acid is often found in cleansers for blemish control. It has anti-inflammatory properties and slows down cell growth.

Benzoyl peroxide, has anti-bacterial properties, which is why it’s useful in treating mild acne.

If you don’t have acne or a skin condition where these compounds have been proven useful, cleansers containing salicylic acid or benzoyl peroxide may be unnecessarily harsh and could harm the skin.

Cleansers containing ceramides, which are naturally-occurring lipids that are an important component of the skin barrier, may be a good option for those looking to protect their skin. The addition of ceramides to a cleanser means less of the skin’s natural oils are lost during cleansing.

Why is using the right cleanser so important?

The skin is delicate. If you use ingredients that are too harsh, it could negatively affect the skin.

For instance, soaps and detergents can be harsh on the skin – specifically to the skin’s lipid components, which are key to the skin’s function as a protective barrier.

Harsh cleansers (or cleansing too often) could also potentially disrupt the skin microbiome – the many different types of bacteria, fungi and viruses that live on our skin and are essential to overall skin health.

If the skin microbiome is disrupted, it could lead to a microbial imbalance, where one bacterial strain grows out of control. This could lead to breakouts or even exacerbate other skin issues, such as eczema.

Dry skin after cleansing may be a sign the skin barrier (the outer layer of dead skin cells that protect the underlying cells from harm) has been damaged. Moisturising after cleansing can combat this. Alternatively, using a cleanser that has a moisturising component – such as ceramides or a micellar water – may be helpful, though it’s still worth monitoring how your skin feels after cleansing.

How do you cleanse properly?

Washing your face with water alone won’t be enough to remove any oil, dirt or makeup that has built up.

Usually a single cleanse will work just fine for removing these things from the surface of the skin – including makeup.

Double cleansing is something that has been popularised by Korean beauty trends. This involves cleansing in two steps – first using an oil-based cleanser, which may work better to remove oily products (such as makeup or sunscreen), and following this up with a water-based cleanser. This procedure is meant to provide a deeper clean, which can be useful.

However, a water cleanser will not be very efficient at removing any residue that may be left behind from the oil cleanser. This could lead to a build-up of the oil-based cleanser which could lead to irritation or breakouts.

When deciding on how to cleanse and which products to use it’s important to consider what will be best for your lifestyle and your skin type. Just be sure your cleanser contains ingredients that allow you to clean your skin without destroying your skin barrier.

Rebecca Wagner receives funding from the Wenner Gren Foundation.

Stone baby: the rare condition that produces a calcified foetus

2026-01-27T16:34:11Z

Miridda/Shutterstock

For some women, pregnancy is a time of profound loss. Not all pregnancies progress as expected. One serious complication is ectopic pregnancy, a condition in which a fertilised egg implants somewhere other than the uterus.

The uterus is the only organ designed to stretch, supply blood and safely support a developing pregnancy. When implantation occurs elsewhere, the pregnancy cannot develop normally and poses significant risks to the mother.

In a very small number of cases, implantation occurs within the abdominal cavity. This is known as an abdominal pregnancy and means the embryo attaches to structures such as the bowel or abdominal lining rather than reproductive organs, often undetected.

There are rare reports of such pregnancies continuing into late gestation and, in extraordinary circumstances, a baby being born healthy. Far more often, however, the outcome is one of the strangest phenomena documented in medicine.

This outcome is known as a lithopaedion, a term derived from Greek that translates literally as “stone baby”. Fewer than 350 to 400 cases have been described in the medical literature, making it exceptionally rare.

In these cases, a woman usually experiences at least the early stages of pregnancy. Some reach full term and even go through labour; the body initiates the physical process of childbirth, but no baby is delivered. In some instances, particularly where access to healthcare is limited, a pregnancy may go entirely unnoticed.

The foetus in these cases has sadly died. After approximately three months of gestation, the foetal skeleton begins to ossify into bone. Ossification is the normal biological process by which soft cartilage turns into hardened bone. Once this has occurred, the foetal remains are too large and structurally complex for the body to break down and absorb.

During a typical pregnancy, the placenta plays a crucial role in regulating the exchange of nutrients and immune signals between mother and foetus. At the same time, the maternal immune system enters a state of immune tolerance: it is partially suppressed to prevent it from attacking the genetically distinct foetus. When the foetus is no longer viable, these protective mechanisms disappear. The immune system then recognises the foetal tissue as foreign and potentially dangerous.

