Neurology Reviews

An alpha-synuclein seed amplification assay (αSyn-SAA) accurately identifies people with Parkinson’s disease, as well as those at risk for Parkinson’s disease and those with early, prodromal symptoms, and provides information on molecular subtypes, new research indicates.

“Identifying an effective biomarker for Parkinson’s disease pathology could have profound implications for the way we treat the condition, potentially making it possible to diagnose people earlier, identify the best treatments for different subsets of patients, and speed up clinical trials,” the study’s co-lead author Andrew Siderowf, MD, of the University of Pennsylvania, Philadelphia, said in a news release.

“Our findings suggest that the αSyn-SAA technique is highly accurate at detecting the biomarker for Parkinson’s disease regardless of the clinical features, making it possible to accurately diagnose the disease in patients at early stages,” added co-lead author Luis Concha-Marambio, PhD, director of research and development at Amprion, San Diego, Calif.

The study was published online in The Lancet Neurology.
 

‘New era’ in Parkinson’s disease

The researchers assessed the usefulness of αSyn-SAA in a cross-sectional analysis of 1,123 participants in the Parkinson’s Progression Markers Initiative (PPMI) cohort from 33 participating academic neurology outpatient practices in 12 countries.

The cohort included individuals with sporadic Parkinson’s disease from LRRK2 or GBA variants, healthy controls, individuals with clinical syndromes prodromal to Parkinson’s disease (rapid eye movement sleep behavior disorder [RBD] or hyposmia), and nonmanifesting carriers of LRRK2 and GBA variants. Cerebrospinal fluid (CSF) samples from each participant were analyzed using αSyn-SAA.

Overall, αSyn-SAA differentiated Parkinson’s disease from healthy controls with 87.7% sensitivity and 96.3% specificity.

Sensitivity of the assay varied across subgroups based on genetic and clinical features. Among genetic Parkinson’s disease subgroups, sensitivity was highest for GBA Parkinson’s disease (95.9%), followed by sporadic Parkinson’s disease (93.3%), and lowest for LRRK2 Parkinson’s disease (67.5%). Among clinical features, hyposmia was the most robust predictor of a positive assay result.

Among all Parkinson’s disease cases with hyposmia, the sensitivity of the assay was 97.2%, compared with 63.0% for Parkinson’s disease without olfactory dysfunction. Combining genetic and clinical features, the sensitivity of positive αSyn-SAA in sporadic Parkinson’s disease with olfactory deficit was 98.6%, compared with 78.3% in sporadic Parkinson’s disease without hyposmia. Most prodromal participants (86%) with RBD and hyposmia had positive αSyn-SAA results, indicating they had α-synuclein aggregates despite not yet being diagnosed with Parkinson’s disease.

Among those recruited based on their loss of smell, 89% (16 of 18 participants) had positive αSyn-SAA results. Similarly, in those with RBD, positive αSyn-SAA results were present in 85% of cases (28 of 33). No other clinical features were associated with a positive αSyn-SAA result.

In participants who carried LRRK2 or GBA variants but had no Parkinson’s disease diagnosis or prodromal symptoms (nonmanifesting carriers), 9% (14 of 159) and 7% (11 of 151), respectively, had positive αSyn-SAA results.

To date, this is the largest analysis of α-Syn-SAA for the biochemical diagnosis of Parkinson’s disease, the researchers said.

The results show that the assay classifies people with Parkinson’s disease with “high sensitivity and specificity, provides information about molecular heterogeneity, and detects prodromal individuals before diagnosis,” they wrote.

“These findings suggest a crucial role for the α-synuclein SAA in therapeutic development, both to identify pathologically defined subgroups of people with Parkinson’s disease and to establish biomarker-defined at-risk cohorts,” they added.

Amprion has commercialized the assay (SYNTap test), which can be ordered online.
 

‘Seminal development’

The authors of an accompanying editorial noted the study “lays the foundation for a biological diagnosis” of Parkinson’s disease. “We have entered a new era of biomarker and treatment development for Parkinson’s disease. The possibility of detecting a misfolded α-synuclein, the pathological hallmark of Parkinson’s disease, by employing an SSA, is a seminal development,” wrote Daniela Berg, MD, PhD, and Christine Klein, MD, with University Hospital Schleswig-Holstein, Germany.

“However, to fully leverage the enormous potential of the α-synuclein seed amplification, the test would have to be performed in blood rather than the CSF, a less invasive approach that has proven to be viable,” they added.

“Although the blood-based method needs to be further elaborated for scalability, α-synuclein SAA is a game changer in Parkinson’s disease diagnostics, research, and treatment trials,” they concluded.

The study was funded by The Michael J. Fox Foundation for Parkinson’s Research and a consortium of more than 40 private and philanthropic partners. Dr. Siderowf has declared consulting for Merck and Parkinson Study Group, and receiving honoraria from Bial. A full list of author disclosures is available with the original article. Dr. Berg and Dr. Klein have reported no relevant financial relationships.
 

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

An alpha-synuclein seed amplification assay (αSyn-SAA) accurately identifies people with Parkinson’s disease, as well as those at risk for Parkinson’s disease and those with early, prodromal symptoms, and provides information on molecular subtypes, new research indicates.

“Identifying an effective biomarker for Parkinson’s disease pathology could have profound implications for the way we treat the condition, potentially making it possible to diagnose people earlier, identify the best treatments for different subsets of patients, and speed up clinical trials,” the study’s co-lead author Andrew Siderowf, MD, of the University of Pennsylvania, Philadelphia, said in a news release.

“Our findings suggest that the αSyn-SAA technique is highly accurate at detecting the biomarker for Parkinson’s disease regardless of the clinical features, making it possible to accurately diagnose the disease in patients at early stages,” added co-lead author Luis Concha-Marambio, PhD, director of research and development at Amprion, San Diego, Calif.

The study was published online in The Lancet Neurology.
 

‘New era’ in Parkinson’s disease

The researchers assessed the usefulness of αSyn-SAA in a cross-sectional analysis of 1,123 participants in the Parkinson’s Progression Markers Initiative (PPMI) cohort from 33 participating academic neurology outpatient practices in 12 countries.

The cohort included individuals with sporadic Parkinson’s disease from LRRK2 or GBA variants, healthy controls, individuals with clinical syndromes prodromal to Parkinson’s disease (rapid eye movement sleep behavior disorder [RBD] or hyposmia), and nonmanifesting carriers of LRRK2 and GBA variants. Cerebrospinal fluid (CSF) samples from each participant were analyzed using αSyn-SAA.

Overall, αSyn-SAA differentiated Parkinson’s disease from healthy controls with 87.7% sensitivity and 96.3% specificity.

Sensitivity of the assay varied across subgroups based on genetic and clinical features. Among genetic Parkinson’s disease subgroups, sensitivity was highest for GBA Parkinson’s disease (95.9%), followed by sporadic Parkinson’s disease (93.3%), and lowest for LRRK2 Parkinson’s disease (67.5%). Among clinical features, hyposmia was the most robust predictor of a positive assay result.

Among all Parkinson’s disease cases with hyposmia, the sensitivity of the assay was 97.2%, compared with 63.0% for Parkinson’s disease without olfactory dysfunction. Combining genetic and clinical features, the sensitivity of positive αSyn-SAA in sporadic Parkinson’s disease with olfactory deficit was 98.6%, compared with 78.3% in sporadic Parkinson’s disease without hyposmia. Most prodromal participants (86%) with RBD and hyposmia had positive αSyn-SAA results, indicating they had α-synuclein aggregates despite not yet being diagnosed with Parkinson’s disease.

Among those recruited based on their loss of smell, 89% (16 of 18 participants) had positive αSyn-SAA results. Similarly, in those with RBD, positive αSyn-SAA results were present in 85% of cases (28 of 33). No other clinical features were associated with a positive αSyn-SAA result.

In participants who carried LRRK2 or GBA variants but had no Parkinson’s disease diagnosis or prodromal symptoms (nonmanifesting carriers), 9% (14 of 159) and 7% (11 of 151), respectively, had positive αSyn-SAA results.

To date, this is the largest analysis of α-Syn-SAA for the biochemical diagnosis of Parkinson’s disease, the researchers said.

The results show that the assay classifies people with Parkinson’s disease with “high sensitivity and specificity, provides information about molecular heterogeneity, and detects prodromal individuals before diagnosis,” they wrote.

“These findings suggest a crucial role for the α-synuclein SAA in therapeutic development, both to identify pathologically defined subgroups of people with Parkinson’s disease and to establish biomarker-defined at-risk cohorts,” they added.

Amprion has commercialized the assay (SYNTap test), which can be ordered online.
 

‘Seminal development’

The authors of an accompanying editorial noted the study “lays the foundation for a biological diagnosis” of Parkinson’s disease. “We have entered a new era of biomarker and treatment development for Parkinson’s disease. The possibility of detecting a misfolded α-synuclein, the pathological hallmark of Parkinson’s disease, by employing an SSA, is a seminal development,” wrote Daniela Berg, MD, PhD, and Christine Klein, MD, with University Hospital Schleswig-Holstein, Germany.

“However, to fully leverage the enormous potential of the α-synuclein seed amplification, the test would have to be performed in blood rather than the CSF, a less invasive approach that has proven to be viable,” they added.

“Although the blood-based method needs to be further elaborated for scalability, α-synuclein SAA is a game changer in Parkinson’s disease diagnostics, research, and treatment trials,” they concluded.

The study was funded by The Michael J. Fox Foundation for Parkinson’s Research and a consortium of more than 40 private and philanthropic partners. Dr. Siderowf has declared consulting for Merck and Parkinson Study Group, and receiving honoraria from Bial. A full list of author disclosures is available with the original article. Dr. Berg and Dr. Klein have reported no relevant financial relationships.
 

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

An alpha-synuclein seed amplification assay (αSyn-SAA) accurately identifies people with Parkinson’s disease, as well as those at risk for Parkinson’s disease and those with early, prodromal symptoms, and provides information on molecular subtypes, new research indicates.

“Identifying an effective biomarker for Parkinson’s disease pathology could have profound implications for the way we treat the condition, potentially making it possible to diagnose people earlier, identify the best treatments for different subsets of patients, and speed up clinical trials,” the study’s co-lead author Andrew Siderowf, MD, of the University of Pennsylvania, Philadelphia, said in a news release.

“Our findings suggest that the αSyn-SAA technique is highly accurate at detecting the biomarker for Parkinson’s disease regardless of the clinical features, making it possible to accurately diagnose the disease in patients at early stages,” added co-lead author Luis Concha-Marambio, PhD, director of research and development at Amprion, San Diego, Calif.

The study was published online in The Lancet Neurology.
 

‘New era’ in Parkinson’s disease

The researchers assessed the usefulness of αSyn-SAA in a cross-sectional analysis of 1,123 participants in the Parkinson’s Progression Markers Initiative (PPMI) cohort from 33 participating academic neurology outpatient practices in 12 countries.

The cohort included individuals with sporadic Parkinson’s disease from LRRK2 or GBA variants, healthy controls, individuals with clinical syndromes prodromal to Parkinson’s disease (rapid eye movement sleep behavior disorder [RBD] or hyposmia), and nonmanifesting carriers of LRRK2 and GBA variants. Cerebrospinal fluid (CSF) samples from each participant were analyzed using αSyn-SAA.

Overall, αSyn-SAA differentiated Parkinson’s disease from healthy controls with 87.7% sensitivity and 96.3% specificity.

Sensitivity of the assay varied across subgroups based on genetic and clinical features. Among genetic Parkinson’s disease subgroups, sensitivity was highest for GBA Parkinson’s disease (95.9%), followed by sporadic Parkinson’s disease (93.3%), and lowest for LRRK2 Parkinson’s disease (67.5%). Among clinical features, hyposmia was the most robust predictor of a positive assay result.

Among all Parkinson’s disease cases with hyposmia, the sensitivity of the assay was 97.2%, compared with 63.0% for Parkinson’s disease without olfactory dysfunction. Combining genetic and clinical features, the sensitivity of positive αSyn-SAA in sporadic Parkinson’s disease with olfactory deficit was 98.6%, compared with 78.3% in sporadic Parkinson’s disease without hyposmia. Most prodromal participants (86%) with RBD and hyposmia had positive αSyn-SAA results, indicating they had α-synuclein aggregates despite not yet being diagnosed with Parkinson’s disease.

Among those recruited based on their loss of smell, 89% (16 of 18 participants) had positive αSyn-SAA results. Similarly, in those with RBD, positive αSyn-SAA results were present in 85% of cases (28 of 33). No other clinical features were associated with a positive αSyn-SAA result.

In participants who carried LRRK2 or GBA variants but had no Parkinson’s disease diagnosis or prodromal symptoms (nonmanifesting carriers), 9% (14 of 159) and 7% (11 of 151), respectively, had positive αSyn-SAA results.

To date, this is the largest analysis of α-Syn-SAA for the biochemical diagnosis of Parkinson’s disease, the researchers said.

The results show that the assay classifies people with Parkinson’s disease with “high sensitivity and specificity, provides information about molecular heterogeneity, and detects prodromal individuals before diagnosis,” they wrote.

“These findings suggest a crucial role for the α-synuclein SAA in therapeutic development, both to identify pathologically defined subgroups of people with Parkinson’s disease and to establish biomarker-defined at-risk cohorts,” they added.

Amprion has commercialized the assay (SYNTap test), which can be ordered online.
 

‘Seminal development’

The authors of an accompanying editorial noted the study “lays the foundation for a biological diagnosis” of Parkinson’s disease. “We have entered a new era of biomarker and treatment development for Parkinson’s disease. The possibility of detecting a misfolded α-synuclein, the pathological hallmark of Parkinson’s disease, by employing an SSA, is a seminal development,” wrote Daniela Berg, MD, PhD, and Christine Klein, MD, with University Hospital Schleswig-Holstein, Germany.

“However, to fully leverage the enormous potential of the α-synuclein seed amplification, the test would have to be performed in blood rather than the CSF, a less invasive approach that has proven to be viable,” they added.

“Although the blood-based method needs to be further elaborated for scalability, α-synuclein SAA is a game changer in Parkinson’s disease diagnostics, research, and treatment trials,” they concluded.

The study was funded by The Michael J. Fox Foundation for Parkinson’s Research and a consortium of more than 40 private and philanthropic partners. Dr. Siderowf has declared consulting for Merck and Parkinson Study Group, and receiving honoraria from Bial. A full list of author disclosures is available with the original article. Dr. Berg and Dr. Klein have reported no relevant financial relationships.
 

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

Food insecurity is linked to a more rapid decline in executive function in older adults, a new study shows.

The findings were reported just weeks after a pandemic-era expansion in Supplemental Nutrition Assistance Program benefits ended, leading to less food assistance for about 5 million people over age 60 who participate in the program.

“Even though we found only a very small association between food insecurity and executive function, it’s still meaningful, because food insecurity is something we can prevent,” lead investigator Boeun Kim, PhD, MPH, RN, postdoctoral fellow at Johns Hopkins University School of Nursing, Baltimore, told this news organization.

The findings were published online  in JAMA Network Open.
 

National data

The number of Americans over 60 with food insecurity has more than doubled since 2007, with an estimated 5.2 million older adults reporting food insecurity in 2020.

Prior studies have linked malnutrition and food insecurity to a decline in cognitive function. Participating in food assistance programs such as SNAP is associated with slower memory decline in older adults.

However, to date, there has been no longitudinal study that has used data from a nationally representative sample of older Americans, which, Dr. Kim said, could limit generalizability of the findings.

To address that issue, investigators analyzed data from 3,037 participants in the National Health and Aging Trends Study, which includes community dwellers age 65 and older who receive Medicare.

Participants reported food insecurity over 7 years, from 2012 to 2019. Data on immediate memory, delayed memory, and executive function were from 2013 to 2020.

Food insecurity was defined as going without groceries due to limited ability or social support; a lack of hot meals related to functional limitation or no help; going without eating because of the inability to feed oneself or no available support; skipping meals due to insufficient food or money; or skipping meals for 5 days or more.

Immediate and delayed recall were assessed using a 10-item word-list memory task, and executive function was measured using a clock drawing test. Each year’s cognitive functions were linked to the prior year’s food insecurity data.

Over 7 years, 417 people, or 12.1%, experienced food insecurity at least once.

Those with food insecurity were more likely to be older, female, part of racial and ethnic minority groups, living alone, obese, and have a lower income and educational attainment, depressive symptoms, social isolation and disability, compared with those without food insecurity.

After adjusting for age, sex, race/ethnicity, educational level, income, marital status, body mass index, functional disability, social isolation, and other potential confounders, researchers found that food insecurity was associated with a more rapid decline in executive function (mean difference in annual change in executive function score, −0.04; 95% confidence interval, −0.09 to −0.003).

Food insecurity was not associated with baseline cognitive function scores or changes in immediate or delayed recall.

“Clinicians should be aware of the experience of food insecurity and the higher risk of cognitive decline so maybe they could do universal screening and refer people with food insecurity to programs that can help them access nutritious meals,” Dr. Kim said.
 

A sign of other problems?

