Category: 8. Health

  • Reuben Saunders Wins Hertz Thesis Prize for Mapping Gene Function in Living Tissues

    Reuben Saunders Wins Hertz Thesis Prize for Mapping Gene Function in Living Tissues

    Newswise — A human body is made up of trillions of cells, each carrying the same set of genes but using them in vastly different ways to form functioning organs and tissues. Understanding the roles of each gene—of which there are around 20,000 that encode proteins—remains one of biology’s greatest challenges.

    Hertz Fellow Reuben Saunders is up to tackling that challenge. As a graduate student, Saunders developed a method to track the precise effects of thousands of genetic changes across millions of individual cells. His approach uses a version of CRISPR called CRISPR interference (CRISPRi) to silence specific genes without cutting or changing their DNA sequence, and then a combination of sequencing and imaging technologies to study the resulting changes to cells. Moreover, it works on many cells at once—not only in lab dishes, but within the rich complexity of living tissues.

    Saunders’s thesis “Pooled genetic screens with rich readouts at scale and in vivo,” describes the method, and its application, and was awarded the 2024 Hertz Thesis Prize from the Hertz Foundation. The Thesis Prize recognizes fellows with exemplary, transformative doctoral theses, and Saunders joins more than 60 fellows who have been previously recognized with the award. Winners are chosen by a vibrant and committed group of volunteers, Hertz Fellows and non-fellows who serve as Thesis Reviewers.

    “We’ve had powerful tools to catalog which genes are active in different cells, but understanding which genes actually control complex tissue behaviors required a new kind of experiment—one that’s quantitative, high-resolution, and scalable in living systems,” said Saunders, who carried out the work under the mentorship of Jonathan Weissman of MIT and the Whitehead Institute for Biomedical Research (previously of University of California, San Francisco).

    At the beginning of graduate school, Saunders was interested in studying molecular pathways activated by cells in the face of stress. Weissman’s lab had developed a technology called Perturb-seq in which scientists silence specific genes in different cells and then profile how each change alters which RNA molecules the cell is producing—a proxy for which other genes are being actively used. The technology had previously been used at a small scale in cell cultures, altering only a handful of genes at once.

    Saunders and his colleagues had a broader vision: to systematically silence nearly every active gene in human cells and study the effects.

    “The early experiments revealed something fundamental: Biology’s complexity isn’t just in having many parts, but in how those parts interact across scales,” said Saunders. “Once I saw that pattern emerging from our data, I knew we had to push beyond cell culture into the messy reality of living tissues.”

    Saunders and his collaborators expanded Perturb-seq to a genome-wide level—profiling the consequences of knocking down nearly every expressed gene in a human cell line, across more than 2.5 million cells.

    That dataset alone surfaced dozens of new biological insights. For example, Saunders and colleagues discovered how altering genes in the nuclei of a cell—where most DNA is located—led to unexpected changes in the activity of genes in the cell’s energy-generating mitochondria.

    “This is what happens when you cast a wide net: You catch things you didn’t know were swimming there. The nuclear-mitochondrial crosstalk emerged from the data like a hidden conversation between two cellular compartments we usually study in isolation,” he said.

    But Saunders’s most ambitious leap came in bringing these techniques into live mouse organs. He developed a “genetic mosaic” liver model in which different genes are randomly switched off in some liver cells, while leaving other parts of the liver normal. That provided a well-controlled experiment as to the effect of each gene within a living animal. By studying the resulting livers with a combination of techniques, his team was able to observe how each gene altered cellular physiology. In one striking result, the group found that multiple different gene perturbations caused fat buildup in liver cells—mimicking early fatty liver disease—but through completely distinct molecular mechanisms.

    “Those kinds of findings just wouldn’t be possible in traditional animal models, where you can only study one gene at a time,” Saunders said. “By doing these pooled, high-content experiments in vivo, we can start to see the true complexity of how gene function plays out in real physiology.”

    Saunders carried out the work not only with members of Weissman’s lab group, but also in collaboration with Xiaowei Zhuang at Harvard and with Will Allen, a Hertz Fellow whom he met through the Hertz community. That connection, Saunders said, was pivotal.

    Now a Junior Fellow in the Harvard Society of Fellows, Saunders is continuing to expand the reach of these methods, optimizing their use in organs other than the liver and integrating new types of readouts beyond RNA and imaging—such as epigenetic markers. These tools could ultimately transform how scientists link genes to disease, paving the way for new drugs and therapies.

    About the Hertz Foundation

    Founded in 1957, the Fannie and John Hertz Foundation accelerates solutions to the world’s most pressing challenges, from enhancing national security to improving human health. Through the Hertz Fellowship, the Foundation identifies the nation’s most promising young innovators and disruptors in science and technology, empowering them to become future leaders who keep our country safe and secure. Today, a community of more than 1,300 Hertz Fellows are a powerful, solution-oriented network of our nation’s top scientific minds, working to address complex problems and contributing to the economic vitality of our country. Learn more at hertzfoundation.org


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  • ‘Autofocus’ specs promise sharp vision, near or far

    ‘Autofocus’ specs promise sharp vision, near or far

    Chris Baraniuk

    Technology Reporter

    IXI Niko Eiden, smiling and wearing IXI's autofocus specs.IXI

    “People don’t want to look like cyborgs,” says Niko Eiden

    They look like an ordinary pair of glasses – but these are tech-packed specs.

    On a Zoom call, Niko Eiden, chief executive and co-founder of Finnish eyewear firm IXI, holds up the frames with lenses containing liquid crystals, meaning their vision-correcting properties can change on the fly.

    This one pair could correct the vision of someone who normally uses totally different pairs of glasses for seeing near or far.

    “These liquid crystals… we can rotate them with an electrical field,” explains Mr Eiden.

    “It’s totally, freely tuneable.” The position of those crystals affects the passage of light through the lenses. A built-in eye-tracker allows the glasses to respond to whatever correction the wearer needs at a given moment.

