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Prenatal Exposure to Depression Linked to Neurodevelopmental Disorders

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Study finds higher risk cannot be attributed entirely to antidepressant exposure

Source: Pixabay CC0

Children of mothers with depression had higher rates of certain neurodevelopmental disorders regardless of whether they were exposed to antidepressants in the womb, reports a new study led by Saraid McIlvride of the University of Glasgow, UK, published September 29th in the open access journal PLOS Medicine.

Antidepressant use during pregnancy is increasing, but currently, the long-term effects of these drugs on child development are unclear. Having untreated depression during pregnancy carries its own risks, however, making it very challenging for someone with depression to make informed decisions about whether to take medication during pregnancy.

In a new study, researchers followed more than 167 000 children born in Wales between 2009 and 2016, until 2022. Using medical and school records, they looked for any links between depression diagnoses or antidepressant use in mothers, and special educational needs in their children, such as diagnoses of autism spectrum disorder or attention deficit hyperactivity disorder, or learning, behavioral, emotional or social difficulties.

They found that children of women who received antidepressant treatment had higher rates of certain neurodevelopmental disorders than women with depression who were untreated. However, these results could be affected by the fact that women with more severe depression are more likely to be prescribed antidepressants. When comparing between treated depression, untreated depression and antidepressant exposure without depression, the analyses showed that antidepressant exposure was associated with an additional 6.3 cases per 100 children in those not exposed to depression, and an additional 2.9 cases per 100 children in those exposed to depression.

The researchers conclude that children of mothers with depression have a higher risk of neurodevelopmental disorders regardless of whether they were exposed to antidepressants, but medication may carry an additional risk. They caution that any potential risk of treatment should be balanced against the risks of untreated depression in mothers, which is associated with a higher risk of postnatal depression.

The authors add, “We showed that if women with depression took antidepressants while pregnant their children were more likely to have special educational needs, but it was only a very slight increase and may have been due to them having more severe depression, rather than an effect of the medicine. 

“Among children of mothers with depression, 24 in every 100 children had special educational needs if she was not on treatment, and this increased by just 3 in every 100 children if she was taking antidepressants. This is compared to 20 in every 100 children for those not exposed to depression or antidepressants in the womb.

“Our results don’t suggest that women should automatically stop taking their antidepressants because depression can harm both mother and baby if not treated. Women should always speak to their doctor about what is best in their situation.

“Our study indicates that exposure to antidepressants during pregnancy could serve as a marker for additional support being needed at school.

“Linking mothers’ and babies’ routinely collected data and being able to follow their health and development over time is an amazing resource which can support research into maternal mental health, an area which urgently needs more attention.

“Further studies are needed to empower women with the knowledge they need to make informed decisions, together with their doctor or midwife, about their own health as well as their baby’s.”

Provided by PLOS

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Existing Drug Helps Bladder Cells to Destroy Hidden UTI

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Urinary tract infections, or UTIs, are among the most common bacterial infections, caused mostly by the uropathogenic bacterium Escherichia coli. But even after antibiotic treatment, a large number of patients experience another UTI.

One reason is that the bacterium can enter the the bladder’s epithelium and hide there, sheltered from both antibiotics and the patient’s immune system. Surviving like this, these bacteria can later multiply again and cause recurrent UTIs, which become a bigger problem since repeated antibiotic treatment risks generating antibiotic resistance.

Researchers led by Kathrin Tomasek and John McKinney at the Laboratory of Microbiology and Microtechnology at EPFL, with Christian Pasquali and Mario Romani from OM Pharma, have now identified a way to strengthen the bladder cells’ own ability to eliminate these hidden bacteria. Their study, published in PLOS Pathogens, shows that the drug OM-89, marketed as Uro-Vaxom®, activates cellular degradation pathways in bladder epithelial cells while also increasing the amount of antibiotic that enters them.

