Scientists track down a protein that may add to lung damage in asthma and related diseases

Your lungs and airways need to be stretchy, sort of like balloons. Take a big breath, and they’ll open right up.

Damaged lungs can’t open properly. Patients with asthma, idiopathic pulmonary fibrosis and systemic sclerosis suffer from fibrosis and tissue remodeling, where a build-up of tissue and immune cells, and proteins that form a glue-like substance, keep the airways from expanding. As fibrosis gets worse, taking a breath feels like blowing up a balloon filled with concrete.

In a new study, researchers at La Jolla Institute for Immunology (LJI) report that a protein called TL1A drives fibrosis in several mouse models, triggering tissue remodeling, and making it harder for lungs and airways to function normally.

“Our new study suggests that TL1A and its receptor on cells could be targets for therapeutics aimed at reducing fibrosis and tissue remodeling in patients with severe lung disease,” says LJI Professor Michael Croft, Ph.D., director of scientific affairs at LJI and senior author of the new study in The Journal of Immunology.

Croft’s laboratory is focused on understanding the importance of a family of proteins, called tumor necrosis factors (TNF) and tumor necrosis factor receptors (TNFR), in inflammatory and autoimmune diseases. By investigating these molecules, researchers hope to track down the root causes of inflammation and stop tissue damage before it’s too late.

Previous research had shown that a TNF protein called TL1A can act on immune cells involved in allergic reactions and drive those immune cells to make inflammatory molecules. The Croft Lab wondered—if TL1A leads to inflammation, could it contribute to fibrosis in the lungs?

For the new study, Croft and his colleagues used genetic and therapeutic interventions, tissue staining, and fluorescence imaging techniques to study protein interactions in mouse models of severe asthma, idiopathic pulmonary fibrosis and systemic sclerosis. They first discovered that TL1A acts directly on a receptor on cells in the lungs and bronchial tubes, which leads to fibrosis and tissue remodeling.

We’re all familiar with the idea of tissue remodeling. When a wound on the skin heals, the new area of skin is sometimes shiner, darker or tougher than the skin around it. The tissue has been remodeled. When lungs and airways try to heal—in response to an asthma attack, for example— the cells in the area also change. The damaged area accumulates cells called fibroblasts, which make several glue-like proteins, including collagen. Too much collagen makes the lungs and airways less elastic—and less functional.

As Croft describes it, tissue remodeling is like wound healing, “but wound healing that goes wrong and becomes so exaggerated that it blocks tissue from behaving in its normal way.” With the new study, scientists now know that TL1A is driving this harmful remodeling in the lungs.

In addition to causing fibroblasts to make collagen, the researchers found that TL1A also helps fibroblasts to behave like smooth muscle cells. A thin layer of smooth muscle cells naturally lines the bronchial tubes allowing them to dilate and constrict, but a thick layer of these smooth muscle cells—that includes fibroblasts—will keep the airways from expanding and contracting normally, making it even hard for a patient to breathe.

The scientists then studied lung tissue remodeling in mice that lacked the receptor for TL1A, called DR3, or were given a reagent that blocked TL1A activity. These mice showed less lung remodeling, less collagen deposition and reduced smooth muscle mass in the lungs.

These animal model data may support recent research in humans. Researchers have found that patients with severe asthma have excessive production of TL1A. This could explain why these patients are more vulnerable to lung fibrosis and remodeling.

“This type of research needs to be expanded to really understand if there are subsets of patients with asthma or other inflammatory lung diseases who might express TL1A at higher levels than other patients—which could potentially guide future therapies for targeting TL1A to reduce remodeling and fibrosis,” says Croft.

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Study shows that rheumatoid arthritis is associated with a 23% increased risk of developing diabetes

A new study presented at this year’s annual meeting of the European Association for the Study of Diabetes (EASD), held online this year, shows that rheumatoid arthritis (RA) is associated with a 23% increased risk of type 2 diabetes (T2D), and may indicate that both diseases are linked to the body’s inflammatory response. The research was conducted by Zixing Tian and Dr. Adrian Heald, University of Manchester, UK, and colleagues.

Inflammation has emerged as a key factor in the onset and progression of T2D, and RA is an autoimmune and inflammatory disease. The team suggest that the systemic inflammation associated with RA might therefore contribute to the risk of an individual developing diabetes in the future.

