Tag: The Conversation

Categories : Environmental EffectsTags :

Rising CO₂ Levels are Reflected in Human Blood. Scientists Don’t Know What it Means

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Alexander Larcombe, The Kids Research Institute Australia; Curtin University and Philip Bierwirth, Australian National University

Humans evolved in an atmosphere containing roughly 200–300 parts per million (ppm) of carbon dioxide (CO₂). Today, that figure sits above 420 ppm, higher than at any point in the history of our species.

We know this extra CO₂ is contributing to climate change, but could it also be changing the chemistry of our bodies?

In our recently published research we looked at two decades of information from one of the biggest health datasets in the world to start answering this question. We found some concerning trends.

What we found

We analysed blood chemistry data from the US National Health and Nutrition Examination Survey (NHANES), which collected samples from about 7000 Americans every two years between 1999 and 2020. We looked at three markers: CO₂, calcium and phosphorus.

CO₂ is mainly carried in blood in the form of bicarbonate (HCO₃⁻).

When CO₂ enters the blood, it is converted to bicarbonate. This process largely occurs inside red blood cells, and also produces hydrogen ions.

During short-term exposure to increased CO₂, this can make blood more acidic, and result in a modest increase in bicarbonate levels in the blood (to reduce acidity).

If the exposure continues for a long time the kidneys reduce the amount of bicarbonate lost in urine and also produce more bicarbonate. This has the net effect of higher bicarbonate levels in the blood, to counteract the persistent acidity.

Levels of calcium and phosphorus in the blood may also be affected, as they too play a role in regulating acidity in the blood. These processes are completely normal.

Over the 21 years from 1999 to 2020, we found that average blood bicarbonate levels rose by about 7%. Over the same period, atmospheric CO₂ concentrations rose by a similar proportion.

Atmospheric CO₂ has risen, along with increases in levels of carbonate in the blood and decreases in calcium and phosphorus. Larcombe & Bierwirth / Air Quality, Atmosphere & Health, CC BY

Meanwhile, blood calcium levels dropped by about 2% and phosphorus by around 7%.

If these trends continue, blood bicarbonate levels may exceed healthy levels in around 50 years. Calcium and phosphorus levels may fall below healthy levels, too, by the end of the century.

Our hypothesis is that rising CO₂ exposure could be contributing to these trends.

What’s causing the changes?

It’s important to be clear about what this study does and doesn’t show. It identifies population-level trends in blood chemistry that parallel rising atmospheric CO₂.

But correlation is not causation. The study does not adjust for factors such as diet, kidney function, diuretic use or obesity, which can influence the measurements and should be considered in future analyses.

There are other plausible contributors. One important consideration is indoor air.

Participants in the NHANES study likely spend most of their time indoors, where CO₂ concentrations often exceed 1000 ppm in poorly ventilated spaces. Other studies show time spent indoors has increased over the past two decades.

The NHANES dataset doesn’t capture this parameter, so we can’t directly assess this contribution. However, if more time indoors is contributing, it means total CO₂ exposure is rising even faster than atmospheric trends suggest. This arguably reinforces rather than alleviates the concern.

Other factors, such as shifting dietary patterns, changing rates of obesity, differences in physical activity and even variations in sample collection or processing across survey cycles, could also be important.

Can our bodies cope?

Some critics have argued that, based on what we know about how our bodies manage blood chemistry, we should have no trouble compensating for future increases in atmospheric CO₂, even under worst-case climate scenarios. For example, the lungs can increase ventilation and the kidneys can adjust to produce more bicarbonate.

For most healthy individuals, small long-term increases in outdoor CO₂ are not expected to meaningfully change the levels of bicarbonate, calcium or phosphorus in the blood.

This makes the population-level trends we observed puzzling. They could reflect a confounding rather than a direct CO₂ effect, but they do highlight how little data we have on long-term, real-world exposure.

A lack of long-term data

The argument that we can cope easily with higher CO₂ is based on short-term responses. Whether the same reasoning applies when CO₂ levels are higher across a person’s entire life remains largely untested.

There is, however, a growing body of evidence across many species which shows that even modest, environmentally relevant increases in CO₂ can produce subtle but measurable physiological effects.

In humans, short-term exposure at concentrations commonly found indoors (1000–2500 ppm) has been linked to reduced cognitive performance and changes in brain activity, though the mechanisms aren’t fully understood.

These new findings highlight a gap in evidence about long-term, real-world CO₂ exposure and human physiology. Unfortunately, there simply aren’t any studies assessing the physiological effects of breathing slightly elevated CO₂ over a lifetime.

This is particularly important for children, who will experience the longest cumulative exposure. And that’s why it’s vital to investigate this area further.

What this means

Our findings are not suggesting people will become suddenly unwell when atmospheric CO₂ reaches a certain level. What the data show is a signal that warrants attention.

If rising atmospheric CO₂ is contributing to gradual shifts in blood chemistry at a population level, then the composition of the atmosphere should be monitored alongside traditional climate indicators as a potential factor in long-term public health.

Reducing CO₂ emissions remains crucial for limiting global warming. Our findings suggest it may also be important for safeguarding aspects of human health that we’re only just beginning to understand.

Alexander Larcombe, Associate Professor and Head of Respiratory Environmental Health, The Kids Research Institute Australia; Curtin University and Philip Bierwirth, Emeritus Research Associate, Australian National University

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

Categories : DermatologyTags :

Copper Peptides: These Powerful Molecules are Worth the Skincare Hype

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Picture by Macrovector on Freepik

Ahmed Elbediwy, Kingston University and Nadine Wehida, Kingston University

Peptides have become one of the skincare industry’s most popular ingredients. It’s no wonder why, with evidence showing these powerful molecules hold the secret to healthier, firmer and more radiant skin.

But out of the many peptides that exist, one in particular has been gaining attention lately in the beauty industry: copper peptides.

It’s not surprising that copper peptides are garnering so much attention. This peptide is special because of its ability to multitask – with research showing that not only does it help make the skin firmer and more supple, it also protects the skin from damage.

