Publisher Health

Most children with a condition that causes a temporary weakness or paralysis of the muscles in the face recover without medication within six months, according to a new study.
The research, led by the Murdoch Children’s Research Institute and published in Neurology, found the steroid prednisolone does not significantly impact on a child’s recovery from Bell’s palsy.
Murdoch Children’s Professor Franz Babl said while studies had shown steroid use in adults with Bell’s palsy helped improve symptoms by minimising facial nerve swelling and damage within the temporal bone, similar research hadn’t been available for children.
The randomised-controlled trial involved 187 participants, aged six months to 17 years, who presented to emergency departments (EDs) with Bell’s palsy. The study was staged in 11 ED’s in the Paediatric Research in Emergency Departments International Collaborative (PREDICT) research network in Australia and New Zealand. They were recruited within 72 hours after symptom onset and received 10 days of treatment with prednisolone or a placebo (no active drug).
The study found 57 per cent of those who didn’t take any medication recovered facial function at one month, 85 per cent at three months and 93 per cent at six months. For those assigned prednisolone, 49 per cent recovered at one month, 90 per cent at three months and 99 per cent at six months. There were no serious side effects recorded during the trial and the most common adverse reactions were temporary changes in behaviour and increased appetite.
Bell’s palsy, which causes half of the face to droop, is the third most common condition causing a sudden change in nerve function in children. In most cases the exact cause of the facial weakness is unknown but may be related to a viral infection.
“The lack of evidence on the use of steroids in children with Bell’s palsy in children has led to variable practice in their treatment,” Professor Babl said. Discovering that early treatment with prednisolone doesn’t hasten recovery will help GPs, emergency physicians and paediatricians in their discussion with affected families and make better informed decisions.”
Story Source:
Materials provided by Murdoch Childrens Research Institute. Note: Content may be edited for style and length.

A team of engineers and doctors at the University of Minnesota Twin Cities have designed a unique 3D-printed light-sensing medical device that is placed directly on the skin and gives real-time feedback to correlate light exposure with disease flare-ups. The device could help millions of people worldwide with lupus and other light-sensitive diseases by providing access to more personalized treatments and information to determine what causes their symptoms.
The research was published in Advanced Science, an interdisciplinary premium open access scientific journal. The researchers have also filed a patent on the device and the technology is available for licensing.
According to the Lupus Foundation of America about 1.5 million Americans, and at least 5 million people worldwide, have a form of lupus. Light sensitivity is common in people with lupus with 40 to 70 percent of people with lupus finding that their disease is made worse by exposure to sunlight or even artificial light indoors. The symptoms of these flare ups for patients with lupus include rashes, joint pain, and fatigue.
“I treat a lot of patients with lupus or related diseases, and clinically, it is challenging to predict when patients’ symptoms are going to flare,” said University of Minnesota Medical School dermatologist Dr. David Pearson and co-author of the study. “We know that ultraviolet light and, in some cases visible light, can cause flares of symptoms — both on their skin, as well as internally — but we don’t always know what combinations of light wavelengths are contributing to the symptoms.”
Pearson had heard about the groundbreaking, customized 3D-printing of wearable devices developed by University of Minnesota mechanical engineering Professor Michael McAlpine and his team and contacted him to collaborate on finding a solution for his problem.
McAlpine’s research group worked with Pearson to develop a first-of-its-kind fully 3D-printed device with a flexible UV-visible light detector that could be placed on the skin. The device is integrated with a custom-built portable console to continuously monitor and correlate light exposure to symptoms.

Scientists have identified a protein known as sulfatase-2 that plays a critical role in the damage caused by rheumatoid arthritis. A chronic disease in which the immune system attacks the body’s own joint tissues, rheumatoid arthritis affects an estimated 1.5 million Americans.
Published in the journal Cellular & Molecular Immunology, the discovery sheds new light on the molecular processes that drive inflammation seen in rheumatoid arthritis. It could also someday lead to improved treatment of the disease, which currently has no cure.