    However, tech-laden eyewear has a troubled history – take Google’s ill-fated “Glass” smart glasses.

    Consumer acceptability is key, acknowledges Mr Eiden. Most people don’t want to look like cyborgs: “We need to make our products actually look like existing eyewear.”

    IXI A pair of IXI glases. On one side you can see through to the electronicsIXI

    IXI glasses have lenses that can be manipulated with an electric field

    The market for eyewear tech is likely to grow.

    Presbyopia, an age-related condition that makes it harder to focus on things close to you, is projected to become more common over time as the world’s population ages. And myopia, or short-sightedness, is also on the rise.

    Spectacles have remained largely the same for decades. Bifocal lenses – in which a lens is split into two regions, usually for either near- or far-sightedness – require the wearer to direct their vision through the relevant region, depending on what they want to look at, in order to see clearly.

    Varifocals do a similar job but the transitions are much smoother.

    In contrast, auto-focus lenses promise to adjust part or all of the lens spontaneously, and even accommodate the wearer’s changing eyesight over time.

    “The first lenses that we produced were horrible,” admits Mr Eiden, candidly.

    Those early prototypes were “hazy”, he says, and with the lens quality noticeably poor at its edges.

    But newer versions have proved promising in tests, says Mr Eiden. Participants in the company’s trials have been asked, for example, to read something on a page, then look at an object in the distance, to see whether the glasses respond smoothly to the transition.

    Mr Eiden says that the eye tracking device within the spectacles cannot determine exactly what a wearer is looking at, though certain activities such as reading are in principle detectable because of the nature of eye movements associated with them.

    Since such glasses respond so closely to the wearer’s eye behaviour, it’s important the frames fit well, says Emilia Helin, product director.

    IXI’s frames are adjustable but not to a great degree, given the delicate electronics inside, she explains: “We have some flexibility but not full flexibility.” That’s why IXI hopes to ensure that the small range of frames it has designed would suit a wide variety of faces.

    The small battery secreted inside IXI’s autofocus frames should last for two days, says Mr Eiden, adding that it’s possible to recharge the specs overnight while the wearer is asleep.

    But he won’t be drawn on a launch date, which he intends to reveal later this year. As for cost, I ask whether £1,000 might be the sort of price tag he has in mind. He merely says, “I’m smiling when you say it but I won’t confirm.”

    Getty Images A mother tries on glasses in a store with her young daughterGetty Images

    Autofocus lenses could help people who struggle with varifocals or bifocals

    Autofocus lenses could help people who struggle with varifocals or bifocals, says Paramdeep Bilkhu, clinical adviser at the College of Optometrists.

    However, he adds, “There is insufficient evidence to state whether they perform as well as traditional options and whether they can be used for safety critical tasks such as driving.”

    Chi-Ho To, an optometry researcher, at the Hong Kong Polytechnic University has a similar concern – what if the vision correction went wrong or was delayed slightly while he was, say, performing surgery on someone?

    “But I think in terms of general use having something that allows autofocusing is a good idea,” he adds.

    Mr Eiden notes that the first version of his company’s lenses will not alter the entire lens area. “One can always glance over the dynamic area,” he says. If wholly self-adjusting lenses emerge then safety will become “a much more serious business”, he adds.

    In 2013, UK firm Adlens released glasses that allowed wearers to manually change the optical power of the lenses via a small dial on the frames. These lenses contained a fluid-filled membrane, which when compressed in response to dial adjustments would alter its curvature.

    Adlens’ current chief executive Rob Stevens says the specs sold for $1,250 (£920) in the US and were “well received by consumers” but not so much by opticians, which he says “strangled sales”.

    Since then, technology has moved on and the concept of lenses that refocus themselves automatically, without manual interventions, has emerged.

    Like IXI and other companies, Adlens is working on glasses that do this. However, Mr Stevens declines to confirm a launch date.

    Joshua Silver, an Oxford University physicist, founded Adlens but no longer works for the company.

    He came up with the idea of fluid-filled adjustable lenses back in 1985 and developed glasses that could be tuned to the wearer’s needs and then permanently set to that prescription.

    Such lenses have enabled roughly 100,000 people in 20 countries to access vision correcting technology. Prof Silver is currently seeking investment for a venture called Vision, which would further rollout these glasses.

    As for more expensive, electronics-filled auto-focus specs, he questions whether they will have broad appeal: “Wouldn’t [people] just go and buy reading glasses, which would more or less do the same thing for them?”

    Hong Kong Polytechnic University Prof Chi-Ho To holding up a lens.Hong Kong Polytechnic University

    Prof Chi-Ho To has developed a lens which slows short-sightedness

    Other specs tech is even slowing down the progression of eye conditions such as myopia, beyond just correcting for them.

    Prof To has developed glasses lenses that have a honeycomb-like ring in them. Light passing through the centre of the ring, focused as normal, reaches the wearer’s retina and allows them to see clearly.

    However, light passing through the ring itself is defocused slightly meaning that the peripheral retina gets a slightly blurred image.

    This appears to slow improper eyeball growth in children, which Prof To says cuts the rate of short-sightedness progression by 60%. Glasses with this technology are now in use in more than 30 countries, he adds.

    British firm SightGlass has a slightly different approach – glasses that gently reduce the contrast of someone’s vision to similarly affect eye growth and myopia progression.

    While autofocus glasses and other high-tech solutions may have promise, Prof To has an even bigger goal: glasses that don’t just slow down myopia but actually reverse it slightly – a tantalising prospect that could improve the vision of potentially billions of people.

    “There is growing evidence that you can do it,” teases Prof To.

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  • expert reaction to observational study of gabapentin and risk of dementia and cognitive impairments

    An observational study published in Regional Anesthesia & Pain Medicine looks at gabapentin prescription for chronic pain and the risk of dementia and cognitive impairment. 