To protect itself from infection or inflammation, the body may respond by calcifying the foetus. Calcification involves the gradual deposition of calcium salts around tissue, effectively isolating it. This process seals the foetus off from surrounding organs, preserving it in place and preventing further harm.

Calcification as a defensive response is not unique to pregnancy. The process of dystrophic calcification occurs when calcium deposits form in dead or damaged tissue. Calcium binds to phospholipids, which are fat-based molecules that make up the outer structure of cells and help hold cell membranes together, stabilising the area and limiting injury. A similar biological mechanism contributes to calcium build-up in blood vessels during atherosclerosis, a condition associated with heart disease.

Lithopaedion formation has also been observed in other species, including rabbits, dogs, cats and monkeys. One of the earliest recorded human cases dates back to 1582, involving a 68-year-old French woman who carried a lithopaedion for 28 years.

Another widely reported case describes a woman in China who carried one for over 60 years. Some lithopaedions have been reported to weigh more than two kilograms, roughly the weight of a full-term newborn. In one exceptionally rare case, a woman was found to have twin lithopaedions.

Symptomless cases

Some women carry a lithopaedion without symptoms for many years. Others develop complications caused by its presence in the abdomen. These include pelvic abscesses, which are collections of infected fluid, twisting or obstruction of the intestines that interfere with digestion, fistula formation – meaning abnormal connections between organs – and other abdominal symptoms such as pain or swelling.

Cases without symptoms are often discovered postmortem – after death during examination. When symptoms do occur, surgical removal is usually required. Because lithopaedions develop outside the uterus, they may attach to nearby organs such as the bowel or bladder.

Each case must therefore be carefully assessed. Surgery may be performed laparoscopically, using small incisions and a camera to minimise recovery time, or may require a more extensive open abdominal procedure.

Diagnosis almost always relies on medical imaging. This often occurs incidentally while investigating other symptoms. Calcified foetal bones can be identified using X-rays, ultrasound or CT scans. CT scans are particularly useful because they provide detailed cross-sectional images that clearly show both bone and surrounding soft tissue.

Lithopaedion cases are now exceptionally rare, likely even more so in modern medicine due to accurate pregnancy testing, early ultrasound scanning and routine antenatal care. Although these cases are medically unusual, they highlight both the vulnerability and resilience of the human body. Whether supporting new life or responding when pregnancy ends unexpectedly, the body works to protect the person carrying the pregnancy, sometimes in ways that continue to surprise medicine centuries later.

Strange Health is hosted by Katie Edwards and Dan Baumgardt. The executive producer is Gemma Ware, with video and sound editing for this episode by Sikander Khan. Artwork by Alice Mason.

In this episode, Dan and Katie talk about a social media clip from tonsilstonessss on TikTok.

Muscle twitches: why they happen and what they mean

2026-01-27T16:34:08Z

Toa55/Shutterstock.com

You’re relaxing on the sofa when suddenly your eyelid starts twitching. Or perhaps it’s a muscle in your arm, your leg, or your foot that begins to spasm – sometimes for a few seconds, sometimes for hours or even days. It’s an unsettling sensation that affects about 70% of people at some point in their lives.

Muscle twitches fall into two main types. There’s myoclonus, where a whole muscle or group of muscles twitch or spasm. Then there’s fasciculation, where single muscle fibres twitch – often too weak to move a limb but visible or sensed beneath the skin.

Many factors can trigger both types of twitching, but people often fear the worst. Some fear it could signal multiple sclerosis – a condition that requires extensive testing, including a lumbar puncture to look for inflammation and MRI scans to detect brain changes.

For many people, however, twitching is simply an annoyance. Once doctors rule out serious causes, everyday features of modern life often turn out to be the trigger.

Too much caffeine, for instance, can cause muscle twitching. As a stimulant, it affects both skeletal and cardiac muscle, increasing heart rate and having a similar effect on skeletal muscle in areas such as the arms and legs. It slows down the time it takes for muscles to relax and increases the amount of calcium ions released within muscles, disrupting normal muscle contraction patterns.