The human body naturally produces many types of peptides. Each supports vital body functions, acting like tiny building blocks of life. Many help form the foundation of essential proteins – such as collagen and elastin, which help keep skin healthy and youthful.

The three main types of peptides in cosmetics are: carrier peptides, signal peptides and neurotransmitter-inhibiting peptides.

Carrier peptides aid in wound repair by physically transporting important minerals into the cells to initiate repair.

Signal peptides can prevent ageing by stimulating the activation of the skin’s fibroblasts – specialised skin cells that produce substances such as collagen, a protein which helps maintain the skin’s elasticity.

Neurotransmitter-inhibiting peptides act like botulinum toxin, relaxing facial muscles by blocking the signals that make them contract. This may reduce wrinkles.

Copper peptides are actually a type of carrier peptide. They’re produced naturally by your body. But as we age, the concentration of copper peptides in our bodies drops. Applying synthetic, lab-made versions – found in creams, serums and masks – can help replenish these molecules and help your skin.

Copper peptides were first discovered in 1973. Research found that these molecules aided wound healing, which is why the first commercialised carrier peptide in 1985 was designed to deliver copper into wounded tissue.

After gaining research attention for this role, further studies examined what other functions copper peptides had on the skin. Researchers found that they had anti-ageing, anti-inflammatory and renewing properties and also supported hair growth.

Copper peptides act as little helpers that tell your skin cells to repair and rebuild themselves. They do this by boosting collagen and elastin, key proteins that keep your skin feeling smooth and firm.

Copper peptides have been also found to reduce inflammation and calm skin redness, too. But perhaps most crucially, they have been found to act as antioxidants, fighting damage caused by pollution and the sun’s ultraviolet rays.

On top of that, copper peptides improve wound healing. This is why they’re often used after cosmetic treatments – such as face and neck lifts and micro-needling – that can damage the skin. Copper infused wound dressings are also used to help chronic wounds heal faster.

Overall, skin cell studies have shown that copper peptides increase collagen production, improve skin thickness and skin elasticity. Clinical trials and lab tests confirm these benefits, making copper peptides one of the most researched anti-ageing ingredients.

For best results, you might want to try applying it twice a day – first in the morning so it can act as a potent antioxidant, then in the evening so it can replenish collagen overnight.

Copper peptides can also penetrate the skin more effectively when delivered with microneedles, which makes them even more useful in advanced skincare products.

Copper peptides v other peptides

Other peptides do work well on the skin – such as palmitoyl-based peptides and acetyl hexapeptide-8 peptide – both of which fight wrinkles. But these both work differently to copper peptides.

Palmitoyl peptides signal the skin to make more collagen, while acetyl hexapeptide-8 relaxes facial muscles to reduce expression lines, acting like a less expensive version of botulinum toxin.

Copper peptides stand out among these other peptides because they can do the work of multiple peptides in one. Copper peptides boost collagen, improve skin healing and fight oxidative stress. This appears to make them better at preventing the signs of ageing.

Some skin cell studies show they work even better when combined with other well known skincare ingredients, such as hyaluronic acid (which boosts hydration).

However, some combinations of peptides can cause copper peptides to be unstable – making them fall apart. This could increase skin sensitivity, especially when combined with peptides, such as vitamin A and C.

Copper peptides themselves can also cause, in a few people, some skin irritation and mild allergic reactions. If you find you experience these symptoms after using copper peptides, stop use immediately.

Copper peptides are more than just a trend – they’re backed by science. They help keep skin healthy and speed up healing. They might even play a role in future cancer treatments.

Research has shown copper peptides turn on genes that tell damaged cancer cells to shut themselves down and stop replicating. They’ve also been shown to fix other genes that control cell growth and repair.

If you’re curious about skincare, copper peptides may be worth incorporating into your daily routine. Just remember that good, healthy skin also needs other measures – such as sunscreen, hydration and a healthy lifestyle.

Ahmed Elbediwy, Senior Lecturer in Cancer Biology & Clinical Biochemistry, Kingston University and Nadine Wehida, Senior Lecturer in Genetics and Molecular Biology, Kingston University

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

Categories : Antibiotics Diet and NutritionTags :

Honey from Australian Wildflowers has Potent Power to Kill Bacteria

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Photo by Benyamin Bohlouli on Unsplash

Kenya Fernandes, University of Sydney

Before antibiotics and antiseptics, healers across ancient Egypt, Greece, and China reached for honey to treat wounds. Archaeological evidence shows humans have been harvesting and collecting honey for thousands of years – and for much of that time, we understood it to be more than just food.

Today, honey sits in most kitchen cupboards as a perfectly ordinary pantry staple. But honey has never entirely shed its medicinal reputation. And modern research shows us why: it possesses genuine antimicrobial properties, capable of killing or inhibiting a wide range of bacteria, including drug-resistant strains.

This matters now more than ever. Antimicrobial resistance – where bacteria evolve to survive drugs designed to kill them – is one of the defining public health crises of our time. Infections caused by these resistant microbes are becoming harder and more expensive to treat, creating an urgent need for alternative therapies.

Our new study, published in the journal MicrobiologyOpen, shows honeys from Australia’s native flora might be a big part of the solution.

What did we do?

We analysed 56 honey samples collected from more than 35 apiaries across New South Wales. Many samples came from landscapes recovering from the 2019–2020 bushfires. Most were derived from native Australian plants such as eucalyptus, leptospermum and melaleuca.

We tested the honeys against two common bacterial pathogens: Staphylococcus aureus (golden staph) and E. coli – both among the six leading causes of deaths associated with antibiotic resistance. For each sample we measured the minimum concentration needed to stop bacterial growth. The lower the concentration, the more potent the honey.

We also carried out comprehensive chemical profiling, measuring sugars, organic acids, amino acids, enzymes and a wide range of plant-derived compounds. Statistical and machine-learning analyses helped us identify which chemical features best explained antibacterial strength.

What did we find?

More than three-quarters of the honey samples stopped bacterial growth even when the honeys were diluted to 10% or less. This places Australian native flora honeys alongside some of the world’s most potent varieties.

The most striking factor was floral diversity.

