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One in Eight Cancers are Likely Caused by an Infection Worldwide – New Study

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John (Eddie) La Marca, WEHI (Walter and Eliza Hall Institute of Medical Research) and Sarah Diepstraten, WEHI (Walter and Eliza Hall Institute of Medical Research)

Around 12% of the world’s total cancer cases in 2024 were likely caused by an infection, according to new research from the World Health Organization (WHO).

The study, published today in The Lancet Oncology, analysed the frequency and causes of different cancers, specifically examining the role of infections.

It linked 2.3 million new cancer cases to an infection. Most were caused by just five pathogens: Helicobacter pylori (4%), human papillomavirus, or HPV (4%), hepatitis B (2%), Epstein-Barr virus (1%) and hepatitis C (under 1%). These infections can cause more than 20 different types of cancer, including stomach, liver, blood and cervical cancers.

So, how can an infection cause cancer? And does this mean these cancers are preventable?

Did we already know about this link?

Some of the study authors have been researching this field for around thirty years. Their previous work investigated cancer cases caused by infections in 1990, 2002, 2008, 2012, and 2018. The proportion of cancer cases caused by infections may appear to have dropped during those years (from a high of 18% in 2002), but the authors stress these comparisons cannot really be made confidently, as the sources and quality of the data have changed over time.

In fact, the latest study wasn’t trying to compare between the years. Instead, it aims to highlight where controlling and preventing infections can help to reduce cancer rates.To make sense of this, it helps to know how infection is linked to cancer. Extensive research has dissected the molecular mechanisms behind this link, and we now know there are various ways infections can cause cancer.

How can a virus cause cancer?

A virus can (directly or indirectly) change the genes of the cell it infects (the host cell), making that cell more likely to grow out of control and eventually become a cancer.There are three main ways viruses can do this.

The first is by turning off the ability of a cell to destroy itself (for example, by inactivating the TP53 protein) or to stop dividing (for example, by inactivating the RB protein). A healthy cell would normally try to do these things if infected by a virus. The second way a virus can cause cancer is by inserting its own DNA into the host cell’s DNA, which can accidentally disrupt genes that control cell death or division (like those above). The third way is when the virus itself carries a gene that causes cancer (an oncogene). In many cases, the virus has picked up these by accident from another organism. The link between viruses and cancer is actually foundational to modern cancer science, and has helped scientists uncover the direct link between genetics and cancer we now take for granted.

What about bacteria and parasites?

It’s not just viruses that cause cancer. Infections from bacteria or parasites – such as Helicobacter pylori (best known for causing stomach ulcers), or Opisthorchis viverrini (a liver fluke, a type of parasitic worm) – can also lead to cancer. However, these work more indirectly than viruses. Long-term (chronic) infection by these types of organisms can cause significant stress to different tissues. Inflammation, normally a part of the body’s immune response, can then become overactive, damaging the tissues further. These stresses can result in cancer-causing DNA damage in cells, or lead to mistakes during cell division as the body tries to rapidly produce new cells to repair tissue damage. In both cases, the cells acquire genetic mutations that put them on the road towards becoming cancer.

Many cancers are preventable

Of course, there may be other mechanisms linking infections and cancer that we don’t know about but, overall, the connection between infections and cancer is indisputable. Critically, what this tells us – and what this new study into the rates of cancers caused by infections reinforces – is that many cancers are preventable.

In Australia, one of the best examples of preventing cancers caused by infections is the human papillomavirus (HPV) vaccine. This vaccine protects against certain strains of HPV strongly associated with cervical cancer, and is available to adolescents in Australia. Since the program began in 2007, HPV infections dropped by 90% among people eligible to receive the vaccine. Because of its success, Australia could be on track to eliminate cervical cancer by 2035. However, vaccination rates among 15-year-olds have fallen from 85.7% in 2020 to 79.5% in 2024, which is concerning. As is the case for all vaccines, a high proportion of the population need to be vaccinated to also protect those who, for health reasons, cannot be vaccinated. For HPV, the WHO and Australian target is to vaccinate 90% of 15-year-old girls by 2030.

Sadly, the new study also highlights that around 75% of cancers caused by infections were found in low- and middle-income countries.Treating infections that can lead to cancer – such as HIV, H. pylori, and hepatitis B and C – is one way to reduce cancer rates. Preventative measures also play a major role, including vaccinations, condoms and disease screening. However, the availability of these programs in poorer countries can be limited, and so access continues to be a major equity issue in combating cancer.

The authors would like to acknowledge the contribution of Amali Cooray from the Olivia Newton-John Cancer Research Institute to this article.

John (Eddie) La Marca, Senior Research Officer, Blood Cells and Blood Cancer, WEHI (Walter and Eliza Hall Institute of Medical Research) and Sarah Diepstraten, Senior Research Officer, Blood Cells and Blood Cancer Division, WEHI (Walter and Eliza Hall Institute of Medical Research) This article is republished from The Conversation under a Creative Commons license. Read the original article.

Categories : Medical Research & TechnologyTags :

The Bias in Medical Research: Africa Carries a Huge Disease Burden but Is Missing from Clinical Trials

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Bamba Gaye, MD, MPH, MSc, PhD, Emory University

Modern medicine prides itself on being a universal science, built on evidence from clinical trials.

But there’s a bias in medical research. While Africa accounts for roughly 25% of the global disease burden and 19% of the global population, the continent’s people are largely invisible in some clinical trials.

The scale of the erasure is revealed in a landmark study of 2,472 randomised controlled trials globally published between 2019 and 2024.

I led this team of researchers, who scrutinised the world’s most influential medical publications to quantify African representation. They included the New England Journal of Medicine, The Lancet, the Journal of the American Medical Association, Nature Medicine, and the British Medical Journal. There were also three leading cardiovascular journals in the study: Circulation, the European Heart Journal and the Journal of the American College of Cardiology.

I am a physician-scientist working at the intersection of cardiometabolic epidemiology and biomedical data science. I also focus on large-scale population studies in Africa and data-driven cardiovascular prevention.

