Publisher Health

A powerful new tool in artificial intelligence is able to predict whether someone is willing to be vaccinated against COVID-19.
The predictive system uses a small set of data from demographics and personal judgments such as aversion to risk or loss.
The findings frame a new technology that could have broad applications for predicting mental health and result in more effective public health campaigns.
A team led by researchers at the University of Cincinnati and Northwestern University created a predictive model using an integrated system of mathematical equations describing the lawful patterns in reward and aversion judgment with machine learning.
“We used a small number of variables and minimal computational resources to make predictions,” said lead author Nicole Vike, a senior research associate in UC’s College of Engineering and Applied Science.
“COVID-19 is unlikely to be the last pandemic we see in the next decades. Having a new form of AI for prediction in public health provides a valuable tool that could help prepare hospitals for predicting vaccination rates and consequential infection rates.”
The study was published in the Journal of Medical Internet Research Public Health and Surveillance.

Researchers surveyed 3,476 adults across the United States in 2021 during the COVID-19 pandemic. At the time of the survey, the first vaccines had been available for more than a year.
Respondents provided information such as where they live, income, highest education level completed, ethnicity and access to the internet. The respondents’ demographics mirrored those of the United States based on U.S. Census Bureau figures.
Participants were asked if they had received either of the available COVID-19 vaccines. About 73% of respondents said they were vaccinated, slightly more than the 70% of the nation’s population that had been vaccinated in 2021.
Further, they were asked if they routinely followed four recommendations designed to prevent the spread of the virus: wearing a mask, social distancing, washing their hands and not gathering in large groups.
Participants were asked to rate how much they liked or disliked a randomly sequenced set of 48 pictures on a seven-point scale of 3 to -3. The pictures were from the International Affective Picture Set, a large set of emotionally evocative color photographs, in six categories: sports, disasters, cute animals, aggressive animals, nature and food.
Vike said the goal of this exercise is to quantify mathematical features of people’s judgments as they observe mildly emotional stimuli. Measures from this task include concepts familiar to behavioral economists — or even people who gamble — such aversion to risk (the point at which someone is willing to accept potential loss for a potential reward) and aversion to loss. This is the willingness to avoid risk by, for example, obtaining insurance.

“The framework by which we judge what is rewarding or aversive is fundamental to how we make medical decisions,” said co-senior author Hans Breiter, a professor of computer science at UC. “A seminal paper in 2017 hypothesized the existence of a standard model of the mind. Using a small set of variables from mathematical psychology to predict medical behavior would support such a model. The work of this collaborative team has provided such support and argues that the mind is a set of equations akin to what is used in particle physics.”
The judgment variables and demographics were compared between respondents who were vaccinated and those who were not. Three machine learning approaches were used to test how well the respondents’ judgment, demographics and attitudes toward COVID-19 precautions predicted whether they would get the vaccine.
The study demonstrates that artificial intelligence can make accurate predictions about human attitudes with surprisingly little data or reliance on expensive and time-consuming clinical assessments.
“We found that a small set of demographic variables and 15 judgment variables predict vaccine uptake with moderate to high accuracy and high precision,” the study said. “In an age of big-data machine learning approaches, the current work provides an argument for using fewer but more interpretable variables.”
“The study is anti-big-data,” said co-senior author Aggelos Katsaggelos, an endowed professor of electrical engineering and computer science at Northwestern University. “It can work very simply. It doesn’t need super-computation, it’s inexpensive and can be applied with anyone who has a smartphone. We refer to it as computational cognition AI. It is likely you will be seeing other applications regarding alterations in judgment in the very near future.”