Honeys from mixed floral sources – where bees foraged across multiple native plant species rather than a single species – were consistently the most antimicrobial.

This potency wasn’t due to any single compound but to a chemically rich combination.

Multiple bioactive factors – substances that have a measurable effect on living cells or tissues – worked together to inhibit bacteria. These included naturally produced hydrogen peroxide, plant-derived phenolic compounds (naturally occurring chemicals that plants produce as part of their own defence systems), and antioxidants.

When bacteria encounter honey, this combination acts on several fronts at once. The low moisture content draws water out of bacterial cells, while the acidity disrupts their metabolism. Hydrogen peroxide damages their cellular structures, and phenolic and antioxidant compounds interfere with their ability to function and reproduce.

The strength of mixed floral honeys may also reflect the health of the bees themselves.

Access to diverse forage keeps colonies well nourished. And healthier bees produce more biologically active honey as their enzymes help integrate and activate the plant compounds into a complex antimicrobial mixture.

What does this mean for antimicrobial resistance?

Honey won’t replace antibiotics for serious or systemic infections.

But for topical applications – chronic wounds, burns, or surgical site infections – it is a genuinely promising option. Because honey attacks bacteria through multiple simultaneous mechanisms, resistance is far less likely to emerge than with single-target drugs. Our team is now exploring these applications in more detail.

Australia is particularly well-placed to lead in bioactive honey production. Around 70% of Australian honey comes from native plants. These plants are found not only in forests but also across farmland, regional landscapes, and urban green spaces.

Our findings show that prioritising floral diversity over monoculture isn’t just good for ecosystems – it produces more potent honey. With the beekeeping industry under serious pressure from bushfires, floods, and now the varroa mite, protecting and restoring florally-rich landscapes is critical: for bee health, for industry resilience, and for expanding our natural antimicrobial toolkit.

In the meantime, the next jar of Australian honey you buy may just be doing more good than you realise.

Kenya Fernandes, Research Fellow, Faculty of Science, University of Sydney

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

Categories : CancerTags :

Ibuprofen: How an Everyday Drug Might Offer Protection Against Cancer

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Photo by Towfiqu barbhuiya: https://www.pexels.com/photo/bottle-with-pills-11361813/

Dipa Kamdar, Kingston University; Ahmed Elbediwy, Kingston University, and Nadine Wehida, Kingston University

Ibuprofen is a household name – the go-to remedy for everything from headaches to period pain. But recent research suggests this everyday drug might be doing more than easing discomfort. It could also have anti-cancer properties.

As scientists uncover more about the links between inflammation and cancer, ibuprofen’s role is coming under the spotlight – raising intriguing questions about how something so familiar might offer unexpected protection.

Ibuprofen belongs to the non-steroidal anti-inflammatory drugs (NSAIDs) family. The connection between NSAIDs and cancer prevention isn’t new: as far back as 1983, clinical evidence linked sulindac – an older prescription NSAID similar to ibuprofen – to a reduced incidence of colon cancer in certain patients. Since then, researchers have been investigating whether these drugs could help prevent or slow other cancers too.

NSAIDs work by blocking enzymes called cyclooxygenases (COX). There are two main types. COX-1 helps protect the stomach lining, maintains kidney function, and plays a role in blood clotting. COX-2, on the other hand, drives inflammation.

Most NSAIDs, including ibuprofen, inhibit both, which is why doctors recommend taking them with food rather than on an empty stomach.

Ibuprofen and endometrial cancer

A 2025 study found that ibuprofen may lower the risk of endometrial cancer, the most common type of womb cancer, which starts in the lining of the uterus (the endometrium) and mainly affects women after menopause.

One of the biggest preventable risk factors for endometrial cancer is being overweight or obese, since excess body fat increases levels of oestrogen – a hormone that can stimulate cancer cell growth.

Other risk factors include older age, hormone replacement therapy (particularly oestrogen-only HRT), diabetes, and polycystic ovary syndrome. Early onset of menstruation, late menopause, or not having children also increase risk. Symptoms can include abnormal vaginal bleeding, pelvic pain, and discomfort during sex.

In the Prostate, Lung, Colorectal, and Ovarian (PLCO) study, data from more than 42,000 women aged 55–74 was analysed over 12 years. Those who reported taking at least 30 ibuprofen tablets per month had a 25% lower risk of developing endometrial cancer than those taking fewer than four tablets monthly. The protective effect appeared strongest among women with heart disease.

Interestingly, aspirin – another common NSAID – did not show the same association with reduced risk in this or other studies. That said, aspirin may help prevent bowel cancer returning.

Other NSAIDs, such as naproxen, have been studied for preventing colon, bladder, and breast cancers. The effectiveness of these drugs seems to depend on cancer type, genetics, and underlying health conditions.

Ibuprofen’s broader potential

Ibuprofen’s possible cancer-protective effects extend beyond endometrial cancer. Studies suggest it may also reduce risk of bowel, breast, lung, and prostate cancers.

For example, people who previously had bowel cancer and took ibuprofen were less likely to experience recurrence. It has also been shown to inhibit colon cancer growth and survival, and some evidence even suggests a protective effect against lung cancer in smokers.

Inflammation is a hallmark of cancer and ibuprofen is, at its core, anti-inflammatory. By blocking COX-2 enzyme activity, the drug reduces production of prostaglandins, chemical messengers that drive inflammation and cell growth – including cancer cell growth. Lower prostaglandin levels may slow or stop tumour development.

But that’s only part of the story. Ibuprofen also appears to influence cancer-related genes such as HIF-1α, NFκB, and STAT3, which help tumour cells survive in low-oxygen conditions and resist treatment.

Ibuprofen seems to reduce the activity of these genes, making cancer cells more vulnerable. It can also alter how DNA is packaged within cells, potentially making cancer cells more sensitive to chemotherapy.

A word of caution

But not all research points in the same direction. A study involving 7,751 patients found that taking aspirin after an endometrial cancer diagnosis was linked to higher mortality, particularly among those who had used aspirin before diagnosis. Other NSAIDs also appeared to increase cancer-related death risk.

