General pediatricians and a multidisciplinary team of specialists agreed most of the time on which children should be diagnosed with autism spectrum disorder (ASD), data from a new study suggest.

But when it came to ruling out ASD, the agreement rate was much lower.

The study by Melanie Penner, MSc, MD, with the Autism Research Centre at Bloorview Research Institute, Toronto, and colleagues found that 89% of the time when a physician determined a child had ASD, the multidisciplinary team agreed. But when a pediatrician thought a child did not have ASD, the multidisciplinary team agreed only 60% of the time. The study was published in JAMA Network Open.

Multidisciplinary team model can’t keep up with demand

The findings are important as many guidelines recommend multidisciplinary teams (MDTs) for all ASD diagnostic assessment. However, the resources for this model can’t meet the demand of children needing a diagnosis and can lead to long waits for ASD therapies.

In Canada, the researchers note, the average wait time from referral to receipt of ASD diagnosis has been reported as 7 months and “has likely lengthened since the COVID-19 pandemic.”

Jennifer Gerdts, PhD, an attending psychologist at the Seattle Children’s Autism Center, said in an interview that the wait there for diagnosis in children older than 4 is “multiple years,” a length of time that’s common across the United States. Meanwhile, in many states families can’t access services without a diagnosis.

Expanding capacity with diagnoses by general pediatricians may improve access, but the diagnostic accuracy is critical.

Dr. Gerdts, who was not part of the study, said this research is “hugely important in the work that is under way to build community capacity for diagnostic evaluation.”

She said this study shows that not all diagnoses need the resources of a multiple-disciplinary team and that “pediatricians can do it, too, and they can do it pretty accurately.” Dr. Gerdts evaluates children for autism and helps train pediatricians to make diagnoses.
 

Pediatricians, specialist team completed blinded assessments

The 17 pediatricians in the study and the specialist team independently completed blinded assessment and each recorded a decision on whether the child had ASD. The prospective diagnostic study was conducted in a specialist assessment center in Toronto and in general pediatrician practices in Ontario from June 2016 to March 2020.

Children were younger than 5.5 years, did not have an ASD diagnosis and were referred because there was a development concern. The pediatricians referred 106 children (75% boys; average age, 3.5 years). More than half (57%) of the participating children were from minority racial and ethnic groups.

The children were randomly assigned to two groups: One included children who had their MDT visits before their pediatrician assessment and the other group included those who had their MDT visits after their pediatrician assessment.

The MDT diagnosed more than two-thirds of the children (68%) with ASD.

Sensitivity and specificity of the pediatrician assessments, compared with that of the specialist team, were 0.75 (95% confidence interval, 0.67-0.83) and 0.79 (95% CI, 0.62-0.91), respectively.
 

A look at pediatricians’ accuracy

Pediatricians reported the decisions they would have made had the child not been in the study.

• In 69% of the true-positive cases, pediatricians would have given an ASD diagnosis.
• In 44% of true-negative cases, they would have told the family the child did not have autism; in 30% of those case, they would give alternative diagnoses (most commonly ADHD and language delay).
• The pediatrician would have diagnosed ASD in only one of the seven false-positive cases and would refer those patients to a subspecialist 71% of the time.
• In false-negative cases, the pediatrician would incorrectly tell the family the child does not have autism 44% of the time.

Regarding the false-negative cases, the authors wrote, “more caution is needed for pediatricians when definitively ruling out ASD, which might result in diagnostic delays.”
 

Confidence is key

Physician confidence was also correlated with accuracy.

The authors wrote: “Among true-positive cases (MDT and pediatrician agree the child has ASD), the pediatrician was certain or very certain 80% of the time (43 cases) and the MDT was certain or very certain 96% of the time (52 cases). As such, if pediatricians conferred ASD diagnoses when feeling certain or very certain, they would make 46 correct diagnoses and 2 incorrect diagnoses.”

The high accuracy of diagnosis when physicians are confident suggests “listening to that sense of certainty is important,” Dr. Gerdts said. Conversely, these numbers show when a physician is uncertain about diagnosing ASD, they should listen to that instinct, too, and refer.

The results of the study support having general pediatricians diagnose and move forward with their patients when the signs of ASD are more definitive, saving the less-certain cases for the more resource-intensive teams to diagnose. Many states are moving toward that “tiered” system, Dr. Gerdts said.

“For many, and in fact most children, general pediatricians are pretty accurate when making an autism diagnosis,” she said.

“Let’s get [general pediatricians] confident in recognizing when this is outside their skill and ability level,” she said. “If you’re not sure, it is better to refer them on than to misdiagnose them.”

The important missing piece she said is how to support them “so they don’t feel pressure to make that call,” Dr. Gerdts said.

This project was funded by a grant from the Bloorview Research Institute, a grant from the Canadian Institutes of Health Research and a grant from the Canadian Institutes of Health. Three coauthors consult for and receive grants from several pharmaceutical companies and other organizations. Dr. Gerdts declared no relevant financial relationships.

General pediatricians and a multidisciplinary team of specialists agreed most of the time on which children should be diagnosed with autism spectrum disorder (ASD), data from a new study suggest.

But when it came to ruling out ASD, the agreement rate was much lower.

The study by Melanie Penner, MSc, MD, with the Autism Research Centre at Bloorview Research Institute, Toronto, and colleagues found that 89% of the time when a physician determined a child had ASD, the multidisciplinary team agreed. But when a pediatrician thought a child did not have ASD, the multidisciplinary team agreed only 60% of the time. The study was published in JAMA Network Open.

Multidisciplinary team model can’t keep up with demand

The findings are important as many guidelines recommend multidisciplinary teams (MDTs) for all ASD diagnostic assessment. However, the resources for this model can’t meet the demand of children needing a diagnosis and can lead to long waits for ASD therapies.

In Canada, the researchers note, the average wait time from referral to receipt of ASD diagnosis has been reported as 7 months and “has likely lengthened since the COVID-19 pandemic.”

Jennifer Gerdts, PhD, an attending psychologist at the Seattle Children’s Autism Center, said in an interview that the wait there for diagnosis in children older than 4 is “multiple years,” a length of time that’s common across the United States. Meanwhile, in many states families can’t access services without a diagnosis.

Expanding capacity with diagnoses by general pediatricians may improve access, but the diagnostic accuracy is critical.

Dr. Gerdts, who was not part of the study, said this research is “hugely important in the work that is under way to build community capacity for diagnostic evaluation.”

She said this study shows that not all diagnoses need the resources of a multiple-disciplinary team and that “pediatricians can do it, too, and they can do it pretty accurately.” Dr. Gerdts evaluates children for autism and helps train pediatricians to make diagnoses.
 

Pediatricians, specialist team completed blinded assessments

The 17 pediatricians in the study and the specialist team independently completed blinded assessment and each recorded a decision on whether the child had ASD. The prospective diagnostic study was conducted in a specialist assessment center in Toronto and in general pediatrician practices in Ontario from June 2016 to March 2020.

Children were younger than 5.5 years, did not have an ASD diagnosis and were referred because there was a development concern. The pediatricians referred 106 children (75% boys; average age, 3.5 years). More than half (57%) of the participating children were from minority racial and ethnic groups.

The children were randomly assigned to two groups: One included children who had their MDT visits before their pediatrician assessment and the other group included those who had their MDT visits after their pediatrician assessment.

The MDT diagnosed more than two-thirds of the children (68%) with ASD.

Sensitivity and specificity of the pediatrician assessments, compared with that of the specialist team, were 0.75 (95% confidence interval, 0.67-0.83) and 0.79 (95% CI, 0.62-0.91), respectively.
 

A look at pediatricians’ accuracy

Pediatricians reported the decisions they would have made had the child not been in the study.

• In 69% of the true-positive cases, pediatricians would have given an ASD diagnosis.
• In 44% of true-negative cases, they would have told the family the child did not have autism; in 30% of those case, they would give alternative diagnoses (most commonly ADHD and language delay).
• The pediatrician would have diagnosed ASD in only one of the seven false-positive cases and would refer those patients to a subspecialist 71% of the time.
• In false-negative cases, the pediatrician would incorrectly tell the family the child does not have autism 44% of the time.

Regarding the false-negative cases, the authors wrote, “more caution is needed for pediatricians when definitively ruling out ASD, which might result in diagnostic delays.”
 

Confidence is key

Physician confidence was also correlated with accuracy.

The authors wrote: “Among true-positive cases (MDT and pediatrician agree the child has ASD), the pediatrician was certain or very certain 80% of the time (43 cases) and the MDT was certain or very certain 96% of the time (52 cases). As such, if pediatricians conferred ASD diagnoses when feeling certain or very certain, they would make 46 correct diagnoses and 2 incorrect diagnoses.”

The high accuracy of diagnosis when physicians are confident suggests “listening to that sense of certainty is important,” Dr. Gerdts said. Conversely, these numbers show when a physician is uncertain about diagnosing ASD, they should listen to that instinct, too, and refer.

The results of the study support having general pediatricians diagnose and move forward with their patients when the signs of ASD are more definitive, saving the less-certain cases for the more resource-intensive teams to diagnose. Many states are moving toward that “tiered” system, Dr. Gerdts said.

“For many, and in fact most children, general pediatricians are pretty accurate when making an autism diagnosis,” she said.

“Let’s get [general pediatricians] confident in recognizing when this is outside their skill and ability level,” she said. “If you’re not sure, it is better to refer them on than to misdiagnose them.”

The important missing piece she said is how to support them “so they don’t feel pressure to make that call,” Dr. Gerdts said.

This project was funded by a grant from the Bloorview Research Institute, a grant from the Canadian Institutes of Health Research and a grant from the Canadian Institutes of Health. Three coauthors consult for and receive grants from several pharmaceutical companies and other organizations. Dr. Gerdts declared no relevant financial relationships.

General pediatricians and a multidisciplinary team of specialists agreed most of the time on which children should be diagnosed with autism spectrum disorder (ASD), data from a new study suggest.

But when it came to ruling out ASD, the agreement rate was much lower.

The study by Melanie Penner, MSc, MD, with the Autism Research Centre at Bloorview Research Institute, Toronto, and colleagues found that 89% of the time when a physician determined a child had ASD, the multidisciplinary team agreed. But when a pediatrician thought a child did not have ASD, the multidisciplinary team agreed only 60% of the time. The study was published in JAMA Network Open.

Multidisciplinary team model can’t keep up with demand

The findings are important as many guidelines recommend multidisciplinary teams (MDTs) for all ASD diagnostic assessment. However, the resources for this model can’t meet the demand of children needing a diagnosis and can lead to long waits for ASD therapies.

In Canada, the researchers note, the average wait time from referral to receipt of ASD diagnosis has been reported as 7 months and “has likely lengthened since the COVID-19 pandemic.”

Jennifer Gerdts, PhD, an attending psychologist at the Seattle Children’s Autism Center, said in an interview that the wait there for diagnosis in children older than 4 is “multiple years,” a length of time that’s common across the United States. Meanwhile, in many states families can’t access services without a diagnosis.

Expanding capacity with diagnoses by general pediatricians may improve access, but the diagnostic accuracy is critical.

Dr. Gerdts, who was not part of the study, said this research is “hugely important in the work that is under way to build community capacity for diagnostic evaluation.”

She said this study shows that not all diagnoses need the resources of a multiple-disciplinary team and that “pediatricians can do it, too, and they can do it pretty accurately.” Dr. Gerdts evaluates children for autism and helps train pediatricians to make diagnoses.
 

Pediatricians, specialist team completed blinded assessments

The 17 pediatricians in the study and the specialist team independently completed blinded assessment and each recorded a decision on whether the child had ASD. The prospective diagnostic study was conducted in a specialist assessment center in Toronto and in general pediatrician practices in Ontario from June 2016 to March 2020.

Children were younger than 5.5 years, did not have an ASD diagnosis and were referred because there was a development concern. The pediatricians referred 106 children (75% boys; average age, 3.5 years). More than half (57%) of the participating children were from minority racial and ethnic groups.

The children were randomly assigned to two groups: One included children who had their MDT visits before their pediatrician assessment and the other group included those who had their MDT visits after their pediatrician assessment.

The MDT diagnosed more than two-thirds of the children (68%) with ASD.

Sensitivity and specificity of the pediatrician assessments, compared with that of the specialist team, were 0.75 (95% confidence interval, 0.67-0.83) and 0.79 (95% CI, 0.62-0.91), respectively.
 

A look at pediatricians’ accuracy

Pediatricians reported the decisions they would have made had the child not been in the study.

• In 69% of the true-positive cases, pediatricians would have given an ASD diagnosis.
• In 44% of true-negative cases, they would have told the family the child did not have autism; in 30% of those case, they would give alternative diagnoses (most commonly ADHD and language delay).
• The pediatrician would have diagnosed ASD in only one of the seven false-positive cases and would refer those patients to a subspecialist 71% of the time.
• In false-negative cases, the pediatrician would incorrectly tell the family the child does not have autism 44% of the time.