OM-89 has been used for several decades to help prevent recurrent UTIs. It is mainly known for stimulating the immune system, but the new in vitro study reveals a second mechanism of action: a direct effect on the cells lining the bladder.

The lysosome connection

The researchers studied mouse and human bladder epithelial cells using organoid models and differentiated cell cultures. They exposed the cells to OM-89, infected them with different strains of uropathogenic E. coli and treated them with antibiotics. They then tracked bacterial survival, antibiotic uptake and changes in cellular pathways involved in destroying intracellular material.

The results pointed to lysosomes, the acidic compartments inside cells that break down unwanted material. OM-89 increased lysosomal acidification as well as the activity of lysosomal enzymes.

When the researchers blocked lysosomal acidification, OM-89’s protective effect was lost. This showed that lysosomal activity is directly involved in reducing bacterial regrowth in recurrent UTIs.

Helping antibiotics reach persistent bacteria

At the same time, OM-89 increased the accumulation of antibiotics inside bladder epithelial cells. When OM-89 and antibiotics were co-administered in the experimental models, bacterial killing increased and bacterial regrowth after antibiotic removal decreased.

This effect extended across different antibiotic classes and several bacterial strains, including clinical samples from patients.

The researchers were also able to reproduce key effects in both mouse and human bladder epithelial models, while analysis of independent human bladder datasets linked lysosomal activity with immune and antibacterial pathways.

“We found that OM-89 doesn’t just stimulate the innate immune system as previously assumed,” says Tomasek. “It acts directly on bladder cells, strengthening their degradation pathways so they can destroy hidden bacteria more effectively while also helping antibiotics reach those bacteria—together reducing regrowth of the bacteria after treatment ends.”

The findings point toward a host-directed approach to recurrent infection: rather than targeting bacteria alone, treatment could also reinforce the antimicrobial machinery of the infected tissue itself.

More broadly, the study identifies lysosomal pathways in the bladder epithelium as a potential target for future treatment combinations designed to improve antibiotic outcomes.

Christian Pasquali, Senior Scientific Liaison Director at OM Pharma and former Head of Preclinical Research says: “While the results come from preclinical models and do not change the approved indication or use of Uro-Vaxom®, they deepen our understanding of how OM-89 may help strengthen the bladder’s natural defenses against recurrent infection and reinforce the scientific foundation supporting its use.”

Original written by Nik Papageorgiou

Source: Ecole Polytechnique Federale de Lausanne (EPFL)

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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.

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Airway Immune Response Kicks out Virus-infected Cells

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3D reconstruction of rhinovirus-infected human airway epithelial cells. Virus-infected cells (multicoloured) can be seen protruding from the epithelial layer during cell extrusion. Credit: Faith Fore. An AI-assisted editing tool was used to sharpen this image.

The epithelium, a layer of cells that forms a protective barrier between the body and the outside world, was the first organised tissue to evolve. Epithelial cells lining our airways are mainly seen as a structural barrier, but cell biologist Jody Rosenblatt, who runs a lab at the Crick and King’s College London, believes their evolutionary history suggests they’re playing a much more active role in infections.

“The airway lining is the body’s first physical barrier against inhaled threats like viruses,” says Jody. “It would make sense for it to take direct action.”

To investigate this, Jody’s team studied rhinoviruses, which are the leading cause of the common cold. They usually cause mild illness, but they can cause more serious respiratory disease in young children, older people, people with weakened immune systems and those with chronic lung conditions such as asthma or COPD.

Their new study, published today in Science Advances, shows that airway cells respond to rhinovirus infection by physically pushing infected cells out of the tissue, in a process the researchers have named ‘virus-induced cell extrusion’ or ‘VICE’.

As first author and Postdoctoral Research Fellow Faith Fore explains, “We studied rhinovirus infection in human epithelial cells grown in the lab, and we observed that when the cells were able to work together as a healthy layer, they could remove infected cells and limit infection within the tissue.