Conversely, a recent review found that NSAIDs, especially aspirin, may reduce the risk of several cancers – though regular use of other NSAIDs could raise the risk of kidney cancer. These conflicting results show how complex the interaction between inflammation, immunity, and cancer really is.

Despite the promise, experts warn against self-medicating with ibuprofen for cancer prevention. Long-term or high-dose NSAID use can cause serious side effects such as stomach ulcers, gut bleeding, and kidney damage.

Less commonly, they may trigger heart problems like heart attacks or strokes. NSAIDs also interact with several medications, including warfarin and certain antidepressants, increasing the risk of bleeding and other complications.

The idea that a humble painkiller could help prevent cancer is both exciting and provocative. If future studies confirm these findings, ibuprofen might one day form part of a broader strategy for reducing cancer risk, especially in high-risk groups.

For now, experts agree it’s wiser to focus on lifestyle-based prevention: eating anti-inflammatory foods, maintaining a healthy weight and staying physically active.

Everyday medicines may yet hold surprising promise, but until the science is settled, the safest prescription for cancer prevention remains the oldest one: eat well, move often, and listen to your doctor before reaching for the pill bottle.

Dipa Kamdar, Senior Lecturer in Pharmacy Practice, Kingston University; Ahmed Elbediwy, Senior Lecturer in Cancer Biology & Clinical Biochemistry, Kingston University, and Nadine Wehida, Senior Lecturer in Genetics and Molecular Biology, Kingston University

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

Categories : Substance Use UrogenitalTags :

Ketamine is Giving More Young People Bladder Problems – An Expert Explains

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A growing number of people in the UK are using ketamine recreationally. Photo by Colin Davis on Unsplash

Heba Ghazal, Kingston University

Urology departments in England and Wales have reported seeing an increase in the number of 16- to 24-year-olds being admitted for bladder inflammation associated with ketamine use.

This appears to coincide with an increase in ketamine use – with the number of adults and teens entering treatment for ketamine abuse last year jumping substantially compared to even just a few years previously.

Ketamine abuse can have many affects on the bladder, causing frequent urination, night-time urination, sudden urges, leakage, inflammation, pain in the bladder or lower back and blood in the urine. These symptoms can be severe, make daily life very difficult and may even be permanent in some cases.

Ketamine was first approved in 1970 for human use as an anaesthetic. More recently, studies have suggested that ketamine used at low doses may have antidepressant effects.

But a growing number of people are now using ketamine recreationally. It acts as a dissociative drug, causing users to feel detached from themselves and their surroundings. It can produce hallucinogenic, stimulant and pain-relieving effects, which last one to two hours.

Users typically snort or smoke powdered ketamine, or inject liquid ketamine or mix it into drinks in order to experience the drug’s effects. Snorting usually produces stronger effects and more noticeable symptoms than swallowing it.

Ketamine users can develop tolerance to the drug quickly, needing higher doses to get the same effects. This is probably due to the body and brain adapting to become more efficient at breaking down the drug. Frequent users often need to take twice the amount of occasional users to get the same effect.

Bladder damage

Frequent, high-dose ketamine use can cause serious damage to the bladder, urinary tract and kidneys. In severe cases, the bladder may need to be removed.

The first recorded cases of ketamine affecting the bladder were reported in Canada in 2007, where nine people who used ketamine recreationally had severe bladder problems and blood in their urine. Later, a bigger study in Hong Kong found the same issues in 59 people who had used ketamine for more than three months.

Ketamine, as with any other drug, is metabolised in the body where it’s broken down and excreted in urine.

When ketamine is broken down, it turns into chemicals that can seriously harm the bladder. When these by-products stay in contact with the urinary tract for a long time, they irritate and damage the tissue.

The bladder is damaged first, because it holds urine the longest. Later, the ureters (tubes connecting the kidney to the bladder) and the kidneys can also be affected.

Over time, the bladder can shrink and become stiff, causing strong urinary symptoms. The ureters can become narrow and bent, sometimes described as looking like a “walking stick.” This can lead to backed-up urine in the kidneys (hydronephrosis).

Ketamine also increases oxidative stress, which damages cells and causes bladder cells to die. This breaks the protective bladder lining, making it leaky and overly sensitive.

All these changes can make the bladder overactive, extremely sensitive and painful, often causing severe urges to urinate and incontinence.

Bladder damage from ketamine use happens in stages.

In the first stage, the bladder becomes inflamed. This can often be reversed by stopping ketamine and taking certain medication – such as anti-inflammatory drugs, pain relievers or prescription drugs that reduce bladder urgency and help the bladder lining heal.

In the second stage, the bladder can shrink or become stiff. In this stage, treatment is similar to stage one, but a bladder wash may also be required. This is where a catheter is used to put liquid medication directly into the bladder. The drug coats the bladder’s inner lining, helping to restore its protective layer and reduce inflammation.

Botulinum toxin injections may also be used to relax the bladder and reduce pain and urgency. Stopping ketamine remains essential to prevent further damage.

In the final stage, permanent damage occurs to the bladder and kidneys. Over time, if the kidneys are affected, it can lead to kidney failure. Dialysis (a treatment where waste products and excess fluid are filtered from the blood) or even surgery may be required to repair kidney function and the urinary system.

Although ketamine has been a class B drug since 2014, it’s unfortunately affordable and accessible – costing as little as £3 per gram in some parts of the UK. Raising awareness about the risks of ketamine use is essential to prevent these serious health problems.

Heba Ghazal, Senior Lecturer, Pharmacy, Kingston University

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

Categories : CancerTags :

The Next Cancer Breakthrough may be Stopping it Before it Starts

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Source: Unsplash CC0

Ahmed Elbediwy, Kingston University and Nadine Wehida, Kingston University

Cancer treatment follows a familiar pattern: doctors spot symptoms, diagnose the disease and start treatment. But scientists are now exploring a radical shift in how we tackle cancer. Instead of waiting for tumours to appear, they want to catch the disease decades before it develops.

This approach is called “cancer interception”. The idea is simple: target the biological processes that cause cancer long before a tumour ever forms.