“Tumor necrosis factor-alpha — or TNF-alpha for short — is one of the main inflammatory proteins that drive rheumatoid arthritis and is targeted by many currently available therapies,” said senior author Salah-Uddin Ahmed, a professor in Washington State University’s College of Pharmacy and Pharmaceutical Sciences. “However, over time patients can develop a resistance to these drugs, meaning they no longer work for them. That is why we were looking for previously undiscovered drug targets in TNF-alpha signaling, so basically proteins that it interacts with that may play a role.”
Though sulfatases such as sulfatase-2 have been extensively studied for their roles in different types of cancer, Ahmed said no one had looked at how they might be involved in inflammatory or autoimmune diseases such as rheumatoid arthritis.
The research team first explored this idea using cells called synovial fibroblasts, which line the joints and keep them lubricated to ensure fluid movement.
“In rheumatoid arthritis, these normally quiescent cells get activated by TNF-alpha and other inflammatory molecules, and they take on this aggressive character,” said first author Ruby J. Siegel, a PhD graduate in the WSU College of Pharmacy and Pharmaceutical Sciences. “They are not dying when they should, and they proliferate in a way that is almost tumor-like, forming this massive synovial tissue that should not be anywhere near that size and at the same time activating proteins that destroy cartilage and bone.”
Using the joint-lining cells of rheumatoid arthritis patients, they removed sulfatase-2 from one group of cells before stimulating all cells with the inflammatory TNF-alpha. What they found was that cells lacking sulfatase-2 did not show the same exaggerated inflammatory response to TNF-alpha as cells that were left intact.
“Looking at sulfatases for their potential role in inflammation was an educated guess, but once we did we saw a very consistent pattern of increased sulfatase-2 expression throughout different tissues and samples we studied,” Ahmed said. “This tells us that TNF-alpha relies on sulfatase-2 to drive inflammation, because as soon as we removed sulfatase-2 the inflammatory effects of TNF-alpha were markedly reduced.”
Resulting from a series of experiments spanning four years, the researchers’ findings open the door to future animal studies to test the effectiveness of inhibiting sulfatase-2 to ease rheumatoid arthritis symptoms. This could someday lead to the development of new combination therapies that along with other inflammatory proteins would also target sulfatase-2 to prevent bone loss, cartilage damage and deformed joints. Such therapies could help address the shortcomings of currently available rheumatoid arthritis drugs, many of which come with significant side effects.
“These drugs shut off TNF-alpha in your whole body, but it does have important immune functions,” Siegel said, adding that patients who take these types of drugs are more susceptible to infection and have an increased risk of developing cancer with long-term use. She also noted that TNF-alpha inhibitors are not effective in all people and are not recommended for patients with certain other health conditions.
Funding support for the study came from the National Institutes of Health and the Rheumatology Research Foundation.
Story Source:
Materials provided by Washington State University. Original written by Judith Van Dongen. Note: Content may be edited for style and length.

Children of women with gestational diabetes and obesity may be twice as likely to develop attention-deficit/hyperactivity disorder (ADHD) compared to those whose mothers did not have obesity, according to new research published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.
The estimated number of children aged 3-17 years ever diagnosed with ADHD is 6 million, according to data from 2016-2019. A major risk factor for ADHD in children is maternal obesity. Roughly 30% of women have obesity at their first doctor’s visit during pregnancy, and this number increases to 47% in women with gestational diabetes. Excessive weight gain during pregnancy in this population is a risk factor for children developing ADHD.
“Our study found pregnant women with obesity and gestational diabetes had children with long-term mental health disorders such as ADHD,” said Verónica Perea, M.D., Ph.D., of the Hospital Universitari MutuaTerrassa in Barcelona, Spain. “We did not find this association when these women gained a healthy amount of weight during pregnancy.”
The researchers studied 1,036 children born to women with gestational diabetes. Thirteen percent of these children were diagnosed with ADHD. The researchers found children of women with gestational diabetes and obesity were twice as likely to have ADHD compared to those born to mothers without obesity.
The researchers only found this association in women with gestational diabetes, obesity and excessive weight gain during pregnancy. The researchers did not observe a higher risk of ADHD in children of women with gestational diabetes and obesity if the amount of weight these women gained during pregnancy was within the normal range.
“It’s important for clinicians to counsel their patients on the importance of healthy weight gain during pregnancy,” Perea said.