“But when we experimentally disrupted the barrier by breaking down junctions between epithelial cells, more virus particles built up in the epithelial layer. We also observed virus-induced cell extrusion in mouse lung tissue, supporting the relevance of the mechanism in a more complex tissue environment.”

The researchers also observed that VICE happens in two distinct waves. The first begins rapidly, before the virus has fully entered the cell, involving the cell’s ability to sense mechanical changes, while a second wave occurs later, triggered by the virus replicating inside the cell, leading to cell death. “These two waves allow the epithelial cells to kick into action straight away, without the need for signals from immune cells that have recognised the virus,” says Jody.

A ‘double-edged defence’

This early defence mechanism helps remove most infected cells from the airway lining within 24 hours, maintaining the integrity of the barrier. But, there’s a downside. “The expelled cells remain alive and infectious, potentially allowing the virus to reach new cells,” explains Faith. The team confirmed this by adding extruded airway cells to healthy cells in a dish, which subsequently were infected with the virus after just six hours.

Faith continues, “The airway gets rid of the infected cell, but it doesn’t destroy the virus. Because the expelled cells can still infect new cells, it creates a double-edged defence. Extrusion helps the tissue clear the immediate infection, but the expelled cells remain a potential source of viral spread.”

An overlooked mechanism

Jody believes that this mechanism should be taken into account when assessing responses to infections. It may have been overlooked because some commonly used laboratory models do not recreate the cell-to-cell junctions that the team has now shown are required for VICE to occur. 

“Understanding these fundamental tissue defence mechanisms could change how we think about the earliest stages of viral infection.”

Jody Rosenblatt
Principal Group Leader

“Our study suggests that cells lining our tissues possess evolutionarily ancient mechanisms for protecting themselves,” she says. “Understanding these fundamental tissue defence mechanisms could change how we think about the earliest stages of viral infection.”

Faith agrees, “We typically think of the cells lining our airways as a simple physical barrier, leaving the heavy lifting of clearing infections to the immune system. What we found is that the epithelium itself actively fights back by physically throwing out infected cells.” 

The researchers are now planning to investigate how widespread this defence mechanism is across respiratory viruses, what determines whether extrusion protects the airway or promotes viral spread, and how viruses might evade or exploit the response.

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Scientists Discover New Gene Boosting the Resistance of C. Diff

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Credit: Desirel Ng

Antibiotic resistance is supercharging dangerous gut bacteria to withstand even hospital-grade disinfectants intended to kill them.

New research from Monash University, published in Nature Communications, reveals the bacteria Clostridioides difficile has picked up a key gene that gives its dormant spores a free pass against antibiotics and cleaning products.

Its spores act like plant seeds, waiting patiently to activate and spread in the right environment, like the human gut.

This is particularly dangerous given this bacterium is commonly found in hospitals and causes diarrhea that can be deadly for already unwell patients.

Lead researcher Professor Dena Lyras, Interim Dean of the Monash Sub-Faculty of Biomedical and Psychological Sciences and Director of Monash Biomedicine Discovery Institute, said the new research is a crucial step forward in what is a dynamic race against antimicrobial resistance.

“Antibiotics are helping bacteria evolve in ways we hadn’t anticipated,” Professor Lyras said.

“Our new research shows just how sophisticated their evolution is, with the potential to have disastrous impacts on humans.

“They are not only better at building tolerance to drugs we develop, but making new versions of themselves that can survive better in particular environments, like surfaces where cleaning products are commonly applied.”

Antimicrobial resistance occurs when bacteria stop responding to antibiotics leading to infections that can be hard or impossible to treat.

The World Health Organization lists this phenomenon as a major global health threat and estimates that it contributes to millions of deaths every year.

This new research, the first to uncover a link between antibiotic resistance and bacterial spores, shows that when Clostridioides difficile picks up this antibiotic resistance gene, the antibiotic block no longer works.