Researchers are hunting for subtle early warning signs. These include genetic mutations that quietly build up in our cells, giving them advantages against our immune defences.

They’re also looking at precancerous lesions like moles or polyps, and early visible changes in tissue. All of these appear long before cancer becomes obvious.

Large genetic studies reveal that as people age, their bodies accumulate small groups of mutated cells called clones that grow silently. Scientists have studied this particularly well in blood. These clones can help predict who might develop blood cancers like leukaemia, and the genetics, inflammation and environmental factors strongly influence them.

Crucially, doctors can measure and track these changes over time. This opens up possibilities for early intervention.

A 16-year study followed around 7,000 women and uncovered how these mutations work. Some mutations helped clones multiply faster, while others made them particularly sensitive to inflammation.

When there was inflammation, these sensitive clones expanded. Breaking down these patterns helps researchers identify people with a higher chance of developing cancer later.

Not a sudden event

The research reveals something fundamental about cancer. It’s not a sudden event that instantly produces a tumour.

Instead, cancer develops through a slow, multi-step process with detectable warning signs along the way. These early signs could become powerful targets for stopping cancer before it starts.

Scientists are developing blood tests to spot cancer long before symptoms appear. These tests, called multi-cancer early detection tests (MCEDs for short), search for tiny fragments of DNA in the blood.

MCEDs work by looking for circulating tumour DNA, or ctDNA – DNA fragments that cancerous or precancerous cells release into the bloodstream. Even very early cancers shed this DNA, so the tests might detect disease long before it shows up on a scan.

The results so far look promising. MCEDs can boost survival rates through early detection, especially for colorectal cancer. When doctors diagnose colorectal cancer at stage one, 92% of patients survive five years. But when they catch it at stage four, only 18% survive that long.

If colon cancer is caught at stage one, most patients are still alive after five years. Credit: National Cancer Institute

The tests aren’t perfect, though. They miss some cancers entirely, and positive results still need follow-up tests to confirm.

Even so, research suggests MCEDs could become crucial for catching cancers that usually go unnoticed until much later. The potential to save lives is significant.

Heart doctors already use a similar approach. They calculate a person’s risk using age, blood pressure, cholesterol and family history, then prescribe drugs like statins years before a heart attack happens.

Cancer researchers want to copy this model. They envision combining genetic mutations, environmental factors and MCED results to guide early cancer prevention.

But cancer differs from heart disease in important ways. Cancer doesn’t follow a predictable path, and some early lesions shrink or never progress.

There’s also the risk of over-diagnosis. Being told you’re at higher risk when you feel perfectly healthy creates anxiety.

Cancer prevention tools also vary widely in their effectiveness, unlike statins that work broadly across different cardiovascular risk groups. The risk-based model shows promise, but needs careful handling.

Treating cancer risk instead of cancer itself raises difficult ethical questions. When someone feels completely healthy, judging whether intervention will truly help them becomes harder.

There’s a danger of causing unnecessary worry or harm. Scientists warn that doctors sometimes overestimate benefits and underestimate risks, particularly for older adults.

MCED tests bring their own ethical concerns. Accuracy isn’t the only issue that matters.

The tests sometimes flag cancer when none exists, leading to follow-up scans and biopsies that patients don’t actually need. The anxiety from all of this carries a high cost, both for patients and the healthcare system.

If these tests are expensive or only available privately, they could make health inequalities worse. This concern hits hardest in low-income countries.

In the US, the medicines regulator is investigating how MCED blood tests should work. They’re examining how reliable the tests need to be and what follow-ups doctors should require to keep patients safe.

The UK is following suit. The National Cancer Plan for England, published on February 4, 2026, commits to providing 9.5 million extra diagnostic tests through the NHS each year by March 2029.

The plan also states that ctDNA biomarker testing will continue in lung and breast cancer. It will extend to other cancers if proven to be cost effective.

What all this shows is clear. Cancer doesn’t suddenly appear; it’s a steady process that begins decades earlier. Catching it before it grows could save countless lives. The question now is how to do that safely, fairly and effectively.

Ahmed Elbediwy, Senior Lecturer in Cancer Biology & Clinical Biochemistry, Kingston University and Nadine Wehida, Senior Lecturer in Genetics and Molecular Biology, Kingston University

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

Categories : Metabolic DisordersTags :

High Cholesterol and Insulin Resistance are Rising Among Young South Africans – What that Means for Public Health

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Photo by Elizeu Dias on Unsplash

Themba Titus Sigudu, University of the Witwatersrand

In a small mining town in South Africa’s Limpopo province, young people are showing worrying signs of diseases that were once thought to affect only older adults.

These include type 2 diabetes, high blood pressure, high cholesterol, obesity and insulin resistance. This is not unique to Limpopo or South Africa. It reflects a global trend, where young adults in many low- and middle-income countries are increasingly experiencing early-onset metabolic diseases due to rapid urbanisation, lifestyle changes, unhealthy diets and reduced physical activity.

The World Health Organization says non-communicable diseases now account for 75% of all non-pandemic-related deaths globally. Also, 82% of premature deaths before age 70 occur in low- and middle-income countries.

I’m a public health researcher specialising in epidemiology, metabolic health, infectious diseases and environmental health. My colleagues and I conducted a study in the town of Lephalale and found that many young adults there have abnormal cholesterol levels. They also have reduced sensitivity to insulin, a condition known as insulin resistance.

Both are key risk factors for type 2 diabetes and heart disease.

Our findings suggest that these health problems are appearing much earlier in life than expected. This is particularly concerning in communities undergoing rapid social and economic change, where access to health services and screening programmes remains limited.

New jobs, new lifestyles

Lephalale, formerly known as Ellisras, offers a window into these transitions. Once a quiet rural area in the north of South Africa, it has changed rapidly over the past two decades. It is now the site of expanding mining and industrial activities, driven by the expansion of coal mining operations and the development of power stations.

This industrial growth has attracted thousands of workers from surrounding provinces and neighbouring countries, bringing new economic opportunities. It is also reshaping daily life. Increasingly, residents are doing sedentary work and eating energy-dense diets, including fast food. These lifestyle transitions make Lephalale an important setting for studying emerging health risks in young adults.