Other authors of this study include Andreu Simó-Servat, Carmen Quirós, Nuria Alonso-Carril, Maite Valverde, Maria-José Barahona, Xavier Urquizu, Eva López and Maria-José Barahona of the Hospital Universitari Mútua de Terrassa; and Antonio J. Amor of the Hospital Clínic de Barcelona in Barcelona, Spain.
The study received funding from the Fundació Docència i Recerca Mútua Terrassa.
Story Source:
Materials provided by The Endocrine Society. Note: Content may be edited for style and length.

Monkeypox, a virus that causes painful rashes and flu-like symptoms, is spreading rapidly throughout many parts of the world, including the U.S. To get a fast understanding of how the virus is moving through communities, researchers reporting in ACS’ Environmental Science & Technology Letters suggest turning to wastewater epidemiology. They show how the method — widely applied to monitor SARS-CoV-2 transmission — could be optimized for monkeypox, potentially detecting as few as seven infections per 100,000 people.
Like SARS-CoV-2, the monkeypox virus can shed from infected people through their feces, urine and saliva. Recently, researchers have detected its DNA in wastewater using polymerase chain reaction (PCR) assays. However, monitoring current monkeypox outbreaks in the U.S. with wastewater-based epidemiology has been limited, despite its success in tracking community-level SARS-CoV-2 prevalence. So, Kyle Bibby and William Chen wanted to evaluate the feasibility of this technique for detecting monkeypox viral DNA in different wastewater scenarios.
The researchers collected information from previous scientific studies about the shedding of monkeypox viral DNA from saliva, stool and urine into wastewater streams. They analyzed that data in combination with people’s daily water usage, concluding that infected people can shed from 13,000 to 208 billion genome copies daily into sewers, with most of that amount coming from stool. These results indicated that a single PCR assay conducted at the lowest level of sensitivity, or 10 genome copies per liter of wastewater, could theoretically detect seven cases out of 100,000 people at the average U.S. wastewater treatment plant. In addition, replicate assays could likely identify even lower infection rates.
Next, the team developed a computer-based strategy to determine the number of PCR assays that would need to be run for wastewater samples collected in the U.S. and other countries, depending on the expected case rates of monkeypox and the desired level of sensitivity. For the U.S., at the average case rate as of July 15, 2022, each sample would need eight replicate assays using a moderately high level of sensitivity to correctly detect monkeypox in the sewage, whereas at a suspected maximum case rate (0.0012%) only four replicates at a lower level of sensitivity would be needed. Since mid-July, case rates have likely increased, so the researchers predict that a lower number of replicates could be implemented now in the U.S. Although there is a lack of information about monkeypox DNA shedding from humans and its persistence wastewater, the researchers say that their computer model can still be a useful framework for developing robust community monitoring programs.
The authors acknowledge funding from a University of Notre Dame Dean’s Fellowship.
Story Source:
Materials provided by American Chemical Society. Note: Content may be edited for style and length.

Published10 hours agoSharecloseShare pageCopy linkAbout sharingImage source, Katie EwerA malaria vaccine with “world-changing” potential has been developed by scientists at the University of Oxford. The team expect it to be rolled out next year after trials showed up to 80% protection against the deadly disease.Crucially, say the scientists, their vaccine is cheap and they already have a deal to manufacture more than 100 million doses a year. The charity Malaria No More said recent progress meant children dying from malaria could end “in our lifetimes”.It has taken more than a century to develop effective vaccines as the malaria parasite, which is spread by mosquitoes, is spectacularly complex and elusive. It is a constantly moving target, shifting forms inside the body, which make it hard to immunise against.Last year, the World Health Organization gave the historic go-ahead for the first vaccine – developed by pharmaceutical giant GSK – to be used in Africa. However, the Oxford team claim their approach is more effective and can be manufactured on a far greater scale. Trial results from 409 children in Nanoro, Burkina Faso, have been published in the Lancet Infectious Diseases. It shows three initial doses followed by a booster a year later gives up to 80% protection. Image source, Katie Ewer”We think these data are the best data yet in the field with any malaria vaccine,” said Prof Adrian Hill, director of the Jenner Institute at the university.The team will start the process of getting their vaccine approved in the next few weeks, but a final decision will hinge on the results of a larger trial of 4,800 