The team conducted a comprehensive search of a range of medical and scientific databases up to 10 March 2020, for cohort studies comparing the incidence of T2D among people with RA to the diabetes risk within the general population. Statistical analyses were performed to calculate the relative risks, as well as to test for possible publication bias (in which the outcome of research influences the decision whether to publish it or not). The eligible studies identified comprised a total of 1,629,854 participants. Most of the studies were population-based and one was hospital-based, while no evidence was found for publication bias in any of them.

The authors found that having RA was associated with a 23% higher chance of developing T2D, compared to the diabetes risk within the general population. They conclude that: “This finding supports the notion that inflammatory pathways are involved in the pathogenesis of diabetes.”

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Researchers succeed with a more inclusive approach to heart transplants

Doctors at Yale New Haven Hospital used a more aggressive selection process to more than quadruple the number of heart transplants performed there while maintaining positive patient outcomes, according to a new study.

The findings suggest that a more inclusive approach to selecting donor hearts and transplant recipients can enable hospitals to successfully treat more patients in need of transplants. The study appears online Sept. 18 in the journal JAMA Network Open.

The study looked at short-term patient outcomes for two groups: 49 patients who received heart transplants from 2014 to 2018, and 58 patients who had their heart transplants in the year after the hospital adopted a more aggressive selection process for donor recipients (2018-2019).

The more aggressive selection process significantly shortened the waiting period for heart patients, from 242 days to 41 days, the researchers said. Importantly, patients’ survival rate at 180 days after the transplant remained nearly unchanged.

The expansion of heart transplant procedures at the hospital, in September 2018, coincided with the implementation of the new United Network for Organ Sharing (UNOS) donor heart allocation system in the United States.

“I think this is the takeaway for other centers—that such a change in the approach could create opportunities for patients in need while maintaining outcomes in the short term,” said Makoto Mori, M.D., a surgical resident at Yale and first author of the study.

The senior author of the study was Harlan Krumholz, M.D., the Harold H. Hines Jr. Professor of Medicine (cardiology) and director of Yale’s Center for Outcomes Research and Evaluation.

In practical terms, the expansion of heart transplant procedures at Yale New Haven Hospital meant accepting hearts from older donors with additional medical conditions, as well as accepting transplant recipients with more severe illnesses.

Yale New Haven Hospital also changed the surgical leadership of its advanced heart failure program, hired a dedicated procurement surgeon and an additional transplant coordinator, and increased the involvement of surgical attending physicians.

The researchers noted that Yale’s increase in heart transplant cases was significantly larger than the volume change seen at other heart transplant centers in the same region during the same period, including Hartford Hospital, Tufts Medical Center, Brigham and Women’s Hospital, and Massachusetts General Hospital.

“We used a multidisciplinary approach and made strategic changes in donor and recipient selection, which allowed us to increase the number of heart transplants performed and therefore help more patients with advanced heart failure in a safe and an effective manner,” said co-author Arnar Geirsson, M.D., chief of cardiac surgery at Yale New Haven Hospital.

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Winter may bring a lot more coronavirus cases, new research finds

Early in the coronavirus pandemic, scientists speculated that warm summer air would dampen its spread.

Then as the virus spread rapidly around the world, racking up more than 27 million cases in the spring and summer, the seasonal impact largely fell out of the public conversation.

But researchers at Johns Hopkins University are coming out with new research that suggests rising temperatures do moderate the spread of the virus—and a big new wave of cases could be coming with the cooler fall air.

“We have made significant inroads in this pandemic, and we can say a lot of that is because of social interventions,” said Dr. Adam Kaplin, assistant Hopkins professor of psychiatry and behavioral sciences and the lead researcher.

The warm weather served as a tail wind for those efforts, he said.

“In the fall and colder months we are going to hit a head wind in the other direction and that will make control much more difficult,” Kaplin said.

The findings were so striking that Kaplin took the unusual step of discussing the work while the research still was under review for publication in a scientific journal.

Maryland and other states, as well as other countries, have been easing restrictions with a drop in cases of COVID-19, the disease caused by the coronavirus. But Kaplin said cases could spike with more virus-friendly cool air even with the same restrictions.

The findings of seasonal variation are not new. The flu, the common cold and other coronaviruses typically moderate during warmer months. This could be due to the direct effects of heat on viruses and because fewer people congregate indoors.

Other recent studies or models on the pandemic coronavirus, from the University of Maryland to Harvard and Princeton universities, have found at least some impact from temperature changes or projected that there would be effects even if they weren’t obvious yet.