Other stimulants such as nicotine, cocaine and amphetamines can cause similar muscular twitching. These substances interfere with the neurotransmitters that control or influence muscle function.

Some prescription medications can also trigger twitching. Antidepressants and anti-seizure drugs, blood pressure medicines, antibiotics and anaesthetics can all cause muscular side-effects.

When minerals run low

Twitching isn’t only caused by what you consume, it can also stem from what your body lacks. Hypocalcaemia, a drop in the amount of calcium in the body, is associated with twitching, particularly in the back and legs.

Calcium is fundamentally important in helping muscle cells rest and remain stable between contractions. When calcium levels fall, sodium channels open more easily. Sodium floods in and, as a result, nerves become hyperactive and muscles contract when they shouldn’t.

There are recognised twitching areas associated with hypocalcaemia, including the Chvostek sign, which is seen in the face and can be triggered by tapping the skin of the cheek just in front of the ear.

Chvostek sign.

Magnesium deficiency can also cause muscle twitching. Some causes of magnesium deficiency are a poor diet or poor absorption in the gut, usually due to conditions such as coeliac disease or other gastrointestinal conditions.

Some medications, particularly when taken over a long period, can cause a drop in magnesium levels in the body. Proton pump inhibitors used to treat reflux and stomach ulcers are recognised for this effect.

Low potassium is another mineral that can cause muscle twitching. Potassium helps muscle cells rest. It’s usually at high levels inside the cell and lower outside, but when potassium levels outside the cell fall, the electrical balance shifts, making muscle cells unstable and prone to misfiring, causing muscle spasms.

If you have no underlying gastrointestinal conditions, eating a healthy, balanced diet is usually enough to ensure you have enough of each of these minerals for normal muscle function.

A healthy water intake is important too, as dehydration affects the balance of sodium and potassium, resulting in abnormal muscle function, such as twitching and spasms. This is even more important during exercise, where overexertion can cause the same phenomenon.

The brain plays a role as well. Stress and anxiety can cause muscles to twitch as a result of overstimulation of the nervous system by hormones and neurotransmitters such as adrenaline.

Adrenaline increases the “alertness” of the nervous system, meaning it’s ready to trigger muscle contraction. It also increases the amount of blood flow and changes the tension of the muscles, which when a surge of energy arrives – or if the muscle is held in suspense for long periods – can result in twitching.

Adrenaline can also result in the nervous system responding to altered levels of neurotransmitters, causing muscle movement when the body is actually at rest.

Infectious agents can cause muscle twitching and spasms, too. The most commonly known is probably tetanus, which causes a phenomenon called lockjaw, where the neck and jaw muscles contract to the point where it becomes difficult to open the mouth and swallow. Lyme disease, from ticks, can also cause muscle spasms.

Many different infections can affect either the nerves or the muscles and can lead to twitching. Cysticercosis, toxoplasmosis, influenza, HIV and herpes simplex have all been linked to muscle twitching.

When doctors rule out these causes, some people receive a diagnosis of benign fasciculation syndrome – involuntary muscle twitching with no identifiable underlying disease.

It’s unknown how common it is, but it’s believed to affect at least 1% of the healthy population. It can persist for months or years, and for many, although benign, it doesn’t resolve completely.

For many people, muscle twitches remain a manageable annoyance rather than a sign of disease. But for others, a healthcare professional may need to rule out more serious causes.

Scientists once thought the brain couldn’t be changed. Now we know different

2026-01-27T12:32:38Z

Master1305/Shutterstock

For much of the 20th century, scientists believed that the adult human brain was largely fixed. According to this view, the brain developed during childhood, settled into a stable form in early adulthood, and then resisted meaningful change for the rest of life.

Today, the concept of neuroplasticity, the brain’s ability to change its structure and function in response to experience, is a central principle of brain science. The brain can change throughout life, but not without limits, not instantly and not effortlessly.

Neuroplasticity therefore reframes the brain as neither rigid nor infinitely malleable, but as a living system shaped by experience, effort and time.

The roots of neuroplasticity can be traced to the mid-20th century. In 1949, psychologist Donald Hebb proposed that connections between neurons, the brain’s nerve cells, become stronger when they are repeatedly activated together.