children due before the end of the year.The world’s largest vaccine manufacturer – the Serum Institute of India – is already lined up to make more than 100 million doses a year. Prof Hill said the vaccine – called R21 – could be made for “a few dollars” and “we really could be looking at a very substantial reduction in that horrendous burden of malaria”.He added: “We hope that this will be deployed and available and saving lives, certainly by the end of next year.” Malaria has been one of the biggest scourges on humanity for millennia and mostly kills babies and infants. The disease still kills more than 400,000 people a year even after dramatic progress with bed nets, insecticides and drugs.This malaria vaccine is the 14th that Prof Katie Ewer has worked on at Oxford as “this is not like Covid where we have seven vaccines straight away that will work… it’s much, much harder”.She told the BBC it was “incredibly gratifying” to get this far and “the potential achievement that this vaccine could have if it’s rolled out could be really world-changing”. Why so effective?The currently approved vaccine – made by GSK – shares similarities with the one developed in Oxford. Both target the first stage of the parasite’s lifecycle by intercepting it before it gets to the liver and establishes a foothold in the body.The vaccines are built using a combination of proteins from the malaria parasite and the hepatitis B virus, but Oxford’s version has a higher proportion of malaria proteins. The team think this helps the immune system to focus on malaria rather than the hepatitis. The success of the GSK vaccine has partly paved the way for Oxford to be optimistic of having their vaccine out next year – such as by assessing how feasible a vaccination programme in Africa would be.It is hard to give a direct comparison of the two vaccines. GSK’s has gone through large real world trials whereas Oxford’s data may appear more effective due to being given just ahead of the peak malaria season in Burkina Faso. Prof Azra Ghani, chair in infectious disease epidemiology at Imperial College London, said the trial results were “very welcome”, but warned it would take money to get vaccines in arms. “Without this investment, we risk losing the gains that have been made over the last decades and witnessing a rising tide of malaria resurgence,” Prof Ghani said. Gareth Jenkins, from the charity Malaria No More UK said: “Today’s R21 vaccine results from Oxford’s renowned Jenner Institute are another encouraging signal that, with the right support, the world could end child deaths from malaria in our lifetimes.”Follow James on Twitter.More on this storyHistoric go-ahead for malaria vaccine in Africa6 October 2021

The findings represent the first time a highly pathogenic form of the virus, which has devastated bird populations this year, has been detected in cetaceans.A bottlenose dolphin found dead in a Florida canal this past spring tested positive for a highly virulent strain of bird flu, scientists said on Wednesday. The announcement came a week after Swedish officials reported that they had found the same type of avian influenza in a stranded porpoise.This version of the virus, which has spread widely among North American and European birds, has affected an unusually broad array of species. But these findings represent the first two documented cases in cetaceans, a group of marine mammals that includes dolphins, porpoises and whales.It is too soon to say how commonly the virus infects cetaceans, but its discovery in two different species on two different continents suggests that there have “almost certainly” been other cases, said Richard Webby, an influenza virologist at St. Jude Children’s Research Hospital in Memphis.“Our surveillance activities on a global scale are never sensitive enough to pick up the only two events of this kind,” said Dr. Webby, who was not involved in the initial detection of the virus but is now working with the Florida team on follow-up studies.The virus has become so widespread in birds that it would not be surprising to see the pathogen pop up in other unexpected species, he added. “Unfortunately, I think this is maybe just sort of a sign of what’s to come should this virus not disappear,” he added.Experts emphasize that the risk to humans remains low. In the United States, the version of the virus that is circulating has caused just one documented human infection, in a person known to have had contact with poultry, according to the Centers for Disease Control and Prevention.But the spread of the virus to new species poses potential risks to wildlife and provides the virus with new chances to mutate and adapt to mammalian hosts.This strain of bird flu, known as Eurasian H5N1, has spread rapidly through domestic poultry, affecting tens of millions of farmed birds, according to the Agriculture Department. Compared to previous versions of the virus, this lineage has taken an especially heavy toll on wild bird populations, felling eagles, owls, pelicans and more.That, in turn, has put mammals