Publisher Health

A University at Buffalo researcher has some good news for athletes and fitness enthusiasts who favor thick, heavily cushioned running shoes. Although these shoes are increasingly popular because they provide comfort and a high degree of shock absorbing protection, those benefits were thought to come at the expense of increased overall leg stiffness, which altered a runner’s normal stride and could increase muscle fatigue.
Plenty of research suggests just such a result when running on a compliant surface, like a synthetic rubber track, but no one had actually tested how the cushioned midsole of a running shoe affects overall leg stiffness.
Until now.
“Our results show that runners do not need to worry about the amount of cushioning,” says Nicholas Holowka, PhD, an assistant professor of anthropology in the UB College of Arts and Sciences and the paper’s first author. “That element of shoe design is not interrupting your normal running style in any significant or meaningful way.”
The findings of the study conducted with Daniel Lieberman, a professor of human evolutionary biology at Harvard University; Emmanuel Virot, a postdoctoral fellow at Harvard; and Stephen Gillinov, a medical school student at Yale University, appear in the Journal of Biomechanics.
Leg stiffness can be compared to a spring’s tension. If the leg alone were modeled as a single spring, that coil would have one level of stiffness. The leg, however, is made up of many muscles that control degrees of stiffness. When running on cushioned surfaces, leg stiffness increases, but that’s not the case when running in heavily cushioned shoes.

Scientists traced how a mouse’s brain gets the signal that it had enough to drink. Something similar may happen in humans.Few pleasures compare to a long cool drink on a hot day. As a glass of water or other tasty drink makes its way to your digestive tract, your brain is tracking it — but how? Scientists have known for some time that thirst is controlled by neurons that send an alert to put down the glass when the right amount has been guzzled. What precisely tells them that it is time, though, is still a bit mysterious.In an earlier study, a team of researchers found that the act of gulping a liquid — really anything from water to oil — is enough to trigger a temporary shutdown of thirst. But they knew that gulping was not the only source of satisfaction. There were signals that shut down thirst coming from deeper within the body.In a paper published Wednesday in Nature, scientists from the same lab report that they’ve followed the signals down the neck, through one of the body’s most important nerves, into the gut, and finally to an unexpected place for this trigger: a set of small veins in the liver.The motion of gulping might provide a quick way for the body to monitor fluid intake. But whatever you swallowed will swiftly arrive in the stomach and gut, and then its identity will become clear to your body as something that can fulfill the body’s need for hydration, or not. Water changes the concentration of nutrients in your blood, and researchers believe that this is the trigger for real satiation.“There is a mechanism to ensure that what you’re drinking is water, not anything else,” said Yuki Oka, a professor at Caltech and an author of both studies. To find out where the body senses changes to your blood’s concentration, Dr. Oka and his colleagues first ran water into the intestines of mice and watched the behavior of nerves that connect the brain to the gut area, which are believed to work similarly in humans. One major nerve, the vagus nerve, fired the closest in time with the water’s arrival in the intestines, suggesting that this is the route the information takes on the way to the brain.Then, the researchers went one by one and sliced each of the nerve’s connections to different regions in the gut. To their surprise, nothing changed when they cut off contact to the intestines.Instead, it was the portal veins of the liver — vessels that carry that blood from around the intestine to the filtering organ — whose isolation silenced the messages back to the brain.These veins ferry nutrients and fluid into the liver, so it’s plausible that they could be a monitoring center for thirst, Dr. Oka said. The team found that just running water through the portal veins was not enough to get the nerve to fire, however. Something about the water’s arrival had to trigger another part of the body’s hydration Rube Goldberg machine.The researchers narrowed it down to a hormone called vasoactive intestinal peptide, or VIP. When water reaches the portal veins, VIP levels go up, and it is VIP, rather than the water itself, that causes the vagus to fire, alerting the brain.As intriguing as that is, the scientists don’t know how the water causes this rise. They are hoping to keep following the signals and identify precisely which cells and molecules connect these unassuming veins and the peptide with the grand acronym.“That is the major thing that we are in a good position to tackle next,” Dr. Oka said.And there is probably even more to learn. While VIP causes the vagus nerve to sound off, the signal isn’t as strong as the researchers would expect if it worked alone. Water is so important to the body’s functioning that Dr. Oka and his team think our brains most likely have multiple, redundant ways to monitor it. With every glass of water you drink, you’re putting that system through its paces.