Regarding the false-negative cases, the authors wrote, “more caution is needed for pediatricians when definitively ruling out ASD, which might result in diagnostic delays.”
 

Confidence is key

Physician confidence was also correlated with accuracy.

The authors wrote: “Among true-positive cases (MDT and pediatrician agree the child has ASD), the pediatrician was certain or very certain 80% of the time (43 cases) and the MDT was certain or very certain 96% of the time (52 cases). As such, if pediatricians conferred ASD diagnoses when feeling certain or very certain, they would make 46 correct diagnoses and 2 incorrect diagnoses.”

The high accuracy of diagnosis when physicians are confident suggests “listening to that sense of certainty is important,” Dr. Gerdts said. Conversely, these numbers show when a physician is uncertain about diagnosing ASD, they should listen to that instinct, too, and refer.

The results of the study support having general pediatricians diagnose and move forward with their patients when the signs of ASD are more definitive, saving the less-certain cases for the more resource-intensive teams to diagnose. Many states are moving toward that “tiered” system, Dr. Gerdts said.

“For many, and in fact most children, general pediatricians are pretty accurate when making an autism diagnosis,” she said.

“Let’s get [general pediatricians] confident in recognizing when this is outside their skill and ability level,” she said. “If you’re not sure, it is better to refer them on than to misdiagnose them.”

The important missing piece she said is how to support them “so they don’t feel pressure to make that call,” Dr. Gerdts said.

This project was funded by a grant from the Bloorview Research Institute, a grant from the Canadian Institutes of Health Research and a grant from the Canadian Institutes of Health. Three coauthors consult for and receive grants from several pharmaceutical companies and other organizations. Dr. Gerdts declared no relevant financial relationships.

For Julia Moore Vogel, PhD, a cup of peppermint tea marked the moment her life would change forever.

One morning in early July 2020, she took a sip of her favorite strongly flavored pick-me-up and couldn’t taste it. She knew loss of taste and smell were symptoms of COVID-19, and she suspected she had contracted the virus. A doctor’s visit confirmed her fears.

“I remember trying the tea and just being so shocked and thinking: How can this be happening to me?” said Dr. Moore Vogel, a COVID-19 researcher with the Scripps Research Translational Institute in San Diego. “I’d been so incredibly careful.”

Her physician assured her that as a healthy woman in her mid-30s, she’d be “back to normal” in 2 weeks’ time and that her loss of taste and smell “very likely will be your only symptom,” she recalled.

But within a week, Dr. Moore Vogel started having trouble breathing. She couldn’t work, and she experienced crushing fatigue, brain fog, and migraines. Now, 2½ years later, Dr. Moore Vogel is among the tens of millions of Americans with long COVID.

As a COVID-19 patient-researcher who still struggles with fatigue and migraines, she has learned to cope with her condition. She directs the Participant Center for the All of Us Research Program, a National Institutes of Health collaboration to build the largest, most diverse health database in history. She relies on a practice called pacing, which helps conserve physical, mental, and emotional energy, to avoid making her symptoms worse.

And she is a coauthor of a landmark 200-study review of long COVID published Jan. 13 in the journal Nature, with Scripps Executive Vice President and Medscape Editor-in-Chief Eric Topol, MD. Two other institute long COVID researchers and patient advocates who have the condition coauthored the review – Lisa McCorkell and Hannah E. Davis, cofounders of the Patient-Led Research Collaborative , a group of long COVID patients who study the virus.

Dr. Moore Vogel discussed the key findings of the new review and her personal experiences with this news organization.
 

Q: When you contracted COVID, no treatments or vaccines existed. Can you talk about what the experience was like for you?

A: “It was July 2020. The loss of taste and smell was the first symptom, and what was interesting was that was my only symptom for a little bit. Being the goal-oriented, work-oriented person that I am, I just worked the rest of the week and hoped that it wasn’t real.

“But that was a Wednesday, and by Friday, I was just getting really tired, and it was really hard to finish my workday. I ended up taking 3 weeks off to recover from the acute phase. At the time, I had read early discussions about long COVID, and it was always on my [mind] – how long was it going to take to recover?”
 

Q: You went to see a doctor that first week?

A: “I called them when I had the loss of taste and smell, and they said, ‘It’s very likely this will be your only symptom.’ And when I first talked to a physician, they were saying, ‘Oh, you’re young and healthy, in 2 weeks you’ll be back to normal.’ But of course that turned out not to be true.

“It’s hard to remember what it was like at that time. There were so few treatments, it was all about rationing ventilators, and it was absolutely terrifying at the time to just not know what was going to happen.”
 

Q: How are you managing your condition today?

A: “I have myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), one of the really common diagnoses that come out of long COVID. So, that’s the biggest thing for me to manage now, and the main management is pacing.

“I also have medications for migraine management. I’ve always had some degree of migraines, like 2 a month, but now it’s like 15 a month, so it’s a totally different scale of management.”
 

Q: It must be frustrating, personally and professionally, that long COVID treatments remain elusive.

A: “I’m disappointed at the pace of testing things in clinical trials. There was so much progress made, so much innovation in the early stages of the pandemic to treat the acute phase, and it led to amazing things. We have all these monoclonal antibodies, the steroids are really effective, not to mention the antivirals and the vaccines, of course, on the prevention side. It’s been amazing.

“But for some reason, long COVID treatment is really lagging. What I hypothesize as part of the reason for that is that it doesn’t feel as dramatic. When you see someone on a ventilator or hear about death, it feels very dramatic, and people really worry about that.”
 

Q: So, let’s talk about the research. How did your personal experiences – and those of the two other coauthors with long COVID – help inform this review?

A: “I work with Eric Topol on a regular basis, and it was amazing that he invited patients to work with him on this review ... I have to say of my other long COVID patient coauthors, Hannah Davis and Lisa McCorkell, it was amazing to work with them.

“It was my first time working with people who have long COVID on a big project. The understanding that we had of each other [where] one of us might say, Oh, I’m crashing today, I can’t work on this. Can you help get us across the finish line for this deadline? That was really amazing to me in terms of how a workplace can be with real disability accommodations.

“It’s really changed my personal outlook on how important it is to have patients involved in the process.”
 

Q: What was the most surprising or significant finding of the review, in your view?

A: “I would say the most impactful thing to me in the process of writing this review is how much research has been done in such a short time. We started with over 250 studies that we wanted to reference in the review, and we actually had to cut out 50 in the editorial process, which was really hard!

“There’s just been so much progress that’s been made in the past couple of years. And then thinking about the progress on long COVID in general, the other things that’s important to acknowledge is all the work that’s been done on other postviral illnesses that present very similarly to long COVID in many patients, ME/CFS, and postural orthostatic tachycardia syndrome (POTS).”
 

Q: One thing that stood out is the review’s finding that long COVID is potentially lifelong COVID and, in some ways, is closer to HIV-AIDS than, say, influenza. Is that right?

A: “Yes. I’m really glad you took that point away from the review because that was one of the things that I felt the most strongly about incorporating. For many people, based on the treatments that we have today, this is likely to lead to lifelong disability. And that’s something, from my personal experience, for sure. I’m seeing no improvement on the horizon.

“That’s part of why I’m so passionate about there being clinical trials because I know there are millions and millions of us. So for me, that wasn’t so surprising, because I’m living it, but I can see how for the general public that was a really surprising finding.”
 

Q: The review breaks down long COVID’s effects on various organs/systems, and it includes the most comprehensive look to date at the effects on pregnant women. Anything you’d care to stress about that?

A: “It really underlies the importance of vaccination, given that it can affect both the pregnant person and child. There is early evidence of development delays if there’s infection while the child is still gestating. So, I think it underscores the need for vaccination to reduce that risk.

“You know, pregnancy is a stressful and terrifying time anyway. So, if there’s anything you can do to reduce the risk to yourself and your unborn child, I think it’s really worthwhile.”
 

Q: Why do you think this exhaustive review was needed?

A: “Because of the massive amount of literature that’s out there, it’s so hard for anybody to sift through. Eric Topol and Hannah Davis, two of the coauthors, are two people who have done it, and they keep up with all the literature, and they are always tweeting about it.

“But most people don’t have the time to be able to sift through it, so what we did was take all of that literature, organize it into sections, and summarize the key findings. Then the other thing that I think is really important for the field right now is the recommendations piece.”
 

Q: What impact do you think the new long COVID review in Nature will have?

A: “The response to our review is way beyond what I expected, and I think that’s in part a sign that there is growing awareness of the issue of long COVID.

“I hope that helps spiral toward more treatment trials. Because there are a lot of great candidates out there. We have a whole table in the review about the different potential treatments that should be tested.”
 

Q: What’s the take-home message for physicians?

A: “One of the key recommendations is about physician education. We know that it is so hard for physicians to keep up with this massive amount of literature, and we really need more physician education that’s meant for busy physicians who really don’t have time to read all of the primary literature themselves.

“So many folks are not getting the care that they need. Because these types of conditions haven’t been seen as much by primary care providers, physical therapists, etc., there’s so much more education that’s needed.

“I think the basic tenets probably could be taught in a weekend course, [including] listening to the patients, believing patients. There are so many times patient symptoms are [dismissed and not] really being taken seriously by their physicians.

“I think part of the challenge behind that is the conflating of mental health issues with these other physiological symptoms. There’s a tendency to say, ‘Oh, all this is this caused by mental health issues’ and that mental health is the root cause, when actually it’s the illness that’s the root cause.”
 

Q: What’s the big picture: How significant is the public health crisis that long COVID represents?

A: “I believe it’s a massive crisis, a massive emergency. A lot of people in the long COVID community are calling it a mass-disabling event. There is concern that if we let the pandemic run unmitigated for long enough – given that we expect about 10% of folks that get COVID will end up with long COVID – we could end up eventually with a majority-disabled society.

“That would be devasting – to individuals, to the economy, the medical system. So, it’s absolutely a public health emergency in my view, and that’s part of why I’ve been so surprised by the lack of trials, the lack of awareness in the public. There hasn’t been as much public education about long COVID as there has about acute COVID. I think we can do more from a public health perspective.”
 

Q: What are the main challenges in combating long COVID?

A: “I think the lack of treatments is the most devastating part because it’s such a hard disease to contract, and there’s no end in sight, and so that time horizon can be really difficult. That’s part of why I’m pushing the treatments so much, because I want to offer hope to the community, you know, I want there to be hope around the corner.

“My hope is that within 5 years we’ll have treatments that can really improve quality of life for the community. And I know that that may seem like a long time for those who are suffering, and I hope that there will be some clinical trials of treatments that improve symptom management within 1-2 years. But I think for really more novel things, it’s really going to take at least 5.”
 

Q: Any advice you’d give to someone with long COVID today?

A: “Connecting with others that are going through the experience is extremely valuable and can really help with that mental component which can be really draining.

“The other thing, in terms of what’s important for the lives of people who are living with long COVID, I would say to everyone who doesn’t have long COVID but knows someone who does, being able to offer support is crucial and can make such a difference in quality of life.

“It is really crucial, for those who don’t have long COVID, to take it into account when you’re making your risk calculations. When you’re thinking: Am I going to wear a mask here? or Am I going to go to that bar?

“Really consider the possibility that if you get COVID, you have a 10% chance of getting long COVID. And if you get long COVID, you have a 25% chance of not being able to work anymore or being so ill that you can’t work anymore and you may lose your health insurance.

“The compounding effects are absolutely devastating, and I think that’s under-factored-in to the general risk calculations of the public.”

A version of this article first appeared on Medscape.com.

For Julia Moore Vogel, PhD, a cup of peppermint tea marked the moment her life would change forever.

One morning in early July 2020, she took a sip of her favorite strongly flavored pick-me-up and couldn’t taste it. She knew loss of taste and smell were symptoms of COVID-19, and she suspected she had contracted the virus. A doctor’s visit confirmed her fears.

“I remember trying the tea and just being so shocked and thinking: How can this be happening to me?” said Dr. Moore Vogel, a COVID-19 researcher with the Scripps Research Translational Institute in San Diego. “I’d been so incredibly careful.”

Her physician assured her that as a healthy woman in her mid-30s, she’d be “back to normal” in 2 weeks’ time and that her loss of taste and smell “very likely will be your only symptom,” she recalled.

But within a week, Dr. Moore Vogel started having trouble breathing. She couldn’t work, and she experienced crushing fatigue, brain fog, and migraines. Now, 2½ years later, Dr. Moore Vogel is among the tens of millions of Americans with long COVID.

