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On the evening of Jan. 15, 2021, in a remote Arizona desert town, Christine Benton saved a life.She and her husband, Brian Benton, were traveling the country in a recreational vehicle and had parked near other R.V.ers at a winery in Willcox. As the couple were eating dinner, someone started shouting from an R.V. behind them. A woman had collapsed and was in cardiac arrest. She had no pulse. Frantic, her husband called 911 while two other people started cardiopulmonary resuscitation.“She looked like she was gone,” said Ms. Benton, a retired paramedic firefighter.But Ms. Benton had made a consequential decision before she and her husband started out: She had bought a personal automated external defibrillator, or A.E.D., which can shock a person’s heart back to life if it suddenly stops beating. Her plan was to to keep it with her, just in case. It was expensive, it was highly unlikely she would ever use it and her husband was hesitant. But she was adamant.“If I were ever in a situation where I could save a life and I didn’t have an A.E.D., I could never live with myself,” she told her husband at the time.As a firefighter, Ms. Benton had been trained to use a defibrillator. She knew that if someone’s heart stopped, a rescuer should start CPR immediately, pushing hard and rhythmically on the chest, while another rescuer went to get an A.E.D. As soon as that second rescuer returned, the A.E.D. should be used.And Ms. Benton knew that A.E.D.s were easy to use, even for someone with no training. The device speaks to rescuers and tells them how to proceed.But even though all states have laws requiring that A.E.D.s be available in public places, Ms. Benton worried that if someone had a cardiac arrest in a place where the nearest A.E.D. was miles away, the person might die — minutes count when reviving someone in cardiac arrest. For every one-minute delay in resuscitation, the likelihood of survival falls by up to 10 percent.For Ms. Benton, the decision to buy an A.E.D. made perfect sense. I also ordered one for myself after reporting on the football player Damar Hamlin’s on-field cardiac arrest. When it arrives I am going to tell my neighborhood’s Google group that I have it.Christine Benton, a retired paramedic firefighter, had been trained to use a defibrillator, but also knew that A.E.D.s are easy to use, even for people with no training.Ash Ponders for The New York TimesBut emergency medicine specialists are divided on whether it makes sense for anyone to buy one.They know that A.E.D.s in public places like airports, where thousands of people pass by every day, can make a difference and they urge people to use them if they see someone who needs help. In the U.S., 85 to 90 percent of people who have sudden cardiac arrests do not survive and many cannot be revived, often because resuscitation attempts start too late.But the situation is different in the home.For one, there is the expense — the devices often cost more than $1,000, making them far less affordable to the average person than home medical devices like a blood pressure monitor or a pulse oximeter. While there are efforts to develop cheaper A.E.D.s, they are still underway, according to Monica Sales, a spokeswoman for the American Heart Association.The price is not the only thing that gives some specialists pause. The odds are so stacked against a dramatic save that it has proved impossible to show that personal A.E.D.’s make a difference.An estimated 1,000 people a day in the U.S. have sudden cardiac arrests, in which the heart stops beating and the person is technically dead. But that represents a minuscule portion of the American population.Even people at high risk of a sudden cardiac arrest were not helped by home A.E.D.s, a large study showed. It involved 7,001 people who had previously had heart attacks and who were randomly assigned to receive an A.E.D. or to be in a control group.Despite the huge number of study participants, very few had cardiac arrests and, even when they did, the arrests often did not occur at home or were not witnessed. In the end, just eight people in each group were resuscitated at home. The authors concluded that even if the study’s size were doubled, there would be too few events to detect an effect of home A.E.D.s.But think of an A.E.D. like a fire extinguisher, said Dr. Benjamin Abella, an emergency medicine specialist at the University of Pennsylvania. You might never use it, but having one might one day save a life.“I think it’s a terrific idea” to own one, Dr. Abella said. He recently ordered an A.E.D. for himself.For the same reason, the American Heart Association supports anyone who wants to get an A.E.D., said Dr. Comilla Sasson, a vice president at the American Heart Association and an emergency medicine physician at the University of Colorado Denver.“If we could just reduce the stigma around, ‘Hey, I can’t do this because I’m not a medical professional,’” she said. “And you don’t need to have CPR certification to use an A.E.D.”But Dr. Sumeet S. Chugh, director of the Center for Cardiac Arrest Prevention at Cedars Sinai in Los Angeles, has his doubts.“I don’t think we have the data to support widespread prophylactic purchases of A.E.D.s even if you can afford it,” he said. And, he added, many who go into cardiac arrest do not have a shockable condition. One example is asystole, a flat line on the heart monitor indicating there is no electrical activity in the heart. An A.E.D. cannot revive people with unshockable rhythms. Other patients are not discovered in time for their heart to be shocked back to life.Karen Schluter, whose life was saved in 2021 after Ms. Benton shocked her heart back into action after she had a cardiac arrest. Without the A.E.D., Ms. Schluter would have died.Andy Manis for The New York TimesThat was the situation that Mary Newman found herself in. Ms. Newman, co-founder of the Sudden Cardiac Arrest Foundation, which promotes awareness of cardiac arrest and has a support group for survivors, has an A.E.D. But when her mother collapsed in the bathroom during a family vacation, no one realized she was missing. By the time the family found her, it was too late to save her.Yet there are rare examples of people who did save a life with a personal A.E.D.One involved Esley Thorton, Jr. of Bismarck, N.D.At about 8 a.m. on Nov. 25, 2019, Mr. Thornton sank into his favorite chair, inexplicably tired.A few minutes later his wife, Melinda, heard an odd noise and came running into the room. “His body was contorted,” she said. “He was gasping for air.”Then he stopped breathing. His heart had stopped.Ms. Thornton screamed for her son Rhannon, who called 911 and grabbed an A.E.D. that another son, who works for the A.E.D. maker Stryker, had given his parents as a gift two years earlier.Rhannon put the device’s pads on his father’s chest. It said, “No pulse, administer shock,” Ms. Thornton recalled.He pressed a button.“Shock administered,” the device said.“We heard him take a deep breath,” Ms. Thornton said. Her husband’s heart was beating again.An ambulance came eight minutes after the 911 call — long enough that without Rhannon’s help, Mr. Thornton might have died or had serious brain damage.One of the paramedics was astonished, telling the family that he had been a paramedic for 22 years but had never before seen a personal A.E.D. used in a patient’s home.In Ms. Benton’s case, the woman whose heart had stopped began breathing again less than 20 seconds after Ms. Benton shocked her heart with the A.E.D.Without the A.E.D., the woman, Karen Schluter, would have died — CPR alone would not have been sufficient in that remote location where it took about half an hour for an ambulance to arrive.Yet no one would have predicted that Ms. Schluter was at risk. She was 52 and athletic — an avid bicyclist.Now Ms. Benton and Ms. Schluter are good friends. Ms. Schluter has purchased an A.E.D. and so have others whose R.V.s were parked there that evening.When the Bentons returned to their R.V. after their A.E.D. saved Ms. Schluter’s life, Mr. Benton looked at his wife and said, “I am sure glad you didn’t listen to me about buying that A.E.D.”