Long hours sitting at work and reduced physical activity create fertile ground for metabolic disorders. When people eat more processed, high-fat, high-sugar foods and move less, the body begins storing excess energy as fat.

Over time, this can lead to weight gain, elevated blood glucose and abnormal cholesterol levels. These changes make it harder for the body to regulate insulin, causing insulin resistance, the first step towards type 2 diabetes. Also, inactivity and poor diet increase unhealthy cholesterol and triglycerides (types of fat in the blood), raising the risk of heart disease. In rapidly transitioning communities, these health shifts can happen quickly.

Non-communicable diseases such as diabetes, hypertension and heart disease are now among the leading causes of death in South Africa. In 2020, diabetes was reported to be the second biggest underlying cause of death in South Africa, accounting for 6.6% of all deaths.

Our research

We examined 781 young adults aged 18 to 29 years living in Lephalale as part of a long-running study. We have been tracking health patterns in this community since 1992.

Participants provided fasting blood samples that were analysed for glucose, insulin and cholesterol levels. We grouped them into diabetic and non-diabetic categories based on clinical definitions used by the American Diabetes Association.

The results were striking:

  • Diabetic participants had significantly higher total cholesterol, low-density lipoprotein (the “bad” cholesterol) and triglycerides, and lower levels of high-density lipoprotein (the “good” cholesterol) than their non-diabetic peers.
  • Over half (52.7%) of the diabetic group had high total cholesterol, compared with 23% of non-diabetic participants.
  • Insulin resistance, when the body needs more insulin to manage blood sugar, was also much higher among diabetics.
  • Even some non-diabetic participants showed early signs of these metabolic changes.

Unhealthy cholesterol patterns and poor insulin sensitivity tend to occur together, each making the other worse. This combination sets the stage for early heart disease, stroke and diabetes.

Why young adults?

Most public-health strategies focus on older adults because that’s when chronic diseases usually become visible.

But our research adds to growing evidence that the seeds of non-communicable diseases are planted early, often in young adulthood or even adolescence.

Young adults in rural or semi-urban areas may seem healthy, yet many are already developing risks due to diet changes, stress and limited exercise opportunities. The modernisation of small towns, while positive economically, brings hidden health costs.

Without early detection, these individuals may enter middle age already carrying high risk of health problems. This will put pressure on health systems that are already stretched.

What makes this community unique?

Lephalale may be changing, but it still lacks many of the urban services, infrastructure and health resources found in South Africa’s big cities.

Health resources are scarce, and screening for cholesterol or insulin resistance is rare. Public clinics focus on infectious diseases such as HIV or tuberculosis. Silent metabolic disorders go unnoticed until symptoms appear.

Our study shows that rapid industrialisation without parallel investment in public-health education and preventive services risks creating a generation of young adults who are chronically unwell by their thirties.

What can be done?

Three priorities stand out:

Early screening and prevention

Regular cholesterol and glucose testing should be part of routine primary-care visits, especially for adults under 30. Mobile health campaigns, school outreach and workplace screenings could help identify those at risk.

Community-based education

Local awareness campaigns must make the link between diet, physical activity and metabolic health easy to understand. They should show, for example, how frequent consumption of fried or sugary foods contributes to cholesterol build-up and insulin resistance.

Healthy-environment policies

Urban planners and municipalities can support healthy lifestyles by ensuring there are safe spaces for exercise. They must also limit marketing of unhealthy foods, and encourage availability of affordable, nutritious options. Similar “health-in-all-policies” approaches have shown success in other countries. such as Finland’s long-running HiAP strategy, which reduced cardiovascular disease rates and improved population health outcomes.

Young people should be in peak health. Without intervention, today’s young adults risk becoming tomorrow’s chronic-disease patients, burdening families, workplaces and health systems.

Themba Titus Sigudu, Lecturer, University of the Witwatersrand

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

Categories : Obstetrics & GynaecologyTags :

Africa’s Hidden Stillbirth Crisis: New Report Exposes Major Policy and Data Gaps

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Mary Kinney, University of Cape Town

Photo by ManuelTheLensman on Unsplash

Nearly one million babies are stillborn in Africa every year. Behind every stillbirth is a mother, a family and a story left untold. Most of these are preventable, many unrecorded, and too often invisible. Each number hides a moment of heartbreak, and every uncounted loss represents a missed opportunity to learn and to act.

As a public health researcher specialising in maternal and newborn health, I have spent the past two decades working on strengthening health systems and quality of care across Africa. My research has focused on understanding how health systems can prevent stillbirths and provide respectful, people-centred care for women and newborns. Most recently, I was part of the team that led a new report called Improving Stillbirth Data Recording, Collection and Reporting in Africa. It is the first continent-wide assessment of how African countries record and use stillbirth data.

The study, conducted jointly by the Africa Centres for Disease Control and Prevention, the University of Cape Town, the London School of Hygiene & Tropical Medicine and the United Nations Children’s Fund, surveyed all 55 African Union member states between 2022 and 2024, with 33 countries responding.

The burden of stillbirths in Africa is staggering. Africa accounts for half of all stillbirths globally, with nearly eight times higher rates than in Europe. Even stillbirths that happen in health facilities may never make it into official statistics despite every maternity registry documenting this birth outcome.

Part of the challenge is that there are multiple data systems for capturing births and deaths, including stillbirths, like routine health information systems, civil registration and other surveillance systems. But these systems often don’t speak to each other either within countries or between countries. This data gap hides both the true burden and the preventable causes.

Despite advances in several countries to prevent stillbirths, large gaps remain, especially on data systems. Only a handful of African countries routinely report stillbirth data to the UN, and many rely on outdated or incomplete records. Without reliable, comparable data, countries cannot fully understand where and why stillbirths occur or which interventions save lives.

Strengthening stillbirth data is not just about numbers; it is about visibility, accountability and change. When countries count every stillbirth and use the data for health system improvement, they can strengthen care at birth for mothers and newborns and give every child a fair start in life.