As a COVID-19 patient-researcher who still struggles with fatigue and migraines, she has learned to cope with her condition. She directs the Participant Center for the All of Us Research Program, a National Institutes of Health collaboration to build the largest, most diverse health database in history. She relies on a practice called pacing, which helps conserve physical, mental, and emotional energy, to avoid making her symptoms worse.

And she is a coauthor of a landmark 200-study review of long COVID published Jan. 13 in the journal Nature, with Scripps Executive Vice President and Medscape Editor-in-Chief Eric Topol, MD. Two other institute long COVID researchers and patient advocates who have the condition coauthored the review – Lisa McCorkell and Hannah E. Davis, cofounders of the Patient-Led Research Collaborative , a group of long COVID patients who study the virus.

Dr. Moore Vogel discussed the key findings of the new review and her personal experiences with this news organization.
 

Q: When you contracted COVID, no treatments or vaccines existed. Can you talk about what the experience was like for you?

A: “It was July 2020. The loss of taste and smell was the first symptom, and what was interesting was that was my only symptom for a little bit. Being the goal-oriented, work-oriented person that I am, I just worked the rest of the week and hoped that it wasn’t real.

“But that was a Wednesday, and by Friday, I was just getting really tired, and it was really hard to finish my workday. I ended up taking 3 weeks off to recover from the acute phase. At the time, I had read early discussions about long COVID, and it was always on my [mind] – how long was it going to take to recover?”
 

Q: You went to see a doctor that first week?

A: “I called them when I had the loss of taste and smell, and they said, ‘It’s very likely this will be your only symptom.’ And when I first talked to a physician, they were saying, ‘Oh, you’re young and healthy, in 2 weeks you’ll be back to normal.’ But of course that turned out not to be true.

“It’s hard to remember what it was like at that time. There were so few treatments, it was all about rationing ventilators, and it was absolutely terrifying at the time to just not know what was going to happen.”
 

Q: How are you managing your condition today?

A: “I have myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), one of the really common diagnoses that come out of long COVID. So, that’s the biggest thing for me to manage now, and the main management is pacing.

“I also have medications for migraine management. I’ve always had some degree of migraines, like 2 a month, but now it’s like 15 a month, so it’s a totally different scale of management.”
 

Q: It must be frustrating, personally and professionally, that long COVID treatments remain elusive.

A: “I’m disappointed at the pace of testing things in clinical trials. There was so much progress made, so much innovation in the early stages of the pandemic to treat the acute phase, and it led to amazing things. We have all these monoclonal antibodies, the steroids are really effective, not to mention the antivirals and the vaccines, of course, on the prevention side. It’s been amazing.

“But for some reason, long COVID treatment is really lagging. What I hypothesize as part of the reason for that is that it doesn’t feel as dramatic. When you see someone on a ventilator or hear about death, it feels very dramatic, and people really worry about that.”
 

Q: So, let’s talk about the research. How did your personal experiences – and those of the two other coauthors with long COVID – help inform this review?

A: “I work with Eric Topol on a regular basis, and it was amazing that he invited patients to work with him on this review ... I have to say of my other long COVID patient coauthors, Hannah Davis and Lisa McCorkell, it was amazing to work with them.

“It was my first time working with people who have long COVID on a big project. The understanding that we had of each other [where] one of us might say, Oh, I’m crashing today, I can’t work on this. Can you help get us across the finish line for this deadline? That was really amazing to me in terms of how a workplace can be with real disability accommodations.

“It’s really changed my personal outlook on how important it is to have patients involved in the process.”
 

Q: What was the most surprising or significant finding of the review, in your view?

A: “I would say the most impactful thing to me in the process of writing this review is how much research has been done in such a short time. We started with over 250 studies that we wanted to reference in the review, and we actually had to cut out 50 in the editorial process, which was really hard!

“There’s just been so much progress that’s been made in the past couple of years. And then thinking about the progress on long COVID in general, the other things that’s important to acknowledge is all the work that’s been done on other postviral illnesses that present very similarly to long COVID in many patients, ME/CFS, and postural orthostatic tachycardia syndrome (POTS).”
 

Q: One thing that stood out is the review’s finding that long COVID is potentially lifelong COVID and, in some ways, is closer to HIV-AIDS than, say, influenza. Is that right?

A: “Yes. I’m really glad you took that point away from the review because that was one of the things that I felt the most strongly about incorporating. For many people, based on the treatments that we have today, this is likely to lead to lifelong disability. And that’s something, from my personal experience, for sure. I’m seeing no improvement on the horizon.

“That’s part of why I’m so passionate about there being clinical trials because I know there are millions and millions of us. So for me, that wasn’t so surprising, because I’m living it, but I can see how for the general public that was a really surprising finding.”
 

Q: The review breaks down long COVID’s effects on various organs/systems, and it includes the most comprehensive look to date at the effects on pregnant women. Anything you’d care to stress about that?

A: “It really underlies the importance of vaccination, given that it can affect both the pregnant person and child. There is early evidence of development delays if there’s infection while the child is still gestating. So, I think it underscores the need for vaccination to reduce that risk.

“You know, pregnancy is a stressful and terrifying time anyway. So, if there’s anything you can do to reduce the risk to yourself and your unborn child, I think it’s really worthwhile.”
 

Q: Why do you think this exhaustive review was needed?

A: “Because of the massive amount of literature that’s out there, it’s so hard for anybody to sift through. Eric Topol and Hannah Davis, two of the coauthors, are two people who have done it, and they keep up with all the literature, and they are always tweeting about it.

“But most people don’t have the time to be able to sift through it, so what we did was take all of that literature, organize it into sections, and summarize the key findings. Then the other thing that I think is really important for the field right now is the recommendations piece.”
 

Q: What impact do you think the new long COVID review in Nature will have?

A: “The response to our review is way beyond what I expected, and I think that’s in part a sign that there is growing awareness of the issue of long COVID.

“I hope that helps spiral toward more treatment trials. Because there are a lot of great candidates out there. We have a whole table in the review about the different potential treatments that should be tested.”
 

Q: What’s the take-home message for physicians?

A: “One of the key recommendations is about physician education. We know that it is so hard for physicians to keep up with this massive amount of literature, and we really need more physician education that’s meant for busy physicians who really don’t have time to read all of the primary literature themselves.

“So many folks are not getting the care that they need. Because these types of conditions haven’t been seen as much by primary care providers, physical therapists, etc., there’s so much more education that’s needed.

“I think the basic tenets probably could be taught in a weekend course, [including] listening to the patients, believing patients. There are so many times patient symptoms are [dismissed and not] really being taken seriously by their physicians.

“I think part of the challenge behind that is the conflating of mental health issues with these other physiological symptoms. There’s a tendency to say, ‘Oh, all this is this caused by mental health issues’ and that mental health is the root cause, when actually it’s the illness that’s the root cause.”
 

Q: What’s the big picture: How significant is the public health crisis that long COVID represents?

A: “I believe it’s a massive crisis, a massive emergency. A lot of people in the long COVID community are calling it a mass-disabling event. There is concern that if we let the pandemic run unmitigated for long enough – given that we expect about 10% of folks that get COVID will end up with long COVID – we could end up eventually with a majority-disabled society.

“That would be devasting – to individuals, to the economy, the medical system. So, it’s absolutely a public health emergency in my view, and that’s part of why I’ve been so surprised by the lack of trials, the lack of awareness in the public. There hasn’t been as much public education about long COVID as there has about acute COVID. I think we can do more from a public health perspective.”
 

Q: What are the main challenges in combating long COVID?

A: “I think the lack of treatments is the most devastating part because it’s such a hard disease to contract, and there’s no end in sight, and so that time horizon can be really difficult. That’s part of why I’m pushing the treatments so much, because I want to offer hope to the community, you know, I want there to be hope around the corner.

“My hope is that within 5 years we’ll have treatments that can really improve quality of life for the community. And I know that that may seem like a long time for those who are suffering, and I hope that there will be some clinical trials of treatments that improve symptom management within 1-2 years. But I think for really more novel things, it’s really going to take at least 5.”
 

Q: Any advice you’d give to someone with long COVID today?

A: “Connecting with others that are going through the experience is extremely valuable and can really help with that mental component which can be really draining.

“The other thing, in terms of what’s important for the lives of people who are living with long COVID, I would say to everyone who doesn’t have long COVID but knows someone who does, being able to offer support is crucial and can make such a difference in quality of life.

“It is really crucial, for those who don’t have long COVID, to take it into account when you’re making your risk calculations. When you’re thinking: Am I going to wear a mask here? or Am I going to go to that bar?

“Really consider the possibility that if you get COVID, you have a 10% chance of getting long COVID. And if you get long COVID, you have a 25% chance of not being able to work anymore or being so ill that you can’t work anymore and you may lose your health insurance.

“The compounding effects are absolutely devastating, and I think that’s under-factored-in to the general risk calculations of the public.”

A version of this article first appeared on Medscape.com.

For Julia Moore Vogel, PhD, a cup of peppermint tea marked the moment her life would change forever.

One morning in early July 2020, she took a sip of her favorite strongly flavored pick-me-up and couldn’t taste it. She knew loss of taste and smell were symptoms of COVID-19, and she suspected she had contracted the virus. A doctor’s visit confirmed her fears.

“I remember trying the tea and just being so shocked and thinking: How can this be happening to me?” said Dr. Moore Vogel, a COVID-19 researcher with the Scripps Research Translational Institute in San Diego. “I’d been so incredibly careful.”

Her physician assured her that as a healthy woman in her mid-30s, she’d be “back to normal” in 2 weeks’ time and that her loss of taste and smell “very likely will be your only symptom,” she recalled.

But within a week, Dr. Moore Vogel started having trouble breathing. She couldn’t work, and she experienced crushing fatigue, brain fog, and migraines. Now, 2½ years later, Dr. Moore Vogel is among the tens of millions of Americans with long COVID.

As a COVID-19 patient-researcher who still struggles with fatigue and migraines, she has learned to cope with her condition. She directs the Participant Center for the All of Us Research Program, a National Institutes of Health collaboration to build the largest, most diverse health database in history. She relies on a practice called pacing, which helps conserve physical, mental, and emotional energy, to avoid making her symptoms worse.

And she is a coauthor of a landmark 200-study review of long COVID published Jan. 13 in the journal Nature, with Scripps Executive Vice President and Medscape Editor-in-Chief Eric Topol, MD. Two other institute long COVID researchers and patient advocates who have the condition coauthored the review – Lisa McCorkell and Hannah E. Davis, cofounders of the Patient-Led Research Collaborative , a group of long COVID patients who study the virus.

Dr. Moore Vogel discussed the key findings of the new review and her personal experiences with this news organization.
 

Q: When you contracted COVID, no treatments or vaccines existed. Can you talk about what the experience was like for you?

A: “It was July 2020. The loss of taste and smell was the first symptom, and what was interesting was that was my only symptom for a little bit. Being the goal-oriented, work-oriented person that I am, I just worked the rest of the week and hoped that it wasn’t real.

“But that was a Wednesday, and by Friday, I was just getting really tired, and it was really hard to finish my workday. I ended up taking 3 weeks off to recover from the acute phase. At the time, I had read early discussions about long COVID, and it was always on my [mind] – how long was it going to take to recover?”
 

Q: You went to see a doctor that first week?

A: “I called them when I had the loss of taste and smell, and they said, ‘It’s very likely this will be your only symptom.’ And when I first talked to a physician, they were saying, ‘Oh, you’re young and healthy, in 2 weeks you’ll be back to normal.’ But of course that turned out not to be true.

“It’s hard to remember what it was like at that time. There were so few treatments, it was all about rationing ventilators, and it was absolutely terrifying at the time to just not know what was going to happen.”
 

Q: How are you managing your condition today?

A: “I have myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), one of the really common diagnoses that come out of long COVID. So, that’s the biggest thing for me to manage now, and the main management is pacing.

“I also have medications for migraine management. I’ve always had some degree of migraines, like 2 a month, but now it’s like 15 a month, so it’s a totally different scale of management.”
 

Q: It must be frustrating, personally and professionally, that long COVID treatments remain elusive.

A: “I’m disappointed at the pace of testing things in clinical trials. There was so much progress made, so much innovation in the early stages of the pandemic to treat the acute phase, and it led to amazing things. We have all these monoclonal antibodies, the steroids are really effective, not to mention the antivirals and the vaccines, of course, on the prevention side. It’s been amazing.

“But for some reason, long COVID treatment is really lagging. What I hypothesize as part of the reason for that is that it doesn’t feel as dramatic. When you see someone on a ventilator or hear about death, it feels very dramatic, and people really worry about that.”
 

Q: So, let’s talk about the research. How did your personal experiences – and those of the two other coauthors with long COVID – help inform this review?