Published7 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy Sean SeddonBBC NewsOne million smokers will be given a free vaping starter kit to encourage them to give up tobacco products.Pregnant women will also be offered up to £400 to stop smoking as part of a package of measures in England to be unveiled by the government on Tuesday.A consultation will be launched on compelling cigarette manufacturers to put advice on quitting inside packs.The government has committed to getting smoking rates in England below 5% by 2030.The plans also include a crackdown on underage and illicit vape sales.Almost one in five smokers in England will receive a kit alongside behavioural support, the government said. In a speech on Tuesday, health minister Neil O’Brien is expected to say the free vape policy – dubbed “swap to stop” – is the first of its kind in the world.”Up to two out of three lifelong smokers will die from smoking. Cigarettes are the only product on sale which will kill you if used correctly,” he will say.It is estimated that 9% of women still smoke during pregnancy in England, and the government says local trials indicate that financial incentives and behavioural support can be effective. The Department of Health and Social Care (DHSC) said it would set out details on how this scheme will work “in due course”.Local authorities are being invited to join the first wave of areas taking part in the free vape policy, before a larger national scheme is rolled out over the next two years.Officials estimate it will cost around £45 million and is set to be funded from the health department’s budget, but administered by local authorities. Deborah Arnott, chief executive of the Action on Smoking and Health campaign, said the policy announcements are “welcome steps in the right direction”.But she warned the moves are “nowhere near sufficient” as the target date for England becoming “smoke free” by 2030 nears.Image source, PA MediaIn 2019, ministers pledged to end smoking – defined as getting rates below 5% – by the end of the decade. As of 2021, smoking prevalence in England was 13%, the lowest on record.But a review of the 2030 target published last year warned it will be missed by at least seven years without further action.Its author, Dr Javed Khan, called for a range of new measures, including a ban on smoking at outdoor spaces such as beaches and beer gardens.He also proposed increasing the age of sale from 18, by one year, every year, “until no one can buy a tobacco product in this country”.The same report recommended promoting vaping as an alternative to tobacco, but said e-cigarettes are not a “silver bullet” or “totally risk free”.While the government wants to encourage adult smokers to swap cigarettes for vapes, there are concerns about the rising popularity of the products among children.NHS figures released last year revealed 9% of secondary school pupils use a vape regularly or occasionally, including almost one in five 15 year olds.The government announced earlier this week it is setting up a new trading standards enforcement squad to crack down on vapes being sold illegally to under-18s.A full consultation on how young people can be discouraged from taking up the habit is also being launched on Tuesday. More on this storyVaping – is it a risk-free option?24 June 2022The secret vault of illegal vapes14 MarchNew measures to crack down on illegal teen vaping2 days ago