Thomas Vidic, MD, said food insecurity often goes hand-in-hand with lack of medication adherence, lack of regular medical care, and a host of other issues. Dr. Vidic is a neurologist at the Elkhart Clinic, Ind., and an adjunct clinical professor of neurology at Indiana University.

“When a person has food insecurity, they likely have other problems, and they’re going to degenerate faster,” said Dr. Vidic, who was not part of the study. “This is one important component, and it’s one more way of getting a handle on people who are failing.”

Dr. Vidic, who has dealt with the issue of food insecurity with his own patients, said he suspects the self-report nature of the study may hide the true scale of the problem.

“I suspect the numbers might actually be higher,” he said, adding that the study fills a gap in the literature with a large, nationally representative sample.

“We’re looking for issues to help with the elderly as far as what can we do to keep dementia from progressing,” he said. “There are some things that make sense, but we’ve never had this kind of data before.”

The study was funded by the National Institute on Aging. Dr. Kim and Dr. Vidic have reported no relevant financial relationships.

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

Food insecurity is linked to a more rapid decline in executive function in older adults, a new study shows.

The findings were reported just weeks after a pandemic-era expansion in Supplemental Nutrition Assistance Program benefits ended, leading to less food assistance for about 5 million people over age 60 who participate in the program.

“Even though we found only a very small association between food insecurity and executive function, it’s still meaningful, because food insecurity is something we can prevent,” lead investigator Boeun Kim, PhD, MPH, RN, postdoctoral fellow at Johns Hopkins University School of Nursing, Baltimore, told this news organization.

The findings were published online  in JAMA Network Open.
 

National data

The number of Americans over 60 with food insecurity has more than doubled since 2007, with an estimated 5.2 million older adults reporting food insecurity in 2020.

Prior studies have linked malnutrition and food insecurity to a decline in cognitive function. Participating in food assistance programs such as SNAP is associated with slower memory decline in older adults.

However, to date, there has been no longitudinal study that has used data from a nationally representative sample of older Americans, which, Dr. Kim said, could limit generalizability of the findings.

To address that issue, investigators analyzed data from 3,037 participants in the National Health and Aging Trends Study, which includes community dwellers age 65 and older who receive Medicare.

Participants reported food insecurity over 7 years, from 2012 to 2019. Data on immediate memory, delayed memory, and executive function were from 2013 to 2020.

Food insecurity was defined as going without groceries due to limited ability or social support; a lack of hot meals related to functional limitation or no help; going without eating because of the inability to feed oneself or no available support; skipping meals due to insufficient food or money; or skipping meals for 5 days or more.

Immediate and delayed recall were assessed using a 10-item word-list memory task, and executive function was measured using a clock drawing test. Each year’s cognitive functions were linked to the prior year’s food insecurity data.

Over 7 years, 417 people, or 12.1%, experienced food insecurity at least once.

Those with food insecurity were more likely to be older, female, part of racial and ethnic minority groups, living alone, obese, and have a lower income and educational attainment, depressive symptoms, social isolation and disability, compared with those without food insecurity.

After adjusting for age, sex, race/ethnicity, educational level, income, marital status, body mass index, functional disability, social isolation, and other potential confounders, researchers found that food insecurity was associated with a more rapid decline in executive function (mean difference in annual change in executive function score, −0.04; 95% confidence interval, −0.09 to −0.003).

Food insecurity was not associated with baseline cognitive function scores or changes in immediate or delayed recall.

“Clinicians should be aware of the experience of food insecurity and the higher risk of cognitive decline so maybe they could do universal screening and refer people with food insecurity to programs that can help them access nutritious meals,” Dr. Kim said.
 

A sign of other problems?

Thomas Vidic, MD, said food insecurity often goes hand-in-hand with lack of medication adherence, lack of regular medical care, and a host of other issues. Dr. Vidic is a neurologist at the Elkhart Clinic, Ind., and an adjunct clinical professor of neurology at Indiana University.

“When a person has food insecurity, they likely have other problems, and they’re going to degenerate faster,” said Dr. Vidic, who was not part of the study. “This is one important component, and it’s one more way of getting a handle on people who are failing.”

Dr. Vidic, who has dealt with the issue of food insecurity with his own patients, said he suspects the self-report nature of the study may hide the true scale of the problem.

“I suspect the numbers might actually be higher,” he said, adding that the study fills a gap in the literature with a large, nationally representative sample.

“We’re looking for issues to help with the elderly as far as what can we do to keep dementia from progressing,” he said. “There are some things that make sense, but we’ve never had this kind of data before.”

The study was funded by the National Institute on Aging. Dr. Kim and Dr. Vidic have reported no relevant financial relationships.

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

Food insecurity is linked to a more rapid decline in executive function in older adults, a new study shows.

The findings were reported just weeks after a pandemic-era expansion in Supplemental Nutrition Assistance Program benefits ended, leading to less food assistance for about 5 million people over age 60 who participate in the program.

“Even though we found only a very small association between food insecurity and executive function, it’s still meaningful, because food insecurity is something we can prevent,” lead investigator Boeun Kim, PhD, MPH, RN, postdoctoral fellow at Johns Hopkins University School of Nursing, Baltimore, told this news organization.

The findings were published online  in JAMA Network Open.
 

National data

The number of Americans over 60 with food insecurity has more than doubled since 2007, with an estimated 5.2 million older adults reporting food insecurity in 2020.

Prior studies have linked malnutrition and food insecurity to a decline in cognitive function. Participating in food assistance programs such as SNAP is associated with slower memory decline in older adults.

However, to date, there has been no longitudinal study that has used data from a nationally representative sample of older Americans, which, Dr. Kim said, could limit generalizability of the findings.

To address that issue, investigators analyzed data from 3,037 participants in the National Health and Aging Trends Study, which includes community dwellers age 65 and older who receive Medicare.

Participants reported food insecurity over 7 years, from 2012 to 2019. Data on immediate memory, delayed memory, and executive function were from 2013 to 2020.

Food insecurity was defined as going without groceries due to limited ability or social support; a lack of hot meals related to functional limitation or no help; going without eating because of the inability to feed oneself or no available support; skipping meals due to insufficient food or money; or skipping meals for 5 days or more.

Immediate and delayed recall were assessed using a 10-item word-list memory task, and executive function was measured using a clock drawing test. Each year’s cognitive functions were linked to the prior year’s food insecurity data.

Over 7 years, 417 people, or 12.1%, experienced food insecurity at least once.

Those with food insecurity were more likely to be older, female, part of racial and ethnic minority groups, living alone, obese, and have a lower income and educational attainment, depressive symptoms, social isolation and disability, compared with those without food insecurity.

After adjusting for age, sex, race/ethnicity, educational level, income, marital status, body mass index, functional disability, social isolation, and other potential confounders, researchers found that food insecurity was associated with a more rapid decline in executive function (mean difference in annual change in executive function score, −0.04; 95% confidence interval, −0.09 to −0.003).

Food insecurity was not associated with baseline cognitive function scores or changes in immediate or delayed recall.

“Clinicians should be aware of the experience of food insecurity and the higher risk of cognitive decline so maybe they could do universal screening and refer people with food insecurity to programs that can help them access nutritious meals,” Dr. Kim said.
 

A sign of other problems?

Thomas Vidic, MD, said food insecurity often goes hand-in-hand with lack of medication adherence, lack of regular medical care, and a host of other issues. Dr. Vidic is a neurologist at the Elkhart Clinic, Ind., and an adjunct clinical professor of neurology at Indiana University.

“When a person has food insecurity, they likely have other problems, and they’re going to degenerate faster,” said Dr. Vidic, who was not part of the study. “This is one important component, and it’s one more way of getting a handle on people who are failing.”

Dr. Vidic, who has dealt with the issue of food insecurity with his own patients, said he suspects the self-report nature of the study may hide the true scale of the problem.

“I suspect the numbers might actually be higher,” he said, adding that the study fills a gap in the literature with a large, nationally representative sample.

“We’re looking for issues to help with the elderly as far as what can we do to keep dementia from progressing,” he said. “There are some things that make sense, but we’ve never had this kind of data before.”

The study was funded by the National Institute on Aging. Dr. Kim and Dr. Vidic have reported no relevant financial relationships.

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

Both pain relief and neurological improvements persisted in patients with diabetic neuropathy 2 years after they began receiving treatment with 10 kHz of spinal cord stimulation, according to research that released early, prior to its presentation at the annual meeting of the American Academy of Neurology.

The data represents the longest follow-up available for spinal cord stimulation at a frequency higher than the 60 Hz initially approved for diabetic neuropathy by the Food and Drug Administration, according to lead author Erika A. Petersen, MD, a professor of neurosurgery and the residency program director at the University of Arkansas for Medical Sciences, Little Rock.

University of Arkansas

“You would expect that somebody who continues to have diabetes for 24 months and has neuropathy would have worse neuropathy after 2 years, and what we’re seeing is that people were stable or better in terms of their nerve function at 2 years,” Dr. Petersen said in an interview. “So that’s really revolutionary.”
 

Encouraging preliminary findings

The findings are “promising and preliminary,” John D. Markman, MD, a professor in neurology and neurosurgery, vice chair for clinical research, and director of the Translational Pain Research Program at the University of Rochester (N.Y.) Medical Center, said in an interview. Dr. Markman, who was not involved in this study, said that, though the results are encouraging, it’s “less clear how much of [the pain improvement] is due to what we would consider to be on-target, pain-relieving benefit from stimulation versus other factors like expectation.” The crossover rate and amount of reduction in pain intensity are promising, but “I think that excitement is weighed against the fact that this is an open-label study.”

An underused treatment

Although spinal cord stimulation has been around since the late 1960s, its use only picked up steam in the 2000s, when it became more frequently used to treat chronic nerve damage related to neuropathic pain syndromes, Dr. Petersen explained. The FDA approved the treatment’s new indication for diabetic neuropathy in 2015, and data from Abbott and Medtronic have shown benefits from spinal cord stimulation at 60 Hz, but some patients are uncomfortable with the vibration or tingling feelings the devices can cause at that frequency.

“They describe creepy crawlies or ants crawling over the feet, or pins and needles, and painful sensitivity,” Dr. Petersen said. “You create a vibration feeling in the same zone where they already have those feelings of buzzing and pain and vibration, and it’s sometimes actually even more uncomfortable and less satisfying to them in terms of relief” with the spinal cord stimulation at 60 Hz, she said, “so there’s a lot of attrition in terms of who will actually use it.”

At 10 kHz, however, “people don’t feel any vibration or tingling associated with it; it just jams the signal of the pain,” she said. The difference between the frequencies is like that between “a lifeguard whistle and a dog whistle.”
 

Testing high-frequency stimulation

The new findings included the 24-month follow-up data from a randomized controlled trial that assessed the effectiveness of high-frequency spinal cord stimulation for painful diabetic neuropathy. The original 216 participants enrolled in the trial had diabetic neuropathy symptoms for at least 12 months and either could no not tolerate or did not respond to medications. Enrollment criteria also included lower-limb pain intensity of at least 5 on a 0-10 visual analogy scale and hemoglobin A1c of no more than 10%.

For the first 6 months of the trial – before crossover was offered – participants were randomly assigned to receive either 10 kHz of spinal cord stimulation along with conventional medical management or to receive conventional medical management alone. The 6-month data from 187 patients, as reported in April 2021 in JAMA Neurology, revealed that 79% of those receiving spinal cord stimulation experienced at least 50% improved pain relief without worsening of their baseline neurologic deficits, compared with only 5% of those receiving only conventional treatments.

Average pain levels increased 2% in the control participants compared with a decrease of 76% in those with the spinal cord stimulation devices. In addition, 62% of the patients receiving spinal cord stimulation demonstration neurologic improvement in reflexes, strength, movement and sensation, compared with 3% of those in the control group. The study’s findings led the FDA to approve the device using 10 kHz.

At 6 months, 93% of control patients crossed over to receiving spinal cord stimulation while none with the devices opted to stop their spinal cord stimulation. The 12-month data revealed that 85% of those receiving spinal cord stimulation experienced at least 50% pain relief, with the average pain relief at 74%. Patients also reported statistically significant improved quality of life as well as less interference with sleep, mood, and daily activities from pain.

Two years after baseline, patients’ pain relief was maintained with average 80% improvement, and 66% of patients showed neurologic improvement since baseline. Though no patients had devices removed because of ineffectiveness, five patients’ devices were removed because of infection while infections in three other patients resolved.

“Being able to offer something that is not a pharmaceutical, without the side effects, that shows an even longer durability to that response is a really important finding at this point,” Dr. Petersen said.
 

Surgical considerations

Among the estimated 37 million Americans with type 1 or 2 diabetes, approximately one quarter of them experience some level of painful diabetic neuropathy, but medication and other medical management strategies are not always adequate in treating their pain. After a 1-week trial of spinal cord stimulation, the devices are implanted under the skin and rechargeable through the skin for up to 10 years, after which they can be replaced.

An appropriate candidate for spinal cord stimulation would be someone for whom existing non-invasive pain relief options, including medications, are ineffective or intolerable, Dr. Petersen and Dr. Markman both said. An adequate trial of medication is not “one size fits all” and will vary by each patient, added Dr. Markman, who is also interested in whether this study’s participants were able to have a reduction in use of pain relief medications.

“I think there’s a significant number of patients out there who can benefit from this, so I think that’s why it’s promising and exciting,” Dr. Markman said. “I do think it’s important to see if this actually allows them to be on less medication or whether stimulation turns out to be another treatment in addition to their baseline treatments.” The challenge is identifying “which patients are most likely to be benefiting from this and which are most likely to be harmed.”

Aside from infection from implantation, other possible risks include pain at the battery site and, in rare cases, a need for reoperation because of migration of the leads, he said.
 

Improvement in symptom severity and quality of life

After the wound from the implant has completely healed, Dr. Petersen said patients using the devices do not have any activity restrictions outside of magnetic interference, such as MRIs. “I’ve had people go back-country kayaking, scuba diving, fishing with their grandkids, all sorts of all sorts of things. If patients need to go through a scanner of any kind, they should ask whether it’s safe for pacemakers since these devices are like a “pacemaker for pain.

“I had a patient bring solar chargers with him so that he could recharge his battery in the backwoods while kayaking because that’s the level of improvement in pain that he got – from barely being able to walk down the hall to feeling comfortable being off the grid and active again,” Dr. Petersen said. “Those kinds of improvements in quality of life are massive.”

The study findings may also suggest that spinal cord stimulation can benefit a broader population of patients experiencing neuropathic pain, Dr. Markman said.

“There’s an extraordinary unmet need for treatments for neuropathy, and one important question here is the extent to which diabetic peripheral neuropathy and the response that we’re seeing here is a proxy for a broader effect across many neuropathies that are caused by other conditions other than diabetes,” Dr. Markman said. “There’s a lot of reason to think that this will be helpful not just for diabetes-related neuropathic pain, but for other types of neuropathic pain that have similar clinical presentations or clinical symptom patterns to diabetic peripheral neuropathy.”

The study was funded by Nevro, who manufactures the devices. Dr. Petersen and Dr. Markman both reported consulting with, receiving support from, holding stock options with, and serving on the data safety monitoring boards and advisory boards of numerous pharmaceutical companies.

Both pain relief and neurological improvements persisted in patients with diabetic neuropathy 2 years after they began receiving treatment with 10 kHz of spinal cord stimulation, according to research that released early, prior to its presentation at the annual meeting of the American Academy of Neurology.

The data represents the longest follow-up available for spinal cord stimulation at a frequency higher than the 60 Hz initially approved for diabetic neuropathy by the Food and Drug Administration, according to lead author Erika A. Petersen, MD, a professor of neurosurgery and the residency program director at the University of Arkansas for Medical Sciences, Little Rock.

University of Arkansas

“You would expect that somebody who continues to have diabetes for 24 months and has neuropathy would have worse neuropathy after 2 years, and what we’re seeing is that people were stable or better in terms of their nerve function at 2 years,” Dr. Petersen said in an interview. “So that’s really revolutionary.”
 

Encouraging preliminary findings

The findings are “promising and preliminary,” John D. Markman, MD, a professor in neurology and neurosurgery, vice chair for clinical research, and director of the Translational Pain Research Program at the University of Rochester (N.Y.) Medical Center, said in an interview. Dr. Markman, who was not involved in this study, said that, though the results are encouraging, it’s “less clear how much of [the pain improvement] is due to what we would consider to be on-target, pain-relieving benefit from stimulation versus other factors like expectation.” The crossover rate and amount of reduction in pain intensity are promising, but “I think that excitement is weighed against the fact that this is an open-label study.”

An underused treatment

Although spinal cord stimulation has been around since the late 1960s, its use only picked up steam in the 2000s, when it became more frequently used to treat chronic nerve damage related to neuropathic pain syndromes, Dr. Petersen explained. The FDA approved the treatment’s new indication for diabetic neuropathy in 2015, and data from Abbott and Medtronic have shown benefits from spinal cord stimulation at 60 Hz, but some patients are uncomfortable with the vibration or tingling feelings the devices can cause at that frequency.

