Publisher Health

B-type procyanidins, made of catechin oligomers, are a class of polyphenols found abundantly in foods like cocoa, apples, grape seeds, and red wine. Several studies have established the benefits of these micronutrients in reducing the risk of cardiovascular diseases and strokes. B-type procyanidins are also successful in controlling hypertension, dyslipidemia, and glucose intolerance. Studies attest to the physiological benefits of their intake on the central nervous system (CNS), namely an improvement in cognitive functions. These physiological changes follow a pattern of hormesis — a phenomenon in which peak benefits of a substance are achieved at mid-range doses, becoming progressively lesser at lower and higher doses.
The dose-response relationship of most bioactive compounds follows a monotonic pattern, in which a higher dose shows a greater response. However, in some exceptional cases, a U-shaped dose-response curve is seen. This U-shaped curve signifies hormesis — an adaptive response, in which a low dose of usually a harmful compound induces resistance in the body to its higher doses. This means that exposure to low levels of a harmful trigger can induce the activation of stress-resistant pathways, leading to greater repair and regeneration capabilities. In case of B-type procyanidins, several in vitro studies support their hormetic effects, but these results have not been demonstrated in vivo.
To address this knowledge gap, researchers from Shibaura Institute of Technology (SIT), Japan, led by Professor Naomi Osakabe from the Department of Bioscience and Engineering, reviewed the data from intervention trials supporting hormetic responses of B-type procyanidin ingestion. The team, comprising Taiki Fushimi and Yasuyuki Fujii from the Graduate School of Engineering and Science (SIT), also conducted in vivo experiments to understand possible connections between B-type procyanidin hormetic responses and CNS neurotransmitter receptor activation. Their article was made available online on June 15, 2022 and has been published in volume 9 of Frontiers of Nutrition on September 7, 2022.
The researchers noted that a single oral administration of an optimal dose of cocoa flavanol temporarily increased the blood pressure and heart rate in rats. But the hemodynamics did not change when the dose was increased or decreased. Administration of B-type procyanidin monomer and various oligomers produced similar results. According to Professor Osakabe, “These results are consistent with those of intervention studies following a single intake of food rich in B-type procyanidin, and support the U-shaped dose-response theory, or hormesis, of polyphenols.”
To observe whether the sympathetic nervous system (SNS) is involved in the hemodynamic changes induced by B-type procyanidins, the team administered adrenaline blockers in test rats. This successfully decreased the temporary increase in heart rate induced by the optimal dose of cocoa flavanol. A different kind of blocker — a1 blocker — inhibited the transient rise in blood pressure. This suggested that the SNS, which controls the action of adrenaline blockers, is responsible for the hemodynamic and metabolic changes induced by a single oral dose of B-type procyanidin.
The researchers next ascertained why optimal doses, and not high doses, are responsible for the thermogenic and metabolic responses. They co-administered a high dose of cocoa flavanol and yohimbine (an α2 blocker) and noted a temporary but distinct increase in blood pressure in test animals. Similar observations were made with the use of B-type procyanidin oligomer and yohimbine. Professor Osakabe surmises, “Since α2 blockers are associated with the down-regulation of the SNS, the reduced metabolic and thermogenic outputs at a high dose of B-type procyanidins seen in our study may have induced α2 auto-receptor activation. Thus, SNS deactivation may be induced by a high dose of B-type procyanidins.”
Previous studies have proven the role of the gut-brain axis in controlling hormetic stress-related responses. The activation of the hypothalamus-pituitary-adrenal (HPA) axis by optimal stress has a strong influence on memory, cognition, and stress tolerance. This article highlights how HPA activation occurs after a single dose of B-type procyanidin, suggesting that stimulation with an oral dose of B-type procyanidin might be a stressor for mammals and cause SNS activation.
Hormesis and its triggering biochemical pathways deliver protection against various pathological and aging processes, enhancing our general health and making us resilient to future stress. Though the exact relation between B-type procyanidins and the CNS needs more research, the health benefits of B-type procyanidin-rich foods remains undisputed.