Published1 hour agoShareclose panelShare pageCopy linkAbout sharingThis video can not be playedTo play this video you need to enable JavaScript in your browser.By Holly HonderichBBC News, WashingtonThe US Department of Justice has appealed against a Texas judge’s decision to suspend approval of the abortion pill mifepristone.The Biden administration lawyers said last week’s “misguided” ruling risked women’s health by blocking access to a pill long cleared as safe.The Texas judge last week halted authorisation of the drug, but gave the government seven days to appeal.Used in most US abortions, the pill has been allowed for over 20 years.The battle looks likely to head for the Supreme Court, placing a question mark over access to the drug for millions of women.The legal showdown could herald the biggest blow to abortion access since the country’s top court last summer ruled there was no nationwide right to terminate a pregnancy.For now, the pill is still available.This video can not be playedTo play this video you need to enable JavaScript in your browser.On Monday, the justice department filed an emergency motion, seeking to temporarily block last Friday’s ruling in Amarillo, Texas.The Biden administration lawyers have asked for a decision by 13 April – one day before the lower court’s decision is set to take effect.The government said the Texas ruling was “especially unwarranted” because it would subvert the scientific judgement of the Food and Drug Administration (FDA), which authorises medication in the US.The government’s motion, if successful, would preserve mifepristone’s approval until an appeal can be heard before the Fifth Circuit Court of Appeals.Lawrence Gostin, a professor of global health law at Georgetown University, told the BBC: “This is such a poorly reasoned decision, I would hope that the Fifth Circuit would immediately stay the injunction and ultimately – on merits – strike down the Texas decision.”But that’s not a certainty. This is probably the most conservative appellate court in America, so it’s possible they will validate the [Texas] decision.””If the FDA can’t approve this drug, I’m not sure what the FDA can approve,” Professor Gostin added. “It’s been on the market for over two decades, it’s got an impeccable health and safety record.”How safe is the abortion pill mifepristone?Man sues women for helping ex-wife get abortion Can these boxes found on US streets save babies’ lives?If the justice department does not win on this emergency motion, called a stay, its lawyers will take the case to the conservative-dominated Supreme Court within hours, legal experts predict.Mifepristone is part of a two-drug regimen that induces abortions.The pill effectively stops a pregnancy, while a second drug, misoprostol, empties the uterus.The Alliance Defending Freedom, a conservative Christian legal advocacy group that represented plaintiffs in the Texas lawsuit, argued that the FDA in its four-year approval process had ignored the potential impacts of mifepristone on the developing bodies of adolescent girls.Its senior counsel, Erin Hawley, said on Monday: “By illegally approving dangerous chemical abortion drugs, and imposing its mail-order abortion regime, the FDA put women in harm’s way, and the agency should be held accountable for its reckless actions.”Pregnancy is not an illness, and chemical abortion drugs don’t provide a therapeutic benefit.”Image source, ReutersMainstream medical organisations such as the American College of Obstetrics and Gynaecologists and the World Health Organization say mifepristone is safe and effective.Friday’s ruling by Judge Matthew Kacsmaryk in Texas declared the FDA’s approval of mifepristone in 2000 to be invalid.In a 67-page opinion, the Trump-appointee said the FDA had violated federal rules that allow for accelerated approval of certain drugs.But just 18 minutes after the Texas decision, another federal judge, this one an Obama appointee in Washington state, ordered that access to mifepristone be preserved in 17 liberal states.William Eskridge, a law professor at Yale University, told the BBC: “The injunction in the Washington case applies to 17 states, and the injunction in the Texas case applies to 50 states.”That puts a lot of pressure on the Supreme Court to take review [of the case] sooner rather than later.”On Monday, more than 300 pharmaceutical executives, including Pfizer CEO Albert Bourla, called for the reversal of the Texas decision, saying it was a “decision to disregard science”.With reporting from Madeline HalpertMore on this storyUS abortion pill access in doubt after court rulings2 days agoHow safe is the abortion pill mifepristone?2 days agoAfter Roe, anti-abortion activists eye new target12 July 2022

Brain development does not occur uniformly across the brain, but follows a newly identified developmental sequence, according to a new Penn Medicine study. Brain regions that support cognitive, social, and emotional functions appear to remain malleable — or capable of changing, adapting, and remodeling — longer than other brain regions, rendering youth sensitive to socioeconomic environments through adolescence. The findings were published recently in Nature Neuroscience.
Researchers charted how developmental processes unfold across the human brain from the ages of 8 to 23 years old through magnetic resonance imaging (MRI). The findings indicate a new approach to understanding the order in which individual brain regions show reductions in plasticity during development.
Brain plasticity refers to the capacity for neural circuits — connections and pathways in the brain for thought, emotion, and movement — to change or reorganize in response to internal biological signals or the external environment. While it is generally understood that children have higher brain plasticity than adults, this study provides new insights into where and when reductions in plasticity occur in the brain throughout childhood and adolescence.
The findings reveal that reductions in brain plasticity occur earliest in “sensory-motor” regions, such as visual and auditory regions, and occur later in “associative” regions, such as those involved in higher-order thinking (problem solving and social learning). As a result, brain regions that support executive, social, and emotional functions appear to be particularly malleable and responsive to the environment during early adolescence, as plasticity occurs later in development.
“Studying brain development in the living human brain is challenging. A lot of neuroscientists’ understanding about brain plasticity during development actually comes from studies conducted with rodents. But rodent brains do not have many of what we refer to as the association regions of the human brain, so we know less about how these important areas develop,” said corresponding author Theodore D. Satterthwaite, MD, the McLure Associate Professor of Psychiatry in the Perelman School of Medicine at the University of Pennsylvania, and director of the Penn Lifespan Informatics and Neuroimaging Center (PennLINC).
To address this challenge, the researchers focused on comparing insights from previous rodent studies to youth MRI imaging insights. Prior research examining how neural circuits behave when they are plastic uncovered that brain plasticity is linked to a unique pattern of “intrinsic” brain activity. Intrinsic activity is the neural activity occurring in a part of the brain when it is at rest, or not being engaged by external stimuli or a mental task. When a brain region is less developed and more plastic, there tends to be more intrinsic activity within the region, and that activity also tends to be more synchronized. This is because more neurons in the region are active, and they tend to be active at the same time. As a result, measurements of brain activity waves show an increase in amplitude(or height).

“Imagine that individual neurons within a region of the brain are like instruments in an orchestra. As more instruments begin to play together in synchrony, the sound level of the orchestra increases, and the amplitude of the sound wave gets higher,” said first author Valerie Sydnor,a Neuroscience PhD student. “Just like decibel meters can measure the amplitude of a sound wave, the amplitude of intrinsic brain activity can be measured with functional MRI while kids are simply resting in the scanner. This allowed our team to study a functional marker of brain plasticity safely and non-invasively in youth.”
Analyzing MRI scans from more than 1,000 individuals, the authors found that the functional marker of brain plasticity declined in earlier childhood in sensory-motor regions but did not decline until mid-adolescence in associative regions.
“These slow-developing associative regions are also those that are vital for children’s cognitive attainment, social interactions, and emotional well-being,” Satterthwaite added. “We are really starting to understand the uniqueness of human’s prolonged developmental program.”
“If a brain region remains malleable for longer, it may also remain sensitive to environmental influences for a longer window of development,” Sydnor said. “This study found evidence for just that.”
The authors studied relationships between youths’ socioeconomic environments and the same functional marker of plasticity. They found that the effects of the environment on the brain were not uniform across regions nor static across development. Rather, the effects of the environment on the brain changed as the identified developmental sequence progressed.