Instead, the bacteria is able to make even tougher spores that can survive hospital grade cleaning products and high laundry temperatures.

The antibiotic resistance gene produces a protein that replaces a key spore-building protein, allowing the bacteria to keep making spores.

First author Dr Yogitha Srikhanta, a Post-Doctoral Research Fellow at Monash Biomedicine Discovery Institute, said targeting the spores could be the key to unlocking a solution.

“Spore survival matters because spores are the main way these pathogens spread between people and through hospitals, homes, and the environment,” Dr Srikhanta said.

“A resistance gene that changes how spores are built could make infections harder to control and help resistant strains spread more easily.

“We are now investigating ways to deal with this new type of antibiotic resistance.”

Read the research paper: http://doi.org/10.1038/s41467-026-75594-5

Source: Monash University

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Genetic Analysis Reveals Potential Benefit of Aspirin for Reducing Dementia Risk

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Low-dose aspirin was associated with a 70 per cent lower risk of dementia among older people with a particular genetic profile, a new Monash University analysis has found, raising the possibility of a more personalised approach to dementia prevention.

The research, published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, analysed genetic data from the landmark ASPREE Trial (Aspirin in Reducing Events in the Elderly), screening genetic scores in more than 13 500 individuals to investigate whether a person’s genes influenced aspirin’s effect on reducing dementia risk.

The strongest finding was linked to genetics that influence platelet count.

Researchers ranked participants according to their platelet-related genetic score.

Among participants in the highest 20 per cent for a platelet count genetic score, only 1 per cent of those taking aspirin developed dementia, compared with 3.3 per cent of those receiving placebo.

This represents about a 70 per cent lower relative risk associated with aspirin use.

However, aspirin also increased the risk of serious bleeding in this group.

Major bleeding occurred in 4.4 per cent of those taking aspirin, compared with 2.1 per cent receiving placebo.

Lead author Dr Peter Fransquet, Research Fellow at Monash’s School of Public Health and Preventive Medicine, said the findings could open the door to a more personalised approach to dementia prevention.

“Previous trials found aspirin didn’t prevent dementia when everyone was considered together,” Dr Fransquet said.

“Our findings suggest there may be more to the story.

“In people with this particular genetic profile, we saw substantially fewer cases of dementia among those taking aspirin.

“It raises the possibility that genetics could one day help us identify who may benefit from a preventive treatment, rather than taking a one-size-fits-all approach.”

Dementia Australia estimates 446 500 Australians are living with dementia in 2026.

It projects this will rise to more than one million by 2065.

While scientists have previously identified a link between platelet activation and aggregation and dementia, the role of a person’s overall platelet count has been less clear.

“What’s particularly interesting is that the signal wasn’t linked to the established genetic risk factors for Alzheimer’s disease and dementia,” Dr Fransquet said.

“Instead, it’s pointing us towards platelet biology and gives us a new avenue to investigate.

“We now need to confirm the finding in other studies and ultimately test it in a trial designed specifically for people with this genetic profile.

“People shouldn’t start taking aspirin to prevent dementia on the basis of this study without consulting with their doctor, particularly given the increased risk of serious bleeding.

“If it holds up, the fact that aspirin is already cheap and widely available could make personalised dementia prevention a real possibility.”

Source: Monash University

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REM and Deep Sleep, not Just Total Sleep Time, Associated with Disease Risk

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Large study used wrist-worn accelerometer data to map associations between real-world sleep patterns and the incidence of more than 1000 health conditions

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Greater amounts of REM and deep sleep were associated with lower risks of dozens of diseases, and less than 5 hours of total sleep was associated with high risks of disease, according to a new study published September 17th in the open access journal PLOS Medicine by Shengzhi Sun of Capital Medical University, China, and colleagues.

There remains limited understanding of how sleep stages and other real-world sleep patterns relate to health outcomes. In part, that is because self-reported sleep measures often show poor correlation with objective assessments, making it difficult to capture real-world sleep patterns.