Randomised controlled trials are a cornerstone of evidence-based medicine. Introduced in the mid-20th century, they rigorously evaluate the safety and effectiveness of treatments by randomly assigning participants to different groups. This is done to minimise bias. Trials like these have been central to major medical breakthroughs, from cardiovascular therapies to vaccines. They continue to guide clinical decisions and the development of new treatments worldwide.

What we discovered

Our findings show a profound imbalance in the global clinical research landscape. Across the five most prestigious general medical journals, only 3.9% of trials were conducted exclusively in Africa. In cardiovascular health, the numbers drop to a statistical whisper. Of the major trials published in leading cardiology journals, just two studies (0.6%) were conducted solely on African soil.

This is a crisis of scientific accuracy. When clinical trials exclude African populations, they produce evidence that lacks “external validity”. This refers to how well the results of a study can be generalised beyond the participants. It asks whether findings from a clinical trial will still hold true when applied to different populations, settings, or real-world conditions.

Without that validity, doctors are essentially conducting unmonitored experiments on millions of patients every day.

Modern medicine cannot claim to be universal if entire populations remain invisible in the evidence base. Biology, health systems and disease patterns are not identical across the world.

The gap and why it matters

Many treatments used across the continent are based on evidence generated in non-African populations, raising concerns about their applicability.

Moreover, most Africa-based trials still focus on infectious diseases, despite the rising burden of non-communicable diseases such as cardiovascular disease.

Emerging evidence shows that genetics, environment and diet can radically alter how a body responds to a drug. It therefore makes no medical sense that an entire continent is left out of the trial net.

There’s also evidence showing that certain treatments have different safety profiles in Black patients. Diabetes and gout are just two examples. So are certain common blood pressure medications, such as angiotensin-converting enzyme (ACE) inhibitors. Research shows that they carry a three- to four-fold higher risk of severe, life-threatening side effects in people of African descent compared to other populations.

When clinical trials exclude populations, doctors are forced to extrapolate findings from one population and apply them to another.

The study also highlights a dangerous lag between global research funding and the evolving reality of African health. The new data show that nearly 76% of trials conducted exclusively in Africa focused on infectious diseases. But the continent is undergoing a massive epidemiological shift. Non-communicable diseases – heart disease, stroke, and diabetes – now account for about 38% of all deaths in many African nations.

The middle class in Africa has tripled to 300 million people from roughly 100 million people in the early 2000s. More people are now living long enough with lifestyles that increase the risk of chronic conditions such as heart disease, diabetes, and hypertension. Consequently, there is a growing need and market for long-term treatments that manage these diseases, rather than short-term therapies for infections. Yet cardiovascular trials continue to be discouraged.

Even within the continent, the data show deep “black holes” of information. South Africa accounted for over 62% of all trials conducted on the continent. Central Africa, a region that’s home to more than 180 million people, was virtually non-existent in the global research record. It contributed less than 3% of the continent’s limited trial output. Possible reasons include South Africa’s decades of cumulative investment, seen in stronger academic hubs, research governance, experienced trial units, and more established sponsor relationships. Other regions face barriers like fewer resourced research institutions, less access to trial platforms, and sometimes language and publication issues that can reduce visibility in top-tier journals.

The inequity extends into the hierarchy of science itself. Even when African sites are included in large, multicontinental trials, they are often relegated to the role of “recruitment hubs” rather than scientific partners. Our study found that African scientists led only 3.6% of multicontinental trials that included an African site.

Towards a new era of African science

Africa should not simply be a location where studies are conducted.

It must be a place where research is conceived, led and interpreted. The current model creates a cycle of external dependence where international institutions manage the funding and the data. This leaves local research systems fragile and unable to translate evidence into national policy.

There is need for “ring-fenced” funding for African-led research, the development of regional trial networks, and a mandate for medical journals to report on the diversity of trial populations.

There are signs of a rising momentum. Organisations like Alliance for Medical Research in Africa are working to equip a new generation of African investigators. Africa must create a research ecosystem that is too important for the global community to ignore.

Bamba Gaye, MD, MPH, MSc, PhD, Adjunct professor, Emory University

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

Categories : Pain ManagementTags :

Melatonin May Help Ease Chronic Muscle and Joint Pain, New Study Suggests

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Dipa Kamdar, Kingston University

Melatonin is best known for helping us sleep. But a new study suggests it might have another surprising use: easing muscle and joint pain.

Produced naturally by the pineal gland in the brain at night, melatonin helps regulate the body’s sleep-wake cycle. That’s why this hormone is widely used as a treatment for insomnia and jet lag.

Sleep and pain are closely linked (poor sleep can make pain feel worse, and pain can make sleep harder). But melatonin may also reduce pain directly. Researchers believe it dampens pain signals in the brain and spinal cord, reduces inflammation, calms overactive nerves and protects cells from oxidative stress – the cellular wear and tear caused when harmful molecules build up.

In the new study, researchers combined the results of 23 clinical trials involving over 2,000 participants to identify overall patterns. These trials looked at melatonin for long-term muscle and joint pain as well as pain after surgery.

Overall, melatonin reduced both pain and sleep problems in people with chronic muscle and joint pain. But the improvements were modest. On average, pain scores fell by about nine points on a 100-point scale. That’s within the range reported for some anti-inflammatory drugs in similar studies, although the two treatments haven’t been directly compared.

Melatonin’s effects may also depend on whether people already have sleep problems or other long-term health conditions. Most of the chronic pain studies included people who already had poor sleep to begin with, but none of the trials looked at results separately for people with and without sleep issues. Because of this, it’s unclear whether melatonin works better for people who struggle with sleep or whether the effects are similar for everyone.

The findings were much less convincing for pain after surgery. Melatonin did not make a noticeable difference to pain or sleep. One analysis found a tiny improvement (about 2.5 points on a 100-point pain scale), but this is far below what would matter to patients recovering from surgery.

The benefits in chronic muscle and joint pain are modest. Based on the current evidence, melatonin should be seen as a possible add-on treatment rather than a replacement for established therapies. The evidence suggests melatonin could complement treatments such as physiotherapy, exercise and anti-inflammatory medicines rather than replace them.