“They describe creepy crawlies or ants crawling over the feet, or pins and needles, and painful sensitivity,” Dr. Petersen said. “You create a vibration feeling in the same zone where they already have those feelings of buzzing and pain and vibration, and it’s sometimes actually even more uncomfortable and less satisfying to them in terms of relief” with the spinal cord stimulation at 60 Hz, she said, “so there’s a lot of attrition in terms of who will actually use it.”

At 10 kHz, however, “people don’t feel any vibration or tingling associated with it; it just jams the signal of the pain,” she said. The difference between the frequencies is like that between “a lifeguard whistle and a dog whistle.”
 

Testing high-frequency stimulation

The new findings included the 24-month follow-up data from a randomized controlled trial that assessed the effectiveness of high-frequency spinal cord stimulation for painful diabetic neuropathy. The original 216 participants enrolled in the trial had diabetic neuropathy symptoms for at least 12 months and either could no not tolerate or did not respond to medications. Enrollment criteria also included lower-limb pain intensity of at least 5 on a 0-10 visual analogy scale and hemoglobin A1c of no more than 10%.

For the first 6 months of the trial – before crossover was offered – participants were randomly assigned to receive either 10 kHz of spinal cord stimulation along with conventional medical management or to receive conventional medical management alone. The 6-month data from 187 patients, as reported in April 2021 in JAMA Neurology, revealed that 79% of those receiving spinal cord stimulation experienced at least 50% improved pain relief without worsening of their baseline neurologic deficits, compared with only 5% of those receiving only conventional treatments.

Average pain levels increased 2% in the control participants compared with a decrease of 76% in those with the spinal cord stimulation devices. In addition, 62% of the patients receiving spinal cord stimulation demonstration neurologic improvement in reflexes, strength, movement and sensation, compared with 3% of those in the control group. The study’s findings led the FDA to approve the device using 10 kHz.

At 6 months, 93% of control patients crossed over to receiving spinal cord stimulation while none with the devices opted to stop their spinal cord stimulation. The 12-month data revealed that 85% of those receiving spinal cord stimulation experienced at least 50% pain relief, with the average pain relief at 74%. Patients also reported statistically significant improved quality of life as well as less interference with sleep, mood, and daily activities from pain.

Two years after baseline, patients’ pain relief was maintained with average 80% improvement, and 66% of patients showed neurologic improvement since baseline. Though no patients had devices removed because of ineffectiveness, five patients’ devices were removed because of infection while infections in three other patients resolved.

“Being able to offer something that is not a pharmaceutical, without the side effects, that shows an even longer durability to that response is a really important finding at this point,” Dr. Petersen said.
 

Surgical considerations

Among the estimated 37 million Americans with type 1 or 2 diabetes, approximately one quarter of them experience some level of painful diabetic neuropathy, but medication and other medical management strategies are not always adequate in treating their pain. After a 1-week trial of spinal cord stimulation, the devices are implanted under the skin and rechargeable through the skin for up to 10 years, after which they can be replaced.

An appropriate candidate for spinal cord stimulation would be someone for whom existing non-invasive pain relief options, including medications, are ineffective or intolerable, Dr. Petersen and Dr. Markman both said. An adequate trial of medication is not “one size fits all” and will vary by each patient, added Dr. Markman, who is also interested in whether this study’s participants were able to have a reduction in use of pain relief medications.

“I think there’s a significant number of patients out there who can benefit from this, so I think that’s why it’s promising and exciting,” Dr. Markman said. “I do think it’s important to see if this actually allows them to be on less medication or whether stimulation turns out to be another treatment in addition to their baseline treatments.” The challenge is identifying “which patients are most likely to be benefiting from this and which are most likely to be harmed.”

Aside from infection from implantation, other possible risks include pain at the battery site and, in rare cases, a need for reoperation because of migration of the leads, he said.
 

Improvement in symptom severity and quality of life

After the wound from the implant has completely healed, Dr. Petersen said patients using the devices do not have any activity restrictions outside of magnetic interference, such as MRIs. “I’ve had people go back-country kayaking, scuba diving, fishing with their grandkids, all sorts of all sorts of things. If patients need to go through a scanner of any kind, they should ask whether it’s safe for pacemakers since these devices are like a “pacemaker for pain.

“I had a patient bring solar chargers with him so that he could recharge his battery in the backwoods while kayaking because that’s the level of improvement in pain that he got – from barely being able to walk down the hall to feeling comfortable being off the grid and active again,” Dr. Petersen said. “Those kinds of improvements in quality of life are massive.”

The study findings may also suggest that spinal cord stimulation can benefit a broader population of patients experiencing neuropathic pain, Dr. Markman said.

“There’s an extraordinary unmet need for treatments for neuropathy, and one important question here is the extent to which diabetic peripheral neuropathy and the response that we’re seeing here is a proxy for a broader effect across many neuropathies that are caused by other conditions other than diabetes,” Dr. Markman said. “There’s a lot of reason to think that this will be helpful not just for diabetes-related neuropathic pain, but for other types of neuropathic pain that have similar clinical presentations or clinical symptom patterns to diabetic peripheral neuropathy.”

The study was funded by Nevro, who manufactures the devices. Dr. Petersen and Dr. Markman both reported consulting with, receiving support from, holding stock options with, and serving on the data safety monitoring boards and advisory boards of numerous pharmaceutical companies.

Both pain relief and neurological improvements persisted in patients with diabetic neuropathy 2 years after they began receiving treatment with 10 kHz of spinal cord stimulation, according to research that released early, prior to its presentation at the annual meeting of the American Academy of Neurology.

The data represents the longest follow-up available for spinal cord stimulation at a frequency higher than the 60 Hz initially approved for diabetic neuropathy by the Food and Drug Administration, according to lead author Erika A. Petersen, MD, a professor of neurosurgery and the residency program director at the University of Arkansas for Medical Sciences, Little Rock.

University of Arkansas

“You would expect that somebody who continues to have diabetes for 24 months and has neuropathy would have worse neuropathy after 2 years, and what we’re seeing is that people were stable or better in terms of their nerve function at 2 years,” Dr. Petersen said in an interview. “So that’s really revolutionary.”
 

Encouraging preliminary findings

The findings are “promising and preliminary,” John D. Markman, MD, a professor in neurology and neurosurgery, vice chair for clinical research, and director of the Translational Pain Research Program at the University of Rochester (N.Y.) Medical Center, said in an interview. Dr. Markman, who was not involved in this study, said that, though the results are encouraging, it’s “less clear how much of [the pain improvement] is due to what we would consider to be on-target, pain-relieving benefit from stimulation versus other factors like expectation.” The crossover rate and amount of reduction in pain intensity are promising, but “I think that excitement is weighed against the fact that this is an open-label study.”

An underused treatment

Although spinal cord stimulation has been around since the late 1960s, its use only picked up steam in the 2000s, when it became more frequently used to treat chronic nerve damage related to neuropathic pain syndromes, Dr. Petersen explained. The FDA approved the treatment’s new indication for diabetic neuropathy in 2015, and data from Abbott and Medtronic have shown benefits from spinal cord stimulation at 60 Hz, but some patients are uncomfortable with the vibration or tingling feelings the devices can cause at that frequency.

“They describe creepy crawlies or ants crawling over the feet, or pins and needles, and painful sensitivity,” Dr. Petersen said. “You create a vibration feeling in the same zone where they already have those feelings of buzzing and pain and vibration, and it’s sometimes actually even more uncomfortable and less satisfying to them in terms of relief” with the spinal cord stimulation at 60 Hz, she said, “so there’s a lot of attrition in terms of who will actually use it.”

At 10 kHz, however, “people don’t feel any vibration or tingling associated with it; it just jams the signal of the pain,” she said. The difference between the frequencies is like that between “a lifeguard whistle and a dog whistle.”
 

Testing high-frequency stimulation

The new findings included the 24-month follow-up data from a randomized controlled trial that assessed the effectiveness of high-frequency spinal cord stimulation for painful diabetic neuropathy. The original 216 participants enrolled in the trial had diabetic neuropathy symptoms for at least 12 months and either could no not tolerate or did not respond to medications. Enrollment criteria also included lower-limb pain intensity of at least 5 on a 0-10 visual analogy scale and hemoglobin A1c of no more than 10%.

For the first 6 months of the trial – before crossover was offered – participants were randomly assigned to receive either 10 kHz of spinal cord stimulation along with conventional medical management or to receive conventional medical management alone. The 6-month data from 187 patients, as reported in April 2021 in JAMA Neurology, revealed that 79% of those receiving spinal cord stimulation experienced at least 50% improved pain relief without worsening of their baseline neurologic deficits, compared with only 5% of those receiving only conventional treatments.

Average pain levels increased 2% in the control participants compared with a decrease of 76% in those with the spinal cord stimulation devices. In addition, 62% of the patients receiving spinal cord stimulation demonstration neurologic improvement in reflexes, strength, movement and sensation, compared with 3% of those in the control group. The study’s findings led the FDA to approve the device using 10 kHz.

At 6 months, 93% of control patients crossed over to receiving spinal cord stimulation while none with the devices opted to stop their spinal cord stimulation. The 12-month data revealed that 85% of those receiving spinal cord stimulation experienced at least 50% pain relief, with the average pain relief at 74%. Patients also reported statistically significant improved quality of life as well as less interference with sleep, mood, and daily activities from pain.

Two years after baseline, patients’ pain relief was maintained with average 80% improvement, and 66% of patients showed neurologic improvement since baseline. Though no patients had devices removed because of ineffectiveness, five patients’ devices were removed because of infection while infections in three other patients resolved.

“Being able to offer something that is not a pharmaceutical, without the side effects, that shows an even longer durability to that response is a really important finding at this point,” Dr. Petersen said.
 

Surgical considerations

Among the estimated 37 million Americans with type 1 or 2 diabetes, approximately one quarter of them experience some level of painful diabetic neuropathy, but medication and other medical management strategies are not always adequate in treating their pain. After a 1-week trial of spinal cord stimulation, the devices are implanted under the skin and rechargeable through the skin for up to 10 years, after which they can be replaced.

An appropriate candidate for spinal cord stimulation would be someone for whom existing non-invasive pain relief options, including medications, are ineffective or intolerable, Dr. Petersen and Dr. Markman both said. An adequate trial of medication is not “one size fits all” and will vary by each patient, added Dr. Markman, who is also interested in whether this study’s participants were able to have a reduction in use of pain relief medications.

“I think there’s a significant number of patients out there who can benefit from this, so I think that’s why it’s promising and exciting,” Dr. Markman said. “I do think it’s important to see if this actually allows them to be on less medication or whether stimulation turns out to be another treatment in addition to their baseline treatments.” The challenge is identifying “which patients are most likely to be benefiting from this and which are most likely to be harmed.”

Aside from infection from implantation, other possible risks include pain at the battery site and, in rare cases, a need for reoperation because of migration of the leads, he said.
 

Improvement in symptom severity and quality of life

After the wound from the implant has completely healed, Dr. Petersen said patients using the devices do not have any activity restrictions outside of magnetic interference, such as MRIs. “I’ve had people go back-country kayaking, scuba diving, fishing with their grandkids, all sorts of all sorts of things. If patients need to go through a scanner of any kind, they should ask whether it’s safe for pacemakers since these devices are like a “pacemaker for pain.

“I had a patient bring solar chargers with him so that he could recharge his battery in the backwoods while kayaking because that’s the level of improvement in pain that he got – from barely being able to walk down the hall to feeling comfortable being off the grid and active again,” Dr. Petersen said. “Those kinds of improvements in quality of life are massive.”

The study findings may also suggest that spinal cord stimulation can benefit a broader population of patients experiencing neuropathic pain, Dr. Markman said.

“There’s an extraordinary unmet need for treatments for neuropathy, and one important question here is the extent to which diabetic peripheral neuropathy and the response that we’re seeing here is a proxy for a broader effect across many neuropathies that are caused by other conditions other than diabetes,” Dr. Markman said. “There’s a lot of reason to think that this will be helpful not just for diabetes-related neuropathic pain, but for other types of neuropathic pain that have similar clinical presentations or clinical symptom patterns to diabetic peripheral neuropathy.”

The study was funded by Nevro, who manufactures the devices. Dr. Petersen and Dr. Markman both reported consulting with, receiving support from, holding stock options with, and serving on the data safety monitoring boards and advisory boards of numerous pharmaceutical companies.

Early detection and management of sleep disorders could reduce asthma incidence, according to a large-scale prospective study that included nearly half a million participants. The study was published in BMJ Open Respiratory Research.

The population-attributable risk analysis indicated that 19% of asthma cases could be prevented through improving sleep traits. The investigators took into consideration polygenic risk scores (PRSs) for asthma and comprehensive sleep scores encompassing five sleep traits.

Sleep quality is generally recognized as a nongenetic driver of asthma. Poor sleep quality and obstructive sleep apnea have been reported particularly among those with severe disease. In addition, asthma is known to adversely affect sleep duration, sleep quality, napping, and daytime sleepiness.

The researchers suggest that the relationship between sleep and asthma is bidirectional, given that sleep disorders (sleep of short duration, insomnia, evening chronotype [“night owl”], snoring, excessive daytime sleepiness) are associated with specific chronic inflammatory reactions. It has remained unclear, however, whether poor sleep reflects a higher risk of early asthma progression.

Genetic factors also contribute to asthma risk, but highly variable heritability suggests that the nongenetic exposures play an important role. “However, whether healthy nongenetic exposure could decrease the risk of asthma and mitigate the adverse effect of genetic risk remains largely unknown,” the authors state. They hypothesize that healthier sleep could decrease future asthma risk and mitigate the hazards of genetic effects.

Using data from the UK Biobank, a national large, prospective cohort drawn from 22 U.K. assessment centers, they investigated the independent and combined effects of sleep pattern and PRSs on asthma incidence.

In the UK Biobank cohort (455,405 adults aged 38-73 years, who were enrolled from 2006 to 2010), 17,836 were diagnosed with asthma over 10 years of follow-up. PRSs were constructed for each participant on the basis of their having any of 17 single-nucleotide polymorphisms that are significantly associated with asthma. Participants were stratified into three groups: those at high genetic risk, those at intermediate genetic risk, and those at low genetic risk. Around 1 in 3 participants were classified as being at high genetic risk (150,429), and another third (151,970) were classified as being at intermediate risk. The remainder were classified as being at low risk. Some 7,105 people at high genetic risk and 5,748 at intermediate genetic risk were diagnosed with asthma during the monitoring period.

Comprehensive sleep scores, which ranged from 0 to 5, were constructed on the basis of self-reported sleep traits. Higher scores represented healthier sleep patterns. A healthy sleep pattern was defined as early chronotype; getting from 7 to 9 hours of sleep every night; never or rare insomnia; no snoring; and no frequent daytime sleepiness. On the basis of their responses, 73,223 people met the criteria for a healthy sleep pattern; 284,267, an intermediate sleep pattern; and 97,915, a poor sleep pattern.

“Compared with non-cases, asthma cases were more likely to have lower education levels, unhealthy sleep traits and patterns, obesity, higher PRS, more smoking, more alcohol consumption, hypertension, diabetes, depression, gastroesophageal reflux. and more air pollution exposure,” the authors report. All five healthy sleep traits were independently associated with lower risk for asthma. Never/rare insomnia and sleep duration of 7-9 hours a night were seemingly the most influential; they were associated with risk reductions of 25% and 20%, respectively.

Analysis showed that, compared with the low-risk group, the hazard ratios and 95% confidence intervals for the highest PRS group and the poor sleep pattern group were 1.47 (95% CI, 1.41-1.52) and 1.55 (95% CI, 1.45-1.65), respectively.

Risk was twofold higher in the presence of a combination of poor sleep and high genetic susceptibility (HR, 2.22; 95% CI, 1.97-2.49; P < .001). Conversely, a healthy sleep pattern was associated with a lower risk of asthma in the low (HR, 0.56; 95% CI, 0.50-0.64), intermediate (HR, 0.59; 95% CI, 0.53-0.67), and high genetic susceptibility groups (HR, 0.63; 95% CI, 0.57-0.70). A population-attributable risk analysis indicated that improving these sleep traits would prevent 19% of asthma cases. Also, a subset analysis suggested that a healthy sleep pattern might reduce the risk of asthma among those at high genetic risk by 37%.

The study findings suggest that analysis of sleep patterns is warranted for all asthma patients, said coauthor Qing Wang, PhD, Cheeloo College of Medicine, Shandong University, Jinan, China, in an interview. “In our results, the effects of sleep and genetics were independent. Therefore, what we learned about the effects of sleep on asthma could be applied to all the patients, including those with a high or low genetic predisposition. In addition, we believe that intervening among those with high genetic predisposition could be more beneficial since they are more likely to have asthma. However, because this study is observational, a large clinical trial is absolutely needed to provide causal evidence, especially before guidelines modifications can be considered.”
 

Complex and multifactorial

“Addressing relevant asthma comorbid conditions continues to be an integral part of asthma care,” commented Diego J. Maselli, MD, associate professor of medicine and interim chief, division of pulmonary diseases and critical care, UT Health, San Antonio, in an interview. “There is mounting evidence that sleep patterns and obstructive sleep apnea may influence asthma control. This association is complex and multifactorial. It is important to remember that obstructive sleep apnea may coexist with other conditions, such as obesity and gastroesophageal reflux disease, that in turn can also worsen asthma control and influence clinical outcomes.

