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A new study adds to a large body of evidence on the effectiveness of movement for treating and preventing pain.Doctors and physical therapists have long incorporated aerobic exercise into treatment programs for lower back pain. Movement can simultaneously ease lower back pain and also strengthen the muscles that support your back. Still, many people with back pain can be hesitant to exercise.A new study, published on Wednesday in The Lancet, offers more evidence on the power of movement. The study found that a regular walking routine can be very effective for preventing the recurrence of back pain. The study focused on adults with a history of low back pain; those who walked regularly went nearly twice as long without their back pain coming back compared to the control group.The new findings are in line with a large body of existing research that has established an association between physical activity and better outcomes for back pain. A 2019 systematic review found that physical activity lowered the prevalence of back pain. And a 2017 study found that yoga worked as well as physical therapy for relieving back pain.The new study builds on this research by following patients outside a tightly controlled clinical setting. Mark Hancock, a professor of physiotherapy at Macquarie University in Australia and a senior author of the study, sought to evaluate the effectiveness of a less expensive intervention that could be easier for many people to access than in-clinic treatment.Dr. Hancock and a team of researchers targeted a relatively sedentary sample group. The researchers collected data on 701 adults who had recently recovered from an episode of low back pain. They were randomly split in two groups: one group received an individualized walking and education program, facilitated by a physiotherapist over six sessions in a six-month period. The other group did not receive any intervention. The researchers followed both groups for the next one to three years.The goal for each person in the walking group was to walk five times per week for at least 30 minutes daily — but the program was highly personalized based on age, body mass index, current activity level, time constraints and personal goals.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

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None of the main political parties has yet set out convincing plans on how they will improve the NHS, a leading health think tank says.

A new study suggests that certain drugs commonly used to treat enlarged prostate may also decrease the risk for dementia with Lewy bodies (DLB). This observational finding may seem surprising, but it mirrors previous work by the University of Iowa Health Care team that links the drugs to a protective effect in another neurodegenerative condition-Parkinson’s disease.
The UI researchers think that a specific side effect of the drugs targets a biological flaw shared by DLB and Parkinson’s disease, as well as other neurodegenerative diseases, raising the possibility that they may have broad potential for treating a wide range of neurodegenerative conditions.
“Diseases like dementia with Lewy bodies, or Parkinson’s disease, or Alzheimer’s disease, are debilitating and we don’t really have any good treatments that can modify the disease progression. We can treat symptoms, but we can’t actually slow the disease,” explains lead study author Jacob Simmering, PhD, UI assistant professor of internal medicine. “One of the most exciting things about this study is that we find that same neuroprotective effect that we saw in Parkinson’s disease. If there is a broadly protective mechanism, these medications could potentially be used to manage or prevent other neurodegenerative diseases.”
The new findings were published online on June 19, 2024, in Neurology®, the medical journal of the American Academy of Neurology.
DLB is a neurodegenerative disease that causes substantial and rapid cognitive decline and dementia. While less common than Parkinson’s disease, DLB affects about one in 1,000 people per year, and accounts for 3 to 7% of all dementia cases. Because aging is a key risk factor for DLB, it is likely to become more common as our population gets older.
For the new study, the UI researchers used a large database of patient information to identify more than 643,000 men with no history of DLB who were newly starting one of six drugs used to treat benign prostatic hyperplasia (enlarged prostate).
Three of the drugs, terazosin, doxazosin, and alfuzosin (Tz/Dz/Az), have an unexpected side effect; they can boost energy production in brain cells. Preclinical studies suggest that this ability may help slow or prevent neurodegenerative diseases like PD and DLB.

