Carbon Chemist

Tag: Liver Disease

  • Nomogram could be a game-changer for predicting alcohol-related liver cancer risk

    Nomogram could be a game-changer for predicting alcohol-related liver cancer risk

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    Liver cancer, unfortunately, is the sixth most common cancer and the third most frequent cause of cancer-related death globally. However, its distribution and causes vary greatly across different regions. While areas like Eastern Asia and sub-Saharan Africa see the most cases, the reasons behind them differ significantly.

    In high-income countries, liver cancer has been on the decline thanks to widespread newborn hepatitis B vaccination and antiviral drugs. Meanwhile, low-income countries witness a worrying rise, often linked to increased hepatitis B and C infections and injectable drug use.

    While viral hepatitis remains a major concern, another factor is gaining attention: alcohol consumption. Studies show that chronic alcohol consumption can directly cause about 10% of cancer cases in men and 3%, respectively, in women. In fact, a study at the Mayo Clinic revealed that alcoholic cirrhosis was the main culprit in 29% of patients with hepatocellular carcinoma (HCC), the most common liver cancer type.

    But the study doesn’t just sound the alarm; it also offers a potential solution. Researchers identified key risk factors for HCC in people with alcohol-related liver disease, including heavy drinking, age, diabetes, male sex, and liver cirrhosis. Based on these factors, they developed a novel tool called a nomogram that can predict HCC risk with high accuracy and ease of use.

    This nomogram could be a game-changer for doctors, allowing them to personalize treatment plans and identify individuals at highest risk for HCC. Early intervention could save lives and prevent unnecessary suffering.

    This study underscores the growing public health concern of alcohol-related liver cancer. The newly developed nomogram offers a valuable tool for doctors to identify high-risk individuals and personalize treatment plans, potentially saving lives and preventing unnecessary suffering.

    While the study provides valuable insights, it acknowledges limitations like its retrospective nature and the need for further validation in larger, prospective studies. Additionally, incorporating other factors like smoking, genetics, and dietary habits could further improve the prediction model.

    The researchers also highlight the need for future research on non-alcoholic fatty liver disease and its link to liver cancer, as this area remains under-investigated.

    Overall, this study shines a light on the rising threat of alcohol-related liver cancer and offers a promising tool for early detection and intervention. Further research and public health efforts are crucial to combat this growing health challenge.

    Source:

    First Hospital of Jilin University

    Journal reference:

    Chang, B., et al. (2024). Prevalence and prediction of hepatocellular carcinoma in alcohol-associated liver disease: a retrospective study of 136 571 patients with chronic liver diseases. eGastroenterology. doi.org/10.1136/egastro-2023-100036.

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  • SickKids study offers new path for pediatric rare disease clinical trials

    SickKids study offers new path for pediatric rare disease clinical trials

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    Using a novel methodology, researchers at The Hospital for Sick Children (SickKids) are the first in pediatric research to use data from an international real-world cohort to overcome the barriers associated with conducting randomized clinical trials in children with rare diseases. 

    The gold standard for evaluating new therapeutics is through randomized clinical trials, where one group of individuals receives treatment while another does not. Unfortunately, conducting this type of clinical trial proves challenging for many rare conditions due to the limited number of individuals with the condition, making meaningful comparisons difficult. Additionally, in pediatrics, it can be unethical to give a potential treatment to some children and not others. 

    In a study published in Hepatology, a team of SickKids scientists developed an innovative and robust statistical approach which may eliminate the need for traditional randomized clinical trials, demonstrating the effectiveness of a medication in reducing disease progression and liver transplants in children with Alagille syndrome (ALGS). 

    By using a global database, we were able to mimic high-quality clinical trial results by comparing present-day outcomes to historical data. Not only do our findings show a marked improvement in liver-related outcomes for children with ALGS treated with this medication, but they also present a path forward for randomized clinical trials for other rare diseases.” 


    Dr. Binita Kamath, Senior Associate Scientist in the Developmental & Stem Cell Biology program and Principal Investigator and senior author of the study

    ALGS is a rare genetic disorder in which a patient has an inadequate number of bile ducts, which usually drain bile from the liver into the intestine. The bile then builds up and causes liver damage. Between 60 to 75 percent of patients with ALGS undergo a liver transplant before they reach adulthood. 

