Category: 8. Health

Walking frequently is linked to reduced back pain, and it’s the total amount of walking that matters most, not how intense it is.

A large research effort examined how daily walking relates to the likelihood of developing chronic lower back problems. If people adopt the simple guidance that emerges, the approach could ease back pain for many and reduce costs for healthcare systems.

The results are clear: people who walk more tend to have fewer lower back issues, and total time on foot matters more than speed or intensity. In practical terms, walking longer is more beneficial than walking faster.

“People who walk more than 100 minutes every day have a 23 per cent lower risk of lower back problems than those who walk 78 minutes or less,” said Rayane Haddadj.

He is a PhD candidate at the Department of Public Health and Nursing at the Norwegian University of Science and Technology (NTNU), and is part of a research group that specifically studies musculoskeletal disorders.

The findings were published in JAMA Network Open and have already drawn significant attention.

Even leisurely strolls are beneficial

It probably comes as no surprise that physical activity is good for your back, but until now, we have not actually known whether the amount of low-intensity walking we do also helps.

“Intensity also plays a role in the risk of long-term back problems, but not as much as the daily amount of walking,” emphasized Haddadj.

A total of 11,194 people participated in the study, which is part of the Trøndelag Health Study (The HUNT Study). What makes this study unique is that the volume and intensity of daily walking were measured using two sensors that participants wore on their thighs and back for up to a week.

The results may be important in relation to preventing chronic back problems. Until now, there has been little research on the prevention of these types of musculoskeletal problems. It is well known that physical activity can prevent a wide range of illnesses and ailments. This study is important because it confirms that physical activity, and especially daily walking, can help prevent long-term lower back problems.

Back pain is a very common ailment

“The findings highlight the importance of finding time to be physically active – to prevent both chronic back problems and a number of other diseases. Over time, this could lead to major savings for society,” said Paul Jarle Mork, a professor at NTNU’s Department of Public Health and Nursing.

Back and neck problems cost society several billion kroner every year. Musculoskeletal disorders are likely the largest expense within the Norwegian healthcare system.

Back pain is one of the most common health problems in Norway. Depending on what you include, between 60 and 80 per cent of us will experience back problems at some point in our lives. At any given time, around one in five Norwegians has back trouble.

The causes are many and complex, but the solution might be as simple as putting on your shoes and going for a walk – each and every day.

Reference: “Volume and Intensity of Walking and Risk of Chronic Low Back Pain” by Rayane Haddadj, Anne Lovise Nordstoga, Tom Ivar Lund Nilsen, Eivind Schjelderup Skarpsno, Atle Kongsvold, Mats Flaaten, Jasper Schipperijn, Kerstin Bach and Paul Jarle Mork, 13 June 2025, JAMA Network Open.
DOI: 10.1001/jamanetworkopen.2025.15592

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Individuals with atopic dermatitis who initiate systemic Janus kinase (JAK)-inhibitors are not at greater risk of developing cardiovascular disease or cancer compared to those initiating interleukin (IL)-4 or IL-13 inhibitors, recent data suggest.¹

These data comparing rates of risk between these 2 patient groups were the result of a recent study authored by investigators such as Sizheng Steven Zhao, MBChB, PhD, a clinical senior lecturer and consultant rheumatologist at the University of Manchester’s Centre for Musculoskeletal Research.

Zhao and colleagues highlighted the well-known efficacy of JAK inhibitors (JAKi) for patients living with atopic dermatitis. They added, however, that cardiovascular and cancer risk concerns have remained persistent, given a prior study pointing to increased risk among patients with rheumatoid arthritis (RA).²

“While the RA and [atopic dermatitis] populations likely differ, [atopic dermatitis] is independently associated with an increased risk of cardiovascular disease and cancer compared with the general population,” Zhao and coauthors wrote.^1,3 “We aimed to compare the risk of cardiovascular disease and cancer between individuals starting systemic JAKi versus IL-4/-13 inhibitors (IL-4/-13i).”

The investigative team used electronic health record data from healthcare systems primarily located in North America to conduct this cohort study. Those deemed eligible to be participants were required to be adults aged ≥18 years and to have an ICD-10 diagnosis code for atopic dermatitis. They also had to have initiated treatment with either a JAKi such as upadacitinib, tofacitinib, or abrocitinib or to have initiated an IL-4/IL-13 inhibitor such as lebrikizumab, dupilumab, or tralokinumab.

