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Researchers from the Max Planck Institute for Human Development, the Institute for Cognitive Sciences and Technologies (ISTC), and the Norwegian University of Science and Technology developed a collective intelligence approach to increase the accuracy of medical diagnoses. Their work was recently presented in the journal PNAS.
An estimated 250,000 people die from preventable medical errors in the U.S. each year. Many of these errors originate during the diagnostic process. A powerful way to increase diagnostic accuracy is to combine the diagnoses of multiple diagnosticians into a collective solution. However, there has been a dearth of methods for aggregating independent diagnoses in general medical diagnostics. Researchers from the Max Planck Institute for Human Development, the Institute for Cognitive Sciences and Technologies (ISTC), and the Norwegian University of Science and Technology have therefore introduced a fully automated solution using knowledge engineering methods.
The researchers tested their solution on 1,333 medical cases provided by The Human Diagnosis Project (Human Dx), each of which was independently diagnosed by 10 diagnosticians. The collective solution substantially increased diagnostic accuracy: Single diagnosticians achieved 46% accuracy, whereas pooling the decisions of 10 diagnosticians increased accuracy to 76%. Improvements occurred across medical specialties, chief complaints, and diagnosticians’ tenure levels. “Our results show the life-saving potential of tapping into the collective intelligence,” says first author Ralf Kurvers. He is a senior research scientist at the Center for Adaptive Rationality of the Max Planck Institute for Human Development and his research focuses on social and collective decision making in humans and animals.
Collective intelligence has been proven to boost decision accuracy across many domains, such as geopolitical forecasting, investment, and diagnostics in radiology and dermatology (e.g., Kurvers et al., PNAS, 2016). However, collective intelligence has been mostly applied to relatively simple decision tasks. Applications in more open-ended tasks, such as emergency management or general medical diagnostics, are largely lacking due to the challenge of integrating unstandardized inputs from different people. To overcome this hurdle, the researchers used semantic knowledge graphs, natural language processing, and the SNOMED CT medical ontology, a comprehensive multilingual clinical terminology, for standardization.
“A key contribution of our work is that, while the human-provided diagnoses maintain their primacy, our aggregation and evaluation procedures are fully automated, avoiding possible biases in the generation of the final diagnosis and allowing the process to be more time- and cost-efficient,” adds co-author Vito Trianni from the Institute for Cognitive Sciences and Technologies (ISTC) in Rome.
The researchers are currently collaborating — along with other partners — within the HACID project to bring their application one step closer to the market. The EU-funded project will explore a new approach that brings together human experts and AI-supported knowledge representation and reasoning in order to create new tools for decision making in various domains. The application of the HACID technology to medical diagnostics showcases one of the many opportunities to benefit from a digitally based health system and accessible data.

A newly developed prediction model may be able to calculate the risk of opioid relapse among individuals in the early stages of medication treatment — as early as three weeks into therapy.
“Medication treatment for opioid use disorder, contrary to popular belief, is very effective and likely to succeed if patients achieve early treatment success,” says Sean X. Luo, MD, PhD, assistant professor of psychiatry at Columbia University Vagelos College of Physicians and Surgeons, who developed the model with Daniel Feaster, PhD, of the University of Miami.
The model, based on data from 2,199 adults enrolled in clinical trials of opioid use medications, estimates in the first few weeks of treatment the likelihood that a patient will return to using opioids before the end of a 12-week treatment program.
More specifically, for patients prescribed buprenorphine, increasing dose of an oral formulation or switching to an extended-release injection formulation could be considered quickly. Physicians should also evaluate patients with high risk of relapse for other factors that may need attention, such as co-occurring psychiatric disorders.
To disseminate the tools developed from this project, the team built a web portal (www.oudriskscore.org) that allows clinicians to estimate the risk of relapse of their patients.
What’s next
Although physicians may modify treatment for patients with a high risk of relapse, no studies have been conducted to determine the optimal strategies. “We need new clinical trials that test different treatment modifications among high-risk individuals,” Luo says.