    Due to the rarity and severity of the condition, clinical trials have historically been difficult to conduct, especially over longer durations of time, since it is unethical and not feasible to have children take a placebo for several years. 

    In a previous study describing an international cohort of children with ALGS, Kamath and Shannon Vandriel established an international database of clinical, genetic and laboratory data in children and young adults with ALGS called The Global ALagille Alliance (GALA) study. 

    In this study, using the data of 469 untreated patients from GALA, the research team were able to compare their long-term outcomes to 84 children being treated with maralixibat, a medication approved in the US and Europe and recently in Canada for symptomatic relief of the severe itching experienced by patients with ALGS. 

    Using this innovative approach, the research team found that over six years, children taking maralixibat showed a 70 per cent improvement in event-free survival and a 67 per cent improvement in transplant-free survival. 

    “While the current indication for maralixibat is for itching, our data showed that over a longer period, the medication actually reduces the rate of liver transplants in patients with ALGS,” says Kamath, who is also a Staff Physician in the Division of Gastroenterology, Hepatology and Nutrition. 

    In addition to these benefits, the methodology used by the research team has ground-breaking implications for the development and implementation of clinical trials for patients with rare diseases. 

    Kamath and Vandriel believe similar approaches could be applied to any rare disease with enough historical data. 

    “Our research provides an alternative to the challenges associated with recruiting patients with life-threatening conditions or debilitating symptoms for long-term clinical trials,” says Kamath. “While our study was specific to patients with ALGS, I hope this sparks a renewed interest in international databases of individuals with rare diseases which can provide real-world data that can be used to help evaluate new therapies.” 

    Funding for The GALA study was provided by grants from The Alagille Syndrome Alliance, Ipsen Pharmaceuticals and Mirum Pharmaceuticals to SickKids Foundation. 

    Source:

    The Hospital for Sick Children

    Journal reference:

    Hansen, B. E., et al. (2023) Event-free survival of maralixibat-treated patients with Alagille syndrome compared to a real-world cohort from GALA. Hepatology. doi.org/10.1097/HEP.0000000000000727.

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  • Understanding obesity’s effects on liver metabolism

    Understanding obesity’s effects on liver metabolism

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    Your liver plays a vital role in your metabolism, the biological process which converts food into energy. We know that being overweight can negatively affect metabolic activity, but not exactly how. To better understand this, researchers compared the livers of mice which were a typical weight with mice which were obese. They were surprised to find that biological regulation of metabolic activity, after a period of feasting and fasting, was reversed between them. In typical mice, allosteric regulation (the process which controls metabolism) was inhibited during feeding and activated when fasting. However, in obese mice, allosteric regulation increased during feeding and decreased when fasting. Investigating the reasons behind this reversed biological behavior could help health professionals understand how obesity affects the body and the development of disease.

    The World Obesity Federation (WOF) estimates that by 2035, over 4 billion people will be overweight or living with obesity. This may lead to a rise in obesity-related health conditions, such as heart disease, nonalcoholic fatty liver disease and Type 2 diabetes. Identifying the causes and effects of obesity, which is now understood to be a complex disease, is key for physicians looking to provide support and help people stay healthy.

    One known way that obesity can affect health is by impacting metabolism, the process by which our bodies take in, store and use energy from our food. Certain organs play key roles in this process, notably the liver. Not only is food processed there to provide energy, but it is one of the places where useful products at the end of the metabolic process are stored until we need them. To better understand the effects of obesity on the liver, researchers compared the livers of typical mice and obese mice after periods of feeding and fasting.

    The team carried out trans-omics analysis, an approach where they gathered data on five sets of biological processes (multi-omics). They then combined these layers of data with information from biological databases to create a trans-omic network. This gave them an overview of how the different layers interacted. “

    We constructed a trans-omic network of metabolic reactions in the livers of mice that could feed freely. We then compared this with data we had previously gathered from mice that had fasted for 16 hours. While enzyme and allosteric regulation which controls metabolism was suppressed in typical mice during feeding, we were surprised to find that the reverse occurred in obese mice and that this activity increased.”