Story Source:
Materials provided by Shibaura Institute of Technology. Note: Content may be edited for style and length.

A new study may have solved a mystery surrounding Crohn’s disease, an inflammatory bowel illness where immune defenses, meant to attack invading microbes, instead mistakenly target the body’s own digestive tract. Norovirus, a common infection that causes vomiting and diarrhea, is one of several viruses and bacteria thought to trigger disease onset in Crohn’s patients, but the field does not know why.
One clue emerged when past studies found that a certain genetic change (mutation) is present in most patients with the condition. This mutation makes gut lining cells more vulnerable to damage. The mystery deepened again, however, when it was learned that half of all Americans have this same risk-conferring genetic mutation, but fewer than a half-million develop Crohn’s.
Publishing online Oct. 5 in the journal Nature, the new work in mice and in human tissue revealed for the first time that in healthy individuals, immune defenders called T cells secrete a protein called apoptosis inhibitor five (API5), which signals the immune system to halt the attack on gut lining cells. This protein adds an extra layer of protection against immune damage, so even those with the mutation can have a healthy gut. However, the researchers also found that norovirus infection blocks T cell secretion of API5 in mice bred to have a rodent form of Crohn’s disease, killing gut-lining cells in the process.
Led by researchers at NYU Grossman School of Medicine, the work supports the theory that API5 protects most people with the mutation against the disease until a second trigger, such as norovirus infection, pushes some across the disease threshold.
In experiments centered on mice genetically modified to have the mutation linked to Crohn’s disease in humans, mice that received an injection of API5 survived, while half of the untreated group died. This confirmed the idea that the protein protects gut cells, say the study authors. In human tissue, the investigators found that those with Crohn’s disease had between fivefold and tenfold fewer API5-producing T cells in their gut tissue than those without the illness.
“Our findings offer new insight into the key role that apoptosis inhibitor five plays in Crohn’s disease,” says study lead author and gastroenterologist Yu Matsuzawa-Ishimoto, MD, PhD. “This molecule may provide a new target for treating this chronic autoimmune illness, which has proven difficult to manage over the long term.”
Matsuzawa-Ishimoto, a postdoctoral research fellow at NYU Langone Health, notes that current therapies, which work by suppressing the immune system, put patients at high risk for infection and often become less effective after a few years of use. A treatment method targeting API5, he adds, might avert those issues.

Scientists have shown that in one in every 4,000 births, some of the genetic code from our mitochondria — the ‘batteries’ that power our cells — inserts itself into our DNA, revealing a surprising new insight into how humans evolve.
In a study published today in Nature, researchers at the University of Cambridge and Queen Mary University of London show that mitochondrial DNA also appears in some cancer DNA, suggesting that it acts as a sticking plaster to try and repair damage to our genetic code.
Mitochondria are tiny ‘organelles’ that sit within our cells, where they act like batteries, providing energy in the form of the molecule ATP to power the cells. Each mitochondrion has its own DNA — mitochondrial DNA — that is distinct to the rest of the human genome, which is comprised of nuclear DNA.
Mitochondrial DNA is passed down the maternal line — that is, we inherit it from our mothers, not our fathers. However, a study published in PNAS in 2018 from researchers at the Cincinnati Children’s Hospital Medical Center in the USA reported evidence that suggested some mitochondrial DNA had been passed down the paternal line.
To investigate these claims, the Cambridge team looked at the DNA from over 11,000 families recruited to Genomics England’s 100,000 Genomes Project, searching for patterns that looked like paternal inheritance. The Cambridge team found mitochondrial DNA ‘inserts’ in the nuclear DNA of some children that were not present in that of their parents. This meant that the US team had probably reached the wrong conclusions: what they had observed were not paternally-inherited mitochondrial DNA, but rather these inserts.
Now, extending this work to over 66,000 people, the team showed that the new inserts are actually happing all the time, showing a new way our genome evolves.