that encounter wild birds at risk. As the outbreaks expanded this spring, the virus turned up in foxes, bobcats, skunks and other species. The virus has also been blamed for a spike in seal strandings in Maine, where bird flu has been detected in both gray and harbor seals.The Florida dolphin, a young male, was found in March in a canal in Dixie County, where area residents noticed that the animal had become trapped between the pilings of a pier and a sea wall, said Dr. Michael Walsh, a veterinarian at the University of Florida College of Veterinary Medicine who leads the university’s marine animal rescue program.By the time rescuers arrived, the dolphin had died, he said. The team, which routinely conducts necropsies, collected a variety of samples from the dolphin and stored them until they could be analyzed in more detail.At the time, the scientists had no reason to suspect that bird flu had made its way into dolphins, and they were not in a particular rush, said Dr. Walsh, who collaborated on the investigation with Dr. Robert Ossiboff, a veterinary pathologist, and Andrew Allison, a veterinary virologist, both at the University of Florida College of Veterinary Medicine.When the results came back this summer, they revealed signs of inflammation in the dolphin’s brain and the surrounding tissues, Dr. Walsh said. Scientists have previously documented brain inflammation in fox kits infected with the virus, which can cause neurological symptoms in birds and mammals.Subsequent laboratory testing turned up Eurasian H5N1 in the dolphin’s brain and lungs. “The brain tissue really showed a high level of virus,” Dr. Walsh said.Whether the virus contributed to the dolphin’s death remains unknown, as does precisely how the animal contracted it. But it is not hard to imagine a young dolphin investigating an ailing bird near the shoreline, Dr. Walsh said, adding: “These animals are always curious about their environment and checking things out. So if he came upon a sick, either dying or dead, bird, he might be very curious about it. He might mouth it.”The virus was also responsible for the death of a porpoise found stranded in Sweden in June, the Swedish National Veterinary Institute said last week. The pathogen was found in several of the animal’s organs, including the brain, according to the agency.So far, there is no evidence that cetaceans are spreading the virus to one another, Dr. Webby said. And Dr. Webby’s team, which has isolated and sequenced the virus detected in the Florida dolphin, has not found any signs that it has picked up mutations associated with adaptation to mammals. “It still very much looks like a virus that you would pick up out of a bird,” he said.But now that dolphins and porpoises are known to be susceptible, researchers can begin to look for the virus more proactively, including in any tissue samples they previously collected.“Now, everybody’s going to be on guard for this,” Dr. Walsh said. “And that’ll help tell us how serious this really is for cetaceans on the coastlines.”

A scientific breakthrough by Tel Aviv University: A team of researchers from the university has demonstrated that antibodies isolated from the immune system of recovered COVID-19 patients are effective in neutralizing all known strains of the virus, including the Delta and the Omicron variants. According to the researchers, this discovery may eliminate the need for repeated booster vaccinations and strengthen the immune system of populations at risk.
The research was led by Dr. Natalia Freund and doctoral students Michael Mor and Ruofan Lee of the Department of Clinical Microbiology and Immunology at the Sackler Faculty of Medicine. The study was conducted in collaboration with Dr. Ben Croker of the University of California San Diego. Prof. Ye Xiang of Tsinghua University in Beijing. Prof. Meital Gal-Tanamy and Dr. Moshe Dessau of Bar-Ilan University also took part in the study. The study was published in the Nature journal Communications Biology.
The present study is a continuation of a preliminary study conducted in October 2020, at the height of the COVID-19 crisis. At that time, Dr. Freund and her colleagues sequenced all the B immune system cells from the blood of people who had recovered from the original COVID strain in Israel, and isolated nine antibodies that the patients produced. The researchers now found that some of these antibodies are very effective in neutralizing the new coronavirus variants, Delta and Omicron.
Dr. Freund: “In the previous study, we showed that the various antibodies that are formed in response to infection with the original virus are directed against different sites of the virus. The most effective antibodies were those that bound to the virus’s ‘spike’ protein, in the same place where the spike binds the cellular receptor ACE2. Of course, we were not the only ones to isolate these antibodies, and the global health system made extensive use of them until the arrival of the different variants of the coronavirus, which in fact rendered most of those antibodies useless.