A: “I work with Eric Topol on a regular basis, and it was amazing that he invited patients to work with him on this review ... I have to say of my other long COVID patient coauthors, Hannah Davis and Lisa McCorkell, it was amazing to work with them.

“It was my first time working with people who have long COVID on a big project. The understanding that we had of each other [where] one of us might say, Oh, I’m crashing today, I can’t work on this. Can you help get us across the finish line for this deadline? That was really amazing to me in terms of how a workplace can be with real disability accommodations.

“It’s really changed my personal outlook on how important it is to have patients involved in the process.”
 

Q: What was the most surprising or significant finding of the review, in your view?

A: “I would say the most impactful thing to me in the process of writing this review is how much research has been done in such a short time. We started with over 250 studies that we wanted to reference in the review, and we actually had to cut out 50 in the editorial process, which was really hard!

“There’s just been so much progress that’s been made in the past couple of years. And then thinking about the progress on long COVID in general, the other things that’s important to acknowledge is all the work that’s been done on other postviral illnesses that present very similarly to long COVID in many patients, ME/CFS, and postural orthostatic tachycardia syndrome (POTS).”
 

Q: One thing that stood out is the review’s finding that long COVID is potentially lifelong COVID and, in some ways, is closer to HIV-AIDS than, say, influenza. Is that right?

A: “Yes. I’m really glad you took that point away from the review because that was one of the things that I felt the most strongly about incorporating. For many people, based on the treatments that we have today, this is likely to lead to lifelong disability. And that’s something, from my personal experience, for sure. I’m seeing no improvement on the horizon.

“That’s part of why I’m so passionate about there being clinical trials because I know there are millions and millions of us. So for me, that wasn’t so surprising, because I’m living it, but I can see how for the general public that was a really surprising finding.”
 

Q: The review breaks down long COVID’s effects on various organs/systems, and it includes the most comprehensive look to date at the effects on pregnant women. Anything you’d care to stress about that?

A: “It really underlies the importance of vaccination, given that it can affect both the pregnant person and child. There is early evidence of development delays if there’s infection while the child is still gestating. So, I think it underscores the need for vaccination to reduce that risk.

“You know, pregnancy is a stressful and terrifying time anyway. So, if there’s anything you can do to reduce the risk to yourself and your unborn child, I think it’s really worthwhile.”
 

Q: Why do you think this exhaustive review was needed?

A: “Because of the massive amount of literature that’s out there, it’s so hard for anybody to sift through. Eric Topol and Hannah Davis, two of the coauthors, are two people who have done it, and they keep up with all the literature, and they are always tweeting about it.

“But most people don’t have the time to be able to sift through it, so what we did was take all of that literature, organize it into sections, and summarize the key findings. Then the other thing that I think is really important for the field right now is the recommendations piece.”
 

Q: What impact do you think the new long COVID review in Nature will have?

A: “The response to our review is way beyond what I expected, and I think that’s in part a sign that there is growing awareness of the issue of long COVID.

“I hope that helps spiral toward more treatment trials. Because there are a lot of great candidates out there. We have a whole table in the review about the different potential treatments that should be tested.”
 

Q: What’s the take-home message for physicians?

A: “One of the key recommendations is about physician education. We know that it is so hard for physicians to keep up with this massive amount of literature, and we really need more physician education that’s meant for busy physicians who really don’t have time to read all of the primary literature themselves.

“So many folks are not getting the care that they need. Because these types of conditions haven’t been seen as much by primary care providers, physical therapists, etc., there’s so much more education that’s needed.

“I think the basic tenets probably could be taught in a weekend course, [including] listening to the patients, believing patients. There are so many times patient symptoms are [dismissed and not] really being taken seriously by their physicians.

“I think part of the challenge behind that is the conflating of mental health issues with these other physiological symptoms. There’s a tendency to say, ‘Oh, all this is this caused by mental health issues’ and that mental health is the root cause, when actually it’s the illness that’s the root cause.”
 

Q: What’s the big picture: How significant is the public health crisis that long COVID represents?

A: “I believe it’s a massive crisis, a massive emergency. A lot of people in the long COVID community are calling it a mass-disabling event. There is concern that if we let the pandemic run unmitigated for long enough – given that we expect about 10% of folks that get COVID will end up with long COVID – we could end up eventually with a majority-disabled society.

“That would be devasting – to individuals, to the economy, the medical system. So, it’s absolutely a public health emergency in my view, and that’s part of why I’ve been so surprised by the lack of trials, the lack of awareness in the public. There hasn’t been as much public education about long COVID as there has about acute COVID. I think we can do more from a public health perspective.”
 

Q: What are the main challenges in combating long COVID?

A: “I think the lack of treatments is the most devastating part because it’s such a hard disease to contract, and there’s no end in sight, and so that time horizon can be really difficult. That’s part of why I’m pushing the treatments so much, because I want to offer hope to the community, you know, I want there to be hope around the corner.

“My hope is that within 5 years we’ll have treatments that can really improve quality of life for the community. And I know that that may seem like a long time for those who are suffering, and I hope that there will be some clinical trials of treatments that improve symptom management within 1-2 years. But I think for really more novel things, it’s really going to take at least 5.”
 

Q: Any advice you’d give to someone with long COVID today?

A: “Connecting with others that are going through the experience is extremely valuable and can really help with that mental component which can be really draining.

“The other thing, in terms of what’s important for the lives of people who are living with long COVID, I would say to everyone who doesn’t have long COVID but knows someone who does, being able to offer support is crucial and can make such a difference in quality of life.

“It is really crucial, for those who don’t have long COVID, to take it into account when you’re making your risk calculations. When you’re thinking: Am I going to wear a mask here? or Am I going to go to that bar?

“Really consider the possibility that if you get COVID, you have a 10% chance of getting long COVID. And if you get long COVID, you have a 25% chance of not being able to work anymore or being so ill that you can’t work anymore and you may lose your health insurance.

“The compounding effects are absolutely devastating, and I think that’s under-factored-in to the general risk calculations of the public.”

A version of this article first appeared on Medscape.com.

Middle-aged adults who spend just 9 additional minutes a day participating in moderate to vigorous physical activity (MVPA) experience improved cognition in new findings that underscore the critical role brisk exercise, such as running and cycling, plays in brain health.

“Even minor differences in daily behavior appeared meaningful for cognition in this study,” researcher John J. Mitchell, MSci and PhD candidate, Medical Research Council, London, told this news organization.

The findings were published online in the Journal of Epidemiology and Community Health.
 

Research gap

Previous research has linked physical activity (PA) with increased cognitive reserve, which delays the onset of cognitive decline in later life. But disentangling the most important components of PA for cognition – such as intensity and volume – has not been well researched.

Previous studies didn’t capture sleep time, which typically takes up the largest component of the day. Sleep is “acutely relevant” when examining cognition, the investigators noted.

In addition, studies in this area often focus on just one or two activity components of the day, which “neglects the growing awareness” that movements “are all tightly interlinked,” said Mr. Mitchell.

The new study included 4,481 participants in the British Cohort Study who were born in 1970 across England, Scotland, and Wales. The participants were followed throughout childhood and adulthood.

The median age of the participants was 47 years, and they were predominantly White, female (52%), married (66%), and well educated. Most were occasional or nonrisky alcohol consumers, and half had never smoked.

The researchers collected biometric measurements and health, demographic, and lifestyle information. Participants wore a thigh-mounted accelerometer at least 7 consecutive hours a day for up to 7 days to track PA, sedentary behavior (SB), and sleep time.

The device used in the study could detect subtle movements as well as speed of accelerations, said Mr. Mitchell. “From this, we can distinguish MVPA from slow walking, standing, and sitting. It’s the current best practice for detecting the more subtle movements we make, such as brisk walking and stair climbing, beyond just ‘exercise,’ “ he added.

Light intensity PA (LIPA) describes movement such as walking and moving around the house or office, while MVPA includes activities such as brisk walking and running that accelerate the heart rate. SB, defined as time spent sitting or lying, is distinguished from standing by the thigh inclination.

On an average day, the cohort spent 51 minutes in MVPA; 5 hours, 42 minutes in LIPA; 9 hours, 16 minutes in SB; and 8 hours, 11 minutes sleeping.

Researchers calculated an overall global score for verbal memory and executive function.

The study used “compositional data analysis,” a statistical method that can examine the associations of cognition and PA in the context of all components of daily movement.

The analysis revealed a positive association between MVPA and cognition relative to all other behaviors, after adjustment for sociodemographic factors that included sex, age, education, and marital status. But the relationship lessened after further adjustment for health status – for example, cardiovascular disease or disability – and lifestyle factors, such as alcohol consumption and smoking status.

SB relative to all other movements remained positively associated with cognition after full adjustment. This, the authors speculated, may reflect engagement in cognitively stimulating activities such as reading.

To better understand the associations, the researchers used a statistical method to reallocate time in the cohort’s average day from one activity component to another.

“We held two of the components static but moved time between the other two and monitored the theoretical ramifications of that change for cognition,” said Mr. Mitchell.
 

Real cognitive change

There was a 1.31% improvement in cognition ranking compared to the sample average after replacing 9 minutes of sedentary activity with MVPA (1.31; 95% confidence interval [CI], 0.09-2.50). There was a 1.27% improvement after replacing 7 minutes of LIPA with MVPA, and a 1.2% improvement after replacing 7 minutes of sleep with MVPA.

Individuals might move up from about the 50th percentile to the 51st or 52nd percentile after just 9 minutes of more moderate to vigorous movement in place of sitting, said Mr. Mitchell. “This highlights how even very modest differences in people’s daily movement – less than 10 minutes – is linked to quite real changes in our cognitive health.”

The impact of physical activity appeared greatest on working memory and mental processes, such as planning and organization.

On the other hand, cognition declined by 1%-2% after replacing MVPA with 8 minutes of SB, 6 minutes of LIPA, or 7 minutes of sleep.

The activity tracking device couldn’t determine how well participants slept, which is “a clear limitation” of the study, said Mr. Mitchell. “We have to be cautious when trying to interpret our findings surrounding sleep.”

Another limitation is that despite a large sample size, people of color were underrepresented, limiting the generalizability of the findings. As well, other healthy pursuits – for example, reading – might have contributed to improved cognition.
 

Important findings

In a comment, Jennifer J. Heisz, PhD, associate professor and Canada research chair in brain health and aging, department of kinesiology, McMaster University, Hamilton, Ont., said the findings from the study are important.

“Through the statistical modelling, the authors demonstrate that swapping just 9 minutes of sedentary behavior with moderate to vigorous physical activity, such as a brisk walk or bike ride, was associated with an increase in cognition.”

She added that this seemed to be especially true for people who sit while at work.

The findings “confer with the growing consensus” that some exercise is better than none when it comes to brain health, said Dr. Heisz.

“Clinicians should encourage their patients to add a brisk, 10-minute walk to their daily routine and break up prolonged sitting with short movement breaks.”

She noted the study was cross-sectional, “so it is not possible to infer causation.”

The study received funding from the Medical Research Council and the British Heart Foundation. Mr. Mitchell and Dr. Heisz have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Middle-aged adults who spend just 9 additional minutes a day participating in moderate to vigorous physical activity (MVPA) experience improved cognition in new findings that underscore the critical role brisk exercise, such as running and cycling, plays in brain health.

“Even minor differences in daily behavior appeared meaningful for cognition in this study,” researcher John J. Mitchell, MSci and PhD candidate, Medical Research Council, London, told this news organization.

The findings were published online in the Journal of Epidemiology and Community Health.
 

Research gap

Previous research has linked physical activity (PA) with increased cognitive reserve, which delays the onset of cognitive decline in later life. But disentangling the most important components of PA for cognition – such as intensity and volume – has not been well researched.

Previous studies didn’t capture sleep time, which typically takes up the largest component of the day. Sleep is “acutely relevant” when examining cognition, the investigators noted.

In addition, studies in this area often focus on just one or two activity components of the day, which “neglects the growing awareness” that movements “are all tightly interlinked,” said Mr. Mitchell.

The new study included 4,481 participants in the British Cohort Study who were born in 1970 across England, Scotland, and Wales. The participants were followed throughout childhood and adulthood.

The median age of the participants was 47 years, and they were predominantly White, female (52%), married (66%), and well educated. Most were occasional or nonrisky alcohol consumers, and half had never smoked.

The researchers collected biometric measurements and health, demographic, and lifestyle information. Participants wore a thigh-mounted accelerometer at least 7 consecutive hours a day for up to 7 days to track PA, sedentary behavior (SB), and sleep time.

The device used in the study could detect subtle movements as well as speed of accelerations, said Mr. Mitchell. “From this, we can distinguish MVPA from slow walking, standing, and sitting. It’s the current best practice for detecting the more subtle movements we make, such as brisk walking and stair climbing, beyond just ‘exercise,’ “ he added.