A molecular test called PancreaSeq accurately classifies pancreatic cysts as potentially cancerous or benign, according to a large, multi-center study led by University of Pittsburgh School of Medicine and UPMC researchers.
Published today in Gastroenterology, the prospective study of more than 1,800 patients found that incorporating molecular markers improved the accuracy of diagnoses compared with current guidelines based on imaging of cysts.
“Based on the results of this study, molecular testing of pancreatic cysts is poised to enter international consensus guidelines for the diagnosis of pancreatic cysts and early detection of pancreatic cancer,” said co-senior author Aatur Singhi, M.D., Ph.D., associate professor of pathology at Pitt and UPMC Hillman Cancer Center investigator. “Our hope is that PancreaSeq will not only improve early detection of pancreatic cancer but also avoid overtreatment and unnecessary surgery of non-cancerous cysts.”
Up to 15% of the U.S. population will develop a pancreatic cyst at some point in their lives. Most of these cysts are benign, but a small fraction will transform into cancer.
“Although rare, pancreatic cancer is a deadly disease: Most patients will die within a few years of diagnosis,” said Singhi. “The only way we can improve outcomes for pancreatic cancer is to find better treatments or detect it earlier. Here at UPMC, our focus has been addressing both of these issues, and especially improving early-stage detection efforts.”
Pittdeveloped PancreaSeq, which accurately distinguishes benign cysts from those that could become cancerous by sequencing 22 pancreatic cyst-associated genes.

Researchers at UNC Lineberger Comprehensive Cancer Center have found a possible way to overcome barriers that block effective anti-cancer immune responses, thereby opening the potential for more effective immunotherapies in people.
The findings are published in Nature.
An unfavorable immune environment immediately surrounding a tumor cell is a major obstacle in using immunotherapy to treat many solid tumors, especially pancreatic and breast cancer, as the suppressive environment can block immune responses that could be helpful in attacking a tumor. One protein, the STimulator of INterferon Genes (STING), has the promise of powerfully provoking multiple parts of the immune system and breaking established barriers.
“Although activating the immune system to control malignant tumors has revolutionized cancer treatment, a sizable portion of patients do not respond to immunotherapy treatments. However, new drugs that target STING have been a high priority for pharmaceutical development yet clinical trials have revealed significant tumor resistance to STING-directed drugs,” said UNC Lineberger’s Jenny PY Ting, PhD, the William R. Kenan Professor of Genetics and professor of microbiology and immunology at the UNC School of Medicine.
“Clinically, to improve the effectiveness of STING-targeted drugs, we need to more deeply understand how these drugs influence different immune cells in the tumor because the beneficial effects of STING on immunity may be outweighed by its unintended immune-suppressive effect,” said Ting, the paper’s co-corresponding author and director of the Center for Translational Immunology at UNC.
The investigators primarily focused on pre-clinical models of pancreatic cancer as the disease has a five-year survival rate of only 10% in people and there are few treatment options. They also expanded the study to other solid tumors, including melanoma, triple-negative breast cancer and lung cancer. Importantly, what they observed in pancreatic cancer is broadly applicable to these additional cancers.

Particle radioactivity, a characteristic of air pollution that reflects the colorless, odorless gas radon found in fine particulate matter (PM2.5) air pollution, enhances PM2.5 toxicity and increases risk of death from cardiovascular disease, especially from heart attack or stroke, according to new research published today in the Journal of the American Heart Association, an open access, peer-reviewed journal of the American Heart Association.
Previous scientific research has confirmed that PM2.5, a component of air pollution, causes cardiovascular disease and death, and that PM2.5 exposure is a modifiable cardiovascular disease risk factor. In 2021, the American Heart Association joined with three other leading cardiovascular organizations urging the medical community and health authorities to mitigate the impact of air pollution on people’s health. According to the statement, an estimated 6.7 million deaths in 2019, or 12 percent of all deaths worldwide, were attributable to outdoor or household air pollution. As many as half of these were due to cardiovascular disease. Air pollution also increases the risk of heart attack, stroke, diabetes and respiratory diseases.