     

    Prof Ian Maidment, Professor in Clinical Pharmacy, Aston University, said:

    “This study found an association between gabapentin and dementia. It was an observation study and therefore conclusions about causality cannot be drawn. Furthermore, the research did not control for length of treatment or dose of gabapentin. Other similar recent studies have failed to find a link. Therefore, overall the jury is out on whether gabapentin causes dementia.”

     

    Prof Martin Prince, Professor of Epidemiological Psychiatry, Institute of Psychiatry, Psychology & Neuroscience, King’s College London, said:

    “This is an interesting pharmaco-epidemiological study, using a retrospective (historical) cohort design, and reporting a significant increased risk of dementia incidence among those prescribed gabapentin for chronic low back pain. The authors are right to stress that they are reporting an association, and not necessarily a causal link. As I will discuss, confounding and reverse causality are tenable explanations for the observed effects. The strengths of the study include a large sample size, a long surveillance period, a state of the art propensity matching on a large number of potential confounding factors, and additional confounders controlled for in the analysis.

    “There are some issues apparent with the research.

    1. The most significant is that the title of the paper (which refers only to chronic low back pain) appears to be misleading. Closer reading of the research methods reveals that the inclusion criteria were actually “chronic pain (ICD- 10- CM G89.29), chronic pain syndrome (ICD- 10- CM G89.4), lumbar radiculopathy (ICD- 10- CM M54.16), or chronic low back pain (ICD- 10- CM M54.5)”. This is a much broader group, and would include, among other conditions, post-herpetic neuralgia and painful diabetic and other peripheral neuropathies, which are particularly common indications for prescription of gabapentin. There is an inconclusive literature linking shingles episodes to an increased risk of dementia (and suggesting that the Shingrix vaccine may lower the risk), and recent research using the UK biobank linking multisite chronic pain with the incidence of dementia and hippocampal atrophy (1). None of this body of potentially relevant research was referenced or discussed in the current paper. Confounding by indication therefore remains a distinct possibility – the condition that gabapentin is treating, rather than the drug itself being responsible for the increased dementia risk. Of note is that use of gabapentin would likely be reserved for those with more severe pain, and therefore a more severe underlying condition. While the investigators clearly sought to limit the potential for confounding by indication (for example by excluding from consideration individuals prescribed gabapentin for epilepsy), their efforts are likely to have been only partially successful. Reverse causality must always be considered in dementia cohort studies given the 20 years or more interval between the earliest detectable signs of Alzheimer’s Disease (from neuroimaging and blood biomarkers) and clinical onset. Those diagnosed with dementia would not, strictly speaking, have been dementia-free at cohort inception. It is possible that the CNS effects of Alzheimer’s disease modulate pain processing and appreciation, leading to more complaints of more severe pain, at multiple sites. Hence that Alzheimer’s disease caused the pain, and, ultimately the Gabapentin prescription, not vice versa. Or that there is an underlying common cause, for example inflammation, that is driving both the neurodegeneration and the neuropathic pain.
    2. I could not understand why mild cognitive impairment, frontotemporal dementia and dementia with Lewy Bodies were listed as factors that were propensity matched at baseline, when the onset of mild cognitive impairment and all cause dementia were outcomes of interest and hence presumably excluded at baseline? It isn’t very clearly explained. It is possible that those with MCI at baseline were left in when assessing dementia as an outcome, but excluded when assessing MCI as an outcome. But leaving FTD and DLB cases in at baseline (with the implicit assumption that they could be considered as remaining at risk for developing AD or vascular dementia), seems to be an odd approach.  
    3. Since, apparently, separate diagnostic codes for Alzheimer’s Disease and Vascular dementia were available, I am surprised that no attempt was made to explore whether the association with gabapentin prescription was similar or different across the two sub-types. The relationship of gabapentin use to both AD polygenic risk scores, and AD-specific blood biomarkers would also be another area for future research.”
    1. W. Zhao, L. Zhao, X. Chang, X. Lu, & Y. Tu, Elevated dementia risk, cognitive decline, and hippocampal atrophy in multisite chronic pain, Proc. Natl. Acad. Sci. U.S.A. 120 (9) e2215192120, https://doi.org/10.1073/pnas.2215192120 (2023).

     

    Prof Tara Spires-Jones, Director of the Centre for Discovery Brain Sciences at the University of Edinburgh, Group Leader in the UK Dementia Research Institute, and Past President of the British Neuroscience Association said:

    “This study by Eghrari and colleagues examined medical records from over 24,000 people in the US and found that prescription of the medication gabapentin for chronic pain was associated with a higher risk of developing dementia.  While authors used statistical methods to try and account for other risk factors, this type of study cannot prove that gabapentin was the cause of increased dementia risk.  One very important factor that was not examined in this study is levels of physical activity.  People with chronic pain requiring gabapentin may have been less physically active, which is a known risk factor for developing dementia.”

     

    Prof Sir John Hardy, Group Leader at the UK Dementia Research Institute at UCL, said:

    “While this is interesting, one has to worry that these types of findings are artefactual and result (for example) from a marginal acute effect on cognitive performance rather than effects on the underlying disease.”

     

    Dr Leah Mursaleen, Head of Clinical Research at Alzheimer’s Research UK, said:

    “Research shows that nearly half (45%) of dementia cases could be prevented or delayed if 14 health and lifestyle risk factors are addressed by people and society. At the moment, there’s not enough evidence to suggest pain medications are linked to higher dementia risk, but this research gives us interesting insights.

    “This large observational study looked at health records of over 26,000 people in the US diagnosed with chronic lower back pain and who were prescribed gabapentin within a 10-year period. They found gabapentin prescription was associated with an increased risk of dementia and mild cognitive impairment, especially in people under the age of 65.

    “Some of the strengths of this research was the large sample size and some dementia risk factors were considered, such as age and high blood pressure.

    “However, this study only shows an association between gabapentin prescriptions and mild cognitive impairment or dementia, so we do not know if the medication is directly causing the higher risk. Gabapentin dosage wasn’t recorded, and there was no information on how long people were on the medication. 