This principle later became known as “Hebbian learning”. At the time, Hebb’s idea was considered relevant mainly to childhood development. Adult brains were still thought to be relatively unchangeable.

That assumption has since been overturned. From the late 20th century onward, studies showed that adult brains can reorganise in response to learning, changes in sensory input, or physical injury. Sensory changes include alterations in vision, hearing or touch due to training, loss of input or environmental change.

More recently, advances in brain imaging have allowed researchers to observe these changes directly in living people. These studies show that learning alters patterns of brain activity and connectivity across the lifespan.

Neuroplasticity is now understood not as a rare exception, but as a basic property of the nervous system. It operates continuously, within biological limits shaped by age, genetics, prior experience and overall brain health.

How the brain changes

Neuroplasticity involves changes in how existing brain cells communicate with one another.

When you learn a new skill, specific synapses, the tiny junctions where neurons pass signals to each other, become stronger and more efficient. Neural networks, which are groups of neurons that work together, become better organised. Communication between brain regions involved in that skill improves.

At the cellular level, plasticity involves changes in synaptic structure, the release of chemical messengers called neurotransmitters, and the sensitivity of receptors that receive those signals. So, it changes how neurons communicate with each other.

In a few areas of the adult brain, particularly the hippocampus, which plays a key role in memory, limited adult neurogenesis, the creation of new neurons, also occurs. Although influenced by factors such as stress, sleep and physical activity, its significance in humans is still debated.

The hippocampus is constantly rewiring to store new information. FocalFinder/Shutterstock

Crucially, neuroplasticity is experience-dependent. The brain changes most reliably in response to repeated, focused and meaningful engagement that requires attention, effort and feedback. Passive exposure to information has far less impact.

What strengthens and weakens plasticity

Over the past decade, research has identified several factors that strongly influence how plastic the brain can be.

1. Practice and challenge are essential.

Repeatedly engaging in tasks that stretch your abilities leads to changes in both brain activity and brain structure, even in older adults.

2. Physical exercise is one of the most powerful enhancers of plasticity.

Aerobic activity increases levels of brain-derived neurotrophic factor, or BDNF, which supports neuron survival and strengthens synaptic connections. Regular exercise is consistently linked to better learning, memory and overall brain health.

3. Sleep plays a critical role in consolidating brain changes.

During deep sleep, important neural connections are strengthened while less useful ones are weakened, supporting learning and emotional regulation, as shown in neuroscience research.

Sleep is essential for brain health. Prostock-studio/Shutterstock

4. Chronic stress can seriously impair plasticity.

Long-term exposure to stress hormones is associated with reduced complexity of neural connections in memory-related brain regions and heightened sensitivity in threat-processing systems, undermining learning and flexibility.

When plasticity works against us

One of the most important and often misunderstood aspects of neuroplasticity is that it is value-neutral. The brain adapts to repeated experiences whether those experiences are helpful or harmful.

This helps explain why conditions such as chronic pain, anxiety disorders and addiction can become self-reinforcing. Through repeated patterns of thought, feeling or behaviour, the brain learns responses that are unhelpful but deeply ingrained, a process known as maladaptive plasticity.

The hopeful side of this insight is that plasticity can also be deliberately directed toward recovery. Psychological therapies such as cognitive behavioural therapy are associated with measurable changes in brain activity and connectivity, particularly in networks involved in emotional regulation. Rehabilitation after stroke or brain injury relies on the same principles, using repeated, task-specific practice to compensate for damaged areas.

Clearing up common myths

Perhaps the most persistent myth is that neuroplasticity means the brain can change rapidly or without limits. In reality, meaningful neural change takes time, repetition and sustained effort, within biological constraints.

Another misconception is that plasticity disappears after childhood. While children’s brains are especially flexible, strong evidence shows that plasticity continues throughout adulthood and into older age.

Claims that brief brain-training programmes dramatically increase intelligence or prevent dementia are not supported by solid scientific evidence. The issue is that meaningful brain change happens most when learning is challenging, varied, and connected to real life.

Activities such as learning a language, exercising regularly, playing a musical instrument, or engaging in complex social interaction are far more effective at strengthening the brain than tapping through app-based puzzles.

In short, brain-training games can be fun and mildly useful, but they train you to play games well, not to think better overall.