Light intensity PA (LIPA) describes movement such as walking and moving around the house or office, while MVPA includes activities such as brisk walking and running that accelerate the heart rate. SB, defined as time spent sitting or lying, is distinguished from standing by the thigh inclination.

On an average day, the cohort spent 51 minutes in MVPA; 5 hours, 42 minutes in LIPA; 9 hours, 16 minutes in SB; and 8 hours, 11 minutes sleeping.

Researchers calculated an overall global score for verbal memory and executive function.

The study used “compositional data analysis,” a statistical method that can examine the associations of cognition and PA in the context of all components of daily movement.

The analysis revealed a positive association between MVPA and cognition relative to all other behaviors, after adjustment for sociodemographic factors that included sex, age, education, and marital status. But the relationship lessened after further adjustment for health status – for example, cardiovascular disease or disability – and lifestyle factors, such as alcohol consumption and smoking status.

SB relative to all other movements remained positively associated with cognition after full adjustment. This, the authors speculated, may reflect engagement in cognitively stimulating activities such as reading.

To better understand the associations, the researchers used a statistical method to reallocate time in the cohort’s average day from one activity component to another.

“We held two of the components static but moved time between the other two and monitored the theoretical ramifications of that change for cognition,” said Mr. Mitchell.
 

Real cognitive change

There was a 1.31% improvement in cognition ranking compared to the sample average after replacing 9 minutes of sedentary activity with MVPA (1.31; 95% confidence interval [CI], 0.09-2.50). There was a 1.27% improvement after replacing 7 minutes of LIPA with MVPA, and a 1.2% improvement after replacing 7 minutes of sleep with MVPA.

Individuals might move up from about the 50th percentile to the 51st or 52nd percentile after just 9 minutes of more moderate to vigorous movement in place of sitting, said Mr. Mitchell. “This highlights how even very modest differences in people’s daily movement – less than 10 minutes – is linked to quite real changes in our cognitive health.”

The impact of physical activity appeared greatest on working memory and mental processes, such as planning and organization.

On the other hand, cognition declined by 1%-2% after replacing MVPA with 8 minutes of SB, 6 minutes of LIPA, or 7 minutes of sleep.

The activity tracking device couldn’t determine how well participants slept, which is “a clear limitation” of the study, said Mr. Mitchell. “We have to be cautious when trying to interpret our findings surrounding sleep.”

Another limitation is that despite a large sample size, people of color were underrepresented, limiting the generalizability of the findings. As well, other healthy pursuits – for example, reading – might have contributed to improved cognition.
 

Important findings

In a comment, Jennifer J. Heisz, PhD, associate professor and Canada research chair in brain health and aging, department of kinesiology, McMaster University, Hamilton, Ont., said the findings from the study are important.

“Through the statistical modelling, the authors demonstrate that swapping just 9 minutes of sedentary behavior with moderate to vigorous physical activity, such as a brisk walk or bike ride, was associated with an increase in cognition.”

She added that this seemed to be especially true for people who sit while at work.

The findings “confer with the growing consensus” that some exercise is better than none when it comes to brain health, said Dr. Heisz.

“Clinicians should encourage their patients to add a brisk, 10-minute walk to their daily routine and break up prolonged sitting with short movement breaks.”

She noted the study was cross-sectional, “so it is not possible to infer causation.”

The study received funding from the Medical Research Council and the British Heart Foundation. Mr. Mitchell and Dr. Heisz have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Middle-aged adults who spend just 9 additional minutes a day participating in moderate to vigorous physical activity (MVPA) experience improved cognition in new findings that underscore the critical role brisk exercise, such as running and cycling, plays in brain health.

“Even minor differences in daily behavior appeared meaningful for cognition in this study,” researcher John J. Mitchell, MSci and PhD candidate, Medical Research Council, London, told this news organization.

The findings were published online in the Journal of Epidemiology and Community Health.
 

Research gap

Previous research has linked physical activity (PA) with increased cognitive reserve, which delays the onset of cognitive decline in later life. But disentangling the most important components of PA for cognition – such as intensity and volume – has not been well researched.

Previous studies didn’t capture sleep time, which typically takes up the largest component of the day. Sleep is “acutely relevant” when examining cognition, the investigators noted.

In addition, studies in this area often focus on just one or two activity components of the day, which “neglects the growing awareness” that movements “are all tightly interlinked,” said Mr. Mitchell.

The new study included 4,481 participants in the British Cohort Study who were born in 1970 across England, Scotland, and Wales. The participants were followed throughout childhood and adulthood.

The median age of the participants was 47 years, and they were predominantly White, female (52%), married (66%), and well educated. Most were occasional or nonrisky alcohol consumers, and half had never smoked.

The researchers collected biometric measurements and health, demographic, and lifestyle information. Participants wore a thigh-mounted accelerometer at least 7 consecutive hours a day for up to 7 days to track PA, sedentary behavior (SB), and sleep time.

The device used in the study could detect subtle movements as well as speed of accelerations, said Mr. Mitchell. “From this, we can distinguish MVPA from slow walking, standing, and sitting. It’s the current best practice for detecting the more subtle movements we make, such as brisk walking and stair climbing, beyond just ‘exercise,’ “ he added.

Light intensity PA (LIPA) describes movement such as walking and moving around the house or office, while MVPA includes activities such as brisk walking and running that accelerate the heart rate. SB, defined as time spent sitting or lying, is distinguished from standing by the thigh inclination.

On an average day, the cohort spent 51 minutes in MVPA; 5 hours, 42 minutes in LIPA; 9 hours, 16 minutes in SB; and 8 hours, 11 minutes sleeping.

Researchers calculated an overall global score for verbal memory and executive function.

The study used “compositional data analysis,” a statistical method that can examine the associations of cognition and PA in the context of all components of daily movement.

The analysis revealed a positive association between MVPA and cognition relative to all other behaviors, after adjustment for sociodemographic factors that included sex, age, education, and marital status. But the relationship lessened after further adjustment for health status – for example, cardiovascular disease or disability – and lifestyle factors, such as alcohol consumption and smoking status.

SB relative to all other movements remained positively associated with cognition after full adjustment. This, the authors speculated, may reflect engagement in cognitively stimulating activities such as reading.

To better understand the associations, the researchers used a statistical method to reallocate time in the cohort’s average day from one activity component to another.

“We held two of the components static but moved time between the other two and monitored the theoretical ramifications of that change for cognition,” said Mr. Mitchell.
 

Real cognitive change

There was a 1.31% improvement in cognition ranking compared to the sample average after replacing 9 minutes of sedentary activity with MVPA (1.31; 95% confidence interval [CI], 0.09-2.50). There was a 1.27% improvement after replacing 7 minutes of LIPA with MVPA, and a 1.2% improvement after replacing 7 minutes of sleep with MVPA.

Individuals might move up from about the 50th percentile to the 51st or 52nd percentile after just 9 minutes of more moderate to vigorous movement in place of sitting, said Mr. Mitchell. “This highlights how even very modest differences in people’s daily movement – less than 10 minutes – is linked to quite real changes in our cognitive health.”

The impact of physical activity appeared greatest on working memory and mental processes, such as planning and organization.

On the other hand, cognition declined by 1%-2% after replacing MVPA with 8 minutes of SB, 6 minutes of LIPA, or 7 minutes of sleep.

The activity tracking device couldn’t determine how well participants slept, which is “a clear limitation” of the study, said Mr. Mitchell. “We have to be cautious when trying to interpret our findings surrounding sleep.”

Another limitation is that despite a large sample size, people of color were underrepresented, limiting the generalizability of the findings. As well, other healthy pursuits – for example, reading – might have contributed to improved cognition.
 

Important findings

In a comment, Jennifer J. Heisz, PhD, associate professor and Canada research chair in brain health and aging, department of kinesiology, McMaster University, Hamilton, Ont., said the findings from the study are important.

“Through the statistical modelling, the authors demonstrate that swapping just 9 minutes of sedentary behavior with moderate to vigorous physical activity, such as a brisk walk or bike ride, was associated with an increase in cognition.”

She added that this seemed to be especially true for people who sit while at work.

The findings “confer with the growing consensus” that some exercise is better than none when it comes to brain health, said Dr. Heisz.

“Clinicians should encourage their patients to add a brisk, 10-minute walk to their daily routine and break up prolonged sitting with short movement breaks.”

She noted the study was cross-sectional, “so it is not possible to infer causation.”

The study received funding from the Medical Research Council and the British Heart Foundation. Mr. Mitchell and Dr. Heisz have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

People hospitalized with viral infections like the flu are more likely to have disorders that degrade the nervous system, like Alzheimer’s or Parkinson’s, later in life, a new analysis shows. 

Researchers found 22 links between viruses and common neurologic conditions often seen in older people. The viruses included influenza, encephalitis, herpes, hepatitis, pneumonia, meningitis, and shingles. Those viruses were linked to one or more of these conditions: Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS), dementia, and multiple sclerosis.

The authors of the study, which was published this month in the journal Neuron, cautioned that their findings stopped short of saying the viruses caused the disorders. 

“Neurodegenerative disorders are a collection of diseases for which there are very few effective treatments and many risk factors,” study author and National Institutes of Health researcher Andrew B. Singleton, PhD, said in a news release from the NIH. “Our results support the idea that viral infections and related inflammation in the nervous system may be common – and possibly avoidable – risk factors for these types of disorders.”

For the study, two data sets were analyzed with a combined 800,000 medical records for people in Finland and the United Kingdom. People who were hospitalized with COVID-19 were excluded from the study.

Generalized dementia was the condition linked to the most viruses. People exposed to viral encephalitis, which causes brain inflammation, were 20 times more likely to be diagnosed with Alzheimer’s, compared with those who were not diagnosed with that virus.

Both influenza and pneumonia were also associated with all of the neurodegenerative disorder diagnoses studied, with the exception of multiple sclerosis. The researchers found that severe flu cases were linked to the most risks.

“Keep in mind that the individuals we studied did not have the common cold. Their infections made them so sick that they had to go to the hospital,” said study author and NIH researcher Michael Nalls, PhD. “Nevertheless, the fact that commonly used vaccines reduce the risk or severity of many of the viral illnesses observed in this study raises the possibility that the risks of neurodegenerative disorders might also be mitigated.”

The researchers examined the time from when someone was infected with a virus to the time when they were diagnosed with one of the neurodegenerative disorders. They found that most had a high risk within 1 year of infection. But in six scenarios, there were significant links that showed up after 5-15 years.

The authors wrote that vaccines that are available for some of the viruses studied may be a way to reduce the risk of getting diseases that degrade the nervous system.

A version of this article first appeared on WebMD.com.

People hospitalized with viral infections like the flu are more likely to have disorders that degrade the nervous system, like Alzheimer’s or Parkinson’s, later in life, a new analysis shows. 

Researchers found 22 links between viruses and common neurologic conditions often seen in older people. The viruses included influenza, encephalitis, herpes, hepatitis, pneumonia, meningitis, and shingles. Those viruses were linked to one or more of these conditions: Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS), dementia, and multiple sclerosis.

The authors of the study, which was published this month in the journal Neuron, cautioned that their findings stopped short of saying the viruses caused the disorders. 

“Neurodegenerative disorders are a collection of diseases for which there are very few effective treatments and many risk factors,” study author and National Institutes of Health researcher Andrew B. Singleton, PhD, said in a news release from the NIH. “Our results support the idea that viral infections and related inflammation in the nervous system may be common – and possibly avoidable – risk factors for these types of disorders.”

For the study, two data sets were analyzed with a combined 800,000 medical records for people in Finland and the United Kingdom. People who were hospitalized with COVID-19 were excluded from the study.

Generalized dementia was the condition linked to the most viruses. People exposed to viral encephalitis, which causes brain inflammation, were 20 times more likely to be diagnosed with Alzheimer’s, compared with those who were not diagnosed with that virus.

Both influenza and pneumonia were also associated with all of the neurodegenerative disorder diagnoses studied, with the exception of multiple sclerosis. The researchers found that severe flu cases were linked to the most risks.

“Keep in mind that the individuals we studied did not have the common cold. Their infections made them so sick that they had to go to the hospital,” said study author and NIH researcher Michael Nalls, PhD. “Nevertheless, the fact that commonly used vaccines reduce the risk or severity of many of the viral illnesses observed in this study raises the possibility that the risks of neurodegenerative disorders might also be mitigated.”

The researchers examined the time from when someone was infected with a virus to the time when they were diagnosed with one of the neurodegenerative disorders. They found that most had a high risk within 1 year of infection. But in six scenarios, there were significant links that showed up after 5-15 years.

The authors wrote that vaccines that are available for some of the viruses studied may be a way to reduce the risk of getting diseases that degrade the nervous system.