    “Because this study only used health records of people with chronic pain, we cannot rule out other factors that might be influencing the findings. And previous studies looking at people prescribed gabapentin for other conditions like seizures, didn’t show a link between the medication and higher dementia risk.

    “Managing chronic pain is very important and if anyone has any concerns about the medication they are receiving, they should speak to their doctor.”

     

     

     

    ‘Risk of dementia following gabapentin prescription in chronic low back pain patients’ by Nafis B Eghrari et al. was published in Regional Anesthesia & Pain Medicine at 23:30 UK time on Thursday 10 July. 

     

    DOI: 10.1136/rapm-2025- 106577

     

     

    Declared interests

    Prof Ian Maidment: No declarations of interest

    Prof Martin Prince: No conflicts of interest to report

    Prof Tara Spires-Jones: I have no conflicts with this study but have received payments for consulting, scientific talks, or collaborative research over the past 10 years from AbbVie, Sanofi, Merck, Scottish Brain Sciences, Jay Therapeutics, Cognition Therapeutics, Ono, and Eisai. I am also Charity trustee for the British Neuroscience Association and the Guarantors of Brain and serve as scientific advisor to several charities and non-profit institutions.

    Prof Sir John Hardy: Have consulted for Eisai

    For all other experts, no reply to our request for DOIs was received.

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  • Does Gabapentin Raise Dementia Risk?

    Does Gabapentin Raise Dementia Risk?

    The anticonvulsant gabapentin has been linked to a significantly increased risk of developing mild cognitive impairment (MCI) or dementia. However, some experts are urging caution in interpreting the study. 

    After adjusting for demographics, comorbidities, and use of other pain medications, adults prescribed gabapentin for chronic low back pain had a 29% higher risk of developing dementia and an 85% higher risk of MCI within 10 years, compared to those with back pain who were not prescribed the drug. 

    This finding provides “a foundation to further research whether gabapentin plays a causal role in the development of dementia and cognitive decline,” the investigators, led by Nafis Eghrari, Case Western Reserve University School of Medicine, Cleveland, Ohio, wrote.

    In the meantime, they said their observations “support the need for close monitoring of adult patients prescribed gabapentin to assess for potential cognitive decline.” 

    The study was published online July 10 in Regional Anesthesia & Pain Management. 

    Hidden Cognitive Cost of Pain Relief?

    Gabapentin has become a common go-to alternative to opioids for chronic pain because of its low abuse potential, but its association with cognitive decline and dementia remain unclear. 

    To investigate, Eghrari and colleagues used the TriNetX national database of de-identified patient records to recreate a propensity-score matched cohort of 26,416 gabapentin users and an equal number of nonusers.

    In the initial analysis of all adults aged 18 and older, gabapentin prescription was associated with a higher incidence of dementia (risk ratio [RR], 1.29) and MCI (RR, 1.85). 

    To explore age-dependent differences, the researchers stratified the cohort into elderly (age ≥ 65) and nonelderly (age 18-64) groups. 

    In the elderly cohort, gabapentin prescription was associated with increased incidence of both dementia and MCI (RR 1.28 and 1.53, respectively). Similarly, dementia and MCI were more commonly diagnosed in nonelderly gabapentin users than nonusers (RR 2.10 and 2.50, respectively).

    The researchers further stratified the nonelderly group into narrower age ranges: 18-34, 35-49 and 50-64 years. Among the 18-34 age group, there was no significant difference in dementia or MCI incidence between gabapentin users and nonusers.

    In contrast, patients aged 35-49 who were prescribed gabapentin had an increased likelihood of both dementia (RR, 2.44) and MCI (RR, 3.50). A similar pattern was observed in the 50-64 age group, where gabapentin exposure was associated with elevated incidence of dementia (RR, 2.28) and MCI (RR, 2.22). 

    The risk increased further with prescription frequency: patients with 12 or more gabapentin prescriptions had a higher incidence of dementia (RR, 1.40) and MCI (RR, 1.65) than those prescribed gabapentin 3-11 times. 

    Interpret With Caution

    Several experts offered perspective on the study in a statement from the UK nonprofit Science Media Centre. 

    Martin Prince, professor of epidemiological psychiatry, King’s College London, cautioned that “confounding and reverse causality are tenable explanations for the observed effects.” 

    Tara Spires-Jones, director of the Centre for Discovery Brain Sciences at the University of Edinburgh in Scotland, noted that “while authors used statistical methods to try and account for other risk factors, this type of study cannot prove that gabapentin was the cause of increased dementia risk.”

    “One very important factor that was not examined in this study is levels of physical activity. People with chronic pain requiring gabapentin may have been less physically active, which is a known risk factor for developing dementia,” Spires-Jones said. 

    Prof Sir John Hardy, group leader at the UK Dementia Research Institute at University College London said while the study is “interesting, one has to worry that these types of findings are artefactual and result (for example) from a marginal acute effect on cognitive performance rather than effects on the underlying disease.”

    Ian Maidment, professor in clinical pharmacy, Aston University, Birmingham, England, noted that the study did not control for length of treatment or dose of gabapentin and further noted that “other similar recent studies have failed to find a link.”

    In Maidment’s view, “the jury is out on whether gabapentin causes dementia.”

    The study had no specific funding. Eghrari, Prince, Maidment, and Spires-Jones declared no conflicts of interest. Hardy has consulted for Eisai. 

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  • Gabapentin Tied to Dementia Risk in Pain Patients

    Gabapentin Tied to Dementia Risk in Pain Patients


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    Gabapentin is often seen as a safer option for treating chronic pain, but new research suggests it may come with cognitive risks.

    A large study using US electronic health records, published in Regional Anesthesia & Pain Medicine, found that adults prescribed gabapentin for low back pain were more likely to develop dementia or mild cognitive impairment.

    Is gabapentin safe for long-term use in treating back pain?

    Chronic low back pain affects millions and puts pressure on healthcare systems worldwide, and treating it isn’t simple. Opioids used to be the go-to option; however, their high risk of dependence and overdose has pushed doctors to look elsewhere.