Particle radioactivity is a characteristic of particulate matter that reflects radon, which primarily comes from radon gas, a radioactive, colorless and odorless gas. The particle radioactivity occurs naturally as a product of radioactive decay of uranium found in soil and rocks. Radon migrates into the atmosphere, decaying to alpha-, beta- and gamma-radiation-emitting isotopes.
“We know that PM2.5 are very small particles in the air that can be inhaled and cause many health problems. However, little is known about which physical, chemical or biological properties of PM2.5 fuel its toxicity,” said study author Shuxin Dong, S.M., a Ph.D. student in population health sciences at Harvard T.H. Chan School of Public Health in Boston. “We studied gross beta-activity, a property of fine particulate matter that is a result of radon that attaches to particles and makes them radioactive, resulting in particle radioactivity. When inhaled, these very small particles penetrate deeply into the lungs and enter the bloodstream and circulate throughout the body.”
The researchers used spatiotemporal predictions of gross beta-activity, a way to use different variables across space and time, to provide refined predictions of exposure. Examining health records from more than 700,000 non-accidental deaths in Massachusetts between 2001 and 2015, they estimated how long-term (months/year) gross beta-activity exposure impacts death from cardiovascular disease, heart attack or stroke and death from all non-accidental causes. They also predicted PM2.5 on cardiovascular disease-related death and examined the interaction between PM2.5 and particle radioactivity.
The study found: Chronic particle radioactivity and PM2.5 exposure were similarly associated with increased risks of death from total cardiovascular disease, heart attack or stroke and all causes of non-accidental death. Based on the middle 50% of the data spread, particle radioactivity exposure alone was associated with a 16% increased risk of death from heart attack; an 11% increased risk of death from stroke; a 7% increased risk of death from all types of cardiovascular disease; and a 4% increased risk of death from all non-accidental causes. Based on the middle 50% of the data spread, PM2.5 exposure alone increased the risk of death from heart attack by 6%; death from stroke by 11%; death from all cardiovascular disease by 12%; and death from all non-accidental causes by 10%.”The risk of death from cardiovascular disease, heart attack or stroke and all causes due to PM2.5 was higher and, therefore, more toxic when gross beta-activity levels were higher,” Dong said. “These findings suggest that particle radioactivity increases the risk of death from cardiovascular disease and enhances the damage from particulate matter. This must be further investigated and may lead to targeted, cost-effective air quality regulations.”
A study limitation is that the research was based on information from one state, Massachusetts, and therefore, the results may not be generalizable to the rest of the U.S.
Co-authors are Petros Koutrakis, Ph.D.; Longxiang Li, Ph.D.; Brent A. Coull, Ph.D.; Joel Schwartz, Ph.D.; Anna Kosheleva, M.S.; and Antonella Zanobetti, Ph.D. Authors’ disclosures are listed in the manuscript.
The study was funded by the U.S. Environmental Protection Agency and the National Institutes of Health.
Story Source:
Materials provided by American Heart Association. Note: Content may be edited for style and length.

A UCLA chemist and colleagues are now a step closer to their goal of developing a handheld tool similar to an alcohol Breathalyzer that can detect THC on a person’s breath after they’ve smoked marijuana.
In a paper published in the journal Organic Letters, UCLA organic chemistry professor Neil Garg and researchers from the UCLA startup ElectraTect Inc. describe the process by which THC introduced, in a solution, into their laboratory-built device can be oxidized, creating an electric current whose strength indicates how much of the psychoactive compound is present.
With the recent legalization or decriminalization of marijuana in many states, including California, the availability of a Breathalyzer-like tool could help make roadways safer, the researchers said. Studies have shown that consumption of marijuana impairs certain driving skills and is associated with a significantly elevated risk of accidents.