Critically, youths’ socioeconomic environments generally had a larger impact on brain development in the late-maturing associative brain regions, and the impact was found to be largest in adolescence.
“This work lays the foundation for understanding how the environment shapes neurodevelopmental trajectories even through the teenage years,” said Bart Larsen, PhD, a PennLINC postdoctoral researcher and co-author.
Sydnor elaborated, “The hope is that studying developmental plasticity will help us to understand when environmental enrichment programs will have a beneficial impact on each child’s neurodevelopmental trajectory. Our findings support that programs designed to alleviate disparities in youths’ socioeconomic environments remain important for brain development throughout the adolescent period.”
This study was supported by the National Institute of Health (R01MH113550, R01MH120482, R01MH112847, R01MH119219, R01MH123563, R01MH119185, R01MH120174, R01NS060910, R01EB022573, RF1MH116920., RF1MH121867, R37MH125829, R34DA050297, K08MH120564, K99MH127293, T32MH014654). The study was also supported by the National Science Foundation Graduate Research Fellowship (DGE-1845298).
Additional support was provided by the Penn-CHOP Lifespan Brain Institute and the Penn Center for Biomedical Image Computing and Analytics.

A new drug, a monoclonal antibody known as enoblituzumab, is safe in men with aggressive prostate cancer and may induce clinical activity against cancer throughout the body, according to a phase 2 study led by investigators at the Johns Hopkins Kimmel Cancer Center and its Bloomberg~Kimmel Institute for Cancer Immunotherapy. If confirmed in additional studies, enoblituzumab could become the first promising antibody-based immunotherapy agent against prostate cancer.
In a clinical trial, 32 men with high-risk or very high-risk prostate cancers who were scheduled for prostate cancer surgery were treated with six weekly infusions of enoblituzumab prior to surgery, and were followed for an average of 30 months thereafter. Twenty-one patients, or 66%, had an undetectable prostate-specific antigen (PSA) level 12 months following surgery, suggesting that there was no sign of residual disease. Additionally, the drug was well-tolerated overall; no patients had any surgical delays or medical complications during or after the operation.
A description of the work was published April 3 in the journal Nature Medicine.
If enoblituzumab continues to perform well in further larger randomized studies, it could represent a new pathway for immunotherapy against multiple cancers, and the first one that may have a role for prostate cancer, says lead study author and cancer immunology researcher Eugene Shenderov, M.D., Ph.D., assistant professor of oncology at the Johns Hopkins University School of Medicine. Other existing antibody-based immunotherapy drugs have targeted immune checkpoints, natural on/off switches mediating immune responses, such as CTLA-4, PD-1 and LAG-3. Cancer cells hijack these checkpoints, turning off the immune response to cancer. “Drugs that block these checkpoints have had success in other types of cancers, including lung cancer and melanoma, but not in prostate cancer,” says Shenderov.
Enoblituzumab works by binding to a protein called B7-H3 that is overexpressed on prostate cancer cells and believed to impede the immune system’s ability to attack cancer cells. The new therapy could pack a one-two punch against cancer, Shenderov says, by blocking B7-H3’s inhibition of the immune system’s recognition and elimination of cancer cells, and also triggering a process called antibody-dependent cellular cytoxicity (ADCC), which leads to tumor cell destruction by activating additional immune cells such as macrophages and natural killer cells.
“Enoblituzumab appears safe and seems to activate the immune system in a way that involves both T-cells and myeloid cells,” Shenderov says. “What this means is if these results can be replicated in a larger, randomized study, it opens the possibility that combining this therapy with local, curative-intent therapies like surgical prostate removal or radiation therapy, would allow this drug to potentially kill micrometastatic disease hiding elsewhere in the body, and therefore prevent a significant number of men from experiencing recurring disease. That could be a paradigm shift in prostate cancer.”
The median age of study participants was 64 (age range 48-74). About half (47%) had a PSA greater than 10 ng/mL at diagnosis, which is abnormally high, and 50% had Gleason grade group 5 at biopsy, meaning they had highly aggressive disease. Patients were enrolled from February 2017 through June 2019. Enoblituzumab was confirmed to penetrate into prostate tumors and to bind to B7-H3 in the vast majority of participants, according to prostate samples studied after surgery.