    Originally developed for epilepsy, gabapentin is now widely prescribed for chronic pain, especially nerve-related pain. Its appeal lies in its low potential for addiction. Some researchers have also suggested it might protect the brain, although concerns are growing.

    There are signs that gabapentin might not be as safe as once thought – at least not for long-term use. Reports have linked it to memory problems and signs of brain aging.

    “Gabapentin is widely used to treat chronic pain, but its association with cognitive decline and dementia remains unclear,” said the authors of the recent study.

    Previous research has been inconsistent: some studies show a link to cognitive decline, whereas others do not. It’s also unclear whether certain age groups are more affected than others.

    Now, a large new study has added weight to those concerns.

    The investigation set out to test the association using real-world medical records, with a focus on how age and prescription frequency might influence risk.

    Study finds increased dementia risk with gabapentin use

    The team used data from TriNetX, a large US database of electronic health records covering 68 healthcare organizations. They looked at 52,828 adults diagnosed with chronic low back pain, half of whom had been prescribed gabapentin and the other half – matched by age, sex, existing conditions and other medications – had not.

    They tracked the patients over 10 years to see who developed dementia or mild cognitive impairment (MCI). The analysis controlled for other painkillers and pre-existing health issues.

    The patients who were prescribed gabapentin 6 times or more were 29% more likely to develop dementia and 85% more likely to develop MCI than those who hadn’t taken the drug.

    However, age also made a difference. Among 18–64-year-olds, the risk of either diagnosis more than doubled compared to non-users. Within that group, the biggest jump was in people aged 35–49 years, who had more than twice the risk of dementia and more than 3 times the risk of MCI. A similar pattern was observed in those aged 50–64 years.

    No added risk was seen in patients aged 18 to 34 years.

    There was also a dose-response trend, with people who’d had 12 or more prescriptions being 40% more likely to develop dementia, and 65% more likely to develop MCI, than those with 3–11 prescriptions.

    What does this mean for gabapentin and dementia research?

    These results raise doubts about the long-term safety of gabapentin as a treatment for chronic pain. While it’s often viewed as a safer alternative to opioids, this study suggests it may carry its own risks.

    “Our findings indicate an association between gabapentin prescription and dementia or cognitive impairment within 10 years. Moreover, increased gabapentin prescription frequency correlated with dementia incidence,” said the team. “Our results support the need for close monitoring of adult patients prescribed gabapentin to assess for potential cognitive decline.”

    However, the results do not mean that gabapentin directly causes dementia. The study doesn’t show cause and effect, nor does it include information on dose or treatment length.

    As the study was retrospective, it’s also possible that early cognitive symptoms led to gabapentin use rather than the reverse.

    There’s a clear need for further research, and prospective studies could help confirm if the link is real. Researchers also need to explore how dosage and duration affect outcomes and how gabapentin might influence the brain over time.

     

    Reference: Eghrari NB, Yazji IH, Yavari B, Acker GMV, Kim CH. Risk of dementia following gabapentin prescription in chronic low back pain patients. Reg Anesth Pain Med. 2025. doi: 10.1136/rapm-2025-106577

     

    This article is a rework of a press release issued by BMJ Group. Material has been edited for length and content. 

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  • A third of UK women who died during or after pregnancy known to children’s services, study finds | Pregnancy

    A third of UK women who died during or after pregnancy known to children’s services, study finds | Pregnancy

    A third of women who have died during, or in the year after, pregnancy were known to children’s social care services, with a fifth of these deaths being the result of suicide, according to research which is the first of its kind.

    Between 2014 and 2022, 1,451 women died during pregnancy or within a year of giving birth, with 420 of these women having been in contact with children’s social care services, according to analysis of data from the maternal, newborn, and infant clinical outcome review programme provided by MBBRACE-UK.

    Of the deaths, a fifth were the result of suicide, while a third were because of “other psychiatric causes” including drug-related deaths, and 5% were because of homicide, according to the analysis published in BMJ Medicine and led by academics at King’s College London and the University of Oxford.

    The report is the first of its kind to detail the high proportion of women with children’s social care involvement who die during and after pregnancy in the UK and the care they receive in that period. Of these women, 65% reported having experienced domestic abuse before or during their pregnancy, while a third had experienced abuse during their childhood.

    The study included a review of anonymised care records for 47 of the women included in the research, which found uncoordinated involvement of maternity and mental health services with social care and other medical specialists, resulting in overwhelming and disjointed appointments.

    Many of the women who died and were in contact with children’s social care services came from “backgrounds of trauma and abuse, and yet despite their efforts to keep up with demanding appointment schedules, they often face scrutiny and judgment rather than receiving support for the issues they are facing”, according to Kaat De Backer, the lead author of the study, from King’s College London.

    She added: “Too often, the professionals the women are in touch with don’t work together to provide holistic care, which increases the pressure on a mother.

    “When women have access to designated multi-disciplinary teams with specialist knowledge and capacity to provide integrated and holistic care, these barriers can be overcome. It makes it easier to understand who is doing what and when, for women and professionals.”

    The researchers called for urgent changes to be made to how mothers with social care involvement are treated by clinicians and other agencies during their pregnancies and early motherhood.

    Naomi Delap, the director of Birth Companions, said the study highlighted the “acute need for better care for women with children’s social care involvement, and the significant barriers that get in the way of providing that care”.

    She added: “To help improve things, we need coordinated national policy and clear expectations across the health and social care systems.”

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  • Is exercise the elixir of youth? It may lower risk of early death by up to 40%, new study finds | Health

    Is exercise the elixir of youth? It may lower risk of early death by up to 40%, new study finds | Health
























    Is exercise the elixir of youth? It may lower risk of early death by up to 40%, new study finds | Health | news8000.com


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  • WHO establishes communities of practice for pathogen genomics surveillance

    WHO establishes communities of practice for pathogen genomics surveillance

    The International Pathogen Surveillance Network (ISPN), set up by the WHO Hub for Pandemic and Epidemic Intelligence, has set up three communities of practice (CoPs), each designed to drive  progress in pathogen genomics surveillance.