Using advanced methodology, scientists in Sweden were able to reveal at the cellular level how lesions in multiple sclerosis develop. The new results are presented in the journal Cell by researchers from Karolinska Institutet and Stockholm University.
Over 1,8 million people worldwide are diagnosed with multiple sclerosis, MS. In this disease, the body’s immune cells attack the cells that form myelin, the so-called oligodendrocytes, which belong to the group of glial cells. Without myelin, signals between nerve cells cannot travel as fast as usual, resulting in symptoms such as reduced sensation and lack of coordination. MS is characterized by lesions in the brain and the spinal cord.
“We wanted to understand which cells are part of the lesions and their dynamics over time,” says Petra Kukanja, co-first author in the study and PhD student at the research group of Professor Gonçalo Castelo-Branco, at Department of Medical Biochemistry and Biophysics, Karolinska Institutet.
The researchers used a technology called in situ sequencing, developed in the research group of Professor Mats Nilsson, at Stockholm University. This involves analyzing and identifying cells that are part of a tissue section by reading which genes are active in a particular cell. This pattern reveals both how different cell types are arranged in the tissue, in this case the spinal cord, and how the cells interact with each other. To study how the lesions develop, samples were taken at different times from mice experimentally induced with MS-like-symptoms and from human MS patients.
“We analyzed simultaneously 239 genes and saw that active lesions in mouse were built up centrifugally in two dimensions, with immune cells in the middle and different types of glial cells around them,” says Christoffer Mattsson Langseth, also co-first author of the study, and PhD student at the Department of Biochemistry and Biophysics, Stockholm University at Professor Mats Nilsson’s group.
In the mice, it was possible to see that the lesions first appeared in the spinal cord and then spread towards the brain. In samples of the spinal cord from four deceased MS patients, 260 genes were simultaneously analyzed and the cellular architecture of the lesions could be determined. The authors also found new lesions and new sub-structures within the lesions.
Previously, oligodendrocytes have mainly been seen as victims of immune cell attacks.

“The fact that they are active in the outer regions of lesions but also in the entire brain and spinal cord raises the question of whether they dampen the disease or drive it,” says Petra Kukanja.
In the next step, the researchers want to use the same methodology to analyze samples from more MS patients, as the disease is very heterogeneous. Another question is what the lesions look like when patients have received different types of treatments.
The two researchers highlight the extensive and fruitful collaboration between their research groups, which has been ongoing since 2019 and to which they have contributed their respective expertise — from Karolinska Institutet on the cell biology behind MS and from Stockholm University with their pioneering technology in situ sequencing and new methodology for complex image analysis.
The study was initially funded by The Strategic Research Area Neuroscience (StratNeuro) and throughout the project by the Swedish Brain Foundation, the Swedish Cancer Society, the Göran Gustafsson Foundation for Research in Natural Sciences and Medicine, the Swedish Society for Medical Research, Olav Thon Foundation, Ming Wai Lau Centre for Reparative Medicine, the Swedish Research Council, the Chan Zuckerberg Initiative, the Erling-Persson Foundation and the Knut and Alice Wallenberg Foundation, European Union (European Research Council). Markus M. Hilscher and Mats Nilsson owned shares in CartaNA AB, which is part of 10x Genomics. Mats Nilsson is a former scientific advisor for 10xGenomics.

A team of infectious diseases experts called for more awareness and preparedness in the medical field to deal with the impact of climate change on the spread of diseases. Their article, published today in JAMA raises the alarm about the emergence and spread of harmful pathogens. The authors also urge the medical community to update their education and training and take steps to combat global warming.
“Clinicians need to be ready to deal with the changes in the infectious disease landscape,” said lead author George R. Thompson. Thompson is a professor at the UC Davis School of Medicine in the Department of Internal Medicine, Division of Infectious Diseases, and the Department of Medical Microbiology and Immunology. “Learning about the connection between climate change and disease behavior can help guide diagnoses, treatment and prevention of infectious diseases.”
Thompson encouraged physicians and practitioners to maintain “a high index of suspicion of diseases on the move.” “I think with improvements in our understanding of the disease, there will be more testing and we’ll miss fewer cases that way,” he said.
Changing infectious diseases landscape
Infectious diseases can be caused by viruses, bacteria, fungi or parasites. Many of these diseases are transmitted from animal to human or from human to human.
One type of infectious disease is vector-borne diseases. They are caused by pathogens carried by vectors like mosquitoes, fleas and ticks. Some diseases caused by vectors aredengue, malaria and Zika.
Changing rain patterns are expanding vectors’ range and their active periods. Shorter, warmer winters and longer summers are also linked to more vector-borne diseases. For example, diseases caused by ticks (like babesiosis and Lyme disease) are now occurring in the winter too. They’re also being found in regions farther west and north than in the past.