Side effects of enoblituzumab were generally mild and included fatigue, neurological symptoms such as headache or dizziness, and flu-like or cold symptoms. One patient developed inflammation of the heart (myocarditis), which fully resolved with steroid treatment, and is a known side effect of other immune checkpoint drugs.
Beyond safety and anti-tumor activity based on PSA dropping to undetectable levels, investigators also looked for changes in the tumor microenvironment before and after enoblituzumab treatment. They found increased markers of cytotoxicity after treatment, consistent with the concept that the immune system was activated against tumor cells. The tumors showed increased infiltration with granulocytes, leukocytes and effector T-cells, and there was roughly a doubling of the density of cytotoxic T cells after treatment.
“The findings are exciting but exploratory, and need to be confirmed in larger study cohorts,” cautions senior study author Emmanuel S. Antonarakis, M.D., the Clark Endowed Professor of Medicine and director of GU Oncology for the University of Minnesota Masonic Cancer Center. Antonarakis was the senior investigator of the study while he was at the Johns Hopkins Kimmel Cancer Center.
“However, these results in high-risk prostate cancer patients, and the broader need for immunotherapeutic strategies with efficacy in prostate cancers, provide justification to further develop multipronged approaches that include targeting B7-H3 to optimize antitumor activity in prostate cancers and other solid malignancies,” he says.
Investigators are now planning a larger, randomized trial of enoblituzumab in newly diagnosed prostate cancer patients to assess clinical activity of the drug compared to current standards of care.
Coauthors of the current study were Angelo M. De Marzo, Tamara L. Lotan, Hao Wang, Sin Chan, Su Jin Lim, Hogkai Ji, Mohamad El Allaf, Carolyn Chapman, Samuel R. Denmeade, Kenneth J. Pienta, Christian P. Pavlovich, and Drew M. Pardoll of Johns Hopkins. Other study authors contributing to the paper were from MacroGenics Inc. of Rockville, Maryland (the maker of enoblituzumab); NanoString Technologies Inc. of Seattle; Adaptive Biotechnologies of Seattle; CDI Labs of Baltimore; the Northwestern University Feinberg School of Medicine in Chicago; and Charles G. Drake formerly at Johns Hopkins, who currently leads Immuno-Oncology at Janssen Research and Development.
The work was supported by the National Institutes of Health (Cancer Center Support Grant P30 CA006973), an NCI SPORE in Prostate Cancer (P50CA58236), a Prostate Cancer Foundation Young Investigator Award, the Department of Defense (grants W81XWH-16-PCRP-CCRSA and W81XWH-18-2-0015), and the Bloomberg~Kimmel Institute for Cancer Immunotherapy and by Macrogenics Inc, of Rockville, Maryland.
E. Shenderov is a paid consultant to GT Biopharma, Guidepoint Global, FirstThought, GLG, and receives institutional research funding from MacroGenics Inc., manufacturer of enoblituzumab. These relationships are managed by The Johns Hopkins University in accordance with its conflict of interest policies. E. Antonarakis has served as a paid consultant for Janssen, Astellas, Sanofi, Bayer, Bristol Myers Squibb, Amgen, Constellation, Blue Earth, Exact Sciences, Invitae, Curium, Pfizer, Merck, AstraZeneca, Clovis and Eli Lilly; and has received research support from MacroGenics, Janssen, Johnson & Johnson, Sanofi, Bristol Myers Squibb, Pfizer, AstraZeneca, Novartis, Curium, Constellation, Celgene, Merck, Bayer, Clovis and Orion. These relationships are managed by the University of Minnesota (Antonarakis’ current institution) in accordance with their conflict of interest policies.

Tulane University researchers have discovered a possible genetic cause for hypermobility (commonly known as double-jointedness) and a range of associated connective tissue disorders such as hypermobile Ehlers-Danlos syndrome, according to preliminary findings published in the journal Heliyon.
You may know someone with overly flexible joints, a friend or family member who can easily slide into a split or bend limbs to impossible angles. But hypermobility is a more serious condition than being “double-jointed.”
For those with hypermobile Ehlers-Danlos syndrome (EDS), the same conditions that create fragile connective tissue can cause a range of symptoms that, on the surface, can seem unrelated: physical conditions such as joint pain, chronic fatigue, thin tooth enamel, dizziness, digestive trouble and migraines; and psychiatric disorders, such as anxiety and depression. Women with hypermobile EDS may also be at increased risk for endometriosis or uterine fibroids.
Researchers have long struggled to find the cause of hypermobility and hypermobile EDS. Of the 13 subtypes of EDS, hypermobile EDS comprises more than 90% of the cases. But until this study, hypermobile EDS was the only subtype without a known genetic correlate. As a result, symptoms have often been treated individually rather than as the result of a single cause.
Researchers at Tulane University School of Medicine have linked hypermobility to a deficiency of folate — the natural form of vitamin B9 — caused by a variation of the MTHFR gene.
“You’ve got millions of people that likely have this, and until now, there’s been no known cause we’ve known to treat,” said Dr. Gregory Bix, director of the Tulane University Clinical Neuroscience Research Center. “It’s a big deal.”
Those with this genetic variant can’t metabolize folate, which causes unmetabolized folate to accumulate in the bloodstream. The folate deficiency may prevent key proteins from binding collagen to the extracellular matrix. This results in more elastic connective tissue, hypermobility, and a potential cascade of associated conditions.

The discovery could help doctors more accurately diagnose hypermobility and hypermobile EDS by looking for elevated folate levels in blood tests as well as the MTHFR genetic variant.
“Hypermobility is widespread and unfortunately under-recognized,” said Dr. Jacques Courseault, medical director of the Tulane Fascia Institute and Treatment Center. “I’m excited about being able to treat the masses where people aren’t going their whole lives being frustrated and not getting the treatment they need.”
Previously, hypermobility could only be diagnosed by the Beighton score, a somewhat controversial physical exam that involves measuring the bend of the spine, fingers and limbs. Combined with a historic lack of acceptance of hypermobility as a distinct body type that requires specialized treatment, the number of people with hypermobility is unclear, though it could comprise more than half the world’s population.
“Hypermobility is not rare,” Courseault said. “Hypermobility is like a Ferrari that requires a lot of maintenance and the best synthetic oil. After knowing a patient’s name and date of birth, I think it’s prudent for clinicians to know which of these body types they have.”
Doctors discovered the connection between folate deficiency and the MTHFR gene by working with patients at Tulane’s Hypermobility and Ehlers-Danlos Clinic, the only such clinic in the U.S. that focuses on fascia disorders. Blood tests of hypermobile patients who showed signs of associated medical conditions revealed elevated levels of unmetabolized folate. Subsequent tests showed that most of those with elevated folate serum levels had the genetic polymorphism.

The good news is a treatment already exists. Methylated folate — folate that is already processed — is FDA-approved and widely available.
“It’s an innocuous treatment,” Bix said. “It’s not dangerous, and it’s a vitamin that can improve people’s lives. That’s the biggest thing: We know what’s going on here, and we can treat it.”
Though Courseault said more lab research and clinical testing needs to be done, patients who have been treated with folate have shown improvement: less pain, less brain fog, fewer allergies and improved gastrointestinal function.
“We’ve discovered something in medicine that can help, not a small group of people, but potentially many across the world,” Courseault said. “This is real, it’s been vetted out well and clinically we’re noticing a difference.”