What we still don’t know

There is also still a lot we don’t know. The trials in this study used a wide range of doses, from 1mg to 10mg, and the researchers couldn’t determine which dose worked best.

There were hints that longer treatment helped more in chronic pain, but this was based on only a few studies. There is also very little evidence on the effectiveness of higher doses, even though they appear safe in other studies.

Melatonin is widely used and generally considered safe for short-term use, but it can cause side-effects, such as daytime sleepiness, dizziness, headaches and nausea.

People with liver or kidney conditions, or those with autoimmune conditions like rheumatoid arthritis, should speak with a doctor or pharmacist before taking it.

It is also worth noting that melatonin is regulated very differently around the world. In the US, melatonin is sold as a dietary supplement, meaning people can buy it easily in supermarkets and online without medical advice. But in the UK, melatonin is a prescription-only medicine and is only licensed for short-term sleep problems and jet lag.

For now, the findings suggest melatonin may offer modest relief for some people with chronic muscle and joint pain, particularly if poor sleep is part of the problem. It’s unlikely to replace established treatments, but it could eventually earn a place alongside them. Larger, well-designed trials will be needed before doctors can say with confidence who is most likely to benefit.

Dipa Kamdar, Senior Lecturer in Pharmacy Practice, Kingston University

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

Categories : Mental HealthTags :

Women Report Poor Sleep Despite a Good Night’s Rest – While Men Overestimate Their Own Sleep Quality

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Men reported sleeping better than they objectively did, while the opposite was true for women. Photo by Ketut Subiyanto on Pexels

Torbjörn Åkerstedt, Karolinska Institutet

Disturbed sleep is a common problem — and one that has many serious consequences beyond feeling tired the next day. Research has linked insomnia and poor sleep to early mortality and diseases including diabetes and cardiovascular disease.

Women often report experiencing disturbed sleep more frequently than men. They also constitute the majority of patients in sleep clinics. Yet strangely, some studies show worse objective sleep quality in men – a bit of a paradox.

To understand what might explain the paradox, my colleagues and I conducted a study that directly compared sleep quality ratings and objective sleep measures between men and women.

We found that women complained more of sleep problems – but slept objectively much better than men. We think this paradox can probably be explained by men overestimating their sleep quality as they’re less able to perceive how often they wake up at night.

A total of 238 randomly selected women participated in the study, plus 238 men who were matched on age and BMI with the women to ensure similar participants were compared against each other.

Sleep was recorded in each participant’s home using a recorder that measured brain waves (electroencephalography – EEG), muscle tension (electromyography – EMG) and eye movements (electrooculography – EOG). These devices tracked what stage of sleep a participant was in and for how long, how much time they spent awake and how quickly they fell asleep.

A researcher visited the participant’s home in the evening, mounted the recording equipment and left. The participant went to bed and awoke at their usual time.

In the morning, the participant rated the degree of difficulty they had falling asleep, if their sleep was restless, if they woke up early, how often they thought they’d woken up, how long it took them to fall asleep, how long they slept and their overall sleep quality.

The sleep recording was scored by a sleep technician based on visual inspection of the EEG, EOG and EMG recordings. The data was then analysed to understand the objective quality of each participant’s sleep and its relation to gender and age.

Analyses were also adjusted for factors such as gender, age and alcohol consumption and smoking, which may affect sleep.

Sleep quality

The results show that women subjectively reported significantly lower sleep quality than men. Yet women actually had considerably fewer nighttime awakenings, less stage one (superficial) sleep and higher sleep efficiency (they spent more time asleep while in bed). Women also experienced more stage three (deep) sleep and slept longer (400 minutes versus 382 minutes for men).

When women did wake up at night, they spent more time awake on average. Photo by Cottonbro on Pexels

The results suggest that women objectively had a good nights’ sleep, compared to men. The only variable that suggests worse sleep in women was that when they did wake up at night, they spent more time awake than men did – around nine minutes each time for women versus just under seven minutes for men.

It only takes around five minutes of being awake at night for a person to remember it the next morning. This may explain why women were better able to remember if they’d woken up the night before and estimate how many times they had. Men, on the other hand, grossly underestimated their number of awakenings (by 72% compared to women’s 37%).

For other quantitative measures, like time to fall asleep, sleep duration and time awake, men and women were equally good at estimating their objective values. And they were relatively correct.

We took this further and found that men who only woke up for a short period of time during the night (around eight minutes or so each time they woke up) often didn’t remember they had.

When this group of men was removed, no gender difference in subjective sleep quality remained. This suggests that men with short nighttime awakenings report better sleep quality than would be expected from their objective sleep measures as they didn’t remember they’d woken up.

It’s also noteworthy that men’s objective sleep deteriorated faster with age than women. This was particularly obvious for stage three sleep. While women aged over 65 got around 80 minutes of stage three sleep each night, men had only 53 minutes. Among those between 30 and 50 years of age, the amount was similar for men and women (around 70 minutes).

Sleep and wellbeing

A key reason women may complain of having a worse nights’ sleep than they objectively had may therefore be the amount of time they spent awake when they woke up, making it easier for them to notice. Likewise, men may overestimate their sleep quality because they’ve spent less time awake when they’ve woken up, so they don’t remember it happening.

Both findings would work towards reducing subjective sleep quality in women and increasing it in men. We assume then, that the experience of awakenings has an important influence on subjective sleep quality.

As our study was only conducted over one night, it will be important for future research to investigate whether these findings remain when participants are studied over longer periods of time.

Future studies may also want to explore the reasons for poor sleep in men – especially since common sources of disturbed sleep, such as alcohol, smoking and BMI, were all adjusted for in our analysis. Researchers may also want to investigate why men’s sleep becomes objectively worse as they get older.

Our research illustrates how sleep quality doesn’t just involve the physiological aspects of sleep. It also includes our own subjective experiences, which can impact our wellbeing and how rested we feel.

It also suggests that because many men overestimate their sleep quality, they may also overlook any sleep problems they’re experiencing. This could mean that some men aren’t getting help for conditions that could be affecting their health and wellbeing.