    Professor Shinya Kuroda, Graduate School of Science, University of Tokyo

    When we eat, our liver builds up stores of energy which is then released as needed, a system known as metabolic homeostasis. However, the researchers saw that in obese mice this equilibrium became dysregulated, i.e., normal function was disrupted, indicating a potential breakdown of the system. This could lead to metabolic disorders such as tiredness, lack of energy and decreased appetite. By contrast, they saw that transcriptional regulation, a process which regulates metabolism and controls cell activity at a genetic level, did not change much between feeding and fasting. This means that, compared to allosteric regulation, it is more stable and less affected by what we eat.

    The team noted that what they observed may not only be evidence of disruption within the liver alone, but a change to broader metabolic cycles throughout the body. “Obesity is a metabolic disease, so to understand it, it is important to construct a trans-omic network with metabolome (the complete set of small-molecule chemicals) at its center,” said Kuroda. “We are interested not only in the liver, but also how the products of metabolic reactions circulate between liver and muscle through the blood in obese mice, which is what we will be working on now.”

    Source:

    Journal reference:

    Bai, Y., et al. (2024) Trans-omic analysis reveals opposite metabolic dysregulation between feeding and fasting in liver associated with obesity. iScience. doi.org/10.1016/j.isci.2024.109121.

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  • Risk of non-alcoholic fatty liver disease for cardiovascular disease and all cause death in patients with type 2 diabetes mellitus

    Risk of non-alcoholic fatty liver disease for cardiovascular disease and all cause death in patients with type 2 diabetes mellitus

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    In a recent study published in the British Medical Journal, researchers investigated the link between non-alcoholic fatty liver disease (NAFLD) in individuals with type 2 diabetes mellitus (T2DM) and all-cause death and cardiovascular disease. They found that individuals with NAFLD and T2DM show an increased risk of cardiovascular disease (CVD) and all-cause death.

    Study: Association of non-alcoholic fatty liver disease with cardiovascular disease and all cause death in patients with type 2 diabetes mellitus: nationwide population based study. Image Credit: Explode/Shutterstock.com
    Study: Association of non-alcoholic fatty liver disease with cardiovascular disease and all cause death in patients with type 2 diabetes mellitus: nationwide population based study. Image Credit: Explode/Shutterstock.com

    Background

    The prevalence of NAFLD is on the rise globally and is often associated with metabolic disorders involving insulin resistance. It poses a significant health concern due to its potential to lead to liver complications and CVD, which is a leading cause of mortality, especially among NAFLD patients.

    T2DM is a major risk factor for CVD and is closely linked to higher NAFLD prevalence and severity. The complex relationship between NAFLD and T2DM suggests a synergistic effect on cardiovascular risk, with a substantial proportion of T2DM patients also having NAFLD. However, studies examining their association with CVD have yielded mixed results. While some found no correlation, others demonstrated a doubled risk of CVD in T2DM patients with NAFLD compared to those without. Additionally, previous studies were limited by their cross-sectional designs and small sample sizes.

    To address this gap, researchers in the present study aimed to assess the risk of CVD and all-cause mortality associated with NAFLD in T2DM patients using a large-scale, population-based longitudinal approach.

    About the study

    This nationwide cohort study utilized data from the National Health Information Database linked t the National Health Screening Program. The exclusion criteria were age ≤ 20 years, consumption of ≥30 g/day alcohol, missing data, or a history of type 1 diabetes mellitus, chronic hepatitis B, and C, liver cirrhosis, hepatocellular carcinoma, or CVD. Additionally, patients who developed CVD within one year were also excluded.

    A total of 7,796,763 participants were selected, and the endpoint was the occurrence of all-cause death, CVD, or until 31 December 2018. CVD included myocardial infarction or ischemic stroke, confirmed through hospital admissions with corresponding claims for brain magnetic resonance imaging or computed tomography. The patients were followed-up for a median of 8.13 years.

    Data on anthropometric measurements and laboratory parameters were collected. Blood pressure was measured in a seated position, and fasting venous blood samples were taken to assess various parameters, including glucose, liver enzymes, lipid profile, and creatinine levels. Additionally, the estimated glomerular filtration rate was determined.

    Information on lifestyle factors such as smoking, alcohol consumption, regular exercise, and socioeconomic status was obtained through a standardized self-assessment questionnaire. Statistical methods included Cox proportional hazards models adjusted for various factors, Kaplan-Meier survival curves, and subgroup analyses.