    The first CoP focuses on addressing the barriers to effectively leverage genomics data for public health decision-making, the second emphasizes strengthening emergency response capabilities using genomics data, and the third is dedicated to developing best-practices for wastewater and environmental surveillance. These targeted communities provide a structured framework for collaboration, ensuring that expertise is shared and applied effectively across critical domains to address challenges.

    CoP on Pathogen Genomics Data

    The implementation of genomic sequencing into public health laboratories has demanded a parallel increase in bioinformatics capacity to store, process, share and integrate genomics data to effectively leverage its public health utility. The CoP on genomics data brings together 60 experts from across the IPSN network representing all WHO regions to envision a scalable, interconnected, and sustainable bioinformatics ecosystem that supports equitable access to pathogen genomic surveillance.

    Since its inception in 2024, ‘CoP Data’ has provided a forum to identify gaps in the pathogen genomics data architecture and has prioritized discussions that will help address them. These discussions have included examining the benefits of and barriers to pathogen data sharing in emergency response, exploring the pathogen data infrastructure landscape, and considering efforts to support equitable access to computational resources for genomic surveillance. The expert group has also guided the development of an upcoming document on defining the principles and attributes pathogen genomic data sharing platforms should aspire to in order to deliver their public health function. 

    From these discussions, it is clear that an optimized data architecture is essential to support both local and global surveillance and to help the community to reimagine how genomic data is most effectively exchanged and utilized to drive public health decision-making. Addressing this data challenge should lead ultimately to a more effective response to current and future infectious disease threats.   

    CoP on Specialised Surveillance for Emergency Response

    Genomic surveillance data is increasingly integral to public health decision-making in emergency response, providing insights into disease transmission and  strain evolution and facilitating analysis of differential strain virulence that contributes to the evidence base for risk assessment. In August 2024, WHO Director-General, Dr Tedros Adhanom Ghebreyesus, determined that the upsurge of mpox in the Democratic Republic of the Congo and adjacent African countries constituted a public health emergency of international concern under the International Health Regulations (2005). To support this response, IPSN established the CoP on Specialized Surveillance for Emergency Response (SSER) to facilitate the coordination of pathogen genomics actors.

    This CoP supports knowledge exchange among members, enabling them to address challenges and identify opportunities for leveraging pathogen genomics and wastewater surveillance in emergency responses. Within the pathogen genomics workstream, the group has focused on supporting harmonization and in-country deployment of the bioinformatics analysis of MPXV genome data to strengthen quality of the analysis. Additionally, the group is developing a guidance document outlining analytical considerations for MPXV genomic surveillance.

    In parallel, the wastewater surveillance workstream convened experts over 5 sessions across 30 countries, to explore the feasibility of detecting MPXV from sewered and unsewered settings; to review the current uptake of wastewater and environmental surveillance (WES) for mpox response,  and to discuss enabling factors for its use, and ongoing technical, regulatory and data utilization constraints. These efforts underscore the need for a more cohesive and consistent wastewater surveillance community for emergency response.

    CoP on Wastewater and Environmental Surveillance

    In June 2025, IPSN launched its newest CoP dedicated to the advancement of genomics in wastewater and environmental surveillance (CoP WES).  The CoP WES aims to enhance global awareness and confidence in the WES capabilities and limitations for genomics, ultimately supporting policy-makers in making evidence-based decisions on how to tailor the use of genomic WES as part of their public health surveillance systems.

    The use of genomics in wastewater and environmental surveillance has significant potential to enhance collaborative surveillance through pathogen detection and tracking, providing situational awareness and supporting early warning capabilities. Scientific developments have also resulted in an enhanced characterization of population pathogen diversity and faster detection of new variants. Yet genomics WES remains a nascent field hindered by barriers to progress, including a fragmented knowledge landscape, limited standardization and consensus on best practices, and uncertainty as to how the data can be leveraged by public health systems.

    The CoP WES offers a structured platform for continuous collaboration and knowledge sharing and capture that tackles many ongoing obstacles faced by the field today. Drawing on existing momentum and activities of other leading experts and organizations in the genomics WES ecosystem, the COP WES will serve as a hub for evidence generation and curation, reducing duplication of efforts, amplifying successful models and creating new products to fill unmet needs.

    Collaboration for effective global public health surveillance

    Communities of Practice are powerful mechanisms for fostering collaboration, driving innovation, and addressing complex challenges in pathogen genomics surveillance. By uniting experts, facilitating knowledge exchange, and developing actionable guidance, these CoPs are laying the groundwork for a more interconnected and effective global public health surveillance system. Moving forward, the IPSN will continue to convene and strengthen these platforms to develop scalable, sustainable solutions that strengthen preparedness and response to infectious disease threats worldwide.

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  • The UN warns millions will die by 2029 if US funding for HIV programs isn’t replaced

    The UN warns millions will die by 2029 if US funding for HIV programs isn’t replaced

    LONDON (AP) — Years of American-led investment into AIDS programs has reduced the number of people killed by the disease to the lowest levels seen in more than three decades and provided life-saving medicines for some of the world’s most vulnerable.

    But in the last six months, the sudden withdrawal of U.S. money has caused a “systemic shock,” U.N. officials warned, adding that if the funding isn’t replaced, it could lead to more than 4 million AIDS-related deaths and 6 million more HIV infections by 2029.

    A new UNAIDS report released Thursday said the funding losses have “already destabilized supply chains, led to the closure of health facilities, left thousands of health clinics without staff, set back prevention programs, disrupted HIV testing efforts and forced many community organizations to reduce or halt their HIV activities.”

    It also said that it feared other major donors scaled back their support, reversing decades of progress against AIDS worldwide — and that the strong multilateral cooperation is in jeopardy because of wars, geopolitical shifts and climate change.