CHEST

“Yet, even after controlling for these factors, sleep disturbances have been associated with poor asthma outcomes. It is reasonable, particularly in patients with uncontrolled and/or severe asthma, to screen for sleep disturbances. There are multiple questionnaires and clinical tools that can be employed to screen for coexisting sleep apnea and other conditions. Although genetic testing has shown some promise in identifying individuals at risk, these assays are not widely available and are not ready yet for routine clinical practice. Therefore, sleep studies should be reserved for patients that have symptoms and test positive for screening questionnaires and other tools.

“The study by Xiang and colleagues adds to the field of study, but further evidence is required to change practice guidelines at this time. Fortunately, sleep studies are readily available now with more widespread use of home testing, so patients can be easily tested. The majority third-party payers have identified that diagnosing these disorders is cost-effective and are able to reimburse sleep studies,” Dr. Maselli concluded.

The research was funded by the Future Program for Young Scholars and National Key Research and Development Program. The study authors and Dr. Maselli have disclosed no relevant financial relationships.
 

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

Early detection and management of sleep disorders could reduce asthma incidence, according to a large-scale prospective study that included nearly half a million participants. The study was published in BMJ Open Respiratory Research.

The population-attributable risk analysis indicated that 19% of asthma cases could be prevented through improving sleep traits. The investigators took into consideration polygenic risk scores (PRSs) for asthma and comprehensive sleep scores encompassing five sleep traits.

Sleep quality is generally recognized as a nongenetic driver of asthma. Poor sleep quality and obstructive sleep apnea have been reported particularly among those with severe disease. In addition, asthma is known to adversely affect sleep duration, sleep quality, napping, and daytime sleepiness.

The researchers suggest that the relationship between sleep and asthma is bidirectional, given that sleep disorders (sleep of short duration, insomnia, evening chronotype [“night owl”], snoring, excessive daytime sleepiness) are associated with specific chronic inflammatory reactions. It has remained unclear, however, whether poor sleep reflects a higher risk of early asthma progression.

Genetic factors also contribute to asthma risk, but highly variable heritability suggests that the nongenetic exposures play an important role. “However, whether healthy nongenetic exposure could decrease the risk of asthma and mitigate the adverse effect of genetic risk remains largely unknown,” the authors state. They hypothesize that healthier sleep could decrease future asthma risk and mitigate the hazards of genetic effects.

Using data from the UK Biobank, a national large, prospective cohort drawn from 22 U.K. assessment centers, they investigated the independent and combined effects of sleep pattern and PRSs on asthma incidence.

In the UK Biobank cohort (455,405 adults aged 38-73 years, who were enrolled from 2006 to 2010), 17,836 were diagnosed with asthma over 10 years of follow-up. PRSs were constructed for each participant on the basis of their having any of 17 single-nucleotide polymorphisms that are significantly associated with asthma. Participants were stratified into three groups: those at high genetic risk, those at intermediate genetic risk, and those at low genetic risk. Around 1 in 3 participants were classified as being at high genetic risk (150,429), and another third (151,970) were classified as being at intermediate risk. The remainder were classified as being at low risk. Some 7,105 people at high genetic risk and 5,748 at intermediate genetic risk were diagnosed with asthma during the monitoring period.

Comprehensive sleep scores, which ranged from 0 to 5, were constructed on the basis of self-reported sleep traits. Higher scores represented healthier sleep patterns. A healthy sleep pattern was defined as early chronotype; getting from 7 to 9 hours of sleep every night; never or rare insomnia; no snoring; and no frequent daytime sleepiness. On the basis of their responses, 73,223 people met the criteria for a healthy sleep pattern; 284,267, an intermediate sleep pattern; and 97,915, a poor sleep pattern.

“Compared with non-cases, asthma cases were more likely to have lower education levels, unhealthy sleep traits and patterns, obesity, higher PRS, more smoking, more alcohol consumption, hypertension, diabetes, depression, gastroesophageal reflux. and more air pollution exposure,” the authors report. All five healthy sleep traits were independently associated with lower risk for asthma. Never/rare insomnia and sleep duration of 7-9 hours a night were seemingly the most influential; they were associated with risk reductions of 25% and 20%, respectively.

Analysis showed that, compared with the low-risk group, the hazard ratios and 95% confidence intervals for the highest PRS group and the poor sleep pattern group were 1.47 (95% CI, 1.41-1.52) and 1.55 (95% CI, 1.45-1.65), respectively.

Risk was twofold higher in the presence of a combination of poor sleep and high genetic susceptibility (HR, 2.22; 95% CI, 1.97-2.49; P < .001). Conversely, a healthy sleep pattern was associated with a lower risk of asthma in the low (HR, 0.56; 95% CI, 0.50-0.64), intermediate (HR, 0.59; 95% CI, 0.53-0.67), and high genetic susceptibility groups (HR, 0.63; 95% CI, 0.57-0.70). A population-attributable risk analysis indicated that improving these sleep traits would prevent 19% of asthma cases. Also, a subset analysis suggested that a healthy sleep pattern might reduce the risk of asthma among those at high genetic risk by 37%.

The study findings suggest that analysis of sleep patterns is warranted for all asthma patients, said coauthor Qing Wang, PhD, Cheeloo College of Medicine, Shandong University, Jinan, China, in an interview. “In our results, the effects of sleep and genetics were independent. Therefore, what we learned about the effects of sleep on asthma could be applied to all the patients, including those with a high or low genetic predisposition. In addition, we believe that intervening among those with high genetic predisposition could be more beneficial since they are more likely to have asthma. However, because this study is observational, a large clinical trial is absolutely needed to provide causal evidence, especially before guidelines modifications can be considered.”
 

Complex and multifactorial

“Addressing relevant asthma comorbid conditions continues to be an integral part of asthma care,” commented Diego J. Maselli, MD, associate professor of medicine and interim chief, division of pulmonary diseases and critical care, UT Health, San Antonio, in an interview. “There is mounting evidence that sleep patterns and obstructive sleep apnea may influence asthma control. This association is complex and multifactorial. It is important to remember that obstructive sleep apnea may coexist with other conditions, such as obesity and gastroesophageal reflux disease, that in turn can also worsen asthma control and influence clinical outcomes.

CHEST

“Yet, even after controlling for these factors, sleep disturbances have been associated with poor asthma outcomes. It is reasonable, particularly in patients with uncontrolled and/or severe asthma, to screen for sleep disturbances. There are multiple questionnaires and clinical tools that can be employed to screen for coexisting sleep apnea and other conditions. Although genetic testing has shown some promise in identifying individuals at risk, these assays are not widely available and are not ready yet for routine clinical practice. Therefore, sleep studies should be reserved for patients that have symptoms and test positive for screening questionnaires and other tools.

“The study by Xiang and colleagues adds to the field of study, but further evidence is required to change practice guidelines at this time. Fortunately, sleep studies are readily available now with more widespread use of home testing, so patients can be easily tested. The majority third-party payers have identified that diagnosing these disorders is cost-effective and are able to reimburse sleep studies,” Dr. Maselli concluded.

The research was funded by the Future Program for Young Scholars and National Key Research and Development Program. The study authors and Dr. Maselli have disclosed no relevant financial relationships.
 

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

Early detection and management of sleep disorders could reduce asthma incidence, according to a large-scale prospective study that included nearly half a million participants. The study was published in BMJ Open Respiratory Research.

The population-attributable risk analysis indicated that 19% of asthma cases could be prevented through improving sleep traits. The investigators took into consideration polygenic risk scores (PRSs) for asthma and comprehensive sleep scores encompassing five sleep traits.

Sleep quality is generally recognized as a nongenetic driver of asthma. Poor sleep quality and obstructive sleep apnea have been reported particularly among those with severe disease. In addition, asthma is known to adversely affect sleep duration, sleep quality, napping, and daytime sleepiness.

The researchers suggest that the relationship between sleep and asthma is bidirectional, given that sleep disorders (sleep of short duration, insomnia, evening chronotype [“night owl”], snoring, excessive daytime sleepiness) are associated with specific chronic inflammatory reactions. It has remained unclear, however, whether poor sleep reflects a higher risk of early asthma progression.

Genetic factors also contribute to asthma risk, but highly variable heritability suggests that the nongenetic exposures play an important role. “However, whether healthy nongenetic exposure could decrease the risk of asthma and mitigate the adverse effect of genetic risk remains largely unknown,” the authors state. They hypothesize that healthier sleep could decrease future asthma risk and mitigate the hazards of genetic effects.

Using data from the UK Biobank, a national large, prospective cohort drawn from 22 U.K. assessment centers, they investigated the independent and combined effects of sleep pattern and PRSs on asthma incidence.

In the UK Biobank cohort (455,405 adults aged 38-73 years, who were enrolled from 2006 to 2010), 17,836 were diagnosed with asthma over 10 years of follow-up. PRSs were constructed for each participant on the basis of their having any of 17 single-nucleotide polymorphisms that are significantly associated with asthma. Participants were stratified into three groups: those at high genetic risk, those at intermediate genetic risk, and those at low genetic risk. Around 1 in 3 participants were classified as being at high genetic risk (150,429), and another third (151,970) were classified as being at intermediate risk. The remainder were classified as being at low risk. Some 7,105 people at high genetic risk and 5,748 at intermediate genetic risk were diagnosed with asthma during the monitoring period.

Comprehensive sleep scores, which ranged from 0 to 5, were constructed on the basis of self-reported sleep traits. Higher scores represented healthier sleep patterns. A healthy sleep pattern was defined as early chronotype; getting from 7 to 9 hours of sleep every night; never or rare insomnia; no snoring; and no frequent daytime sleepiness. On the basis of their responses, 73,223 people met the criteria for a healthy sleep pattern; 284,267, an intermediate sleep pattern; and 97,915, a poor sleep pattern.

“Compared with non-cases, asthma cases were more likely to have lower education levels, unhealthy sleep traits and patterns, obesity, higher PRS, more smoking, more alcohol consumption, hypertension, diabetes, depression, gastroesophageal reflux. and more air pollution exposure,” the authors report. All five healthy sleep traits were independently associated with lower risk for asthma. Never/rare insomnia and sleep duration of 7-9 hours a night were seemingly the most influential; they were associated with risk reductions of 25% and 20%, respectively.

Analysis showed that, compared with the low-risk group, the hazard ratios and 95% confidence intervals for the highest PRS group and the poor sleep pattern group were 1.47 (95% CI, 1.41-1.52) and 1.55 (95% CI, 1.45-1.65), respectively.

Risk was twofold higher in the presence of a combination of poor sleep and high genetic susceptibility (HR, 2.22; 95% CI, 1.97-2.49; P < .001). Conversely, a healthy sleep pattern was associated with a lower risk of asthma in the low (HR, 0.56; 95% CI, 0.50-0.64), intermediate (HR, 0.59; 95% CI, 0.53-0.67), and high genetic susceptibility groups (HR, 0.63; 95% CI, 0.57-0.70). A population-attributable risk analysis indicated that improving these sleep traits would prevent 19% of asthma cases. Also, a subset analysis suggested that a healthy sleep pattern might reduce the risk of asthma among those at high genetic risk by 37%.

The study findings suggest that analysis of sleep patterns is warranted for all asthma patients, said coauthor Qing Wang, PhD, Cheeloo College of Medicine, Shandong University, Jinan, China, in an interview. “In our results, the effects of sleep and genetics were independent. Therefore, what we learned about the effects of sleep on asthma could be applied to all the patients, including those with a high or low genetic predisposition. In addition, we believe that intervening among those with high genetic predisposition could be more beneficial since they are more likely to have asthma. However, because this study is observational, a large clinical trial is absolutely needed to provide causal evidence, especially before guidelines modifications can be considered.”
 

Complex and multifactorial

“Addressing relevant asthma comorbid conditions continues to be an integral part of asthma care,” commented Diego J. Maselli, MD, associate professor of medicine and interim chief, division of pulmonary diseases and critical care, UT Health, San Antonio, in an interview. “There is mounting evidence that sleep patterns and obstructive sleep apnea may influence asthma control. This association is complex and multifactorial. It is important to remember that obstructive sleep apnea may coexist with other conditions, such as obesity and gastroesophageal reflux disease, that in turn can also worsen asthma control and influence clinical outcomes.

CHEST

“Yet, even after controlling for these factors, sleep disturbances have been associated with poor asthma outcomes. It is reasonable, particularly in patients with uncontrolled and/or severe asthma, to screen for sleep disturbances. There are multiple questionnaires and clinical tools that can be employed to screen for coexisting sleep apnea and other conditions. Although genetic testing has shown some promise in identifying individuals at risk, these assays are not widely available and are not ready yet for routine clinical practice. Therefore, sleep studies should be reserved for patients that have symptoms and test positive for screening questionnaires and other tools.

“The study by Xiang and colleagues adds to the field of study, but further evidence is required to change practice guidelines at this time. Fortunately, sleep studies are readily available now with more widespread use of home testing, so patients can be easily tested. The majority third-party payers have identified that diagnosing these disorders is cost-effective and are able to reimburse sleep studies,” Dr. Maselli concluded.

The research was funded by the Future Program for Young Scholars and National Key Research and Development Program. The study authors and Dr. Maselli have disclosed no relevant financial relationships.
 

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

In my most recent column, “ ‘They All Laughed When I Spoke of Greedy Doctors,’ ” I attempted to provide a global understanding of some of the economic forces that have made American medicine what it is, how that happened, and why it is still happening.

I did not propose a fix. I have been proposing fixes for more than 30 years, on the pages of JAMA until 1999 and then for this news organization, most recently in 2019 with “Healthcare for All in a Land of Special Interests.”

Where you stand depends a lot on where you sit.

Is this good news or bad news? When William Hubbard was the dean of the University of Michigan School of Medicine in 1969, he said that “an academic medical center is the most efficient energy and resource trapping device that has ever been created” (personal communication, 1969).

To me as a faculty member of an academic medical center for many years, that was great news. We could grow faculty, erect buildings, take the best care of sick people, churn out research papers, mint new physicians and specialists, and get paid well in the process for doing “the Lord’s work.” What’s not to like? At that time, the proportion of the country’s gross national product expended for medical and health care was about 7%. And the predicted life span of an American at birth was 70.5 years.

Is this good news or bad news? In 2021, the proportion of our annual gross domestic product (GDP) consumed by health care was 18.3%, totaling $4.3 trillion, or $12,914 per person. For perspective, in 2021, the median income per capita was $37,638. Because quite a few Americans have very high incomes, the mean income per capita is much higher: $63,444. Predicted life span in 2021 was 76.4 years.

Thus, in a span of 53 years (1969-2022), only 5.9 years of life were gained per person born, for how many trillions of dollars expended? To me as a tax-paying citizen and payer of medical insurance premiums, that is bad news.

Is this good news or bad news? If we compare developed societies globally, our medical system does a whole lot of things very well indeed. But we spend a great deal more than any other country for health care and objectively achieve poorer outcomes. Thus, we are neither efficient nor effective. We keep a lot of workers very busy doing stuff, and they are generally well paid. As a worker, that’s good news; as a manager who values efficiency, it’s bad news indeed.

Is this good news or bad news? We’re the leader at finding money to pay people to do “health care work.” More Americans work in health care than any other field. In 2019, the United States employed some 21,000,000 people doing “health care and social assistance.” Among others, these occupations include physicians, dentists, dental hygienists and assistants, pharmacists, registered nurses, LVNs/LPNs, nursing aides, technologists and technicians, home health aides, respiratory therapists, occupational and speech therapists, social workers, childcare workers, and personal and home care aides. For a patient, parent, grandparent, and great-grandparent, it is good news to have all those folks available to take care of us when we need it.

So, while I have cringed at the frequent exposés from Roy Poses of what seem to me to be massive societal betrayals by American health care industry giants, it doesn’t have to be that way. Might it still be possible to do well while doing good?
 

A jobs program

Consider such common medical procedures as coronary artery stents or bypass grafts for stable angina (when optimal medical therapy is as good, or better than, and much less expensive); PSAs on asymptomatic men followed by unnecessary surgery for localized cancer; excess surgery for low back pain; and the jobs created by managing the people caught up in medical complications of the obesity epidemic.

Don’t forget the number of people employed simply to “follow the money” within our byzantine cockamamie medical billing system. In 2009, this prompted me to describe the bloated system as a “health care bubble” not unlike Enron, the submarket real estate financing debacle, or the dot-com boom and bust. I warned of the downside of bursting that bubble, particularly lost jobs.

The Affordable Care Act (ACA) provided health insurance to some 35 million Americans who had been uninsured. It retarded health care inflation. But it did nothing to trim administrative costs or very high pay for nonclinical executives, or shareholder profits in those companies that were for-profit, or drug and device prices. Without the support of all those groups, the ACA would never have passed Congress. The ACA has clearly been a mixed blessing.

If any large American constituency were ever serious about reducing the percentage of our GDP expended on health care, we have excellent ways to do that while improving the health and well-being of the American people. But remember, one person’s liability (unnecessary work) is another person’s asset (needed job).
 