A paper published in the Journal of the American Medical Association by the Maryland researchers found, for example, the virus acted in a way “consistent with the behavior of a seasonal respiratory virus,” spreading along with temperature and humidity levels. The College Park researchers said it would be possible to develop a weather model to predict places most likely at higher risk for spread.

Rachel Baker from the Princeton Environmental Institute downplayed how much the weather was a factor, instead pointing to the importance of other measures such as wearing masks and physical distancing.

“I think it is possible that upcoming wintertime conditions could increase transmission, particularly in locations with more severe winters,” she said. “However, if we have effective control measures in place, we should be able to limit large secondary outbreaks.”

Baker said studies suggest the effects would be more clear over time. For now, a lot of the studies face challenges, such as differences in how cases are reported around the world.

Dr. Michael Ryan, executive director of the World Health Organization’s Health Emergencies Programme, was even less sure there would be a visible impact from temperature changes.

“This virus has demonstrated no seasonal pattern as such so far,” he said during an Aug. 10 news conference.

But other studies have raised concerns that a cold winter will lead to more cases if steps aren’t taken now to tamp down cases and keep them low.

That includes Dr. David Rubin at the Children’s Hospital of Philadelphia’s PolicyLab, which has incorporated weather into models it regularly produces. (The model suggests a slight uptick in Baltimore in the fall due to various factors including students returning to college campuses.)

The PolicyLab’s own weather study found a narrow range of springlike temperatures were the safest, 60-65 degrees. The researchers hypothesize that colder weather may facilitate more virus transmission but warmer weather may encourage more social gatherings conducive to spread.

The study, published in July in JAMA Network Open, also found distancing measures were the most effective means of controlling the virus no matter the temperature.

“There is a reason the meatpacking industry was hit so hard by this pandemic,” Rubin said. “They do live in congregate housing, but they also work in freezers. … We need to start now and get a good control of the virus so we don’t go into winter already in a surge.”

Kaplin at Hopkins agreed that measures taken now will matter.

A psychiatrist, Kaplin doesn’t normally do weather-related research, but wanted to sound early alarms to get the public’s attention while there is still time.

The issue became clear to him while in Brazil for his wedding in February, a summer month. He noticed a lower rate of viral transmission compared with the infection rate in the United States during a winter month.

Kaplin enlisted statistician colleagues and used data collected by other Hopkins researchers for their public coronavirus dashboard as well as available government weather data. The researchers got information from 50 countries that had reporting early in their outbreaks, before controls such as mask-wearing and physical distancing. The researchers accounted for population and land area in their calculations and looked for a pattern.

They found from January to April, places such as Singapore with average temperatures in the 80s had much lower rates of viral spread than places such as Turkey with average temperatures in the 20s.

Kaplin didn’t want to weigh in on specific actions to get ahead of another big wave of cases. But he said policymakers likely would have to consider tougher restrictions when the temperature drops just to maintain the same level of spread.

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A primer on viruses, vaccines and therapies

Since the novel coronavirus SARS-Cov-2 emerged late last year, it has been virtually impossible to consume any news without encountering stories about the virus and how it spreads, potential treatments, and the development of new vaccines.

This deluge of news can be overwhelming, especially for those who aren’t well-versed in virology or immunology. To help equip people to interpret the new information we learn about SARS-Cov-2 every day, Arup Chakraborty, the Robert T. Haslam Professor in Chemical Engineering at MIT, and Andrey Shaw at Genentech sat down early in the pandemic to write a slim book containing an overview of viruses and how they emerge to cause pandemics. The book also explains how our immune system fights viruses, the science of epidemiological models, and how vaccines and therapies work.

The resulting book, “Viruses, Pandemics, and Immunity,” provides important context for anyone who wants to better understand the complexities of the COVID-19 outbreak, as well as past and possible future pandemics, Chakraborty says. The book also provides an outline for creating a more pandemic-resilient world.

“People who read the book will now have a conceptual framework and facts to think about how viruses emerge to cause infectious diseases, how they spread, how we combat them naturally, and how we can combat them with vaccines and therapeutics,” says Chakraborty, who is also a professor of physics and of chemistry, a member of MIT’s Institute for Medical Engineering and Science, and a member of the Ragon Institute of MGH, MIT, and Harvard. “It will give them the framework that they need to debate and consider the current issues, and how we might build a more pandemic-resilient world.”