    A ‘lifeline’ removed

    AP AUDIO: UN says if US funding for HIV programs is not replaced, millions more will die by 2029

    AP correspondent Karen Chammas reports on the impact of cuts to US funding for international HIV programs.

    The $4 billion that the United States pledged for the global HIV response for 2025 disappeared virtually overnight in January, when U.S. President Donald Trump ordered that all foreign aid be suspended and later moved to shutter the U.S. AID agency.

    Andrew Hill, an HIV expert at the University of Liverpool who is not connected to the United Nations, said that while Trump is entitled to spend U.S. money as he sees fit, “any responsible government would have given advance warning so countries could plan,” instead of stranding patients in Africa where clinics were closed overnight.

    The U.S. President’s Emergency Plan for AIDS Relief, or PEPFAR, was launched in 2003 by U.S. President George W. Bush, the biggest-ever commitment by any country focused on a single disease.

    UNAIDS called the program a “lifeline” for countries with high HIV rates, and said that it supported testing for 84.1 million people, treatment for 20.6 million, among other initiatives. According to data from Nigeria, PEPFAR also funded 99.9% of the country’s budget for medicines taken to prevent HIV.

    U.N. Assistant Secretary-General Angeli Achrekar, a UNAIDS deputy executive director who was PEPFAR’s principal deputy coordinator until January 2023, said the program is under review by the Trump administration though Secretary of State Marco Rubio issued a waiver “to continue life-saving treatment.”

    ““The extent to which it will continue in the future, we don’t know,” she told a video news conference with U.N. reporters in New York. “We are cautiously hopeful that PEPFAR will continue to support both prevention and treatment services.”

    A gap impossible to fill

    In 2024, there were about 630,000 AIDS-related deaths worldwide, per a UNAIDS estimate — the figure has remained about the same since 2022 after peaking at about 2 million deaths in 2004.

    Even before the U.S. funding cuts, progress against curbing HIV was uneven. UNAIDS said that half of all new infections are in sub-Saharan Africa.

    Tom Ellman of Doctors Without Borders said that while some poorer countries were now moving to fund more of their own HIV programs, it would be impossible to fill the gap left by the U.S.

    “There’s nothing we can do that will protect these countries from the sudden, vicious withdrawal of support from the U.S.,” said Ellman, head of the group’s South Africa medical unit.

    Experts also fear another significant loss — data.

    The U.S. paid for most HIV surveillance in African countries, including hospital, patient and electronic records, all of which has now abruptly ceased, according to Dr. Chris Beyrer, director of the Global Health Institute at Duke University.

    “Without reliable data about how HIV is spreading, it will be incredibly hard to stop it,” he said.

    A new drug revives hope

    The uncertainty comes in the wake of a twice-yearly injectable that many hope could end HIV. Studies published last year showed that the drug from pharmaceutical maker Gilead was 100% effective in preventing the virus.

    At a launch event Thursday, South Africa’s health minister Aaron Motsoaledi said the country would “move mountains and rivers to make sure every adolescent girl who needs it will get it,” saying that the continent’s past dependence upon US aid was “scary.”

    Last month, the U.S. Food and Drug Administration approved the drug, called Yeztugo, a move that should have been a “threshold moment” for stopping the AIDS epidemic, said Peter Maybarduk of the advocacy group Public Citizen.

    But activists like Maybarduk said Gilead’s pricing will put it out of reach of many countries that need it. Gilead has agreed to sell generic versions of the drug in 120 poor countries with high HIV rates but has excluded nearly all of Latin America, where rates are far lower but increasing.

    “We could be ending AIDS,” Maybarduk said. “Instead, the U.S. is abandoning the fight.”

    ___

    Associated Press writer Edith M. Lederer at the United Nations contributed to this report.

    ___

    The Associated Press Health and Science Department receives support from the Howard Hughes Medical Institute’s Department of Science Education and the Robert Wood Johnson Foundation. The AP receives financial support for global health and development coverage in Africa from the Gates Foundation. The AP is solely responsible for all content. Find AP’s standards for working with philanthropies, a list of supporters and funded coverage areas at AP.org.

    ___

    A previous version of this story was corrected to show that the name of the drug is Yeztugo, not Sunlenca.


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  • This influencer shares her active life. Offline, she’s fighting for treatment of a painful condition.

    This influencer shares her active life. Offline, she’s fighting for treatment of a painful condition.

    A scroll through Aurora McCausland’s wildly popular social media accounts — she has more than 300,000 followers across TikTok and Instagram — shows an active young mom dancing, cleaning and tackling major renovation projects in her Utah home.

    Behind the scenes, though, is a painful reality: McCausland has lipedema, a progressive and debilitating disease that causes fat in connective tissue to build up disproportionately, most often in the legs, ankles and hips.

    She said her legs throb with pain, swell unpredictably and feel heavy, like they’re filled with cement. It’s a major source of frustration for the mother of two young children. Standing up can cause her to black out.

    “Things that I feel like I should be able to do cause pain pretty quickly, and then I kind of have to tap out,” said McCausland, 30, of West Valley City, Utah. “Getting down to play with my kids is really hard.”

    Aurora McCausland first noticed symptoms of lipedema as a teenager. It took more than a decade for her to be diagnosed.Courtesy Aurora McCausland

    She’s tried to manage the pain with compression garments, lymphatic drainage and anti-inflammatory diets.

    “Those are helpful at potentially slowing down the disease,” her physician, Dr. David Smart, said. “But really, only surgery helps to reverse the disease process.”

    Smart is a dermatologic surgeon at the Roxbury Institute in Murray, Utah. He performs a specialized type of liposuction that removes the diseased tissue to restore mobility.

    The procedure is not cosmetic, and despite the buildup of fat, lipedema is not related to obesity. It’s not caused by overeating or inactivity. It’s a hormonally-driven inflammatory condition, one that’s largely resistant to diet and exercise.

    “It goes against the more traditional health dogma that’s out there about normal fat,” Smart said.