Findings

The report was based on a regional survey of ministries of health. This was followed by document reviews and expert consultations to assess national systems, policies and practices for stillbirth reporting and review.

The report reveals that 60% of African countries have national and sub-national committees responsible for collecting and using stillbirth data, which produce national reports to respective health ministries. But data use remains limited. Capacity gaps, fragmented systems and insufficient funding prevents many countries from translating information into action.

To guide investment and accountability, the report categorises countries into three readiness levels:

  1. Mature systems needing strengthening, such as Kenya, Rwanda and Uganda. These countries have consistent data flows but need more analysis and use.
  2. Partial systems requiring support, where reporting mechanisms exist but are not systematically implemented, like Ghana, Malawi and Tanzania.
  3. Foundational systems still being built, including fragile or conflict-affected countries like South Sudan and Somalia. Here, policies and structures for data collection and use remain absent.

The findings show both progress and persistent gaps. Two-thirds of African countries now include stillbirths in their national health strategies, and more than half have set reduction targets. Nearly all countries report that they routinely record stillbirths through their health sectors using standard forms and definitions, yet these definitions vary widely. Most systems depend on data reported from health facilities. But the lack of integration between health, civil registration and other data systems means that countless losses never enter national statistics.

For example, if a woman delivers at home alone in Mozambique and the baby is stillborn, the loss is only known to the family and community. Without a facility register entry or civil registration notification, the death never reaches district or national statistics. Even when a stillbirth occurs in a health centre, the health worker may log it in a facility register but not report it to the civil registration system. This means the loss of the baby remains invisible in official data.

What this means

Stillbirths are a sensitive measure of how health systems are performing. They reflect whether women can access timely, quality care during pregnancy and at birth. But unlike maternal deaths, which are often a benchmark for health system strength, stillbirths remain largely absent from accountability frameworks.

Their causes, like untreated infections, complications during labour, or delays in accessing emergency caesarean sections, are often preventable. The same interventions that prevent a stillbirth also reduce maternal deaths. These improve newborn survival, and lay the foundation for better health and development outcomes in early childhood.

Accurate data on stillbirths can guide clinical care and direct scarce resources to where they are needed most. When data systems are strong, leaders can identify where and why stillbirths occur, track progress and make informed decisions to prevent future tragedies.

The analysis also highlights promising signs of momentum. Over two-thirds of countries now reference stillbirths in national health plans, an important marker of growing political attention. Several countries are moving from isolated data collection to more coordinated, system-wide approaches. This progress shows that change is possible when stillbirths are integrated into national health information systems and supported by investment in workforce capacity, supervision and data quality.

What’s needed

Africa has the knowledge, evidence and experience to make change happen.

The report calls for harmonised definitions, national targets and stronger connections and data use between the different data sources within and across African countries. Above all, it calls for collective leadership and investment to turn information into impact, so that every stillbirth is counted, every death review leads to learning and no parent grieves alone.

The author acknowledges and appreciates the partners involved in developing the report and the support from the Global Surgery Division at UCT.

Mary Kinney, Senior Lecturer with the Global Surgery Division, University of Cape Town

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

Categories : Neurodegenerative Diseases New Compounds and TreatmentsTags :

A New Treatment for Huntington’s Disease Is Genuinely Promising – But Here’s Why We Still Need Caution

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Photo by Anna Shvets

Bryce Vissel, UNSW Sydney

Imagine knowing in your 20s or 30s that you carry a gene which will cause your mind and body to slowly unravel. Huntington’s disease is inherited, relentless and fatal, and there is no cure. Families live with the certainty of decline stretching across generations.

Now, a new treatment is being widely reported as a breakthrough.

Last week, gene therapy company uniQure announced that a one-time brain infusion appeared to slow the disease in a small clinical study.

If confirmed, this would not only be a landmark for Huntington’s disease but potentially the first time a gene therapy has shown promise in any adult-onset neurodegenerative disorder.

But the results, which were announced in a press release, are early, unreviewed and based on external comparisons. So, while these findings offer families hope after decades of failure, we need to remain cautious.

What is Huntington’s disease?

Huntington’s is a rare but devastating disease, affecting around five to ten people in 100,000 in Western countries. That means thousands in Australia and hundreds of thousands worldwide.

Symptoms usually start in mid-life. They include involuntary movements, depression, irritability and progressive decline in thinking and memory. People lose the ability to work, manage money, live independently and eventually care for themselves. Most die ten to 20 years after onset.

The disease is caused by an expanded stretch of certain DNA repeats (CAG) in the huntingtin gene. The number of repeats strongly influences when symptoms begin, with longer expansions usually linked to earlier onset.

Looking for a treatment

The gene that causes Huntington’s disease was identified in 1993, 32 years ago. Soon afterwards, mouse studies showed that switching off the mutant huntingtin protein even after symptoms had begun could reverse signs and improve behaviour.

This suggested lowering the toxic protein might slow or even partly reverse the disease. Yet for three decades, every attempt to develop a therapy for people has failed to show convincing clinical benefit. Trials of huntingtin-lowering drugs and other approaches did not slow progression.

What is the new treatment?

The one-time gene therapy, called AMT-130, involves brain surgery guided by MRI. Surgeons infuse an engineered virus directly into the caudate and putamen brain regions, which are heavily affected in Huntington’s.

The virus carries a short genetic “microRNA” designed to reduce production of the affected huntingtin protein.

By delivering it straight into the brain, the treatment bypasses the blood–brain barrier. This natural wall usually prevents medicines from entering the central nervous system. That barrier helps explain why so many brain-targeted drugs have failed.

What did they find?

Some 29 patients received treatment, with 12 in each group (one low-dose, and one high-dose) followed for three years. According to uniQure, those given the higher dose declined much slower than expected.

The study compared how much participants’ movement, thinking and daily function declined, compared to a matched external group from a global Huntington’s registry (meaning they weren’t part of the study). The company claimed those given the higher dose had a 75% slowing in their decline.

On a functional scale focused on independence, the company reported a 60% slowing in decline for the higher dose group.