The same risk factors that contribute to making heart disease the leading cause of death worldwide also impact the rising global prevalence of brain disease, including stroke, Alzheimer’s disease and dementia, according to the American Heart Association’s Heart Disease and Stroke Statistics — 2022 Update, published today in the Association’s flagship, peer-reviewed journal Circulation. Experts say maintaining a healthy weight, managing your blood pressure and following other heart-healthy lifestyle behaviors can also support good brain health.
Optimal brain health includes the functional ability to perform all the diverse tasks for which the brain is responsible, including movement, perception, learning and memory, communication, problem solving, judgment, decision making and emotion. Cognitive decline and dementia are often seen following stroke and cerebrovascular disease and indicate a decline in brain health. Conversely, studies show maintaining good vascular health is associated with healthy aging and retained cognitive function.
The global death rate from Alzheimer’s disease and other dementias is increasing considerably — even more than the rate of heart disease death: Globally, more than 54 million people had Alzheimer’s disease and other dementias in 2020, that’s a 37% increase since 2010 and a 144% increase over the past 30 years (1990-2020). More than 1.89 million deaths were attributed to Alzheimer’s disease and other dementias worldwide in 2020, compared to nearly 9 million deaths from heart disease. Global deaths from Alzheimer’s disease and other dementias increased more than 44% from 2010 to 2020, compared to a 21% increase in deaths from heart disease. Deaths from Alzheimer’s disease and other dementias increased 184% over the past 30 years (1990-2020), compared to a 66% increase in heart disease deaths during that same time.Because prevalence and mortality data are tracked differently by the Centers for Disease Control and Prevention, in the U.S. compared to other countries, the Statistical Update does not offer comparable national data for 2020. However, nearly 2.9 million people in the U.S. were reported to have Alzheimer’s disease and other dementias in 2017. Alzheimer’s disease and other dementias combined were the leading cause of death among all neurological disorders, including stroke.
“The global rate of brain disease is quickly outpacing heart disease. The rate of deaths from Alzheimer’s disease and other dementias rose more than twice as much in the past decade compared to the rate of deaths from heart disease, and that is something we must address,” said Mitchell S.V. Elkind, M.D. M.S., FAHA, the immediate past president of the American Heart Association, a professor of neurology and epidemiology at Columbia University Vagelos College of Physicians and Surgeons and attending neurologist at New York-Presbyterian/Columbia University Irving Medical Center, New York, NY. “We are learning more about how some types of dementia are related to the aging, and how some types are due to poor vascular health. Many studies show that the same healthy lifestyle behaviors that can help improve a person’s heart health can also preserve or even improve their brain health. It’s becoming more evident that reducing vascular disease risk factors can make a real difference in helping people live longer, healthier lives, free of heart disease and brain disease.”
The 2022 Statistical Update highlights some of that research: In a meta-analysis of 139 studies, people with midlife hypertension were five times more likely to experience impairment on global cognition and about twice as likely to experience reduced executive function, dementia and Alzheimer’s disease. Nearly half of all adults (47% or 121.5 million) in the U.S. have elevated blood pressure, based on 2015 to 2018 data. In a meta-analysis of longitudinal studies with up to 42 years of follow-up, people with obesity had three times the risk of dementia. Current smoking was associated with a 30%-40% increased risk of dementia, Alzheimer’s disease and vascular dementia, based on a meta-analysis of 37 prospective studies.Having cardiovascular disease also increases the chances of developing brain disease: In a meta-analysis of four longitudinal studies, the risk for dementia associated with heart failure was nearly two-fold. In the ARIC Neurocognitive study (12,515 participants, average age of 57 years, 24% Black participants, 56% women), atrial fibrillation was associated with greater cognitive decline and dementia over 20 years. A meta-analysis of 10 prospective studies (including 24,801 participants) found that coronary heart disease was associated with a 40% increased risk of poor cognitive outcomes including dementia, cognitive impairment or cognitive decline.

Strict COVID-19 lockdown policies such as workplace closures in European cities reduced levels of air pollution and the number of associated deaths, according to new estimates published in Nature’s Scientific Reports.