In the new study, researchers analysed data from 95 559 UK Biobank participants who wore wrist accelerometers for seven consecutive days and nights. The researchers used a deep-learning algorithm to calculate sleep stages (REM, deep, and light sleep), total sleep duration, wakefulness after sleep onset, and night-to-night sleep irregularity. Participants were followed for a median of 8.9 years, and health records were available to test for associations with more than 1000 disease outcomes.

Greater REM sleep (per interquartile range, 47.6 minutes) was associated with a lower risk of 83 diseases, including heart failure (hazard ratio 0.74), dementia (hazard ratio 0.54), and Parkinson’s disease (hazard ratio 0.20), while greater deep sleep was linked to lower risk of 7 conditions, including type 2 diabetes and major depressive disorder. Greater sleep irregularity and wakefulness after sleep onset were each linked to higher risk of several conditions, including anxiety and substance use disorders. Total sleep duration showed a non-linear relationship with disease risk for many conditions, with the lowest risk concentrated in a 6-to-8-hour window; people sleeping less than 5 hours faced the most elevated clinical vulnerability, with an increased risk of 37 conditions. However, as an observational study, this research cannot establish that sleep patterns directly cause disease risk.

“The findings provide additional evidence supporting the role of a 6-8 hours’ sleep duration as a health safeguard for middle-aged and older adults, likely attributable to more favourable distributions of sleep stages,” the authors say. “Maintaining a sleep duration of 6-8 hours can effectively reduce the risk of multiple diseases, providing new insights for health promotion and preventive practice.”

The authors add, “Phenome-wide association analysis identified 156 significant associations between sleep patterns and incident diseases after Bonferroni correction.”

“Sleep duration exhibited significant non-linear associations with 86 disease phenotypes, with the minimum-risk duration for the majority of these conditions (69 phenotypes) precisely concentrated within a 6-8 hour window.”

Provided by PLOS

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Rare Pregnancy Infections Linked to Autism

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Infections that, in rare cases, can be transmitted from the pregnant woman to the foetus are linked to an increased risk of autism and intellectual disability in the child. This is shown by a study from the Karolinska Institute published in JAMA Pediatrics.

”It is important to emphasise that it is unusual for these infections to be transmitted from mother to child. They account for a very small proportion of all cases of autism in the population, but for those children who are actually affected, we see a clearly elevated risk of both autism and intellectual disability,” says Reneé Gardner, a researcher at the Department of Global Public Health at Karolinska Institutet, who contributed to the study. 

The researchers have investigated how so-called TORCH infections affect children’s later development. TORCH is a group of infections that can be transmitted from a pregnant woman to the foetus and includes, amongst others, cytomegalovirus, rubella, toxoplasma and herpesvirus. Unlike many common infections, these pathogens can sometimes cross the placenta and directly infect the foetus.

Were followed for three decades

The study included 3.7 million people born in Sweden between 1987 and 2021. Of these, 975 had been diagnosed with a congenital TORCH infection. The researchers followed the participants for up to three decades to investigate whether the infections were linked to later diagnoses and educational outcomes.

The results show that children with a congenital TORCH infection were approximately three times more likely to be diagnosed with autism later in life and more than seven times more likely to be diagnosed with an intellectual disability compared with children without the infection. The risk of severe to profound intellectual disability was up to 30 times higher.

However, despite the high relative risks, the significance of these infections at a population level is limited, as they are rare in newborns. The researchers estimate that congenital TORCH infections may be linked to approximately 1.2 per cent of all cases of severe intellectual disability, whilst around 0.034 per cent of all cases of autism in Sweden can be explained by these infections. They also estimate that approximately one in five children born with a TORCH infection may later develop autism.