Researchers at DZNE and Charité — Universitätsmedizin Berlin have pioneered a novel treatment for the most common autoimmune encephalitis. By reprogramming white blood cells to target and eliminate disease-causing cells, the approach offers a new level of precision and efficiency. The technique has proven successful in laboratory studies, clinical trials in humans are already being planned.
NMDA receptor encephalitis is the most common form of antibody-caused brain disease, in which antibodies suddenly attack the brain, thus turning against the patient’s own body. “In pre-clinical testing, we have succeeded in switching off selectively the cells in which these misdirected antibodies are formed,” says Professor Harald Prüss, who conducts research at DZNE’s Berlin site and at Charité — Universitätsmedizin Berlin. The team has engineered specialized CAAR-T cells, designed for injection into patients. These “chimeric autoantibody receptor T cells” are programmed to identify and eliminate, with high precision, the cells responsible for producing harmful antibodies. In mouse models, this innovative approach has already demonstrated its accuracy. The findings have been published by Prüss and colleagues in the scientific journal CELL.
New treatment method
Around 200 to 300 people are estimated to develop NMDA receptor encephalitis in Germany every year — with severe symptoms: They experience memory impairment, epileptic seizures, impaired consciousness, and psychosis. Severe cases may even require treatment in an intensive care unit. The new procedure would be an enormous improvement over current therapy. “Instead of suppressing the entire immune system and eliminating not only the misdirected antibodies, but also the more than 99 percent of beneficial antibodies, as we have done in the past, we set out to find a targeted approach.” That has now been achieved. “You can think of it like a surgical procedure, where the scalpel cuts out only what is harmful and the healthy tissue is left untouched,” Prüss says.
The disease, against which the therapy is directed, is insidious: the patient’s own immune system becomes the enemy, attacking the body instead of protecting it. While antibodies designed to eliminate viruses or bacteria are abundant in human blood, problems arise when some of these antibodies mistakenly target the body’s own tissues. If they cross the so-called blood-brain barrier, they can attack the brain. It is known by now that there is a whole range of such “autoimmune encephalopathies,” each triggered by different antibodies.
Reprogrammed cells
For their new, targeted therapy, the researchers had to develop an elaborate procedure: “We use human T cells, which we can obtain from patients’ blood, and modify them by adding a coupling molecule,” explains Dr. Momsen Reincke, one of the study’s first authors, who also researches at DZNE and Charité. This genetic reprogramming turns the T cells — a special type of white blood cells — into what is known as CAAR T cells. Once reintroduced into the body, these CAAR T cells now specifically attack those body cells that produce the misdirected antibodies. “The surface of these cells is shaped in such a way that the CAAR T cells precisely dock onto them and kill them.” Importantly, cells producing other antibodies and therefore have a different surface, remain untouched.
The term “chimera” behind the acronym CAAR refers to the principle of artificially building a molecule from different components. A treatment that follows a similar pattern already exists in cancer therapy. The Berlin researchers are the first to successfully apply this concept to an autoimmune disease of the brain.
Prospects for cure?
In a next step, the scientists aim to test the new therapy in a human clinical trial. This could start in one to two years, according to current estimates. “In the beginning, we will take a blood sample from every affected person in order to obtain T cells from them individually,” says Harald Prüss. “Given the rapid developments in the field of cell therapies, however, the next step could presumably be to use cells with which treatment no longer has to be patient-specific. That would be far less costly.” The hope of the DZNE researchers: A single application of the reprogrammed cells could definitively cure this type of autoimmune encephalitis — because according to current knowledge, once killed, the cells that generate the problematic antibodies usually do not reproduce. Moreover, the method could be adapted to work in other autoimmune encephalopathies and not only in the NMDA receptor variant.