The main outcomes Zhao et al assessed were the occurrence of coronary artery disease or stroke, and the incidence of any form of cancer among patients. In their evaluation of secondary endpoints, outcomes included coronary artery disease alone, skin cancer, stroke alone, and 2 control outcomes—herpes zoster and conjunctivitis.

The investigative team applied 1:1 propensity score (PS)-matched Cox proportional hazards models to draw comparisons of time-to-event outcomes between treatment cohorts in their analysis. Zhao and colleagues included matching variables such as participants’ sex, age at initiation of treatment, sex, and ethnicity. The team assessed other covariates within the 12 months before initiation of these medications, including C-reactive protein (CRP) levels, ischemic heart disease, body mass index (BMI), cerebrovascular disease, cardiovascular risk factors, proxies for atopic dermatitis severity, and cancer history.

Zhao and coauthors’ follow-up period continued until the last available record or the conclusion of the study period, whichever occurred first. Individuals involved in the analysis who shifted to 1 drug from another treatment class during follow-up were not included. The analyses were repeated for 1-, 3-, and 5-year follow-up intervals, with investigators hoping to address potential differences in exposure duration. They also conducted sensitivity analyses, excluding participants who reported a prior history of the outcome of interest. They would also remove events that took place within the first month of follow-up to limit reverse causation.

In total, there were 1978 subjects who began using a JAK inhibitor and were successfully matched to 1978 IL-4/IL-13 inhibitor initiators. Mean follow-up duration was shown by the investigative team to have been slightly longer for IL-4/IL-13 inhibitor users (e.g., 291 days versus 264 days at the 1-year timepoint). All covariates at the point of baseline were well-balanced across the different cohorts of patients. Overall, the team found no statistically significant differences observed between drug classes in risk of any cancers (HR 0.81; 95% CI 0.60–1.08), cardiovascular events (HR 1.41; 95% CI 0.78–2.56), or skin cancers specifically (HR 1.07; 95% CI 0.61–1.89).¹

Zhao et al’s findings in this study were consistent across 1-, 3-, and 5-year follow-up periods and across their sensitivity analyses. However, JAKi therapy was linked with a decreased risk of conjunctivitis and an increased risk of herpes zoster. Nevertheless, this large real-world study’s findings indicate that, among adult patients with atopic dermatitis, JAK inhibitors do not appear to raise their risk of developing cardiovascular disease or cancer when compared with IL-4/IL-13 inhibitors.¹

Such conclusions may allow for reassurance among patients and clinicians, and the findings were consistent with both atopic dermatitis clinical trial data and previous observational research in RA. The investigators did acknowledge, however, the relatively limited number of outcome events and the consequent constraint on the data’s statistical power, highlighting the value of continued monitoring and replication in future studies.

“The main limitation is the inability to accurately ascertain the drug cessation date using administrative data and the differences in follow-up time between exposure groups,” Zhao et al concluded.¹ “However, results were similar across different durations of follow-up. As with all observational studies, residual confounding may bias our results. Nonetheless, reassurance comes from using IL-4/-13i as an active comparator and from the use of control outcomes.”

References

1. Zhao SS, Hernandez G, Alam U. Risk of Cardiovascular Disease and Cancer in Patients Initiating JAK Versus IL-4/-13 Inhibitors for Atopic Dermatitis. Int J Dermatol. 2025 Apr 28. doi: 10.1111/ijd.17815. Epub ahead of print. PMID: 40293104. Accessed September 5, 2025.

2. Ytterberg SR, Bhatt DL, Mikuls TR, Connell CA, et al; ORAL Surveillance Investigators. Cardiovascular and Cancer Risk with Tofacitinib in Rheumatoid Arthritis. N Engl J Med. 2022 Jan 27;386(4):316-326. doi: 10.1056/NEJMoa2109927. PMID: 35081280. Accessed September 5, 2025.