The research, which was funded by the European Centre for Medium-Range Weather Forecasts (ECMWF) on behalf of the Copernicus Atmosphere Monitoring Service (CAMS), was led by a team of statistical health and earth observation satellite modellers based at the London School of Hygiene & Tropical Medicine (LSHTM), with colleagues from CAMS.
The study compared government policies from 47 European cities from February to July 2020 and estimated the changes in pollution levels and related number of deaths avoided during the first wave of COVID-19 pandemic.
Government measures for COVID-19 such as school and workplace closure, cancelling public events, and stay-at-home requirements had the strongest effect on reducing NO2 levels. This is linked to the reduction in road transport and local mobility which is known to be a contributor to NO2 air pollution. Spanish, French and Italian cities had the largest decrease in NO2 of between 50% and 60% during the period.
Although strong decreases in NO2 were observed, levels of fine particulate matter PM2.5 and PM10 were reduced more modestly since they are also produced by natural sources (wildfires and dust), and other emission sources like residential activities, that were slightly increased during lockdown.
Antonio Gasparrini, Professor of Biostatistics and Epidemiology at LSHTM and senior author of the study, said: “The lockdown during the first wave of the COVID-19 pandemic created immense health and social costs, however, it has offered unique conditions to investigate potential effects of strict policies to reduce pollution levels in urban areas. This ‘natural experiment’ has given us a glimpse of how air quality can be improved by drastic public health measures that would be difficult to implement in normal times. The information can be important to design effective policies to tackle the problem of pollution in our cities.

It is unlikely that a cancer-causing chemical inside your car can be dusted or wiped way, according to new UC Riverside research.
This finding has now been published in the journal Environmental Research. It follows on the heels of a related study showing the longer your commute, the more you’re exposed to this chemical.
TDCIPP, or chlorinated tris, is a chemical flame retardant widely used in automobile seat foam. In addition to TDCIPP being on California’s Prop. 65 list because it is carcinogenic, UCR environmental toxicologist David Volz has found that TDCIPP prevents zebrafish embryos from developing normally. Other studies have associated it with infertility in certain women.
Some research suggests that dust removal could lead to lower exposure to chemicals. Volz and his colleagues hoped that was true for car interiors.
The researchers divided nearly 50 study participants, all of them heavy commuters, into four groups they tracked for two weeks. One group did not wipe dust in their cars at all, another wiped the dust both weeks, and two other groups wiped for only one of the two weeks.
All participants were given silicone wristbands to wear continuously during the two-week testing period. The molecular structure of silicone makes it ideal for capturing airborne contaminants such as TDCIPP.
“Going into this, our hypothesis was that the no-wipe group would have the highest concentration, the two-week wipe group would be lower, and the partial wipe groups would be somewhere in between,” Volz said. “But what we found was that there was basically no difference between any of the groups.”
Previously, the researchers assumed that commuters’ primary exposure to TDCIPP is through contaminated dust. One possible explanation for this study’s result, Volz said, was the possibility that TDCIPP is not coming from dust that can be cleaned. Instead, it could have moved directly from car seats into wristbands in gas or aerosol form.
“This result suggests dust may not be the primary route of exposure,” Volz said. “Dust is definitely something compounds like TDCIPP attach to, however, we can’t rule out that people are just inhaling airborne compounds.”
Another possibility is that the flame retardant is coming in through the air vents from outside, but the researchers do not think this scenario is likely.
Until there is more data, Volz has a suggestion for concerned readers.
“Outside of a major policy change that replaces TDCIPP with something else, it might not hurt to wear a mask in your car,” Volz said. “Just like wearing a mask mitigates COVID-19 transmission, so too would aerosol-phase flame retardants be mitigated. N95s are probably best for this purpose.”
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Materials provided by University of California – Riverside. Original written by Jules Bernstein. Note: Content may be edited for style and length.

A bad dye job is bad enough on its own, but an itchy and irritating allergic reaction to it is even worse. And people who become allergic to hair dye can develop reactions to many other common substances, transforming a simple cosmetic treatment into a big problem. Now, researchers reporting in ACS Sustainable Chemistry & Engineering have developed a range of permanent hair dyes that avoid the allergenic properties of traditional formulations.