    Results and discussion

    Among the participants, 6.49% of the participants had T2DM. Grade 1 and 2 NAFLD were found in 22.04% and 11.11% of participants, respectively. A higher proportion of T2DM patients had grade 2 NAFLD (26.73%) and grade 1 NAFLD (34.06%) compared to those without T2DM. Among participants with T2DM, 6.77% had CVD, and about 8.38% of participants died. In contrast, among those without T2DM, 2.24% had CVD, and about 2.71% of participants died.

    Incidence rates for CVD, myocardial infarction, ischemic stroke, and all-cause mortality increased with the severity of NAFLD and were higher in patients with T2DM than in those without. Hazard ratios for these outcomes were also higher with grade 1 and grade 2 NAFLD compared to no NAFLD, regardless of T2DM status. Moreover, the five-year absolute risk for these outcomes increased with NAFLD severity, particularly in patients with T2DM. Risk differences for CVD, myocardial infarction, ischemic stroke, and all-cause death were higher between no NAFLD and grade 2 NAFLD than between no NAFLD and grade 1 NAFLD. Additionally, these risk differences were higher in patients with T2DM compared to those without T2DM.

    NAFLD was linked to an increased risk of cardiovascular disease, myocardial infarction, ischemic stroke, and all-cause death in both T2DM and non-T2DM patients (p<0.001). Among NAFLD patients, those with grade 2 NAFLD exhibited the highest risk, followed by grade 1 NAFLD.

    Further, the incidence rates of CVD, myocardial infarction, ischemic stroke, and all-cause death increased sequentially from no NAFLD to grade 1 NAFLD and to grade 2 NAFLD across all age groups, with higher rates observed in T2DM patients.

    The study’s limitations include the use of the fatty liver index for NAFLD definition, lack of assessment of glycated hemoglobin variability and changes in diabetes drugs, limited generalizability to other ethnicities, and the inability to evaluate hepatic fibrosis.

    Conclusion

    In conclusion, patients with T2DM and even mild NAFLD have a higher risk of cardiovascular disease and all-cause death. The risk gap between no NAFLD and grade 1 or grade 2 NAFLD is more significant in T2DM patients than in those without. The findings emphasize the need for NAFLD screening and prevention in T2DM patients to reduce subsequent cardiovascular risk and mortality.

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  • Study may open up new ways of approaching metabolic diseases

    Study may open up new ways of approaching metabolic diseases

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    A study led by the University of Barcelona and the Biomedical Research Networking Center in Diabetes and Associated Metabolic Disorders (CIBERDEM) reveals how a new mechanism could improve the efficiency of currently available treatments for diabetes. The study, carried out on mice and cell cultures, may open up new ways of approaching metabolic diseases that are a global health problem.

    The study, published in the journal Metabolism, focuses on the GDF15 protein, a factor that is expressed at high levels in many diseases, such as heart failure, cancer and fatty liver disease. Obese patients also have elevated levels of this protein, but its function is altered and those affected may develop resistance to GDF15 — that is, a reduction in the effectiveness of its activity.

    The study is led by Professor Manuel Vázquez-Carrera, from the Faculty of Pharmacy and Food Sciences of the UB, the Institute of Biomedicine of the UB (IBUB), the Sant Joan de Déu Research Institute (IRSJD) and CIBERDEM. The study also highlights the participation of researchers Patricia Rada and ángela María Valverde, also collaborators at CIBERDEM, the Spanish National Research Council (CSIC) and the Autonomous University of Madrid (UAM). The work has the collaboration of Professor Walter Wahli of the University of Lausanne (Switzerland), among other experts.

    New alternatives to reduce glucose synthesis in the liver

    Our study reveals that GDF15 inhibits glucose synthesis in the liver. This pathway plays a decisive role in the generation of hyperglycemia (increased blood glucose levels) in patients with type 2 diabetes mellitus.”

    Professor Manuel Vázquez-Carrera

    “The action of the protein would also help reduce the presence of liver fibrosis, a condition associated with increased mortality in patients with fatty liver disease”, the researcher notes.

    The study reveals that mice deficient in GDF15 have glucose intolerance and low levels of AMPK protein in the liver, which is a sensor of energy metabolism in the cell against type 2 diabetes.

    Moreover, increased glucose synthesis in the liver (hepatic gluconeogenesis) was also detected in these study models, as well as increased liver fibrosis.