3. Silverwood RJ, Forbes HJ, Langan SM, et al. Severe and predominantly active atopic eczema in adulthood and long term risk of cardiovascular disease: population based cohort study. BMJ. 2018 May 23;361:k1786. doi: 10.1136/bmj.k1786. PMID: 29792314; PMCID: PMC6190010. Accessed September 5, 2025.

When a medicine is added to the WHO’s EML, it signals that it is vital for public health and should be made affordable and accessible, that countries should include it in national policies, and that corporations should register it in-country so more people can access it. Currently, rapid-acting insulins and GLP-1s are generally unaffordable and often unavailable in the places MSF operates.

Rapid-acting insulin analogues and GLP-1s help manage blood sugar levels, reducing the likelihood of potential diabetes-related health complications and the need for additional care—something that can be difficult to access for people in low- and middle-income countries.

For over 40 years, beta blockers have been prescribed to heart attack survivors as a standard treatment. But the massive REBOOT trial has revealed they provide no benefit for patients with preserved heart function — and may actually increase risks for women.

Standard Treatment Questioned After 40 Years

Beta blockers, commonly prescribed for heart conditions including heart attacks, have now been shown to offer no measurable benefit for patients who experience an uncomplicated myocardial infarction while maintaining normal heart function. Despite being recommended for this group for four decades, their effectiveness in such cases is now being called into question.

The finding comes from the REBOOT Trial, a major study led by Valentin Fuster, MD, PhD, President of Mount Sinai Fuster Heart Hospital and General Director of Spain’s Centro Nacional de Investigaciones Cardiovasculares (CNIC). The results, which challenge one of cardiology’s longest-standing practices, were presented on August 30, during a “Hot Line” session at the European Society of Cardiology Congress in Madrid and published at the same time in The New England Journal of Medicine.

Higher Risks for Women Exposed

A companion substudy of REBOOT, released the same day in the European Heart Journal, revealed an important difference between men and women. Women who were treated with beta blockers after a heart attack faced a higher likelihood of dying, suffering another heart attack, or being hospitalized for heart failure when compared with women who did not receive the medication. This increased risk was not observed in men.

“This trial will reshape all international clinical guidelines. It joins other previous landmark trials led by CNIC and Mount Sinai – such as SECURE with the polypill and DapaTAVI, with SLT2 inhibition associated to TAVI –that have already transformed some global approaches to cardiovascular disease,” says Dr. Fuster.

The SECURE trial showed a polypill, a single pill that combines three medications – which contains aspirin, ramipril, and atorvastatin – reduces cardiovascular events by 33 percent in patients treated with this after a heart attack. The DapaTAVI trial showed that both dapagliflozin and the related medication empagliflozin – drugs used to treat diabetes – improve the prognosis of patients with aortic stenosis treated by transcatheter aortic valve implantation.

Global Impact on Heart Attack Care

“REBOOT will change clinical practice worldwide,” says Principal Investigator Borja Ibáñez, MD, CNIC’s Scientific Director, who presented the results. “Currently, more than 80 percent of patients with uncomplicated myocardial infarction are discharged on beta blockers. The REBOOT findings represent one of the most significant advances in heart attack treatment in decades.”

Although generally considered safe, beta blockers can cause side effects such as fatigue, bradycardia (low heart rate), and sexual dysfunction. For more than 40 years, beta blockers have been prescribed as a standard treatment after a heart attack, but their benefit in the context of modern treatments was unproven. The REBOOT trial, is the largest clinical trial on this subject. The international study was coordinated by CNIC in collaboration with the Mario Negri Institute for Pharmacological Research in Milan.

Largest Beta Blocker Study to Date

Researchers enrolled 8,505 patients across 109 hospitals in Spain and Italy. Participants were randomly assigned to receive or not receive beta blockers after hospital discharge. All patients otherwise received the current standard of care and were followed for a median of nearly four years. The results showed no significant differences between the two groups in rates of death, recurrent heart attack, or hospitalization for heart failure.

A REBOOT subgroup analysis found that women treated with beta blockers experienced more adverse events. Results show women treated with beta-blockers had a 2.7 percent higher absolute risk of mortality compared to those not treated with beta-blockers during the 3.7 years of follow-up of the study. The elevated risk when treated with beta-blockers was restricted to women with completely normal cardiac function after a heart attack (left ventricular ejection fraction of 50 percent or higher). Those with a mild deterioration in cardiac function did not have an excess risk of adverse outcomes when treated with beta-blockers.