“It’s very difficult for the public to really get an understanding of the whole picture, and so that’s what our attempt was here,” Shaw says. “We felt that it was important to lay out the scientific framework so that people could make their own decisions about what is going on.”

The book, which was illustrated by Philip J.S. Stork of Oregon Health and Science University, was published by the MIT Press as an ebook on Sept. 8 and will be published as a paperback in February.

Historical perspective

Pandemics have played major roles in the course of human history, especially since humans began living together in closer quarters following the development of agriculture more than 10,000 years ago. Periodic outbreaks of bubonic plague, smallpox, yellow fever, influenza, and other infectious diseases have taken a huge toll on human populations.

During the 20th century, humankind made great strides against infectious disease, due to three major factors: improvements in sanitation, the discovery of antibiotics, and the development of vaccines against many deadly diseases. Because of those advances, many people, especially those living in developed countries, tended to think of major disease outbreaks as a thing of the past.

“This pandemic has reminded us that infectious diseases are an existential threat to humankind and have always been,” Chakraborty says.

As he and Shaw outline in their book, viruses, especially RNA viruses, are well-suited to cause pandemics. One reason for this is that RNA viruses are much more prone to make mistakes in copying their genetic material than DNA viruses are. This allows them to occasionally generate mutations that allow them to jump between species. The SARS-Cov-2 virus is believed to have done just that, likely jumping from bats to humans.

While humans have not previously encountered this particular virus, our immune system does have myriad defenses that can help fend off viral infection. These defenses fall into two main branches—innate and adaptive immunity.

The innate immune system is constantly on the lookout for foreign invaders. Upon encountering viral particles, it deploys a variety of cellular responses that can control the virus. The innate immune system also sends out a distress signal that attracts the specialized cells of the adaptive immune system. These cells, such as “killer T cells,” can launch a response tailored specifically for a particular virus or any pathogen. However, this response takes longer to develop. Once a pathogen has been vanquished, memory T cells, B cells, and antibodies specific to that pathogen continue to circulate, providing immunity to future infection.

Medical advances

While the human body has its own defenses against infection, these don’t always get the job done. Technological advances, especially vaccination, have proven to be a major weapon against infectious disease. The first modern vaccine, which was developed in 1796 to prevent smallpox, consisted of a virus called cowpox, which doesn’t harm humans but is similar enough to smallpox to provoke an immune response against the disease. The term vaccine comes from the Latin word “vaccinus,” meaning “of or from cows.”

The book describes the many types of vaccines, including attenuated vaccines, which consist of a weakened form of a virus or bacterium; vaccines that consist of killed pathogens; and subunit vaccines, which contain just a fragment of a pathogen.

One promising new type of subunit vaccine is RNA vaccines, which are made from RNA that encodes a viral protein. A major advantage of this type of vaccine is that they can be designed very quickly—one pharmaceutical company, Moderna, was able to start phase 1 clinical trials of an RNA vaccine against SARS-Cov-2 just over two months after the virus’ genetic sequence was published. That vaccine is now in phase 3 clinical trials, while dozens more, many based on other strategies, are also in development.

Because we don’t know yet which approaches will work the best for COVID-19, “it is wonderful that many vaccine ideas are being pursued in parallel,” the authors write in their chapter on vaccine development.

One factor that makes the authors optimistic about a SARS-Cov-2 vaccine is that the virus does not mutate rapidly, unlike other RNA viruses such as HIV and influenza. “It may not be so difficult to make a vaccine against it, especially with the extraordinary efforts people are putting into it,” Chakraborty says. He adds that the lessons learned from these intense efforts, and current research on vaccines against highly mutable pathogens, could lead to future advances that make possible vaccines against more difficult viruses such as HIV, which has no effective vaccine even after many decades of research, as well as vaccines against novel mutable viruses that may emerge in the future.

Antiviral drugs have also proven successful against some diseases, such as HIV and hepatitis C. These drugs can target many different stages of the viral life cycle. Some prevent viruses from binding to cell receptors that let them enter cells, while others, such as the reverse transcriptase inhibitors used to treat HIV, prevent the virus from replicating inside cells.

Because it takes so long to develop a new antiviral drug, scientists often try repurposing old drugs when a new virus emerges. Recently the U.S. Food and Drug Administration granted emergency-use authorization for remdesivir, a drug that is believed to interfere with viral replication, to treat COVID-19. Dexamethasone, a corticosteroid that helps reduce inflammation, has also been shown to improve symptoms in some patients.