A version of this article first appeared on WebMD.com.

People hospitalized with viral infections like the flu are more likely to have disorders that degrade the nervous system, like Alzheimer’s or Parkinson’s, later in life, a new analysis shows. 

Researchers found 22 links between viruses and common neurologic conditions often seen in older people. The viruses included influenza, encephalitis, herpes, hepatitis, pneumonia, meningitis, and shingles. Those viruses were linked to one or more of these conditions: Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS), dementia, and multiple sclerosis.

The authors of the study, which was published this month in the journal Neuron, cautioned that their findings stopped short of saying the viruses caused the disorders. 

“Neurodegenerative disorders are a collection of diseases for which there are very few effective treatments and many risk factors,” study author and National Institutes of Health researcher Andrew B. Singleton, PhD, said in a news release from the NIH. “Our results support the idea that viral infections and related inflammation in the nervous system may be common – and possibly avoidable – risk factors for these types of disorders.”

For the study, two data sets were analyzed with a combined 800,000 medical records for people in Finland and the United Kingdom. People who were hospitalized with COVID-19 were excluded from the study.

Generalized dementia was the condition linked to the most viruses. People exposed to viral encephalitis, which causes brain inflammation, were 20 times more likely to be diagnosed with Alzheimer’s, compared with those who were not diagnosed with that virus.

Both influenza and pneumonia were also associated with all of the neurodegenerative disorder diagnoses studied, with the exception of multiple sclerosis. The researchers found that severe flu cases were linked to the most risks.

“Keep in mind that the individuals we studied did not have the common cold. Their infections made them so sick that they had to go to the hospital,” said study author and NIH researcher Michael Nalls, PhD. “Nevertheless, the fact that commonly used vaccines reduce the risk or severity of many of the viral illnesses observed in this study raises the possibility that the risks of neurodegenerative disorders might also be mitigated.”

The researchers examined the time from when someone was infected with a virus to the time when they were diagnosed with one of the neurodegenerative disorders. They found that most had a high risk within 1 year of infection. But in six scenarios, there were significant links that showed up after 5-15 years.

The authors wrote that vaccines that are available for some of the viruses studied may be a way to reduce the risk of getting diseases that degrade the nervous system.

A version of this article first appeared on WebMD.com.

Several decades ago, a new patient came to my office with her family. She was elderly, in good health, spoke no English, and her extended family translated for her. Their request: “Don’t tell her that she has cancer.” Sharing her diagnosis with her would cause too much stress, they said. Their mother would not be able to tolerate the bad news, they said. She would “give up.”

I asked her (through her family and an interpreter) how much she wanted to know about what was going on, or would she prefer I confine my remarks to her family? It turns out that she did want to know her diagnosis and prognosis, and after a thorough discussion in front of her family about her treatment options, she decided she did not want to proceed with additional therapy. She wanted to focus on quality of life. I did not get the impression that this is what her family would have opted for.

The patient’s voice can take multiple directions, such as making informed decisions about their own care. When empowered, patients can and will express their wants, needs, feelings, and priorities to their providers, and they’ll participate in directing their own care. There is a growing body of evidence that shows patients who are more engaged and share decision-making with their health care professionals have better health outcomes and care experiences. Engaged patients feel more empowered and are more motivated to take action. They’re also more likely to follow treatment plans, take their medications, and heed their provider’s recommendations. By virtue of better treatments for lung cancer, many patients are living longer and better lives. Some of these patients even become “experts” on their own care, often bringing questions about research and clinical trials to the attention of their providers.
 

The patient’s voice in research and advocacy

The patient’s perspective is also key to a meaningful, successful clinical research project. Rather than being carried out to, about, or for the patient, patient involvement means research being carried out with or by patients. A patient and researcher may have different research goals. For example, patients may value being able to work, be with family, and live without pain, whereas a clinical researcher’s goal may be inducing responses. Patient involvement is important in both laboratory research and clinical research. The best-designed projects involve patient advocates from the beginning of the project to help make research relevant and meaningful to patients and include these perspectives through project completion.

More and more pharmaceutical companies are actively involving patients at all levels of protocol development, including protocol design and selection of relevant outcomes to patients. Benefits of engaging patients as partners in research include inclusion of real-world data, increased study enrollment, and translation of results to the cancer community in an understandable and accessible manner.
 

Accelerated research

Advocating for accelerated research is another area where the patient’s voice is important. Patients can and do identify research priorities for researchers, funding agencies, and pharma. Patients who support research advocacy are frequently part of meetings and panel discussions with researchers, the Food and Drug Administration, and the National Cancer Institute. And, they serve on advisory boards for pharmaceutical companies. They participate in grant reviews and institutional review boards, review manuscripts, and are active members of the cooperative groups and other professional societies. In fact, patient-led advocacy groups are raising money to help fund research they feel is most important to them. In lung cancer, for example, there are many groups organized around biomarkers, including the EGFR Resisters, ALK Positive, ROS1ders, MET Crusaders, and KRAS Kickers, who have raised hundreds of thousands of dollars to fund investigator-led translational research that would not have occurred without their involvement.

It is important to recognize that all patients are different and have different values and motivations that are important to them and influence their life decisions. Some patients want to know more about their condition and their preferences should be respected. Similarly, it’s critical to understand that not every patient is an advocate and not every advocate is a research advocate. Research advocates have more in-depth knowledge about the science of lung cancer and focus on representing the patient perspective for all lung cancer patients.

So, getting back to my original story: Did my patient “give up” by choosing palliative care without chemotherapy? Perhaps, but I don’t think she considered her decision “giving up.” Instead, she made the best decision possible for herself. What would have happened had she not been told of her diagnosis? She probably would not have spent extra quality time with her family, as they tried to ignore the obvious. And, after all, quality time with her family was all she wanted.

Dr. Schiller is a medical oncologist and founding member of Oncologists United for Climate and Health. She is a former board member of the International Association for the Study of Lung Cancer and a current board member of the Lung Cancer Research Foundation. Ivy Elkins, cofounder of EGFR Resisters, a patient, survivor, and caregiver advocacy group, contributed to this article.

Several decades ago, a new patient came to my office with her family. She was elderly, in good health, spoke no English, and her extended family translated for her. Their request: “Don’t tell her that she has cancer.” Sharing her diagnosis with her would cause too much stress, they said. Their mother would not be able to tolerate the bad news, they said. She would “give up.”

I asked her (through her family and an interpreter) how much she wanted to know about what was going on, or would she prefer I confine my remarks to her family? It turns out that she did want to know her diagnosis and prognosis, and after a thorough discussion in front of her family about her treatment options, she decided she did not want to proceed with additional therapy. She wanted to focus on quality of life. I did not get the impression that this is what her family would have opted for.

The patient’s voice can take multiple directions, such as making informed decisions about their own care. When empowered, patients can and will express their wants, needs, feelings, and priorities to their providers, and they’ll participate in directing their own care. There is a growing body of evidence that shows patients who are more engaged and share decision-making with their health care professionals have better health outcomes and care experiences. Engaged patients feel more empowered and are more motivated to take action. They’re also more likely to follow treatment plans, take their medications, and heed their provider’s recommendations. By virtue of better treatments for lung cancer, many patients are living longer and better lives. Some of these patients even become “experts” on their own care, often bringing questions about research and clinical trials to the attention of their providers.
 

The patient’s voice in research and advocacy

The patient’s perspective is also key to a meaningful, successful clinical research project. Rather than being carried out to, about, or for the patient, patient involvement means research being carried out with or by patients. A patient and researcher may have different research goals. For example, patients may value being able to work, be with family, and live without pain, whereas a clinical researcher’s goal may be inducing responses. Patient involvement is important in both laboratory research and clinical research. The best-designed projects involve patient advocates from the beginning of the project to help make research relevant and meaningful to patients and include these perspectives through project completion.

More and more pharmaceutical companies are actively involving patients at all levels of protocol development, including protocol design and selection of relevant outcomes to patients. Benefits of engaging patients as partners in research include inclusion of real-world data, increased study enrollment, and translation of results to the cancer community in an understandable and accessible manner.
 

Accelerated research

Advocating for accelerated research is another area where the patient’s voice is important. Patients can and do identify research priorities for researchers, funding agencies, and pharma. Patients who support research advocacy are frequently part of meetings and panel discussions with researchers, the Food and Drug Administration, and the National Cancer Institute. And, they serve on advisory boards for pharmaceutical companies. They participate in grant reviews and institutional review boards, review manuscripts, and are active members of the cooperative groups and other professional societies. In fact, patient-led advocacy groups are raising money to help fund research they feel is most important to them. In lung cancer, for example, there are many groups organized around biomarkers, including the EGFR Resisters, ALK Positive, ROS1ders, MET Crusaders, and KRAS Kickers, who have raised hundreds of thousands of dollars to fund investigator-led translational research that would not have occurred without their involvement.

It is important to recognize that all patients are different and have different values and motivations that are important to them and influence their life decisions. Some patients want to know more about their condition and their preferences should be respected. Similarly, it’s critical to understand that not every patient is an advocate and not every advocate is a research advocate. Research advocates have more in-depth knowledge about the science of lung cancer and focus on representing the patient perspective for all lung cancer patients.

So, getting back to my original story: Did my patient “give up” by choosing palliative care without chemotherapy? Perhaps, but I don’t think she considered her decision “giving up.” Instead, she made the best decision possible for herself. What would have happened had she not been told of her diagnosis? She probably would not have spent extra quality time with her family, as they tried to ignore the obvious. And, after all, quality time with her family was all she wanted.

Dr. Schiller is a medical oncologist and founding member of Oncologists United for Climate and Health. She is a former board member of the International Association for the Study of Lung Cancer and a current board member of the Lung Cancer Research Foundation. Ivy Elkins, cofounder of EGFR Resisters, a patient, survivor, and caregiver advocacy group, contributed to this article.

Several decades ago, a new patient came to my office with her family. She was elderly, in good health, spoke no English, and her extended family translated for her. Their request: “Don’t tell her that she has cancer.” Sharing her diagnosis with her would cause too much stress, they said. Their mother would not be able to tolerate the bad news, they said. She would “give up.”

I asked her (through her family and an interpreter) how much she wanted to know about what was going on, or would she prefer I confine my remarks to her family? It turns out that she did want to know her diagnosis and prognosis, and after a thorough discussion in front of her family about her treatment options, she decided she did not want to proceed with additional therapy. She wanted to focus on quality of life. I did not get the impression that this is what her family would have opted for.

The patient’s voice can take multiple directions, such as making informed decisions about their own care. When empowered, patients can and will express their wants, needs, feelings, and priorities to their providers, and they’ll participate in directing their own care. There is a growing body of evidence that shows patients who are more engaged and share decision-making with their health care professionals have better health outcomes and care experiences. Engaged patients feel more empowered and are more motivated to take action. They’re also more likely to follow treatment plans, take their medications, and heed their provider’s recommendations. By virtue of better treatments for lung cancer, many patients are living longer and better lives. Some of these patients even become “experts” on their own care, often bringing questions about research and clinical trials to the attention of their providers.
 

The patient’s voice in research and advocacy

The patient’s perspective is also key to a meaningful, successful clinical research project. Rather than being carried out to, about, or for the patient, patient involvement means research being carried out with or by patients. A patient and researcher may have different research goals. For example, patients may value being able to work, be with family, and live without pain, whereas a clinical researcher’s goal may be inducing responses. Patient involvement is important in both laboratory research and clinical research. The best-designed projects involve patient advocates from the beginning of the project to help make research relevant and meaningful to patients and include these perspectives through project completion.

More and more pharmaceutical companies are actively involving patients at all levels of protocol development, including protocol design and selection of relevant outcomes to patients. Benefits of engaging patients as partners in research include inclusion of real-world data, increased study enrollment, and translation of results to the cancer community in an understandable and accessible manner.
 

Accelerated research

Advocating for accelerated research is another area where the patient’s voice is important. Patients can and do identify research priorities for researchers, funding agencies, and pharma. Patients who support research advocacy are frequently part of meetings and panel discussions with researchers, the Food and Drug Administration, and the National Cancer Institute. And, they serve on advisory boards for pharmaceutical companies. They participate in grant reviews and institutional review boards, review manuscripts, and are active members of the cooperative groups and other professional societies. In fact, patient-led advocacy groups are raising money to help fund research they feel is most important to them. In lung cancer, for example, there are many groups organized around biomarkers, including the EGFR Resisters, ALK Positive, ROS1ders, MET Crusaders, and KRAS Kickers, who have raised hundreds of thousands of dollars to fund investigator-led translational research that would not have occurred without their involvement.