Other tests of movement and thinking also favoured treatment. Nerve-cell damage in spinal fluid was lower for study participants than would be expected for untreated patients.

Why should we be cautious?

These findings are an early snapshot of results reported by the company, not yet peer-reviewed. The study compared treated patients to an external matched control group, not people randomised to placebo at the same time. This design can introduce bias. The numbers are also small – only 12 patients at the three-year mark – so we can’t draw solid conclusions.

The company reports the therapy was generally well tolerated, with no new serious adverse events related to the drug since late 2022. Most problems were related to the neurosurgical infusion itself, and resolved. But in a disease that already causes such severe symptoms, it is often hard to know what counts as a side effect.

The company uniQure has said it plans to seek regulatory approval in 2026 on the basis of this dataset.

Regulators will face difficult decisions: whether to allow access sooner before all the questions and uncertainties are addressed – based on the needs of a community with no effective options – and wait for further data while people are being treated, or to insist on larger trials that confirm results before approval.

What does it mean?

If upheld, these results represent the first convincing signs that a gene-targeted therapy can slow Huntington’s disease. They may also be the first evidence of benefit from a gene therapy in any adult-onset neurodegenerative disorder. That would be a milestone after decades of failure.

But these results do not prove success. Only larger, longer and fully peer-reviewed studies will show whether this treatment truly changes lives. Even if approved, a complex neurosurgical gene therapy may not be easily accessible to all patients.

The company has said the drug’s price would be similar to other gene therapies – which can cost over A$3 million per patient – and will have the added cost of brain surgery.

The takeaway

For families who carry this gene, the hope is profound. But caution is just as important.

We may be witnessing the first credible step toward slowing an inherited adult-onset neurodegenerative disease, or just an early signal that may not hold up.

Ultimately, only time and rigorous science will show whether this treatment delivers the benefits so urgently needed.

Bryce Vissel, Cojoint Professor, School of Clinical Medicine, UNSW Sydney

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

Categories : UncategorizedTags :

Prediabetes Remission Possible Without Dropping Pounds, Our New Study Finds

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Photo by Kenny Eliason on Unsplash

Andreas L. Birkenfeld, University of Tübingen and Reiner Jumpertz-von Schwartzenberg, University of Tübingen

There’s a long-held belief in diabetes prevention that weight loss is the main way to lower disease risk. Our new study challenges this.

For decades, people diagnosed with prediabetes – a condition affecting up to one in three adults depending on age – have been told the same thing by their doctors: eat healthily and lose weight to avoid developing diabetes.

This approach hasn’t been working for all. Despite unchanged medical recommendations for more than 20 years, diabetes prevalence continues rising globally. Most people with prediabetes find weight-loss goals hard to reach, leaving them discouraged and still at high risk of diabetes.

Our latest research, published in Nature Medicine, reveals a different approach entirely. We found that prediabetes can go into remission – with blood sugar returning to normal – even without weight loss.

About one in four people in lifestyle intervention programmes bring their blood sugar back to normal without losing any weight. Remarkably, this weight-stable remission protects against future diabetes just as effectively as remission achieved through weight loss.

This represents a significant shift in how doctors might treat overweight or obese patients at high risk for diabetes. But how is it possible to reduce blood glucose levels without losing weight, or even while gaining weight?

The answer lies in how fat is distributed throughout the body. Not all body fat behaves the same way.

The visceral fat deep in our abdomen, surrounding our internal organs, acts as a metabolic troublemaker. This belly fat drives chronic inflammation that interferes with insulin – the hormone responsible for controlling blood sugar levels. When insulin can’t function properly, blood glucose rises.

In contrast, subcutaneous fat – the fat directly under our skin – can be beneficial. This type of fat tissue produces hormones that help insulin work more effectively. Our study shows that people who reverse prediabetes without weight loss shift fat from deep within their abdomen to beneath their skin, even if their total weight stays the same.

Subcutaneous fat can be beneficial. Photo by Andres Ayrton on Pexels

We’ve also uncovered another piece of the puzzle. Natural hormones that are mimicked by new weight-loss medications like Wegovy and Mounjaro appear to play a crucial role in this process. These hormones, particularly GLP-1, help pancreatic beta cells secrete insulin when blood sugar levels rise.

People who reverse their prediabetes without losing weight seem to naturally enhance this hormone system, while simultaneously suppressing other hormones that typically drive glucose levels higher.

Targeting fat redistribution, not just weight loss

The practical implications are encouraging. Instead of focusing only on the scales, people with prediabetes can aim to shift body fat with diet and exercise.

Research shows that polyunsaturated fatty acids, abundant in Mediterranean diets rich in fish oil, olives and nuts, may help reduce visceral belly fat. Similarly, endurance training can decrease abdominal fat even without overall weight loss.

This doesn’t mean weight loss should be abandoned as a goal – it remains beneficial for overall health and diabetes prevention. However, our findings suggest that achieving normal blood glucose levels, regardless of weight changes, should become a primary target for prediabetes treatment.

This approach could help millions of people who have struggled with traditional weight-loss programmes but might still achieve meaningful health improvements through metabolic changes.

For healthcare providers, this research suggests a need to broaden treatment approaches beyond weight-focused interventions. Monitoring blood glucose improvements and encouraging fat redistribution through targeted nutrition and exercise could provide alternative pathways to diabetes prevention for patients who find weight loss particularly difficult.

The implications extend globally, where diabetes represents one of the fastest-growing health problems. By recognising that prediabetes can improve without weight loss, we open new possibilities for preventing a disease that affects hundreds of millions worldwide and continues rapidly expanding.

This research fundamentally reframes diabetes prevention, suggesting that metabolic health improvements – not just weight reduction – should be central to clinical practice. For the many people living with prediabetes who have felt discouraged by unsuccessful weight-loss attempts, this offers renewed hope and practical alternative strategies for reducing their diabetes risk.

Andreas L. Birkenfeld, Professor, Diabetology, Endocrinology and Nephrology, University of Tübingen and Reiner Jumpertz-von Schwartzenberg, Professorship for Clinical Metabolism and Obesity Research, University Hospital and Medical Faculty, University of Tübingen

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