The MBAization of medicine

Meanwhile, back at Dean Hubbard’s voracious academic medical center, the high intellect and driven nature of those who are attracted to medicine as a career has had other effects. The resulting organizations reflect not only the glorious calling of caring for the sick and the availability of lots of money to recruit and compensate leaders, but also the necessity to develop strong executive types who won’t be “eaten alive” by the high-powered workforce of demanding physicians and the surrounding environment.

Thus, it came as no great surprise that in its 2021 determination of America’s top 25 Best Large Employers, Forbes included five health care organizations and seven universities. Beating out such giants as NASA, Cisco, Microsoft, Netflix, and Google, the University of Alabama Birmingham Hospital was ranked first. Mayo Clinic and Yale University came in third and fifth, respectively, and at the other end of the list were Duke (23), MIT (24), and MD Anderson (25).

My goodness! Well done.

Yet, as a country attempting to be balanced, Warren Buffett’s descriptive entreaty on the 2021 failure of Haven, the Amazon-Chase-Berkshire Hathaway joint initiative, remains troubling. Calling upon Haven to change the U.S. health care system, Buffet said, “We learned a lot about the difficulty of changing around an industry that’s 17% of the GDP. We were fighting a tapeworm in the American economy, and the tapeworm won.” They had failed to tame the American health care cost beast.

I am on record as despising the “MBAization” of American medicine. Unfairly, I blamed a professional and technical discipline for what I considered misuse. I hereby repent and renounce my earlier condemnations.
 

Take it all over?

Here’s an idea: If you can’t beat them, join them.

Medical care is important, especially for acute illnesses and injuries, early cancer therapy, and many chronic conditions. But the real determinants of health writ large are social: wealth, education, housing, nutritious food, childcare, climate, clean air and water, meaningful employment, safety from violence, exercise schemes, vaccinations, and so on.

Why doesn’t the American medical-industrial complex simply bestow the label of “health care” on all health-related social determinants? Take it all over. Good “health care” jobs for everyone. Medical professionals will still be blamed for the low health quality and poor outcome scores, the main social determinants of health over which we have no control or influence.

Let that tapeworm grow to encompass all social determinants of health, and measure results by length and quality of life, national human happiness, and, of course, jobs. We can do it. Let that bubble glow. Party time.

And that’s the way it is. That’s my opinion.

George Lundberg, MD, is editor-in-chief at Cancer Commons, president of the Lundberg Institute, executive advisor at Cureus, and a clinical professor of pathology at Northwestern University. Previously, he served as editor-in-chief of JAMA (including 10 specialty journals), American Medical News, and Medscape.

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

In my most recent column, “ ‘They All Laughed When I Spoke of Greedy Doctors,’ ” I attempted to provide a global understanding of some of the economic forces that have made American medicine what it is, how that happened, and why it is still happening.

I did not propose a fix. I have been proposing fixes for more than 30 years, on the pages of JAMA until 1999 and then for this news organization, most recently in 2019 with “Healthcare for All in a Land of Special Interests.”

Where you stand depends a lot on where you sit.

Is this good news or bad news? When William Hubbard was the dean of the University of Michigan School of Medicine in 1969, he said that “an academic medical center is the most efficient energy and resource trapping device that has ever been created” (personal communication, 1969).

To me as a faculty member of an academic medical center for many years, that was great news. We could grow faculty, erect buildings, take the best care of sick people, churn out research papers, mint new physicians and specialists, and get paid well in the process for doing “the Lord’s work.” What’s not to like? At that time, the proportion of the country’s gross national product expended for medical and health care was about 7%. And the predicted life span of an American at birth was 70.5 years.

Is this good news or bad news? In 2021, the proportion of our annual gross domestic product (GDP) consumed by health care was 18.3%, totaling $4.3 trillion, or $12,914 per person. For perspective, in 2021, the median income per capita was $37,638. Because quite a few Americans have very high incomes, the mean income per capita is much higher: $63,444. Predicted life span in 2021 was 76.4 years.

Thus, in a span of 53 years (1969-2022), only 5.9 years of life were gained per person born, for how many trillions of dollars expended? To me as a tax-paying citizen and payer of medical insurance premiums, that is bad news.

Is this good news or bad news? If we compare developed societies globally, our medical system does a whole lot of things very well indeed. But we spend a great deal more than any other country for health care and objectively achieve poorer outcomes. Thus, we are neither efficient nor effective. We keep a lot of workers very busy doing stuff, and they are generally well paid. As a worker, that’s good news; as a manager who values efficiency, it’s bad news indeed.

Is this good news or bad news? We’re the leader at finding money to pay people to do “health care work.” More Americans work in health care than any other field. In 2019, the United States employed some 21,000,000 people doing “health care and social assistance.” Among others, these occupations include physicians, dentists, dental hygienists and assistants, pharmacists, registered nurses, LVNs/LPNs, nursing aides, technologists and technicians, home health aides, respiratory therapists, occupational and speech therapists, social workers, childcare workers, and personal and home care aides. For a patient, parent, grandparent, and great-grandparent, it is good news to have all those folks available to take care of us when we need it.

So, while I have cringed at the frequent exposés from Roy Poses of what seem to me to be massive societal betrayals by American health care industry giants, it doesn’t have to be that way. Might it still be possible to do well while doing good?
 

A jobs program

Consider such common medical procedures as coronary artery stents or bypass grafts for stable angina (when optimal medical therapy is as good, or better than, and much less expensive); PSAs on asymptomatic men followed by unnecessary surgery for localized cancer; excess surgery for low back pain; and the jobs created by managing the people caught up in medical complications of the obesity epidemic.

Don’t forget the number of people employed simply to “follow the money” within our byzantine cockamamie medical billing system. In 2009, this prompted me to describe the bloated system as a “health care bubble” not unlike Enron, the submarket real estate financing debacle, or the dot-com boom and bust. I warned of the downside of bursting that bubble, particularly lost jobs.

The Affordable Care Act (ACA) provided health insurance to some 35 million Americans who had been uninsured. It retarded health care inflation. But it did nothing to trim administrative costs or very high pay for nonclinical executives, or shareholder profits in those companies that were for-profit, or drug and device prices. Without the support of all those groups, the ACA would never have passed Congress. The ACA has clearly been a mixed blessing.

If any large American constituency were ever serious about reducing the percentage of our GDP expended on health care, we have excellent ways to do that while improving the health and well-being of the American people. But remember, one person’s liability (unnecessary work) is another person’s asset (needed job).
 

The MBAization of medicine

Meanwhile, back at Dean Hubbard’s voracious academic medical center, the high intellect and driven nature of those who are attracted to medicine as a career has had other effects. The resulting organizations reflect not only the glorious calling of caring for the sick and the availability of lots of money to recruit and compensate leaders, but also the necessity to develop strong executive types who won’t be “eaten alive” by the high-powered workforce of demanding physicians and the surrounding environment.

Thus, it came as no great surprise that in its 2021 determination of America’s top 25 Best Large Employers, Forbes included five health care organizations and seven universities. Beating out such giants as NASA, Cisco, Microsoft, Netflix, and Google, the University of Alabama Birmingham Hospital was ranked first. Mayo Clinic and Yale University came in third and fifth, respectively, and at the other end of the list were Duke (23), MIT (24), and MD Anderson (25).

My goodness! Well done.

Yet, as a country attempting to be balanced, Warren Buffett’s descriptive entreaty on the 2021 failure of Haven, the Amazon-Chase-Berkshire Hathaway joint initiative, remains troubling. Calling upon Haven to change the U.S. health care system, Buffet said, “We learned a lot about the difficulty of changing around an industry that’s 17% of the GDP. We were fighting a tapeworm in the American economy, and the tapeworm won.” They had failed to tame the American health care cost beast.

I am on record as despising the “MBAization” of American medicine. Unfairly, I blamed a professional and technical discipline for what I considered misuse. I hereby repent and renounce my earlier condemnations.
 

Take it all over?

Here’s an idea: If you can’t beat them, join them.

Medical care is important, especially for acute illnesses and injuries, early cancer therapy, and many chronic conditions. But the real determinants of health writ large are social: wealth, education, housing, nutritious food, childcare, climate, clean air and water, meaningful employment, safety from violence, exercise schemes, vaccinations, and so on.

Why doesn’t the American medical-industrial complex simply bestow the label of “health care” on all health-related social determinants? Take it all over. Good “health care” jobs for everyone. Medical professionals will still be blamed for the low health quality and poor outcome scores, the main social determinants of health over which we have no control or influence.

Let that tapeworm grow to encompass all social determinants of health, and measure results by length and quality of life, national human happiness, and, of course, jobs. We can do it. Let that bubble glow. Party time.

And that’s the way it is. That’s my opinion.

George Lundberg, MD, is editor-in-chief at Cancer Commons, president of the Lundberg Institute, executive advisor at Cureus, and a clinical professor of pathology at Northwestern University. Previously, he served as editor-in-chief of JAMA (including 10 specialty journals), American Medical News, and Medscape.

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

In my most recent column, “ ‘They All Laughed When I Spoke of Greedy Doctors,’ ” I attempted to provide a global understanding of some of the economic forces that have made American medicine what it is, how that happened, and why it is still happening.

I did not propose a fix. I have been proposing fixes for more than 30 years, on the pages of JAMA until 1999 and then for this news organization, most recently in 2019 with “Healthcare for All in a Land of Special Interests.”

Where you stand depends a lot on where you sit.

Is this good news or bad news? When William Hubbard was the dean of the University of Michigan School of Medicine in 1969, he said that “an academic medical center is the most efficient energy and resource trapping device that has ever been created” (personal communication, 1969).

To me as a faculty member of an academic medical center for many years, that was great news. We could grow faculty, erect buildings, take the best care of sick people, churn out research papers, mint new physicians and specialists, and get paid well in the process for doing “the Lord’s work.” What’s not to like? At that time, the proportion of the country’s gross national product expended for medical and health care was about 7%. And the predicted life span of an American at birth was 70.5 years.

Is this good news or bad news? In 2021, the proportion of our annual gross domestic product (GDP) consumed by health care was 18.3%, totaling $4.3 trillion, or $12,914 per person. For perspective, in 2021, the median income per capita was $37,638. Because quite a few Americans have very high incomes, the mean income per capita is much higher: $63,444. Predicted life span in 2021 was 76.4 years.

Thus, in a span of 53 years (1969-2022), only 5.9 years of life were gained per person born, for how many trillions of dollars expended? To me as a tax-paying citizen and payer of medical insurance premiums, that is bad news.

Is this good news or bad news? If we compare developed societies globally, our medical system does a whole lot of things very well indeed. But we spend a great deal more than any other country for health care and objectively achieve poorer outcomes. Thus, we are neither efficient nor effective. We keep a lot of workers very busy doing stuff, and they are generally well paid. As a worker, that’s good news; as a manager who values efficiency, it’s bad news indeed.

Is this good news or bad news? We’re the leader at finding money to pay people to do “health care work.” More Americans work in health care than any other field. In 2019, the United States employed some 21,000,000 people doing “health care and social assistance.” Among others, these occupations include physicians, dentists, dental hygienists and assistants, pharmacists, registered nurses, LVNs/LPNs, nursing aides, technologists and technicians, home health aides, respiratory therapists, occupational and speech therapists, social workers, childcare workers, and personal and home care aides. For a patient, parent, grandparent, and great-grandparent, it is good news to have all those folks available to take care of us when we need it.

So, while I have cringed at the frequent exposés from Roy Poses of what seem to me to be massive societal betrayals by American health care industry giants, it doesn’t have to be that way. Might it still be possible to do well while doing good?
 

A jobs program

Consider such common medical procedures as coronary artery stents or bypass grafts for stable angina (when optimal medical therapy is as good, or better than, and much less expensive); PSAs on asymptomatic men followed by unnecessary surgery for localized cancer; excess surgery for low back pain; and the jobs created by managing the people caught up in medical complications of the obesity epidemic.

Don’t forget the number of people employed simply to “follow the money” within our byzantine cockamamie medical billing system. In 2009, this prompted me to describe the bloated system as a “health care bubble” not unlike Enron, the submarket real estate financing debacle, or the dot-com boom and bust. I warned of the downside of bursting that bubble, particularly lost jobs.

The Affordable Care Act (ACA) provided health insurance to some 35 million Americans who had been uninsured. It retarded health care inflation. But it did nothing to trim administrative costs or very high pay for nonclinical executives, or shareholder profits in those companies that were for-profit, or drug and device prices. Without the support of all those groups, the ACA would never have passed Congress. The ACA has clearly been a mixed blessing.

If any large American constituency were ever serious about reducing the percentage of our GDP expended on health care, we have excellent ways to do that while improving the health and well-being of the American people. But remember, one person’s liability (unnecessary work) is another person’s asset (needed job).
 

The MBAization of medicine

Meanwhile, back at Dean Hubbard’s voracious academic medical center, the high intellect and driven nature of those who are attracted to medicine as a career has had other effects. The resulting organizations reflect not only the glorious calling of caring for the sick and the availability of lots of money to recruit and compensate leaders, but also the necessity to develop strong executive types who won’t be “eaten alive” by the high-powered workforce of demanding physicians and the surrounding environment.

Thus, it came as no great surprise that in its 2021 determination of America’s top 25 Best Large Employers, Forbes included five health care organizations and seven universities. Beating out such giants as NASA, Cisco, Microsoft, Netflix, and Google, the University of Alabama Birmingham Hospital was ranked first. Mayo Clinic and Yale University came in third and fifth, respectively, and at the other end of the list were Duke (23), MIT (24), and MD Anderson (25).

My goodness! Well done.

Yet, as a country attempting to be balanced, Warren Buffett’s descriptive entreaty on the 2021 failure of Haven, the Amazon-Chase-Berkshire Hathaway joint initiative, remains troubling. Calling upon Haven to change the U.S. health care system, Buffet said, “We learned a lot about the difficulty of changing around an industry that’s 17% of the GDP. We were fighting a tapeworm in the American economy, and the tapeworm won.” They had failed to tame the American health care cost beast.

I am on record as despising the “MBAization” of American medicine. Unfairly, I blamed a professional and technical discipline for what I considered misuse. I hereby repent and renounce my earlier condemnations.
 

Take it all over?

Here’s an idea: If you can’t beat them, join them.

Medical care is important, especially for acute illnesses and injuries, early cancer therapy, and many chronic conditions. But the real determinants of health writ large are social: wealth, education, housing, nutritious food, childcare, climate, clean air and water, meaningful employment, safety from violence, exercise schemes, vaccinations, and so on.

Why doesn’t the American medical-industrial complex simply bestow the label of “health care” on all health-related social determinants? Take it all over. Good “health care” jobs for everyone. Medical professionals will still be blamed for the low health quality and poor outcome scores, the main social determinants of health over which we have no control or influence.

Let that tapeworm grow to encompass all social determinants of health, and measure results by length and quality of life, national human happiness, and, of course, jobs. We can do it. Let that bubble glow. Party time.

And that’s the way it is. That’s my opinion.

George Lundberg, MD, is editor-in-chief at Cancer Commons, president of the Lundberg Institute, executive advisor at Cureus, and a clinical professor of pathology at Northwestern University. Previously, he served as editor-in-chief of JAMA (including 10 specialty journals), American Medical News, and Medscape.

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

You and me and baby makes 10,003

If you were a virus hunter, looking for your next big virus discovery, where would you go? The wholesale seafood market in Wuhan? A gathering of unmasked anti-vaxxers in the heartland of America? The frozen snot fields of northwest Siberia?

Comstock/Thinkstock

How about babies? Well, it’s too late now, because that’s what Dennis Sandris Nielsen, PhD, of the University of Copenhagen, and his associates did, and they hit the mother lode. Actually, it was more like the infant load, if we’re being honest here.

“We found an exceptional number of unknown viruses in the faeces of these babies,” Dr. Nielsen said in a written statement from the university. (The study was published in Nature Microbiology, so we get the English spelling of feces.)

The investigators mapped the gut “viromes” of 647 healthy Danish 1-year-old children over the course of 5 years and found 10,000 species of viruses distributed across 248 different viral families, of which only 16 were already known. Incredible stuff, but then things took a turn for the cute. “The researchers named the remaining 232 unknown viral families after the children whose diapers made the study possible. As a result, new viral families include names like Sylvesterviridae, Rigmorviridae and Tristanviridae,” the university said.

About 90% of the viruses found in the feces are bacterial viruses, aka bacteriophages, which have bacteria as their hosts and don’t attack the children’s cells, so they don’t cause disease. The other 10%, however, are eukaryotic: They use human cells as hosts, so they can be either friend or foe. “It is thought-provoking that all children run around with 10-20 of these virus types that infect human cells. So, there is a constant viral infection taking place, which apparently doesn’t make them sick,” Dr. Nielsen said.

Doesn’t make them sick? Riiiight. The thought that this gives rise to now? People love babies. Everyone wants to pick up the baby. Now we know why. Because the viruses want us to! Well, those cute little faces aren’t fooling us anymore. No more babies for us. Everyone should stay away from babies and their evil little eukaryotic viruses. STOP THE BABIES!

[Editor’s note: After a short timeout, we explained to the staff that the human species actually needs babies for its survival. They calmed down, picked up their crayons, and quietly went back to work.]