“When COVID-19 first burst onto the scene, many physicians were really unprepared to treat this. But as the months have passed, we’ve become much more familiar with what’s going on, and we have a better idea how to treat these problems,” Shaw says.

The road ahead

In addition to offering the general public a better understanding of the scientific principles behind viruses, immunity, vaccines, therapies, and epidemiology, Chakraborty and Shaw hope to inspire young people to pursue careers related to those topics. They also hope that the book will help people in policymaking positions to gain a better understanding of the science behind pandemics, to aid them in making decisions that will help combat COVID-19 and potential future disease outbreaks.

“The authors provide a readily accessible introduction to viruses, a class of tiny human pathogens of surprising potential to cause transmissible, sometimes fatal, disease. They speak from a deep understanding of the viruses and the body’s response to viral infections. A great book for people who want to understand why viruses are such a challenge to human life,” says David Baltimore, president emeritus and professor of biology at Caltech, and winner of the 1975 Nobel Prize in Medicine.

Chakraborty and Shaw believe there are many ways to make the world more resilient to future pandemics, including improving early diagnostics, surveillance, and epidemiological modeling; creating more targeted approaches to the development of vaccines and antiviral drugs; making vaccine manufacturing more flexible; and making living spaces, workplaces, and hospitals safer. Success in these areas will require partnerships between government, the pharmaceutical industry and academia, with investments by the government to stimulate the necessary advances, the authors say.

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Study takes us a step closer to a universal antibody test for COVID-19

A new study released by Houston Methodist takes researchers a significant step closer to developing a uniform, universal COVID-19 antibody test. The multicenter collaboration tested alternative ways to measure COVID-19 antibody levels that is faster and easier and can inexpensively be used on a larger scale to accurately identify potential donors with the best chance of helping patients infected with the SARS-CoV-2 virus with convalescent plasma therapy.

The findings will also have applications beyond determining who the best plasma donors are. The consensus among the study authors is that, following donor identification, it will most likely next be used in practice to establish target levels of COVID-19 antibodies individuals will need to be considered candidates for vaccines and passive immune therapies.

Additional uses coming later that are likely to have the biggest societal impact, the researchers say, are to assess relative immunity in those previously infected by the SARS-CoV-2 virus and identifying asymptomatic individuals with high levels of neutralizing antibodies against SARS-CoV-2.

It was also found that donors who experienced shortness of breath (or dyspnea) while infected with COVID-19 and those who were hospitalized or had severe disease were more likely to have a robust immune response and, thus, had higher levels of neutralizing antibodies in all the tests. In the absence of available testing, identifying such donor characteristics may be used as a contingency plan to determine which patients have developed higher antibody levels and inform efforts to recruit plasma donors for therapeutic purposes.

In collaboration with Penn State, University of Texas at Austin and U.S. Army Medical Research Institute of Infectious Diseases, study authors James M. Musser, M.D., Ph.D., and Eric Salazar, M.D., Ph.D., physician scientists at Houston Methodist, sought to find alternatives to measuring virus neutralization (VN) titers, which is the gold standard of COVID-19 antibody testing, as VN antibodies in the blood correlate with immunity. This kind of antibody testing, however, is not widely available, because it’s technically complex, requires days to set up, run and interpret, and needs to be performed in a biosafety level 3 laboratory. This leads to most donor plasma virus antibody levels remaining unknown prior to transfusions, so an easier, more readily available method is needed to identify more suitable convalescent plasma donors.

The research team, therefore, looked to another type of test, called ELISA assays, which can be implemented and performed with relative ease in a high-throughput fashion and are widely available and extensively used in clinical labs across the world. The ELISA tests, or enzyme-linked immunosorbent assays, look at whether antibodies against the SARS-CoV-2 proteins are present and produce a quantitative measure of those antibodies. The UT Austin research team developed the ELISA antibody test for SARS-CoV-2 and provided the viral antigens for this study.

Specifically, scientists looked at the relationship of anti-spike ectodomain (ECD) and anti-receptor binding domain (RBD) IgG bloodstream antibody titers. The spike ECD and RBD proteins are physiological parts of the much-talked-about spike protein made by SARS-CoV-2 and critical to how the virus finds its way into the body, spreads and causes COVID-19 disease, so they are prime targets for antibody testing and vaccine development. The blood samples for the study were identified during an institutional surveillance program involving 2,814 Houston Methodist employees.