Non-biological factors and social determinants of health are important to include in CVD risk assessment for women, particularly for women of diverse races and ethnicities other than white, according to a new American Heart Association scientific statement published today in Circulation, the Association’s flagship, peer-reviewed journal.
“Risk assessment is the first step in preventing heart disease, yet there are many limitations to traditional risk factors and their ability to comprehensively estimate a woman’s risk for cardiovascular disease,” said Jennifer H. Mieres, M.D., FAHA, vice chair of the scientific statement writing committee and a professor of cardiology at the Zucker School of Medicine at Hofstra Northwell in Hempstead, N.Y. Of note, large patient data registries used to develop cardiovascular risk assessment formulas or algorithms lack racial and ethnic diversity, so they may not accurately reflect risk for women of underrepresented groups.
A 2022 American Heart Association presidential advisory deemed it critical to understand the impact of race and ethnicity on cardiovascular risk factors in women in order to incorporate those specific risks into prevention plans and reduce the high burden of CVD among women from diverse backgrounds. This new scientific statement responds to the presidential advisory as a review of the current evidence on racial and ethnic differences in cardiovascular risk factors for women in the U.S.
What traditional risk formulas miss about women in general
Traditional formulas to determine cardiovascular disease risk include Type 2 diabetes, blood pressure, cholesterol, family history, smoking status, physical activity level, diet and weight. These formulas do not account for sex-specific biological influences on cardiovascular risk or medications and conditions that are more common among women than men.
Female-specific factors that should be included in assessing cardiovascular risk are: Pregnancy-related conditions, such as preeclampsia (dangerous high blood pressure that develops late in pregnancy), preterm delivery, gestational diabetes, gestational high blood pressure or miscarriage. According to the Association of Black Cardiologists, 2 out of 3 women who experience preeclampsia will die of heart disease. Menstrual cycle history, such as age at first period and at menopause. Types of birth control and/or hormone replacement therapy used. History of chemotherapy or radiation therapy. Polycystic ovarian syndrome (PCOS) — a condition that results in hormone imbalance and irregular ovulation. PCOS affects up to 10% of women of reproductive age and is associated with higher risk for cardiovascular disease. Autoimmune disorders — women are twice as likely as men to develop autoimmune disorders such as rheumatoid arthritis or lupus. These conditions are associated with faster build-up of plaque in the arteries, higher risk of cardiovascular disease and worse outcomes after heart attacks and strokes. Depression and posttraumatic stress disorder — both are more common among women and associated with a higher risk of developing CVD.”The delivery of equitable cardiovascular health care for women depends on improving the knowledge and awareness of all members of the health care team about the full spectrum of cardiovascular risk factors for women, including female-specific and female-predominant risk factors,” said Mieres, who is also the chief diversity and inclusion officer at Northwell Health.

Importance of social determinants of health in risk assessment
Social determinants of health play a significant role in the development of CVD among women, with disproportionate effects on women from diverse racial and ethnic backgrounds. These determinants include economic stability, neighborhood safety, working conditions, environmental hazards (such as exposure to air pollution), education level and access to quality health care. The impact of social factors is recognized in how they affect behavioral risk factors, such as smoking status, physical activity, diet and proper medication use.
“It is critical that risk assessment be expanded to include social determinants of health as risk factors if we are to improve health outcomes in all women,” said Laxmi S. Mehta, M.D., FAHA, chair of the writing group and director of preventative cardiology and women’s cardiovascular health at The Ohio State University Wexner Medical Center in Columbus, Ohio. “It is also important for the health care team to consider social determinants of health when working with women on shared decisions about cardiovascular disease prevention and treatment.”
Differences in women’s cardiovascular disease risk by race and ethnicity
Although cardiovascular disease is the leading cause of death for all women, the statement highlights significant racial and ethnic differences in cardiovascular risk profiles: Non-Hispanic Black women (an umbrella term encompassing African American, African and Caribbean) in the U.S. have the highest prevalence of high blood pressure in the world, above 50%. They are also more likely to develop Type 2 diabetes; have obesity or extreme obesity; and to die of smoking-related diseases. Non-Hispanic Black women are disproportionately affected by traditional risk factors and experience the onset of CVD at younger ages. Social determinants of health are a key driver for this disparity, as detailed in the AHA’s 2022 Cardiovascular Disease Statistical Update. Hispanic/Latina women (referring to women of any racial and ethnic background whose ancestry is from Mexico, Central America, South America, the Caribbean or other Spanish-speaking countries) have a higher rate of obesity compared with Hispanic/Latino men. Hispanic/Latina women born in the U.S. also have higher rates of smoking than those who were born in another country and immigrated to the U.S. Paradoxically, despite higher rates of Type 2 diabetes, obesity and metabolic syndrome, CVD death rates are 15-20% lower in Hispanic/Latina women than among non-Hispanic white women. It’s possible that this “Hispanic paradox” is due to grouping diverse Hispanic subcultures together in research data, which does not account for different levels of risk among individual subgroups of Hispanic/Latino people or the possibility of healthy immigrant bias. American Indian and Alaska Native women (a diverse population including hundreds of federally recognized and non-recognized tribes across the U.S.) have a higher rate of tobacco use than other groups, with 1 in 3 American Indian or Alaska Native women currently smoking. Type 2 diabetes is the primary risk factor for heart disease among American Indian women; however, rates vary by region, with up to 72% prevalence among American Indian women in Arizona, and just over 40% among those in Oklahoma, North Dakota and South Dakota. Unfortunately, understanding the cardiovascular health of American Indian/Alaska Native people is challenging due to small sample sizes in national data, racial and/or ethnic misclassification or other factors. Asian American women (having origins in the Far East, Southeast Asia or the Indian subcontinent) have varied rates of CVD risk within Asian subgroups: high blood pressure rates are 30% among Chinese women and 53% among Filipino women; rates of low HDL (good) cholesterol and high triglycerides are highest among Asian Indian and Filipino women; and Type 2 diabetes prevalence is highest among Southeast Asian women. The BMI level for increased risk of Type 2 diabetes is lower for Asian people than for other racial groups. Asian Americans are less likely to be overweight or have obesity compared to other racial groups, however, at the same BMI they have higher rates of high blood pressure, CVD and Type 2 diabetes. Higher body fat levels and the distribution of body fat may explain these differences: Recent research shows that Asian people generally have a higher percentage of body fat than non-Hispanic white people of the same age, sex and body mass index. In addition, studies have shown that Chinese, Filipino and Asian Indian people have more abdominal fat compared with non-Hispanic white and Black people.”When customizing CVD prevention and treatment strategies to improve cardiovascular health for women, a one-size-fits-all approach is unlikely to be successful,” Mieres said. “We must be cognizant of the complex interplay of sex, race and ethnicity, as well as social determinants of health, and how they impact the risk of cardiovascular disease and adverse outcomes in order to avert future CVD morbidity and mortality.”
Future cardiovascular disease prevention guidelines may be strengthened by urging culturally specific lifestyle recommendations tailored to the cultural norms and expectations that influence behaviors, beliefs and attitudes about diet, physical activity and healthy weight, according to the statement. The writing committee calls for community-based approaches, faith-based community partnerships and peer support in encouraging a healthy lifestyle to improve the primary prevention of cardiovascular disease among women from underrepresented groups. The statement also urges more research to address gaps in our knowledge about risk factors among women, including gathering data specific to subgroups of each race and ethnicity.
This scientific statement was prepared by the volunteer writing group on behalf of the American Heart Association’s Cardiovascular Disease and Stroke in Women and Underrepresented Populations Committee of the Council on Clinical Cardiology; the Council on Cardiovascular and Stroke Nursing; the Council on Hypertension; the Council on Lifelong Congenital Heart Disease and Heart Health in the Young; the Council on Lifestyle and Cardiometabolic Health; the Council on Peripheral Vascular Disease; and the Stroke Council. American Heart Association scientific statements promote greater awareness about cardiovascular diseases and stroke issues and help facilitate informed health care decisions. Scientific statements outline what is currently known about a topic and what areas need additional research. While scientific statements inform the development of guidelines, they do not make treatment recommendations. American Heart Association guidelines provide the Association’s official clinical practice recommendations.