It is important to recognize that all patients are different and have different values and motivations that are important to them and influence their life decisions. Some patients want to know more about their condition and their preferences should be respected. Similarly, it’s critical to understand that not every patient is an advocate and not every advocate is a research advocate. Research advocates have more in-depth knowledge about the science of lung cancer and focus on representing the patient perspective for all lung cancer patients.

So, getting back to my original story: Did my patient “give up” by choosing palliative care without chemotherapy? Perhaps, but I don’t think she considered her decision “giving up.” Instead, she made the best decision possible for herself. What would have happened had she not been told of her diagnosis? She probably would not have spent extra quality time with her family, as they tried to ignore the obvious. And, after all, quality time with her family was all she wanted.

Dr. Schiller is a medical oncologist and founding member of Oncologists United for Climate and Health. She is a former board member of the International Association for the Study of Lung Cancer and a current board member of the Lung Cancer Research Foundation. Ivy Elkins, cofounder of EGFR Resisters, a patient, survivor, and caregiver advocacy group, contributed to this article.

High levels of high-density lipoprotein cholesterol (HDL-C) in older adults are associated with a higher risk of sustaining a fracture than lower HDL-C levels, a new study suggests.

Raycat/Getty Images

“Two animal studies showing that HDL-C reduces bone mineral density by reducing osteoblast number and function provide a plausible explanation for why high HDL-C may increase the risk of fractures,” Monira Hussain, MBBS, MPH, PhD, of Monash University in Melbourne, told this news organization. “So, it was not surprising when our analyses provided evidence that amongst those in the highest quintile of HDL-C (> 74 mg/dL), there was a [33%] increased risk of fractures.”

After adjustment, one standard deviation increment in HDL-C level was associated with a 14% higher risk of fracture during a 4-year follow-up.

Based on this and other studies, Dr. Hussain said, “I believe that the finding of a very high HDL-C [should] alert clinicians to a higher risk of mortality, fractures, and possibly other threats to their patient’s health.”

The study was published online in JAMA Cardiology.
 

Independent risk factor

For this report, the researchers conducted a post hoc analysis of data from the Aspirin in Reducing Events in the Elderly (ASPREE) clinical trial and the ASPREE-Fracture substudy.

ASPREE was a double-blind, randomized, placebo-controlled primary prevention trial of aspirin. Participants were 16,703 community-dwelling Australians and 2,411 individuals from the United States with a mean age of 75 and without evident cardiovascular disease, dementia, physical disability, or life-limiting chronic illness.

The ASPREE-Fracture substudy collected data on fractures reported post randomization from the Australian participants. Fractures were confirmed by imaging and adjudicated by an expert panel and included both traumatic and minimal trauma fractures.

Of the 16,262 participants who had a plasma HDL-C measurement at baseline (55% women), 1,659 (10.2%) experienced at least one fracture over a median of 4 years. This included 711 minimal trauma fractures (for example, falls from standing height) and 948 other trauma fractures, mainly falls on stairs, ladders, or stools.

Higher rates of fractures occurred in the highest quintile of HDL-C level where the mean level was 89 mg/dL. At baseline, participants in that quintile had a lower BMI, a high prevalence of current/former smoking and current alcohol use, 12 years or longer of school, more physical activity, and higher use of antiosteoporosis medication. They also had less chronic kidney disease, diabetes, prefrailty/frailty, or treatment with lipid-lowering drugs.

In a fully adjusted model, each standard deviation increment in HDL-C level was associated with a 14% higher risk of fractures (hazard ratio, 1.14). When analyzed in quintiles, compared with participants in Q1, those in Q5 had a 33% higher risk for fracture (HR, 1.33).

Prevalence rates were similar between the sexes. The increase in fracture risk appeared to be independent of traditional risk factors for fractures, including age, sex, physical activity, alcohol use, frailty, BMI, smoking status, diabetes, chronic kidney disease, use of lipid-lowering or antiosteoporosis drugs, and education, the authors note.

The results persisted in sensitivity analyses in restricted subgroups of interest and in stratified analyses – including, for example, only minimal fractures; participants not taking antiosteoporosis drugs or statins; never smokers; nondrinkers; and those engaging in minimal physical activity (walking less than 30 minutes per day).

No association was observed between non–HDL-C levels and fractures.

The authors conclude that the study “provides robust evidence that higher levels of HDL-C are associated with incident fractures in both male and female individuals, independent of conventional risk factors.”
 

Clinically useful?

Commenting on the study for this news organization, Marilyn Tan, MD, clinic chief of the Endocrine Clinic and clinical associate professor of medicine at Stanford (Calif.) University, said, “I certainly would not recommend anyone do anything to actively lower their HDL levels. HDL levels are largely determined by genetics, diet, and lifestyle, with some effects from certain medications/supplements. Studies have demonstrated that moderately higher HDL levels may be protective for atherosclerosis.”

In the current study, she said, “Causation has not been proven, and importantly there is no evidence that reducing HDL levels reduces fracture risk. Also, this association between raised HDL levels and fracture risk has not been demonstrated consistently in other studies.”

Furthermore, she noted, the preclinical trials on which the authors based their hypothesis – that is, an association between HDL and a reduction in the number and function of osteoblasts – “has not been demonstrated widely in human subjects.”

“We have a large armamentarium of FDA-approved treatments for osteoporosis that have been clinically proven to reduce fracture risk very significantly, and these are the tools [in addition to lifestyle changes] we should use to reduce fracture risk,” Dr. Tan concluded.

John Wilkins, MD, of Northwestern University, Chicago, and Anand Rohatgi, MD, MSCS, of UT Southwestern Medical Center, Dallas, also point out some limitations of the study in a related editorial.

They note the inclusion of predominantly healthy adults with a mean age of 75, a population that could yield different findings from middle-aged cohorts with chronic illnesses, as well as a lack of clarity regarding the possible role of alcohol intake among the study participants.

Furthermore, the editorialists write, although significant associations were shown in this study, “models were not adjusted for detailed measures of exercise/activity, triglycerides, or any other lipids, including other HDL compositional measures such as HDL-P or ApoA-I levels. There was no assessment of whether HDL-C improved discrimination, reclassification, or any other validated measures of risk prediction performance.

“Taken together,” they conclude, “this study alone leaves several unanswered questions as to whether high HDL-C could be a useful biomarker to detect fracture risk.”

No commercial funding was disclosed. The authors report no relevant financial relationships.

A version of this article originally appeared on Medscape.com.

High levels of high-density lipoprotein cholesterol (HDL-C) in older adults are associated with a higher risk of sustaining a fracture than lower HDL-C levels, a new study suggests.

Raycat/Getty Images

“Two animal studies showing that HDL-C reduces bone mineral density by reducing osteoblast number and function provide a plausible explanation for why high HDL-C may increase the risk of fractures,” Monira Hussain, MBBS, MPH, PhD, of Monash University in Melbourne, told this news organization. “So, it was not surprising when our analyses provided evidence that amongst those in the highest quintile of HDL-C (> 74 mg/dL), there was a [33%] increased risk of fractures.”

After adjustment, one standard deviation increment in HDL-C level was associated with a 14% higher risk of fracture during a 4-year follow-up.

Based on this and other studies, Dr. Hussain said, “I believe that the finding of a very high HDL-C [should] alert clinicians to a higher risk of mortality, fractures, and possibly other threats to their patient’s health.”

The study was published online in JAMA Cardiology.
 

Independent risk factor

For this report, the researchers conducted a post hoc analysis of data from the Aspirin in Reducing Events in the Elderly (ASPREE) clinical trial and the ASPREE-Fracture substudy.

ASPREE was a double-blind, randomized, placebo-controlled primary prevention trial of aspirin. Participants were 16,703 community-dwelling Australians and 2,411 individuals from the United States with a mean age of 75 and without evident cardiovascular disease, dementia, physical disability, or life-limiting chronic illness.

The ASPREE-Fracture substudy collected data on fractures reported post randomization from the Australian participants. Fractures were confirmed by imaging and adjudicated by an expert panel and included both traumatic and minimal trauma fractures.

Of the 16,262 participants who had a plasma HDL-C measurement at baseline (55% women), 1,659 (10.2%) experienced at least one fracture over a median of 4 years. This included 711 minimal trauma fractures (for example, falls from standing height) and 948 other trauma fractures, mainly falls on stairs, ladders, or stools.

Higher rates of fractures occurred in the highest quintile of HDL-C level where the mean level was 89 mg/dL. At baseline, participants in that quintile had a lower BMI, a high prevalence of current/former smoking and current alcohol use, 12 years or longer of school, more physical activity, and higher use of antiosteoporosis medication. They also had less chronic kidney disease, diabetes, prefrailty/frailty, or treatment with lipid-lowering drugs.

In a fully adjusted model, each standard deviation increment in HDL-C level was associated with a 14% higher risk of fractures (hazard ratio, 1.14). When analyzed in quintiles, compared with participants in Q1, those in Q5 had a 33% higher risk for fracture (HR, 1.33).

Prevalence rates were similar between the sexes. The increase in fracture risk appeared to be independent of traditional risk factors for fractures, including age, sex, physical activity, alcohol use, frailty, BMI, smoking status, diabetes, chronic kidney disease, use of lipid-lowering or antiosteoporosis drugs, and education, the authors note.

The results persisted in sensitivity analyses in restricted subgroups of interest and in stratified analyses – including, for example, only minimal fractures; participants not taking antiosteoporosis drugs or statins; never smokers; nondrinkers; and those engaging in minimal physical activity (walking less than 30 minutes per day).

No association was observed between non–HDL-C levels and fractures.

The authors conclude that the study “provides robust evidence that higher levels of HDL-C are associated with incident fractures in both male and female individuals, independent of conventional risk factors.”
 

Clinically useful?

Commenting on the study for this news organization, Marilyn Tan, MD, clinic chief of the Endocrine Clinic and clinical associate professor of medicine at Stanford (Calif.) University, said, “I certainly would not recommend anyone do anything to actively lower their HDL levels. HDL levels are largely determined by genetics, diet, and lifestyle, with some effects from certain medications/supplements. Studies have demonstrated that moderately higher HDL levels may be protective for atherosclerosis.”

In the current study, she said, “Causation has not been proven, and importantly there is no evidence that reducing HDL levels reduces fracture risk. Also, this association between raised HDL levels and fracture risk has not been demonstrated consistently in other studies.”

Furthermore, she noted, the preclinical trials on which the authors based their hypothesis – that is, an association between HDL and a reduction in the number and function of osteoblasts – “has not been demonstrated widely in human subjects.”

“We have a large armamentarium of FDA-approved treatments for osteoporosis that have been clinically proven to reduce fracture risk very significantly, and these are the tools [in addition to lifestyle changes] we should use to reduce fracture risk,” Dr. Tan concluded.

John Wilkins, MD, of Northwestern University, Chicago, and Anand Rohatgi, MD, MSCS, of UT Southwestern Medical Center, Dallas, also point out some limitations of the study in a related editorial.

They note the inclusion of predominantly healthy adults with a mean age of 75, a population that could yield different findings from middle-aged cohorts with chronic illnesses, as well as a lack of clarity regarding the possible role of alcohol intake among the study participants.

Furthermore, the editorialists write, although significant associations were shown in this study, “models were not adjusted for detailed measures of exercise/activity, triglycerides, or any other lipids, including other HDL compositional measures such as HDL-P or ApoA-I levels. There was no assessment of whether HDL-C improved discrimination, reclassification, or any other validated measures of risk prediction performance.

“Taken together,” they conclude, “this study alone leaves several unanswered questions as to whether high HDL-C could be a useful biomarker to detect fracture risk.”

No commercial funding was disclosed. The authors report no relevant financial relationships.

A version of this article originally appeared on Medscape.com.

High levels of high-density lipoprotein cholesterol (HDL-C) in older adults are associated with a higher risk of sustaining a fracture than lower HDL-C levels, a new study suggests.

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“Two animal studies showing that HDL-C reduces bone mineral density by reducing osteoblast number and function provide a plausible explanation for why high HDL-C may increase the risk of fractures,” Monira Hussain, MBBS, MPH, PhD, of Monash University in Melbourne, told this news organization. “So, it was not surprising when our analyses provided evidence that amongst those in the highest quintile of HDL-C (> 74 mg/dL), there was a [33%] increased risk of fractures.”

After adjustment, one standard deviation increment in HDL-C level was associated with a 14% higher risk of fracture during a 4-year follow-up.

Based on this and other studies, Dr. Hussain said, “I believe that the finding of a very high HDL-C [should] alert clinicians to a higher risk of mortality, fractures, and possibly other threats to their patient’s health.”

The study was published online in JAMA Cardiology.
 

Independent risk factor

For this report, the researchers conducted a post hoc analysis of data from the Aspirin in Reducing Events in the Elderly (ASPREE) clinical trial and the ASPREE-Fracture substudy.