Why the Old Standard No Longer Fits

“After a heart attack, patients are typically prescribed multiple medications, which can make adherence difficult,” explains Dr. Ibáñez. “Beta blockers were added to standard treatment early on because they significantly reduced mortality at the time. Their benefits were linked to reduced cardiac oxygen demand and arrhythmia prevention. But therapies have evolved. Today, occluded coronary arteries are reopened rapidly and systematically, drastically lowering the risk of serious complications such as arrhythmias. In this new context, where the extent of heart damage is smaller, the need for beta blockers is unclear. While we often test new drugs, it’s much less common to rigorously question the continued need for older treatments.”

REBOOT Trial Motivation

That was the motivation behind REBOOT.

“The trial was designed to optimize heart attack care based on solid scientific evidence and without commercial interests. These results will help streamline treatment, reduce side effects, and improve quality of life for thousands of patients every year,” Dr. Ibanez adds.

References:

“Beta-Blockers after Myocardial Infarction without Reduced Ejection Fraction” by Borja Ibanez, Roberto Latini, Xavier Rossello, Alberto Dominguez-Rodriguez, Felipe Fernández-Vazquez, Valentina Pelizzoni, Pedro L. Sánchez, Manuel Anguita, José A. Barrabés, Sergio Raposeiras-Roubín, Stuart Pocock, Noemí Escalera, Lidia Staszewsky, Carlos Nicolás Pérez-García, Pablo Díez-Villanueva, Jose-Angel Pérez-Rivera, Oscar Prada-Delgado, Ruth Owen, Gonzalo Pizarro, Onofre Caldes, Sandra Gómez-Talavera, José Tuñón, Matteo Bianco, Jesus Zarauza, Alfredo Vetrano, Ana Campos, Susana Martínez-Huertas, Héctor Bueno, Miguel Puentes, Giulietta Grigis, Juan L. Bonilla-Palomas, Elvira Marco, José R. González-Juanatey, Roi Bangueses, Carlos González-Juanatey, Ana García-Álvarez, Juan Ruiz-García, Anna Carrasquer, Juan C. García-Rubira, Domingo Pascual-Figal, Carlos Tomás-Querol, J. Alberto San Román, Pasquale Baratta, Jaume Agüero, Roberto Martín-Reyes, Furio Colivicchi, Rosario Ortas-Nadal, Pablo Bazal, Alberto Cordero, Antonio Fernández-Ortiz, Pierangelo Basso, Eva González, Fabrizio Poletti, Giulia Bugani, Marzia Debiasio, Deborah Cosmi, Alessandro Navazio, Javier Bermejo, Giovanni Tortorella, Marco Marini, Javier Botas, José M. de la Torre-Hernández, Filippo Ottani and Valentín Fuster, 29 August 2025, New England Journal of Medicine.
DOI: 10.1056/NEJMoa2504735

“Beta-blockers after myocardial infarction: effects according to sex in the REBOOT trial” by Xavier Rossello, Alberto Dominguez-Rodriguez, Roberto Latini, Pedro L Sánchez, Sergio Raposeiras-Roubín, Manuel Anguita, José A Barrabés, Giulietta Grigis, Ruth Owen, Stuart Pocock, Sandra Gómez-Talavera, Ines García-Lunar, Noemí Escalera, Carlos Nicolás Pérez-García, Stefania Angela Di Fusco, Gonzalo Pizarro, María López Benito, Giulia Pongetti, Luis M Rincón-Díaz, Irene Buera, José Rozado, María Jesús García, Oscar Prada-Delgado, Deborah Cosmi, Valentín Fuster and Borja Ibanez, 30 August 2025, European Heart Journal.
DOI: 10.1093/eurheartj/ehaf673

Meeting: ESC Congress 2025

REBOOT was conducted without pharmaceutical industry funding.

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If Wenjun Zhang has her way, no one will ever have to brush or floss again.

Zhang, a UC Berkeley professor of chemical and biomolecular engineering, is trying to distinguish the healthy bacteria in our mouths from the unhealthy bacteria – those that cause cavities – so that she can boost the proportion of the former and promote a probiotic oral microbiome.