Our understanding of neuroplasticity has come a long way since Hebb’s early ideas. What was once thought impossible is now accepted scientific fact. Embracing neuroplasticity means recognising that brains can change, while remaining realistic about how slowly and selectively that change occurs.

More than a century ago, Spanish neuroscientist Santiago Ramón y Cajal wrote that every person can become the sculptor of their own brain. Modern science shows that this sculpting never truly ends. It simply requires effort, patience and persistence.

Siobhan Mc lernon receives funding from The Burdett trust for Nursing

Laura Elin Pigott does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Tonsils, kidneys and gall: where and why your body makes stones

2026-01-27T10:00:37Z

Video_Stock _Production/Shutterstock

The human body, it turns out, is surprisingly good at making stone.

Give it enough time and the right conditions and it will go about crystallising minerals, hardening secretions and, in rare cases, turning tragedy into rock. Gallstones. Kidney stones. Tonsil stones. Salivary stones. And, in one of the strangest and saddest corners of medical history, stone babies.

In the second episode of The Conversation’s Strange Health podcast, we take a tour through the stony side of human anatomy and ask why this keeps happening, where these stones form and which ones you actually need to worry about.

Strange Health explores the weird, surprising and sometimes alarming things our bodies do. Each episode takes a bodily mystery or viral health claim and traces it back to anatomy, chemistry and evidence, drawing on researchers with first-hand experience of these processes. Some discoveries are not ideal mealtime material.

This episode’s guide is Adam Taylor, professor of anatomy at Lancaster University and long-time contributor to The Conversation. Taylor has spent years studying stones in both everyday and extraordinary contexts, including a rare genetic condition called alkaptonuria. In people with this condition, the body cannot properly break down certain proteins, leading to blackened cartilage, dark urine and an unusually high risk of stone formation throughout the body. It is exactly as unsettling as it sounds.

Stones, Taylor explains, form when substances that normally stay dissolved stop behaving themselves. Calcium, phosphate, uric acid and one of the building blocks of protein called cysteine can all crystallise if conditions are right. Once a few molecules stick, more follow. The process snowballs. Over time, a stone appears.

Kidney stones and gallstones are the most familiar examples, and among the most painful. Their jagged crystal edges scrape delicate tissues, trigger spasms and cause bleeding as the body desperately tries to force them through narrow ducts never designed for sharp objects. Larger stones can block urine flow entirely, damaging the kidneys and, if left untreated, causing serious harm.

Smaller stones can form elsewhere. Tonsil stones develop when food debris, bacteria and dead cells collect in the crevices of the tonsils and harden. Salivary stones can form when ducts become blocked by bacteria or foreign material, sometimes something as mundane as a stray toothbrush bristle. These stones are rarely dangerous, but they are often unpleasant, painful and, judging by social media, irresistibly watchable when removed.

Then there are stone babies, or lithopedions. In extremely rare cases, a pregnancy that cannot continue is not expelled from the body. Instead, the immune system encases the remains in calcium, effectively mummifying them to prevent infection. Some have been discovered decades later, only after death.

What unites all of these stones is not toxins or detoxing, but chemistry and fluid balance, and sometimes bad luck. Taylor stresses that dehydration is one of the biggest risk factors. When fluids slow down, materials that are normally carried in fluid begin to solidify. Stones follow.

Listen to Strange Health to understanding why solid things form inside something that is mostly water, and why some stones are medical emergencies while others are just deeply, memorably gross. You have been warned about watching while eating.

Strange Health is hosted by Katie Edwards and Dan Baumgardt. The executive producer is Gemma Ware, with video and sound editing for this episode by Sikander Khan. Artwork by Alice Mason.

In this episode, Dan and Katie talk about a social media clip from tonsilstonessss on TikTok.

Katie Edwards works for The Conversation.

Adam Taylor and Dan Baumgart do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.

People from sexual minorities really do die younger, new data suggests

2026-01-26T17:12:12Z

Okrasiuk/Shutterstock

New data has revealed something the UK has never seen before: clear evidence that sexual minority people die earlier, and at higher rates, than their straight or heterosexual peers.