A child psychologist, he argued that behavioral therapy had to come first in addressing attention deficit hyperactivity disorder, with drugs like Ritalin as a supplement.William E. Pelham Jr., a child psychologist who challenged how his field approached attention deficit hyperactivity disorder in children, arguing for a therapy-based regimen that used drugs like Ritalin and Adderall as an optional supplement, died on Oct. 21 in Miami. He was 75.His son, William E. Pelham III, who is also a child psychologist, confirmed the death, in a hospital, but did not provide a cause.Dr. Pelham began his career in the mid-1970s, when the modern understanding of mental health was emerging and psychologists were only just beginning to understand A.D.H.D. — and with it a new generation of medication to treat it.Through the 1980s and ’90s, doctors and many parents embraced A.D.H.D. drugs like Ritalin and Adderall as miracle medications, though some, including Dr. Pelham, raised concerns about their efficacy and side effects.Dr. Pelham was not opposed to medication. He recognized that drugs were effective at rapidly addressing the symptoms of A.D.H.D., like fidgeting, impulsiveness and lack of concentration. But in a long string of studies and papers, he argued that for most children, behavioral therapy, combined with parental intervention techniques, should be the first line of attack, followed by low doses of drugs, if necessary.And yet, as he pointed out repeatedly, the reality was far different: The Centers for Disease Control and Prevention reported in 2016 that while six in 10 children diagnosed with A.D.H.D. were on medication, fewer than half received behavioral therapy.In one major study, which he published in 2016 along with Susan Murphy, a statistician at the University of Michigan, he demonstrated the importance of treatment sequencing — that behavioral therapy should come first, then medication.He and Dr. Murphy split a group of 146 children with A.D.H.D., from ages 5 to 12, into two groups. One group received a low dose of generic Ritalin; the other received nothing, but their parents were given instruction in behavioral-modification techniques.After two months, children from both groups who showed no improvement were arranged into four new groups: The children given generic Ritalin received either more medication or behavioral modification therapy, and the children given behavioral modification therapy received either more intense therapy or a dose of medication.“We showed that the sequence in which you give treatments makes a big difference in outcomes,” Dr. Pelham told The New York Times. “The children who started with behavioral modification were doing significantly better than those who began with medication by the end, no matter what treatment combination they ended up with.”In 1980, Dr. Pelham started an innovative summer camp for children with A.D.H.D. and associated disorders.FIU Center for Children and FamiliesNot everyone agreed with Dr. Pelham’s conclusions, many on practical grounds. Medication was easy to administer, they said, and proper behavioral therapy could be time-consuming and expensive and therefore hard to maintain over a long stretch of time, both for parents and children — especially teenagers, who were more likely to resist it.Dr. Pelham’s influence can perhaps best be seen in the 2019 guidelines for A.D.H.D. diagnosis and treatment issued by the American Academy of Pediatrics, the group’s most recent recommendations. For very young children, it recommends treatment first, with medication as an option; for children 6 to 12, it recommends both simultaneously. But for adolescents, it concludes that behavioral treatment is unproven, and recommends medication only.Dr. Pelham began his career at Washington State University but spent most of it at the State University of New York at Buffalo. He moved his research program, the Center for Children and Families, to Florida International University, in Miami, in 2010.At both schools he ran an innovative summer camp for children with A.D.H.D. and associated disorders. The camp, which he created in 1980, served as a space for both therapy and research. It has since been the model for similar programs nationwide and internationally, including in Japan.“Dr. Pelham was one of the original giants in the field of A.D.H.D. research,” Dr. James McGough, a professor of psychology at the University of California, Los Angeles, said in a phone interview.FIU Center for Children and FamiliesWilliam Ellerbe Pelham Jr. was born on Jan. 22, 1948, in Atlanta, the son of William and Kitty Copeland (Kay) Pelham. The family moved often for William Sr.’s work, first to Kensington, Md., where he managed a Canada Dry facility, and later to Montgomery, Ala., where he sold securities. His mother was a homemaker and an artist.William Jr. received a bachelor’s degree in psychology from Dartmouth in 1970. He spent a year teaching special education in Amsterdam, N.Y., northwest of Albany, before enrolling in the doctoral program in psychology at the State University of New York at Stony Brook, on Long Island. He received his Ph.D. in 1976.In addition to his son, Dr. Pelham is survived by his wife, Maureen (Cullinan) Pelham, whom he married in 1990; his daughter, Caroline Pelham; and his brothers, Gayle and John.Dr. Pelham insisted on a therapy-first approach in part because it equipped children with the skills they needed to manage what was often a lifelong struggle.“Our research has found time and time again that behavioral and educational intervention is the best first-line treatment for children with A.D.H.D.,” he said in an interview with the podcast The Academic Minute in 2022. “They, their teachers and parents learn skills and strategies that will help them succeed at home, in school and in their relationships.”