    Lipedema is almost exclusively seen in women, but scientists don’t have a good handle on how many are affected. Some estimates suggest it may affect up to 11% of women.

    “There are no large-scale, population-based epidemiologic estimates. We don’t have blood tests. We don’t have imaging studies,” said Dr. Aaron Aday, co-director of vascular medicine at Vanderbilt University Medical Center in Nashville, Tennessee.

    Denied relief

    Many women first notice symptoms of lipedema at puberty, and the disease often worsens during major hormonal shifts like pregnancy or menopause.

    McCausland said her symptoms first appeared during her early teens: leg pain, swelling and bruising from the slightest touch. “I thought it was just growing pains,” she said. Fat built up around her ankles. No matter how physically active she was — dancing and CrossFit were two hobbies — she couldn’t make the fat in her lower legs go away.

    Still, she was told it was just excess weight. “That if I worked out more, ate less, it would go away,” she said. “But no matter what I did, my legs just hurt more. I was doing everything right and getting worse.”

    If you are dealing with bills that seem to be out of line or a denial of coverage, care or repairs, whether for health, home or auto, please email us at Costofdenial@nbcuni.com.

    McCausland’s five sisters experienced similar symptoms. She said none knew what the problem was until one of the sisters got liposuction to slim down her lower legs.

    But lipedema fat isn’t the same as typical fat. Instead of feeling soft, it can feel like hard nodules under the skin. Regular liposuction can be risky to use on lipedema patients.

    It took far longer than it should have for her sister’s doctor to do the procedure, McCausland said.

    “The doctor ended up giving her third-degree internal burns all on her legs, because he didn’t know that it wasn’t normal fat. He just kept going, having to go over and over and over trying to remove it,” she said. “It was just this horrible thing that happened. Obviously the doctor had no idea that she had this condition, and neither did my sister.”

    Aday — who hasn’t treated McCausland — said that a specialized type of liposuction, performed by a surgeon with extensive knowledge of lipedema, is the most effective way to treat the disorder. It can reverse symptoms in many people. Some patients, he said, may have to have the procedure repeated.

    The Roxbury Institute said that McCausland would need two liposuction surgeries, totaling more than $35,000. But her former insurance provider, Cigna Healthcare, denied coverage for the procedure twice.

    In an emailed statement, a Cigna representative said: “Lipedema is a painful condition that disproportionately impacts women, and we cover a range of treatment options, including liposuction, for patients that meet evidence-based clinical criteria. Ms. McCausland’s case was carefully reviewed by multiple doctors, including a plastic surgeon with expertise in lipedema. Based on the information submitted by her doctor, she did not meet the clinical criteria for liposuction at that time.”

    McCausland believes her coverage was denied because she didn’t look sick enough, adding that she suspects it’s based on her social media posts.

    They said “that it’s not medically necessary,” McCausland said. “That’s absurd. They’re not looking at how I live. They’re looking at a photo and deciding I don’t look bad enough to be helped.”

    Cigna told NBC News that social media isn’t considered when making coverage decisions. “Our coverage decisions are based on the clinical information submitted by a patient’s treating physician in accordance with coverage policies and the patient’s plan design,” the representative said.

    Her health insurance has since switched to MotivHealth, because of her husband’s new job. McCausland said MotivHealth has already suggested to her in a phone call that it’s not a procedure it usually covers but she can submit additional documentation. A representative for the company did not respond to several requests for comment.

    A long under-recognized disease

    Lipedema is categorized in four stages, based on visual appearance. Stage 1 looks like minor fat accumulation and Stage 4 appears as severe leg disfigurement. Appearance, however, doesn’t always match the severity of symptoms.

    “You can have a Stage 1 patient that has very severe and crippling symptoms of pain and swelling, and somebody who is maybe more progressed visibly that doesn’t have such severe symptoms,” Smart said.

    McCausland is a prime example. She doesn’t look sick, according to some commenters on her social media videos.

    Aurora McCausland.
    McCausland said her legs throb with pain, swell unpredictably and feel heavy, like they’re filled with cement.Courtesy Aurora McCausland

    “I’ve gotten a handful of people saying, ‘Well, I’ve looked at your other videos, and I agree with your insurance company,’” she said.

    “This is very likely the reason why lipedema has been so under-recognized for such a long time,” Smart said. “So many people, so many insurance companies, so many physicians, have been telling lipedema patients for decades to just ‘work out, eat better, lose weight,’ when that’s not actually the problem.”

    He said waiting until the condition progresses is dangerous. Without treatment, lipedema advances, causing more inflammation, worsening pain and permanent joint damage. The longer surgery is delayed, the harder it is to restore mobility in later stages.

    “It’s really unfortunate for Aurora, because at that early stage, it is less likely that she gets insurance coverage,” Smart said. “They’re not looking at the severity of her symptoms. They’re not looking at the severity of her pain, the decrease in mobility, her lack of ability to be able to perform those daily activities of living.”

    Jonathan Kartt, chief executive officer of the Lipedema Foundation, said that the pain experienced by women with lipedema can be measured objectively.

    Using a tool to measure how patients perceive stimuli like temperature and touch, researchers in Germany found that women with lipedema had a lower pain threshold compared with other women. The pain was specific to areas affected by the disease.

    “The differences were so stark,” Kartt said, that it’s possible to use “this test to actually diagnose or confirm a diagnosis of lipedema.”

    Aday, of Vanderbilt, is leading an effort to create a national biobank of information on lipedema patients. The team takes blood samples and urine, as well as fat and skin biopsies.

    “It’s meant to be a living research resource,” he said. “We want other investigators to use these data, build upon it and generate new data.”

    There is also growing excitement in the lipedema field to see whether the blockbuster GLP-1 drugs, like Ozempic and Wegovy, might be useful. The drugs are mainly used to treat Type 2 diabetes and obesity, but have been shown to provide benefits for other diseases. Aday is working to secure funding for such a study.

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