The goal of the study was to test the hypothesis that anti-ECD and anti-RBD IgG bloodstream antibody titers are correlated with VN titer, making these more accessible, easier-to-perform ELISA tests a surrogate marker to identify plasma donors with titers above the recommended U.S. Food and Drug Administration threshold for convalescent plasma donation.

In assessing the correlation between VN antibody levels and anti-RBD and anti-ECD ELISA protein titer data, the researchers found that the ELISA tests had an 80% probability or greater of comparable antibody level to VN titers at or above the FDA-recommended levels for COVID-19 convalescent plasma. These results affirm that all three types of tests could potentially serve as a quantitative target for therapeutic and prophylactic treatments.

They also found that convalescent donors maintain high levels of immunity over the course of many weeks and that frequent plasma donations did not cause a significant decrease in antibody or virus neutralization levels.

Perhaps most surprising is that they also identified 27 individuals from the surveillance cohort with high enough antibody titers across all three tests to indicate that some asymptomatic individuals may have plasma suitable for therapeutic use and may have a degree of relative immunity against SARS-CoV-2.

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How even a short walk can boost your memory

How even a short walk can boost your memory: Exercise improves concentration and problem-solving skills, scientists discover

  • Scientific review found people improved on memory tests after exercising 
  • Findings come from 13 studies which were analysed by Swedish researchers 
  • Exercise is believed to increase levels of a protein called ‘brain-derived neurotrophic factor’ which is thought to be important for memory function

A short walk, run or bike ride could provide a memory boost in less than an hour.

A scientific review looked at people aged 18 to 35 who walked, ran or cycled at moderate to high intensity and then took tests such as remembering a list of 15 words.

The participants, who exercised in bursts of two minutes, or 15 minutes, half an hour or an hour, improved on tests and showed better concentration and problem-solving skills.

The findings come from 13 studies which were analysed by Swedish researchers.

A short walk, run or bike ride could provide a memory boost in less than an hour

The authors, from Jonkoping and Linkoping universities, conclude: ‘This systematic review strongly suggests that aerobic, physical exercise followed by a brief recovery… improves attention, concentration, and learning and memory functions in young adults.’

Exercise is believed to increase levels of a protein called ‘brain-derived neurotrophic factor’ which is thought to be important for memory.

But not everyone is a natural athlete or has hours to work out. 

The review wanted to see if a single bout of exercise could have an effect, so looked at studies exploring this with young adults over ten years.

The review, published in the journal Translational Sports Medicine, found exercise from two minutes to an hour improved memory and thinking skills for up to two hours.

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If sitting at a desk all day is bad during coronavirus, could I lie down to work instead?

Most of us have heard that too much sitting is bad for you. Studies show sitting increases the risk for cardiovascular disease and mortality, Type 2 diabetes and cancer.

With Americans more sedentary than ever, that’s particularly alarming. Even before COVID-19, many of us had managed to engineer physical activity out of our lives. But now, the pandemic has made things worse. Going outside less, missing the gym, working from home and countless hours on Zoom has meant, for most of us, even more sitting.

One question that occasionally comes up about this, perhaps from couch potatoes looking for a loophole, or maybe just those who prefer a more precise definition: Is reclining better? Instead of sitting upright (or slumped over) at a desk all day, is it somehow healthier to lie on the sofa, or relax in a hammock, or lean back in the easy chair? After all, your body is positioned differently. Does that distinction matter?

As an exercise physiologist, I can give you a short answer to that: No. (Sorry.) And instead of “sitting,” maybe we should use the term “sedentary behavior,” which is any waking behavior (note the word “waking”) that’s associated with low levels of energy expenditure. That includes sitting, reclining or lying down, according to the 2018 Physical Activity guidelines.

Move, move, move

Does physical activity help reduce, even eliminate, the negative impact of sedentary behavior? A 2016 study reviewed data from more than 1 million men and women. Those who sat a lot, and had little moderate or vigorous physical activity, had the highest risk of mortality from all causes. Those who sat only a little, and had high levels of moderate or vigorous physical activity, had the lowest risk.

What about someone in between? Someone who sits a lot but also engages in plenty of physical activity? The findings show mortality risk decreases as long as physical activity increases, regardless of sitting time. But the best way to go: high levels of activity, low levels of sedentary behavior.

How much activity do you need? The current estimate is 60 to 75 minutes a day of moderate activity, or 30 to 40 minutes of vigorous activity; do at least one of the two.