Torbjörn Åkerstedt, Senior Professor of Psychology, Department of Clinical Neuroscience, Karolinska Institutet

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

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South African Scientists Make Breakthrough in Decoding Cancer’s Most Effective Survival Strategy

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Scanning electron micrograph of just-divided HeLa cells. Zeiss Merlin HR-SEM. Credit: National Center for Microscopy and Imaging Research

Kevin Naidoo, University of Cape Town

In the intricate biology of the human body, organs such as the breast, the colon and the lungs are lined with a defensive barrier known as the epithelium. At the heart of this barrier sits a remarkable protein called Mucin-1 (MUC1). In a healthy body, MUC1 is like a sentinel.

It stands on the cell wall, draped in a complex “armour” of long chains of sugar molecules (carbohydrates), where it serves as a physical shield against bacteria, viruses and toxins. Crucially, it communicates with the immune system, telling our natural defences when the body is under threat.

But in the case of cancer, this guardian exchanges its sugar coat armour for shorter sugar chains and so turns into a traitor. It stops sending danger signals to the immune system and instead binds to the immune cells, creating an anti-inflammatory microenvironment that promotes tumours.

The team I lead at the Scientific Computing Research Unit at the University of Cape Town is home to computer modelling experts and experimental chemical biology research scientists. The molecular details of this MUC1 alteration, which contributes to the transformation of normal cells into tumour cells, were recently published in Nature Communications, and provide a new look at exactly how this process happens.

By developing a novel “test-tube” synthetic biology approach, we modelled and decoded the molecular assembly line reorganisation that allows cancer to “redecorate” MUC1, turning it from a protective shield into a cloak of invisibility. We used our own computational chemistry algorithms to map the exact sugar coating positions that create a tumour-promoting environment.

Understanding the location and nature of the MUC1 sugars that prevent the immune system from detecting tumours provides the foundation for our laboratory and others in the field to develop cancer vaccines, biomarkers and therapeutics.

This South African-led discovery represents a major leap forward in our ability to decode one of cancer’s most effective survival strategies.

The problem: a malignant makeover

In a normal cell, the sugar molecules attached to MUC1 are long and complex. The process of attaching sugars is called glycosylation. In cancer cells, however, this process goes haywire. The sugar molecules are often cut short or altered, creating “aberrant” structures like the Tn and sialyl-Tn (sTn) antigens. These are specific types of sugar-protein combinations that are tags for tumour cells.

These altered sugars do two dangerous things: they allow the tumour to evade detection by the immune system, and they actively trigger the process of turning a normal cell into a cancerous one.

Because MUC1 is found in so many different types of cancer, the US National Cancer Institute has ranked it as the most accesible target.

To stop the cascading effect of the MUC1 changes from normal to tumour cells, scientists first had to understand exactly how the “assembly line” breaks down.

The discovery: relocating the factory

Our research team set out to do something ambitious: recreate the transition from a healthy sugar coating to a cancerous one in a laboratory setting.

In normal cells, the enzymes that build these sugar chains (long molecules) live in a part of the cell called the Golgi apparatus, the cell’s “packaging and delivery centre”. We built an in vitro (test-tube) model to simulate what happens when these conditions change. We discovered that in tumour cells, the enzymes responsible for starting the sugar chains are relocated to another part of the cell, the endoplasmic reticulum, essentially the cell’s “factory floor”.

This relocation changes everything. Here, the enzymes are no longer inhibited by the usual cellular checks and balances. They take over the sugar sites on the MUC1 protein, creating the foundation for the cancerous Tn antigen.

To take the study even further, we used quantum chemistry. We simulated the behaviour of atoms and molecules at the most fundamental level to find out where these changes are most likely to happen. We identified a specific location on the MUC1 protein, known as the T13 site, which cancer enzymes prefer. This specific interaction is what drives the massive increase in the sTn antigen seen in malignant tumours.

Why this matters: from lab to patient

Understanding the “how” and the “where” of these sugar changes is the first step towards stopping them. The research didn’t stop at the test tube; the team is already looking at what this means for patients.

The next phase of the research, as detailed in a recent paper in Glycobiology, involves building a sophisticated “systems biology” computational model. A model can connect the changes in the MUC1 sugar coating to the behaviour of immune cells. For example, scientists found that when these cancerous sugars interact with macrophages (a type of white blood cell), they trigger the release of specific signals that tell the tumour to grow and spread.

We are refining these details for various types of cancer. We are comparing common forms of breast cancer with more aggressive, currently untreatable types to see if the “sugar code” differs between them.

By using this accurate, atomic-level data to build computer models of the entire biological system, we hope to identify new drugs that can block these signals. The goal is to move towards precision medicine: treatments that can strip away cancer’s sugar shield, allowing the patient’s own immune system to finally see and destroy the tumour.

Kevin Naidoo, Professor of Scientific Computing and Physical Chemistry, University of Cape Town

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

Categories : Mental HealthTags :

What Causes Depression? What We Know, Don’t Know and Suspect

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Photo by Sydney Sims on Unsplash

Caroline Gurvich, Monash University; Eveline Mu, Monash University, and Jayashri Kulkarni, Monash University

Depression is a complex and deeply personal experience. While almost everyone has periods of sadness, low mood or grief, depression is different. Major depressive disorder is persistent, interferes with day-to-day activities, and can affect work, life and relationships.

One in five people will experience depression in their lifetime. Women are nearly twice as likely as men to develop it – a disparity that emerges around puberty and persists into adulthood.

But what causes it? The short answer is: many different things.

While there are various theories, we know brain chemistry, genes, hormones, stress, lifestyle and personality can all play a role. How these interact can vary greatly from one person to another.

An imbalance of brain chemicals?

The traditional “monoamine hypothesis” of depression was proposed more than half a century ago, in the 1950s. This theory suggests the root cause of depression is a deficiency in certain brain chemicals (or neurotransmitters) called monoamines – serotonin, dopamine and norepinephrine.

Several antidepressants have been developed based on this. They primarily work by increasing levels of monoamines such as serotonin.

However, it has become clear that the “chemical imbalance” explanation is an oversimplification.

Research over the past few decades has not found consistent evidence that individuals with depression always have lower levels of serotonin, or any single neurotransmitter.