”It has long been known that these infections can cause intellectual disability. However, the link to autism has been less clear in previous research, which has often been based on small patient groups. This study is the largest to date in this field and is based on national register data covering almost the entire population of Sweden,” says Hugo Sjöqvist, a PhD student and lead author of the study.

To better determine whether the associations were due to the infections themselves, the researchers also compared children who had had a TORCH infection with their own siblings who had not had the infection. The results were similar in the sibling comparisons, which suggests that the associations cannot be explained solely by factors shared within families.

The researchers found no clear links between TORCH infections and other neuropsychiatric conditions, such as ADHD or obsessive-compulsive disorder. However, an impact on academic performance was observed. Even children who had not been diagnosed with autism or an intellectual disability had, on average, lower grades than their peers without the infection.

“Our results suggest that certain infections transmitted to the foetus during pregnancy may have long-term effects on brain development. Although these congenital infections are rare, some of them can be prevented, which makes them important from a public health perspective,” says Reneé Gardner.

The researchers particularly emphasise the importance of preventive measures. For example, the study points out that rubella has virtually disappeared in Sweden following the introduction of national vaccination programmes. According to the researchers, the results underline the importance of maintaining vaccination programmes and other strategies to prevent infections that can be transmitted from the pregnant woman to the foetus.

The research was funded by the Swedish Research Council. Co-author David Mataix-Cols states that he has received author’s fees from UpToDate Inc and that he is a partner in Scandinavian E-Health AB, which is unrelated to the publication.

Publication

”Congenital TORCH infections and neurodevelopmental outcomes: A population- and sibling-based cohort study”, Hugo Sjöqvist, Christina Dalman, David Mataix-Cols, Reneé M Gardner, Håkan Karlsson. JAMA Pediatrics, online 21 September 2026, doi: 10.1001/jamapediatrics.2026.4229.

Facts on how TORCH infections can be prevented

• T = Toxoplasma: Avoid raw or undercooked meat, wash vegetables, and take care when handling cat faeces. 

• O = Other (including infections such as syphilis): Screening during pregnancy and antibiotic treatment. 

• R = Rubella: Vaccination before pregnancy (MMR vaccine). 

• C = Cytomegalovirus (CMV): Good hand hygiene; avoid contact with young children’s saliva and urine. 

• H = Herpes simplex (HSV): Identification and treatment of infection during pregnancy; sometimes a caesarean section is performed in the event of active genital herpes prior to delivery.

Source: Karolinska Institutet

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Major Trial Examines Artificial Sweeteners in Soft Drinks

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Researchers at the University of Liverpool have conducted the longest and most comprehensive randomised controlled trial on non-nutritive sweetened (NNS) soft drinks.

Non-nutritive sweeteners are low- or no-calorie alternatives to sugar used to sweeten foods and drinks. The 104-week clinical trial shows NNS beverages ie, diet beverages are equivalent to water for long term weight management.

Professor Jo Harrold, Dean of Psychology at the University of Liverpool alongside Professor Jason Halford, Professor, Biological Psychology & Health Behaviours at the University of Leeds (formerly of the University of Liverpool) conducted the peer-reviewed research funded by the American Beverage Association. The research team was independent of the funder and had full control over the analysis and reporting of their findings.

The major new study was published in the British Journal of Nutrition and provides long-term clinical evidence that NNS beverages – specifically those containing aspartame, acesulfame potassium (acesulfame‑K), and sucralose – are equivalent to water in supporting weight loss and long‑term weight maintenance.

The SWITCH trial followed 493 adults with overweight or obesity through a structured behavioural weight management programme. Participants were randomised to consume either water or commercially available diet beverages, daily, with sweeteners provided at levels well within established European Food Safety Authority (EFSA) safety thresholds.

Overall, the results do not support concerns that NNS beverages disrupt appetite regulation or have long term metabolic harm.