    All indications are that all the described alterations were triggered by increased hepatic levels of transforming growth factor-beta 1 (TGF-β1) and an SMAD3mediator protein, which are the main inducers of liver fibrosis. Thus, treatment with recombinant CDF15 can activate AMPK and decrease levels of active SMAD3 in mouse liver and in primary hepatocyte cultures.

    “In conclusion, the results indicate that GDF15 activates AMPK protein and inhibits hepatic gluconeogenesis and fibrosis through the reduction of the TGF-β1/SMAD3 pathway”, says Vázquez-Carrera.

    “These results suggest that modulation of GDF15 levels could be useful to improve the effectiveness of current anti-diabetic treatments, as hepatic gluconeogenesis is key in hyperglycaemia in patients with type 2 diabetes mellitus, and serum TGF-β1 levels are also increased in these patients”, concludes the researcher.

    Source:

    Journal reference:

    Jurado-Aguilar, J., et al. (2024). GDF15 activates AMPK and inhibits gluconeogenesis and fibrosis in the liver by attenuating the TGF-β1/SMAD3 pathway. Metabolism. doi.org/10.1016/j.metabol.2023.155772.

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  • Males born to obese women more likely to develop metabolic complications in later life

    Males born to obese women more likely to develop metabolic complications in later life

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    Males born to obese women are more likely to be overweight at birth and develop metabolic complications in later life, including liver disease and diabetes.

    Image Credit: University of South Australia

    The way that male sex hormones activate pathways in the developing liver is partly to blame.

    That’s the finding from a new study led by University of South Australia (UniSA) researchers looking at the impact of maternal obesity on fetal liver androgen signalling.

    Male fetuses of obese pregnant women have different signals that are activated by male sex hormones in the liver, which encourages them to prioritize growth at the expense of their health.

    UniSA researcher Dr Ashley Meakin says androgens give men their male characteristics and are crucial in their development, but if there are too many, male fetuses grow too large, causing not only problems at birth, but impacting liver function as an adult.

    Female fetuses exposed to excess testosterone from an obese pregnancy are wired to switch off the androgen pathway in the liver, restricting their growth and lowering the risks of metabolic disorders in adulthood.

    We know there are sex differences in metabolic disorders in later life in response to maternal obesity. Men are more prone to non-alcohol fatty liver diseases and diabetes as an adult if their mother is obese during pregnancy and their birth weight is above 4 kg (9 lb 15 oz). They are genetically wired to prioritize androgens because it supports the development of male characteristics – including size – but too much androgen is bad.”

    Dr Ashley Meakin, UniSA Researcher

    Study lead author Professor Janna Morrison, Head of the Early Origins of Adult Health Research Group at UniSA, says it’s a fine balance for women getting the right nutrition in pregnancy to ensure optimal conditions for their unborn child to flourish.

    “There are also risks for offspring being malnourished during pregnancy,” she says. “If you are too little, too big, born too early, or a male, you are more vulnerable to negative outcomes later in life. You need the Goldilocks pregnancy: you must be the right size, born at the right time.”

    Prof Morrison says unless society changes its approach to nutrition, it will be an uphill battle to reduce obesity and associated health issues, from the womb into adulthood.

    “As a society, we urgently need to address obesity. If children were taught early on about the importance of healthy eating, it would carry through into adulthood, including during pregnancy, where the right nutrition is so important.”

    Dr Meakin says in the intervening period, supplements that address nutritional imbalances in pregnancy could provide the fetus with the best chance of optimal development.

    The liver androgen signalling study, recently published in Life Sciences, is among a series of studies by Prof Morrison and colleagues that investigates the impact of maternal under- and over-nutrition on the placenta, heart, lung, and liver.

    Males born to obese women at higher risk of liver diseases as adults

    Video Credit: University of South Australia

    Source:

    University of South Australia

    Journal reference:

    Meakin, A. S., et al. (2024). Maternal obesity impacts fetal liver androgen signalling in a sex-specific manner. Life Sciences. doi.org/10.1016/j.lfs.2023.122344.

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  • Up to 10% of dementia cases in veterans may be caused by liver disease

    Up to 10% of dementia cases in veterans may be caused by liver disease

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    As many as 10% of older U.S. veterans diagnosed with dementia may suffer instead from reversible cognitive decline caused by advanced liver disease, according to an analysis from the Virginia Commonwealth University’s School of Medicine and the Richmond VA Medical Center. 