And while antidepressants can increase serotonin levels within hours, improvements in mood typically take days or weeks to emerge. This delay suggests depression cannot be explained by neurotransmitter levels alone.

Current understanding recognises depression as a complex condition influenced by multiple interacting factors, including genetics, trauma, medications, diet, sleep patterns and social interactions.

Genetic factors can increase your risk

According to one 2021 review, around 30 to 50% of the risk someone will develop depression may be inherited.

No single “depression gene” has been found. But large studies have identified over 100 genetic risk markers on chromosomes.

The genetic risk of depression is also thought to be “polygenic”. This means multiple genetic variants (each carrying a small effect) interact and collectively contribute to someone’s genetic risk.

One important and longstanding research question has been whether there is a genetic reason women are more likely than men to develop depression.

In 2025, a large study revealed substantial overlap between men and women’s genetic risk. However, on average, women with depression tend to carry more of the genetic variants linked to depression.

This suggests that there may be a greater genetic risk for depression in women and perhaps a stronger environmental influence on depression risk in men.

Still, carrying a genetic risk does not mean someone will necessarily develop depression. The interplay between genetic and non-genetic factors is complex.

Hormones and biological sex

Hormones – the body’s chemical messengers – also play an important role in mood and wellbeing.

In women, estrogen and progesterone levels naturally fluctuate across different life stages, including the menstrual cycle, pregnancy, the period after childbirth and menopause.

Our 2025 review found some women are more sensitive to these normal hormonal shifts, and more vulnerable to mood disturbances.

For instance, in the premenstrual phase of their cycle, around 8% of women experience a severe depression, with intense mood swings and irritability, called premenstrual dysphoric disorder.

Similarly, the dramatic hormonal changes during pregnancy and after childbirth (combined with sleep loss and stress) can contribute to postnatal depression.

Later in life, fluctuating and falling estrogen levels during the menopause transition years may also increase the risk of developing depressive symptoms or intensify existing ones.

Hormonal contraceptives – which contain synthetic forms of estrogen and progesterone – have also been linked to mood changes and depression symptoms. In fact, these are some of the most common reasons women stop taking them.

These effects appear to depend on the specific type and amount of progesterone used in the formulation.

These findings show how hormones can act as biological triggers, and help explain why women are statistically more likely to experience depression at certain stages of life.

The effect of hormones on depression in men has predominantly focused on the protective role of testosterone, but findings remain inconclusive.

Stress is another important factor

Chronic or repeated stress can have lasting effects on both the brain and body.

When we experience stress, our bodies activate the hypothalamic–pituitary–adrenal (HPA) axis, also known as the “stress-response system”. This helps us cope by maintaining balance in our body – what scientists call physiological homeostasis.

But when stress is constant or overwhelming, this system can become dysregulated. Stressful or traumatic experiences in childhood – such as neglect, abuse or severe adversity – can also disrupt the stress-response system.

As a result, we overproduce the stress hormone cortisol. High or persistent cortisol levels can alter the structure and functioning of key brain areas (the hippocampus and pre-frontal cortex) which are important for regulating mood and memory.

Cortisol can also trigger the release of inflammatory chemicals, which then cross into the brain or influence neural signals, leading to mood changes and depressive symptoms.

Importantly though, not everyone who experiences stressful life events becomes depressed.

Some people may be more vulnerable due to genetic factors, early life adversity or differences in brain chemistry. Others might cope with the same stress without developing depression or other conditions.

Does personality play a role?

Personality traits also influence how people respond to stress and may affect their risk of developing depression.

People who tend to experience anxiety, sadness and self-doubt are more likely to develop depressive symptoms, especially after stressful events. In contrast, traits such as resilience, optimism, and emotional stability seem to protect against depression.

This suggests that personality plays an important role in shaping both vulnerability and resilience to depression.

Lifestyle choices can help lower your risk

These include not smoking, limiting alcohol use, eating a balanced diet, staying physically active, getting enough sleep, maintaining a healthy body weight and having social supports.

Research shows these healthy habits and lifestyle factors can have a protective effect on mental health. They may even reduce the impact of genetic risk factors for depression.

There’s no single cause – and no universal treatment

Depression arises from a mix of factors – biological (genes and hormones), psychological (personality and thoughts) and social (stress and life events).

Treatment options are based on all of these factors, as well as considering how severe the depression is and whether a person has responded to previous treatments.

While science has made some progress in understanding depression, what underpins each person’s experience is unique.

Caroline Gurvich, Associate Professor and Clinical Neuropsychologist, Monash University; Eveline Mu, Research Fellow in Women’s Mental Health, Monash University, and Jayashri Kulkarni, Professor of Psychiatry, Monash University

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

Categories : CancerTags :

Breakthrough Drug Nearly Doubles Survival with Advanced Pancreatic Cancer

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– an Oncologist Explains how Daraxonrasib Overcame an ‘Undruggable’ Disease

Pancreatic cancer. Credit: Scientific Animations CC BY-SA 4.0

Christopher Lieu, University of Colorado Anschutz

For a long time, the likelihood of surviving pancreatic cancer has been extremely low. For patients who were diagnosed with metastatic pancreatic cancer between 2015 and 2021, about 97% died within five years of their diagnosis.

Pancreatic cancer is so deadly in part because there are no effective screening tests, and it rarely causes noticeable symptoms in its earliest stages. By the time a patient experiences signs, such as jaundice – a yellowing of the skin – or abdominal pain, the cancer has often already spread to other organs.

As a gastrointestinal oncologist and researcher specialising in early-phase clinical trials, I have seen the critical need for more effective therapies for patients with pancreatic cancer. For decades, successfully targeting the central mechanism that causes the vast majority of pancreatic cancers was considered impossible.

However, that narrative is rapidly changing with a new drug that can shut down the key protein that drives pancreatic cancer, nearly doubling survival rates for patients with advanced stages of the disease.

‘Undruggable’ tumours

The standard treatment for advanced pancreatic cancer has historically relied on chemotherapy, potent drugs designed to kill rapidly dividing cells. While chemotherapy can slow the progression of the disease, its effectiveness is often limited by the ability of pancreatic cancer cells to develop resistance against these drugs.