“We’re seeing cases of tick-borne diseases in January and February,” said first author of the study Matthew Phillips. Phillips is an infectious diseases fellow at Massachusetts General Hospital and Harvard Medical School. “The tick season is starting earlier and with more active ticks in a wider range. This means that the number of tick bites is going up and with it, the tick-borne diseases.”
Another concern is malaria. The mosquitos that transmit the disease are expanding northward, a climate-induced change. Changing rain patterns have led to more mosquitos and a higher disease transmission rate.
“As an infectious disease clinician, one of the scariest things that happened last summer was the locally acquired cases of malaria. We saw cases in Texas and Florida and then all the way north in Maryland, which was really surprising. They happened to people who didn’t travel outside the U.S.,” Phillips said.
Zoonotic diseases, such as plague and hantavirus (carried by rodents), are also showing changes in incidence and location. The experts noted changes in animal migration patterns and natural ranges. Due to their habitat loss, wild animals are coming closer to humans. With that comes a higher risk of animal diseases spilling over to humans and for new pathogens to develop.
The study also pointed to the emergence of new fungal infections, such as Candida auris (C. auris), and changes in the location of some fungal pathogens. For example, the fungal infection Coccidioides (also known as Valley fever) was endemic to hot, dry areas in California and Arizona. But Valley fever was recently diagnosed as far north as Washington State.
Changes in rain patterns and coastal water temperature can also affect the spread of waterborne diseases, such as E. coli and Vibrio. According to the team, the sea level is rising, and storm surges and coastal flooding that used to be rare or extreme events are happening more frequently.

Call for medical community to take steps
Over the last few years, infectious diseases, such as COVID-19, impacted the world enormously.
“They can spring up and cause absolute chaos for the whole world and then we kind of forget about them for a while. Yet, the epidemic and pandemic potential of infections really mandates that we stay involved with federal funding agencies and advisory groups to make sure that infectious diseases don’t slip back too far on the public’s radar,” Thomspon explained.
The team called for stronger measures for infectious disease surveillance and urged medical educators to train clinicians to anticipate the changes in infectious disease patterns.
“It’s not a hopeless situation. There are distinct steps that we can take to prepare for and help deal with these changes. Clinicians see first-hand the impact of climate change on people’s health. As such, they have a role in advocating for policies that can slow climate change,” Phillips said.
Regina C. LaRocque, associate professor of medicine at Harvard Medical School and infectious diseases physician at Harvard Medical School, is a coauthor of this study.
This study was partially supported by National Institutes of Health grants T32AI007061 and 5U19AI166798.

Abdominal pain, diarrhea, weight loss — these and the other symptoms of inflammatory bowel disease (IBD) can be disruptive and debilitating. And while scientists have figured out that IBD has a genetic component, not everyone with a family history develops the disease. To date, the environmental triggers for Crohn’s disease and ulcerative colitis, known together as IBD, remain largely unknown.
A new U-M study finds a complex interplay between diet, genes, and the gut microbiota that could explain why IBD develops. Led by the labs of Eric Martens, Ph.D. and Mahesh Desai, Ph.D. and first authors Gabriel Pereira, Ph.D., Marie Boudaud, Ph.D. and their colleagues, the newest study builds on previous work that found that a low fiber diet led to a proliferation of mucin degrading bacteria — bacteria that thrive by eating the mucus lining of the intestine.
IBD genes
In some people, genetic loss of a cytokine — a protein that affects the immune system — known as interleukin-10 (IL-10), or its receptor leads to early onset of IBD in infants and children. The new study set out to examine this genetic connection more closely, using mice with the same immune alteration.
While some of these mice spontaneously developed inflammation in their intestinal tracts as well, the level of severity varied and appeared to be made worse by the presence of certain bacteria and a low fiber diet. In fact, mice bred to lack any bacteria had no evidence of disease.
By adjusting the presence or absence of a model human gut microbiome and the dietary fiber content for their mouse models, the team found they could turn up or down inflammation. What’s more is the inflammation triggered by fiber free diets appeared to increase in reaction to the increased abundance of mucin degrading bacteria Akkermansia mucinphila and Bacteroides caccae.
“These bacteria start foraging on the mucus layer for nutrients, reducing its thickness and barrier function and brings microbes just 10-100 microns closer to the host tissue. That was enough in the context of the mice with IBD genetics to make them sick,” said Martens, professor of microbiology and immunology at U-M Medical School.