Our mouth’s microbiome consists of hundreds of different species of bacteria, many of which form a community that sticks to teeth to form plaque. Previous studies have focused on which of those species are associated with cavities, producing acid that eats away at tooth enamel. But researchers have found that each species is not uniformly good or bad – individual species can have hundreds of different varieties, called strains, that differ in their cavity-promoting qualities.

Instead of focusing on species or strains, Zhang and her team scan the DNA sequences of all the bacteria in the mouth – the metagenome – in search of clusters of genes associated with cavities.

In a paper published Aug. 19 in the journal Proceedings of the National Academy of Sciences, she and her colleagues reported the discovery of one such gene cluster that produces two molecules that together help the mouth’s community of bacteria – good and bad – stick together and form a strong biofilm on teeth.

They found this gene cluster in some but not all strains of several known bad actors in the mouth, including Streptococcus mutans – the main villain in tooth decay. Zhang sees an opportunity to stick this gene cluster into good bacteria to help them attach better to teeth and push out the acid-producing bacteria that pave the way for cavities.

Particular strains belonging to the same species can be a pathogen or a commensal or even probiotic. After we better understand these molecules’ activity and how they can promote strong biofilm formation, we can introduce them to the good bacteria so that the good bacteria can now form strong biofilms and outcompete all the bad ones.”

Wenjun Zhang, professor of chemical and biomolecular engineering, UC Berkeley 

The work was supported by the National Institute of Dental & Craniofacial Research of the National Institutes of Health (R01DE032732).

“Specialized” metabolism

The gene cluster was discovered by searching through an online database of a large number of metagenomic sequences of the microbial communities in the mouths of human volunteers. Berkeley graduate student McKenna Yao conducted a statistical analysis to identify clusters associated with oral disease and then cultivated the bacteria to analyze and identify the metabolites produced by these clusters.

The metabolites are small molecules composed of short strands of amino acids – peptides – and fatty acids, or lipids. One molecule works like glue, helping cells clump together into blobs, while the other acts more like string, letting them form chains. Together they give bacteria the ability to build communities – the sticky substance on your teeth – instead of floating alone.

The newfound gene cluster contains about 15 DNA segments coding for proteins, enhancers and transcription factors that act like a self-contained metabolic cassette – an alternative metabolic pathway that is not essential for survival of the bacteria but which, Zhang has found, has major impacts on the surrounding environment, such as teeth. These gene clusters are sometimes referred to as a microbe’s secondary metabolism, but Zhang prefers the term “specialized” because they can produce interesting molecules. Specialized metabolic networks in soil bacteria have proved a fertile source of antibiotics, for example.

“These specialized metabolites enhance survival in certain ways,” said Yao, one of three Berkeley graduate students who contributed to the work and are first authors of the paper. “Many, for example, are antibiotics, so they can kill other bugs, or others are involved in metal acquisition – they help the bacteria monopolize the resources in their environmental niche. Being able to produce these, especially in a microbial community, helps the bacteria boot out the other guy and guard their resources.”

Yet the role of specialized metabolic networks and secondary metabolites in the human microbiome have largely remained unstudied, Zhang said. Two years ago, she and her colleagues found a gene cluster in oral bacteria that produces a previously unknown antibiotic. They found another gene cluster that produced a different set of sticky molecules that help to form biofilms.

The newly reported gene cluster is another demonstration of the importance of the microbiome’s secondary metabolites in human health, whether in the mouth, gut, skin or any organ. Understanding these sticky metabolites in the mouth, dubbed mutanoclumpins, could help reduce cavities.

“We are looking for something which is correlated with cavities, with disease. If one day we can prove that, under certain conditions, this is really a bad molecule you want to prevent, we might develop genetic or chemical inhibitors to inhibit their production, so hopefully the bacteria will not make them, and you have fewer cavities,” Zhang said. “Meanwhile, we also look at other molecules correlated with health, allowing a simple strategy to directly engineer the microbes to make more of them.”

One species of bacteria that could use a boost is Streptococcus salivarius, which appears to promote oral health and is currently marketed as an oral probiotic. Unfortunately, even if it proves to be probiotic, it doesn’t form a strong biofilm that sticks to teeth and rapidly dissipates. Zhang suggests adding strong biofilm-forming molecules to S. salivarius to see if the bacteria can work better as probiotics.