When applied as hair color, paraphenylenediamine (PPD) — a common ingredient in permanent dyes — undergoes a chemical reaction that turns the hair a dark color that won’t wash out over time. This reaction, however, can also produce compounds that bind proteins in the user’s skin, causing allergic responses, such as eczema and facial swelling. PPD can also sensitize users to other substances, including a compound commonly found in sunscreens and cosmetics, as well as common pigment and ink compounds. Alternatives have been proposed, but they generally are not water-soluble, and the safety of some of the compounds are not well understood. Gopalakrishnan Venkatesan and colleagues wanted to create new alternatives that would avoid the problems of PPD while still providing permanent hair coloring.
The team prepared seven dyes based on PPD with modifications to the aromatic amine core. The modifications were chosen to potentially make the compounds less reactive toward proteins and less able to be absorbed into skin. All seven compounds permanently colored hair samples, producing a range of hues from rosy pinks to deep blacks that did not fade, even after three weeks of daily washing. The team then examined the dyes in a test commonly used in the cosmetics industry to determine if a product is a skin sensitizer. Five of the modified dyes were “weak” sensitizers, whereas PPD was “moderate.” Another test showed that the new compounds generated a reduced inflammatory response in cells compared to PPD. These results suggest that the new dyes can effectively color hair while also avoiding the potential allergenic and sensitization risks of more traditional ones.
The authors acknowledge funding from the National University of Singapore.
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Materials provided by American Chemical Society. Note: Content may be edited for style and length.

At a time when we are concerned about health, the smart ring, which can track sleep and body temperature, is too flawed to recommend.There couldn’t be a better time for wearable technology to shine. In the coronavirus era, we’re all concerned about our well-being. So wearable computers with tiny sensors that offer insight into our health seem particularly useful.One such gadget that stands out as intriguing is the third-generation Oura Ring, which was unveiled last November. It’s a tiny $300 health-monitoring device worn on a finger as if it were a piece of jewelry.The ring, according to Oura Health, offers the unique ability to measure minute changes in body temperature to help women accurately predict their menstrual cycles and potentially detect when a person is getting sick. That might even reveal early symptoms of Covid-19, the company has said.Who wouldn’t want that these days?The Oura Ring has also made a splashy debut. You may have seen it in a recent episode of “And Just Like That,” the reboot of “Sex and the City.” Prince Harry, Kim Kardashian and Jennifer Aniston have been seen wearing one. And ads for it have surfaced on Instagram and other social media, portraying the ring as a replacement for devices like the Apple Watch.Despite all the hype, I’m disappointed to report after two weeks of wearing an Oura that it was a letdown. The ring failed to accurately measure basic data like my footsteps, which raised broader questions about my general health data. (More on this later.) And while the charts about my heart rate and sleep patterns sure looked neat, I didn’t feel more enlightened about my overall health.I also can’t confirm whether the Oura can detect Covid-19 or any disease because I (fortunately) haven’t gotten ill.For a second opinion, I turned to Dr. Ethan Weiss, a cardiologist at the University of California, San Francisco, who owns an older version of the Oura Ring that he used to track sleep, body temperature and fitness activity. Dr. Weiss said he had stopped wearing it years ago.“It didn’t give me anything I could use to help me,” he said. “A lot of these technologies are looking for problems to solve. This is one of them.”There might be some people who would like the Oura Ring — body hackers and competitive athletes who are striving to optimize their fitness levels jump to mind — but I wouldn’t recommend it for most of us.Here’s what I found.Off on the Wrong FootThe Oura smart ring comes in four finishes.Oura HealthGetting started with an Oura Ring is a multistep process. First, you order a free sizing kit from the company’s website to measure your finger. Then you tell the company your size. When the ring arrives, you place it on a dock to charge it and sync it with a smartphone app. Once worn, it takes about two weeks for the software to calculate the baseline of your health data and make accurate estimates.After Week 1 of testing, something unusual came up. A relative needed help with an emergency, so I hopped on my motorcycle and rode 50 miles to his house.After I rode home, I opened the Oura app. It said I had walked 20 miles. This was obviously wrong. I had walked only a mile that day when I took my dogs out for an afternoon stroll.Brian X. ChenIt was clear what had happened. The Oura had incorrectly logged a portion of my 100-mile motorcycle ride as footsteps.A quick web search revealed that Oura customers complained about this issue last year with the ring’s previous version. The company’s response at the time, posted on Reddit, was that the ring falsely detected “excess motion” from motorcycling as a fitness activity, and it suggested removing the ring and putting it in a pocket while riding a motorcycle.Chris Becherer, Oura Health’s head of product, told me that the company was aware of the problem and researching a fix. He suggested that in the meantime, I could go back and delete workouts to inform the app that I wasn’t walking.This didn’t work. The app had permanently recorded my movements as walking, and the data could not be purged. I ride motorcycles regularly, including for errands around town, so that meant nearly a week of activity data was ruined. Having to manually edit my data would also have defeated the purpose of an automatic tracker.For comparison, I also wore an Apple Watch while testing the Oura. Even after my 100-mile trip, the Apple Watch correctly reported that I had walked only about a mile and had not exercised much that day.The Coronavirus Pandemic: Key Things to KnowCard 1 of 4Omicron in retreat.