    It can be difficult for physicians to differentiate dementia from the cognitive decline caused by cirrhosis, called hepatic encephalopathy. If undetected, patients may not receive appropriate treatment that can reverse or halt the impairment. The study, published in the journal JAMA Network Open, sought to learn more about the prevalence and risk factors of undiagnosed cirrhosis and potential encephalopathy in veterans with dementia.

    The findings suggest that physicians treating veterans with dementia, even without a cirrhosis diagnosis, should consider assessing their patients for liver disease. Identifying cirrhosis early on may unveil reversible causes of cognitive impairment, potentially improving the lives of these patients.

    This unexpected link between dementia and liver health emphasizes the importance of screening patients for potentially treatable contributors to cognitive decline.”


    Jasmohan Bajaj, M.D., lead author, gastroenterologist and world-renowned expert in hepatic encephalopathy with the VCU Stravitz-Sanyal Institute for Liver Disease and Metabolic Health and the Richmond VA Medical Center

    The researchers believe the findings would apply to non-veterans with dementia, but further research is needed. Bajaj urges clinicians, especially those who encounter patients with dementia, to incorporate liver assessments into routine care for their patients. 

    “Early detection of liver issues allows for targeted interventions and opens avenues for addressing treatable factors contributing to cognitive decline,” he said.

    Hepatic encephalopathy is a nervous system disorder brought on by cirrhosis, an advanced form of liver disease in which patients experience severe scarring of the liver. When the liver doesn’t work properly, toxins build up in the blood. These toxins can travel to the brain and affect brain function, leaving patients confused or delirious. Widely available medications can readily rid the body of toxins and reverse this condition, but without treatment, patients can lapse into coma or die. 

    Bajaj said the study was sparked by the cases of two older men who were thought to have dementia and Parkinson’s disease, but whose symptoms dramatically improved after being treated for hepatic encephalopathy. One of the men recovered to the point where he resumed driving. Bajaj and colleagues continued to pursue this link between dementia and cirrhosis, publishing findings in 2023 that about 8% of U.S. veterans with cirrhosis had dementia.

    To look at the flip side, the new study’s authors reviewed medical records of 177,422 U.S. veterans diagnosed with dementia but not cirrhosis between 2009 and 2019. The veterans studied were patients from all across the VA medical system. Roughly 30% of veterans suffer from some form of liver disease.

    Participants were overwhelmingly male, with an average age of 78, and evaluated using the Fibrosis-4, or FIB-4, score. The FIB-4 score, an initial screening index for most liver diseases that is based on multiple measurements, including age, is recommended by leading liver, gastroenterology and endocrinology associations as a first-line test to screen for liver fibrosis in the general population. The FIB-4 score was developed by VCU Health hepatologist Richard Sterling, M.D., who is the chief clinical officer of the Stravitz-Sanyal Institute for Liver Disease and Metabolic Health.

    The study revealed that 10.3% of veterans with dementia had high FIB-4 scores, meaning they were very likely to have cirrhosis. Factors that increase the risk of cirrhosis include older age, being male, congestive heart failure, viral hepatitis, alcohol use and certain health conditions. 

    Notably, the data showed that dementia disproportionately affected Black and Hispanic veterans, who also were more likely to be diagnosed later in the disease course. Non-Hispanic white veterans who did not use tobacco or had diabetes were less likely to have elevated FIB-4 scores.

    The researchers conducted a follow up study at the Richmond VA Medical Center to validate their findings and found similar results, with as many as 11.2% of the patients having high FIB-4 scores. 

    “The next step is to ensure that health care providers taking care of patients with cirrhosis and well as those with dementia are made aware of a potential overlap with hepatic encephalopathy, which is treatable,” said Bajaj, who has spent the past several years focusing on hepatic encephalopathy and the gut-brain axis. 

    “Routinely using the FIB-4 index to evaluate dementia could help a significant number of patients, families and physicians by providing an opportunity to treat and potentially reverse cognitive impairment brought on by liver disease,” he added. 

    Source:

    Virginia Commonwealth University

    Journal reference:

    Bajaj, J. S., et al. (2024). Undiagnosed Cirrhosis and Hepatic Encephalopathy in a National Cohort of Veterans With Dementia. JAMA Network Open. doi.org/10.1001/jamanetworkopen.2023.53965.

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