In 2020, Garg and UCLA postdoctoral researcher Evan Darzi discovered that removing a hydrogen molecule from the larger THC molecule caused it to change colors in a detectable way. The process, known as oxidation, is similar to that used in alcohol breath analyzers, which convert ethanol into an organic chemical compound through the loss of hydrogen. In most modern alcohol breath analyzer devices, this oxidation leads to an electric current that shows the presence and concentration of ethanol in the breath.
Since their 2020 finding, the researchers have been working with their patent-pending oxidation technology to develop a THC breath analyzer that works similarly. ElectraTect has exclusively licensed the patent rights from UCLA.
How the new device works
In the new paper, Darzi, now the CEO of ElectraTect, Garg, and ElectraTect researchers detail how their new laboratory-scale THC-powered fuel cell sensor functions. When THC (known scientifically as Delta-9-tetrahydrocannabinol) comes into contact with a negatively charged electrode, or anode, on one side of the device’s H-shaped glass chamber, it oxidizes into a new compound called THCQ, sending electrons across the chamber to a positively charged electrode, or cathode, on the other side, generating a measurable electric current. The higher the concentration of THC molecules, the stronger the current.
The advance marks the first time THC has been used to power a fuel cell sensor. The researchers said they expect that the relatively simple, inexpensive technology, once perfected, can be scaled up for economical mass production, and they are currently working to refine the device to detect and measure THC in exhaled breath and to shrink it to a more compact size suitable for use in a handheld breath analyzer or ignition interlock device — a breath analyzer connected to a vehicle’s ignition that prevents it from starting if THC is detected.
Making marijuana testing easier — and fairer
Beyond the implications for improved roadway safety, the technology has the potential to make marijuana law-enforcement fairer, the researchers said. Generally, urine or blood tests are used to detect the presence of THC in drivers. Not only are such tests difficult to administer at the roadside, but because the compound can linger in the body for weeks after marijuana use without any residual cognitive effects, these tests aren’t always useful for identifying impaired drivers. This ambiguity can lead to fines, imprisonment or loss of employment, even if an individual is not high when tested.
Such issues, the researchers said, highlight the need for innovative forensic technologies that are easier to use and more accurate for detecting recent marijuana use. And while a commercial marijuana breath analyzer based on their technology would still be several years off, Darzi and Garg stressed that such a tool could ultimately have benefits beyond traffic safety and law enforcement. Their technological breakthrough, they said, could ultimately be used in any situation where fair marijuana testing is critical, including in the workplace, where employees might be operating machinery, or even at home, where individuals may one day be able to use it proactively — before they ever get behind the wheel.

Published1 day agoSharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesBy Philippa RoxbyHealth reporterEating meals within set hours of the day may be a good way for shift workers to feel better and stay healthier, researchers say.Their working patterns are known to play havoc with the body’s rhythms, raising the risk of disease.In a study, firefighters working 24-hour shifts reduced their “bad” cholesterol and blood pressure, by eating within a 10-hour window.And those with existing health conditions benefited the most.The researchers said parents who are kept up at night looking after a new baby, and health workers, could also benefit from time-restricted eating.”Many of us eat all the time, right up until we go to bed – but the body doesn’t need it,” says Prof Pam Taub, study co-author and professor of medicine at the University of California, San Diego School of Medicine.Instead, the body needs a rest period to allow cells to repair and rejuvenate so the body becomes more efficient, she explains.Image source, Getty ImagesThe researchers, writing in the journal Cell Metabolism, asked 150 firefighters from the San Diego Fire Rescue Department to track everything they ate for three months on an app.Half ate all their calories within a 10-hour window of 9am to 7pm, without skipping meals, while the other half didn’t change their normal routine and ate within a 14-hour window, on average.Both groups were encouraged to follow a Mediterranean diet – full of fresh vegetables, fruit, fish and olive oil – which is known to be healthy. Firefighters who were overweight or had health issues such as high blood pressure, high cholesterol or type 2 diabetes, were included in the study.The health of those following a time-restricted eating regime improved more than the health of those in the comparison group, the study found.Tests showed their