Ten minutes of moderate exercise daily would prevent more than 111,000 premature deaths a year, a new analysis found.If almost all of us started walking for an extra 10 minutes a day, we could, collectively, prevent more than 111,000 deaths every year, according to an enlightening new study of movement and mortality. Published this week in JAMA Internal Medicine, the study used data about physical activity and death rates for thousands of American adults to estimate how many deaths every year might be averted if everyone exercised more. The results indicate that even a little extra physical activity by each of us could potentially stave off hundreds of thousands of premature deaths over the coming years.Already, science offers plenty of evidence that how much we exercise influences how long we live. In a telling 2019 study published by the Centers for Disease Control and Prevention, more than 8 percent of all deaths in the United States were attributed to “inadequate levels of activity.” A British study from 2015 likewise found that men and women who exercised for at least 150 minutes per week — the standard recommendation in Britain, Europe and the United States — reduced their risk of premature death by at least 25 percent compared to people who exercised less. More dramatically, a 2020 examination of the lifestyles and death risks of about 44,000 adults in the United States and Europe concluded that the most sedentary men and women in the study, who sat almost all day, were as much as 260 percent more likely to die prematurely as the most highly active people studied, who exercised for at least 30 minutes most days.But much of this past research relied on people’s often unreliable memories of their exercise and sitting habits. In addition, many of the studies that delved into the broader, population-level impacts of exercise on longevity tended to use formal exercise guidelines as their goal. In those studies, researchers modeled what would happen if everyone started working out for at least 150 minutes a week, an ambitious and perhaps unachievable goal for the many people who previously have exercised rarely, if at all.In the new study, researchers at the National Cancer Institute and the C.D.C. decided instead to explore what might happen to death rates if people started moving around more, even if they did not necessarily meet the formal exercise guidelines. But, first, the researchers needed to establish a baseline of how many deaths might be related to too-little movement. So, they began gathering data from the ongoing National Health and Nutrition Examination Survey, or NHANES, which periodically asks a representative sample of the population about their lives and health. It also provides some of them with activity trackers, to objectively measure how much they move.The researchers now pulled information from 4,840 participants of different ethnicities, male and female, who ranged in age from 40 to 85. All had joined the survey between 2003 and 2006 and worn an activity monitor for a week. Based on that data, the researchers grouped people according to how many minutes they walked or otherwise moved most days. They also checked people’s names against a national death registry to establish mortality risks for the various activity levels.Using those results, they began creating a series of statistical what-if’s. Suppose, the researchers asked, everyone who was capable of exercising began exercising moderately, such as by walking briskly, for an extra 10 minutes per day, on top of how much or little they currently worked out? How many deaths might not happen?The researchers made adjustments to account statistically for those people who were too frail or otherwise unable to walk or easily move around. They also considered age, education, smoking status, diet, body mass index and other health factors in their calculations.Then, the researchers ran the same statistical scenario with everyone working out for an extra 20 minutes a day and, finally, for an extra 30 minutes a day and checked the mortality outcomes.Quite a few people would live longer in any of those scenarios, they found. According to the modeling, if every capable adult walked briskly or otherwise exercised for an additional 10 minutes a day, 111,174 deaths annually across the country — or about 7 percent of all deaths in a typical year — might be avoided.When they doubled the imagined exercise time to an extra 20 minutes a day, the number of potentially averted deaths rose to 209,459. Tripling the exercise to 30 extra minutes a day averted 272,297 deaths, or almost 17 percent of typical annual totals. (The data was gathered before the pandemic, which has skewed mortality numbers.)Those figures might seem abstract, but, in practice, those hundreds of thousands of deaths forestalled could turn out to be deeply personal. They could mean avoiding the early death of a spouse, parent, friend, grown child, co-worker or, of course, us, said Pedro Saint-Maurice, an epidemiologist at the National Cancer Institute, who led the new study. “There is a message in this data for public health entities” about the importance of promoting physical activity to reduce premature deaths, he said. And the message applies equally to each of us.So get up and walk or engage in some kind of moderate physical activity for an extra 10 minutes today. Invite your friends, colleagues and aging parents to do the same. “In this context, a little additional physical activity can have a huge impact,” Dr. Saint-Maurice said.