Published13 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy Michelle RobertsDigital health editorFour women giving birth by Caesarean have had surgery to cut their risk of ovarian cancer at the same time, in what doctors say is a documented first. The pioneering two-in-one operations, at a London hospital, all went wellExperts say it is not a decision to be taken lightly, as removing the ovaries puts a woman into early menopause. Doing the surgery at the time of Caesarean delivery also risks greater blood loss, due to the physical changes that occur during pregnancy.However, it can avoid an anxious wait for the standard cancer risk-reducing operation to remove the fallopian tubes and ovaries, which is usually a standalone procedure.Prof Adam Rosenthal, who performed the procedure at University College London Hospital, said this type of simultaneous surgery has not previously been reported in a medical journal. The results are published in the latest edition of Obstetrics and Gynecology journal.Image source, Claire Rodrigues LeeClaire Rodrigues Lee, 45, from London, was one of the four women to have the pioneering dual procedure, which took surgeons about an hour to complete. She was awake for the entire operation, but had a spinal anaesthetic, meaning she felt no pain.Her operation in 2019, when she had just turned 41, was at the same time as the birth of her son – her second child. She told BBC News: “They handed him to me, so I had a cuddle with him – I think it was before they started on the next procedure. Then I passed him to my husband and they started the second part.”Explaining what the procedure entails, Prof Rosenthal said: “We lift the top of the uterus out of the abdomen to bring the tubes and ovaries out of the abdominal incision so they are easily accessible. “The only real issue is that the blood vessels get much bigger in pregnancy so extra care has to be taken to avoid damaging them. We ligate or cauterise them very carefully.”No regretsClaire says she knew she was at higher risk of ovarian cancer due to a gene she had inherited, and wanted to have the risk-reducing surgery as soon as possible after giving birth for the second time, knowing she had had all the children she wanted. “I was looking up online how quickly I could have the surgery after giving birth, and I came across the combined surgery as the first case had just been done. So I wanted to know if it would be possible for me.”She says she has no regrets about the surgery. “It saved me having to go into surgery twice…and the worry – this cloud of fear that I would get ovarian cancer.”She had her daughter by Caesarean too, and says the recovery and experience with her son was “no different really”. “It’s probably the best decision I’ve made, simply because I didn’t have to take out more time away from my children to go in for another procedure. “Why would I put myself through two surgeries when I could have everything done all at once and then I heal?”A woman who inherits a BRCA1 or BRCA2 gene variant has an increased risk of developing breast and ovarian cancer during her lifetime. It is not inevitable that she will get cancer, but her odds are higher than average.For example:Of 100 women in the general population, two will develop ovarian cancer before the age of 80Of 100 women with a BRCA2 variant, 11 to 25 will get ovarian cancer by age 80With a BRCA1 variant, 36 to 53 in every 100 will get ovarian cancer by 80Source: Macmillan Cancer SupportThere is a one-in-two, or 50-50, chance she will pass the variant to each of her children.Claire says she discovered that she had the BRCA2 variant when she was 36. “I had just got married. I started to look at what my options were. “It was quite scary. You sail through life thinking everything is fine… then all of a sudden this thing hits you in the face. You’ve got this gene and it means you are at a higher risk for cancer.”Claire has also had a double mastectomy to reduce her risk of getting breast cancer. She says when her children grow up they will be able to chose whether or not to get tested for the gene. “With all the luck in the world hopefully neither of them have it, but if they do, then they have choices.”Athena Lamnisos, from The Eve Appeal charity which works to raise awareness about women’s cancers, said: “These case studies tell a powerful story about what preventative surgery can deliver for women at high risk of ovarian cancer.” Sign up for our morning newsletter and get BBC News in your inbox.More on this storyBreast cancer gene linked to Orkney islandsPublished16 MarchAngelina Jolie gene testing for all?Published18 January 2018Related Internet LinksGynaecological Cancer Research Charity – The Eve AppealUniversity College London Hospitals NHS Foundation TrustObstetrics and Gynecology journalThe BBC is not responsible for the content of external sites.