Model of the 3D structure of KRAS, resembling a rough-looking blob with a molecule tucked inside
KRAS (blue) has been difficult for drugs to target. Fvasconcellos/Wikimedia Commons

Pancreatic cancer’s success lies in its genetics. More than 90% of pancreatic tumours are driven by mutations in a gene called KRAS. This gene codes for proteins that function as switches that turn cell growth on and off. When the KRAS gene is mutated, the switch becomes permanently stuck in the “on” position, commanding cancer cells to multiply endlessly.

For decades, scientists considered KRAS to be “undruggable.” The surface of the protein is exceptionally smooth, lacking the molecular pockets that standard drugs require to bind to and turn the switch off.

Because existing drugs haven’t been able to target this protein, treatment for pancreatic cancer has primarily relied on toxic drugs that act more like blunt instruments than precise tools. Chemotherapy attempts to control the disease through widespread cell destruction, causing significant collateral damage to healthy tissues that lead to side effects.

What is daraxonrasib?

A new drug called daraxonrasib offers a critical advance in treating metastatic pancreatic cancer.

Daraxonrasib is taken daily by mouth. Instead of binding to KRAS directly, it attaches to a molecule called cyclophilin A in cells that helps fold proteins into their final 3D structures. This protein complex is then able to bind to the active KRAS protein and shut down its ability to signal cancer cells to multiply.

The company developing the drug, Revolution Medicines, presented results on May 31, 2026, from its Phase 3 clinical trial of 500 patients with metastatic pancreatic cancer who had received prior treatment. Compared to standard chemotherapy, daraxonrasib nearly doubled overall survival from 6.7 months to 13.2 months after diagnosis. Overall, daraxonrasib reduced the risk of death for metastatic pancreatic cancer patients by 60%. https://www.youtube.com/embed/sIspXSWQn1w?wmode=transparent&start=0 Daraxonrasib nearly doubled survival for patients with advanced pancreatic cancer compared to chemotherapy.

The most common side effect is a prominent skin rash, which affected more than 86% of patients in the study. Patients also frequently dealt with stomatitis – painful swelling and sores inside the mouth – as well as diarrhoea, nausea and vomiting. However, patients taking daraxonrasib were far less likely to stop treatment due to severe side effects compared to chemotherapy, and they had improved quality of life with reduced pain.

Next steps for daraxonrasib

By successfully targeting the specific genetic mutation that drives the vast majority of pancreatic cancers, researchers have demonstrated that this “undruggable” disease is treatable with targeted therapy.

The immediate next step is regulatory review of the drug’s readiness for the clinic. With data now officially published, Revolution Medicines will use these findings to seek formal approval from the Food and Drug Administration and other global regulatory bodies.

Because advanced pancreatic cancer is notoriously difficult to treat, breakthrough therapies that demonstrate this kind of significant survival benefit are often granted expedited or priority review. When daroxonrasib becomes available to patients will depend on the review timeline. Should the drug obtain approval, it could be available in clinics within months.

For the broader landscape of drug development, this milestone represents a likely shift in pancreatic cancer treatment. I expect more clinical trials exploring combination therapies pairing KRAS inhibitors with other drugs to prevent tumours from developing resistance to treatment.

Should daraxonrasib succeed, it could help set the stage for more precise, personalised and effective treatments for pancreatic cancer in the years to come.

Christopher Lieu, Professor of Medical Oncology, University of Colorado Anschutz

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

Categories : Infection ControlTags :

Why Africa – and the World – Remain Dangerously Unprepared for the Next Pandemic

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Oyewale Tomori, Nigerian Academy of Science

As the news spread about the outbreak of Ebola in mid-May 2026, the World Health Organization (WHO) released a report about pandemics. The title was: A World on the Edge: Priorities for a Pandemic-Resilient Future.

The document was prepared by the WHO’s Global Preparedness Monitoring Board. It sets out why the world isn’t better prepared for pandemics a decade after Ebola exposed dangerous gaps. And six years after COVID-19 turned those gaps into a global catastrophe.

It adds that investment in pandemic preparedness has not kept pace with the rising risk of pandemics.

The Global Preparedness Monitoring Board is an independent monitoring and accountability body established in 2018 by the WHO and the World Bank. The aim was to strengthen preparedness for global health crises. It is composed of political leaders, agency principals and world-class experts. Its task is to provide assessments of global progress in building and sustaining the capacity to prevent, detect and respond to health emergencies.

The report was released during another Ebola epidemic. This time starting in the Democratic Republic of Congo. On 17 May the WHO declared the outbreak a public health emergency of international concern. This means that it is a risk to many countries through international spread and hence requires global coordinated efforts.

As a virologist and former global health administrator, I believe the monitoring board’s diagnosis and recommendations are vitally important for managing pandemics.

My first observation about the report is that its recommendations remain largely unimplemented by many countries. This is particularly true in Africa, where pandemics thrive and disease epidemics rage and ravage.

Africa needs to specially build trust in its own ability to prepare for and prevent disease outbreaks, and control them when they do occur.

To achieve this, and in line with the recommendations, Africa must sustain:

  • independent pandemic risk monitoring
  • health workforce capability and retention
  • equitable access to countermeasures such as vaccines
  • financing
  • political attention.

Independent pandemic risk monitoring

Using local resources and financing, African countries must own the solution to health through establishing data systems that uphold health sovereignty.

They must also ensure that data derived from surveillance, research and pathogen processing are securely managed and accountable to African institutions rather than foreign entities. Recent agreements with the US have brought this issue to the fore. Some were asking African countries to sign away their health data or prodigally release their precious pathogens in a barter exchange for donor funding.

But health data are an invaluable asset for public health, clinical management and research. They help countries identify diseases and develop vaccines and treatments.

What African countries should be doing instead is mobilising locally sourced counterpart funds. These should be used to create the local environment to support and enhance the capacity of indigenous scientists and researchers to develop innovations from national/natural pathogens for global benefits.