“In the current study, we proved that two other antibodies, TAU-1109 and TAU-2310, which bind the viral spike protein in a different area from the region where most of the antibodies were concentrated until now (and were therefore less effective in neutralizing the original strain) are actually very effective in neutralizing the Delta and Omicron variants. According to our findings, the effectiveness of the first antibody, TAU-1109, in neutralizing the Omicron strain is 92%, and in neutralizing the Delta strain, 90%. The second antibody, TAU-2310, neutralizes the Omicron variant with an efficacy of 84%, and the Delta variant with an efficacy of 97%.”
According to Dr. Freund, the surprising effectiveness of these antibodies might be related to the evolution of the virus: “The infectivity of the virus increased with each variant because each time, it changed the amino acid sequence of the part of the spike protein that binds to the ACE2 receptor, thereby increasing its infectivity and at the same time evading the natural antibodies that were created following vaccinations. In contrast, the antibodies TAU-1109 and TAU-2310 don’t bind to the ACE2 receptor binding site, but to another region of the spike protein — an area of the viral spike that for some reason does not undergo many mutations — and they are therefore effective in neutralizing more viral variants. These findings emerged as we tested all the known COVID strains to date.”
The two antibodies, cloned in Dr. Freund’s laboratory at Tel Aviv University, were sent for tests to check their effectiveness against live viruses in laboratory cultures at the University of California San Diego, and against pseudoviruses in the laboratories of the Faculty of Medicine of Bar-Ilan University in the Galilee; the results were identical and equally encouraging in both tests.
Dr. Freund believes that the antibodies can bring about a real revolution in the fight against COVID-19: “We need to look at the COVID-19 pandemic in the context of previous disease outbreaks that humankind has witnessed. People who were vaccinated against smallpox at birth and who today are 50 years old still have antibodies, so they are probably protected, at least partially, from the monkeypox virus that we have recently been hearing about. Unfortunately, this is not the case with the coronavirus. For reasons we still don’t yet fully understand, the level of antibodies against COVID-19 declines significantly after three months, which is why we see people getting infected again and again, even after being vaccinated three times. In our view, targeted treatment with antibodies and their delivery to the body in high concentrations can serve as an effective substitute for repeated boosters, especially for at-risk populations and those with weakened immune systems. COVID-19 infection can cause serious illness, and we know that providing antibodies in the first days following infection can stop the spread of the virus. It is therefore possible that by using effective antibody treatment, we will not have to provide booster doses to the entire population every time there is a new variant.”
Story Source:
Materials provided by Tel-Aviv University. Note: Content may be edited for style and length.

A newly developed agonistic antibody reduced the amyloid pathology in mice with Alzheimer’s disease, signaling its promise as a potential treatment for the disease, according to a team of researchers at UTHealth Houston.
Research led by senior author Zhiqiang An, PhD, professor and Robert A. Welch Distinguished University Chair in Chemistry at McGovern Medical School at UTHealth Houston, found that a tetra-variable domain antibody targeting thetriggering receptor expressed on myeloid 2 (TREM2) — dubbed TREM2 TVD-lg — reduced amyloid burden, eased neuron damage, and alleviated cognitive decline in mice with Alzheimer’s disease. The study was published today in Science Translational Medicine.
“Antibody-based therapy is a viable drug modality for the treatment of Alzheimer’s disease,” said An, director of the Texas Therapeutics Institute with The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases (IMM). “One of the major areas of focus at the Texas Therapeutics Institute is developing technologies to deliver antibody-based therapies across the blood-brain barrier for potential treatment of the disease.”
TREM2 is a single-pass receptor expressed by microglia — supportive cells that function as scavengers in the central nervous system. Microglia play a crucial role in the removal of amyloids that cluster around amyloid-beta plaques, a hallmark of Alzheimer’s disease.
While previous research has shown that TREM2 plays an important role in the pathophysiology of Alzheimer’s disease, the recent findings suggest that increasing TREM2 activation could have therapeutic effects such as improved cognition.
“By leveraging the unique antibody drug discovery capabilities at UTHealth Houston and collaborating with scientists with complementary expertise, we demonstrated the feasibility of engineering multivalent TREM2 agonistic antibodies coupled with TfR-mediated brain delivery to enhance microglia functions and reduce amyloid pathology in vitro and in vivo,” said co-senior author Ningyan Zhang, PhD, professor at the Texas Therapeutics Institute at IMM at McGovern Medical School. “This antibody engineering approach enables the development of effective TREM2-targeting therapies for AD.”