Key outcomes include:

  • Equivalent weight loss between NNS beverages and water at 104 weeks (−4.8 kg vs −3.7 kg; nonsignificant difference).
  • Sustained weight reduction over two years in both groups, even during the final unassisted year.
  • Decrease in waist and hip circumference and improvement in body composition, and several metabolic biomarkers in both groups.
  • No clinically meaningful difference in effects such as blood pressure and cholesterol, associated with long-term consumption of either aspartame, acesulfame‑K, or sucralose or water.
  • Sugar intake decreased in both groups, with slightly greater reductions in the NNS group.

Importantly, the findings directly address recent World Health Organization (WHO) guidance, which advised against using non-sugar sweeteners for weight control due to uncertainty in observational studies. The SWITCH trial provides long-duration, randomised controlled evidence which can be used to inform global guidelines.

Professor Joanne Harrold, said: “The University of Liverpool is one of the UK’s leading research-intensive higher education institutions, with a key focus on public health. These latest findings show that concerns about sweeteners disrupting appetite or causing weight gain are not supported when tested in a rigorous, long-term randomised trial. We hope this evidence informs future WHO guidance and public health policy.

The effectS of non-nutritive sWeetened beverages on appetITe during aCtive weigHt loss (SWITCH) trial was conceived and designed by researchers in the context of the need to reduce sugar in the diet and to address questions about the potential effects on appetite regulation of using sweeteners as a substitute. This latest published work continues from previously published evidence in the International Journal of Obesity in 2023.

Professor Jason Halford, University of Leeds and University of Liverpool, concluded: “This study provides the long‑term clinical evidence that has been missing from international discussions. For people trying to manage their weight, non‑nutritive sweetened beverages offer an effective alternative to sugar‑sweetened drinks – and perform equivalently to water over two years.”

Source: University of Liverpool

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Blood Test Trends may Help Identify Patients at Increased Risk of Cancer

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Among patients with unexplained weight loss, changes over time in routine blood test results were associated with overall and site-specific cancer diagnoses

Photo: Pixabay

Blood test trends alongside unexplained weight loss can improve triage for cancer testing, according to a study by Brian Nicholson and colleagues from the University of Oxford, UK, published September 17th in the open access journal PLOS Medicine.

Abnormal blood test results, such as low haemoglobin or increased platelet counts, can provide clues about a patient’s risk of developing cancer. However, monitoring trends over repeat tests could provide further clues in some instances, by identifying cancer-related changes in blood test results that do not appear abnormal. Assessing patterns in blood test abnormalities and trends alongside unexplained weight loss could enhance cancer risk assessment and support earlier diagnosis.

In this study, researchers examined trends in blood test results among patients with unexplained weight loss, a common non-specific symptom associated with multiple cancer types. The goal was to determine whether trends in 26 commonly used blood tests in primary care could improve cancer risk stratification compared to abnormalities on single blood tests.

Among the more than 275 000 patients included in the study, nearly 14 000 were subsequently diagnosed with cancer within six months, allowing researchers to relate abnormalities on single tests and trends over repeat blood tests to cancer diagnosis. Overall, 23 blood test trends were associated with overall cancer risk. Several abnormalities were also associated with specific cancer types. After accounting for age and sex, several blood test trends were more discriminative for cancer diagnosis than individual abnormal test results. For example, trends in white blood count and neutrophils were linked to lung cancer while trends in red blood cell count, haematocrit, and platelet-to-lymphocyte ratio were associated with prostate cancer.

The findings suggest that monitoring changes in routine blood test results in patients with unexplained weight loss could identify patients in primary care who would benefit from additional cancer testing.

Author Brian Nicholson adds, “We show how blood test results are made more accurate for cancer by adding patient age and sex. This relatively simple calculation could easily be performed at the laboratory.”

Author Pradeep Virdee states, “In some instances, monitoring how a patient’s blood test results change over time could offer further value. We plan to assess how well blood test abnormalities and trends inform cancer risk in patients with other types of non-specific symptoms, such as fatigue and vomiting.”

Provided by PLOS