Two African health institutions should be at the centre of these endeavours: the WHO-Africa Region and the Africa Centers for Disease Control, an agency of the African Union. They must not compete, but collaborate and spearhead these efforts through centralised disease control and tracking scorecards.

Health workers

Fostering the well-being of health workforce results in growth, higher productivity, national pride and loyalty.

It also helps in long-term retention of health workers.

African countries need to prioritise capacity retention over capacity building. They must build and sustain a conducive work environment which involves physical workspace and psychological safety.

Availability of adequate resources is needed to function effectively and productively. This includes materials, laboratory facilities, supplies, reagents and consumables for a trained African health workforce and researchers.

Under such enabling conditions, the health workforce can focus on relevant and local health issues and find appropriate solutions to them.

Equitable access to countermeasures

Africa must not compromise on the ratification of international health pacts that guarantee fair technology transfer, intellectual property waivers, and robust regional manufacturing.

Countries must equally expand local production of laboratory diagnostic kits, vaccines and medical supplies as well as non-medical products. Such include gloves, personal protective equipment and masks.

This will reduce reliance on external donation and supply chains in and out of global crises.

Sustainable financing

The greater challenge for many African countries is the waste of available resources and spending on misplaced priorities.

To address this, governments must commit to sustained domestic investment in healthcare. At the same time they must use blended financing (involving both the public and private sectors) to close remaining gaps. Initiatives such as the African Epidemic Fund offer a practical model for building financial reserves for rapid, locally led responses. The fund, launched in 2025, is designed to mobilise funding to support preparedness and response efforts to combat public health threats on the continent. The African Epidemic Fund, though relatively new, must operate at the highest level of accountability. It must provide regular updates on contributions, projects supported and their impact on disease preparedness, prevention and control in Africa.

Sustained political attention

African leaders must keep pandemic preparedness high on the political agenda to ensure continuous resource allocation and accountability. The advocacy for preparedness must go beyond political campaign slogans. It must be driven by regional bodies like the African Union. Countries must then translate commitments into tangible national policies.

There can be no recess or holiday from pandemic preparedness.

African political leaders and elites, at the continental, national and sub-national levels, have crucial roles to play in achieving trusted community engagement and involvement for successful and reliable pandemic preparedness. Above all, there must be active community engagement and involvement.

Oyewale Tomori, Fellow, Nigerian Academy of Science

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

Categories : Mental HealthTags :

Why Lithium is Still the Gold Standard in Treating Bipolar Disorder

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Julia E. Marquez Arrico, Universitat de Barcelona

According to recent data from the Global Bipolar Cohort, only 29% of people with bipolar disorder are prescribed lithium. Despite being the “gold standard” for treating this mental health condition, we often prioritise perceptions over scientific reality, and neglect the best available treatment.

Lithium is not some complex molecule synthesised in a state-of-the-art laboratory. It is just an element, the third in the periodic table, and ever since the Australian psychiatrist John Cade discovered its therapeutic properties in 1949, it has maintained a relevance that no other psychotropic drug has been able to match.

This longevity is not a relic of the past, but a reflection of its clinical robustness. Despite decades of research and the constant emergence of new drugs, no alternative has shown comparable efficacy in the long-term prevention of manic and depressive episodes in bipolar disorder.

According to a review published in 2024, lithium is still “the mainstay treatment of mood disorders in general and in bipolar disorder specifically”. It is also the benchmark against which all other treatment options are compared, both for stabilising mood and reducing the risk of relapse.

It is the only mood stabiliser with proven efficacy in treating mania and depression, as well as in preventing relapses. Furthermore, recent studies confirm that it may also have neuroprotective properties, from the modulation of cellular pathways involved in neural plasticity to potential effects in preventing mild cognitive impairment and dementia.

These characteristics explain why international guidelines still rank it as the first-line treatment for bipolar disorder. A consensus published in 2025 stated that it should be prescribed more frequently, contrary to the unfounded reservations that still persist in clinical practice.

Suicide reduction

Above all, there is one aspect that sets lithium apart from other psychopharmaceutical drugs: its ability to reduce the risk of suicide. No other medication has demonstrated such a consistently protective effect.

A 2024 review highlighted that, despite the methodological difficulties in studying this statistically rare event, the body of evidence from clinical trials, observational studies and meta-analyses all points in the same direction: lithium reduces mortality and suicide attempts.

This is likely due to its ability to reduce impulsivity, stabilise extreme mood swings and prevent depressive relapses, all of which create the moments of greatest risk.

Beyond episodic treatment

Current research is also looking into lithium’s ability to alter the course of bipolar disorder. Not only does it stop episodes, but it also protects the brain, and evidence suggests that, unlike some antipsychotics, it improves brain connectivity and preserves verbal fluency.

In fact, there is very interesting data suggesting that it could reduce the risk of dementia by up to 50%. Even residual levels in drinking water appear to have a protective effect at a population level. Lithium is, in short, a molecule with exceptional neuroprotective potential.

But the neuroprotective effects do not stop there. Recent studies also suggest that lithium stimulates the production of brain-derived neurotrophic factor, a protein essential for neuronal survival and growth that is often reduced in patients with bipolar disorder.

In other words, it doesn’t just prevent the brain from deteriorating – it actively helps it to heal.

Blood monitoring and ‘precision medicine’

It is often argued that the need for blood tests to monitor lithium levels (the optimal therapeutic range is 0.6-0.8 millimoles per litre) is an inconvenience. However, from a rigorous clinical perspective, this monitoring is a safeguard, not a risk. It is what allows the dose to be adjusted to the exact biology of each patient, a form of “precision medicine” that we were already practising long before the term became fashionable.

We should also remember that many commonly used medicines – from anticoagulants to immunosuppressants – require the same kind of laboratory monitoring, yet they are not considered dangerous for that reason.

What lithium management requires is not fear, but rigour. So why is it prescribed less often? The answer is complex. It is partly due to pressure from the pharmaceutical industry to promote new, patentable molecules – lithium, being a natural element, cannot be patented. There is also a degree of clinical reluctance due to its narrow therapeutic window – it needs to be carefully controlled to ensure a safe yet effective dose.