The other drugs, tamsulosin and two 5-alpha-reductase inhibitors (5ARIs) called finasteride and dutasteride, do not enhance energy production in the brain and therefore provide a good comparison to test the effect of the Tz/Dz/Az drugs.
The team then followed the data on these men from when they started taking the medication until they left the database or developed dementia with Lewy bodies, whichever happened first. On average, the men were followed for about three years.
Because all the participants were selected to start a drug that treats the same condition, the researchers reasoned that the men were likely similar to each other at the outset of the treatment. The researchers also matched the men using propensity scores for characteristics like age, the year they started the medication, and other illnesses they had before staring the treatment, to further reduce the differences between the groups.
“We found that men who took Tz/Az/Dz drugs were less likely to develop a diagnosis of dementia with Lewy bodies,” Simmering says. “Overall, men taking terazosin-type medications had about a 40% lower risk of developing a DLB diagnosis compared to men taking tamsulosin, and about a 37% reduction in risk compared to men taking five alpha reductase inhibitors.”
Meanwhile, there wasn’t a statistically significant difference in risk between men taking tamsulosin and 5-alpha reductase inhibitors.
This was an observational study and therefore the results show only an association between taking the Tz/Dz/Az drugs and a reduced risk of developing DLB rather than a causal relationship. In addition, the study only included men because the drugs are prescribed for prostate problems, which means that the researchers don’t know if the findings would apply to women. However, Simmering and his colleagues are excited by the potential of these drugs, which are already FDA approved, inexpensive, and have been used safely for decades.
“If terazosin and these similar medications can help slow this progression — if not outright preventing the disease — this would be important to preserving cognitive function and quality of life in people with DLB,” Simmering says.
In addition to Simmering, the team included UI neuroscience researchers Nandakumar Narayanan, MD, PhD, Georgina Aldridge, MD, PhD, and Qiang Zhang, MD, and Alexander Hart, MD, who is now at University of Michigan.

A scientific story that began with a discovery in just one extraordinary patient is now panning out. In 2019, an international team that included researchers from two Mass General Brigham hospitals — Mass Eye and Ear and Massachusetts General Hospital (MGH) — reported on the case of a patient who did not develop cognitive impairment until her late 70s, despite being part of a family at extremely high genetic risk for developing early-onset Alzheimer’s disease. In addition to having the genetic variant that causes an autosomal dominant form of Alzheimer’s disease, the woman had two copies of a rare variant of the APOE3 gene, called Christchurch (APOE3Ch). Now, the research team reports on an additional 27 members of the family who carry just one copy of the variant and experienced delayed disease onset.
The study, published in The New England Journal of Medicine, represents the first evidence that having one copy of the Christchurch variant may confer some level of protection against autosomal dominant Alzheimer’s disease, even if less pronounced compared to when two copies are present. The findings have important implications for drug development, suggesting the potential effects of targeting this genetic pathway.
“As a clinician, I am highly encouraged by our findings, as they suggest the potential for delaying cognitive decline and dementia in older individuals. Now we must leverage this new knowledge to develop effective treatments for dementia prevention,” said co-first author Yakeel T. Quiroz, PhD, clinical neuropsychologist and neuroimaging researcher and director of the Familial Dementia Neuroimaging Lab in the Departments of Psychiatry and Neurology at Massachusetts General Hospital.” As a neuroscientist, I’m thrilled by our findings because they underscore the complex relationship between APOE and a deterministic mutation for Alzheimer’s disease, potentially paving the way for innovative treatment approaches for Alzheimer’s disease, including targeting APOE-related pathways.”
Quiroz and her team at MGH and co-senior study author Joseph Arboleda-Velasquez, MD, PhD, of Mass Eye and Ear, have been working with their colleagues in Colombia as part of the MGH Colombia-Boston (COLBOS) biomarker study to examine family members of the world’s largest-known kindred with a genetic variant called the “Paisa” mutation (Presenilin-1 E280A). The Paisa mutation is an autosomal dominant variant, meaning that inheriting just one copy of the mutated gene from a parent is enough to cause a genetic condition. The family consists of about 6,000 blood relatives, and about 1,200 carry the variant. Carriers of this Paisa variant are destined to develop Alzheimer’s disease; most develop mild cognitive impairment in their 40s, dementia in their 50s, and die from complications of dementia in their 60s. Francisco Lopera, MD, director of the Grupo de Neurociencias de Antioquia in Medellín, Colombia, and co-senior author of the NEJM paper, is the neurologist who discovered this family and has been following them for the last 40 years.
In addition to the 2019 case report about a family member with two copies of the Christchurch variant, molecular studies have added further biological evidence that the variant could be playing a protective role. In 2023, the research team identified another “resiliency gene variant” called Reelin-COLBOS that appeared to delay the onset of symptoms in other family members. The new study in NEJM reports on a larger group of individuals from this family who carry a copy of the Christchurch variant.
“Our original study told us that protection was possible, and that was an important insight. But if a person needs two copies of a rare genetic variant, it just comes down to luck,” said co-senior author Joseph F. Arboleda-Velasquez, MD, PhD, an associate scientist at Mass Eye and Ear. “Our new study is significant because it increases our confidence that this target is not only protective, but druggable. We think that therapeutics inspired by protected humans are much more likely to work and to be safer.”
The research team assessed 1,077 descendants of the Colombian family. They identified 27 family members who carried both Paisa mutation and one copy of the Christchurch variant. On average, these family members began showing signs of cognitive impairment at age 52, compared to a matched group of family members who did not have the variant, who began showing signs at age 47. The family members also showed signs of dementia four years later than those who did not carry the variant.
Two of these individuals had functional brain imaging performed. Scans showed lower levels of tau and preserved metabolic activity in areas typically involved in Alzheimer’s disease, even in the presence of amyloid plaques — proteins considered a hallmark of Alzheimer’s disease. The team also analyzed autopsy samples from four deceased individuals that showed less pathology in blood vessels, a characteristic that appears important for the protective effects of APOE3 Christchurch.
The authors note that their study was limited to a relatively small number of people carrying both the Paisa and Christchurch variants, and to a single, extended family. They write that further studies involving larger and more ethnically diverse samples of Alzheimer’s disease may shed further light on the protective effect of the Christchurch variant and help determine if findings from the family in Colombia could translate into discoveries relevant for treating sporadic forms of Alzheimer’s disease.
“As a next step, we are currently focused on improving our understanding of the brain resilience among the remaining family members who carry one copy of the Christchurch variant. This involves conducting structural and functional MRI scans and cognitive evaluations, as well as analyzing blood samples to assess their protein and biomarker profiles,” said Quiroz. “The unwavering commitment to research shown by our Colombian patients with autosomal dominant Alzheimer’s and their families has been indispensable in making this study possible and allowing us to continue to work toward interventions for this devastating disease.”