For more than 100 million Americans who are obese, bariatric surgery may reverse complications related to diabetes, including regenerating damaged nerves, a Michigan Medicine study shows.
A research team led by the University of Michigan Health Department of Neurology followed more than 120 patients who underwent bariatric surgery for obesity over two years after the procedure. They found that all metabolic risk factors for developing diabetes, such as high glucose and lipid levels, improved outside of blood pressure and total cholesterol, according to results published in Diabetologia.
Investigators also found that patients two years removed from bariatric surgery showed improvements in peripheral neuropathy, a condition marked by damage to the nerves that go from the spinal cord all the way to the hands and feet.
“Our findings suggest that bariatric surgery likely enables the regeneration of the peripheral nerves and, therefore, may be an effective treatment for millions of individuals with obesity who are at risk of developing diabetes and peripheral neuropathy,” said senior author Brian C. Callaghan, M.D., M.S., a neurologist at University of Michigan Health and the Eva L. Feldman, M.D., Ph.D., Professor of Neurology at U-M Medical School.
Obesity is the second leading risk factor for peripheral neuropathy after diabetes, which affects more than 30 million Americans.
Researchers assessed two primary measures for peripheral neuropathy in patients with obesity by taking skin biopsies that show the nerve fiber density in the thigh and the leg. Two years after bariatric surgery, nerve fiber density improved in the thigh and remained stable in the leg.
Compared to previous studies of medical weight loss, when providers guide a patient’s weight loss goals, bariatric surgery led to better metabolic improvements and even greater improvements in peripheral neuropathy.
“Given the natural history of peripheral neuropathy decline in patients with obesity, even stability in nerve fiber density may be considered a successful result,” said first author Evan Reynolds, Ph.D., lead statistician for the NeuroNetwork for Emerging Therapies at Michigan Medicine. “Therefore, our findings of stability of nerve fiber density in the leg and improvement in nerve fiber density at the thigh indicate that bariatric surgery may be a successful therapy to improve or reverse peripheral neuropathy for patients with long-term metabolic impairment.”
Treatment for peripheral neuropathy currently focuses on pain, including oral medications such gabapentin and sodium channel blockers, topical analgesics and non-medical treatments, like exercise and cognitive behavioral therapy.
Additional authors include Maya Watanabe B.S., Mousumi Banerjee, Ph.D, Ericka Chant M.P.H., Emily Villegas-Umana B.S.N., R.N., Melissa A. Elafros M.D, Ph.D., Thomas W. Gardner M.D., M.S., Rodica Pop-Busui M.D., Ph.D., Subramaniam Pennathur M.D. and Eva Feldman, M.D., Ph.D., all of University of Michigan.