For the first time, the Office for National Statistics (ONS) has published overall mortality rates by sexual orientation in England and Wales. The findings come from a new bulletin that links voluntary sexual orientation data collected in the 2021 census with death registrations between March 2021 and November 2024. The linkage was possible for people with valid NHS identification numbers, allowing researchers to examine patterns of death across a population of nearly 29 million adults.

Evidence on whether sexual minority people experience higher overall mortality has been mixed, with many previous studies limited by small sample sizes, indirect measures of sexual orientation or a focus on specific causes of death rather than all-cause mortality. The new ONS analysis is the first UK study to link self-reported sexual orientation from the census with national death registrations, allowing population-level mortality rates to be examined across millions of people.

The headline result is difficult to ignore. People identifying as lesbian, gay, bisexual or another minority sexual orientation were 30% more likely to die from any cause during the study period than those identifying as straight or heterosexual. In age-standardised terms, this equates to 982.8 deaths per 100,000 people in the LGB+ group, compared with 752.6 per 100,000 among straight or heterosexual people.

Sexual orientation was included in the census for the first time in 2021. Around 92.5% of people aged 16 and over answered the question, representing roughly 44.9 million people.

Most respondents (89.4%) identified as straight or heterosexual, while 3.2% identified with an LGB+ orientation. A further 7.5% chose not to answer. After linking census responses to death records, the final ONS analysis covered just under 28.7 million people.

While this is the first UK release to examine all-cause mortality by sexual orientation, it builds on earlier ONS findings. In April 2025, the agency reported that people identifying as LGB+ had more than double the risk of suicide and two-and-a-half times the risk of intentional self-harm compared with straight or heterosexual people.

What the new data shows is that higher mortality among sexual minority people extends well beyond mental health.

Heart disease, for example, was the leading cause of death in both groups together and specifically in men (the leading cause of death in LGB+ women was intentional self-harm, and heart disease was the second leading cause). It accounted for 11.9% of deaths among LGB+ people and 10.7% among straight or heterosexual people.

This might not sound surprising until age is taken into account. On average, people in the LGB+ group were much younger, with a mean age of 35.6 years, compared with 48.6 years in the straight or heterosexual group.

Because the risk of ischaemic heart disease rises steeply with age, a higher share of deaths from this cause in a younger population is particularly troubling.

The ONS does not attempt to explain why these differences exist, and the data alone cannot establish cause. But the broader evidence base offers important clues. Smoking, high blood pressure, high cholesterol, diabetes, obesity and physical inactivity are all well-established risk factors for cardiovascular disease, and some are known to be more common among sexual minority populations.

Earlier ONS analysis has shown that lesbian, gay and bisexual people are more likely to smoke than heterosexual people, especially women, even after accounting for factors such as age, ethnicity and socioeconomic status.

Other research suggests higher rates of obesity among sexual minority women, though not consistently among men. Evidence for differences in conditions such as high blood pressure and diabetes is more mixed.

Beyond individual behaviour, decades of research point to the health effects of minority stress on heart disease. Exposure to discrimination, stigma and violence is associated with higher levels of smoking and alcohol use, disrupted sleep, obesity and hypertension, all of which accumulate over time to increase the risk of serious illness and early death.

The most distressing findings in the new ONS release concern young people. Among those aged 16 to 24 who identified as LGB+, suicide accounted for 45.3% of all deaths. Among straight or heterosexual people of the same age, the figure was 26.6%.

Suicide is preventable, but it rarely has a single cause. What these findings make clear is that living in today’s society still places a heavier burden on sexual minority people, particularly the young. That burden shows up not only in mental health statistics, but in patterns of physical illness and early death.

If sexual minority young people were able to grow up in safer, more inclusive environments, these stark inequalities might not exist. The emerging evidence suggests they are not inevitable. They are shaped by social conditions and, at least in part, they can be changed.

Catherine Meads volunteers occasionally for the Liberal Democrat political party in the UK but is not a member.

On Being Ill at 100: Virginia Woolf’s ‘best essay’ still shapes how we read sickness

2026-01-26T17:12:07Z

The year is 1926. Queen Elizabeth II is christened. Wage cuts and increased working hours for coal miners precipitate a general strike of workers. A.A. Milne publishes Winnie-the-Pooh. The League of Nations accepts Germany as the sixth permanent member on the council deeming it a “peace-loving country”.