If further study confirms the findings, they could lead to ways to prevent and treat the complex condition.It is one of many mysteries about long Covid: Who is more prone to developing it? Are some people more likely than others to experience physical, neurological or cognitive symptoms than can emerge, or linger for, months after their coronavirus infections have cleared?Now, a team of researchers who followed more than 200 patients for two to three months after their Covid diagnoses report that they have identified biological factors that might help predict if a person will develop long Covid.The study, published Tuesday by the journal Cell, found four factors that could be identified early in a person’s coronavirus infection that appeared to correlate with increased risk of having lasting symptoms weeks later.The researchers said they had found that there was an association between these factors and long Covid (which goes by the medical name post-acute sequelae of Covid-19, or PASC) whether the initial infection was serious or mild. They said that the findings might suggest ways to prevent or treat some cases of long Covid, including the possibility of giving people antiviral medications soon after an infection has been diagnosed.“It’s the first real solid attempt to come up with some biologic mechanisms for long Covid,” said Dr. Steven Deeks, a professor of medicine at the University of California, San Francisco, who was not involved in the study.He and other experts, along with the study authors themselves, cautioned that the findings were exploratory and would need to be verified by considerably more research.Still, Dr. Deeks said: “They’ve identified these four major factors. Each is biologically plausible, consistent with theories that other people are pursuing, and importantly, each is actionable. If these pathways get confirmed, we as clinicians can actually design interventions to make people better. That is the take-home message.”One of the four factors researchers identified is the level of coronavirus RNA in the blood early in the infection, an indicator of viral load. Another is the presence of certain autoantibodies — antibodies that mistakenly attack tissues in the body as they do in conditions like lupus and rheumatoid arthritis. A third factor is the reactivation of Epstein-Barr virus, a virus that infects most people, often when they are young, and then usually becomes dormant.The final factor is having Type 2 diabetes, although the researchers and other experts said that in studies involving larger numbers of patients, it might turn out that diabetes is only one of several medical conditions that increase the risk of long Covid.“I think this research stresses the importance of doing measurements early in the disease course to figure out how to treat patients, even if we don’t really know how we’re going to use all that information yet,” said Jim Heath, the principal investigator of the study and president of the Institute for Systems Biology, a nonprofit biomedical research organization in Seattle.“Once you can measure something, then you may be able to start doing something about it,” Dr. Heath said, adding: “We did this analysis because we know patients will go to physicians and they’ll say that they’re tired all the time or whatever, and the physician just tells them to get more sleep. That’s not very helpful. So, we wanted to actually have a way to quantify and say that there’s actually something wrong with these patients.”The complex study had several components and involved dozens of researchers at several universities and centers including the Institute for Systems Biology, the University of Washington and Swedish Medical Center in Seattle, where the study’s lead medical author, Dr. Jason Goldman, is an infectious disease specialist.The primary group of patients included 209 people, ages 18 to 89, who were infected with the coronavirus during 2020 or early 2021 and were seen at Swedish Medical Center or an affiliated clinic. Many were hospitalized for their initial infections, but some were seen only as outpatients. Researchers analyzed blood and nasal swabs when patients were diagnosed, during the acute phase of their infections and two to three months later.A tattoo of the demon Mr. Gillotte hallucinated during the Covid delirium he experienced after he was taken off the ventilator.Joshua Bright for The New York TimesThey surveyed the patients about 20 symptoms associated with long Covid, including fatigue, brain fog and shortness of breath, and corroborated those reports with electronic health records, Dr. Heath said.He said that 37 percent of the patients had reported three or more symptoms of long Covid two or three months after infection. A further 24 percent reported one or two symptoms, and 39 percent reported no symptoms. Of patients reporting three or more symptoms, 95 percent had one or more of the four biological factors identified in the study when they were diagnosed with Covid-19, Dr. Heath said.The most influential factor appeared to be autoantibodies, which were associated with two-thirds of the cases of long Covid, Dr. Heath said. Each of the other three factors showed up in about a third of the cases, he said, and there was considerable overlap, with several factors identified in some patients.The researchers corroborated some of their findings in a separate group of 100 patients, many with mild initial infections, from research led by Dr. Helen Chu at the University of Washington. The researchers also compared their results to data from 457 healthy people.“The study is large and comprehensive and is a great resource for the community studying long Covid,” said Akiko Iwasaki, an immunologist at Yale, who was not involved in the research.Dr. Avindra Nath, who is chief of the section on infections of the nervous system at the National Institute of Neurological Disorders and Stroke and was not involved in the study, called the study well designed but pointed out several weaknesses, including the fact that patients had been followed for only two to three months. “This might be too short a time frame,” he said. “Some might just improve spontaneously with time.”Dr. Iwasaki noted that 71 percent of the patients in the primary group had been hospitalized, limiting the ability to conclude that the biological factors were equally relevant for people with mild initial infections. The Coronavirus Pandemic: Key Things to KnowCard 1 of 4Omicron in retreat.