Characterized by extensive damage to joints and debilitating pain, osteoarthritis (OA) impacts millions of people worldwide and has long posed a substantial clinical and economic burden.
In spite of advances in diagnosis, medications, and short-term pain management solutions, the elusive goal of a disease-modifying OA drug has remained out of reach. In recent years though, the use of stem cell therapy has gained traction as a promising alternative to surgery and for improving patients’ quality of life.
Through a grant from the Marcus Foundation, an Emory team of investigators in collaboration with other recruitment sites throughout the nation explored the potential of mesenchymal stem cells as a game-changing treatment option for knee OA, one of the most common causes of chronic knee pain. This type of treatment seeks to harness the ability of a patient’s own cells to repair damaged tissue. However, the availability of robust data from well-designed randomized controlled trials has been limited, particularly in comparison to the gold-standard of treatment for knee OA, corticosteroid injections (CSI).
The initial findings of this study, which were just published in Nature Medicine, describe a first-of-its-kind randomized clinical trial to identify the most effective source of cellular injections for knee OA. The research team compared three types of cellular preparations, including autologous bone marrow aspirate concentrate (BMAC), autologous stromal vascular fraction (SVF), and allogenic human umbilical cord tissue MSCs (UCT) against CSI. The primary outcome measures were the visual analog scale (VAS) and the Knee Injury and Osteoarthritis Outcome Score (KOOS) for pain from baseline to one year. The question driving the research was whether cell therapies could outperform corticosteroids in the treatment of knee osteoarthritis at the one-year mark.
While the findings showed each group had a measurable improvement in pain and function, there was no significant advantage to using any of the tested cell products compared to the gold standard anti-inflammatory corticosteroid treatment at the 12-month follow-up regarding the change in VAS pain score from baseline. Similarly, the analysis of the KOOS pain score produced consistent results, with no significant differences between groups at the 12-month mark in the change in score from baseline.
“The study demonstrated no superiority of any cell therapy over corticosteroids in reducing pain intensity over the course of a year,” says Scott D. Boden, MD, director of the Emory Orthopaedics and Spine Center, and a senior author on the study. “While there is much enthusiasm about the regenerative capacity of stem cells, the findings call into question the comparative effectiveness of various injections for knee osteoarthritis and underscores the importance of a personalized approach in selecting the right treatment for each patient’s unique needs.”
The study’s extensive reach also extended to evaluating the safety of these procedures measuring every adverse reaction, ranging from mild joint discomfort and swelling to unrelated hospitalizations. Importantly, the study found no study-related serious adverse events or symptomatic knee infections across any of the treatment groups at any point during the follow-up.
According to Dr. Boden, future papers from the ongoing analysis of our data will determine if certain subgroups of patients might preferentially benefit from one of these treatments more than another. The findings offer an important step forward in answering key questions about the comparative effectiveness of certain OA treatment options, but more in-depth analysis using MRIs and cellular analysis of each injectate will continue to help inform standards of care.

Using a technique that has shown promise in targeting cancer tumors, a Duke Health team has found a way to deploy a molecular warhead that can annihilate the bacterium that causes Lyme disease.
Tested in cell cultures using the Borrelia burgdoferi bacterium, the approach holds the potential to target not only bacteria, but also fungi such as yeast and viruses. The findings appear in the journal Cell Chemical Biology.
“This transport mechanism gets internalized in the bacterium and brings in a molecule that causes what we’ve described as a berserker reaction — a programmed death response,” said lead author Timothy Haystead, Ph.D., professor in Duke’s Department of Pharmacology and Cancer Biology. “It wipes out the bacteria — sterilizes the culture with a single dose of light. And then when you look at what occurs with electron microscopy, you see the collapse of the chromosome.”
Haystead and colleagues used a molecular facilitator called high-temperature protein G (HtpG), which is involved in protecting cells that are undergoing heat stress. This family of proteins has been the focus of drug development programs for possible cancer therapies.
Studies of this protein as an antimicrobial have also been encouraging, but the Duke team’s work appears to be the first to tether an HtpG inhibitor to a drug that enhances sensitivity to light.
The researchers found that the HtpG inhibitor, armed with the photosensitive drug, was rapidly absorbed into the cells of the Lyme bacteria. When hit with light, the bacteria’s cells went into disarray and ultimately collapsed, killing them.
“Our findings point to a new, alternate antibiotic development strategy, whereby one
can exploit a potentially vast number of previously unexplored druggable areas within bacteria to deliver cellular toxins,” Haystead said.
In addition to Haystead, study authors include Dave L. Carlson, Mark Kowalewski, Khaldon Bodoor, Adam D. Lietzan, Philip Hughes, David Gooden, David L. Loiselle, David Alcorta, Zoey Dingman, Elizabeth A. Mueller, Irnov Irnov, Shannon Modla, Tim Chaya, Jeffrey Caplan, Monica Embers, Jennifer C. Miller, Christine Jacobs-Wagner, Matthew R. Redinbo, and Neil Spector (deceased).
The study received funding support from the Steven and Alexander Cohen foundation and Bay Area Lyme Foundation.

Americans who have a tooth pulled or another painful dental procedure in the United States today are far less likely to get opioid painkillers than they were just a few years ago, a new study shows.
That’s good news, since research shows that opioids are not necessary for most dental procedures.
But the COVID-19 pandemic seems to have thrown a wrench into the effort to reduce opioid use in dental care — and not just in the few months after dentists and oral surgeons started providing routine care again after a pause in spring 2020.
The decline in opioid prescriptions filled by dental patients was much faster in the pre-pandemic years 2016 through 2019, compared with the rate of decline from June 2020 to December 2022, the study shows.
In all, dental opioids dispensed to U.S. patients of all ages declined 45% from 2016 to the end of 2022, according to the new findings published in PLoS One by a team from the University of Michigan Medical School and School of Dentistry.
But even with the decline, 7.4 million dental patients of all ages filled opioid prescriptions in 2022.
Fortunately, opioid prescriptions to teens and young adults — who face especially high risks related to opioids — kept declining at a rapid rate after the pandemic pause in dental care, the study finds. But for other groups, the rate of decline slowed after June 2020.

An international team of researchers has discovered that formaldehyde, a widely spread pollutant and common metabolite in our body, interferes in the epigenetic programming of the cell. This finding expands the knowledge of formaldehyde, previously considered only as a DNA mutagen, and helps establishing a further link with cancer. Dr. Lucas Pontel, group leader at the Josep Carreras Leukaemia Research Institute and Dr. Manel Esteller, group leader and director of the institution, sign the paper as collaborator authors, which has been published at Science.
Epigenetics, the chemical mechanisms that controls the activity of genes, allows our cells, tissues and organs to adapt to the changing circumstances of the environment around us. This advantage can become a drawback, though, as this epigenetic regulation can be more easily altered by toxins than the more stable genetic sequence of the DNA.