Physical activity: Good for everyone

Now let’s define physical activity: body movements that require energy expenditure, according to the World Health Organization. That covers plenty of ground: Any movement while working or playing counts, whether chores around the house or walks around the neighborhood. Your benefits from this activity begin immediately, and any amount helps. It doesn’t matter if you’re very young, very old or if you have chronic disabilities.

Notice I haven’t yet used the word “exercise”—until now. Exercise, obviously, is a type of physical activity, structured to improve flexibility, balance and speed, along with cardio and muscular fitness. It’s one of the best things you can do to improve your health and quality of life.

Benefits include a lower risk of mortality from all causes: heart disease, stroke, Type 2 diabetes, cancer, obesity, hypertension and osteoporosis. Your brain health will be better, perhaps enough to help ward off depression, anxiety, dementia and Alzheimer’s. And your sleep will improve.

Sleep on it

About sleep: The sedentary behavior referenced earlier does not include sleep. For optimal health, sleep is an absolute must.

Everyone is compromised by sleep deficiency, sometimes known as short sleep, or fewer than six hours per day. Difficulties with behavior, emotional control, decision-making and problem-solving are just some of the effects in people of all ages.

Poor sleep can also affect the immune system in people of all ages, leading to vulnerability to infections. It can be a factor in suicide, depression and high-risk behavior. And poor sleep also promotes obesity; essentially, a deficiency increases your “hunger hormone” (ghrelin) and decreases the “satiety hormone” (leptin). This makes you more likely to overeat.

In adults, sleep deficiency is associated with an increased risk of heart disease, high blood pressure, stroke and kidney disease. Adults need seven to eight hours per day.

Kids also suffer when they do not get enough sleep. Lack of sleep slows the release of growth hormone. Teens need 8-10 hours of sleep, and children age 6-12 need 9-12 hours.

Physical activity and good sleep go hand in hand. Moderate to vigorous activity lets you fall asleep faster and get more deep sleep; it reduces daytime sleepiness and use of sleep medications.

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Need a pep talk? Here are ten rules to live by if you want to make a change

Sometimes in life all we need is someone to sit us down, give us a good talking to and offer some advice.

Whether it’s motivation to workout, reasons to change career, how to overcome adversity or to boost your confidence, talking to someone who has ‘been there and done that’ can have a hugely positive impact on your own life.

PepTalk is a new online coaching platform that allows you to connect with people such as entrepreneurs, industry experts, award-winning adventurers and gold-medal athletes.

The aim is to motivate, educate and inspire you to be bigger and better than you were before.

We’ve asked ten of their experts to share the rules they live by, in order to lead a healthier and happier life.

Rule 1: When making changes, understand why

‘I encourage moderation and understanding when making lifestyle changes,’ says Marina Kirik, stress buster, joy finder and meditation coach.

‘Whether it’s changes to diet and exercise, improving hydration or mindfulness, I encourage sustainable shifts.

‘Don’t go on a diet, instead understand why you should eat more fruit and vegetables and incorporate them in your life in a way that’s feasible.

‘If you start drinking more water, make sure you know the why of what water does for your body.

‘I find this approach encourages people to make changes that fit their lifestyle and that they feel motivated to keep up.’

Rule 2: Take steps every day to care for your skin

‘Remember that caring for your health as a whole prevents ageing and brings about beautiful skin,’ says Katy Burris, skincare physician.

‘Eat a diet filled with antioxidants, aim to drink at least eight to ten cups of water each day and be sure to exercise.

‘Take a vitamin D supplement to keep your bones strong and your immune system supported.

‘In addition, hydrate your skin with moisturiser twice daily and always wear sunscreen — it’s the best anti-ageing remedy we have.’

Rule 3: Don’t hesitate to take time off

‘Before starting my business, I worked remotely and found it challenging to switch off at the end of the day,’ says Emma Dechoux, a straight-talking leadership coach and inspirational mentor.

‘What helped was switching devices off and going for a walk or run.

‘This allowed me to decompress and reflect and return home re-energised.

‘It’s also important to be proactive with your self-care and I schedule at least one wellbeing day off per month.’

Rule 4: Get into a good sleep routine

‘Sleep plays an essential role in wellbeing and performance,’ says Matt Lovell, performance, nutrition and wellbeing specialist.