As teacher shortages continue to worsen across the United States, a new study at the University of Missouri gives insight into why so many stressed and burnt-out teachers are leaving the profession. The study found teachers who struggle to cope with the stress of their job report far lower job satisfaction compared to teachers who find ways to manage the pressure.
Seth Woods, a former doctoral student at MU, collaborated with Keith Herman, a Curators’ Distinguished Professor in the MU College of Education and Human Development, and others to analyze survey data of 2,300 teachers from Missouri and Oklahoma who were asked to rate how stressed they were at work, if they found ways to cope with work stress and how satisfied they were with their jobs.
Woods said while the findings were not particularly surprising, the study highlights how the ability — or inability — to cope with work stress can be a significant factor contributing to teacher burnout, which ultimately leads many teachers to leave the profession.
“In my 20 years as an educator, I’ve seen many great people leave the profession unfortunately, and this research confirms that we need to start devoting more time and resources into helping teachers identify and adopt healthy coping mechanisms,” said Woods, who is now principal at Beulah Ralph Elementary School in Columbia, Missouri. “Finding ways to mitigate teacher stress and investing in ways to help them cope with stress in positive manners will pay us back in not having to constantly hire and train new teachers all the time. In addition, retaining experienced teachers will likely benefit student achievement as well.”
The researchers explained that positive, healthy coping mechanisms can be quick, easy and free. One healthy coping mechanism Woods suggests for stressed teachers is writing and delivering a short letter of gratitude to a colleague they enjoy working with. Herman, who authored a book titled, “Stress Management for Teachers: A Proactive Guide,” said simple things like increasing positive interactions with students and peers, improving classroom management skills, and avoiding gossip at work can also help.
Herman added that while systematic issues, such as low teacher pay and overburdened teacher workloads remain critical topics to address, school principals, district superintendents and school administrators can all play in a role in supporting stressed teachers who may be struggling to cope.
“Communicating with teachers about their concerns, demonstrating empathy and checking in on their health and well-being shows that you care,” Herman said. “Our overall goal is to create school environments that allow teachers to thrive and give them the tools they need to be successful.”
“The relationship between teacher stress and job satisfaction as moderated by coping” was published in Psychology in the Schools. Funding for the study was provided by the U.S. Department of Education and the National Institute of Justice.

A recently developed amino acid compound successfully treats nonalcoholic fatty liver disease in non-human primates — bringing scientists one step closer to the first human treatment for the condition that is rapidly increasing around the world, a study suggests.
Researchers at Michigan Medicine developed DT-109, a glycine-based tripeptide, to treat the severe form of fatty liver disease called nonalcoholic steatohepatitis. More commonly known as NASH, the disease causes scarring and inflammation in the liver and is estimated to affect up to 6.5% of the global population.
Results reveal that DT-109 reversed fat buildup and prevented scarring in the livers of both mice and primates that had developed NASH. The study, completed in partnership with an international team including the Laboratory Animal Center at Xi’an Jiaotong University Health Science Center and the Institute of Cardiovascular Sciences at Peking University Health Science Center, is published in Cell Metabolism.
“For years, scientists have been trying to develop a medication that treats NASH, but many attempts have failed to show an improvement or have raised safety concerns in clinical trials,” said Eugene Chen, M.D., Ph.D., senior author of the study and Frederick G. L. Huetwell Professor of Cardiovascular Medicine at University of Michigan Medical School. “NASH is rising at a staggering rate, and successful treatment of non-human primates with our drug candidate, DT-109, brings us closer than ever to treating the millions of people suffering from this condition.”
NASH is the second stage of nonalcoholic fatty liver disease, which is estimated to affect 32% of people worldwide. While fatty liver disease can be treated with exercise and nutritional intervention, the liver damage from NASH is more permanent. It has become the primary cause of chronic liver disease, and NASH-related cirrhosis is now one of the most common reasons for liver transplantation.
Chen and his team developed DT-109 for treating NASH in non-human primates after reports showed that impaired glycine metabolism emerged as a cause of nonalcoholic fatty liver disease and NASH.
While hundreds of compounds have successfully treated NASH in mice, including DT-109, Chen says mouse NASH models are limited because not all aspects of the human disease are accurately mimicked and, therefore, are not easily translatable to the clinic. The research team’s non-human primate model for NASH, confirmed using multiomics profiling studies, is among the first to accomplish the feat.
In both non-human primates and mice, investigators in the international collaboration found that treatment with DT-109 reverses fat buildup and prevents fibrosis progression by stimulating fatty acid degradation and antioxidant formation. The drug also inhibited the production of lithocholic acid, a toxic secondary bile acid closely linked to nonalcoholic fatty liver disease.
“With this significant breakthrough in preclinical models, we can now consider evaluating DT-109 as a potential drug candidate for the treatment of NASH in future clinical trials,” said Jifeng Zhang, Ph.D., co-corresponding author and research associate professor of cardiovascular medicine at Michigan Medicine. “With millions of people suffering from NASH, the need for an effective treatment is more pressing than ever.”
Additional authors include Oren Rom, Ying Zhao, Chao Xue, Yang Zhao, Bo Wen, Duxin Sun, Jiandie Lin, all of University of Michigan, Pengxiang Qu, Linying Jia, Wenbin Cao, Jinpeng Zhao, Liang Bai, Sihai Zhao, Enqi Liu, all of Xi’an Jiaotong University Health Science Center, Ke Li, Shusi Ding, Beijing Tiantan Hospital, Mingming Zhao, Huiqing Wang, Lemin Zheng, all of Peking University, Xiaojing Gao, Chengshuang Chu, Rong Zeng, all of Shanghai Institute of Biochemistry and Cell Biology, Zhipeng Lui, Purdue University, Shuangshuang Chen and Xuelian Xiong, both of Fudan University, Alexandra C. Finney, Louisiana State University Health Sciences Center-Shreveport, Zuowen Zheng, Spring Biological Technology Development Co., Wanqing Liu, Wayne State University.
Disclosure: Chen is an inventor of the compound DT-109. The University of Michigan has patented it and licensed it to Diapin Therapeutics. Chen and the university have an ownership interest in Diapin. Diapin provided DT-109 for this study. The company is further developing the compound.
All procedures performed in mice were approved by the Institutional Animal Care and Use Committee at the University of Michigan and performed in accordance with the institutional guidelines. All experimental protocols involving non-human primates were approved by the Laboratory Animal Care Committee of Xi’an Jiaotong University (approval number: 20191278) and the Institutional Animal Care and Use Committee of Spring Biological Technology Development Co., Ltd. (approval number: 201901). The study was performed in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals.