Neurology

The first US clinical guidelines to diagnose and treat attention-deficit/hyperactivity disorder (ADHD) in adults are expected to be released this fall, providing patients, clinicians, insurers, and policymakers with a long overdue and much-needed standardized framework.

The initiative comes under the auspices of the American Professional Society of ADHD and Related Disorders (APSARD). David Goodman, MD, a member of the APSARD guidelines executive committee and assistant professor in the Department of Psychiatry and Behavioral Sciences at Johns Hopkins School of Medicine in Baltimore, Maryland, noted that the US lags behind several other nations, including Canada, the United Kingdom, Australia, and New Zealand who already have guidelines in place.

Dr. Goodman would not go into any detail as to why the country has been so slow off the mark but told this news organization that in part it has been due to a lack of specific funding. In addition, he said, “adult psychiatry abdicated responsibility for ADHD in adults.”

The American Psychiatric Association (APA) would not comment, although a spokesperson said two of its members are working with APSARD on the guidelines.

Estimates show that there are 10-11 million American adults (4.4%) with ADHD, making it the second most common psychiatric disorder in adults.

Surveys show that mental health professionals, including psychiatrists, report a lack of familiarity with ADHD in adults, said Margaret Sibley, PhD, professor of psychiatry and behavioral sciences at the University of Washington School of Medicine in Seattle and chair of the APSARD guidelines diagnostic and screening committee.

Many don’t consider an ADHD diagnosis in adults “because they were always trained to conceptualize it as something that’s relevant only in childhood,” Dr. Sibley told this new organization. However, research shows that people with ADHD do not outgrow the disorder.

“ADHD itself is still present and has unique problems associated with it in adults,” Dr. Sibley said.
 

Filling the Leadership Gap

Laurie Kulikosky, CEO of the advocacy group CHADD, said that the organization views the development of guidelines “as a huge step forward in the ability for more people to understand ADHD, particularly on the adult side.”

Oren Mason, MD, a primary care physician who specializes in ADHD at his Grand Rapids, Michigan-based practice, said “there hasn’t been a single specialty that has taken lead responsibility in adult ADHD,” which has contributed to the lag in guideline development.

In addition, Dr. Mason said, “trying to come up with adult guidelines even 5 or 10 years ago wouldn’t have yielded nearly as robust a set of guidelines because it’s taken awhile to have the evidence base to be able to make a few pronouncements really confidently.”

Not only has the evidence base grown but so has telehealth, especially during the height of the COVID-19 pandemic. That led to concerns that ADHD was not rigorously evaluated and that stimulants were prescribed too easily, said Dr. Goodman.

Several telehealth providers came under federal scrutiny, with the DEA accusing Cerebral’s pharmacy of dispensing stimulants for nonmedical reasons. The agency said that some 72,000 prescriptions for controlled substances, mostly stimulants, were written between 2020 and 2022.

APSARD felt it was time to act, said Dr. Goodman.

“We could not allow entrepreneurs who felt there was a business opportunity here to, under the auspices of advocating for mental health, increase the distribution of potentially addictive medications in the community,” he said
 

Ensuring Psychiatrist Buy-In

Development of the APSARD guidelines is led by Thomas Spencer, MD, a retired associate professor of psychiatry at Harvard Medical School, and Frances Rudnick Levin, MD, the Kennedy-Leavy Professor of Psychiatry at Columbia University, both of whom have decades of experience and clinical work in adults with ADHD.

Dr. Goodman is joined on the executive committee by Lenard Adler, MD (NYU Grossman School of Medicine), and Stephen Faraone, PhD (SUNY Upstate Medical University), along with 30 others who have expertise in psychiatry, psychology, primary care, and other health professions.

To participate in the development of the guidelines, experts had to agree to disengage from any potential conflicts and devote themselves — unpaid — to the process, said Dr. Goodman. The goal is to head off any charges of conflicts or biases, he said.

Three subcommittees — diagnosis and assessment, medical treatment, and nonmedical treatment — will review the literature, grade the evidence base, and use the Delphi consensus method to write the draft guidelines.

The draft will go out to the public and to medical specialties for comment, which will be considered for inclusion in the final publication, said Dr. Goodman.

The guidelines panel has been working closely with the APA and following the APA guideline development process in an effort to get buy-in from psychiatrists, he said.
 

Critical Educational Tool

“Doctors are often surprised to hear that there are no guidelines for adult ADHD in the US,” said Ann Childress, MD, APSARD president, when the group announced its effort in 2023. “Whether diagnosis and treatment are provided in office or online, the standard of care should be the same throughout the country,” she said.

Guidelines will “reduce mythology and error or at least when we run into mythology and error we can say no, there’s a giant consensus with hundreds of experts that disagree with that and so if you want to counter that you better bring some heavy machinery, you can’t just throw out an opinion and leave it unsupported,” said Dr. Mason.

Dr. Sibley said that, although there are no good data, anecdotally it appears many clinicians rely on the Diagnostic and Statistical Manual of Mental Disorders (DSM) when treating adults with ADHD.

The DSM “tells people what they should do but it doesn’t exactly tell them what’s the best way to do it,” she said, adding that often physicians follow what they learned from whoever they were trained by.

“Some people have been trained by people who are well versed in best practices and so they might be doing things that we would say have a research support to them, and other people might be doing things based on people who developed their own opinions about the best way to diagnose ADHD based on lived experience which may or may not be best practices,” Dr. Sibley said.

Her subcommittee aims to offer guidance on screening “that will be helpful in primary care, in terms of what are the most efficient ways to do it” and to help with accuracy, she said. Currently, there are likely some clinicians who are making too liberal a diagnosis and others who are making too conservative a diagnosis, she said.

With so many clinicians — especially in primary care — having a lack of experience, the guidelines could increase “the ability for more different kinds of providers to help,” said Dr. Kulikosky.

Guidelines should also provide a template for ongoing education, especially for clinicians who have never received any training in ADHD.

Dr. Goodman said it is increasingly likely that primary care physicians will be writing more prescriptions for ADHD medications than psychiatrists. “If that is the trajectory, the education of those providers seeing these patients is critical,” he said.
 

Offering Standards, Dispelling Myths

Guidelines can also help “shorten the learning curve,” said Dr. Mason, who said that he’s had to piece together evidence over the last few decades. Once published, the standards can be used in residency, for board exams, and continuing medical education, he said.

Not only do they offer a “kind of a shortcut to what we all know and agree on,” they also specify where the edges of knowledge are, he said.

Guidelines can also dissuade clinicians from practices that have no evidence to support them, such as “medication holidays,” said Dr. Mason. That has been employed to give children, especially, a break from side effects, but studies have shown that it actually increases side effects, he said.

Dr. Goodman and Dr. Sibley expect the guidelines to help with the challenge of diagnosis. Approximately 38% of adults with ADHD have a mood disorder and 48% have anxiety, said Dr. Goodman. Many others have coexisting posttraumatic stress disorder, substance use disorders, or medical illnesses that compound cognitive problems.

If an individual has several psychiatric conditions, “the question is how do you diagnostically prioritize which you treat first, second, and third, with the goal of treating one without making the others worse,” said Dr. Goodman.

“ADHD takes more detective work than other disorders,” said Dr. Sibley, adding that without an objective diagnostic and with overlaps with other comorbid disorders, “there are very complex issues that all of us wrestle with.”

While the guidelines will not provide algorithms, they will provide information that “will help guide them in the tougher diagnostic context,” she said.

Dr. Mason agreed. “It’s a complicated disorder to diagnose and treat. It’s hard for somebody to jump into it. [The guidelines] are going to give us — here’s what you really have to know, here’s what you have to do,” he said.

And it won’t just be clinicians who look to the guidelines. Calls to National Resource Center on ADHD — which CHADD runs for the federal government — from adults wanting to know more about their own condition “have increased exponentially” in the last few years, said Dr. Kulikosky. “We know adults are seeking out information, they are seeking out diagnosis and treatment,” she said.

Dr. Goodman and Dr. Sibley reported no relevant financial relationships. Dr. Mason reported that he consults for Otsuka and is a speaker for Iron Shore.

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

The first US clinical guidelines to diagnose and treat attention-deficit/hyperactivity disorder (ADHD) in adults are expected to be released this fall, providing patients, clinicians, insurers, and policymakers with a long overdue and much-needed standardized framework.

The initiative comes under the auspices of the American Professional Society of ADHD and Related Disorders (APSARD). David Goodman, MD, a member of the APSARD guidelines executive committee and assistant professor in the Department of Psychiatry and Behavioral Sciences at Johns Hopkins School of Medicine in Baltimore, Maryland, noted that the US lags behind several other nations, including Canada, the United Kingdom, Australia, and New Zealand who already have guidelines in place.

Dr. Goodman would not go into any detail as to why the country has been so slow off the mark but told this news organization that in part it has been due to a lack of specific funding. In addition, he said, “adult psychiatry abdicated responsibility for ADHD in adults.”

The American Psychiatric Association (APA) would not comment, although a spokesperson said two of its members are working with APSARD on the guidelines.

Estimates show that there are 10-11 million American adults (4.4%) with ADHD, making it the second most common psychiatric disorder in adults.

Surveys show that mental health professionals, including psychiatrists, report a lack of familiarity with ADHD in adults, said Margaret Sibley, PhD, professor of psychiatry and behavioral sciences at the University of Washington School of Medicine in Seattle and chair of the APSARD guidelines diagnostic and screening committee.

Many don’t consider an ADHD diagnosis in adults “because they were always trained to conceptualize it as something that’s relevant only in childhood,” Dr. Sibley told this new organization. However, research shows that people with ADHD do not outgrow the disorder.

“ADHD itself is still present and has unique problems associated with it in adults,” Dr. Sibley said.
 

Filling the Leadership Gap

Laurie Kulikosky, CEO of the advocacy group CHADD, said that the organization views the development of guidelines “as a huge step forward in the ability for more people to understand ADHD, particularly on the adult side.”

Oren Mason, MD, a primary care physician who specializes in ADHD at his Grand Rapids, Michigan-based practice, said “there hasn’t been a single specialty that has taken lead responsibility in adult ADHD,” which has contributed to the lag in guideline development.

In addition, Dr. Mason said, “trying to come up with adult guidelines even 5 or 10 years ago wouldn’t have yielded nearly as robust a set of guidelines because it’s taken awhile to have the evidence base to be able to make a few pronouncements really confidently.”

Not only has the evidence base grown but so has telehealth, especially during the height of the COVID-19 pandemic. That led to concerns that ADHD was not rigorously evaluated and that stimulants were prescribed too easily, said Dr. Goodman.

Several telehealth providers came under federal scrutiny, with the DEA accusing Cerebral’s pharmacy of dispensing stimulants for nonmedical reasons. The agency said that some 72,000 prescriptions for controlled substances, mostly stimulants, were written between 2020 and 2022.

APSARD felt it was time to act, said Dr. Goodman.

“We could not allow entrepreneurs who felt there was a business opportunity here to, under the auspices of advocating for mental health, increase the distribution of potentially addictive medications in the community,” he said
 

Ensuring Psychiatrist Buy-In

Development of the APSARD guidelines is led by Thomas Spencer, MD, a retired associate professor of psychiatry at Harvard Medical School, and Frances Rudnick Levin, MD, the Kennedy-Leavy Professor of Psychiatry at Columbia University, both of whom have decades of experience and clinical work in adults with ADHD.

Dr. Goodman is joined on the executive committee by Lenard Adler, MD (NYU Grossman School of Medicine), and Stephen Faraone, PhD (SUNY Upstate Medical University), along with 30 others who have expertise in psychiatry, psychology, primary care, and other health professions.

To participate in the development of the guidelines, experts had to agree to disengage from any potential conflicts and devote themselves — unpaid — to the process, said Dr. Goodman. The goal is to head off any charges of conflicts or biases, he said.

Three subcommittees — diagnosis and assessment, medical treatment, and nonmedical treatment — will review the literature, grade the evidence base, and use the Delphi consensus method to write the draft guidelines.

The draft will go out to the public and to medical specialties for comment, which will be considered for inclusion in the final publication, said Dr. Goodman.

The guidelines panel has been working closely with the APA and following the APA guideline development process in an effort to get buy-in from psychiatrists, he said.
 

Critical Educational Tool

“Doctors are often surprised to hear that there are no guidelines for adult ADHD in the US,” said Ann Childress, MD, APSARD president, when the group announced its effort in 2023. “Whether diagnosis and treatment are provided in office or online, the standard of care should be the same throughout the country,” she said.

Guidelines will “reduce mythology and error or at least when we run into mythology and error we can say no, there’s a giant consensus with hundreds of experts that disagree with that and so if you want to counter that you better bring some heavy machinery, you can’t just throw out an opinion and leave it unsupported,” said Dr. Mason.

Dr. Sibley said that, although there are no good data, anecdotally it appears many clinicians rely on the Diagnostic and Statistical Manual of Mental Disorders (DSM) when treating adults with ADHD.

The DSM “tells people what they should do but it doesn’t exactly tell them what’s the best way to do it,” she said, adding that often physicians follow what they learned from whoever they were trained by.

“Some people have been trained by people who are well versed in best practices and so they might be doing things that we would say have a research support to them, and other people might be doing things based on people who developed their own opinions about the best way to diagnose ADHD based on lived experience which may or may not be best practices,” Dr. Sibley said.

Her subcommittee aims to offer guidance on screening “that will be helpful in primary care, in terms of what are the most efficient ways to do it” and to help with accuracy, she said. Currently, there are likely some clinicians who are making too liberal a diagnosis and others who are making too conservative a diagnosis, she said.

With so many clinicians — especially in primary care — having a lack of experience, the guidelines could increase “the ability for more different kinds of providers to help,” said Dr. Kulikosky.

Guidelines should also provide a template for ongoing education, especially for clinicians who have never received any training in ADHD.

Dr. Goodman said it is increasingly likely that primary care physicians will be writing more prescriptions for ADHD medications than psychiatrists. “If that is the trajectory, the education of those providers seeing these patients is critical,” he said.
 

Offering Standards, Dispelling Myths

Guidelines can also help “shorten the learning curve,” said Dr. Mason, who said that he’s had to piece together evidence over the last few decades. Once published, the standards can be used in residency, for board exams, and continuing medical education, he said.

Not only do they offer a “kind of a shortcut to what we all know and agree on,” they also specify where the edges of knowledge are, he said.

Guidelines can also dissuade clinicians from practices that have no evidence to support them, such as “medication holidays,” said Dr. Mason. That has been employed to give children, especially, a break from side effects, but studies have shown that it actually increases side effects, he said.

Dr. Goodman and Dr. Sibley expect the guidelines to help with the challenge of diagnosis. Approximately 38% of adults with ADHD have a mood disorder and 48% have anxiety, said Dr. Goodman. Many others have coexisting posttraumatic stress disorder, substance use disorders, or medical illnesses that compound cognitive problems.

If an individual has several psychiatric conditions, “the question is how do you diagnostically prioritize which you treat first, second, and third, with the goal of treating one without making the others worse,” said Dr. Goodman.

“ADHD takes more detective work than other disorders,” said Dr. Sibley, adding that without an objective diagnostic and with overlaps with other comorbid disorders, “there are very complex issues that all of us wrestle with.”

While the guidelines will not provide algorithms, they will provide information that “will help guide them in the tougher diagnostic context,” she said.

Dr. Mason agreed. “It’s a complicated disorder to diagnose and treat. It’s hard for somebody to jump into it. [The guidelines] are going to give us — here’s what you really have to know, here’s what you have to do,” he said.

And it won’t just be clinicians who look to the guidelines. Calls to National Resource Center on ADHD — which CHADD runs for the federal government — from adults wanting to know more about their own condition “have increased exponentially” in the last few years, said Dr. Kulikosky. “We know adults are seeking out information, they are seeking out diagnosis and treatment,” she said.

Dr. Goodman and Dr. Sibley reported no relevant financial relationships. Dr. Mason reported that he consults for Otsuka and is a speaker for Iron Shore.

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

The first US clinical guidelines to diagnose and treat attention-deficit/hyperactivity disorder (ADHD) in adults are expected to be released this fall, providing patients, clinicians, insurers, and policymakers with a long overdue and much-needed standardized framework.

The initiative comes under the auspices of the American Professional Society of ADHD and Related Disorders (APSARD). David Goodman, MD, a member of the APSARD guidelines executive committee and assistant professor in the Department of Psychiatry and Behavioral Sciences at Johns Hopkins School of Medicine in Baltimore, Maryland, noted that the US lags behind several other nations, including Canada, the United Kingdom, Australia, and New Zealand who already have guidelines in place.

Dr. Goodman would not go into any detail as to why the country has been so slow off the mark but told this news organization that in part it has been due to a lack of specific funding. In addition, he said, “adult psychiatry abdicated responsibility for ADHD in adults.”

The American Psychiatric Association (APA) would not comment, although a spokesperson said two of its members are working with APSARD on the guidelines.

Estimates show that there are 10-11 million American adults (4.4%) with ADHD, making it the second most common psychiatric disorder in adults.

Surveys show that mental health professionals, including psychiatrists, report a lack of familiarity with ADHD in adults, said Margaret Sibley, PhD, professor of psychiatry and behavioral sciences at the University of Washington School of Medicine in Seattle and chair of the APSARD guidelines diagnostic and screening committee.

Many don’t consider an ADHD diagnosis in adults “because they were always trained to conceptualize it as something that’s relevant only in childhood,” Dr. Sibley told this new organization. However, research shows that people with ADHD do not outgrow the disorder.

“ADHD itself is still present and has unique problems associated with it in adults,” Dr. Sibley said.
 

Filling the Leadership Gap

Laurie Kulikosky, CEO of the advocacy group CHADD, said that the organization views the development of guidelines “as a huge step forward in the ability for more people to understand ADHD, particularly on the adult side.”

Oren Mason, MD, a primary care physician who specializes in ADHD at his Grand Rapids, Michigan-based practice, said “there hasn’t been a single specialty that has taken lead responsibility in adult ADHD,” which has contributed to the lag in guideline development.

In addition, Dr. Mason said, “trying to come up with adult guidelines even 5 or 10 years ago wouldn’t have yielded nearly as robust a set of guidelines because it’s taken awhile to have the evidence base to be able to make a few pronouncements really confidently.”

Not only has the evidence base grown but so has telehealth, especially during the height of the COVID-19 pandemic. That led to concerns that ADHD was not rigorously evaluated and that stimulants were prescribed too easily, said Dr. Goodman.

Several telehealth providers came under federal scrutiny, with the DEA accusing Cerebral’s pharmacy of dispensing stimulants for nonmedical reasons. The agency said that some 72,000 prescriptions for controlled substances, mostly stimulants, were written between 2020 and 2022.

APSARD felt it was time to act, said Dr. Goodman.

“We could not allow entrepreneurs who felt there was a business opportunity here to, under the auspices of advocating for mental health, increase the distribution of potentially addictive medications in the community,” he said
 

Ensuring Psychiatrist Buy-In

Development of the APSARD guidelines is led by Thomas Spencer, MD, a retired associate professor of psychiatry at Harvard Medical School, and Frances Rudnick Levin, MD, the Kennedy-Leavy Professor of Psychiatry at Columbia University, both of whom have decades of experience and clinical work in adults with ADHD.

Dr. Goodman is joined on the executive committee by Lenard Adler, MD (NYU Grossman School of Medicine), and Stephen Faraone, PhD (SUNY Upstate Medical University), along with 30 others who have expertise in psychiatry, psychology, primary care, and other health professions.

To participate in the development of the guidelines, experts had to agree to disengage from any potential conflicts and devote themselves — unpaid — to the process, said Dr. Goodman. The goal is to head off any charges of conflicts or biases, he said.

Three subcommittees — diagnosis and assessment, medical treatment, and nonmedical treatment — will review the literature, grade the evidence base, and use the Delphi consensus method to write the draft guidelines.

The draft will go out to the public and to medical specialties for comment, which will be considered for inclusion in the final publication, said Dr. Goodman.

The guidelines panel has been working closely with the APA and following the APA guideline development process in an effort to get buy-in from psychiatrists, he said.
 

Critical Educational Tool

“Doctors are often surprised to hear that there are no guidelines for adult ADHD in the US,” said Ann Childress, MD, APSARD president, when the group announced its effort in 2023. “Whether diagnosis and treatment are provided in office or online, the standard of care should be the same throughout the country,” she said.

Guidelines will “reduce mythology and error or at least when we run into mythology and error we can say no, there’s a giant consensus with hundreds of experts that disagree with that and so if you want to counter that you better bring some heavy machinery, you can’t just throw out an opinion and leave it unsupported,” said Dr. Mason.

Dr. Sibley said that, although there are no good data, anecdotally it appears many clinicians rely on the Diagnostic and Statistical Manual of Mental Disorders (DSM) when treating adults with ADHD.

The DSM “tells people what they should do but it doesn’t exactly tell them what’s the best way to do it,” she said, adding that often physicians follow what they learned from whoever they were trained by.

“Some people have been trained by people who are well versed in best practices and so they might be doing things that we would say have a research support to them, and other people might be doing things based on people who developed their own opinions about the best way to diagnose ADHD based on lived experience which may or may not be best practices,” Dr. Sibley said.

Her subcommittee aims to offer guidance on screening “that will be helpful in primary care, in terms of what are the most efficient ways to do it” and to help with accuracy, she said. Currently, there are likely some clinicians who are making too liberal a diagnosis and others who are making too conservative a diagnosis, she said.

With so many clinicians — especially in primary care — having a lack of experience, the guidelines could increase “the ability for more different kinds of providers to help,” said Dr. Kulikosky.

Guidelines should also provide a template for ongoing education, especially for clinicians who have never received any training in ADHD.

Dr. Goodman said it is increasingly likely that primary care physicians will be writing more prescriptions for ADHD medications than psychiatrists. “If that is the trajectory, the education of those providers seeing these patients is critical,” he said.
 

Offering Standards, Dispelling Myths

Guidelines can also help “shorten the learning curve,” said Dr. Mason, who said that he’s had to piece together evidence over the last few decades. Once published, the standards can be used in residency, for board exams, and continuing medical education, he said.

Not only do they offer a “kind of a shortcut to what we all know and agree on,” they also specify where the edges of knowledge are, he said.

Guidelines can also dissuade clinicians from practices that have no evidence to support them, such as “medication holidays,” said Dr. Mason. That has been employed to give children, especially, a break from side effects, but studies have shown that it actually increases side effects, he said.

Dr. Goodman and Dr. Sibley expect the guidelines to help with the challenge of diagnosis. Approximately 38% of adults with ADHD have a mood disorder and 48% have anxiety, said Dr. Goodman. Many others have coexisting posttraumatic stress disorder, substance use disorders, or medical illnesses that compound cognitive problems.

If an individual has several psychiatric conditions, “the question is how do you diagnostically prioritize which you treat first, second, and third, with the goal of treating one without making the others worse,” said Dr. Goodman.

“ADHD takes more detective work than other disorders,” said Dr. Sibley, adding that without an objective diagnostic and with overlaps with other comorbid disorders, “there are very complex issues that all of us wrestle with.”

While the guidelines will not provide algorithms, they will provide information that “will help guide them in the tougher diagnostic context,” she said.

Dr. Mason agreed. “It’s a complicated disorder to diagnose and treat. It’s hard for somebody to jump into it. [The guidelines] are going to give us — here’s what you really have to know, here’s what you have to do,” he said.

And it won’t just be clinicians who look to the guidelines. Calls to National Resource Center on ADHD — which CHADD runs for the federal government — from adults wanting to know more about their own condition “have increased exponentially” in the last few years, said Dr. Kulikosky. “We know adults are seeking out information, they are seeking out diagnosis and treatment,” she said.

Dr. Goodman and Dr. Sibley reported no relevant financial relationships. Dr. Mason reported that he consults for Otsuka and is a speaker for Iron Shore.

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

Delirium is tied to a significantly increased risk for dementia and death in older adults, with men at particular risk, new research showed.

Incident dementia risk was more than three times higher in those who experienced just one episode of delirium, with each additional episode linked to a further 20% increase in dementia risk. The association was strongest in men.

Patients with delirium also had a 39% higher mortality risk than those with no history of delirium.

“We have known for a long time that delirium is dangerous, and this provides evidence that it’s even more dangerous than perhaps we had appreciated,” said study investigator Emily H. Gordon, PhD, MBBS, a geriatrician and senior lecturer at the University of Queensland, Brisbane, Australia.

“But we also know delirium is preventable. There are no excuses anymore; we really need to work together to improve the hospital system, to implement what are known to be effective interventions,” she added.

The findings were published online in The BMJ.
 

Close Matching

Prior studies that suggested an association between delirium and dementia were relatively small with short follow-up and varied in their adjustment for confounders. They also didn’t account for the competing risk for death, researchers noted.

Investigators used a linked New South Wales (NSW) statewide dataset that includes records of care episodes from all NSW hospitals as well as personal, administrative, clinical, and death information.

The study included an eligible sample of 626,467 older adults without dementia at baseline with at least one hospital admission between 2009 and 2014. For these patients, researchers calculated a hospital frailty risk score and collected other information including primary diagnosis and mean length of hospital stay and stay in the intensive care unit. From diagnostic codes, they categorized patients into no delirium and delirium groups and determined the number of delirium episodes.

Investigators matched patients in the delirium group to patients with no delirium according to characteristics with potential to confound the association between delirium and risk for dementia, including age, gender, frailty, reason for hospitalization, and length of stay in hospital and intensive care.

The matched study sample included 55,211 (mean age, 83 years) each in the delirium and the no delirium groups. Despite matching, the length of hospital stay for the index episode was longer for the delirium group than the no delirium group (mean, 9 days vs 6 days).

The primary outcomes were death and incident dementia, determined via diagnostic codes. During a follow-up of 5.25 years, 58% of patients died, and 17% had a new dementia diagnosis.

Among patients with at least one episode of delirium, the rate of incident dementia was 3.4 times higher than in those without delirium. After accounting for the competing risk for death, incident dementia risk remained three times higher among the delirium group (hazard ratio [HR], 3.00; 95% CI, 2.91-3.10).

This association was stronger for men than women (HR, 3.17 and 2.88, respectively; P = .004).
 

Sex Differences

The study is thought to be the first to identify a difference between sexes in dementia risk and delirium, Dr. Gordon said. It’s possible delirium in men is more severe in intensity or lasts longer than in women, or the male brain is, for whatever reason, more vulnerable to the effects of delirium, said Dr. Gordon. But she stressed these are only theories.

Investigators also found a mortality rate 1.4 times higher in the delirium group versus those without delirium, equating to a 39% increased risk for death (HR, 1.39; 95% CI, 1.37-1.41). The risk was similar for men and women (interaction P = .62).

When researchers categorized delirium by number of episodes, they found each additional episode was associated with a 10% increased risk for death (HR, 1.10; 95% CI, 1.09-1.12).

In addition to its large size, long follow-up, and close matching, what sets this new study apart from previous research is it accounted for the competing risk for death, said Dr. Gordon.

“This is really important because you’re not going to get dementia if you die, and in this population, the rate of death is incredibly high,” she said. “If we just assume people who died didn’t get dementia, then that screws the results.”
 

Causal Link?

For those who experienced at least one episode of delirium within the first 12 months, each additional episode of delirium was associated with a 20% increased risk for dementia (HR, 1.20; 95% CI, 1.18-1.23).

That dose-response association suggests a causal link between the two, Dr. Gordon said.

“The number one way to prove causality is to do a randomized controlled trial,” which isn’t feasible with delirium, she said. “By demonstrating a dose-response relationship suggests that it could be a causal pathway.”

Exact mechanisms linking delirium with dementia are unclear. Delirium might uncover preexisting or preclinical dementia, or it might cause dementia by accelerating underlying neuropathologic processes or de novo mechanisms, the authors noted.

Study limitations included the potential for residual confounding from unmeasured variables in the matching criteria. Delirium and dementia diagnoses depended on clinical coding of medical information recorded in the administrative dataset, and under-coding of dementia during hospitalization is well-recognized.

Although the study controlled for length of stay in hospital and in intensive care, this may not have fully captured differences in severity of medical conditions. Data about the duration and severity of delirium episodes were also unavailable, which limited the dose-response analysis.

Commenting on the findings, Christopher Weber, PhD, Alzheimer’s Association as director of Global Science Initiatives, said the results are consistent with other research on the association between delirium and incidents of dementia.

The increased risk for dementia following delirium in males is “an interesting finding,” said Dr. Weber. “This suggests a need for more research to understand the impact of sex differences in delirium, as well as research to see if preventing incidents of delirium could ultimately reduce rates of dementia.”

The study received support from the National Health and Medical Research Council: Partnership Centre for Health System Sustainability. Dr. Gordon and Dr. Weber reported no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

Delirium is tied to a significantly increased risk for dementia and death in older adults, with men at particular risk, new research showed.

Incident dementia risk was more than three times higher in those who experienced just one episode of delirium, with each additional episode linked to a further 20% increase in dementia risk. The association was strongest in men.

Patients with delirium also had a 39% higher mortality risk than those with no history of delirium.

“We have known for a long time that delirium is dangerous, and this provides evidence that it’s even more dangerous than perhaps we had appreciated,” said study investigator Emily H. Gordon, PhD, MBBS, a geriatrician and senior lecturer at the University of Queensland, Brisbane, Australia.

“But we also know delirium is preventable. There are no excuses anymore; we really need to work together to improve the hospital system, to implement what are known to be effective interventions,” she added.

The findings were published online in The BMJ.
 

Close Matching

Prior studies that suggested an association between delirium and dementia were relatively small with short follow-up and varied in their adjustment for confounders. They also didn’t account for the competing risk for death, researchers noted.

Investigators used a linked New South Wales (NSW) statewide dataset that includes records of care episodes from all NSW hospitals as well as personal, administrative, clinical, and death information.

The study included an eligible sample of 626,467 older adults without dementia at baseline with at least one hospital admission between 2009 and 2014. For these patients, researchers calculated a hospital frailty risk score and collected other information including primary diagnosis and mean length of hospital stay and stay in the intensive care unit. From diagnostic codes, they categorized patients into no delirium and delirium groups and determined the number of delirium episodes.

Investigators matched patients in the delirium group to patients with no delirium according to characteristics with potential to confound the association between delirium and risk for dementia, including age, gender, frailty, reason for hospitalization, and length of stay in hospital and intensive care.

The matched study sample included 55,211 (mean age, 83 years) each in the delirium and the no delirium groups. Despite matching, the length of hospital stay for the index episode was longer for the delirium group than the no delirium group (mean, 9 days vs 6 days).

The primary outcomes were death and incident dementia, determined via diagnostic codes. During a follow-up of 5.25 years, 58% of patients died, and 17% had a new dementia diagnosis.

Among patients with at least one episode of delirium, the rate of incident dementia was 3.4 times higher than in those without delirium. After accounting for the competing risk for death, incident dementia risk remained three times higher among the delirium group (hazard ratio [HR], 3.00; 95% CI, 2.91-3.10).

This association was stronger for men than women (HR, 3.17 and 2.88, respectively; P = .004).
 

Sex Differences

The study is thought to be the first to identify a difference between sexes in dementia risk and delirium, Dr. Gordon said. It’s possible delirium in men is more severe in intensity or lasts longer than in women, or the male brain is, for whatever reason, more vulnerable to the effects of delirium, said Dr. Gordon. But she stressed these are only theories.

Investigators also found a mortality rate 1.4 times higher in the delirium group versus those without delirium, equating to a 39% increased risk for death (HR, 1.39; 95% CI, 1.37-1.41). The risk was similar for men and women (interaction P = .62).

When researchers categorized delirium by number of episodes, they found each additional episode was associated with a 10% increased risk for death (HR, 1.10; 95% CI, 1.09-1.12).

In addition to its large size, long follow-up, and close matching, what sets this new study apart from previous research is it accounted for the competing risk for death, said Dr. Gordon.

“This is really important because you’re not going to get dementia if you die, and in this population, the rate of death is incredibly high,” she said. “If we just assume people who died didn’t get dementia, then that screws the results.”
 

Causal Link?

For those who experienced at least one episode of delirium within the first 12 months, each additional episode of delirium was associated with a 20% increased risk for dementia (HR, 1.20; 95% CI, 1.18-1.23).

That dose-response association suggests a causal link between the two, Dr. Gordon said.

“The number one way to prove causality is to do a randomized controlled trial,” which isn’t feasible with delirium, she said. “By demonstrating a dose-response relationship suggests that it could be a causal pathway.”

Exact mechanisms linking delirium with dementia are unclear. Delirium might uncover preexisting or preclinical dementia, or it might cause dementia by accelerating underlying neuropathologic processes or de novo mechanisms, the authors noted.

Study limitations included the potential for residual confounding from unmeasured variables in the matching criteria. Delirium and dementia diagnoses depended on clinical coding of medical information recorded in the administrative dataset, and under-coding of dementia during hospitalization is well-recognized.

Although the study controlled for length of stay in hospital and in intensive care, this may not have fully captured differences in severity of medical conditions. Data about the duration and severity of delirium episodes were also unavailable, which limited the dose-response analysis.

Commenting on the findings, Christopher Weber, PhD, Alzheimer’s Association as director of Global Science Initiatives, said the results are consistent with other research on the association between delirium and incidents of dementia.

The increased risk for dementia following delirium in males is “an interesting finding,” said Dr. Weber. “This suggests a need for more research to understand the impact of sex differences in delirium, as well as research to see if preventing incidents of delirium could ultimately reduce rates of dementia.”

The study received support from the National Health and Medical Research Council: Partnership Centre for Health System Sustainability. Dr. Gordon and Dr. Weber reported no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

Delirium is tied to a significantly increased risk for dementia and death in older adults, with men at particular risk, new research showed.

Incident dementia risk was more than three times higher in those who experienced just one episode of delirium, with each additional episode linked to a further 20% increase in dementia risk. The association was strongest in men.

Patients with delirium also had a 39% higher mortality risk than those with no history of delirium.

“We have known for a long time that delirium is dangerous, and this provides evidence that it’s even more dangerous than perhaps we had appreciated,” said study investigator Emily H. Gordon, PhD, MBBS, a geriatrician and senior lecturer at the University of Queensland, Brisbane, Australia.

“But we also know delirium is preventable. There are no excuses anymore; we really need to work together to improve the hospital system, to implement what are known to be effective interventions,” she added.

The findings were published online in The BMJ.
 

Close Matching

Prior studies that suggested an association between delirium and dementia were relatively small with short follow-up and varied in their adjustment for confounders. They also didn’t account for the competing risk for death, researchers noted.

Investigators used a linked New South Wales (NSW) statewide dataset that includes records of care episodes from all NSW hospitals as well as personal, administrative, clinical, and death information.

The study included an eligible sample of 626,467 older adults without dementia at baseline with at least one hospital admission between 2009 and 2014. For these patients, researchers calculated a hospital frailty risk score and collected other information including primary diagnosis and mean length of hospital stay and stay in the intensive care unit. From diagnostic codes, they categorized patients into no delirium and delirium groups and determined the number of delirium episodes.

Investigators matched patients in the delirium group to patients with no delirium according to characteristics with potential to confound the association between delirium and risk for dementia, including age, gender, frailty, reason for hospitalization, and length of stay in hospital and intensive care.

The matched study sample included 55,211 (mean age, 83 years) each in the delirium and the no delirium groups. Despite matching, the length of hospital stay for the index episode was longer for the delirium group than the no delirium group (mean, 9 days vs 6 days).

The primary outcomes were death and incident dementia, determined via diagnostic codes. During a follow-up of 5.25 years, 58% of patients died, and 17% had a new dementia diagnosis.

Among patients with at least one episode of delirium, the rate of incident dementia was 3.4 times higher than in those without delirium. After accounting for the competing risk for death, incident dementia risk remained three times higher among the delirium group (hazard ratio [HR], 3.00; 95% CI, 2.91-3.10).

This association was stronger for men than women (HR, 3.17 and 2.88, respectively; P = .004).
 

Sex Differences

The study is thought to be the first to identify a difference between sexes in dementia risk and delirium, Dr. Gordon said. It’s possible delirium in men is more severe in intensity or lasts longer than in women, or the male brain is, for whatever reason, more vulnerable to the effects of delirium, said Dr. Gordon. But she stressed these are only theories.

Investigators also found a mortality rate 1.4 times higher in the delirium group versus those without delirium, equating to a 39% increased risk for death (HR, 1.39; 95% CI, 1.37-1.41). The risk was similar for men and women (interaction P = .62).

When researchers categorized delirium by number of episodes, they found each additional episode was associated with a 10% increased risk for death (HR, 1.10; 95% CI, 1.09-1.12).

In addition to its large size, long follow-up, and close matching, what sets this new study apart from previous research is it accounted for the competing risk for death, said Dr. Gordon.

“This is really important because you’re not going to get dementia if you die, and in this population, the rate of death is incredibly high,” she said. “If we just assume people who died didn’t get dementia, then that screws the results.”
 

Causal Link?

For those who experienced at least one episode of delirium within the first 12 months, each additional episode of delirium was associated with a 20% increased risk for dementia (HR, 1.20; 95% CI, 1.18-1.23).

That dose-response association suggests a causal link between the two, Dr. Gordon said.

“The number one way to prove causality is to do a randomized controlled trial,” which isn’t feasible with delirium, she said. “By demonstrating a dose-response relationship suggests that it could be a causal pathway.”

Exact mechanisms linking delirium with dementia are unclear. Delirium might uncover preexisting or preclinical dementia, or it might cause dementia by accelerating underlying neuropathologic processes or de novo mechanisms, the authors noted.

Study limitations included the potential for residual confounding from unmeasured variables in the matching criteria. Delirium and dementia diagnoses depended on clinical coding of medical information recorded in the administrative dataset, and under-coding of dementia during hospitalization is well-recognized.

Although the study controlled for length of stay in hospital and in intensive care, this may not have fully captured differences in severity of medical conditions. Data about the duration and severity of delirium episodes were also unavailable, which limited the dose-response analysis.

Commenting on the findings, Christopher Weber, PhD, Alzheimer’s Association as director of Global Science Initiatives, said the results are consistent with other research on the association between delirium and incidents of dementia.

The increased risk for dementia following delirium in males is “an interesting finding,” said Dr. Weber. “This suggests a need for more research to understand the impact of sex differences in delirium, as well as research to see if preventing incidents of delirium could ultimately reduce rates of dementia.”

The study received support from the National Health and Medical Research Council: Partnership Centre for Health System Sustainability. Dr. Gordon and Dr. Weber reported no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

The consequences of chronic musculoskeletal pain (CMP) may extend well beyond physical discomfort, potentially leading to faster aging of the brain, new research showed.

Using structural MRI data from more than 9000 adults with knee osteoarthritis (KOA) from the UK Biobank, investigators developed a brain age model to compare an individual’s brain age with their chronological age. Those with KOA showed a much faster rate of brain aging than healthy individuals.

The acceleration in brain aging was largely driven by the hippocampus and predicted memory decline and incident dementia during follow-up. Researchers identified a gene highly expressed in glial cells as a possible genetic factor for accelerated brain aging.

“We demonstrate the accelerated brain aging and cognitive decline in chronic musculoskeletal pain, in particular knee osteoarthritis, and provide a neural marker for early detection and intervention,” said co-first author Jiao Liu, PhD candidate, Chinese Academy of Sciences, Beijing.

“We are interested to know how to slow down the aging brain in chronic musculoskeletal pain patients. Proper exercise and lifestyle may reduce the risk,” Dr. Liu said.

The study was published online in Nature Mental Health.
 

Common Condition

CMP affects more than 40% of the world’s population and has been shown to have a harmful impact on cognitive function, although the exact mechanisms remain unclear. Prior research suggests that inflammatory markers associated with brain aging are higher in patients with CMP, suggesting a link between brain aging and CMP.

To investigate further, researchers explored patterns of brain aging in healthy cohorts and cohorts with four common types of CMP — chronic knee pain, chronic back pain, chronic neck pain, and chronic hip pain.

Using their brain age model, investigators observed significantly increased brain aging, or “predicted age difference,” only in individuals with KOA (P < .001). The observation was validated in an independent dataset (P = .020), suggesting a pattern of brain aging acceleration specific to KOA.

This acceleration was primarily driven by key brain regions involved in cognitive processing, including hippocampus and orbitofrontal cortex, and was correlated with longitudinal memory decline and dementia risk.

These data also suggest that the SLC39A8 gene, which is highly expressed in glial cells, might be a key genetic factor underpinning this acceleration.

“We not only revealed the specificity of accelerated brain aging in knee osteoarthritis patients, but importantly, we also provided longitudinal evidence suggesting the ability of our brain aging marker to predict future memory decline and increased dementia risk,” corresponding author Yiheng Tu, PhD, also with Chinese Academy of Sciences, Beijing, said in a news release.
 

A Future Treatment Target?

Commenting on this research, Shaheen Lakhan, MD, PhD, a neurologist and researcher based in Miami, noted that in this study, people with KOA showed signs of “faster brain aging on scans. Think of it as your brain wearing a disguise, appearing older than its actual years,” Dr. Lakhan said.

“Inflammation, a key player in osteoarthritis, might be playing a double agent, wreaking havoc not just on your joints but potentially on your memory too. Researchers even identified a specific gene linked to both knee pain and faster brain aging, hinting at a potential target for future treatments,” he added.

“Importantly, the increased risk of cognitive decline and dementia associated with chronic pain is likely one of many factors, and probably not a very high one on its own,” Dr. Lakhan noted.

The “good news,” he said, is that there are many “well-established ways to keep your brain sharp. Regular exercise, a healthy diet, and staying mentally stimulated are all proven strategies to reduce dementia risk. Think of chronic pain management as another tool you can add to your brain health toolbox.”

Support for the study was provided by the STI-2030 Major Project, the National Natural Science Foundation of China, the Scientific Foundation of the Institute of Psychology, Chinese Academy of Sciences, and the Young Elite Scientist Sponsorship Program by the China Association for Science and Technology. Dr. Liu and Dr. Lakhan had no relevant disclosures.

A version of this article appeared on Medscape.com.

The consequences of chronic musculoskeletal pain (CMP) may extend well beyond physical discomfort, potentially leading to faster aging of the brain, new research showed.

Using structural MRI data from more than 9000 adults with knee osteoarthritis (KOA) from the UK Biobank, investigators developed a brain age model to compare an individual’s brain age with their chronological age. Those with KOA showed a much faster rate of brain aging than healthy individuals.

The acceleration in brain aging was largely driven by the hippocampus and predicted memory decline and incident dementia during follow-up. Researchers identified a gene highly expressed in glial cells as a possible genetic factor for accelerated brain aging.

“We demonstrate the accelerated brain aging and cognitive decline in chronic musculoskeletal pain, in particular knee osteoarthritis, and provide a neural marker for early detection and intervention,” said co-first author Jiao Liu, PhD candidate, Chinese Academy of Sciences, Beijing.

“We are interested to know how to slow down the aging brain in chronic musculoskeletal pain patients. Proper exercise and lifestyle may reduce the risk,” Dr. Liu said.

The study was published online in Nature Mental Health.
 

Common Condition

CMP affects more than 40% of the world’s population and has been shown to have a harmful impact on cognitive function, although the exact mechanisms remain unclear. Prior research suggests that inflammatory markers associated with brain aging are higher in patients with CMP, suggesting a link between brain aging and CMP.

To investigate further, researchers explored patterns of brain aging in healthy cohorts and cohorts with four common types of CMP — chronic knee pain, chronic back pain, chronic neck pain, and chronic hip pain.

Using their brain age model, investigators observed significantly increased brain aging, or “predicted age difference,” only in individuals with KOA (P < .001). The observation was validated in an independent dataset (P = .020), suggesting a pattern of brain aging acceleration specific to KOA.

This acceleration was primarily driven by key brain regions involved in cognitive processing, including hippocampus and orbitofrontal cortex, and was correlated with longitudinal memory decline and dementia risk.

These data also suggest that the SLC39A8 gene, which is highly expressed in glial cells, might be a key genetic factor underpinning this acceleration.

“We not only revealed the specificity of accelerated brain aging in knee osteoarthritis patients, but importantly, we also provided longitudinal evidence suggesting the ability of our brain aging marker to predict future memory decline and increased dementia risk,” corresponding author Yiheng Tu, PhD, also with Chinese Academy of Sciences, Beijing, said in a news release.
 

A Future Treatment Target?

Commenting on this research, Shaheen Lakhan, MD, PhD, a neurologist and researcher based in Miami, noted that in this study, people with KOA showed signs of “faster brain aging on scans. Think of it as your brain wearing a disguise, appearing older than its actual years,” Dr. Lakhan said.

“Inflammation, a key player in osteoarthritis, might be playing a double agent, wreaking havoc not just on your joints but potentially on your memory too. Researchers even identified a specific gene linked to both knee pain and faster brain aging, hinting at a potential target for future treatments,” he added.

“Importantly, the increased risk of cognitive decline and dementia associated with chronic pain is likely one of many factors, and probably not a very high one on its own,” Dr. Lakhan noted.

The “good news,” he said, is that there are many “well-established ways to keep your brain sharp. Regular exercise, a healthy diet, and staying mentally stimulated are all proven strategies to reduce dementia risk. Think of chronic pain management as another tool you can add to your brain health toolbox.”

Support for the study was provided by the STI-2030 Major Project, the National Natural Science Foundation of China, the Scientific Foundation of the Institute of Psychology, Chinese Academy of Sciences, and the Young Elite Scientist Sponsorship Program by the China Association for Science and Technology. Dr. Liu and Dr. Lakhan had no relevant disclosures.

A version of this article appeared on Medscape.com.

The consequences of chronic musculoskeletal pain (CMP) may extend well beyond physical discomfort, potentially leading to faster aging of the brain, new research showed.

Using structural MRI data from more than 9000 adults with knee osteoarthritis (KOA) from the UK Biobank, investigators developed a brain age model to compare an individual’s brain age with their chronological age. Those with KOA showed a much faster rate of brain aging than healthy individuals.

The acceleration in brain aging was largely driven by the hippocampus and predicted memory decline and incident dementia during follow-up. Researchers identified a gene highly expressed in glial cells as a possible genetic factor for accelerated brain aging.

“We demonstrate the accelerated brain aging and cognitive decline in chronic musculoskeletal pain, in particular knee osteoarthritis, and provide a neural marker for early detection and intervention,” said co-first author Jiao Liu, PhD candidate, Chinese Academy of Sciences, Beijing.

“We are interested to know how to slow down the aging brain in chronic musculoskeletal pain patients. Proper exercise and lifestyle may reduce the risk,” Dr. Liu said.

The study was published online in Nature Mental Health.
 

Common Condition

CMP affects more than 40% of the world’s population and has been shown to have a harmful impact on cognitive function, although the exact mechanisms remain unclear. Prior research suggests that inflammatory markers associated with brain aging are higher in patients with CMP, suggesting a link between brain aging and CMP.

To investigate further, researchers explored patterns of brain aging in healthy cohorts and cohorts with four common types of CMP — chronic knee pain, chronic back pain, chronic neck pain, and chronic hip pain.

Using their brain age model, investigators observed significantly increased brain aging, or “predicted age difference,” only in individuals with KOA (P < .001). The observation was validated in an independent dataset (P = .020), suggesting a pattern of brain aging acceleration specific to KOA.

This acceleration was primarily driven by key brain regions involved in cognitive processing, including hippocampus and orbitofrontal cortex, and was correlated with longitudinal memory decline and dementia risk.

These data also suggest that the SLC39A8 gene, which is highly expressed in glial cells, might be a key genetic factor underpinning this acceleration.

“We not only revealed the specificity of accelerated brain aging in knee osteoarthritis patients, but importantly, we also provided longitudinal evidence suggesting the ability of our brain aging marker to predict future memory decline and increased dementia risk,” corresponding author Yiheng Tu, PhD, also with Chinese Academy of Sciences, Beijing, said in a news release.
 

A Future Treatment Target?

Commenting on this research, Shaheen Lakhan, MD, PhD, a neurologist and researcher based in Miami, noted that in this study, people with KOA showed signs of “faster brain aging on scans. Think of it as your brain wearing a disguise, appearing older than its actual years,” Dr. Lakhan said.

“Inflammation, a key player in osteoarthritis, might be playing a double agent, wreaking havoc not just on your joints but potentially on your memory too. Researchers even identified a specific gene linked to both knee pain and faster brain aging, hinting at a potential target for future treatments,” he added.

“Importantly, the increased risk of cognitive decline and dementia associated with chronic pain is likely one of many factors, and probably not a very high one on its own,” Dr. Lakhan noted.

The “good news,” he said, is that there are many “well-established ways to keep your brain sharp. Regular exercise, a healthy diet, and staying mentally stimulated are all proven strategies to reduce dementia risk. Think of chronic pain management as another tool you can add to your brain health toolbox.”

Support for the study was provided by the STI-2030 Major Project, the National Natural Science Foundation of China, the Scientific Foundation of the Institute of Psychology, Chinese Academy of Sciences, and the Young Elite Scientist Sponsorship Program by the China Association for Science and Technology. Dr. Liu and Dr. Lakhan had no relevant disclosures.

A version of this article appeared on Medscape.com.

The prevalence of dementia among homeless people is almost twice as high as that in housed populations in Ontario, Canada, according to the results of a new study.

The findings suggested that dementia occurs earlier in homeless individuals, and that these patients could benefit from proactive screening and housing interventions.

“Whether dementia caused the homelessness or homelessness caused the dementia, it’s a bidirectional relationship,” said lead author Richard G. Booth, PhD, RN, adjunct scientist at ICES (formerly Institute for Clinical Evaluative Sciences) and associate professor of nursing at Western University in London, Ontario, Canada.

The study was published in the April issue of The Lancet Public Health.

 

Dementia at Early Ages

The investigators used health administrative data from Ontario to compare the prevalence of dementia among homeless people with that among housed individuals in the general population and those living in low-income neighborhoods.

They included individuals aged 45 years or older on January 1, 2019, who visited hospital-based ambulatory care (such as emergency departments), were hospitalized, or visited a community health center in 2019. The researchers identified people as experiencing homelessness if they had one or more healthcare records with an indication of homelessness or unstable housing. The prevalence of dementia was ascertained as of December 31, 2019.

Included in the population-based, cross-sectional comparative analysis were 12,863 homeless people, 475,544 people in the low-income group, and 2,273,068 people in the general population group.

Dementia prevalence was 68.7 per 1000 individuals among the homeless population, 62.6 per 1000 in the low-income group, and 51.0 per 1000 in the general population group.

After adjustments for age, sex, geographical location of residence (urban vs rural), and health conditions associated with dementia, the prevalence ratio of dementia among homeless people was 1.71, compared with the low-income group, and 1.90, compared with the general population group.

Dementia also was detected in the 45- to 55-year age group among homeless people. This age is much earlier than the age at which doctors start screening their patients for cognitive decline (65 years).

“The study was not designed to define the causality but consider: If you have early-stage dementia and you are not intact enough to do basic functions of life, the likelihood of you becoming homeless is definitely increased, and vice versa. If you are homeless and suffer significant environmental and physical traumas just living on the street, you age much quicker, and you will experience geriatric symptoms such as dementia earlier in your life trajectory,” said Dr. Booth.

“The main takeaway here is that if you don’t have housing, bad things are going to happen in life.”
 

Public Health Problem

In an accompanying editorial, William J. Panenka, MD, associate professor of psychiatry at the University of British Columbia in Vancouver, British Columbia, Canada, and colleagues cited modifiable risk factors for dementia, including lower education, traumatic brain injury, substance use, smoking, mood disorders, and social isolation, many of which are disproportionately prevalent among homeless individuals.

“Ultimately, dementia could contribute to the cycle of homelessness, whereby housing instability increases the risk for brain impairment, and brain impairment makes breaking the cycle of homelessness progressively more challenging,” they wrote.

Dr. Panenka and colleagues also pointed out that the average age of homeless people is increasing. In the United States, it is now approximately 50 years. This fact underscores “the immediacy and gravity of the public health problem. A multifaceted approach that integrates healthcare, housing, and social services is needed to better understand and alleviate the health consequences of homelessness. A concerted effort at all levels is vital to inform future public health efforts and stem the tide of increasing morbidity, compromised function, and early mortality in homelessness,” they concluded.

Stephen Hwang, MD, director of the MAP Centre for Urban Health Solutions at St. Michael’s Hospital and Unity Health in Toronto, said that the study may underestimate the magnitude of the problem of dementia among homeless people.

“The methods used in this research study are very strong because they draw upon data for everyone living in the entire province of Ontario, and this is a very powerful way of looking at this challenging problem. The study probably underestimates the magnitude of the problem because to be diagnosed with dementia, patients have to have contact with healthcare providers that make that diagnosis. Often, people experiencing homelessness don’t have extensive contact with the healthcare system, and so their condition may go undiagnosed,” said Dr. Hwang.

A specialist in internal medicine, Dr. Hwang has provided healthcare for homeless people, and his research focuses on homelessness, housing, and health. He said that the findings from the Canadian study are applicable to the United States.

Forced clearances of homeless people and placing them in encampments, something that has been discussed in Florida, is unlikely to solve the problem, he said.

“The approach that has been shown to be beneficial is to engage with people and offer them housing and services that will allow them to exit homelessness without criminalizing the fact that they’re homeless. There really is no reason to think that this approach of forced clearances is going to help anyone.”

This study was supported by ICES (formerly the Institute for Clinical Evaluative Sciences), which is funded by the Ontario Ministry of Health and Ontario Ministry of Long-Term Care. Dr. Booth and Dr. Hwang reported no relevant financial relationships. Dr. Panenka reported receiving a research grant from the Canadian Institutes of Health Research.
 

A version of this article appeared on Medscape.com.

The prevalence of dementia among homeless people is almost twice as high as that in housed populations in Ontario, Canada, according to the results of a new study.

The findings suggested that dementia occurs earlier in homeless individuals, and that these patients could benefit from proactive screening and housing interventions.

“Whether dementia caused the homelessness or homelessness caused the dementia, it’s a bidirectional relationship,” said lead author Richard G. Booth, PhD, RN, adjunct scientist at ICES (formerly Institute for Clinical Evaluative Sciences) and associate professor of nursing at Western University in London, Ontario, Canada.

The study was published in the April issue of The Lancet Public Health.

 

Dementia at Early Ages

The investigators used health administrative data from Ontario to compare the prevalence of dementia among homeless people with that among housed individuals in the general population and those living in low-income neighborhoods.

They included individuals aged 45 years or older on January 1, 2019, who visited hospital-based ambulatory care (such as emergency departments), were hospitalized, or visited a community health center in 2019. The researchers identified people as experiencing homelessness if they had one or more healthcare records with an indication of homelessness or unstable housing. The prevalence of dementia was ascertained as of December 31, 2019.

Included in the population-based, cross-sectional comparative analysis were 12,863 homeless people, 475,544 people in the low-income group, and 2,273,068 people in the general population group.

Dementia prevalence was 68.7 per 1000 individuals among the homeless population, 62.6 per 1000 in the low-income group, and 51.0 per 1000 in the general population group.

After adjustments for age, sex, geographical location of residence (urban vs rural), and health conditions associated with dementia, the prevalence ratio of dementia among homeless people was 1.71, compared with the low-income group, and 1.90, compared with the general population group.

Dementia also was detected in the 45- to 55-year age group among homeless people. This age is much earlier than the age at which doctors start screening their patients for cognitive decline (65 years).

“The study was not designed to define the causality but consider: If you have early-stage dementia and you are not intact enough to do basic functions of life, the likelihood of you becoming homeless is definitely increased, and vice versa. If you are homeless and suffer significant environmental and physical traumas just living on the street, you age much quicker, and you will experience geriatric symptoms such as dementia earlier in your life trajectory,” said Dr. Booth.

“The main takeaway here is that if you don’t have housing, bad things are going to happen in life.”
 

Public Health Problem

In an accompanying editorial, William J. Panenka, MD, associate professor of psychiatry at the University of British Columbia in Vancouver, British Columbia, Canada, and colleagues cited modifiable risk factors for dementia, including lower education, traumatic brain injury, substance use, smoking, mood disorders, and social isolation, many of which are disproportionately prevalent among homeless individuals.

“Ultimately, dementia could contribute to the cycle of homelessness, whereby housing instability increases the risk for brain impairment, and brain impairment makes breaking the cycle of homelessness progressively more challenging,” they wrote.

Dr. Panenka and colleagues also pointed out that the average age of homeless people is increasing. In the United States, it is now approximately 50 years. This fact underscores “the immediacy and gravity of the public health problem. A multifaceted approach that integrates healthcare, housing, and social services is needed to better understand and alleviate the health consequences of homelessness. A concerted effort at all levels is vital to inform future public health efforts and stem the tide of increasing morbidity, compromised function, and early mortality in homelessness,” they concluded.

Stephen Hwang, MD, director of the MAP Centre for Urban Health Solutions at St. Michael’s Hospital and Unity Health in Toronto, said that the study may underestimate the magnitude of the problem of dementia among homeless people.

“The methods used in this research study are very strong because they draw upon data for everyone living in the entire province of Ontario, and this is a very powerful way of looking at this challenging problem. The study probably underestimates the magnitude of the problem because to be diagnosed with dementia, patients have to have contact with healthcare providers that make that diagnosis. Often, people experiencing homelessness don’t have extensive contact with the healthcare system, and so their condition may go undiagnosed,” said Dr. Hwang.

A specialist in internal medicine, Dr. Hwang has provided healthcare for homeless people, and his research focuses on homelessness, housing, and health. He said that the findings from the Canadian study are applicable to the United States.

Forced clearances of homeless people and placing them in encampments, something that has been discussed in Florida, is unlikely to solve the problem, he said.

“The approach that has been shown to be beneficial is to engage with people and offer them housing and services that will allow them to exit homelessness without criminalizing the fact that they’re homeless. There really is no reason to think that this approach of forced clearances is going to help anyone.”

This study was supported by ICES (formerly the Institute for Clinical Evaluative Sciences), which is funded by the Ontario Ministry of Health and Ontario Ministry of Long-Term Care. Dr. Booth and Dr. Hwang reported no relevant financial relationships. Dr. Panenka reported receiving a research grant from the Canadian Institutes of Health Research.
 

A version of this article appeared on Medscape.com.

The prevalence of dementia among homeless people is almost twice as high as that in housed populations in Ontario, Canada, according to the results of a new study.

The findings suggested that dementia occurs earlier in homeless individuals, and that these patients could benefit from proactive screening and housing interventions.

“Whether dementia caused the homelessness or homelessness caused the dementia, it’s a bidirectional relationship,” said lead author Richard G. Booth, PhD, RN, adjunct scientist at ICES (formerly Institute for Clinical Evaluative Sciences) and associate professor of nursing at Western University in London, Ontario, Canada.

The study was published in the April issue of The Lancet Public Health.

 

Dementia at Early Ages

The investigators used health administrative data from Ontario to compare the prevalence of dementia among homeless people with that among housed individuals in the general population and those living in low-income neighborhoods.

They included individuals aged 45 years or older on January 1, 2019, who visited hospital-based ambulatory care (such as emergency departments), were hospitalized, or visited a community health center in 2019. The researchers identified people as experiencing homelessness if they had one or more healthcare records with an indication of homelessness or unstable housing. The prevalence of dementia was ascertained as of December 31, 2019.

Included in the population-based, cross-sectional comparative analysis were 12,863 homeless people, 475,544 people in the low-income group, and 2,273,068 people in the general population group.

Dementia prevalence was 68.7 per 1000 individuals among the homeless population, 62.6 per 1000 in the low-income group, and 51.0 per 1000 in the general population group.

After adjustments for age, sex, geographical location of residence (urban vs rural), and health conditions associated with dementia, the prevalence ratio of dementia among homeless people was 1.71, compared with the low-income group, and 1.90, compared with the general population group.

Dementia also was detected in the 45- to 55-year age group among homeless people. This age is much earlier than the age at which doctors start screening their patients for cognitive decline (65 years).

“The study was not designed to define the causality but consider: If you have early-stage dementia and you are not intact enough to do basic functions of life, the likelihood of you becoming homeless is definitely increased, and vice versa. If you are homeless and suffer significant environmental and physical traumas just living on the street, you age much quicker, and you will experience geriatric symptoms such as dementia earlier in your life trajectory,” said Dr. Booth.

“The main takeaway here is that if you don’t have housing, bad things are going to happen in life.”
 

Public Health Problem

In an accompanying editorial, William J. Panenka, MD, associate professor of psychiatry at the University of British Columbia in Vancouver, British Columbia, Canada, and colleagues cited modifiable risk factors for dementia, including lower education, traumatic brain injury, substance use, smoking, mood disorders, and social isolation, many of which are disproportionately prevalent among homeless individuals.

“Ultimately, dementia could contribute to the cycle of homelessness, whereby housing instability increases the risk for brain impairment, and brain impairment makes breaking the cycle of homelessness progressively more challenging,” they wrote.

Dr. Panenka and colleagues also pointed out that the average age of homeless people is increasing. In the United States, it is now approximately 50 years. This fact underscores “the immediacy and gravity of the public health problem. A multifaceted approach that integrates healthcare, housing, and social services is needed to better understand and alleviate the health consequences of homelessness. A concerted effort at all levels is vital to inform future public health efforts and stem the tide of increasing morbidity, compromised function, and early mortality in homelessness,” they concluded.

Stephen Hwang, MD, director of the MAP Centre for Urban Health Solutions at St. Michael’s Hospital and Unity Health in Toronto, said that the study may underestimate the magnitude of the problem of dementia among homeless people.

“The methods used in this research study are very strong because they draw upon data for everyone living in the entire province of Ontario, and this is a very powerful way of looking at this challenging problem. The study probably underestimates the magnitude of the problem because to be diagnosed with dementia, patients have to have contact with healthcare providers that make that diagnosis. Often, people experiencing homelessness don’t have extensive contact with the healthcare system, and so their condition may go undiagnosed,” said Dr. Hwang.

A specialist in internal medicine, Dr. Hwang has provided healthcare for homeless people, and his research focuses on homelessness, housing, and health. He said that the findings from the Canadian study are applicable to the United States.

Forced clearances of homeless people and placing them in encampments, something that has been discussed in Florida, is unlikely to solve the problem, he said.

“The approach that has been shown to be beneficial is to engage with people and offer them housing and services that will allow them to exit homelessness without criminalizing the fact that they’re homeless. There really is no reason to think that this approach of forced clearances is going to help anyone.”

This study was supported by ICES (formerly the Institute for Clinical Evaluative Sciences), which is funded by the Ontario Ministry of Health and Ontario Ministry of Long-Term Care. Dr. Booth and Dr. Hwang reported no relevant financial relationships. Dr. Panenka reported receiving a research grant from the Canadian Institutes of Health Research.
 

A version of this article appeared on Medscape.com.

Experts say pediatricians and primary care clinicians should do more to prevent the toxic effects of lead in their young patients following a 2023 outbreak of elevated levels of lead in children associated with consumption of contaminated applesauce.

Federal legislation in the 1970s eliminated lead from gasoline, paints, and other consumer products, and resulted in significantly reduced blood lead levels (BLLs) in children throughout the United States.

But recently published studies highlight persistent issues with lead in drinking water and consumer products, suggesting that the fight is not over.
 

It’s in the Water

In 2014 the city of Flint, Michigan, changed its water supply and high levels of lead were later found in the municipal water supply.

Effects of that crisis still plague the city today. An initial study found that elevated BLLs had doubled among children between 2013 and 2015.

Lead exposure in young children is associated with several negative outcomes, including decreased cognitive ability, brain volume, and social mobility, and increased anxiety/depression and impulsivity, and higher rates of criminal offenses later in life. 

Many other water systems still contain lead pipes, despite a 1986 ban by the US Environmental Protection Agency on using them for installing or repairing public water systems. The mayor of Chicago announced a plan to start replacing lead service lines in 2020; however, 400,000 households are still served by these pipes, the most in the nation.

Benjamin Huynh, a native of Chicago, was curious about the impact of all those lead service lines. Now an assistant professor in the Department of Environmental Health and Engineering at Johns Hopkins University in Baltimore, Maryland, he and his colleagues researched how many children under the age of 6 years were exposed to contaminated water.

The results showed that lead contamination of water is widespread. 

“We’re estimating that 68% of kids under the age of 6 in Chicago were exposed to lead-contaminated drinking water,” Mr. Huynh said. 

He added that residents in predominantly Black and Latino neighborhoods had the highest risk for lead contamination in their water, but children living on these blocks were less likely to get tested, suggesting a need for more outreach to raise awareness.

Meanwhile, a little over one third of Chicago residents reported drinking bottled water as their main source of drinking water.

But even bottled water could contain lead. The US Food and Drug Administration (FDA) has set a limit for lead in bottled water to five parts per billion. The FDA threshold for taking action in public drinking water systems is 15 parts per billion. But the American Academy of Pediatrics states that no amount of lead in drinking water is considered safe for drinking. 

Mr. Huynh also pointed out that not all home water filters remove lead. Only devices that meet National Sanitation Foundation 53 standards are certified for lead removal. Consumers should verify that the filter package specifically lists the device as certified for removing contaminant lead.
 

Lead-tainted Cinnamon 

Last fall, the North Carolina Department of Health and Human Services identified several children with elevated levels of lead who had consumed WanaBana Apple Cinnamon Fruit Puree pouches.

An investigation by the FDA identified additional brands containing lead and issued a recall of applesauce pouches sold by retailers like Dollar Tree and Amazon.

According to the US Centers for Disease Control and Prevention, nearly 500 children were affected by the tainted applesauce. The FDA traced the source of the lead to cinnamon from a supplier in Ecuador.

An FDA spokesperson told this news organization the episode appears to have resulted from “economically motivated adulteration,” which occurs when a manufacturer leaves out or substitutes a valuable ingredient or part of a food. In the case of spices, lead may be added as a coloring agent or to increase the product weight.

“When we look at domestically made products from large, reputable companies, in general, they do a pretty good job of following safe product guidelines and regulations,” said Kevin Osterhoudt, MD, professor of pediatrics at the Perelman School of Medicine at the University of Pennsylvania in Philadelphia. “But when we use third-party sellers and we import things from other countries that aren’t regulated as closely, we certainly take a lot more risk in the products that we receive.”

While the Food Safety Modernization Act of 2011 aimed to improve agency’s capacity to manage the ever-rising volume of food produced domestically and imported from overseas, the funding has stayed flat while the volume of inspections has increased. In the early 1990s, the number of shipments screened by the agency numbered in the thousands annually. Last year the FDA screened 15 million shipments from more than 200 countries, according to the agency.

Prompted by the finding of lead in applesauce, the FDA began a wider investigation into ground cinnamon by sampling the product from discount retail stores. It recalled an additional six brands of cinnamon sold in the United States containing lead.

Dr. Osterhoudt’s message to families who think their child might have been exposed to a contaminated product is to dispose of it as directed by FDA and CDC guidelines. 

In Philadelphia, where Dr. Osterhoudt practices as an emergency room physician, baseline rates of childhood lead poisoning are already high, so he advises families to “do a larger inventory of all the source potential sources of lead in their life and to reduce all the exposures as low as possible.” 

He also advises parents that a nutritious diet high in calcium and iron can protect their children from the deleterious effects of lead.
 

Current Standards for Lead Screening and Testing

Lead is ubiquitous. The common routes of exposure to humans include use of fossil fuels such as leaded gasoline, some types of industrial facilities, and past use of lead-based paint in homes. In addition to spices, lead has been found in a wide variety of products such as toys, jewelry, antiques, cosmetics, and dietary supplements imported from other countries.

Noah Buncher, DO, is a primary care pediatrician in South Philadelphia at Children’s Hospital of Pennsylvania and the former director of a lead clinic in Boston that provides care for children with lead poisoning. He follows guidelines from the American Academy of Pediatrics that define an elevated BLL as ≥ 3.5 µg/dL. The guidelines recommend screening children for lead exposures during well child visits starting at age 6 months up to 6 years and obtaining a BLL if risks for lead exposure are present. 

Dr. Buncher starts with a basic environmental history that covers items like the age, condition, zip code of home, parental occupations, or hobbies that might result in exposing family members to lead, and if another child in the home has a history of elevated BLLs. 

But a careful history for potential lead exposures can be time-consuming. 

“There’s a lot to cover in a routine well child visit,” Dr. Buncher said. “We have maybe 15-20 minutes to cover a lot.” 

Clinics also vary on whether lead screening questions are put into workflows in the electronic medical record. Although parents can complete a written questionnaire about possible lead exposures, they may have difficulty answering questions about the age of their home or not know whether their occupation is high risk.

Transportation to a clinic is often a barrier for families, and sometimes patients must travel to a separate lab to be tested for lead. 

Dr. Buncher also pointed to the patchwork of local and state requirements that can lead to confusion among providers. Massachusetts, where he formerly practiced, has a universal requirement to test all children at ages 1, 2, and 3 years. But in Pennsylvania, screening laws vary from county to county. 

“Pennsylvania should implement universal screening recommendations for all kids under 6 regardless of what county you live in,” Dr. Buncher said.
 

Protective Measures 

Alan Woolf, MD, a professor of pediatrics at Harvard Medical School, Boston, Massachusetts, and director of the Pediatric Environmental Health Center at Boston Children’s Hospital, has a few ideas about how providers can step up their lead game, including partnering with their local health department. 

The CDC funds Childhood Lead Poisoning Prevention Programs based in state and local health departments to work with clinicians to improve rates of blood lead testing, monitor the prevalence of lead in their jurisdictions, and ensure that a system of referral is available for treatment and lead remediation services in the home.

Dr. Woolf also suggested that clinicians refer patients under age 3 years with high BLLs to their local Early Intervention Program. 

“They’ll assess their child’s development, their speech, their motor skills, their social skills, and if they qualify, it’s free,” Dr. Woolf said. 

He cited research showing children with elevated lead levels who received early intervention services performed better in grade school than equally exposed children who did not access similar services.

Another key strategy for pediatric clinicians is to learn local or state regulations for testing children for lead and how to access lead surveillance data in their practice area. Children who reside in high-risk areas are automatic candidates for screening. 

Dr. Woolf pointed out that big cities are not the only localities with lead in the drinking water. If families are drawing water from their own well, they should collect that water annually to have it tested for lead and microbes.

At the clinic-wide level, Dr. Woolf recommends the use of blood lead testing as a quality improvement measure. For example, Akron Children’s Hospital developed a quality improvement initiative using a clinical decision support tool to raise screening rates in their network of 30 clinics. One year after beginning the project, lead screenings during 12-month well visits increased from 71% to 96%. 

“What we’re interested in as pediatric health professionals is eliminating all background sources of lead in a child’s environment,” Dr. Woolf said. “Whether that’s applesauce pouches, whether that’s lead-containing paint, lead in water, lead in spices, or lead in imported pottery or cookware — there are just a tremendous number of sources of lead that we can do something about.”

None of the subjects reported financial conflicts of interest.

A former pediatrician, Dr. Thomas is a freelance science writer living in Portland, Oregon.

A version of this article appeared on Medscape.com.

Experts say pediatricians and primary care clinicians should do more to prevent the toxic effects of lead in their young patients following a 2023 outbreak of elevated levels of lead in children associated with consumption of contaminated applesauce.

Federal legislation in the 1970s eliminated lead from gasoline, paints, and other consumer products, and resulted in significantly reduced blood lead levels (BLLs) in children throughout the United States.

But recently published studies highlight persistent issues with lead in drinking water and consumer products, suggesting that the fight is not over.
 

It’s in the Water

In 2014 the city of Flint, Michigan, changed its water supply and high levels of lead were later found in the municipal water supply.

Effects of that crisis still plague the city today. An initial study found that elevated BLLs had doubled among children between 2013 and 2015.

Lead exposure in young children is associated with several negative outcomes, including decreased cognitive ability, brain volume, and social mobility, and increased anxiety/depression and impulsivity, and higher rates of criminal offenses later in life. 

Many other water systems still contain lead pipes, despite a 1986 ban by the US Environmental Protection Agency on using them for installing or repairing public water systems. The mayor of Chicago announced a plan to start replacing lead service lines in 2020; however, 400,000 households are still served by these pipes, the most in the nation.

Benjamin Huynh, a native of Chicago, was curious about the impact of all those lead service lines. Now an assistant professor in the Department of Environmental Health and Engineering at Johns Hopkins University in Baltimore, Maryland, he and his colleagues researched how many children under the age of 6 years were exposed to contaminated water.

The results showed that lead contamination of water is widespread. 

“We’re estimating that 68% of kids under the age of 6 in Chicago were exposed to lead-contaminated drinking water,” Mr. Huynh said. 

He added that residents in predominantly Black and Latino neighborhoods had the highest risk for lead contamination in their water, but children living on these blocks were less likely to get tested, suggesting a need for more outreach to raise awareness.

Meanwhile, a little over one third of Chicago residents reported drinking bottled water as their main source of drinking water.

But even bottled water could contain lead. The US Food and Drug Administration (FDA) has set a limit for lead in bottled water to five parts per billion. The FDA threshold for taking action in public drinking water systems is 15 parts per billion. But the American Academy of Pediatrics states that no amount of lead in drinking water is considered safe for drinking. 

Mr. Huynh also pointed out that not all home water filters remove lead. Only devices that meet National Sanitation Foundation 53 standards are certified for lead removal. Consumers should verify that the filter package specifically lists the device as certified for removing contaminant lead.
 

Lead-tainted Cinnamon 

Last fall, the North Carolina Department of Health and Human Services identified several children with elevated levels of lead who had consumed WanaBana Apple Cinnamon Fruit Puree pouches.

An investigation by the FDA identified additional brands containing lead and issued a recall of applesauce pouches sold by retailers like Dollar Tree and Amazon.

According to the US Centers for Disease Control and Prevention, nearly 500 children were affected by the tainted applesauce. The FDA traced the source of the lead to cinnamon from a supplier in Ecuador.

An FDA spokesperson told this news organization the episode appears to have resulted from “economically motivated adulteration,” which occurs when a manufacturer leaves out or substitutes a valuable ingredient or part of a food. In the case of spices, lead may be added as a coloring agent or to increase the product weight.

“When we look at domestically made products from large, reputable companies, in general, they do a pretty good job of following safe product guidelines and regulations,” said Kevin Osterhoudt, MD, professor of pediatrics at the Perelman School of Medicine at the University of Pennsylvania in Philadelphia. “But when we use third-party sellers and we import things from other countries that aren’t regulated as closely, we certainly take a lot more risk in the products that we receive.”

While the Food Safety Modernization Act of 2011 aimed to improve agency’s capacity to manage the ever-rising volume of food produced domestically and imported from overseas, the funding has stayed flat while the volume of inspections has increased. In the early 1990s, the number of shipments screened by the agency numbered in the thousands annually. Last year the FDA screened 15 million shipments from more than 200 countries, according to the agency.

Prompted by the finding of lead in applesauce, the FDA began a wider investigation into ground cinnamon by sampling the product from discount retail stores. It recalled an additional six brands of cinnamon sold in the United States containing lead.

Dr. Osterhoudt’s message to families who think their child might have been exposed to a contaminated product is to dispose of it as directed by FDA and CDC guidelines. 

In Philadelphia, where Dr. Osterhoudt practices as an emergency room physician, baseline rates of childhood lead poisoning are already high, so he advises families to “do a larger inventory of all the source potential sources of lead in their life and to reduce all the exposures as low as possible.” 

He also advises parents that a nutritious diet high in calcium and iron can protect their children from the deleterious effects of lead.
 

Current Standards for Lead Screening and Testing

Lead is ubiquitous. The common routes of exposure to humans include use of fossil fuels such as leaded gasoline, some types of industrial facilities, and past use of lead-based paint in homes. In addition to spices, lead has been found in a wide variety of products such as toys, jewelry, antiques, cosmetics, and dietary supplements imported from other countries.

Noah Buncher, DO, is a primary care pediatrician in South Philadelphia at Children’s Hospital of Pennsylvania and the former director of a lead clinic in Boston that provides care for children with lead poisoning. He follows guidelines from the American Academy of Pediatrics that define an elevated BLL as ≥ 3.5 µg/dL. The guidelines recommend screening children for lead exposures during well child visits starting at age 6 months up to 6 years and obtaining a BLL if risks for lead exposure are present. 

Dr. Buncher starts with a basic environmental history that covers items like the age, condition, zip code of home, parental occupations, or hobbies that might result in exposing family members to lead, and if another child in the home has a history of elevated BLLs. 

But a careful history for potential lead exposures can be time-consuming. 

“There’s a lot to cover in a routine well child visit,” Dr. Buncher said. “We have maybe 15-20 minutes to cover a lot.” 

Clinics also vary on whether lead screening questions are put into workflows in the electronic medical record. Although parents can complete a written questionnaire about possible lead exposures, they may have difficulty answering questions about the age of their home or not know whether their occupation is high risk.

Transportation to a clinic is often a barrier for families, and sometimes patients must travel to a separate lab to be tested for lead. 

Dr. Buncher also pointed to the patchwork of local and state requirements that can lead to confusion among providers. Massachusetts, where he formerly practiced, has a universal requirement to test all children at ages 1, 2, and 3 years. But in Pennsylvania, screening laws vary from county to county. 

“Pennsylvania should implement universal screening recommendations for all kids under 6 regardless of what county you live in,” Dr. Buncher said.
 

Protective Measures 

Alan Woolf, MD, a professor of pediatrics at Harvard Medical School, Boston, Massachusetts, and director of the Pediatric Environmental Health Center at Boston Children’s Hospital, has a few ideas about how providers can step up their lead game, including partnering with their local health department. 

The CDC funds Childhood Lead Poisoning Prevention Programs based in state and local health departments to work with clinicians to improve rates of blood lead testing, monitor the prevalence of lead in their jurisdictions, and ensure that a system of referral is available for treatment and lead remediation services in the home.

Dr. Woolf also suggested that clinicians refer patients under age 3 years with high BLLs to their local Early Intervention Program. 

“They’ll assess their child’s development, their speech, their motor skills, their social skills, and if they qualify, it’s free,” Dr. Woolf said. 

He cited research showing children with elevated lead levels who received early intervention services performed better in grade school than equally exposed children who did not access similar services.

Another key strategy for pediatric clinicians is to learn local or state regulations for testing children for lead and how to access lead surveillance data in their practice area. Children who reside in high-risk areas are automatic candidates for screening. 

Dr. Woolf pointed out that big cities are not the only localities with lead in the drinking water. If families are drawing water from their own well, they should collect that water annually to have it tested for lead and microbes.

At the clinic-wide level, Dr. Woolf recommends the use of blood lead testing as a quality improvement measure. For example, Akron Children’s Hospital developed a quality improvement initiative using a clinical decision support tool to raise screening rates in their network of 30 clinics. One year after beginning the project, lead screenings during 12-month well visits increased from 71% to 96%. 

“What we’re interested in as pediatric health professionals is eliminating all background sources of lead in a child’s environment,” Dr. Woolf said. “Whether that’s applesauce pouches, whether that’s lead-containing paint, lead in water, lead in spices, or lead in imported pottery or cookware — there are just a tremendous number of sources of lead that we can do something about.”

None of the subjects reported financial conflicts of interest.

A former pediatrician, Dr. Thomas is a freelance science writer living in Portland, Oregon.

A version of this article appeared on Medscape.com.

Experts say pediatricians and primary care clinicians should do more to prevent the toxic effects of lead in their young patients following a 2023 outbreak of elevated levels of lead in children associated with consumption of contaminated applesauce.

Federal legislation in the 1970s eliminated lead from gasoline, paints, and other consumer products, and resulted in significantly reduced blood lead levels (BLLs) in children throughout the United States.

But recently published studies highlight persistent issues with lead in drinking water and consumer products, suggesting that the fight is not over.
 

It’s in the Water

In 2014 the city of Flint, Michigan, changed its water supply and high levels of lead were later found in the municipal water supply.

Effects of that crisis still plague the city today. An initial study found that elevated BLLs had doubled among children between 2013 and 2015.

Lead exposure in young children is associated with several negative outcomes, including decreased cognitive ability, brain volume, and social mobility, and increased anxiety/depression and impulsivity, and higher rates of criminal offenses later in life. 

Many other water systems still contain lead pipes, despite a 1986 ban by the US Environmental Protection Agency on using them for installing or repairing public water systems. The mayor of Chicago announced a plan to start replacing lead service lines in 2020; however, 400,000 households are still served by these pipes, the most in the nation.

Benjamin Huynh, a native of Chicago, was curious about the impact of all those lead service lines. Now an assistant professor in the Department of Environmental Health and Engineering at Johns Hopkins University in Baltimore, Maryland, he and his colleagues researched how many children under the age of 6 years were exposed to contaminated water.

The results showed that lead contamination of water is widespread. 

“We’re estimating that 68% of kids under the age of 6 in Chicago were exposed to lead-contaminated drinking water,” Mr. Huynh said. 

He added that residents in predominantly Black and Latino neighborhoods had the highest risk for lead contamination in their water, but children living on these blocks were less likely to get tested, suggesting a need for more outreach to raise awareness.

Meanwhile, a little over one third of Chicago residents reported drinking bottled water as their main source of drinking water.

But even bottled water could contain lead. The US Food and Drug Administration (FDA) has set a limit for lead in bottled water to five parts per billion. The FDA threshold for taking action in public drinking water systems is 15 parts per billion. But the American Academy of Pediatrics states that no amount of lead in drinking water is considered safe for drinking. 

Mr. Huynh also pointed out that not all home water filters remove lead. Only devices that meet National Sanitation Foundation 53 standards are certified for lead removal. Consumers should verify that the filter package specifically lists the device as certified for removing contaminant lead.
 

Lead-tainted Cinnamon 

Last fall, the North Carolina Department of Health and Human Services identified several children with elevated levels of lead who had consumed WanaBana Apple Cinnamon Fruit Puree pouches.

An investigation by the FDA identified additional brands containing lead and issued a recall of applesauce pouches sold by retailers like Dollar Tree and Amazon.

According to the US Centers for Disease Control and Prevention, nearly 500 children were affected by the tainted applesauce. The FDA traced the source of the lead to cinnamon from a supplier in Ecuador.

An FDA spokesperson told this news organization the episode appears to have resulted from “economically motivated adulteration,” which occurs when a manufacturer leaves out or substitutes a valuable ingredient or part of a food. In the case of spices, lead may be added as a coloring agent or to increase the product weight.

“When we look at domestically made products from large, reputable companies, in general, they do a pretty good job of following safe product guidelines and regulations,” said Kevin Osterhoudt, MD, professor of pediatrics at the Perelman School of Medicine at the University of Pennsylvania in Philadelphia. “But when we use third-party sellers and we import things from other countries that aren’t regulated as closely, we certainly take a lot more risk in the products that we receive.”

While the Food Safety Modernization Act of 2011 aimed to improve agency’s capacity to manage the ever-rising volume of food produced domestically and imported from overseas, the funding has stayed flat while the volume of inspections has increased. In the early 1990s, the number of shipments screened by the agency numbered in the thousands annually. Last year the FDA screened 15 million shipments from more than 200 countries, according to the agency.

Prompted by the finding of lead in applesauce, the FDA began a wider investigation into ground cinnamon by sampling the product from discount retail stores. It recalled an additional six brands of cinnamon sold in the United States containing lead.

Dr. Osterhoudt’s message to families who think their child might have been exposed to a contaminated product is to dispose of it as directed by FDA and CDC guidelines. 

In Philadelphia, where Dr. Osterhoudt practices as an emergency room physician, baseline rates of childhood lead poisoning are already high, so he advises families to “do a larger inventory of all the source potential sources of lead in their life and to reduce all the exposures as low as possible.” 

He also advises parents that a nutritious diet high in calcium and iron can protect their children from the deleterious effects of lead.
 

Current Standards for Lead Screening and Testing

Lead is ubiquitous. The common routes of exposure to humans include use of fossil fuels such as leaded gasoline, some types of industrial facilities, and past use of lead-based paint in homes. In addition to spices, lead has been found in a wide variety of products such as toys, jewelry, antiques, cosmetics, and dietary supplements imported from other countries.

Noah Buncher, DO, is a primary care pediatrician in South Philadelphia at Children’s Hospital of Pennsylvania and the former director of a lead clinic in Boston that provides care for children with lead poisoning. He follows guidelines from the American Academy of Pediatrics that define an elevated BLL as ≥ 3.5 µg/dL. The guidelines recommend screening children for lead exposures during well child visits starting at age 6 months up to 6 years and obtaining a BLL if risks for lead exposure are present. 

Dr. Buncher starts with a basic environmental history that covers items like the age, condition, zip code of home, parental occupations, or hobbies that might result in exposing family members to lead, and if another child in the home has a history of elevated BLLs. 

But a careful history for potential lead exposures can be time-consuming. 

“There’s a lot to cover in a routine well child visit,” Dr. Buncher said. “We have maybe 15-20 minutes to cover a lot.” 

Clinics also vary on whether lead screening questions are put into workflows in the electronic medical record. Although parents can complete a written questionnaire about possible lead exposures, they may have difficulty answering questions about the age of their home or not know whether their occupation is high risk.

Transportation to a clinic is often a barrier for families, and sometimes patients must travel to a separate lab to be tested for lead. 

Dr. Buncher also pointed to the patchwork of local and state requirements that can lead to confusion among providers. Massachusetts, where he formerly practiced, has a universal requirement to test all children at ages 1, 2, and 3 years. But in Pennsylvania, screening laws vary from county to county. 

“Pennsylvania should implement universal screening recommendations for all kids under 6 regardless of what county you live in,” Dr. Buncher said.
 

Protective Measures 

Alan Woolf, MD, a professor of pediatrics at Harvard Medical School, Boston, Massachusetts, and director of the Pediatric Environmental Health Center at Boston Children’s Hospital, has a few ideas about how providers can step up their lead game, including partnering with their local health department. 

The CDC funds Childhood Lead Poisoning Prevention Programs based in state and local health departments to work with clinicians to improve rates of blood lead testing, monitor the prevalence of lead in their jurisdictions, and ensure that a system of referral is available for treatment and lead remediation services in the home.

Dr. Woolf also suggested that clinicians refer patients under age 3 years with high BLLs to their local Early Intervention Program. 

“They’ll assess their child’s development, their speech, their motor skills, their social skills, and if they qualify, it’s free,” Dr. Woolf said. 

He cited research showing children with elevated lead levels who received early intervention services performed better in grade school than equally exposed children who did not access similar services.

Another key strategy for pediatric clinicians is to learn local or state regulations for testing children for lead and how to access lead surveillance data in their practice area. Children who reside in high-risk areas are automatic candidates for screening. 

Dr. Woolf pointed out that big cities are not the only localities with lead in the drinking water. If families are drawing water from their own well, they should collect that water annually to have it tested for lead and microbes.

At the clinic-wide level, Dr. Woolf recommends the use of blood lead testing as a quality improvement measure. For example, Akron Children’s Hospital developed a quality improvement initiative using a clinical decision support tool to raise screening rates in their network of 30 clinics. One year after beginning the project, lead screenings during 12-month well visits increased from 71% to 96%. 

“What we’re interested in as pediatric health professionals is eliminating all background sources of lead in a child’s environment,” Dr. Woolf said. “Whether that’s applesauce pouches, whether that’s lead-containing paint, lead in water, lead in spices, or lead in imported pottery or cookware — there are just a tremendous number of sources of lead that we can do something about.”

None of the subjects reported financial conflicts of interest.

A former pediatrician, Dr. Thomas is a freelance science writer living in Portland, Oregon.

A version of this article appeared on Medscape.com.

Three recent publications highlight the ability of telestroke protocols not only to match the quality of in-person care, but in some instances to exceed it. These studies set the stage for larger studies comparing outcomes and efficiency of various telemedicine and transport models and gauging stakeholder satisfaction, authors said.

Surprising Results

In a single-site retrospective comparison of 252 patients with acute stroke assessed under an in-house telestroke protocol and 2437 assessed in person, telestroke provided statistically significant advantages in the following areas:

• Door-to-imaging times (median: 38 minutes vs 44)
• Rates of intravenous (18.2% vs 8.6%) and mechanical (10.4% vs 5.1%) treatment
• Length of stay (median: 6 days vs 8)
• Symptomatic hemorrhagic transformation rate (1.1% vs 5.1%)
• Mortality (6.7% vs 11.1%)

The better metrics observed in the telestroke group were especially surprising, said lead author Rodrigo Meirelles Massaud, MD, because the same team of neurologists conducted both types of evaluations. “This consistency ensures that the quality and expertise of medical care were maintained across both groups,” said Dr. Massaud, a neurologist at the Hospital Israelita Albert Einstein in São Paulo, Brazil. The study appeared online in Frontiers in Neurology.

The findings also counter the preconceived notion that distance medicine could be inferior because of the inability to conduct direct physical examinations and the potential for communication failures, he said. The telestroke group’s younger average age (63.5 years vs 69.5 years) and lower initial National Institutes of Health Stroke Scale (NIHSS) scores — 2 versus 3 — might explain the disparity, Dr. Massaud added, because both factors augur improved outcomes.

Conversely, the authors wrote that the in-person group’s lower median door-to-groin puncture time in ischemic stroke (103.5 minutes vs 151.5 for telemedicine) likely resulted from the need to transport patients from satellite facilities to a hub hospital with neurologists on continuous standby. After adjustment for initial NIHSS score and age, both groups achieved similar percentages of patients with modified Rankin Scale (mRS) scores of 0-2 at discharge: 58.5% for in-person evaluation versus 61.9% for telemedicine (P = .028).
 

Acute Ischemic Stroke

In another study, a systematic review that included 7396 thrombolysed patients with acute ischemic stroke, odds ratios (ORs) revealed no significant differences between telestroke and in-person care for the percentage of mRS scores 0-2 at discharge (1.06; P = .5), 90-day mortality (OR, 1.16; P = .17), and symptomatic intracranial hemorrhage (OR, 0.99; P = .93). The study appeared in the March International Journal of Stroke.

The lack of significant differences between telestroke and in-person care regarding mortality and mRS scores of 0-2 (which defines a good outcome) surprised researchers, said lead author Ahmed Mohamed, who is completing a master of health sciences degree in medical physiology at the University of Toronto Temerty Faculty of Medicine, Toronto, Ontario, Canada.

“When we were starting this project,” he said, “we thought that telemedicine would probably take longer than conventional treatment.” And waiting longer for treatment — especially for patients with acute ischemic stroke — leads to worse outcomes. “However,” Mr. Mohamed said, “that wasn’t the case.” Additional measures that showed no significant differences included rates of intravenous tissue plasminogen activator (ivtPA) use and endovascular mechanical thrombectomy.
 

Telestroke Expansion

Authors of a study that analyzed the impact of expanding telestroke coverage beyond community ERs credited many postexpansion improvements to the addition of advanced practice providers (APPs). ProMedica Stroke Network, Toledo, Ohio, added seven APPs in June 2020 to provide two-way audiovisual inpatient stroke and TIA consultations and follow-ups at 19 spoke facilities supported by vascular neurologists at the hub comprehensive stroke center (CSC).

Revamping the TS workflow resulted in a threefold increase in TS cart utilization, a 31% decrease in transfers to the CSC, and a higher home discharge rate from spoke hospitals than from the CSC (57.38% versus 52.8%, respectively). Diagnostic sensitivity also improved, with overall decreases in stroke and TIA diagnosis of 11.5% and 39.8%, respectively, and a 12.9% increase in identification of stroke mimics. The study was published in the March Annals of Neurology.
 

Future Directions

All three author groups called for larger, more granular follow-up studies. Mr. Mohamed said that the 7396-patient review of 33 studies does not show whether video consultations with neurologists produce better outcomes than phone calls, for example, or whether utilizing different telestroke modalities such as a third-party telemedicine service provides better outcomes than other methods. Additionally, authors wrote, future research should compare telestroke versus non-telestroke patient transport models to optimize treatment plans and outcomes and validate potential advantages and disadvantages of telemedicine for patients with acute ischemic stroke.

“There is also a need to understand the long-term outcomes of patients treated via telestroke versus in-person care,” said Dr. Massaud. Future studies could include randomized, controlled trials comparing telestroke to traditional care in various settings with larger sample sizes, he said. “Additionally, research into the cost-effectiveness of telestroke services, patient satisfaction, and the impact of telestroke on different subtypes of stroke could provide a more comprehensive understanding of its benefits and limitations.”

Dr. Massaud and Mr. Mohamed reported no relevant financial interests. Authors of all three studies reported no funding sources or potential conflicts of interest.

Three recent publications highlight the ability of telestroke protocols not only to match the quality of in-person care, but in some instances to exceed it. These studies set the stage for larger studies comparing outcomes and efficiency of various telemedicine and transport models and gauging stakeholder satisfaction, authors said.

Surprising Results

In a single-site retrospective comparison of 252 patients with acute stroke assessed under an in-house telestroke protocol and 2437 assessed in person, telestroke provided statistically significant advantages in the following areas:

• Door-to-imaging times (median: 38 minutes vs 44)
• Rates of intravenous (18.2% vs 8.6%) and mechanical (10.4% vs 5.1%) treatment
• Length of stay (median: 6 days vs 8)
• Symptomatic hemorrhagic transformation rate (1.1% vs 5.1%)
• Mortality (6.7% vs 11.1%)

The better metrics observed in the telestroke group were especially surprising, said lead author Rodrigo Meirelles Massaud, MD, because the same team of neurologists conducted both types of evaluations. “This consistency ensures that the quality and expertise of medical care were maintained across both groups,” said Dr. Massaud, a neurologist at the Hospital Israelita Albert Einstein in São Paulo, Brazil. The study appeared online in Frontiers in Neurology.

The findings also counter the preconceived notion that distance medicine could be inferior because of the inability to conduct direct physical examinations and the potential for communication failures, he said. The telestroke group’s younger average age (63.5 years vs 69.5 years) and lower initial National Institutes of Health Stroke Scale (NIHSS) scores — 2 versus 3 — might explain the disparity, Dr. Massaud added, because both factors augur improved outcomes.

Conversely, the authors wrote that the in-person group’s lower median door-to-groin puncture time in ischemic stroke (103.5 minutes vs 151.5 for telemedicine) likely resulted from the need to transport patients from satellite facilities to a hub hospital with neurologists on continuous standby. After adjustment for initial NIHSS score and age, both groups achieved similar percentages of patients with modified Rankin Scale (mRS) scores of 0-2 at discharge: 58.5% for in-person evaluation versus 61.9% for telemedicine (P = .028).
 

Acute Ischemic Stroke

In another study, a systematic review that included 7396 thrombolysed patients with acute ischemic stroke, odds ratios (ORs) revealed no significant differences between telestroke and in-person care for the percentage of mRS scores 0-2 at discharge (1.06; P = .5), 90-day mortality (OR, 1.16; P = .17), and symptomatic intracranial hemorrhage (OR, 0.99; P = .93). The study appeared in the March International Journal of Stroke.

The lack of significant differences between telestroke and in-person care regarding mortality and mRS scores of 0-2 (which defines a good outcome) surprised researchers, said lead author Ahmed Mohamed, who is completing a master of health sciences degree in medical physiology at the University of Toronto Temerty Faculty of Medicine, Toronto, Ontario, Canada.

“When we were starting this project,” he said, “we thought that telemedicine would probably take longer than conventional treatment.” And waiting longer for treatment — especially for patients with acute ischemic stroke — leads to worse outcomes. “However,” Mr. Mohamed said, “that wasn’t the case.” Additional measures that showed no significant differences included rates of intravenous tissue plasminogen activator (ivtPA) use and endovascular mechanical thrombectomy.
 

Telestroke Expansion

Authors of a study that analyzed the impact of expanding telestroke coverage beyond community ERs credited many postexpansion improvements to the addition of advanced practice providers (APPs). ProMedica Stroke Network, Toledo, Ohio, added seven APPs in June 2020 to provide two-way audiovisual inpatient stroke and TIA consultations and follow-ups at 19 spoke facilities supported by vascular neurologists at the hub comprehensive stroke center (CSC).

Revamping the TS workflow resulted in a threefold increase in TS cart utilization, a 31% decrease in transfers to the CSC, and a higher home discharge rate from spoke hospitals than from the CSC (57.38% versus 52.8%, respectively). Diagnostic sensitivity also improved, with overall decreases in stroke and TIA diagnosis of 11.5% and 39.8%, respectively, and a 12.9% increase in identification of stroke mimics. The study was published in the March Annals of Neurology.
 

Future Directions

All three author groups called for larger, more granular follow-up studies. Mr. Mohamed said that the 7396-patient review of 33 studies does not show whether video consultations with neurologists produce better outcomes than phone calls, for example, or whether utilizing different telestroke modalities such as a third-party telemedicine service provides better outcomes than other methods. Additionally, authors wrote, future research should compare telestroke versus non-telestroke patient transport models to optimize treatment plans and outcomes and validate potential advantages and disadvantages of telemedicine for patients with acute ischemic stroke.

“There is also a need to understand the long-term outcomes of patients treated via telestroke versus in-person care,” said Dr. Massaud. Future studies could include randomized, controlled trials comparing telestroke to traditional care in various settings with larger sample sizes, he said. “Additionally, research into the cost-effectiveness of telestroke services, patient satisfaction, and the impact of telestroke on different subtypes of stroke could provide a more comprehensive understanding of its benefits and limitations.”

Dr. Massaud and Mr. Mohamed reported no relevant financial interests. Authors of all three studies reported no funding sources or potential conflicts of interest.

Three recent publications highlight the ability of telestroke protocols not only to match the quality of in-person care, but in some instances to exceed it. These studies set the stage for larger studies comparing outcomes and efficiency of various telemedicine and transport models and gauging stakeholder satisfaction, authors said.

Surprising Results

In a single-site retrospective comparison of 252 patients with acute stroke assessed under an in-house telestroke protocol and 2437 assessed in person, telestroke provided statistically significant advantages in the following areas:

• Door-to-imaging times (median: 38 minutes vs 44)
• Rates of intravenous (18.2% vs 8.6%) and mechanical (10.4% vs 5.1%) treatment
• Length of stay (median: 6 days vs 8)
• Symptomatic hemorrhagic transformation rate (1.1% vs 5.1%)
• Mortality (6.7% vs 11.1%)

The better metrics observed in the telestroke group were especially surprising, said lead author Rodrigo Meirelles Massaud, MD, because the same team of neurologists conducted both types of evaluations. “This consistency ensures that the quality and expertise of medical care were maintained across both groups,” said Dr. Massaud, a neurologist at the Hospital Israelita Albert Einstein in São Paulo, Brazil. The study appeared online in Frontiers in Neurology.

The findings also counter the preconceived notion that distance medicine could be inferior because of the inability to conduct direct physical examinations and the potential for communication failures, he said. The telestroke group’s younger average age (63.5 years vs 69.5 years) and lower initial National Institutes of Health Stroke Scale (NIHSS) scores — 2 versus 3 — might explain the disparity, Dr. Massaud added, because both factors augur improved outcomes.

Conversely, the authors wrote that the in-person group’s lower median door-to-groin puncture time in ischemic stroke (103.5 minutes vs 151.5 for telemedicine) likely resulted from the need to transport patients from satellite facilities to a hub hospital with neurologists on continuous standby. After adjustment for initial NIHSS score and age, both groups achieved similar percentages of patients with modified Rankin Scale (mRS) scores of 0-2 at discharge: 58.5% for in-person evaluation versus 61.9% for telemedicine (P = .028).
 

Acute Ischemic Stroke

In another study, a systematic review that included 7396 thrombolysed patients with acute ischemic stroke, odds ratios (ORs) revealed no significant differences between telestroke and in-person care for the percentage of mRS scores 0-2 at discharge (1.06; P = .5), 90-day mortality (OR, 1.16; P = .17), and symptomatic intracranial hemorrhage (OR, 0.99; P = .93). The study appeared in the March International Journal of Stroke.

The lack of significant differences between telestroke and in-person care regarding mortality and mRS scores of 0-2 (which defines a good outcome) surprised researchers, said lead author Ahmed Mohamed, who is completing a master of health sciences degree in medical physiology at the University of Toronto Temerty Faculty of Medicine, Toronto, Ontario, Canada.

“When we were starting this project,” he said, “we thought that telemedicine would probably take longer than conventional treatment.” And waiting longer for treatment — especially for patients with acute ischemic stroke — leads to worse outcomes. “However,” Mr. Mohamed said, “that wasn’t the case.” Additional measures that showed no significant differences included rates of intravenous tissue plasminogen activator (ivtPA) use and endovascular mechanical thrombectomy.
 

Telestroke Expansion

Authors of a study that analyzed the impact of expanding telestroke coverage beyond community ERs credited many postexpansion improvements to the addition of advanced practice providers (APPs). ProMedica Stroke Network, Toledo, Ohio, added seven APPs in June 2020 to provide two-way audiovisual inpatient stroke and TIA consultations and follow-ups at 19 spoke facilities supported by vascular neurologists at the hub comprehensive stroke center (CSC).

Revamping the TS workflow resulted in a threefold increase in TS cart utilization, a 31% decrease in transfers to the CSC, and a higher home discharge rate from spoke hospitals than from the CSC (57.38% versus 52.8%, respectively). Diagnostic sensitivity also improved, with overall decreases in stroke and TIA diagnosis of 11.5% and 39.8%, respectively, and a 12.9% increase in identification of stroke mimics. The study was published in the March Annals of Neurology.
 

Future Directions

All three author groups called for larger, more granular follow-up studies. Mr. Mohamed said that the 7396-patient review of 33 studies does not show whether video consultations with neurologists produce better outcomes than phone calls, for example, or whether utilizing different telestroke modalities such as a third-party telemedicine service provides better outcomes than other methods. Additionally, authors wrote, future research should compare telestroke versus non-telestroke patient transport models to optimize treatment plans and outcomes and validate potential advantages and disadvantages of telemedicine for patients with acute ischemic stroke.

“There is also a need to understand the long-term outcomes of patients treated via telestroke versus in-person care,” said Dr. Massaud. Future studies could include randomized, controlled trials comparing telestroke to traditional care in various settings with larger sample sizes, he said. “Additionally, research into the cost-effectiveness of telestroke services, patient satisfaction, and the impact of telestroke on different subtypes of stroke could provide a more comprehensive understanding of its benefits and limitations.”

Dr. Massaud and Mr. Mohamed reported no relevant financial interests. Authors of all three studies reported no funding sources or potential conflicts of interest.

TOPLINE:

Earlier treatment with erenumab was associated with significantly better migraine prevention than that with nonspecific oral migraine preventive medications (OMPMs) in patients with resistant episodic migraine. Based on this research, the investigators suggest clinicians should start erenumab early and not prolong use of OMPMs.

METHODOLOGY:

• The 12-month prospective, international, multicenter, phase 4 randomized clinical APPRAISE trial included 621 adult patients (mean age, 41 years; 88% female) with a ≥ 12-month history of migraine and between 4 and 15 monthly migraine days (MMDs).
• Primary endpoint was the proportion of patients who completed 12 months of the initially assigned treatment and experiencing a reduction of ≥ 50% from baseline in MMDs at the end of the year.
• Secondary endpoints included cumulative mean change from baseline in MMDs during the treatment period and the proportion of responders (based on the Patients’ Global Impression of Change scale) at month 12 for patients taking the initially assigned treatment.

TAKEAWAY:

• At month 12, patients receiving erenumab were six times more likely to report a ≥ 50% reduction in MMDs than those receiving OMPMs (odds ratio [OR], 6.48; P < .001).
• Compared with OMPMs, treatment with erenumab yielded a higher responder rate at 1 year (76% vs 19%; OR, 13.75; P < .001) and a significantly greater reduction in cumulative average MMDs (−4.32 days vs −2.65 days; P < .001).
• Substantially, fewer patients in the erenumab vs the OMPM group switched medication (2% vs 35%) or discontinued treatment due to adverse events (3% vs 23%).
• Incidence of treatment-emergent adverse events was similar between the treatment arms (75% vs 76%) until the researchers adjusted for exposure to treatment, which revealed a roughly 30% lower exposure-adjusted rate (per 100 patient-years) in the erenumab group.

IN PRACTICE:

“Earlier initiation of erenumab may ultimately lead to fewer patients discontinuing or switching medication in a real-world clinical practice,” the authors wrote. In addition, the findings “lend further support to the recent guideline update issued by the European Headache Federation, in which CGRP-targeted mAbs are considered a first-line treatment option for patients with migraine who require preventive treatment.”

SOURCE:

Patricia Pozo-Rosich, MD, PhD, of the Headache and Neurological Pain Research Group, Vall d’Hebron Institute of Research, Department of Medicine, Universitat Autònoma de Barcelona, Spain, and the Headache Unit, Neurology Department, Vall d’Hebron University Hospital, Barcelona, Spain, was the lead and corresponding author of the study. It was published online in JAMA Neurology.

LIMITATIONS:

Only locally approved and marketed OMPMs at study onset were used as comparators. The open-label study design might have led to a placebo response, which could have played a role in the findings because erenumab can only be administered in a clinic and was administered subcutaneously.

DISCLOSURES:

This study was funded by Novartis Pharma AG, Basel, Switzerland. Dr. Pozo-Rosich reported receiving grants from AbbVie, Novartis, and Teva and personal fees from AbbVie, Eli Lilly, Lundbeck, Novartis, Pfizer, and Teva outside the submitted work. The other authors’ disclosures were listed on the original paper.

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

TOPLINE:

Earlier treatment with erenumab was associated with significantly better migraine prevention than that with nonspecific oral migraine preventive medications (OMPMs) in patients with resistant episodic migraine. Based on this research, the investigators suggest clinicians should start erenumab early and not prolong use of OMPMs.

METHODOLOGY:

• The 12-month prospective, international, multicenter, phase 4 randomized clinical APPRAISE trial included 621 adult patients (mean age, 41 years; 88% female) with a ≥ 12-month history of migraine and between 4 and 15 monthly migraine days (MMDs).
• Primary endpoint was the proportion of patients who completed 12 months of the initially assigned treatment and experiencing a reduction of ≥ 50% from baseline in MMDs at the end of the year.
• Secondary endpoints included cumulative mean change from baseline in MMDs during the treatment period and the proportion of responders (based on the Patients’ Global Impression of Change scale) at month 12 for patients taking the initially assigned treatment.

TAKEAWAY:

• At month 12, patients receiving erenumab were six times more likely to report a ≥ 50% reduction in MMDs than those receiving OMPMs (odds ratio [OR], 6.48; P < .001).
• Compared with OMPMs, treatment with erenumab yielded a higher responder rate at 1 year (76% vs 19%; OR, 13.75; P < .001) and a significantly greater reduction in cumulative average MMDs (−4.32 days vs −2.65 days; P < .001).
• Substantially, fewer patients in the erenumab vs the OMPM group switched medication (2% vs 35%) or discontinued treatment due to adverse events (3% vs 23%).
• Incidence of treatment-emergent adverse events was similar between the treatment arms (75% vs 76%) until the researchers adjusted for exposure to treatment, which revealed a roughly 30% lower exposure-adjusted rate (per 100 patient-years) in the erenumab group.

IN PRACTICE:

“Earlier initiation of erenumab may ultimately lead to fewer patients discontinuing or switching medication in a real-world clinical practice,” the authors wrote. In addition, the findings “lend further support to the recent guideline update issued by the European Headache Federation, in which CGRP-targeted mAbs are considered a first-line treatment option for patients with migraine who require preventive treatment.”

SOURCE:

Patricia Pozo-Rosich, MD, PhD, of the Headache and Neurological Pain Research Group, Vall d’Hebron Institute of Research, Department of Medicine, Universitat Autònoma de Barcelona, Spain, and the Headache Unit, Neurology Department, Vall d’Hebron University Hospital, Barcelona, Spain, was the lead and corresponding author of the study. It was published online in JAMA Neurology.

LIMITATIONS:

Only locally approved and marketed OMPMs at study onset were used as comparators. The open-label study design might have led to a placebo response, which could have played a role in the findings because erenumab can only be administered in a clinic and was administered subcutaneously.

DISCLOSURES:

This study was funded by Novartis Pharma AG, Basel, Switzerland. Dr. Pozo-Rosich reported receiving grants from AbbVie, Novartis, and Teva and personal fees from AbbVie, Eli Lilly, Lundbeck, Novartis, Pfizer, and Teva outside the submitted work. The other authors’ disclosures were listed on the original paper.

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

TOPLINE:

Earlier treatment with erenumab was associated with significantly better migraine prevention than that with nonspecific oral migraine preventive medications (OMPMs) in patients with resistant episodic migraine. Based on this research, the investigators suggest clinicians should start erenumab early and not prolong use of OMPMs.

METHODOLOGY:

• The 12-month prospective, international, multicenter, phase 4 randomized clinical APPRAISE trial included 621 adult patients (mean age, 41 years; 88% female) with a ≥ 12-month history of migraine and between 4 and 15 monthly migraine days (MMDs).
• Primary endpoint was the proportion of patients who completed 12 months of the initially assigned treatment and experiencing a reduction of ≥ 50% from baseline in MMDs at the end of the year.
• Secondary endpoints included cumulative mean change from baseline in MMDs during the treatment period and the proportion of responders (based on the Patients’ Global Impression of Change scale) at month 12 for patients taking the initially assigned treatment.

TAKEAWAY:

• At month 12, patients receiving erenumab were six times more likely to report a ≥ 50% reduction in MMDs than those receiving OMPMs (odds ratio [OR], 6.48; P < .001).
• Compared with OMPMs, treatment with erenumab yielded a higher responder rate at 1 year (76% vs 19%; OR, 13.75; P < .001) and a significantly greater reduction in cumulative average MMDs (−4.32 days vs −2.65 days; P < .001).
• Substantially, fewer patients in the erenumab vs the OMPM group switched medication (2% vs 35%) or discontinued treatment due to adverse events (3% vs 23%).
• Incidence of treatment-emergent adverse events was similar between the treatment arms (75% vs 76%) until the researchers adjusted for exposure to treatment, which revealed a roughly 30% lower exposure-adjusted rate (per 100 patient-years) in the erenumab group.

IN PRACTICE:

“Earlier initiation of erenumab may ultimately lead to fewer patients discontinuing or switching medication in a real-world clinical practice,” the authors wrote. In addition, the findings “lend further support to the recent guideline update issued by the European Headache Federation, in which CGRP-targeted mAbs are considered a first-line treatment option for patients with migraine who require preventive treatment.”

SOURCE:

Patricia Pozo-Rosich, MD, PhD, of the Headache and Neurological Pain Research Group, Vall d’Hebron Institute of Research, Department of Medicine, Universitat Autònoma de Barcelona, Spain, and the Headache Unit, Neurology Department, Vall d’Hebron University Hospital, Barcelona, Spain, was the lead and corresponding author of the study. It was published online in JAMA Neurology.

LIMITATIONS:

Only locally approved and marketed OMPMs at study onset were used as comparators. The open-label study design might have led to a placebo response, which could have played a role in the findings because erenumab can only be administered in a clinic and was administered subcutaneously.

DISCLOSURES:

This study was funded by Novartis Pharma AG, Basel, Switzerland. Dr. Pozo-Rosich reported receiving grants from AbbVie, Novartis, and Teva and personal fees from AbbVie, Eli Lilly, Lundbeck, Novartis, Pfizer, and Teva outside the submitted work. The other authors’ disclosures were listed on the original paper.

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

TOPLINE:

Certain stimulants prescribed for attention-deficit/hyperactivity disorder (ADHD) are associated with a decreased risk for psychiatric and nonpsychiatric hospitalization and suicide, new data from a national cohort study showed.

METHODOLOGY:

• Investigators used various medical and administrative databases in Sweden to identify individuals aged 16-65 years who were diagnosed with ADHD between January 2006 and December 2021.
• Participants were followed for up to 15 years (mean duration, 7 years) from date of diagnosis until death, emigration, or end of data linkage in December 2021.
• Researchers wanted to explore the link between ADHD meds and psychiatric hospitalization, nonpsychiatric hospitalization, and suicidal behavior.

TAKEAWAY:

• The cohort included 221,700 individuals with ADHD (mean age, 25 years; 54% male), and 56% had a psychiatric comorbidity such as an anxiety or stress-related disorder (24%), and depression or bipolar disorder (20%).
• Investigators found significantly lower risk for psychiatric hospitalization for the several medications. These included amphetamine (adjusted hazard ratio [aHR], 0.74), lisdexamphetamine (aHR, 0.80), dexamphetamine (aHR, 0.88), methylphenidate (aHR, 0.93), and polytherapy (aHR, 0.85). All but atomoxetine was significant at the P < .001 level.
• ADHD medications associated with a significantly lower risk for nonpsychiatric hospitalization included amphetamine (aHR, 0.62), lisdexamphetamine (aHR, 0.64), polytherapy (aHR, 0.67), dexamphetamine (aHR, 0.72), methylphenidate (aHR, 0.80), and atomoxetine (aHR, 0.84). All but atomoxetine was significant at the P < .001 level.
• Use of dexamphetamine (aHR, 0.69; P < .001), lisdexamphetamine (aHR, 0.76; P = .43), polytherapy (aHR, 0.85; P = .02), and methylphenidate (aHR, 0.92; P = .007) were associated with a significantly lower risk for suicidal behavior.

IN PRACTICE:

“Although concerns have been raised about the potential of amphetamines and methylphenidate for increasing the risk of adverse psychiatric outcomes, such as psychosis and mania, our results show that overall, the net effect on psychiatric outcomes is positive,” study authors wrote.

SOURCE:

Heidi Taipale, PhD, of Karolinska Institutet, led the study, which was published online in JAMA Network Open. 

LIMITATIONS:

Due to the use of nationwide registers, there was a lack of detailed clinical data, including type and severity of symptoms. There was also no data on nonpharmacologic treatments.

DISCLOSURES:

The study was funded by the AFA Insurance Agency. Dr. Taipale reported receiving personal fees from Gedeon Richter, Janssen, Lundbeck, and Otsuka and grants from Janssen and Eli Lilly outside of the submitted work. Other disclosures are noted in the original article.

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

TOPLINE:

Certain stimulants prescribed for attention-deficit/hyperactivity disorder (ADHD) are associated with a decreased risk for psychiatric and nonpsychiatric hospitalization and suicide, new data from a national cohort study showed.

METHODOLOGY:

• Investigators used various medical and administrative databases in Sweden to identify individuals aged 16-65 years who were diagnosed with ADHD between January 2006 and December 2021.
• Participants were followed for up to 15 years (mean duration, 7 years) from date of diagnosis until death, emigration, or end of data linkage in December 2021.
• Researchers wanted to explore the link between ADHD meds and psychiatric hospitalization, nonpsychiatric hospitalization, and suicidal behavior.

TAKEAWAY:

• The cohort included 221,700 individuals with ADHD (mean age, 25 years; 54% male), and 56% had a psychiatric comorbidity such as an anxiety or stress-related disorder (24%), and depression or bipolar disorder (20%).
• Investigators found significantly lower risk for psychiatric hospitalization for the several medications. These included amphetamine (adjusted hazard ratio [aHR], 0.74), lisdexamphetamine (aHR, 0.80), dexamphetamine (aHR, 0.88), methylphenidate (aHR, 0.93), and polytherapy (aHR, 0.85). All but atomoxetine was significant at the P < .001 level.
• ADHD medications associated with a significantly lower risk for nonpsychiatric hospitalization included amphetamine (aHR, 0.62), lisdexamphetamine (aHR, 0.64), polytherapy (aHR, 0.67), dexamphetamine (aHR, 0.72), methylphenidate (aHR, 0.80), and atomoxetine (aHR, 0.84). All but atomoxetine was significant at the P < .001 level.
• Use of dexamphetamine (aHR, 0.69; P < .001), lisdexamphetamine (aHR, 0.76; P = .43), polytherapy (aHR, 0.85; P = .02), and methylphenidate (aHR, 0.92; P = .007) were associated with a significantly lower risk for suicidal behavior.

IN PRACTICE:

“Although concerns have been raised about the potential of amphetamines and methylphenidate for increasing the risk of adverse psychiatric outcomes, such as psychosis and mania, our results show that overall, the net effect on psychiatric outcomes is positive,” study authors wrote.

SOURCE:

Heidi Taipale, PhD, of Karolinska Institutet, led the study, which was published online in JAMA Network Open. 

LIMITATIONS:

Due to the use of nationwide registers, there was a lack of detailed clinical data, including type and severity of symptoms. There was also no data on nonpharmacologic treatments.

DISCLOSURES:

The study was funded by the AFA Insurance Agency. Dr. Taipale reported receiving personal fees from Gedeon Richter, Janssen, Lundbeck, and Otsuka and grants from Janssen and Eli Lilly outside of the submitted work. Other disclosures are noted in the original article.

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

TOPLINE:

Certain stimulants prescribed for attention-deficit/hyperactivity disorder (ADHD) are associated with a decreased risk for psychiatric and nonpsychiatric hospitalization and suicide, new data from a national cohort study showed.

METHODOLOGY:

• Investigators used various medical and administrative databases in Sweden to identify individuals aged 16-65 years who were diagnosed with ADHD between January 2006 and December 2021.
• Participants were followed for up to 15 years (mean duration, 7 years) from date of diagnosis until death, emigration, or end of data linkage in December 2021.
• Researchers wanted to explore the link between ADHD meds and psychiatric hospitalization, nonpsychiatric hospitalization, and suicidal behavior.

TAKEAWAY:

• The cohort included 221,700 individuals with ADHD (mean age, 25 years; 54% male), and 56% had a psychiatric comorbidity such as an anxiety or stress-related disorder (24%), and depression or bipolar disorder (20%).
• Investigators found significantly lower risk for psychiatric hospitalization for the several medications. These included amphetamine (adjusted hazard ratio [aHR], 0.74), lisdexamphetamine (aHR, 0.80), dexamphetamine (aHR, 0.88), methylphenidate (aHR, 0.93), and polytherapy (aHR, 0.85). All but atomoxetine was significant at the P < .001 level.
• ADHD medications associated with a significantly lower risk for nonpsychiatric hospitalization included amphetamine (aHR, 0.62), lisdexamphetamine (aHR, 0.64), polytherapy (aHR, 0.67), dexamphetamine (aHR, 0.72), methylphenidate (aHR, 0.80), and atomoxetine (aHR, 0.84). All but atomoxetine was significant at the P < .001 level.
• Use of dexamphetamine (aHR, 0.69; P < .001), lisdexamphetamine (aHR, 0.76; P = .43), polytherapy (aHR, 0.85; P = .02), and methylphenidate (aHR, 0.92; P = .007) were associated with a significantly lower risk for suicidal behavior.

IN PRACTICE:

“Although concerns have been raised about the potential of amphetamines and methylphenidate for increasing the risk of adverse psychiatric outcomes, such as psychosis and mania, our results show that overall, the net effect on psychiatric outcomes is positive,” study authors wrote.

SOURCE:

Heidi Taipale, PhD, of Karolinska Institutet, led the study, which was published online in JAMA Network Open. 

LIMITATIONS:

Due to the use of nationwide registers, there was a lack of detailed clinical data, including type and severity of symptoms. There was also no data on nonpharmacologic treatments.

DISCLOSURES:

The study was funded by the AFA Insurance Agency. Dr. Taipale reported receiving personal fees from Gedeon Richter, Janssen, Lundbeck, and Otsuka and grants from Janssen and Eli Lilly outside of the submitted work. Other disclosures are noted in the original article.

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

Studies in preclinical models hint that familial Alzheimer’s disease (AD) may be transmissible via bone marrow transplant, but the researchers and outside experts caution against making the immediate leap to humans. 

The researchers observed that adoptive transplantation of donor bone marrow stem cells harboring a mutant human amyloid precursor protein (APP) transgene into both APP-deficient and healthy wild-type mice resulted in the rapid development of AD pathologic hallmarks. 

These pathologic features included compromised blood-brain barrier integrity, heightened cerebral vascular neoangiogenesis, elevated brain-associated beta-amyloid levels, and cognitive impairment.

In addition, symptoms of cognitive decline presented rapidly — 6 months after transplant in the APP-knockout mice and 9 months in the wild-type mice vs 12 months shown previously in AD transgenic mice.

“Contrary to prevailing beliefs regarding AD occurring solely in familial or sporadic forms, our study reveals an unexpected transplantable form of AD in a preclinical model, suggesting potential iatrogenic transmission in AD patients,” the investigators, led by Wilfred Jefferies, DPhil, write. 

Although this is probably an “infrequent” occurrence, it’s still “concerning,” Dr. Jefferies told this news organization, and it suggests that “human donors of blood, tissue, organ, and stem cells should be screened to prevent its inadvertent transfer of disease during blood product transfusions and cellular therapies.”

The study was published March 28 in Stem Cell Reports. 

Intriguing, but Limited Human Relevance

The researchers note the study also demonstrates that beta-amyloid accumulation originating outside of the central nervous system contributes to AD pathology, providing an opportunity for the development of new biomarkers for AD. 

Several experts weighed in on this research in a statement from the UK-based nonprofit and independent Science Media Centre (SMC).

David Curtis, MBBS, MD, PhD, with University College London’s Genetics Institute, United Kingdom, noted that the study suggests that “theoretically there could be a risk of acquiring Alzheimer’s disease if one received a stem cell transplant from somebody carrying the severe, familial form of the disease. However, this form is extremely rare so in practice the risk seems low and there are many safeguards around stem cell transplantation. I do not see that the risks extend to other areas such as organ transplantation or blood transfusion because these procedures do not involve large numbers of stem cells which can go on to form glial cells.”

Paul Morgan, PhD, with UK Dementia Research Institute Cardiff, Cardiff University, said the study is “scientifically intriguing” in demonstrating in this “very specific experimental situation, that bone marrow cells are sufficient to transfer the gene and the disease. Relevance to human organ and cell transplant is limited.”

Morgan cautioned against making the “gargantuan leap to propose that tissue, organ and cell transplantation, and even blood transfusion, carry a risk of transferring Alzheimer’s disease and other neuropathologies in man.”

Bart De Strooper, MD, PhD, with University College London, agreed. “There is not sufficient evidence here to suggest that anyone receiving a bone marrow transplant is at risk of developing Alzheimer’s disease as a result of the procedure, and nobody should forgo a transplant for this reason,” he said in the SMC release. 

The study had no specific funding. The authors hold equity in the start-up company, Cava Healthcare, which possesses intellectual property related to these findings. This had no role in the study design, data collection, analysis, or interpretation of data, or in the writing of the paper. Morgan, De Strooper, and Curtis have no relevant disclosures.

A version of this article appeared on Medscape.com.

Studies in preclinical models hint that familial Alzheimer’s disease (AD) may be transmissible via bone marrow transplant, but the researchers and outside experts caution against making the immediate leap to humans. 

The researchers observed that adoptive transplantation of donor bone marrow stem cells harboring a mutant human amyloid precursor protein (APP) transgene into both APP-deficient and healthy wild-type mice resulted in the rapid development of AD pathologic hallmarks. 

These pathologic features included compromised blood-brain barrier integrity, heightened cerebral vascular neoangiogenesis, elevated brain-associated beta-amyloid levels, and cognitive impairment.

In addition, symptoms of cognitive decline presented rapidly — 6 months after transplant in the APP-knockout mice and 9 months in the wild-type mice vs 12 months shown previously in AD transgenic mice.

“Contrary to prevailing beliefs regarding AD occurring solely in familial or sporadic forms, our study reveals an unexpected transplantable form of AD in a preclinical model, suggesting potential iatrogenic transmission in AD patients,” the investigators, led by Wilfred Jefferies, DPhil, write. 

Although this is probably an “infrequent” occurrence, it’s still “concerning,” Dr. Jefferies told this news organization, and it suggests that “human donors of blood, tissue, organ, and stem cells should be screened to prevent its inadvertent transfer of disease during blood product transfusions and cellular therapies.”

The study was published March 28 in Stem Cell Reports. 

Intriguing, but Limited Human Relevance

The researchers note the study also demonstrates that beta-amyloid accumulation originating outside of the central nervous system contributes to AD pathology, providing an opportunity for the development of new biomarkers for AD. 

Several experts weighed in on this research in a statement from the UK-based nonprofit and independent Science Media Centre (SMC).

David Curtis, MBBS, MD, PhD, with University College London’s Genetics Institute, United Kingdom, noted that the study suggests that “theoretically there could be a risk of acquiring Alzheimer’s disease if one received a stem cell transplant from somebody carrying the severe, familial form of the disease. However, this form is extremely rare so in practice the risk seems low and there are many safeguards around stem cell transplantation. I do not see that the risks extend to other areas such as organ transplantation or blood transfusion because these procedures do not involve large numbers of stem cells which can go on to form glial cells.”

Paul Morgan, PhD, with UK Dementia Research Institute Cardiff, Cardiff University, said the study is “scientifically intriguing” in demonstrating in this “very specific experimental situation, that bone marrow cells are sufficient to transfer the gene and the disease. Relevance to human organ and cell transplant is limited.”

Morgan cautioned against making the “gargantuan leap to propose that tissue, organ and cell transplantation, and even blood transfusion, carry a risk of transferring Alzheimer’s disease and other neuropathologies in man.”

Bart De Strooper, MD, PhD, with University College London, agreed. “There is not sufficient evidence here to suggest that anyone receiving a bone marrow transplant is at risk of developing Alzheimer’s disease as a result of the procedure, and nobody should forgo a transplant for this reason,” he said in the SMC release. 

The study had no specific funding. The authors hold equity in the start-up company, Cava Healthcare, which possesses intellectual property related to these findings. This had no role in the study design, data collection, analysis, or interpretation of data, or in the writing of the paper. Morgan, De Strooper, and Curtis have no relevant disclosures.

A version of this article appeared on Medscape.com.

Studies in preclinical models hint that familial Alzheimer’s disease (AD) may be transmissible via bone marrow transplant, but the researchers and outside experts caution against making the immediate leap to humans. 

The researchers observed that adoptive transplantation of donor bone marrow stem cells harboring a mutant human amyloid precursor protein (APP) transgene into both APP-deficient and healthy wild-type mice resulted in the rapid development of AD pathologic hallmarks. 

These pathologic features included compromised blood-brain barrier integrity, heightened cerebral vascular neoangiogenesis, elevated brain-associated beta-amyloid levels, and cognitive impairment.

In addition, symptoms of cognitive decline presented rapidly — 6 months after transplant in the APP-knockout mice and 9 months in the wild-type mice vs 12 months shown previously in AD transgenic mice.

“Contrary to prevailing beliefs regarding AD occurring solely in familial or sporadic forms, our study reveals an unexpected transplantable form of AD in a preclinical model, suggesting potential iatrogenic transmission in AD patients,” the investigators, led by Wilfred Jefferies, DPhil, write. 

Although this is probably an “infrequent” occurrence, it’s still “concerning,” Dr. Jefferies told this news organization, and it suggests that “human donors of blood, tissue, organ, and stem cells should be screened to prevent its inadvertent transfer of disease during blood product transfusions and cellular therapies.”

The study was published March 28 in Stem Cell Reports. 

Intriguing, but Limited Human Relevance

The researchers note the study also demonstrates that beta-amyloid accumulation originating outside of the central nervous system contributes to AD pathology, providing an opportunity for the development of new biomarkers for AD. 

Several experts weighed in on this research in a statement from the UK-based nonprofit and independent Science Media Centre (SMC).

David Curtis, MBBS, MD, PhD, with University College London’s Genetics Institute, United Kingdom, noted that the study suggests that “theoretically there could be a risk of acquiring Alzheimer’s disease if one received a stem cell transplant from somebody carrying the severe, familial form of the disease. However, this form is extremely rare so in practice the risk seems low and there are many safeguards around stem cell transplantation. I do not see that the risks extend to other areas such as organ transplantation or blood transfusion because these procedures do not involve large numbers of stem cells which can go on to form glial cells.”

Paul Morgan, PhD, with UK Dementia Research Institute Cardiff, Cardiff University, said the study is “scientifically intriguing” in demonstrating in this “very specific experimental situation, that bone marrow cells are sufficient to transfer the gene and the disease. Relevance to human organ and cell transplant is limited.”

Morgan cautioned against making the “gargantuan leap to propose that tissue, organ and cell transplantation, and even blood transfusion, carry a risk of transferring Alzheimer’s disease and other neuropathologies in man.”

Bart De Strooper, MD, PhD, with University College London, agreed. “There is not sufficient evidence here to suggest that anyone receiving a bone marrow transplant is at risk of developing Alzheimer’s disease as a result of the procedure, and nobody should forgo a transplant for this reason,” he said in the SMC release. 

The study had no specific funding. The authors hold equity in the start-up company, Cava Healthcare, which possesses intellectual property related to these findings. This had no role in the study design, data collection, analysis, or interpretation of data, or in the writing of the paper. Morgan, De Strooper, and Curtis have no relevant disclosures.

A version of this article appeared on Medscape.com.

Two classes of chemicals present in common household products may impair the development of oligodendrocytes, the myelinating cells of the central nervous system (CNS), which are critical to brain development and function. However, the researchers as well as outside experts agree more research is needed before any firm conclusions can be drawn. 

Quaternary ammonium compounds, ubiquitous in disinfecting agents and personal care products, and organophosphate flame retardants, which are commonly found in household items such as furniture and electronics had “surprising effects specifically on the non-nerve cells in the brain,” said lead researcher Paul Tesar, PhD, professor and director of the Institute for Glial Sciences, Case Western Reserve University School of Medicine, Cleveland. 

“Other studies have shown that our exposures to the chemicals in disinfecting agents nearly doubled during the pandemic,” Dr. Tesar noted. The finding that quaternary ammonium chemicals in disinfecting agents are harmful to specific brain cells suggests “we need to think about our increased utilization and exposure,” he added.

The results were published online on March 25 in Nature Neuroscience. 
 

Motor Dysfunction

Exposure to various chemicals in the environment has been shown to impair brain development. However, most of this research has focused on neurons. Less is known about effects on oligodendrocytes, which form the electrical insulation around the axons of CNS cells. Oligodendrocyte development continues from before birth into adulthood, thus these cells may be particularly vulnerable to damage from toxic chemicals.

The researchers analyzed the effects of 1823 chemicals on mouse oligodendrocyte development in cell cultures. They identified 292 chemicals that cause oligodendrocytes to die and 47 that inhibit oligodendrocyte generation. These chemicals belonged to two different classes.

They found that quaternary compounds were potently and selectively cytotoxic to developing oligodendrocytes and that organophosphate flame retardants prematurely arrested oligodendrocyte maturation. These effects were confirmed in mice and cultured human oligodendrocytes.

In addition, an analysis of epidemiologic data from the National Health and Nutrition Examination Survey (2013-2018) showed that one flame retardant metabolite, bis(1,3-dichloro-2-propy) phosphate (BDCIPP), was present in nearly all urine samples of children aged 3-11 years who were examined (1753 out of 1763 children).

After adjustment for multiple confounding factors, results showed that compared with children with urinary BDCIPP concentration in the lowest quartile, those with concentrations in the highest quartile were twice as likely to require special education (adjusted odds ratio [aOR], 2.0; 95% CI, 1.0-3.8) and were six times as likely to have gross motor dysfunction (aOR, 6.0; 95% CI, 1.7-21.9).

Children with urinary BDCIPP concentration within the third quartile also had significantly increased odds of motor dysfunction (aOR, 4.2; 95% CI, 1.1-16.2). 

“These results suggest that the identified chemicals are potentially hazardous to human health. However, we want to be clear that more studies are needed to make definitive connections between chemical exposure and human disease,” said Dr. Tesar.

“Future studies will need to deepen our understanding of the duration and timing of exposure required to initiate or exacerbate disease. This information is needed before specific recommendations, such as behavioral interventions, can be made to reduce exposure. Some of these chemicals have useful roles in our homes, but we need to consider how they’re being used and what level of exposure might be considered safe,” Dr. Tesar said. 

In his view, the results “provide a starting point to understand what exposure levels to these chemicals might be putting ourselves or kids at risk for toxicity.”
 

Too Soon to Tell

Commenting for this news organization, Shaheen Lakhan, MD, a neurologist and researcher based in Miami, who was not involved in the study, echoed the need for more research. 

“The biological mechanisms uncovered provide plausible pathways by which these chemicals could potentially impact human brain development related to oligodendrocytes and myelination. Oligodendrocytes play a critical role in plastic neurological processes throughout life, not just early neurodevelopment. So, disrupting their maturation and function theoretically could contribute to neurodevelopmental disorders as well as adult conditions like multiple sclerosis,” Dr. Lakhan said. 

“This study alone shouldn’t sound neurotoxicant alarms yet. We’ve seen many past chemical scares like saccharin and phthalates fizzle despite alarming lab results when real-world human brain impacts failed to materialize,” Dr. Lakhan cautioned. 

“Far more rigorous research directly linking household chemical exposures to cognitive deficits in people is still needed before drawing firm conclusions or prompting overreactions from the general public. Policymakers will eventually need to weigh potential risks vs benefits, but no definitive human health threat has currently been established,” Dr. Lakhan said. 

Sarah Evans, PhD, MPH, assistant professor in the Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai in New York, also emphasized the need for further study.

“Given that most of the experiments in this study were conducted in isolated cells and a mouse model, further research is needed to determine whether exposure to these chemicals at levels experienced by the general population during critical windows of development impairs myelination and leads to adverse health outcomes like learning and behavior problems in humans,” said Dr. Evans, who was involved in the study.

“The authors’ finding of an association between higher urinary levels of the organophosphate flame-retardant metabolite BDCIPP and gross motor problems or need for special education in children aged 3-11 years in the CDC National Health and Nutrition Examination Survey strengthens their laboratory findings and warrants further investigation,” Dr. Evans added. 

The research was supported by grants from the National Institutes of Health, National Multiple Sclerosis Society, Howard Hughes Medical Institute and New York Stem Cell Foundation, and philanthropic support by sTF5 Care and the Long, Walter, Peterson, Goodman, and Geller families. Dr. Tesar, Dr. Lakhan, and Dr. Evans report no relevant disclosures. 
 

A version of this article appeared on Medscape.com.

Two classes of chemicals present in common household products may impair the development of oligodendrocytes, the myelinating cells of the central nervous system (CNS), which are critical to brain development and function. However, the researchers as well as outside experts agree more research is needed before any firm conclusions can be drawn. 

Quaternary ammonium compounds, ubiquitous in disinfecting agents and personal care products, and organophosphate flame retardants, which are commonly found in household items such as furniture and electronics had “surprising effects specifically on the non-nerve cells in the brain,” said lead researcher Paul Tesar, PhD, professor and director of the Institute for Glial Sciences, Case Western Reserve University School of Medicine, Cleveland. 

“Other studies have shown that our exposures to the chemicals in disinfecting agents nearly doubled during the pandemic,” Dr. Tesar noted. The finding that quaternary ammonium chemicals in disinfecting agents are harmful to specific brain cells suggests “we need to think about our increased utilization and exposure,” he added.

The results were published online on March 25 in Nature Neuroscience. 
 

Motor Dysfunction

Exposure to various chemicals in the environment has been shown to impair brain development. However, most of this research has focused on neurons. Less is known about effects on oligodendrocytes, which form the electrical insulation around the axons of CNS cells. Oligodendrocyte development continues from before birth into adulthood, thus these cells may be particularly vulnerable to damage from toxic chemicals.

The researchers analyzed the effects of 1823 chemicals on mouse oligodendrocyte development in cell cultures. They identified 292 chemicals that cause oligodendrocytes to die and 47 that inhibit oligodendrocyte generation. These chemicals belonged to two different classes.

They found that quaternary compounds were potently and selectively cytotoxic to developing oligodendrocytes and that organophosphate flame retardants prematurely arrested oligodendrocyte maturation. These effects were confirmed in mice and cultured human oligodendrocytes.

In addition, an analysis of epidemiologic data from the National Health and Nutrition Examination Survey (2013-2018) showed that one flame retardant metabolite, bis(1,3-dichloro-2-propy) phosphate (BDCIPP), was present in nearly all urine samples of children aged 3-11 years who were examined (1753 out of 1763 children).

After adjustment for multiple confounding factors, results showed that compared with children with urinary BDCIPP concentration in the lowest quartile, those with concentrations in the highest quartile were twice as likely to require special education (adjusted odds ratio [aOR], 2.0; 95% CI, 1.0-3.8) and were six times as likely to have gross motor dysfunction (aOR, 6.0; 95% CI, 1.7-21.9).

Children with urinary BDCIPP concentration within the third quartile also had significantly increased odds of motor dysfunction (aOR, 4.2; 95% CI, 1.1-16.2). 

“These results suggest that the identified chemicals are potentially hazardous to human health. However, we want to be clear that more studies are needed to make definitive connections between chemical exposure and human disease,” said Dr. Tesar.

“Future studies will need to deepen our understanding of the duration and timing of exposure required to initiate or exacerbate disease. This information is needed before specific recommendations, such as behavioral interventions, can be made to reduce exposure. Some of these chemicals have useful roles in our homes, but we need to consider how they’re being used and what level of exposure might be considered safe,” Dr. Tesar said. 

In his view, the results “provide a starting point to understand what exposure levels to these chemicals might be putting ourselves or kids at risk for toxicity.”
 

Too Soon to Tell

Commenting for this news organization, Shaheen Lakhan, MD, a neurologist and researcher based in Miami, who was not involved in the study, echoed the need for more research. 

“The biological mechanisms uncovered provide plausible pathways by which these chemicals could potentially impact human brain development related to oligodendrocytes and myelination. Oligodendrocytes play a critical role in plastic neurological processes throughout life, not just early neurodevelopment. So, disrupting their maturation and function theoretically could contribute to neurodevelopmental disorders as well as adult conditions like multiple sclerosis,” Dr. Lakhan said. 

“This study alone shouldn’t sound neurotoxicant alarms yet. We’ve seen many past chemical scares like saccharin and phthalates fizzle despite alarming lab results when real-world human brain impacts failed to materialize,” Dr. Lakhan cautioned. 

“Far more rigorous research directly linking household chemical exposures to cognitive deficits in people is still needed before drawing firm conclusions or prompting overreactions from the general public. Policymakers will eventually need to weigh potential risks vs benefits, but no definitive human health threat has currently been established,” Dr. Lakhan said. 

Sarah Evans, PhD, MPH, assistant professor in the Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai in New York, also emphasized the need for further study.

“Given that most of the experiments in this study were conducted in isolated cells and a mouse model, further research is needed to determine whether exposure to these chemicals at levels experienced by the general population during critical windows of development impairs myelination and leads to adverse health outcomes like learning and behavior problems in humans,” said Dr. Evans, who was involved in the study.

“The authors’ finding of an association between higher urinary levels of the organophosphate flame-retardant metabolite BDCIPP and gross motor problems or need for special education in children aged 3-11 years in the CDC National Health and Nutrition Examination Survey strengthens their laboratory findings and warrants further investigation,” Dr. Evans added. 

The research was supported by grants from the National Institutes of Health, National Multiple Sclerosis Society, Howard Hughes Medical Institute and New York Stem Cell Foundation, and philanthropic support by sTF5 Care and the Long, Walter, Peterson, Goodman, and Geller families. Dr. Tesar, Dr. Lakhan, and Dr. Evans report no relevant disclosures. 
 

A version of this article appeared on Medscape.com.

Two classes of chemicals present in common household products may impair the development of oligodendrocytes, the myelinating cells of the central nervous system (CNS), which are critical to brain development and function. However, the researchers as well as outside experts agree more research is needed before any firm conclusions can be drawn. 

Quaternary ammonium compounds, ubiquitous in disinfecting agents and personal care products, and organophosphate flame retardants, which are commonly found in household items such as furniture and electronics had “surprising effects specifically on the non-nerve cells in the brain,” said lead researcher Paul Tesar, PhD, professor and director of the Institute for Glial Sciences, Case Western Reserve University School of Medicine, Cleveland. 

“Other studies have shown that our exposures to the chemicals in disinfecting agents nearly doubled during the pandemic,” Dr. Tesar noted. The finding that quaternary ammonium chemicals in disinfecting agents are harmful to specific brain cells suggests “we need to think about our increased utilization and exposure,” he added.

The results were published online on March 25 in Nature Neuroscience. 
 

Motor Dysfunction

Exposure to various chemicals in the environment has been shown to impair brain development. However, most of this research has focused on neurons. Less is known about effects on oligodendrocytes, which form the electrical insulation around the axons of CNS cells. Oligodendrocyte development continues from before birth into adulthood, thus these cells may be particularly vulnerable to damage from toxic chemicals.

The researchers analyzed the effects of 1823 chemicals on mouse oligodendrocyte development in cell cultures. They identified 292 chemicals that cause oligodendrocytes to die and 47 that inhibit oligodendrocyte generation. These chemicals belonged to two different classes.

They found that quaternary compounds were potently and selectively cytotoxic to developing oligodendrocytes and that organophosphate flame retardants prematurely arrested oligodendrocyte maturation. These effects were confirmed in mice and cultured human oligodendrocytes.

In addition, an analysis of epidemiologic data from the National Health and Nutrition Examination Survey (2013-2018) showed that one flame retardant metabolite, bis(1,3-dichloro-2-propy) phosphate (BDCIPP), was present in nearly all urine samples of children aged 3-11 years who were examined (1753 out of 1763 children).

After adjustment for multiple confounding factors, results showed that compared with children with urinary BDCIPP concentration in the lowest quartile, those with concentrations in the highest quartile were twice as likely to require special education (adjusted odds ratio [aOR], 2.0; 95% CI, 1.0-3.8) and were six times as likely to have gross motor dysfunction (aOR, 6.0; 95% CI, 1.7-21.9).

Children with urinary BDCIPP concentration within the third quartile also had significantly increased odds of motor dysfunction (aOR, 4.2; 95% CI, 1.1-16.2). 

“These results suggest that the identified chemicals are potentially hazardous to human health. However, we want to be clear that more studies are needed to make definitive connections between chemical exposure and human disease,” said Dr. Tesar.

“Future studies will need to deepen our understanding of the duration and timing of exposure required to initiate or exacerbate disease. This information is needed before specific recommendations, such as behavioral interventions, can be made to reduce exposure. Some of these chemicals have useful roles in our homes, but we need to consider how they’re being used and what level of exposure might be considered safe,” Dr. Tesar said. 

In his view, the results “provide a starting point to understand what exposure levels to these chemicals might be putting ourselves or kids at risk for toxicity.”
 

Too Soon to Tell

Commenting for this news organization, Shaheen Lakhan, MD, a neurologist and researcher based in Miami, who was not involved in the study, echoed the need for more research. 

“The biological mechanisms uncovered provide plausible pathways by which these chemicals could potentially impact human brain development related to oligodendrocytes and myelination. Oligodendrocytes play a critical role in plastic neurological processes throughout life, not just early neurodevelopment. So, disrupting their maturation and function theoretically could contribute to neurodevelopmental disorders as well as adult conditions like multiple sclerosis,” Dr. Lakhan said. 

“This study alone shouldn’t sound neurotoxicant alarms yet. We’ve seen many past chemical scares like saccharin and phthalates fizzle despite alarming lab results when real-world human brain impacts failed to materialize,” Dr. Lakhan cautioned. 

“Far more rigorous research directly linking household chemical exposures to cognitive deficits in people is still needed before drawing firm conclusions or prompting overreactions from the general public. Policymakers will eventually need to weigh potential risks vs benefits, but no definitive human health threat has currently been established,” Dr. Lakhan said. 

Sarah Evans, PhD, MPH, assistant professor in the Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai in New York, also emphasized the need for further study.

“Given that most of the experiments in this study were conducted in isolated cells and a mouse model, further research is needed to determine whether exposure to these chemicals at levels experienced by the general population during critical windows of development impairs myelination and leads to adverse health outcomes like learning and behavior problems in humans,” said Dr. Evans, who was involved in the study.

“The authors’ finding of an association between higher urinary levels of the organophosphate flame-retardant metabolite BDCIPP and gross motor problems or need for special education in children aged 3-11 years in the CDC National Health and Nutrition Examination Survey strengthens their laboratory findings and warrants further investigation,” Dr. Evans added. 

The research was supported by grants from the National Institutes of Health, National Multiple Sclerosis Society, Howard Hughes Medical Institute and New York Stem Cell Foundation, and philanthropic support by sTF5 Care and the Long, Walter, Peterson, Goodman, and Geller families. Dr. Tesar, Dr. Lakhan, and Dr. Evans report no relevant disclosures. 
 

A version of this article appeared on Medscape.com.