‘Ensure you follow the obvious rules: power down and try to be in restful mode a couple of hours before you want to sleep and steer clear of “blue light” devices like computers and phones.

‘Try some slow breathing, and if you have a pet, it can be quieting to spend time with them.

‘Being restful before sleep can help regulate your stress hormones, so when you do wake, you’re ready to go.’

Rule 5: Don’t be afraid to make a change

‘I work with many clients who feel unfulfilled in their work,’ says Lauren Phelps, change and accountability coach.

‘If you feel disengaged, uninspired and spend your spare time playing mindless games on your phone, it’s a sign you need a change.

‘Your past doesn’t dictate your future. Rise out of that rut.

‘There is a more compelling future waiting for you. Making tiny changes are small steps towards a better life.’

Rule 6: Get your ‘five-a-day’ for the mind

‘Each person is different in terms of how they support their mental health and wellbeing — meditation, mindfulness, exercise or therapy,’ says Charlie Hoare, positive psychologist and wellbeing consultant.

‘Try out some of these practices to determine what works for you.

‘Just as you’d aim to eat five fruit and vegetables per day to keep your body healthy, try to do five things to keep your mind healthy, whether that’s a moment of mindfulness or stepping into nature.

‘Try not to feel you need to be productive all the time; a rest is also good for the soul.’

Rule 7: Look up, around and forward

‘I have lived by this rule every day of my life since I retired from international rugby,’ says Catherine Spencer, former England rugby captain and female empowerment coach.

‘I use it to fuel my future in a positive way. It helps me to be focused, confident and ultimately happy.

‘It is important to have the confidence to try different things, to aim for goals and to aspire to our dreams; some we will achieve, some we won’t but that is OK.

‘It takes all of our experiences to push us forward.’

Rule 8: Prioritise your health

‘Make sure your health is always a top priority,’ says Peter Dale, Sky Sports presenter and inspirational broadcaster.

‘As someone who suffered a major heart attack aged 36 — even though I worked out and felt fit — I’ve learned it’s crucial to care for yourself and get your heart checked regularly.

‘If your body doesn’t feel quite right, don’t put off going to see the doctor.

‘Young people today have the pressure of high expectations and this can really impact their health.’

Rule 9: For happiness, find ways to serve others

‘During challenging times, turn off national and international news and tune into your community,’ says communications expert Jenifer Sarver.

‘Obsessing over global events which you have little control over can be overwhelming.

‘My solution is to prioritise what’s going on in my city, in my neighbourhood and take direct action to help.

‘I find serving others alleviates my own stress and anxiety.

‘Reaching out and helping others makes our lives richer and more meaningful and has a positive impact on our world.’

Rule 10: Make sure to listen to yourself

‘Take time and space to consider what’s working in your life and what isn’t,’ explains Dierdre Wolownick, language professor and inspirational motivator.

‘It’s important to make sure we’re living the life we want, not the life others think we should be.

‘Try journaling and reflecting on your entries. Or, get outside to experience nature and exercise; you don’t have to run a marathon.

‘Committing to physical activity can provide clarity on who you are and who you want to be.’

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A tool that automatically scores dream reports used to test the ‘continuity hypothesis’

A team of researchers from Università degli studi di Roma Tre and Nokia Bell Laboratories has developed a tool that automatically scores dream reports, greatly speeding what is normally a slow and time-consuming manual process. In their paper published in the journal Royal Society Open Science, the group describes the factors that went into the development of their tool and how well it compared to reports done manually.

Human beings have pondered the meaning of their dreams for thousands of years, and scientists have been studying them for centuries. As a way to interpret their meaning in the modern age, scientists have created systems to score dreams based on a variety of factors such as which characters were in them, and how they interacted. Such systems have led many in the field to conclude that dreams are nothing more than a continuum of our daily lives.

This “continuity hypothesis” suggests that our dreams are the mind’s way of processing events during the day. Prior research has shown the reverse to be true, as well—stressful dreams lead to reduced stress throughout the day. One of the most well-known sleep systems developed for creating dream reports (for therapists treating patients) is called the Hall and Van de Castle system. It is a system for codifying dreams, which allows for standardized assessments.

The team with this new effort based their tool on the Hall and Van de Castle system—the tool automatically scores dream reports. The researchers operationalized those factors they felt were most important in the system in a way that could be crunched by a computer. They then validated their tool by running it on 24,000 dream accounts and compared what it produced with those that had been done manually. They found it to have an error rate of just 0.24 percent.

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