Researchers at the National Institutes of Health (NIH) have developed a non-chemotherapy treatment regimen that is achieving full remissions for some people with aggressive B-cell lymphoma that has come back or is no longer responding to standard treatments. The five-drug combination targets multiple molecular pathways that diffuse large B-cell lymphoma (DLBCL) tumors use to survive.
In a clinical trial at NIH’s National Cancer Institute, researchers tested the combination of venetoclax, ibrutinib, prednisone, obinutuzumab, and lenalidomide (called ViPOR) in 50 patients with DLBCL, the most common type of lymphoma. The treatment shrank tumors substantially in 26 of 48 (54%) evaluable patients, with 18 (38%) of those patients’ tumors disappearing entirely, known as a complete response. At two years, 36% of all patients were alive and 34% were free of disease. These benefits were seen mainly in people with two specific subtypes of DLBCL.
The findings were published June 20, 2024, in the New England Journal of Medicine.
“Many of these patients who stopped responding to standard treatments would have otherwise died within a year, and now we have a good proportion who are still alive past two years, and some past four years,” said Christopher J. Melani, M.D., of NCI’s Center for Cancer Research, who co-led the study. “It’s gratifying to see these long-term remissions and potential cures in patients.”
Previous studies have identified various genetic pathways involved in the development and survival of the different molecular subtypes of DLBCL, such as activated B cell-like (ABC) DLBCL and germinal center B cell-like (GCB) DLBCL. Targeted drugs have shown effectiveness in blocking some of these pathways, but individual drugs rarely produced lasting responses in patients because the tumors may be resistant due to alternative survival pathways. Dr. Melani and his colleagues hypothesized that combining targeted drugs that block multiple survival pathways would lead to more durable responses.
Based on laboratory studies in which they analyzed which targeted drugs could best be combined to kill DLBCL cells in a synergistic manner, the researchers designed the five-drug regimen to test in human trials. To allow for the targeted drugs to work synergistically in patients, the researchers gave the drugs simultaneously in two-week cycles. To limit the accumulation of side effects, they scheduled a weeklong break between each cycle.
“DLBCL is one of the most genetically heterogeneous forms of cancer, and as a result we don’t yet have the ability to identify exactly which combination of drugs would be most effective for any given patient,” Dr. Melani said. “By putting five drugs together, we believe that there will be some drug combination — either two, three, or more drugs — that will be particularly effective against that patient’s tumor.”
In the phase 1b/2 trial, 50 people with DLBCL that had relapsed or stopped responding to treatment were given six cycles of the ViPOR regimen. Responses to ViPOR varied by DLBCL subtype, with complete responses concentrated in two subtypes, including in 8 of 13 (62%) people with non-GCB DLBCL and 8 of 15 (53%) people with a form of GCB DLBCL known as high-grade B-cell lymphoma “double hit.”

At two years, people with non-GCB DLBCL and double-hit GCB DLBCL had higher rates of both progression-free and overall survival than other people in the study. Non-GCB DLBCL and double-hit GCB DLBCL are highly reliant on the survival mechanisms targeted by ViPOR, so it makes sense that they responded particularly well to the combination therapy. ViPOR also helped 6 of 20 (30%) patients whose lymphomas had not responded to or had come back after CAR T-cell therapy — the current standard of care for people with relapsed DLBCL — achieve lasting remissions.
Side effects of the five-drug regimen were generally mild to moderate when compared with those of standard treatments and improved during the treatment breaks. Only five patients had to stop treatment early for various reasons, including side effects. Given these relatively mild to moderate side effects, additional drugs could potentially be added to ViPOR to improve its efficacy, the researchers said. The team is also studying the ViPOR regimen in people with other types of lymphoma that are resistant to previous therapies.
The researchers have developed a larger phase 2 study, which will be conducted at multiple centers, to confirm the activity of ViPOR in people with non-GCB DLBCL and double-hit GCB DLBCL. More work is needed to develop therapies for GCB DLBCL subtypes that aren’t as responsive to ViPOR.
NCI’s Center for Cancer Research investigators Wyndham H. Wilson, M.D., Ph.D., Mark Roschewski, M.D., and Louis M. Staudt, M.D., Ph.D., co-led the study with Dr. Melani. Investigators from NIH’s National Center for Advancing Translational Sciences and other institutions contributed to the study.

Roughly one in four U.S. households have soil exceeding the new U.S. Environmental Protection Agency’s lead screening levels of 200 parts per million (ppm), halved from the previous level of 400 ppm, a new study found. For households with exposure from multiple sources, the EPA lowered the guidance to 100 ppm; nearly 40% of households exceed that level, the study also found.
“I was shocked at how many households were above the new 200 ppm guideline,” said Gabriel Filippelli, a biochemist at Indiana University who led the new study. “I assumed it was going to be a more modest number. And results for the 100 ppm guideline are even worse.”
Remediating the roughly 29 million affected households using traditional “dig and dump” soil removal methods could cost upward of $1 trillion, the study calculated. The study was published in GeoHealth, an open-access AGU journal that publishes research investigating the intersection of human and planetary health for a sustainable future. Filippelli is the former editor-in-chief of GeoHealth.
National lead problem “nowhere near over”
Lead is a heavy metal that can accumulate in the human body, with toxic effects. In children, exposure to lead is associated with lower educational outcomes. In the United States, the burden of lead exposure has historically fallen on lower-income communities and communities of color because of redlining and other discriminatory practices. Lead pollution can come from aging water pipes, old paint, and remnant gasoline and industrial pollution, but today, most lead exposure are from contaminated soils and dust, even after lead-containing infrastructure was removed.
The Centers for Disease Control and Prevention first set a limit on the concentration of lead in blood in 1991 at 10 micrograms per deciliter, and it lowered that limit several times until reaching the current limit of 3.5 micrograms per deciliter. But the EPA’s soil lead screening level remained unchanged for more than 30 years until the January announcement. Some states had established their own lower guidelines; California has the lowest screening level, at 80 ppm.
The lag is likely due to “the immensity and ubiquity of the problem,” the study authors wrote. “The scale is astounding, and the nation’s lead and remediation efforts just became substantially more complicated.” That’s because once the EPA lowers a screening limit, they need to tell people what to do if their soils exceed it.

When the EPA lowered the screening level, Filippelli and his co-authors decided to make use of the database of 15,595 residential soil samples from the contiguous United States that they’d collected over the years to find out how many exceeded the new guideline.
Household health hazard
About 25% of the residential soil samples, collected from yards, gardens, alleys, and other residential spots, exceeded the new 200 ppm level, the study found. (Only 12% of samples had exceeded the older, 400 ppm level.) Extrapolating across the country, that equates to roughly 29 million households.
The EPA issued separate guidance for households with multiple sources of exposure, such as both lead-contaminated soil and lead pipes, setting the level in those situations at 100 ppm. In practice, that’s most urban households, Filippelli said. Forty percent of households exceed that limit, increasing the number of affected households to nearly 50 million, the study found.
Typically, contaminated soils are remediated with removal — colloquially, “dig and dump.” But the practice is costly and typically only used after an area is placed on the National Priority List for remediation, a process that can take years. To remediate all contaminated households with “dig and dump” would cost between $290 billion and $1.2 trillion, the authors calculated.
A cheaper option is “capping”: burying the contaminated soil with about a foot of soil or mulch. A geotechnical fabric barrier can also be installed. Most lead contamination is in the top 10 to 12 inches of soil, Filippelli said, so this simple method either covers up the problem or dilutes it to an acceptable level.

“Urban gardeners have been doing this forever anyway, with raised beds, because they’re intuitively concerned about the history of land use at their house,” Filippelli said.
And capping is quicker.
“A huge advantage of capping is speed. It immediately reduces exposure,” Filippelli said. “You’re not waiting two years on a list to have your yard remediated while your child is getting poisoned. It’s done in a weekend.”
Capping still requires time and effort; residents must find clean soil, transport it to their home and spread it out. But the health benefits likely outweigh those costs, Filippelli said.
Because capping has been done more informally, there’s still a lot to be learned about its lifespan and sustainability, Filippelli said. That’s where the research will go next.
Despite the “staggering” scale of the problem, “I’m really optimistic,” Filippelli said. “Lead is the most easily solvable problem that we have. We know where it is, and we know how to avoid it. It’s just a matter of taking action.”
Maps: https://www.mapmyenvironment.com/

In low- and middle-income countries, anemia reduction efforts are often touted as a way to improve educational outcomes and reduce poverty. A new study, co-authored by a global health economics expert from the University of Notre Dame, evaluates the relationship between anemia and school attendance in India, debunking earlier research that could have misguided policy interventions.
Santosh Kumar, associate professor of development and global health economics at Notre Dame’s Keough School of Global Affairs, is co-author of the study, published in Communications Medicine. Kumar’s research explores the intersection of global health and poverty reduction. His latest work evaluates the relationship between anemia and school attendance in India.
The study investigated whether there was a link between anemia and school attendance in more than 250,000 adolescents ages 15 to 18. Earlier observational studies have shown a link between anemia and attendance, even after accounting for variables such as gender and household wealth, according to Kumar. But the new study, which applied more rigorous econometric statistical analysis, did not find such a link, he said.
“Most previous research on this topic has used conventional study designs or focused on small geographical areas, which limits its policy relevance,” Kumar said. “Earlier estimates may have been distorted by unobserved household factors related to both anemia and school attendance. So in this study, we focused on the relationship between anemia and attendance among adolescents who were living in the same household.
“Ultimately,” Kumar said, “we found that the link between anemia and schooling is more muted than previously suggested by studies that did not consider household-level factors.”
The findings have important implications for policymakers seeking to improve education in low- and middle-income countries like India, Kumar said. India has widespread school attendance issues and struggles with health conditions such as anemia caused by iron deficiency, particularly in children and adolescents. The country has pushed to improve educational outcomes, in keeping with the United Nations’ Sustainable Development Goals, Kumar said. But to achieve that, he said, more research is needed to pinpoint an evidence-based intervention.
This study is part of an ongoing project to do that work and was co-authored with Jan-Walter De Neve of the University of Heidelberg, Omar Karlsson of Lund University in Sweden, Rajesh Kumar Rai of Harvard University and Sebastian Vollmer of the University of Göttingen. The project received funding from the Alexander von Humboldt Foundation, the Swedish Research Council and the West Bengal State Department of Health and Family Welfare in India.
The latest study builds on an earlier one in which Kumar and fellow researchers helped evaluate the results of an iron fortification school lunch program for students ages 7 and 8 in India. That study showed that fortification reduced anemia but did not affect students’ performance in school. A forthcoming study, set to launch in summer 2024, will look at iron fortification for children ages 3 to 5. The research hypothesis is that an early-age nutritional intervention among preschoolers would make a significant impact on physical and cognitive development.
“Our findings have implications for policymakers who want to improve educational outcomes and reduce poverty,” Kumar said. “Effective policies are based on evidence. We need more rigorous statistical analysis to examine the causal relationship between anemia and education.
“This work ties into my larger research agenda, which explores the intersection of global health and poverty reduction. I want to use my academic research to support human dignity by helping to identify evidence-based health policies that will make a tangible difference in people’s lives.”