However, international guidelines are clear: lithium should be the first choice. We cannot overlook it in favour of less effective alternatives simply because they appear more modern. This kind of mistake should not influence clinical practice.

Newer is not always better

Good psychopharmacology is not a question of chasing the latest developments, but of using the most appropriate treatment for each individual at every stage of their illness.

Lithium has a proven track record that spans decades, across areas that no other mood stabiliser can address simultaneously. It controls manic and depressive episodes, prevents suicide, and provides active neuroprotection. Three areas, in one single drug.

This does not mean it is right for absolutely everyone. Good psychopharmacology should always push back against fads and dogma alike, but discarding lithium’s use without ever seriously considering it deprives patients of an option that is, according to the evidence, categorically the best therapeutic option.

Our challenge today is not to reinvent the wheel, but to understand how best to use the therapeutic tools we already have. A drug doesn’t become outdated just because time has passed; it becomes outdated when new evidence emerges and supersedes it. In the case of lithium, new evidence only confirms its value.

Julia E. Marquez Arrico, Professora Lectora, Universitat de Barcelona

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

Categories : Diet and NutritionTags :

Iodine Deficiency Is Creeping Back. Vegans, Vegetarians and Pregnant Women Are Most at Risk

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José Miguel Soriano del Castillo, Universitat de València

Iodine deficiency is often seen as a problem of the past, but this isn’t entirely true. During the 20th century, the iodisation of salt became one of the most effective public health interventions for preventing conditions caused by a lack of this mineral, including goiter (enlargement of the thyroid gland) and preventable damage to neurological development.

The World Health Organization (WHO) still views iodised salt as a safe and effective strategy, while UNICEF notes that it is the most widely used way of improving iodine intake worldwide.

However, the success of this simple measure means iodine has all but disappeared from public debate. And today, in several countries, signs of insufficient intake are once again being detected in certain groups, particularly in pregnant or breastfeeding women and people on restrictive or poorly planned diets.

What we are witnessing is not a dramatic resurgence of the most severe symptoms everywhere, but rather a silent risk of deficiency in contexts where vigilance has waned.

Iodine’s role in the body

Iodine is an essential micronutrient for the synthesis of thyroxine (T4) and triiodothyronine (T3), hormones that regulate metabolism, growth, and many physiological processes. Adequate intake during pregnancy and early childhood is particularly important for the normal development of the central nervous system and for the early stages of brain maturation.

In addition, the body’s needs increase during pregnancy and breastfeeding due to increased maternal production of thyroid hormones, greater renal excretion of iodine, and the transfer of this mineral to the fetus and the infant.

Why deficiency is on the rise again

The issue is not that people have stopped consuming salt, but rather that the type of salt they consume has changed, as have the sources of sodium in their diet. In recent years, iodised salt has been replaced in many households by “gourmet” or “natural” salts. These include sea salt, pink Himalayan salt, flaked salt and kosher salt, which are often perceived as more sophisticated or healthier, even though they are not always iodised.

In a way, iodised salt has an image problem. Compared to the culinary prestige of its trendy rivals, it has come to be viewed as something ordinary, outdated even.

Today, lot of our salt intake also comes from processed and ultraprocessed foods, meaning the use of iodised salt cannot be guaranteed. For this reason, the World Health Organization has called for coordination between policies that aim to reduce sodium intake and those that promote iodised salt.

The makeup of our diets has also changed a lot. Iodine is naturally present in all seafood, some dairy products and in eggs, though the quantity may vary from one region or food system to another. When a person reduces or cuts out several of these sources at once while not also consuming iodised salt or fortified foods, the risk of deficiency increases.

The result is that a basic, inexpensive, and effective micronutrient has fallen out of the spotlight just as certain groups are once again at risk of not getting enough iodine.

Plant-based diets

Vegetarian and vegan diets can be healthy, but they must take iodine into consideration. A 2023 review in the British Journal of Nutrition concluded that people following a plant-based diet, especially vegans, may find it hard to get the recommended amount of iodine from these foods alone.

This does not mean a plant-based diet is inherently lacking – and the solution is straightforward. Just as vitamin B12 is is commonly recommended for those who reduce their consumption of fish or dairy – or when people replace animal products with unfortified plant-based alternatives – so too should iodine.

Pregnancy and breastfeeding

Iodine deserves special attention during pregnancy. There is strong evidence that a severe deficiency of this micronutrient can affect fetal development and thyroid function, which is why many organisations use specific thresholds to assess iodine status in pregnant women. The US National Institutes of Health states that a urinary concentration of 150–249 micrograms per liter (μg/L) in pregnant women is considered adequate for the general population.

But there is a caveat to this. Concerns about mild or moderate deficiency are legitimate, but there is no conclusive evidence as to the cognitive benefits of supplementing all pregnant women who show a mild deficiency. Reviews and trials have indicated that there is plausible biological concern, and some studies suggest an association with poorer outcomes, but controlled experiments have not unanimously shown clear improvements in infant neurodevelopment.

Nevertheless, several scientific societies have adopted a cautious stance. The American Thyroid Association, for instance, states that women who are planning to conceive, pregnant or breastfeeding should receive 150 μg of iodine daily in prenatal or multivitamin supplements, usually in the form of potassium iodide, to help meet increased requirements.

Why ‘more salt’ is not the answer

Another important clarification is needed here. Advocating for iodised salt does not mean recommending a higher salt intake. The WHO maintains its recommendation to reduce sodium intake due to its link with high blood pressure and cardiovascular disease. In terms of public health, the solution is not “more salt”, but less – though the salt we do eat should be iodised.

In fact, the WHO itself has emphasised that reducing salt intake and fortifying salt with iodine are compatible, provided the concentration of the mineral is properly adjusted and salt used by the food industry is also fortified.

This point is key because it avoids two common pitfalls: turning the issue into a nostalgic defence of table salt, or the other extreme of assuming that any reduction in sodium intake will automatically solve all health problems without any nutritional consequences. But it is possible to strike a balance between preventing cardiovascular disease and iodine deficiency.

José Miguel Soriano del Castillo, Catedrático de Nutrición y Bromatología del Departamento de Medicina Preventiva y Salud Pública, Universitat de València

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