blood pressure levels, blood sugar and cholesterol levels all improved by eating within a set timeframe and then fasting for the rest of their shift.Even healthy firefighters with no underlying health risks experienced a boost to their quality of life and a reduction in “bad” cholesterol, by eating that way.And the study found no decrease in energy levels or other negative side-effects.Disrupted sleep”We’ve shown that time-restricted eating is a feasible way for shift workers, such as firefighters, to improve their cardiovascular health and wellbeing,” said Prof Taub.Shift workers, who make up more than a quarter of working people in many countries, are at increased risk of heart disease, type 2 diabetes and cancer.This is because the body’s natural circadian rhythms are regularly disrupted by being awake at night and sleeping during the day.And yet shift workers are often left out of clinical trials and little is understood about how to improve their health, Prof Taub says.Dr Linia Patel, a registered dietitian and spokesperson for the British Dietetic Association, said anyone could try time-restricted eating and see if it worked for them. “But one size doesn’t fit all – shift working is very hard and finding out the best time to fast is key,” she said.There were some limitations to the research – the study was made up mostly of men and only one particular shift pattern was analysed. But the research team says time-restricted eating should be tested in other groups of shift workers.”These findings can likely be extended to a wider population, including health care workers like nurses and others who experience abnormal sleep-wake patterns,” Prof Taub said.

Published1 day agoSharecloseShare pageCopy linkAbout sharingThis video can not be playedTo play this video you need to enable JavaScript in your browser.An expert has called for “immediate research” after a study suggested that elite rugby union players could be at increased risk of brain conditions like motor neurone disease.The study examined a link between sport and neurodegenerative diseases such as Parkinson’s, MND and dementia.The MND Association said the study raised “more questions than answers”.Scientists said the study should encourage “dramatic changes” in rugby to reduce the risks of brain injury.Rugby authorities have been told they should look to minimise contact training and reduce the global calendar. The research team was led by consultant neuropathologist Professor Willie Stewart, honorary professor at the University of Glasgow.More stories on Scottish sportThe Sports Desk – Rugby’s concussion crisis – BBC SoundsIt looked at former Scotland rugby international players from both the amateur and the professional period.The research team compared health outcomes among 412 former Scotland international male rugby players with more than 1,200 individuals from the general population. The results showed that the rugby players, all of whom were born before 1991, were more likely to die at a slightly older age than peers of similar age and socioeconomic status. Urgent action neededWhile they had a higher risk of death overall from neurodegenerative disease, they were less likely to die of respiratory disease. Their chances of being diagnosed with a neurodegenerative disease were 2.67 times higher.By far the biggest risk was for MND, with rugby players 15.17 times more likely to be diagnosed than people of the same age range in the general population.The overall number of MND cases in the study is not known, although it is understood to be small. Former internationalists were also three times more likely to develop Parkinson’s and two times more likely to develop dementia.The debate on brain health and contact sports such as rugby and football is gathering momentum. There are no definitive answers but a series of research studies, including this latest one from the University of Glasgow, add weight to the suspicion that elite players are more at risk than those in the wider population. Care has to be taken about drawing firm conclusions especially if the numbers of players surveyed is relatively small. But the research team, led by Professor Willie Stewart, having previously carried out a landmark study of the dementia risk among former professional footballers, has now further underlined the need for further research on the impact of concussion and other head injuries on the longer-term health of rugby players.The results have been published as part of the FIELD study, which was funded by the Football Association and the Professional Footballers Association.Prof Stewart – who led previous research that found former footballer professionals are three-and-a-half times more likely to die of dementia than the general population – called for further investigation.”Of particular concern are the data on motor neurone disease risk among our rugby players, which is even higher than that for former professional footballers,” he said. “This finding requires immediate research attention to explore the specific association between rugby and the devastating condition of motor neurone disease.” Image source, Getty ImagesAt at briefing ahead of the study’s publication, the academic said urgent action was needed by rugby authorities.He welcomed moves to reduce high-impact training between matches, but said the pace of change was “slow”. “This should be a stimulus to them to really pick up their heels and start making pretty dramatic changes as quickly as possible to try and reduce risk,” Prof Stewart said.”Instead of talking about extending seasons and introducing new competitions and global seasons, they should be talking about restricting it as much as possible. “So cutting back on the amount of rugby we’re seeing, getting rid of as much training as possible. Things like that have to be addressed pretty, pretty rapidly.”