“Our future work will be to create a broad map of the collection of these specialized metabolites to look at collectively what this dynamic, complex community on your teeth is making,” Zhang said.

Yao noted, however, that “the best way you can remove the biofilm on your teeth is to brush. We believe that there’s actually a better way of disrupting that biofilm, but we’re just beginning to understand what the complexity is within the mouth.”

Nicholas Zill and Colin Charles Barber are first co-authors with Yao. Other co-authors are Yongle Du, Rui Zhai, Eunice Yoon and Dunya Al Marzooqi of Berkeley’s Department of Chemical and Biomolecular Engineering and Peijun Lin, a visiting student in the College of Computing, Data Science, and Society.

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There’s an old joke about the Daily Mail that is timeless: The tabloid likes to categorize every substance known to humankind as either a cause or cure of cancer. There was even a song put out by the BBC 15 years ago making fun of this trend.

The problem is that it’s not just the Daily Mail. In reality, we all love stories about causing or preventing cancer, so much so that most media sources are guilty of misrepresenting the evidence that appears in the many cancer-related studies published each year.

The latest series of articles is a wonderful example. A recent scientific publication has come out noting that there is a relationship between the intake of cruciferous vegetables—a large group that includes everything from broccoli to bok choi—and a reduced risk of colon cancer. The media has, predictably, gone wild. If you believe the headlines, it would mean that we can slash our risk of a really nasty form of cancer with just a few florets of cauliflower a day.

Sadly, as an epidemiologist, I can tell you that the data are not nearly strong enough to draw such a meaningful conclusion.

The new study is a systematic review of observational research. Observational research in this context means that scientists ask people what they eat, and then look at whether the foods they consume are linked to their long-term risk of cancer. A systematic review is a type of study that aggregates all of the studies on a topic and then combines them into a single analysis of some kind.

In this case, if you look at all of the observational research on cruciferous vegetables and colon cancer, it appears that people who eat more of the veggies have less cancer. The highest levels of veggie-munching were associated with a 17 percent reduction in colon cancer risk across 17 studies compared to eating no cruciferous vegetables at all.

The problem here is with that word association. Thanks to this study and the predecessors it aggregates, we can say with some certainty that if you ask large groups of people what they eat, the people who say that they eat more broccoli each week are less likely to get colon cancer as time goes on. But what does that really mean?

It’s very hard to know from studies like this whether eating more of the vegetables actually causes improved health or whether there is some other factor going on that isn’t measured properly in the study. People regularly lie on surveys about what they eat, or they forget and make mistakes. People who eat more vegetables are systematically different from people who eat fewer veggies, in ways that are hard to control for in studies like this. It might just be that rich people have more access to vegetables and are less likely to get cancer because they exercise more, or have less exposure to known carcinogens, rather than anything specific to cabbage or Brussels sprouts.

The authors of this systematic review did try to account for some of these issues, but a fundamental problem with large nutrition studies that simply ask people what they eat is that it’s really hard to eliminate the problems entirely. That’s why we run randomized clinical trials, which can account for all of these problems.

Or, to quote the authors of the new review: “This meta-analysis suggests a potential inverse association between higher CV [cruciferous vegetables] intake and CC [colon cancer] incidence. However, these findings should be interpreted cautiously due to methodological limitations.” This is basically science-speak for: “We don’t know if broccoli prevents cancer or not.”

This feels like just another case of the media blowing unimportant findings way out of proportion. Yes, there is some association between broccoli and good health, but we already knew that. There are probably dozens, if not hundreds, of diseases where you could find some positive association like this, but in my humble opinion, that news isn’t interesting or useful to your life.

When it comes to the question of individual foods causing or curing cancer, I don’t think we’ll ever have good answers. Even for red meat—which has been researched for decades—there’s no clear proof of a cancer link.

It’s definitely true that your diet as a whole can raise or lower your risk of various diseases, but when it comes to specific foods, the evidence is much murkier. Don’t start spooning up coleslaw because you think it’ll stop you from getting cancer. If you like cabbage, eat it.

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