An article recently published at Science with the collaboration of the groups of Dr. Manel Esteller, Director of the Josep Carreras Leukaemia Research Institute (IJC-CERCA), ICREA Research Professor and Chairman of Genetics at the University of Barcelona, and Dr. Lucas Pontel, Ramon y Cajal Fellow also of the Josep Carreras Institute, demonstrates that the substance called formaldehyde, commonly present in various household and cosmetic products, in polluted air, and widely used in construction, is a powerful modifier of normal epigenetic patterns.
The publication is led by Dr. Christopher J. Chang, of the University of California Berkeley in the United States, whose research group is pioneer in the study of the effects of various chemical products on cell metabolism. The research has focused on investigating the effects of high concentrations of formaldehyde in the body, a substance already been associated with an increased risk of developing cancer (nasopharyngeal tumours and leukaemia), hepatic degeneration due to fatty liver (steatosis) and asthma. Dr. Esteller points out that this is relevant because “formaldehyde enters our body mainly during our breathing and, because it dissolves well in an aqueous medium, it ends up reaching all the cells of our body.”
“This substance is especially concentrated in various products used in construction, furniture manufacturing, the textile industry and some hair products,” comments Dr. Esteller. Going a step further, Dr. Pontel stresses this vision pointing out that “formaldehyde is not only a significant environmental hazard, often found in polluted fumes, but it can also be generated within our bodies through the metabolism of common dietary substances like the sweetener aspartame. Moreover, our cells are continually producing formaldehyde, a known mutagen that can lead to cancer.”
As an overview of the research, Dr. Esteller points out that “we have discovered that formaldehyde is an inhibitor of the MAT1A protein, which is the main producer of S-Adenosyl-L-Methionine (SAM) and this last molecule is the universal donor of the chemical group “methyl” that regulates epigenetic activity. Specifically, we found that exposure to formaldehyde induced a reduction in SAM content and caused the loss of methylation of histones, proteins that package our DNA and control the function of thousands of genes.”
Altogether, this work reveals an even more concerning aspect of formaldehyde’s toxicity. Dr. Pontel summarizes it as “we have discovered that formaldehyde has the capacity to modify the epigenetic landscape of our cells, which might contribute to the well-documented carcinogenic properties of formaldehyde.”
The epigenetic changes caused by the toxic agent could directly contribute to the origin of the mentioned diseases, beyond its known mutagenic properties. On this regard, Dr. Esteller informs that “International health authorities are already restricting the use of formaldehyde as much as possible, but there are still areas of work where high levels of it are used, such as in the manufacture of resins, the production of plastic, industrial foundries or the cosmetics industry. In addition, it also originates during the combustion of automobile gasoline and in tobacco smoke, thus, environmental and health policies aimed at reducing our exposure to the characterized substance should be promoted.”

One in seven people in the US reported having had long Covid by the end of 2022, suggests a large-scale investigation of long Covid and symptom prevalence by academics at UCL and Dartmouth.
Having had long Covid is associated with anxiety and low mood, as well as an increased likelihood of continued physical mobility problems and challenges with memory, concentration or understanding, according to the findings published in PLOS ONE.
The risk of anxiety and low mood appeared to be lower for those who have been vaccinated, including for those who have had long Covid.
Co-author Professor Alex Bryson (UCL Social Research Institute) said: “Little is known about long Covid and its impact on health and wellbeing, but there is a growing body of evidence that many people experience persistent and concerning symptoms.
“Here, we have found that long Covid continues to affect millions of people in the US, with some groups much more affected than others. Those who have ever had long Covid remain more likely to report low mood, challenges in carrying out daily tasks, and challenges with memory, concentration and understanding, compared to people who have never had long Covid.”
The researchers reviewed data from 461,550 people who responded to the US Census Bureau’s Household Pulse Survey from June to December 2022. They were comparing people who said they had never had Covid-19, with those who had had a Covid-19 infection without lingering symptoms, and those who currently or previously had long Covid.
In line with the World Health Organization (WHO), they defined long Covid as the continuation or development of new symptoms at least three months after the initial infection.