SharecloseShare pageCopy linkAbout sharingImage source, PA MediaTwo-thirds of people recently infected with the Omicron variant say they had already had Covid previously. The findings come from a large, continuing study, React, swab-testing thousands of volunteers in England. More work is needed to know how many are true reinfections – but the results reveal the groups that appear to be more likely to catch Covid again. They include healthcare workers and households with children or lots of members under one roof. Winter waveMore than two million people have been tested in the study. The latest findings, for the first two weeks of 2022 – round 17 – are based on about 100,000 polymerase chain reaction (PCR) tests posted to volunteers and then returned.About 4,000 were positive, by far the highest rate seen since the pandemic began. And when a selection of them were sequenced to check what type of Covid was to blame, virtually all were Omicron – the highly infectious variant, first identified in South Africa, causing a big winter wave of infections in the UK. Severe diseaseIt is not yet clear how many of the volunteers who tested positive had been fully vaccinated. Two shots offer little protection against catching Omicron, although protection against severe disease wanes less. But booster doses have been rolled out at speed since Omicron hit, to top up people’s protection. Two out of every three (65%) of the infected volunteers said they had already previously tested positive for Covid.Many of these could have been reinfected.Although, in some instances, the latest PCR tests might be picking up old traces of virus.Other estimates have suggested one in every 10 Omicron case is a possible reinfection. Currently, daily Covid case figures reported by the government – which reflect the number of infections picked up by people coming forward for testing – do not include reinfections for all countries of the UK. Coronavirus infections have slowed recently but remain high, particularly among children and young teenagers, the React findings also suggest. React programme director Prof Paul Elliott, from Imperial College London, said: “There is rapidly increasing prevalence among children now they are mixing more following the start of the school term and, compared with December, prevalence in older people, aged 65 plus, has increased… which may lead to increased hospitalisations. “It’s therefore vital that we continue to monitor the situation closely.”‘Get boosted’UK Health Security Agency chief executive Dr Jenny Harries said although vaccines may not stop every infection, they were doing a great job at protecting lives. “Vaccination remains the best way to protect yourself from severe disease and hospitalisation from Omicron, and I would urge anyone who has not done so to come forward for their primary and booster doses as soon as possible,” she said.”The impact the vaccination is having on preventing severe disease and hospitalisations is clear to see.”To ensure we continue on the downward trend and protect our communities, it is still important for us all to follow public-health advice, particularly in crowded spaces and areas of poor ventilation.”If you are visiting friends and family, make sure to take a test before going out.”Health and Social Care Secretary Sajid Javid said: “It’s reassuring to see Covid-19 infections beginning to slow across the country, as we move back to Plan A.”Rates are still high, so as we learn to live with the virus it is vital we continue to be vigilant – wash your hands, let in fresh air, get tested and, if you haven’t already, get boosted.”LOOK-UP TOOL: How many cases in your area?YOUR QUESTIONS: We answer your queriesTHE R NUMBER: What it means and why it mattersNEW VARIANTS: How worried should we be?COVID IMMUNITY: Can you catch it twice?