It is also the year that Virginia Woolf published her essay, On Being Ill, in January’s volume of The New Criterion – the literary review headed up by T.S. Eliot. The essay had been written from her sickbed, as Woolf lay recovering after fainting at her nephew Quentin’s 15th birthday dinner months before.

In the essay, Woolf argues that illness is “the great confessional” which is never talked about in literature because of the “poverty” of language when it comes to sickness and disease. Books on influenza, poetry on pneumonia and tomes on toothache and typhoid are “null, negligible and non-existent”, she declares, reckoning with Shakespeare, Milton, Pope, Proust, Donne and Keats.

Eliot was ‘not enthusiastic’ about Woolf’s essay. National Portrait Gallery

Recounting a conversation with her husband Leonard Woolf about the essay in her diary a month before its publication, she remarked it was the “article which I, & Leonard too, thought one of my best”. However, not everyone was of the same opinion.

Woolf’s diaries reveal that a postcard sent by Eliot illustrated that he was “not enthusiastic” about the piece, prompting her to write: “So, reading the proof just now, I saw wordiness, feebleness, & all the vices in it.” It “increased” her “distaste” for her own writing and “dejection at the thought of writing another novel”.

Nevertheless, a revised version of On Being Ill was published months later, in April 1926, in an American magazine called The Forum. This time it was under the title Illness: An Unexploited Mine. Despite her critics, Woolf persisted with the topic, believing the absence of our ailments in literature called for censure.

In November 1930, a slim quarto of 250 numbered and signed copies of On Being Ill was hand-printed by the Woolfs’ printing press, The Hogarth Press. It was printed in an original vellum-backed green cloth with marbled endpapers, woodcut vignette on final leaf and an original dust jacket designed by her sister, Vanessa Bell. Woolf set the type herself. She spent Sunday June 15 1926, in the full swing of summer doing so, writing in her diary: “I was so methodically devoting my morning to finishing the last page of type setting: On Being Ill.”

On or about December 2019, human character changed

Two years before the writing of On Being Ill, in one of the most quoted lines in literature, Woolf wrote “on or about December 1910, human character changed”, in her essay, Mr Bennett and Mrs. Brown (1924), continuing that when “human relations change there is at the same time a change in religion, conduct, politics, and literature”.

Human character changed in December 2019, when SARS-CoV-2 was discovered and the COVID pandemic began in earnest.

Pandemic Pages, the podcast that I founded and co-host with Dr Catherine Wynne at the University of Hull, charts this tectonic shift in our lives and literature through interviews with authors, creatives, academics and medical professionals. Previous guests include Booker Prize winner and chair Roddy Doyle; NHS doctor and award-winning author, Dr Roopa Farooki and Professor Lucy Easthope, the UK’s leading expert on disaster recovery and advisor to the Prime Minister’s office during COVID.

The podcast has just launched its third season, which aims to create a living dialogue with the centenary of Woolf’s On Being Ill. In one episode, I chat to associate professor of Graphic Design from the Oslo National Academy of the Arts, Ane Thon Knutsen, a letter press print artist who printed one sentence of On Being Ill every day in the early days of lockdown.

Knutsen, whose wedding was postponed due to COVID, said this project “fell into her life” when lockdown began in Norway after everything she had planned fell apart: “A couple of days into the pandemic, I read On Being Ill. I’d read it before and I had planned to work on it, but I read it again and I was just like, my God, this essay is about just what’s happening right now.”

In the introduction to Knutsen’s book, Mark Hussey, emeritus professor of English at Pace University in New York, writes that her daily meditations on a single sentence painstakingly rebuild Woolf’s words one letter at a time, resulting in a collective slow reading. Her work urges us to savour words, to ponder them, to roll them around on the tongue before swallowing.

In the UK’s National Year of Reading 2026 – a UK-wide campaign designed to inspire more people to make reading a regular part of their lives – Woolf’s essay and Knutsen’s diary feel particularly poignant to press books into the hands of everyone we can – to regift ourselves the slowness of suspended pandemic time, the stillness in that season of survival.

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This article features references to books that have been included for editorial reasons, and may contain links to bookshop.org. If you click on one of the links and go on to buy something from bookshop.org The Conversation UK may earn a commission.

Lucyl Harrison does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.