Diet effects
On the other hand, feeding the mice a fiber rich diet prevented inflammation from developing and even returning mice fed low fiber to a high fiber diet led to a peak in inflammation followed by a decline, suggesting fiber can reverse the deleterious effects of mucus erosion on inflammation. But ironically, IBD, especially in children, is often treated with a formula-based diet called exclusive enteral nutrition (EEN), which lacks fiber. Despite a lack of fiber, this diet does result in reduced inflammation in people, for reasons unexplained.
To answer why, the team dried down the formula to administer it to the mice with IBD genetics. Interestingly, these mice had varying levels of inflammation following the diet, with some experiencing considerably less inflammation than the mice fed the fiber free diet, even though the EEN diet also reduced mucus thickness.
The team then discovered that elevated amounts of a single branched-chain fatty acid, isobutyrate, was elevated in EEN fed mice and might suppress inflammation. Isobutyrate is produced through fermentation by some bacteria in the gut. “It seems one of the ways these exclusive enteral nutrition diets could possibly work in people is by triggering certain bacteria to make beneficial metabolites,” said Martens.
Spurred by these findings, the team plans to further interrogate how diet and bacteria interact to improve on therapies for pediatric IBD as well as answer how to potentially reverse or prevent the onset of these diseases by manipulation of these environmental triggers. “Our findings suggest a potential new path for treating IBD. By tailoring specific dietary interventions to influence gut microbiome function, we may be able to manipulate these bacterial communities to alleviate inflammation.” said Pereira.
Additional authors include Mathis Wolter, Celeste Alexander, Alessandro De Sciscio, Erica Grant, Bruno Caetano Trindade, Nicholas Pudlo, Shaleni Singh, Austin Campbell, Mengrou Shan, Li Zhang, Qinnan Yang, Stephanie Willieme, Kwi Kim, Trisha Denike-Duval, Jamie Fuentes, Andre Bleich, Thomas Schmidt, Lucy Kennedy, Costas A. Lyssiotis, Grace Y. Chen, Kathryn A. Eaton, and Mahesh S. Desai.

Published8 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, PA MediaBy Nick TriggleHealth correspondentJunior doctors in England have voted in favour of continuing strike action in their pay dispute.Some 98% of members of the British Medical Association who voted backed further walkouts on a turnout of 62%.There have been 10 walkouts so far by junior doctors since the first one in March last year.The British Medical Association (BMA) has asked for a 35% pay rise, but ministers have described the pay claim as unreasonable.Two-thirds of junior doctors are members of the BMA.The vote result means the union has a strike mandate for another six months.Junior doctors committee co-chairs Dr Robert Laurenson and Dr Vivek Trivedi said:   ”It has now been a year since we began strike action. “That is a year of too many strikes. The government believed it could ignore, delay, and offer excuses long enough that we would simply give up.”We ask the health secretary to come forward as soon as possible with a new offer – and make sure not a single further strike day need be called,” they said. What are junior doctors paid – and how much to settle?Why talk of a UK doctor exodus is prematureJunior doctors received a pay rise averaging nearly 9% this financial year – and during talks at the end of last year, the option of an extra 3% on top of that was discussed.But those talks ended in early December without a deal being reached.The BMA is after a 35% pay increase to make up for what it says is 15 years of below-inflation pay rises.There have been no formal talks since those negotiations ended and the BMA is boycotting the pay review process for next year, refusing to provide evidence to the independent pay review body that makes recommendations on pay rises.Junior doctors in Wales and Northern Ireland are also involved in strike action.But consultants in England are voting on whether to accept a revised pay offer from ministers after putting their strike action on pause.More than 1.4 million operations and appointments in total have been cancelled because of strike action by health workers including doctors, nurses and other healthcare professionals since December 2022.The disputes involving the majority of the other health workers have been resolved. More on this storyInside top hospital as it deals with doctors’ strikePublished6 JanuaryHospitals call on junior doctors to return to workPublished4 JanuaryGive us credible offer and we’ll end strikes – BMAPublished3 JanuaryJunior doctor strikes return, after talks collapsePublished5 December 2023Thousands of appointments hit by doctor walkoutPublished27 December 2023Junior doctors and consultants to strike togetherPublished25 September 2023Related Internet LinksBritish Medical AssociationHospital Consultants and Specialists AssociationNHS ConfederationThe BBC is not responsible for the content of external sites.