‘Truly remarkable’ drug helps motor neurone diseasePlayers suing governing bodies over brain damageRugby season should be cut in half – PophamNew dementia study to reduce footballers’ riskThe study, published in the Journal of Neurology, Neurosurgery and Psychiatry, showed about three out of four of the rugby players with dementia had chronic traumatic encephalopathy, a specific pathology linked to brain injury exposure.It also found that unlike in football, there was no sign of increased risk depending on position on the field. Dr Brian Dickie, director of research development at the Motor Neurone Disease Association, said the new study added weight to previous reports from the FIELD team on increased risk of neurodegeneration in football players, although the new study was considerably smaller. However, he said it raised “more questions than answers”.Image source, Getty Images”For example, it is not clear exactly how many players were diagnosed with MND, though from the information provided, that absolute number will be small,” he said.”It is also surprising that there were no cases reported in the larger control group, as MND is the most common neurodegenerative disease of mid-life and the study population appears to include people in the ‘high risk’ age range of 50-80 years. “Moreover, we know that the vast majority of cases of MND involve a complex mix of genetic and environmental risk factors, so the level of genetic risk may be different in high-performance athletes compared with the general population.”Dr Jane Haley, director of research at MND Scotland, said: “We welcome this very interesting piece of research. While the initial results do seem concerning, the study is based on a small sample size which means that, because MND is a relatively uncommon condition, larger studies will be needed to determine whether this result can be confirmed more widely. “A connection between elite level sports and MND has been proposed before, but this is the first time an increased risk has been indicated for rugby players. The reasons for these apparent increases are not yet known and need to be explored further.” Dr James Robson, chief medical officer for the Scottish Rugby Union, said: “Work continues in Scotland, on and off the field, to address player safety, taking the issues involved seriously.”He added: “Rugby continues to have many health and social benefits. Important research like this can help us continue to improve safety and mitigate risks associated with contact sport.” More on this story’Truly remarkable’ drug helps motor neurone disease21 SeptemberRugby season should be cut in half – Popham25 JulyPlayers suing governing bodies over brain damage25 JulyNew dementia study to reduce footballers’ risk26 AprilCharity says housing system fails people with MND7 MarchAround the BBCThe Sports Desk – Rugby’s concussion crisis

A new study led by UC Davis Comprehensive Cancer Center researchers shows that current smokers have a 12% increased risk of a laboratory-confirmed viral infection and a 48% increased risk of being diagnosed with respiratory illnesses. These results did not vary by type of virus, including a coronavirus.
In combination with past findings, the current findings published today in the Nicotine and Tobacco Research journal support urgent recommendations to increase tobacco control efforts for countering COVID-19.
“Past research has shown that smoking increases the risk of COVID-19 disease severity, but the risk of infection had been less clear,” said UC Davis tobacco researcher and lead author of the study Melanie Dove. “Our study findings show smokers have an increased risk of viral infection, including a coronavirus and respiratory illness.”
Study results
The researchersre-analyzed data from the British Cold Study (BCS), a 1986-1989 challenge study that exposed 399 healthy adults to 1 of 5 “common cold” viruses. This included a type of common coronavirus (coronavirus 229E) that existed prior to the novel coronavirus (SARS-CoV-2 virus), which causes COVID-19 disease. Data from the British Cold Study is available on the Carnegie Mellon University The Common Cold Project website
The UC Davis researchers calculated overall and coronavirus-specific unadjusted and adjusted relative risks for current smokers and each outcome (infection and illness), testing whether each association was modified by type of respiratory virus.