Additional authors from UTHealth Houston’s IMM include Peng Zhao, PhD, postdoctoral research fellow; Yuanzhong Xu, PhD, assistant professor; Xuejun Fan, MD, PhD, research scientist; Leike Li, PhD, postdoctoral research fellow; Xin Li, research associate; and Qingchun Tong, PhD, professor and Cullen Chair in Molecular Medicine. Wei Cao, PhD, the Roy M. and Phyllis Gough Huffington Distinguished Professor of anesthesiology with McGovern Medical School, also contributed to the study. An, Tong, and Cao are also faculty members at The University of Texas MD Anderson Cancer Center UTHealth Houston Graduate School of Biomedical Sciences.
Other co-authors include LuLin Jiang, PhD, with Sanford Burnham Prebys Medical Discovery Institute in California; Hisashi Arase, MD, with Osaka University in Japan; Hui Zheng, PhD, with Baylor College of Medicine in Houston; Yingjun Zhao, PhD, with Xiamen University in China; and Huaxi Xu, PhD, with Xiamen University and Chongqing Medical University in China.
The work was in part supported by grants from the Cancer Prevention and Research Institute of Texas (RP150551 and RP190561) and Welch Foundation.

You know drinking alcohol isn’t the best thing for your health, but just how bad is it? After all, in the United States, two thirds of adults report some degree of alcohol use.
When we do picture health harms from drinking, we’re more likely to think of car crashes than cancer. This is largely because the alcohol industry has suppressed efforts to educate consumers about drinking-related health risks while championing the idea that alcohol can be beneficial to health, say two researchers with ties to the University of North Carolina at Chapel Hill.
In a New England Journal of Medicine perspective piece, co-authors Anna H. Grummon, PhD, and Marissa G. Hall, PhD, propose updating alcohol container warning labels as a strategy to help consumers make more informed decisions about how much they imbibe.
In April 2022, the U.S. Centers for Disease Control and Prevention published statistics showing that alcohol consumption is responsible for more than 140,000 deaths per year — that’s over 380 deaths every day. COVID-19 has exacerbated the situation, with alcohol-related deaths increasing by 25% during just the first year of the pandemic.
Still, a recent national survey found that almost 70% of U.S. adults have no idea that even light or moderate alcohol consumption can increase their risk of cancer.
“Many people are unaware of the full range of risks from alcohol consumption,” said Grummon, the study’s lead author and a Gillings alum — now a research scientist in the Department of Nutrition at Harvard University’s T.H. Chan School of Public Health. “For example, there is now scientific consensus that alcohol increases the risk of several types of cancer, including head and neck cancer, breast cancer and colorectal cancer. But two-thirds of Americans are not aware of these risks.”
One strategy for addressing these knowledge gaps could be to update the required warning labels on alcohol containers. Such warnings are a low-cost, sustainable public health strategy for informing consumers and encouraging healthier behaviors.
For example, more than 150 countries require warning labels on cigarette packages, and the policy has contributed to remarkable decreases in smoking rates over the past several decades.
Based on previous research findings, the most effective warnings labels are shown prominently on the front of product packaging, include visual elements like photos or illustrations, and come in a variety of rotating designs so they avoid becoming “stale” to consumers.
The alcohol warning currently used in the U.S. has none of these elements and was written when there was far less evidence about the harms associated with alcohol consumption.
“The current U.S. warning label hasn’t been updated in more than 30 years and largely goes unnoticed,” said Hall, the study’s senior author and an assistant professor in the Gillings School’s Department of Health Behavior. (She is also a member of the Lineberger Comprehensive Cancer Center and a faculty fellow at the Carolina Population Center.) “Also, the warning says that alcohol ‘may cause health problems,’ a phrase so vague that it borders on being misleading. Given the mounting evidence about the harms caused by alcohol, the government has a duty to inform its citizens about these risks.”
The warning label strategy has strong precedent: Remember those two thirds of American adults — most of us! — who were unaware alcohol has ties with cancer? Research also has found that two thirds of Americans also support requiring new, more specific health-related warning labels for alcohol products.