ASPREE was a double-blind, randomized, placebo-controlled primary prevention trial of aspirin. Participants were 16,703 community-dwelling Australians and 2,411 individuals from the United States with a mean age of 75 and without evident cardiovascular disease, dementia, physical disability, or life-limiting chronic illness.

The ASPREE-Fracture substudy collected data on fractures reported post randomization from the Australian participants. Fractures were confirmed by imaging and adjudicated by an expert panel and included both traumatic and minimal trauma fractures.

Of the 16,262 participants who had a plasma HDL-C measurement at baseline (55% women), 1,659 (10.2%) experienced at least one fracture over a median of 4 years. This included 711 minimal trauma fractures (for example, falls from standing height) and 948 other trauma fractures, mainly falls on stairs, ladders, or stools.

Higher rates of fractures occurred in the highest quintile of HDL-C level where the mean level was 89 mg/dL. At baseline, participants in that quintile had a lower BMI, a high prevalence of current/former smoking and current alcohol use, 12 years or longer of school, more physical activity, and higher use of antiosteoporosis medication. They also had less chronic kidney disease, diabetes, prefrailty/frailty, or treatment with lipid-lowering drugs.

In a fully adjusted model, each standard deviation increment in HDL-C level was associated with a 14% higher risk of fractures (hazard ratio, 1.14). When analyzed in quintiles, compared with participants in Q1, those in Q5 had a 33% higher risk for fracture (HR, 1.33).

Prevalence rates were similar between the sexes. The increase in fracture risk appeared to be independent of traditional risk factors for fractures, including age, sex, physical activity, alcohol use, frailty, BMI, smoking status, diabetes, chronic kidney disease, use of lipid-lowering or antiosteoporosis drugs, and education, the authors note.

The results persisted in sensitivity analyses in restricted subgroups of interest and in stratified analyses – including, for example, only minimal fractures; participants not taking antiosteoporosis drugs or statins; never smokers; nondrinkers; and those engaging in minimal physical activity (walking less than 30 minutes per day).

No association was observed between non–HDL-C levels and fractures.

The authors conclude that the study “provides robust evidence that higher levels of HDL-C are associated with incident fractures in both male and female individuals, independent of conventional risk factors.”
 

Clinically useful?

Commenting on the study for this news organization, Marilyn Tan, MD, clinic chief of the Endocrine Clinic and clinical associate professor of medicine at Stanford (Calif.) University, said, “I certainly would not recommend anyone do anything to actively lower their HDL levels. HDL levels are largely determined by genetics, diet, and lifestyle, with some effects from certain medications/supplements. Studies have demonstrated that moderately higher HDL levels may be protective for atherosclerosis.”

In the current study, she said, “Causation has not been proven, and importantly there is no evidence that reducing HDL levels reduces fracture risk. Also, this association between raised HDL levels and fracture risk has not been demonstrated consistently in other studies.”

Furthermore, she noted, the preclinical trials on which the authors based their hypothesis – that is, an association between HDL and a reduction in the number and function of osteoblasts – “has not been demonstrated widely in human subjects.”

“We have a large armamentarium of FDA-approved treatments for osteoporosis that have been clinically proven to reduce fracture risk very significantly, and these are the tools [in addition to lifestyle changes] we should use to reduce fracture risk,” Dr. Tan concluded.

John Wilkins, MD, of Northwestern University, Chicago, and Anand Rohatgi, MD, MSCS, of UT Southwestern Medical Center, Dallas, also point out some limitations of the study in a related editorial.

They note the inclusion of predominantly healthy adults with a mean age of 75, a population that could yield different findings from middle-aged cohorts with chronic illnesses, as well as a lack of clarity regarding the possible role of alcohol intake among the study participants.

Furthermore, the editorialists write, although significant associations were shown in this study, “models were not adjusted for detailed measures of exercise/activity, triglycerides, or any other lipids, including other HDL compositional measures such as HDL-P or ApoA-I levels. There was no assessment of whether HDL-C improved discrimination, reclassification, or any other validated measures of risk prediction performance.

“Taken together,” they conclude, “this study alone leaves several unanswered questions as to whether high HDL-C could be a useful biomarker to detect fracture risk.”

No commercial funding was disclosed. The authors report no relevant financial relationships.

A version of this article originally appeared on Medscape.com.

A recent change in Medicare policy designed to increase access to left ventricular assist devices (LVADs) may have had the unintended consequence of increasing inequalities in access to heart transplant for patients with advanced heart failure.

In December 2020, the Centers for Medicare & Medicaid Services relaxed restrictions on centers that implant LVADs but don’t perform heart transplants. Specifically, they dropped the requirement that LVAD-only centers obtain permission from a Medicare-approved heart transplant center authorizing LVAD implantation with “bridge-to-transplant” (BTT) intent, meaning the patient is a transplant candidate.

zimmytws/gettyimages

While the relaxed requirement has the potential to increase access to LVADs for appropriate patients, a look back at 22,221 LVAD recipients found that patients who received LVADs at transplant-capable centers had a 79% higher likelihood of receiving a BTT LVAD designation.

The 2-year heart transplant rate following LVAD implant was 25.6% for patients who received an LVAD at a heart transplant center, compared with 11.9% at LVAD-only centers.

Thomas Cascino, MD, with University of Michigan Health Frankel Cardiovascular Center, Ann Arbor, and colleagues reported their findings in JAMA Network Open.
 

Differential assessment?

Nontransplant LVAD centers are increasing in number in the United States now that the CMS has made establishing an LVAD-only center easier.

“Although there should be enthusiasm for the potential of LVAD-only centers to increase access to LVAD, it appears that receiving an LVAD at a center that does not perform transplants results in differential assessment of transplant eligibility at the time of LVAD implant and inequities in receipt of transplant,” Dr. Cascino and colleagues said.

“Being cared for at a center that does not perform heart transplant should not result in a lesser chance to receive a heart transplant,” Dr. Cascino added in a university news release. “Our study shows that this disparity existed before the policy change, and we think it will likely grow larger now that there is less collaboration.”

The CMS policy will likely “further challenge equity in access to transplant for patients seeking care at nontransplant centers and may have the unintended consequence of contributing to increasing inequities in access to transplants, as has been feared,” the researchers wrote.

They also note that recent changes in the adult heart allocation system under the United Network for Organ Sharing have significantly reduced the likelihood of transplant after durable LVAD implant unless candidates are listed as being at higher urgency status owing to an LVAD complication or clinical deterioration.

“The reality is that durable LVADs are much less likely to be a bridge to the best therapy (that is, transplant) in the current allocation system. As a result, there is a critical need to select appropriate durable LVAD and transplant candidates at the initial evaluation,” the authors said.

“This puts the onus on the transplant community to select appropriate LVAD and transplant candidates during the initial evaluation. We need a system in which any patient can walk into the same hospital and get the right therapy for them,” Dr. Cascino added in the news release.

The research was supported in part through funding from the University of Michigan Health department of cardiac surgery and the National Institutes of Health, National Heart, Lung, and Blood Institute. Dr. Cascino has received grants from Johnson & Johnson.

A version of this article first appeared on Medscape.com.

A recent change in Medicare policy designed to increase access to left ventricular assist devices (LVADs) may have had the unintended consequence of increasing inequalities in access to heart transplant for patients with advanced heart failure.

In December 2020, the Centers for Medicare & Medicaid Services relaxed restrictions on centers that implant LVADs but don’t perform heart transplants. Specifically, they dropped the requirement that LVAD-only centers obtain permission from a Medicare-approved heart transplant center authorizing LVAD implantation with “bridge-to-transplant” (BTT) intent, meaning the patient is a transplant candidate.

zimmytws/gettyimages

While the relaxed requirement has the potential to increase access to LVADs for appropriate patients, a look back at 22,221 LVAD recipients found that patients who received LVADs at transplant-capable centers had a 79% higher likelihood of receiving a BTT LVAD designation.

The 2-year heart transplant rate following LVAD implant was 25.6% for patients who received an LVAD at a heart transplant center, compared with 11.9% at LVAD-only centers.

Thomas Cascino, MD, with University of Michigan Health Frankel Cardiovascular Center, Ann Arbor, and colleagues reported their findings in JAMA Network Open.
 

Differential assessment?

Nontransplant LVAD centers are increasing in number in the United States now that the CMS has made establishing an LVAD-only center easier.

“Although there should be enthusiasm for the potential of LVAD-only centers to increase access to LVAD, it appears that receiving an LVAD at a center that does not perform transplants results in differential assessment of transplant eligibility at the time of LVAD implant and inequities in receipt of transplant,” Dr. Cascino and colleagues said.

“Being cared for at a center that does not perform heart transplant should not result in a lesser chance to receive a heart transplant,” Dr. Cascino added in a university news release. “Our study shows that this disparity existed before the policy change, and we think it will likely grow larger now that there is less collaboration.”

The CMS policy will likely “further challenge equity in access to transplant for patients seeking care at nontransplant centers and may have the unintended consequence of contributing to increasing inequities in access to transplants, as has been feared,” the researchers wrote.

They also note that recent changes in the adult heart allocation system under the United Network for Organ Sharing have significantly reduced the likelihood of transplant after durable LVAD implant unless candidates are listed as being at higher urgency status owing to an LVAD complication or clinical deterioration.

“The reality is that durable LVADs are much less likely to be a bridge to the best therapy (that is, transplant) in the current allocation system. As a result, there is a critical need to select appropriate durable LVAD and transplant candidates at the initial evaluation,” the authors said.

“This puts the onus on the transplant community to select appropriate LVAD and transplant candidates during the initial evaluation. We need a system in which any patient can walk into the same hospital and get the right therapy for them,” Dr. Cascino added in the news release.

The research was supported in part through funding from the University of Michigan Health department of cardiac surgery and the National Institutes of Health, National Heart, Lung, and Blood Institute. Dr. Cascino has received grants from Johnson & Johnson.

A version of this article first appeared on Medscape.com.

A recent change in Medicare policy designed to increase access to left ventricular assist devices (LVADs) may have had the unintended consequence of increasing inequalities in access to heart transplant for patients with advanced heart failure.

In December 2020, the Centers for Medicare & Medicaid Services relaxed restrictions on centers that implant LVADs but don’t perform heart transplants. Specifically, they dropped the requirement that LVAD-only centers obtain permission from a Medicare-approved heart transplant center authorizing LVAD implantation with “bridge-to-transplant” (BTT) intent, meaning the patient is a transplant candidate.

zimmytws/gettyimages

While the relaxed requirement has the potential to increase access to LVADs for appropriate patients, a look back at 22,221 LVAD recipients found that patients who received LVADs at transplant-capable centers had a 79% higher likelihood of receiving a BTT LVAD designation.

The 2-year heart transplant rate following LVAD implant was 25.6% for patients who received an LVAD at a heart transplant center, compared with 11.9% at LVAD-only centers.

Thomas Cascino, MD, with University of Michigan Health Frankel Cardiovascular Center, Ann Arbor, and colleagues reported their findings in JAMA Network Open.
 

Differential assessment?

Nontransplant LVAD centers are increasing in number in the United States now that the CMS has made establishing an LVAD-only center easier.

“Although there should be enthusiasm for the potential of LVAD-only centers to increase access to LVAD, it appears that receiving an LVAD at a center that does not perform transplants results in differential assessment of transplant eligibility at the time of LVAD implant and inequities in receipt of transplant,” Dr. Cascino and colleagues said.

“Being cared for at a center that does not perform heart transplant should not result in a lesser chance to receive a heart transplant,” Dr. Cascino added in a university news release. “Our study shows that this disparity existed before the policy change, and we think it will likely grow larger now that there is less collaboration.”

The CMS policy will likely “further challenge equity in access to transplant for patients seeking care at nontransplant centers and may have the unintended consequence of contributing to increasing inequities in access to transplants, as has been feared,” the researchers wrote.

They also note that recent changes in the adult heart allocation system under the United Network for Organ Sharing have significantly reduced the likelihood of transplant after durable LVAD implant unless candidates are listed as being at higher urgency status owing to an LVAD complication or clinical deterioration.

“The reality is that durable LVADs are much less likely to be a bridge to the best therapy (that is, transplant) in the current allocation system. As a result, there is a critical need to select appropriate durable LVAD and transplant candidates at the initial evaluation,” the authors said.

“This puts the onus on the transplant community to select appropriate LVAD and transplant candidates during the initial evaluation. We need a system in which any patient can walk into the same hospital and get the right therapy for them,” Dr. Cascino added in the news release.

The research was supported in part through funding from the University of Michigan Health department of cardiac surgery and the National Institutes of Health, National Heart, Lung, and Blood Institute. Dr. Cascino has received grants from Johnson & Johnson.

A version of this article first appeared on Medscape.com.