Imagine being able to count the different types of blood cells being formed inside the tiny bones of a mouse and pinpointing the strings and clusters of cells within the bone marrow that are responsible for producing specific types of blood cells.
That’s exactly what a team of scientists led by experts at Cincinnati Children’s achieved in a far-reaching study published March 20, 2024, in the journal Nature. Their work adds unprecedented new understanding of the “elegant” and “resilient” anatomy of bone marrow while also generating evidence of unexpected variations in how the skeleton responds to stresses such as infection or blood loss.
“Stunningly, we found that the response to hematopoietic insults varies across the skeleton. We speculate that certain bones have specialized to preferentially respond to some insults, and this will be the focus of future studies,” the co-authors state.
The research was led by co-first authors Qingqing Wu, PhD, and Jizhou Zhang, PhD, and corresponding author Daniel Lucas, PhD, all with the Division of Experimental Hematology and Cancer Biology at Cincinnati Children’s. Overall, 23 researchers from five institutions contributed to this groundbreaking study.
The discovery of specific blood cell production sites within the bone marrow raises new challenges and opportunities for diagnosing and treating a number of blood-related conditions.
“For example, our data shows that biopsies that draw marrow from just one type of bone may not provide a full picture of how the blood production system has been affected by a disease or other insult,” Lucas says. “Meanwhile, efforts to stimulate production of certain blood cell types may be dramatically improved by focusing on specific bone types.”
Highlights of the findings
The key discoveries reported in the paper include: New tools allowing visualization of blood production inside the bone, allowing defining the basic anatomy of blood cell formation. These revealed that bone marrow functions are highly responsive and durable, but not uniform. The paper describes how strings and clusters of cells form within the marrow to act as blood cell production factories. Location matters, even during normal blood cell production. The team demonstrated that different key types of progenitor cells move through different microenvironments as they mature. These microenvironments significantly influence which types of mature blood cells get produced. Different microenvironments give rise to oxygen-carrying red blood cells versus infection-fighting white blood cells, and so on. Unexpected variations in stress responses. The researchers compared how the system responded to three acute kinds of stress: blood loss, L. monocytogenes infection, and granulocyte-colony stimulating factor (G-CSF) treatment (often given to boost white blood cell production after chemotherapy). They also measured how aging changed the process.

The team meticulously measured how different bones responded to these insults. Among several examples: blood loss triggered rapid red blood cell production in the sternum, tibia, vertebrae, and humerus — but not in the skull. Blood loss also temporarily reduced the number of B cell production sites across the skeleton.
Meanwhile, when exposed to G-CSF, long bones rapidly increased formation of granulocyte progenitors and mature neutrophils. But in sharp contrast, the sternum from the same mice displayed “profound reductions” in these cell types as well as loss of neutrophil production sites.
“These variations are important because until now, mouse studies of blood cell biology have depended almost entirely upon material collected from the femur and tibia,” Lucas says.
Innovation required just to conduct the study
The research team first needed to conduct a research project-within-the-project to establish a method for imaging and counting the different cell types at work within the mouse bone marrow.
Counting the cells involved a process called confocal imaging microscopy. This uses specialized microscopes relying on lasers to detect specific tags in the cells. When “tagged” properly, the cells emit different colors under the laser, which allows them to be imaged and counted.

The challenge is coming up with the right tag so that the laser accurately detects the targeted cells of interest, while not counting other cells. In this study, the team started with a vast library of potential markers, then they whittled the list down to 35 promising genetic markers.
Ultimately, they found that detecting cells that express the gene marker ESAM, in combination with other markers, allowed distinguishing between six different types of blood progenitor cells. The marker also proved capable of showing information about the microenvironment, such as whether blood cell production was occurring within sinusoids or arterioles, two distinct types of blood channels found within bone marrow. Importantly, the process developed for this study allowed the team to analyze blood cell development in multiple parts of the skeleton.
Next steps
Looking ahead, Lucas says much more research will be needed to fully detail how different parts of the skeleton become specialized producers of specific blood components. Also, more studies will be needed to confirm how much of the bone marrow stress response observed in mice also occurs in humans.
It will likely require several years of development, but understanding more about the mechanics of blood cell production may allow a wide range of improvements in the precision and effectiveness of treatments to support healthy blood cell production.
“It might even allow to build artificial bones capable of producing red blood cells for transfusion,” Lucas says.
About the study
Achieving these findings required significant support from the Bio-Imaging Analysis Facility and the Research Flow Cytometry Core at Cincinnati Children’s.
In addition to Wu, Zhang and Lucas, Cincinnati Children’s co-authors included: Sumit Kumar, Siyu Shen, Morgan Kincaid, Courtney B. Johnson, Yanan Sophia Zhang, and Shelli Homan, Marie Dominique Filippi, PhD, and H. Leighton Grimes, PhD, all with Experimental Hematology and Cancer Biology; Anastasiya Slaughter, Benjamin Weinhaus, and Baobao Song from the Immunology Graduate Program; Bryan Sherman, Tzu-Yu Shao, and Sing Sing Way, MD, PhD, from Infectious Diseases; and Matt Kofron, PhD, a member of Developmental Biology and director of the Bio-Imaging and Analysis Facility.
The study also included contributions from researchers with the Charles P. Lin lab at Massachusetts General Hospital, Harvard Medical School, and Keisuke Ito at the Albert Einstein College of Medicine in Bronx, NY.
The study was supported with funds from several grants from the National Institutes of Health. Individual co-authors also receive support from the Leukemia and Lymphoma Society, the Edward P. Evans Foundation, the HHMI Faculty Scholar’s Program, the Burroughs Wellcome Fund, and the March of Dimes Foundation Ohio Collaborative.

An analysis of over 20,000 U.S. adults found that people who limited their eating across less than 8 hours per day, a time-restricted eating plan, were more likely to die from cardiovascular disease compared to people who ate across 12-16 hours per day, according to preliminary research presented at the American Heart Association’s Epidemiology and Prevention Lifestyle and Cardiometabolic Scientific Sessions 2024, March 18- 21, in Chicago. The meeting offers the latest science on population-based health and wellness and implications for lifestyle.
Time-restricted eating, a type of intermittent fasting, involves limiting the hours for eating to a specific number of hours each day, which may range from a 4- to 12-hour time window in 24 hours. Many people who follow a time-restricted eating diet follow a 16:8 eating schedule, where they eat all their foods in an 8-hour window and fast for the remaining 16 hours each day, the researchers noted. Previous research has found that time-restricted eating improves several cardiometabolic health measures, such as blood pressure, blood glucose and cholesterol levels.
“Restricting daily eating time to a short period, such as 8 hours per day, has gained popularity in recent years as a way to lose weight and improve heart health,” said senior study author Victor Wenze Zhong, Ph.D., a professor and chair of the department of epidemiology and biostatistics at the Shanghai Jiao Tong University School of Medicine in Shanghai, China. “However, the long-term health effects of time-restricted eating, including risk of death from any cause or cardiovascular disease, are unknown.”
In this study, researchers investigated the potential long-term health impact of following an 8-hour time-restricted eating plan. They reviewed information about dietary patterns for participants in the annual 2003-2018 National Health and Nutrition Examination Surveys (NHANES) in comparison to data about people who died in the U.S., from 2003 through December 2019, from the Centers for Disease Control and Prevention’s National Death Index database.
The analysis found: People who followed a pattern of eating all of their food across less than 8 hours per day had a 91% higher risk of death due to cardiovascular disease. The increased risk of cardiovascular death was also seen in people living with heart disease or cancer. Among people with existing cardiovascular disease, an eating duration of no less than 8 but less than 10 hours per day was also associated with a 66% higher risk of death from heart disease or stroke. Time-restricted eating did not reduce the overall risk of death from any cause. An eating duration of more than 16 hours per day was associated with a lower risk of cancer mortality among people with cancer.”We were surprised to find that people who followed an 8-hour, time-restricted eating schedule were more likely to die from cardiovascular disease. Even though this type of diet has been popular due to its potential short-term benefits, our research clearly shows that, compared with a typical eating time range of 12-16 hours per day, a shorter eating duration was not associated with living longer,” Zhong said.
“It’s crucial for patients, particularly those with existing heart conditions or cancer, to be aware of the association between an 8-hour eating window and increased risk of cardiovascular death. Our study’s findings encourage a more cautious, personalized approach to dietary recommendations, ensuring that they are aligned with an individual’s health status and the latest scientific evidence,” he continued. “Although the study identified an association between an 8-hour eating window and cardiovascular death, this does not mean that time-restricted eating caused cardiovascular death.” Study details and background: The study included approximately 20,000 adults in the U.S. with an average age of 49 years. Study participants were followed for a median length of 8 years and maximum length of 17 years. The study included data for NHANES participants who were at least 20 years old at enrollment, between 2003-2018, and had completed two 24-hour dietary recall questionnaires within the first year of enrollment. Approximately half of the participants self-identified as men, and half self-identified as women. 73.3% of the participants self-identified as non-Hispanic white adults, 11% self-identified as Hispanic adults, 8% self-identified as non-Hispanic Black adults and 6.9% of adults self-identified as another racial category, including mixed-race adults and adults of other non-Hispanic races.The study’s limitations included its reliance on self-reported dietary information, which may be affected by participant’s memory or recall and may not accurately assess typical eating patterns. Factors that may also play a role in health, outside of daily duration of eating and cause of death, were not included in the analysis.

Future research may examine the biological mechanisms that underly the associations between a time-restricted eating schedule and adverse cardiovascular outcomes, and whether these findings are similar for people who live in other parts of the world, the authors noted.
“Overall, this study suggests that time-restricted eating may have short-term benefits but long-term adverse effects. When the study is presented in its entirety, it will be interesting and helpful to learn more of the details of the analysis,” said Christopher D. Gardner, Ph.D., FAHA, the Rehnborg Farquhar Professor of Medicine at Stanford University in Stanford, California, and chair of the writing committee for the Association’s 2023 scientific statement, Popular Dietary Patterns: Alignment with American Heart Association 2021 Dietary Guidance.
“One of those details involves the nutrient quality of the diets typical of the different subsets of participants. Without this information, it cannot be determined if nutrient density might be an alternate explanation to the findings that currently focus on the window of time for eating. Second, it needs to be emphasized that categorization into the different windows of time-restricted eating was determined on the basis of just two days of dietary intake,” he said.
“It will also be critical to see a comparison of demographics and baseline characteristics across the groups that were classified into the different time-restricted eating windows — for example, was the group with the shortest time-restricted eating window unique compared to people who followed other eating schedules, in terms of weight, stress, traditional cardiometabolic risk factors or other factors associated with adverse cardiovascular outcomes? This additional information will help to better understand the potential independent contribution of the short time-restricted eating pattern reported in this interesting and provocative abstract.”

Cases this year have already topped the total in 2023. Unvaccinated travelers account for most infections.Measles, a highly contagious but preventable disease, is resurging in pockets of the United States, a warning of the dangers of the strengthening anti-vaccine movement.The Centers for Disease Control and Prevention has recorded more cases this year than the 58 tallied in all of 2023, although the agency is not expected to release exact numbers until Friday. On Monday, the agency advised health care providers to ensure that unvaccinated patients, especially those traveling internationally, stay updated on their immunizations.The number of cases is likely to keep rising because of a sharp spike in measles worldwide, along with spring travel to some regions with outbreaks, including Britain, said Dr. Manisha Patel, chief medical officer at the C.D.C.’s respiratory disease division.Nearly all the cases in the United States so far are related to unvaccinated travelers. “We’re not going to see widespread measles cases going throughout the country,” Dr. Patel said. “But we do expect additional cases and outbreaks to happen.”Measles is among the most contagious of diseases; each infected person can spread the virus to as many as 18 others. The virus is airborne and can stay aloft up to two hours after an infected person has left the room, spreading rapidly through homes, schools and child care facilities.In Chicago, one case of measles at a migrant shelter has grown to 13, prompting the C.D.C. to send a team to help contain the outbreak. (Two additional cases in the city appear to be unrelated.)We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

A number of case studies published after recent total solar eclipses highlight the importance of safe viewing.A young woman visited New York Eye & Ear Infirmary of Mount Sinai Hospital shortly after the eclipse of Aug. 21, 2017. She told Dr. Avnish Deobhakta, an ophthalmologist, that she had a black area in her vision, and then drew a crescent shape for him on a piece of paper.When Dr. Deobhakta examined her eyes, he was astonished. He saw a burn on her retina that was exactly the same shape. It was “almost like a branding,” he said.She had looked at the sun during the eclipse without any protection. The burn was an image of the sun’s corona, its halo-like outer rim.With every eclipse, ophthalmologists see patients who looked at the sun and complain afterward that their vision is distorted: They see small black spots, their eyes are watery and sensitive to light. Usually, the symptoms resolve, although it may take several weeks to a year.But the woman’s retinal burns, which Dr. Deobhakta and colleagues described in a medical case write-up, would not heal. Her retina was permanently scarred and a sign of the severity of injuries that can follow looking at an eclipse without proper precautions.With the coming eclipse in April, ophthalmologists advise people to be careful and not assume that short glances at the sun are safe. Damage can occur, they say, in less than a minute.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Published2 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, TOLGA AKMEN/EPA-EFE/REX/ShutterstockBy Brian WheelerPolitical reporterRishi Sunak’s plan to ban anyone born after 2009 from buying cigarettes is starting its journey into law.The Tobacco and Vapes Bill means anyone turning 15 this year, or younger, will never legally be sold cigarettes.The government says smoking itself will not be criminalised, so anyone who can legally buy tobacco now will not be prevented from doing so in future.But if the bill is passed it will give the UK some of the world’s toughest anti-tobacco laws.It will effectively raise the legal age people can buy cigarettes by one year every year, with the aim of stopping today’s young people from taking up the habit in the first place.The planned new law also aims to reduce youth vaping, by restricting vape flavours and packaging intentionally marketed at children.A quick guide to smoking bans across the worldRishi Sunak defends his plan to phase out smokingWill Rishi Sunak’s plan to ban smoking in UK work?This could change how vapes, which contain nicotine, are displayed in shops, moving them out of sight of children and away from other products such as sweets.Figures show that one in five children has tried vaping despite it being illegal for under-18s, while the number of children using vapes has tripled in the past three years.’Nanny state’Other powers in the Tobacco and Vapes Bill mean shops that fail to clamp down on underage sales of tobacco and vapes will be given £100 on-the-spot fines. This is in addition to the maximum £2,500 fine that local councils can already impose. It will also be illegal for retailers to give free samples of vapes to under-18s.Separately, the government has committed to ban disposable vapes from April 2025 under environmental laws.Labour is backing the ban, meaning it is likely to become law later this year.But MPs will get a free vote on it – meaning they will not be told which way to vote by party bosses – and some Conservative MPs are expected to oppose it.Earlier, this year, former Prime Minister Liz Truss said: “A Conservative government should not be seeking to extend the nanny state. It only gives succour to those who wish to curtail freedom.”‘Reduce illness’But Rishi Sunak, who announced the plan last year, said tackling smoking would save lives and billions of pound for the NHS.”If we want to build a better future for our children we need to tackle the single biggest entirely preventable cause of ill-health, disability and death: smoking,” he said.”That is why, alongside new measures to curb the alarming rise in youth vaping, we are delivering on our commitment to create a smoke-free generation and stop our kids from getting hooked on harmful cigarettes and other nicotine products.”England’s chief medical officer, Professor Chris Whitty, said: “If passed this will be a major public health measure which reduce illness, disability, and premature deaths for children today and future generations.”Smokers’ rights group Forest, which is funded by the tobacco industry, said: “No-one wants children to smoke, but the idea that government should take away people’s freedom to choose long after they have grown up is absurd.”The UK government’s plan to phase out tobacco sales is based on a similar scheme in New Zealand, which has since been scrapped. The Tobacco and Vapes Bill will be introduced in the Commons later on Wednesday, but the date when MPs first debate the measures is yet to be announced.