Fooled them. _{Stop the babies!}

At least someone out there appreciates hospital food

Life in Alaska is not for the meek. It’s dark half the year. Summer is 3 weeks in July. And somehow, there’s a moose in line ahead of you at the doctor’s office. To make matters worse, it’s arguing about insurance. “What do you mean, you’ve heard the Moo Cross Moo Shield joke before?”

Jean Beaufort/PublicDomainPictures.net

One might expect that Providence Alaska Health Park, located near downtown Anchorage, the largest city in Alaska by a massive margin, might be safe from ungulate invasion. Nope. In recent days, a young moose has taken to hanging around Providence campus, and it just could not find anything to eat. Remember, it may be early April, but this is Alaska. It’s still winter there. The ground’s still covered in snow.

Eventually, the gears in our young moose friend’s mind turned and it settled on a course of action: “Hey, those are some nice-looking plants behind that door over there. …” And that’s how Providence Alaska Health ended up with a moose munching on decorative potted plants in the hospital lobby.

Funnily enough, the moose didn’t even make a big scene. It just walked through the automatic doors and started chowing down. Security only found out because a tenant called them. Naturally though, once security made the announcement that a massive wild animal had been spotted in the building, the lobby was evacuated. … What do you mean, half the hospital came around to see it? Apparently, even though Alaskans have to fight moose herds on their daily commute, a lot of people wanted to see our moose friend do its thing.

“That’s crazy,” a woman in scrubs said in a video as she snapped a photo with her phone.

“This is the best. Like, what’s the code for this?” asked another bystander.

Despite security’s best efforts to shoo the moose out with barricades and offers of tasty branches, our furry friend left of its own volition, presumably irritated that his breakfast had become a spectator sport. But it didn’t go far. It hung around the front drive for a while, then went around the back of the building for a nap. What has four hooves and still doesn’t give a crap? Bob Moose-o! How you doing?
 

That click sounded stressed

How can people tell that you’re stressed? Maybe you get irritable and a little snappy. Some people have an inability to concentrate or focus. Eating that muffin when you weren’t really hungry could be a sign you’re not relaxed.

Georgijevic/E+/Getty Images

Did you know that your computer can be an indicator of your stress levels?

We tend to be working when we’re using computers, right? That can be a stressor in itself. Well, some researchers at ETH Zürich decided to have a look at the situation. Surprisingly, at least to us, one in three Swiss employees experience workplace stress, which makes us wonder what the percentage is in this country.

The Swiss researchers developed a model that tells how stressed someone is just by the way they use their computer mouse or type. The results of their study showed that those who were stressed clicked and tapped differently than participants who were more relaxed.

Stressed people click “more often and less precisely and cover longer distances on the screen,” while the relaxed take “shorter, more direct routes to reach their destination and take more time doing so,” study author Mara Nägelin explained in a written statement from ETH (Eidgenössische Technische Hochschule, or Swiss Federal Institute of Technology) Zürich.

Ever find when you’re frustrated and in a rush you end up making more mistakes? Same deal. Coauthor Jasmine Kerr noted that “increased levels of stress negatively impact our brain’s ability to process information.” Which totally is going to affect how we move.

Hopefully, these results can give insight to companies on how stressed their employees are and the effect it has on their work performance, eventually leading to, guess what, more research on how to alleviate workplace stress in general, which can benefit us all.

So if you find yourself in the office working on your computer like it’s a game of Perfection and time is running out, take a beat. Maybe try a stress-relieving breathing technique. Nonstressed people, according to the study, take fewer and longer pauses on their computers. Perfection on the job may mean relaxing first.

You and me and baby makes 10,003

If you were a virus hunter, looking for your next big virus discovery, where would you go? The wholesale seafood market in Wuhan? A gathering of unmasked anti-vaxxers in the heartland of America? The frozen snot fields of northwest Siberia?

Comstock/Thinkstock

How about babies? Well, it’s too late now, because that’s what Dennis Sandris Nielsen, PhD, of the University of Copenhagen, and his associates did, and they hit the mother lode. Actually, it was more like the infant load, if we’re being honest here.

“We found an exceptional number of unknown viruses in the faeces of these babies,” Dr. Nielsen said in a written statement from the university. (The study was published in Nature Microbiology, so we get the English spelling of feces.)

The investigators mapped the gut “viromes” of 647 healthy Danish 1-year-old children over the course of 5 years and found 10,000 species of viruses distributed across 248 different viral families, of which only 16 were already known. Incredible stuff, but then things took a turn for the cute. “The researchers named the remaining 232 unknown viral families after the children whose diapers made the study possible. As a result, new viral families include names like Sylvesterviridae, Rigmorviridae and Tristanviridae,” the university said.

About 90% of the viruses found in the feces are bacterial viruses, aka bacteriophages, which have bacteria as their hosts and don’t attack the children’s cells, so they don’t cause disease. The other 10%, however, are eukaryotic: They use human cells as hosts, so they can be either friend or foe. “It is thought-provoking that all children run around with 10-20 of these virus types that infect human cells. So, there is a constant viral infection taking place, which apparently doesn’t make them sick,” Dr. Nielsen said.

Doesn’t make them sick? Riiiight. The thought that this gives rise to now? People love babies. Everyone wants to pick up the baby. Now we know why. Because the viruses want us to! Well, those cute little faces aren’t fooling us anymore. No more babies for us. Everyone should stay away from babies and their evil little eukaryotic viruses. STOP THE BABIES!

[Editor’s note: After a short timeout, we explained to the staff that the human species actually needs babies for its survival. They calmed down, picked up their crayons, and quietly went back to work.]

Fooled them. _{Stop the babies!}

At least someone out there appreciates hospital food

Life in Alaska is not for the meek. It’s dark half the year. Summer is 3 weeks in July. And somehow, there’s a moose in line ahead of you at the doctor’s office. To make matters worse, it’s arguing about insurance. “What do you mean, you’ve heard the Moo Cross Moo Shield joke before?”

Jean Beaufort/PublicDomainPictures.net

One might expect that Providence Alaska Health Park, located near downtown Anchorage, the largest city in Alaska by a massive margin, might be safe from ungulate invasion. Nope. In recent days, a young moose has taken to hanging around Providence campus, and it just could not find anything to eat. Remember, it may be early April, but this is Alaska. It’s still winter there. The ground’s still covered in snow.

Eventually, the gears in our young moose friend’s mind turned and it settled on a course of action: “Hey, those are some nice-looking plants behind that door over there. …” And that’s how Providence Alaska Health ended up with a moose munching on decorative potted plants in the hospital lobby.

Funnily enough, the moose didn’t even make a big scene. It just walked through the automatic doors and started chowing down. Security only found out because a tenant called them. Naturally though, once security made the announcement that a massive wild animal had been spotted in the building, the lobby was evacuated. … What do you mean, half the hospital came around to see it? Apparently, even though Alaskans have to fight moose herds on their daily commute, a lot of people wanted to see our moose friend do its thing.

“That’s crazy,” a woman in scrubs said in a video as she snapped a photo with her phone.

“This is the best. Like, what’s the code for this?” asked another bystander.

Despite security’s best efforts to shoo the moose out with barricades and offers of tasty branches, our furry friend left of its own volition, presumably irritated that his breakfast had become a spectator sport. But it didn’t go far. It hung around the front drive for a while, then went around the back of the building for a nap. What has four hooves and still doesn’t give a crap? Bob Moose-o! How you doing?
 

That click sounded stressed

How can people tell that you’re stressed? Maybe you get irritable and a little snappy. Some people have an inability to concentrate or focus. Eating that muffin when you weren’t really hungry could be a sign you’re not relaxed.

Georgijevic/E+/Getty Images

Did you know that your computer can be an indicator of your stress levels?

We tend to be working when we’re using computers, right? That can be a stressor in itself. Well, some researchers at ETH Zürich decided to have a look at the situation. Surprisingly, at least to us, one in three Swiss employees experience workplace stress, which makes us wonder what the percentage is in this country.

The Swiss researchers developed a model that tells how stressed someone is just by the way they use their computer mouse or type. The results of their study showed that those who were stressed clicked and tapped differently than participants who were more relaxed.

Stressed people click “more often and less precisely and cover longer distances on the screen,” while the relaxed take “shorter, more direct routes to reach their destination and take more time doing so,” study author Mara Nägelin explained in a written statement from ETH (Eidgenössische Technische Hochschule, or Swiss Federal Institute of Technology) Zürich.

Ever find when you’re frustrated and in a rush you end up making more mistakes? Same deal. Coauthor Jasmine Kerr noted that “increased levels of stress negatively impact our brain’s ability to process information.” Which totally is going to affect how we move.

Hopefully, these results can give insight to companies on how stressed their employees are and the effect it has on their work performance, eventually leading to, guess what, more research on how to alleviate workplace stress in general, which can benefit us all.

So if you find yourself in the office working on your computer like it’s a game of Perfection and time is running out, take a beat. Maybe try a stress-relieving breathing technique. Nonstressed people, according to the study, take fewer and longer pauses on their computers. Perfection on the job may mean relaxing first.

You and me and baby makes 10,003

If you were a virus hunter, looking for your next big virus discovery, where would you go? The wholesale seafood market in Wuhan? A gathering of unmasked anti-vaxxers in the heartland of America? The frozen snot fields of northwest Siberia?

Comstock/Thinkstock

How about babies? Well, it’s too late now, because that’s what Dennis Sandris Nielsen, PhD, of the University of Copenhagen, and his associates did, and they hit the mother lode. Actually, it was more like the infant load, if we’re being honest here.

“We found an exceptional number of unknown viruses in the faeces of these babies,” Dr. Nielsen said in a written statement from the university. (The study was published in Nature Microbiology, so we get the English spelling of feces.)

The investigators mapped the gut “viromes” of 647 healthy Danish 1-year-old children over the course of 5 years and found 10,000 species of viruses distributed across 248 different viral families, of which only 16 were already known. Incredible stuff, but then things took a turn for the cute. “The researchers named the remaining 232 unknown viral families after the children whose diapers made the study possible. As a result, new viral families include names like Sylvesterviridae, Rigmorviridae and Tristanviridae,” the university said.

About 90% of the viruses found in the feces are bacterial viruses, aka bacteriophages, which have bacteria as their hosts and don’t attack the children’s cells, so they don’t cause disease. The other 10%, however, are eukaryotic: They use human cells as hosts, so they can be either friend or foe. “It is thought-provoking that all children run around with 10-20 of these virus types that infect human cells. So, there is a constant viral infection taking place, which apparently doesn’t make them sick,” Dr. Nielsen said.

Doesn’t make them sick? Riiiight. The thought that this gives rise to now? People love babies. Everyone wants to pick up the baby. Now we know why. Because the viruses want us to! Well, those cute little faces aren’t fooling us anymore. No more babies for us. Everyone should stay away from babies and their evil little eukaryotic viruses. STOP THE BABIES!

[Editor’s note: After a short timeout, we explained to the staff that the human species actually needs babies for its survival. They calmed down, picked up their crayons, and quietly went back to work.]

Fooled them. _{Stop the babies!}

At least someone out there appreciates hospital food

Life in Alaska is not for the meek. It’s dark half the year. Summer is 3 weeks in July. And somehow, there’s a moose in line ahead of you at the doctor’s office. To make matters worse, it’s arguing about insurance. “What do you mean, you’ve heard the Moo Cross Moo Shield joke before?”

Jean Beaufort/PublicDomainPictures.net

One might expect that Providence Alaska Health Park, located near downtown Anchorage, the largest city in Alaska by a massive margin, might be safe from ungulate invasion. Nope. In recent days, a young moose has taken to hanging around Providence campus, and it just could not find anything to eat. Remember, it may be early April, but this is Alaska. It’s still winter there. The ground’s still covered in snow.

Eventually, the gears in our young moose friend’s mind turned and it settled on a course of action: “Hey, those are some nice-looking plants behind that door over there. …” And that’s how Providence Alaska Health ended up with a moose munching on decorative potted plants in the hospital lobby.

Funnily enough, the moose didn’t even make a big scene. It just walked through the automatic doors and started chowing down. Security only found out because a tenant called them. Naturally though, once security made the announcement that a massive wild animal had been spotted in the building, the lobby was evacuated. … What do you mean, half the hospital came around to see it? Apparently, even though Alaskans have to fight moose herds on their daily commute, a lot of people wanted to see our moose friend do its thing.

“That’s crazy,” a woman in scrubs said in a video as she snapped a photo with her phone.

“This is the best. Like, what’s the code for this?” asked another bystander.

Despite security’s best efforts to shoo the moose out with barricades and offers of tasty branches, our furry friend left of its own volition, presumably irritated that his breakfast had become a spectator sport. But it didn’t go far. It hung around the front drive for a while, then went around the back of the building for a nap. What has four hooves and still doesn’t give a crap? Bob Moose-o! How you doing?
 

That click sounded stressed

How can people tell that you’re stressed? Maybe you get irritable and a little snappy. Some people have an inability to concentrate or focus. Eating that muffin when you weren’t really hungry could be a sign you’re not relaxed.

Georgijevic/E+/Getty Images

Did you know that your computer can be an indicator of your stress levels?

We tend to be working when we’re using computers, right? That can be a stressor in itself. Well, some researchers at ETH Zürich decided to have a look at the situation. Surprisingly, at least to us, one in three Swiss employees experience workplace stress, which makes us wonder what the percentage is in this country.

The Swiss researchers developed a model that tells how stressed someone is just by the way they use their computer mouse or type. The results of their study showed that those who were stressed clicked and tapped differently than participants who were more relaxed.

Stressed people click “more often and less precisely and cover longer distances on the screen,” while the relaxed take “shorter, more direct routes to reach their destination and take more time doing so,” study author Mara Nägelin explained in a written statement from ETH (Eidgenössische Technische Hochschule, or Swiss Federal Institute of Technology) Zürich.

Ever find when you’re frustrated and in a rush you end up making more mistakes? Same deal. Coauthor Jasmine Kerr noted that “increased levels of stress negatively impact our brain’s ability to process information.” Which totally is going to affect how we move.

Hopefully, these results can give insight to companies on how stressed their employees are and the effect it has on their work performance, eventually leading to, guess what, more research on how to alleviate workplace stress in general, which can benefit us all.

So if you find yourself in the office working on your computer like it’s a game of Perfection and time is running out, take a beat. Maybe try a stress-relieving breathing technique. Nonstressed people, according to the study, take fewer and longer pauses on their computers. Perfection on the job may mean relaxing first.

Older adults in cities are at lower risk of serious psychological distress – and potentially of later cognitive impairment and dementia – when they live close to so-called green and blue spaces, which can include public parks, community gardens, cemeteries, and bodies of water.

The findings of the study, which was released ahead of its scheduled presentation at the annual meeting of the American Academy of Neurology, build on a growing understanding of the relationship between types and qualities of urban environments and dementia risk.

Adithya Vegaraju, a student at Washington State University, Spokane, led the study, which looked at data from the Washington State Behavioral Risk Factor Surveillance System to assess prevalence of serious psychological distress among 42,980 Washington state residents aged 65 and over.

The data, collected between 2011 and 2019, used a self-reported questionnaire to determine serious psychological distress, which is defined as a level of mental distress considered debilitating enough to warrant treatment.

Mr. Vegaraju and his coauthor Solmaz Amiri, DDes, also of Washington State University, used ZIP codes, along with U.S. census data, to approximate the urban adults’ proximity to green and blue spaces.

After controlling for potential confounders of age, sex, ethnicity, education, and marital status, the investigators found that people living within half a mile of green or blue spaces had a 17% lower risk of experiencing serious psychological distress, compared with people living farther from these spaces, the investigators said in a news release.
 

Implications for cognitive decline and dementia?

Psychological distress in adults has been linked in population-based longitudinal studies to later cognitive decline and dementia. One study in older adults found the risk of dementia to be more than 50% higher among adults aged 50-70 with persistent depression. Blue and green spaces have also been investigated in relation to neurodegenerative disease among older adults; a 2022 study looking at data from some 62 million Medicare beneficiaries found those living in areas with more vegetation saw lower risk of hospitalizations for Alzheimer’s disease and related dementias.

“Since we lack effective prevention methods or treatments for mild cognitive impairment and dementia, we need to get creative in how we look at these issues,” Dr. Amiri commented in a press statement about her and Mr. Vegaraju’s findings. “Our hope is that this study showing better mental health among people living close to parks and water will trigger other studies about how these benefits work and whether this proximity can help prevent or delay mild cognitive impairment and dementia.”

The investigators acknowledged that their findings were limited by reliance on a self-reported measure of psychological distress.
 

A bidirectional connection with depression and dementia

In a comment, Anjum Hajat, PhD, an epidemiologist at University of Washington School of Public Health in Seattle who has also studied the relationship between green space and dementia risk in older adults, noted some further apparent limitations of the new study, for which only an abstract was available at publication.

“It has been shown that people with depression are at higher risk for dementia, but the opposite is also true,” Dr. Hajat commented. “Those with dementia are more likely to develop depression. This bidirectionality makes this study abstract difficult to interpret since the study is based on cross-sectional data: Individuals are not followed over time to see which develops first, dementia or depression.”

Additionally, Dr. Hajat noted, the data used to determine proximity to green and blue spaces did not allow for the calculation of precise distances between subjects’ homes and these spaces.

Mr. Vegaraju and Dr. Amiri’s study had no outside support, and the investigators declared no conflicts of interest. Dr. Hajat declared no conflicts of interest.

Older adults in cities are at lower risk of serious psychological distress – and potentially of later cognitive impairment and dementia – when they live close to so-called green and blue spaces, which can include public parks, community gardens, cemeteries, and bodies of water.

The findings of the study, which was released ahead of its scheduled presentation at the annual meeting of the American Academy of Neurology, build on a growing understanding of the relationship between types and qualities of urban environments and dementia risk.

Adithya Vegaraju, a student at Washington State University, Spokane, led the study, which looked at data from the Washington State Behavioral Risk Factor Surveillance System to assess prevalence of serious psychological distress among 42,980 Washington state residents aged 65 and over.

The data, collected between 2011 and 2019, used a self-reported questionnaire to determine serious psychological distress, which is defined as a level of mental distress considered debilitating enough to warrant treatment.

Mr. Vegaraju and his coauthor Solmaz Amiri, DDes, also of Washington State University, used ZIP codes, along with U.S. census data, to approximate the urban adults’ proximity to green and blue spaces.

After controlling for potential confounders of age, sex, ethnicity, education, and marital status, the investigators found that people living within half a mile of green or blue spaces had a 17% lower risk of experiencing serious psychological distress, compared with people living farther from these spaces, the investigators said in a news release.
 

Implications for cognitive decline and dementia?

Psychological distress in adults has been linked in population-based longitudinal studies to later cognitive decline and dementia. One study in older adults found the risk of dementia to be more than 50% higher among adults aged 50-70 with persistent depression. Blue and green spaces have also been investigated in relation to neurodegenerative disease among older adults; a 2022 study looking at data from some 62 million Medicare beneficiaries found those living in areas with more vegetation saw lower risk of hospitalizations for Alzheimer’s disease and related dementias.

“Since we lack effective prevention methods or treatments for mild cognitive impairment and dementia, we need to get creative in how we look at these issues,” Dr. Amiri commented in a press statement about her and Mr. Vegaraju’s findings. “Our hope is that this study showing better mental health among people living close to parks and water will trigger other studies about how these benefits work and whether this proximity can help prevent or delay mild cognitive impairment and dementia.”

The investigators acknowledged that their findings were limited by reliance on a self-reported measure of psychological distress.
 

A bidirectional connection with depression and dementia

In a comment, Anjum Hajat, PhD, an epidemiologist at University of Washington School of Public Health in Seattle who has also studied the relationship between green space and dementia risk in older adults, noted some further apparent limitations of the new study, for which only an abstract was available at publication.

“It has been shown that people with depression are at higher risk for dementia, but the opposite is also true,” Dr. Hajat commented. “Those with dementia are more likely to develop depression. This bidirectionality makes this study abstract difficult to interpret since the study is based on cross-sectional data: Individuals are not followed over time to see which develops first, dementia or depression.”

Additionally, Dr. Hajat noted, the data used to determine proximity to green and blue spaces did not allow for the calculation of precise distances between subjects’ homes and these spaces.

Mr. Vegaraju and Dr. Amiri’s study had no outside support, and the investigators declared no conflicts of interest. Dr. Hajat declared no conflicts of interest.

Older adults in cities are at lower risk of serious psychological distress – and potentially of later cognitive impairment and dementia – when they live close to so-called green and blue spaces, which can include public parks, community gardens, cemeteries, and bodies of water.

The findings of the study, which was released ahead of its scheduled presentation at the annual meeting of the American Academy of Neurology, build on a growing understanding of the relationship between types and qualities of urban environments and dementia risk.

Adithya Vegaraju, a student at Washington State University, Spokane, led the study, which looked at data from the Washington State Behavioral Risk Factor Surveillance System to assess prevalence of serious psychological distress among 42,980 Washington state residents aged 65 and over.

The data, collected between 2011 and 2019, used a self-reported questionnaire to determine serious psychological distress, which is defined as a level of mental distress considered debilitating enough to warrant treatment.

Mr. Vegaraju and his coauthor Solmaz Amiri, DDes, also of Washington State University, used ZIP codes, along with U.S. census data, to approximate the urban adults’ proximity to green and blue spaces.

After controlling for potential confounders of age, sex, ethnicity, education, and marital status, the investigators found that people living within half a mile of green or blue spaces had a 17% lower risk of experiencing serious psychological distress, compared with people living farther from these spaces, the investigators said in a news release.
 

Implications for cognitive decline and dementia?

Psychological distress in adults has been linked in population-based longitudinal studies to later cognitive decline and dementia. One study in older adults found the risk of dementia to be more than 50% higher among adults aged 50-70 with persistent depression. Blue and green spaces have also been investigated in relation to neurodegenerative disease among older adults; a 2022 study looking at data from some 62 million Medicare beneficiaries found those living in areas with more vegetation saw lower risk of hospitalizations for Alzheimer’s disease and related dementias.

“Since we lack effective prevention methods or treatments for mild cognitive impairment and dementia, we need to get creative in how we look at these issues,” Dr. Amiri commented in a press statement about her and Mr. Vegaraju’s findings. “Our hope is that this study showing better mental health among people living close to parks and water will trigger other studies about how these benefits work and whether this proximity can help prevent or delay mild cognitive impairment and dementia.”

The investigators acknowledged that their findings were limited by reliance on a self-reported measure of psychological distress.
 

A bidirectional connection with depression and dementia

In a comment, Anjum Hajat, PhD, an epidemiologist at University of Washington School of Public Health in Seattle who has also studied the relationship between green space and dementia risk in older adults, noted some further apparent limitations of the new study, for which only an abstract was available at publication.

“It has been shown that people with depression are at higher risk for dementia, but the opposite is also true,” Dr. Hajat commented. “Those with dementia are more likely to develop depression. This bidirectionality makes this study abstract difficult to interpret since the study is based on cross-sectional data: Individuals are not followed over time to see which develops first, dementia or depression.”

Additionally, Dr. Hajat noted, the data used to determine proximity to green and blue spaces did not allow for the calculation of precise distances between subjects’ homes and these spaces.

Mr. Vegaraju and Dr. Amiri’s study had no outside support, and the investigators declared no conflicts of interest. Dr. Hajat declared no conflicts of interest.

The presence of antiphospholipid antibodies is associated with an increased risk for future cardiovascular events, according to a new study.

The findings point to possible new approaches to risk stratification and the potential for new therapeutic targets in heart disease.

“In this study of the general population, we found that two antiphospholipid antibodies were associated with an increased risk of having a serious cardiovascular event over a follow-up of 8 years,” coauthor Jason Knight, MD, University of Michigan, Ann Arbor, said in an interview.

“If confirmed in further studies, these findings could be used to identify a subgroup of patients who need more careful monitoring and more aggressive risk-factor modification, and if the increased risk linked to these antibodies is high enough, it may also justify preemptive treatments such as the anticoagulants that are routinely used in antiphospholipid syndrome,” Dr. Knight said.

“The long-term vision is that we may identify some people in the general population who would benefit from treating the immune system for the prevention and treatment of cardiovascular disease instead of, or in addition to, using typical cardiovascular medications,” he added.

The study was published online in JAMA Network Open.

Individuals with autoimmune and inflammatory diseases have a greater risk for cardiovascular events than expected based on traditional cardiovascular risk factors, with mechanisms proposed to explain this risk including inflammation-mediated disruption of vascular integrity and activation of platelets and coagulation pathways, the authors explained. However, the role of autoantibodies remains unclear.

They noted that antiphospholipid antibodies can activate endothelial cells, platelets, and neutrophils, and some patients with persistently circulating antiphospholipid antibodies can develop antiphospholipid syndrome – an acquired thromboinflammatory disease characterized by arterial, venous, and microvascular thrombotic events and obstetric complications.

Cross-sectional studies have shown that antiphospholipid antibodies are acutely present in up to 17.4% of patients with stroke or transient ischemic attack, and small cohort studies have suggested that such antibodies may be present in 1%-12% of seemingly healthy individuals. However, the impact of sex, race, and ethnicity on the prevalence of antiphospholipid antibodies and their association with atherosclerotic cardiovascular disease is not known.

The researchers conducted the current study to look at the association between antiphospholipid antibodies and future risk for atherosclerotic cardiovascular events.

They analyzed data from 2,427 participants in the population-based Dallas Heart Study who had no history of atherosclerotic cardiovascular disease or autoimmune diseases requiring immunosuppressive medications at the time of blood sampling at study entry in 2007-2009.

Eight different types of antiphospholipid antibodies were measured, and data on cardiovascular events over the next 8 years was recorded.

Results showed that 14.5% of the cohort tested positive for one of these antiphospholipid antibodies at the start of the study, with approximately one-third of those detected at a moderate or high titer.

The researchers also found that the IgA isotypes of two antiphospholipid antibodies – anticardiolipin and anti-beta-2 glycoprotein – were associated with future atherosclerotic cardiovascular events.

After adjustment for other known risk factors, individuals testing positive for the IgA isotype of anticardiolipin had an almost five times increased risk (hazard ratio, 4.92) of the primary endpoint (myocardial infarction, stroke, coronary revascularization, or cardiovascular death); while those testing positive for anti–beta₂-glycoprotein had an almost three times increased risk (HR, 2.91).

Furthermore, there was what appeared to be a dose effect. People with the highest levels of these antibodies also had the highest risk for cardiovascular events, with up to an almost 10-fold increased risk with the higher level of anticardiolipin. 

Dr. Knight said that more research into the IgA isotypes of these antiphospholipid antibodies is needed.

“Most of the mechanistic work in the antiphospholipid syndrome field has focused on IgG antiphospholipid antibodies. While we commonly find these IgA antibodies in patients with APS, the extent to which they contribute to disease has not been firmly established,” he said. “The fact that IgA was the primary hit in our unbiased screen suggests that there is more to the story and we need to better understand the implications of having these antibodies in circulation, and what specific problems they may be causing.”

Noting that antiphospholipid antibodies can form transiently after certain situations, such as infections, Dr. Knight said that further studies were needed with repeat blood testing to detect the chronic presence of the antibodies.

He added that information of venous thromboses was not available in this study and “perhaps some of the other antibodies might have stood out if we were able to analyze for different outcomes.”

This study was supported by a Pfizer Aspire Award. Dr. Knight reported receiving research funding and consulting fees from Jazz Pharmaceuticals outside the submitted work.

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

The presence of antiphospholipid antibodies is associated with an increased risk for future cardiovascular events, according to a new study.

The findings point to possible new approaches to risk stratification and the potential for new therapeutic targets in heart disease.

“In this study of the general population, we found that two antiphospholipid antibodies were associated with an increased risk of having a serious cardiovascular event over a follow-up of 8 years,” coauthor Jason Knight, MD, University of Michigan, Ann Arbor, said in an interview.

“If confirmed in further studies, these findings could be used to identify a subgroup of patients who need more careful monitoring and more aggressive risk-factor modification, and if the increased risk linked to these antibodies is high enough, it may also justify preemptive treatments such as the anticoagulants that are routinely used in antiphospholipid syndrome,” Dr. Knight said.

“The long-term vision is that we may identify some people in the general population who would benefit from treating the immune system for the prevention and treatment of cardiovascular disease instead of, or in addition to, using typical cardiovascular medications,” he added.

The study was published online in JAMA Network Open.

Individuals with autoimmune and inflammatory diseases have a greater risk for cardiovascular events than expected based on traditional cardiovascular risk factors, with mechanisms proposed to explain this risk including inflammation-mediated disruption of vascular integrity and activation of platelets and coagulation pathways, the authors explained. However, the role of autoantibodies remains unclear.

They noted that antiphospholipid antibodies can activate endothelial cells, platelets, and neutrophils, and some patients with persistently circulating antiphospholipid antibodies can develop antiphospholipid syndrome – an acquired thromboinflammatory disease characterized by arterial, venous, and microvascular thrombotic events and obstetric complications.

Cross-sectional studies have shown that antiphospholipid antibodies are acutely present in up to 17.4% of patients with stroke or transient ischemic attack, and small cohort studies have suggested that such antibodies may be present in 1%-12% of seemingly healthy individuals. However, the impact of sex, race, and ethnicity on the prevalence of antiphospholipid antibodies and their association with atherosclerotic cardiovascular disease is not known.

The researchers conducted the current study to look at the association between antiphospholipid antibodies and future risk for atherosclerotic cardiovascular events.

They analyzed data from 2,427 participants in the population-based Dallas Heart Study who had no history of atherosclerotic cardiovascular disease or autoimmune diseases requiring immunosuppressive medications at the time of blood sampling at study entry in 2007-2009.

Eight different types of antiphospholipid antibodies were measured, and data on cardiovascular events over the next 8 years was recorded.

Results showed that 14.5% of the cohort tested positive for one of these antiphospholipid antibodies at the start of the study, with approximately one-third of those detected at a moderate or high titer.

The researchers also found that the IgA isotypes of two antiphospholipid antibodies – anticardiolipin and anti-beta-2 glycoprotein – were associated with future atherosclerotic cardiovascular events.

After adjustment for other known risk factors, individuals testing positive for the IgA isotype of anticardiolipin had an almost five times increased risk (hazard ratio, 4.92) of the primary endpoint (myocardial infarction, stroke, coronary revascularization, or cardiovascular death); while those testing positive for anti–beta₂-glycoprotein had an almost three times increased risk (HR, 2.91).

Furthermore, there was what appeared to be a dose effect. People with the highest levels of these antibodies also had the highest risk for cardiovascular events, with up to an almost 10-fold increased risk with the higher level of anticardiolipin. 

Dr. Knight said that more research into the IgA isotypes of these antiphospholipid antibodies is needed.

“Most of the mechanistic work in the antiphospholipid syndrome field has focused on IgG antiphospholipid antibodies. While we commonly find these IgA antibodies in patients with APS, the extent to which they contribute to disease has not been firmly established,” he said. “The fact that IgA was the primary hit in our unbiased screen suggests that there is more to the story and we need to better understand the implications of having these antibodies in circulation, and what specific problems they may be causing.”

Noting that antiphospholipid antibodies can form transiently after certain situations, such as infections, Dr. Knight said that further studies were needed with repeat blood testing to detect the chronic presence of the antibodies.

He added that information of venous thromboses was not available in this study and “perhaps some of the other antibodies might have stood out if we were able to analyze for different outcomes.”

This study was supported by a Pfizer Aspire Award. Dr. Knight reported receiving research funding and consulting fees from Jazz Pharmaceuticals outside the submitted work.

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

The presence of antiphospholipid antibodies is associated with an increased risk for future cardiovascular events, according to a new study.

The findings point to possible new approaches to risk stratification and the potential for new therapeutic targets in heart disease.

“In this study of the general population, we found that two antiphospholipid antibodies were associated with an increased risk of having a serious cardiovascular event over a follow-up of 8 years,” coauthor Jason Knight, MD, University of Michigan, Ann Arbor, said in an interview.

“If confirmed in further studies, these findings could be used to identify a subgroup of patients who need more careful monitoring and more aggressive risk-factor modification, and if the increased risk linked to these antibodies is high enough, it may also justify preemptive treatments such as the anticoagulants that are routinely used in antiphospholipid syndrome,” Dr. Knight said.

“The long-term vision is that we may identify some people in the general population who would benefit from treating the immune system for the prevention and treatment of cardiovascular disease instead of, or in addition to, using typical cardiovascular medications,” he added.

The study was published online in JAMA Network Open.

Individuals with autoimmune and inflammatory diseases have a greater risk for cardiovascular events than expected based on traditional cardiovascular risk factors, with mechanisms proposed to explain this risk including inflammation-mediated disruption of vascular integrity and activation of platelets and coagulation pathways, the authors explained. However, the role of autoantibodies remains unclear.

They noted that antiphospholipid antibodies can activate endothelial cells, platelets, and neutrophils, and some patients with persistently circulating antiphospholipid antibodies can develop antiphospholipid syndrome – an acquired thromboinflammatory disease characterized by arterial, venous, and microvascular thrombotic events and obstetric complications.

Cross-sectional studies have shown that antiphospholipid antibodies are acutely present in up to 17.4% of patients with stroke or transient ischemic attack, and small cohort studies have suggested that such antibodies may be present in 1%-12% of seemingly healthy individuals. However, the impact of sex, race, and ethnicity on the prevalence of antiphospholipid antibodies and their association with atherosclerotic cardiovascular disease is not known.

The researchers conducted the current study to look at the association between antiphospholipid antibodies and future risk for atherosclerotic cardiovascular events.

They analyzed data from 2,427 participants in the population-based Dallas Heart Study who had no history of atherosclerotic cardiovascular disease or autoimmune diseases requiring immunosuppressive medications at the time of blood sampling at study entry in 2007-2009.

Eight different types of antiphospholipid antibodies were measured, and data on cardiovascular events over the next 8 years was recorded.

Results showed that 14.5% of the cohort tested positive for one of these antiphospholipid antibodies at the start of the study, with approximately one-third of those detected at a moderate or high titer.

The researchers also found that the IgA isotypes of two antiphospholipid antibodies – anticardiolipin and anti-beta-2 glycoprotein – were associated with future atherosclerotic cardiovascular events.

After adjustment for other known risk factors, individuals testing positive for the IgA isotype of anticardiolipin had an almost five times increased risk (hazard ratio, 4.92) of the primary endpoint (myocardial infarction, stroke, coronary revascularization, or cardiovascular death); while those testing positive for anti–beta₂-glycoprotein had an almost three times increased risk (HR, 2.91).

Furthermore, there was what appeared to be a dose effect. People with the highest levels of these antibodies also had the highest risk for cardiovascular events, with up to an almost 10-fold increased risk with the higher level of anticardiolipin. 

Dr. Knight said that more research into the IgA isotypes of these antiphospholipid antibodies is needed.

“Most of the mechanistic work in the antiphospholipid syndrome field has focused on IgG antiphospholipid antibodies. While we commonly find these IgA antibodies in patients with APS, the extent to which they contribute to disease has not been firmly established,” he said. “The fact that IgA was the primary hit in our unbiased screen suggests that there is more to the story and we need to better understand the implications of having these antibodies in circulation, and what specific problems they may be causing.”

Noting that antiphospholipid antibodies can form transiently after certain situations, such as infections, Dr. Knight said that further studies were needed with repeat blood testing to detect the chronic presence of the antibodies.

He added that information of venous thromboses was not available in this study and “perhaps some of the other antibodies might have stood out if we were able to analyze for different outcomes.”

This study was supported by a Pfizer Aspire Award. Dr. Knight reported receiving research funding and consulting fees from Jazz Pharmaceuticals outside the submitted work.

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

Phototherapy is a safe, effective, noninvasive, and inexpensive way of boosting cognition for patients with dementia, new research suggests. It may be “one of the most promising interventions for improving core symptoms” of the disease.

A new meta-analysis shows that patients with dementia who received phototherapy experienced significant cognitive improvement, compared with those who received usual treatment. However, there were no differences between study groups in terms of improved depression, agitation, or sleep problems.

“Our meta-analysis indicates that phototherapy improved cognitive function in patients with dementia. ... This suggests that phototherapy may be one of the most promising non-pharmacological interventions for improving core symptoms of dementia,” wrote the investigators, led by Xinlian Lu, Peking University, Beijing.

The study was published online in Brain and Behavior.
 

A new treatment option?

“As drug treatment for dementia has limitations such as medical contraindications, limited efficacy, and adverse effects, nonpharmacological therapy has been increasingly regarded as a critical part of comprehensive dementia care,” the investigators noted.

Phototherapy, which utilizes full-spectrum bright light (usually > 600 lux) or wavelength-specific light (for example, blue-enriched or blue-green), is a “promising nonpharmacological therapy” that is noninvasive, inexpensive, and safe.

Most studies of phototherapy have focused on sleep. Findings have shown “high heterogeneity” among the interventions and the populations in the studies, and results have been “inconsistent.” In addition, the effect of phototherapy on cognitive function and behavioral and psychological symptoms of dementia (BPSD) “still need to be clarified.”

In the systematic review and meta-analysis, the investigators examined the effects of phototherapy on cognitive function, BPSD, and sleep in older adults with dementia.

They searched several databases for randomized controlled trials that investigated phototherapy interventions for elderly patients. The primary outcome was cognitive function, which was assessed via the Mini-Mental State Examination (MMSE).

Secondary outcomes included BPSD, including agitation, anxiety, irritability, depression, anxiety, and sleep disturbances, as assessed by the Cornell Scale for Depression in Dementia (CSDD), the Cohen-Mansfield Agitation Inventory (CMAI), the Neuropsychiatric Inventory (NPI), and measures of sleep, including total sleep time (TST), sleep efficiency (SE), and sleep disorders, as assessed by the Sleep Disorder Inventory (SDI).

To be included in the analysis, individual studies had to focus on elderly adults who had some form of dementia. In addition, a group receiving a phototherapy intervention had to be compared with a nonintervention group, and the study had to specify one of the above-defined outcomes.

The review included phototherapy interventions of all forms, frequencies, and durations, including use of bright light, LED light, and blue or blue-green light.
 

Regulating circadian rhythm

Twelve studies met the researchers’ criteria. They included a total of 766 patients with dementia – 426 in the intervention group and 340 in the control group. The mean ages ranged from 73.73 to 85.9 years, and there was a greater number of female than male participants.

Of the studies, seven employed routine daily light in the control group, while the others used either dim light (≤ 50 lux) or devices without light.

The researchers found “significant positive intervention effects” for global cognitive function. Improvements in postintervention MMSE scores differed significantly between the experimental groups and control groups (mean difference, 2.68; 95% confidence interval, 1.38-3.98; I2 = 0%).

No significant differences were found in the effects of intervention on depression symptoms, as evidenced in CSDD scores (MD, −0.70; 95% CI, −3.10 to 1.70; I² = 81%).

Among patients with higher CMAI scores, which indicate more severe agitation behaviors, there was a “trend of decreasing CMAI scores” after phototherapy (MD, −3.12; 95% CI, −8.05 to 1.82; I² = 0%). No significant difference in NPI scores was observed between the two groups.

Similarly, no significant difference was found between the two groups in TST, SE, or SDI scores.

Adverse effects were infrequent and were not severe. Two of the 426 patients in the intervention group experienced mild ocular irritation, and one experienced slight transient redness of the forehead.

Light “may compensate for the reduction in the visual sensory input of patients with dementia and stimulate specific neurons in the suprachiasmatic nucleus of the hypothalamus to regulate circadian rhythm,” the researchers suggested.

“As circadian rhythms are involved in optimal brain function, light supplementation may act on the synchronizing/phase-shifting effects of circadian rhythms to improve cognitive function,” they added.

They note that the light box is the “most commonly used device in phototherapy.” Light boxes provide full-spectrum bright light, usually greater than 2,500 lux. The duration is 30 minutes in the daytime, and treatment lasts 4-8 weeks.

The investigators cautioned that the light box should be placed 60 cm away from the patient or above the patient’s eye level. They said that a ceiling-mounted light is a “good choice” for providing whole-day phototherapy, since such lights do not interfere with the patient’s daily routine, reduce the demand on staff, and contribute to better adherence.

Phototherapy helmets and glasses are also available. These portable devices “allow for better control of light intensity and are ergonomic without interfering with patients’ normal activities.”

The researchers noted that “further well-designed studies are needed to explore the most effective clinical implementation conditions, including device type, duration, frequency, and time.”
 

Easy to use

Mariana Figueiro, PhD, professor and director of the Light and Health Research Center, department of population health medicine, Icahn School of Medicine at Mount Sinai, New York, said light is the “major stimulus for the circadian system, and a robust light-dark pattern daily (which can be given by light therapy during the day) improves sleep and behavior and reduces depression and agitation.”

Dr. Figueiro, who was not involved with the current study, noted that patients with dementia “have sleep issues, which can further affect their cognition; improvement in sleep leads to improvement in cognition,” and this may be an underlying mechanism associated with these results.

The clinical significance of the study “is that this is a nonpharmacological intervention and can be easily applied in the homes or controlled facilities, and it can be used with any other medication,” she pointed out.

“More importantly, sleep medications have negative side effects, so the use of nonpharmacological interventions improving sleep and cognition is great for clinical practice,” she added.

However, she took issue with the finding that phototherapy was not effective for depression and agitation, noting that there were “too few studies to say for sure that light therapy is ineffective at improving these outcomes.”

The research received no external funding. The authors and Dr. Figueiro disclosed no relevant financial relationships.

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

Phototherapy is a safe, effective, noninvasive, and inexpensive way of boosting cognition for patients with dementia, new research suggests. It may be “one of the most promising interventions for improving core symptoms” of the disease.

A new meta-analysis shows that patients with dementia who received phototherapy experienced significant cognitive improvement, compared with those who received usual treatment. However, there were no differences between study groups in terms of improved depression, agitation, or sleep problems.

“Our meta-analysis indicates that phototherapy improved cognitive function in patients with dementia. ... This suggests that phototherapy may be one of the most promising non-pharmacological interventions for improving core symptoms of dementia,” wrote the investigators, led by Xinlian Lu, Peking University, Beijing.

The study was published online in Brain and Behavior.
 

A new treatment option?

“As drug treatment for dementia has limitations such as medical contraindications, limited efficacy, and adverse effects, nonpharmacological therapy has been increasingly regarded as a critical part of comprehensive dementia care,” the investigators noted.

Phototherapy, which utilizes full-spectrum bright light (usually > 600 lux) or wavelength-specific light (for example, blue-enriched or blue-green), is a “promising nonpharmacological therapy” that is noninvasive, inexpensive, and safe.

Most studies of phototherapy have focused on sleep. Findings have shown “high heterogeneity” among the interventions and the populations in the studies, and results have been “inconsistent.” In addition, the effect of phototherapy on cognitive function and behavioral and psychological symptoms of dementia (BPSD) “still need to be clarified.”

In the systematic review and meta-analysis, the investigators examined the effects of phototherapy on cognitive function, BPSD, and sleep in older adults with dementia.

They searched several databases for randomized controlled trials that investigated phototherapy interventions for elderly patients. The primary outcome was cognitive function, which was assessed via the Mini-Mental State Examination (MMSE).

Secondary outcomes included BPSD, including agitation, anxiety, irritability, depression, anxiety, and sleep disturbances, as assessed by the Cornell Scale for Depression in Dementia (CSDD), the Cohen-Mansfield Agitation Inventory (CMAI), the Neuropsychiatric Inventory (NPI), and measures of sleep, including total sleep time (TST), sleep efficiency (SE), and sleep disorders, as assessed by the Sleep Disorder Inventory (SDI).

To be included in the analysis, individual studies had to focus on elderly adults who had some form of dementia. In addition, a group receiving a phototherapy intervention had to be compared with a nonintervention group, and the study had to specify one of the above-defined outcomes.

The review included phototherapy interventions of all forms, frequencies, and durations, including use of bright light, LED light, and blue or blue-green light.
 

Regulating circadian rhythm

Twelve studies met the researchers’ criteria. They included a total of 766 patients with dementia – 426 in the intervention group and 340 in the control group. The mean ages ranged from 73.73 to 85.9 years, and there was a greater number of female than male participants.

Of the studies, seven employed routine daily light in the control group, while the others used either dim light (≤ 50 lux) or devices without light.

The researchers found “significant positive intervention effects” for global cognitive function. Improvements in postintervention MMSE scores differed significantly between the experimental groups and control groups (mean difference, 2.68; 95% confidence interval, 1.38-3.98; I2 = 0%).

No significant differences were found in the effects of intervention on depression symptoms, as evidenced in CSDD scores (MD, −0.70; 95% CI, −3.10 to 1.70; I² = 81%).

Among patients with higher CMAI scores, which indicate more severe agitation behaviors, there was a “trend of decreasing CMAI scores” after phototherapy (MD, −3.12; 95% CI, −8.05 to 1.82; I² = 0%). No significant difference in NPI scores was observed between the two groups.

Similarly, no significant difference was found between the two groups in TST, SE, or SDI scores.

Adverse effects were infrequent and were not severe. Two of the 426 patients in the intervention group experienced mild ocular irritation, and one experienced slight transient redness of the forehead.

Light “may compensate for the reduction in the visual sensory input of patients with dementia and stimulate specific neurons in the suprachiasmatic nucleus of the hypothalamus to regulate circadian rhythm,” the researchers suggested.

“As circadian rhythms are involved in optimal brain function, light supplementation may act on the synchronizing/phase-shifting effects of circadian rhythms to improve cognitive function,” they added.

They note that the light box is the “most commonly used device in phototherapy.” Light boxes provide full-spectrum bright light, usually greater than 2,500 lux. The duration is 30 minutes in the daytime, and treatment lasts 4-8 weeks.

The investigators cautioned that the light box should be placed 60 cm away from the patient or above the patient’s eye level. They said that a ceiling-mounted light is a “good choice” for providing whole-day phototherapy, since such lights do not interfere with the patient’s daily routine, reduce the demand on staff, and contribute to better adherence.

Phototherapy helmets and glasses are also available. These portable devices “allow for better control of light intensity and are ergonomic without interfering with patients’ normal activities.”

The researchers noted that “further well-designed studies are needed to explore the most effective clinical implementation conditions, including device type, duration, frequency, and time.”
 

Easy to use

Mariana Figueiro, PhD, professor and director of the Light and Health Research Center, department of population health medicine, Icahn School of Medicine at Mount Sinai, New York, said light is the “major stimulus for the circadian system, and a robust light-dark pattern daily (which can be given by light therapy during the day) improves sleep and behavior and reduces depression and agitation.”

Dr. Figueiro, who was not involved with the current study, noted that patients with dementia “have sleep issues, which can further affect their cognition; improvement in sleep leads to improvement in cognition,” and this may be an underlying mechanism associated with these results.

The clinical significance of the study “is that this is a nonpharmacological intervention and can be easily applied in the homes or controlled facilities, and it can be used with any other medication,” she pointed out.

“More importantly, sleep medications have negative side effects, so the use of nonpharmacological interventions improving sleep and cognition is great for clinical practice,” she added.

However, she took issue with the finding that phototherapy was not effective for depression and agitation, noting that there were “too few studies to say for sure that light therapy is ineffective at improving these outcomes.”

The research received no external funding. The authors and Dr. Figueiro disclosed no relevant financial relationships.

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

Phototherapy is a safe, effective, noninvasive, and inexpensive way of boosting cognition for patients with dementia, new research suggests. It may be “one of the most promising interventions for improving core symptoms” of the disease.

A new meta-analysis shows that patients with dementia who received phototherapy experienced significant cognitive improvement, compared with those who received usual treatment. However, there were no differences between study groups in terms of improved depression, agitation, or sleep problems.

“Our meta-analysis indicates that phototherapy improved cognitive function in patients with dementia. ... This suggests that phototherapy may be one of the most promising non-pharmacological interventions for improving core symptoms of dementia,” wrote the investigators, led by Xinlian Lu, Peking University, Beijing.

The study was published online in Brain and Behavior.
 

A new treatment option?

“As drug treatment for dementia has limitations such as medical contraindications, limited efficacy, and adverse effects, nonpharmacological therapy has been increasingly regarded as a critical part of comprehensive dementia care,” the investigators noted.

Phototherapy, which utilizes full-spectrum bright light (usually > 600 lux) or wavelength-specific light (for example, blue-enriched or blue-green), is a “promising nonpharmacological therapy” that is noninvasive, inexpensive, and safe.

Most studies of phototherapy have focused on sleep. Findings have shown “high heterogeneity” among the interventions and the populations in the studies, and results have been “inconsistent.” In addition, the effect of phototherapy on cognitive function and behavioral and psychological symptoms of dementia (BPSD) “still need to be clarified.”

In the systematic review and meta-analysis, the investigators examined the effects of phototherapy on cognitive function, BPSD, and sleep in older adults with dementia.

They searched several databases for randomized controlled trials that investigated phototherapy interventions for elderly patients. The primary outcome was cognitive function, which was assessed via the Mini-Mental State Examination (MMSE).

Secondary outcomes included BPSD, including agitation, anxiety, irritability, depression, anxiety, and sleep disturbances, as assessed by the Cornell Scale for Depression in Dementia (CSDD), the Cohen-Mansfield Agitation Inventory (CMAI), the Neuropsychiatric Inventory (NPI), and measures of sleep, including total sleep time (TST), sleep efficiency (SE), and sleep disorders, as assessed by the Sleep Disorder Inventory (SDI).

To be included in the analysis, individual studies had to focus on elderly adults who had some form of dementia. In addition, a group receiving a phototherapy intervention had to be compared with a nonintervention group, and the study had to specify one of the above-defined outcomes.

The review included phototherapy interventions of all forms, frequencies, and durations, including use of bright light, LED light, and blue or blue-green light.
 

Regulating circadian rhythm

Twelve studies met the researchers’ criteria. They included a total of 766 patients with dementia – 426 in the intervention group and 340 in the control group. The mean ages ranged from 73.73 to 85.9 years, and there was a greater number of female than male participants.

Of the studies, seven employed routine daily light in the control group, while the others used either dim light (≤ 50 lux) or devices without light.

The researchers found “significant positive intervention effects” for global cognitive function. Improvements in postintervention MMSE scores differed significantly between the experimental groups and control groups (mean difference, 2.68; 95% confidence interval, 1.38-3.98; I2 = 0%).

No significant differences were found in the effects of intervention on depression symptoms, as evidenced in CSDD scores (MD, −0.70; 95% CI, −3.10 to 1.70; I² = 81%).

Among patients with higher CMAI scores, which indicate more severe agitation behaviors, there was a “trend of decreasing CMAI scores” after phototherapy (MD, −3.12; 95% CI, −8.05 to 1.82; I² = 0%). No significant difference in NPI scores was observed between the two groups.

Similarly, no significant difference was found between the two groups in TST, SE, or SDI scores.

Adverse effects were infrequent and were not severe. Two of the 426 patients in the intervention group experienced mild ocular irritation, and one experienced slight transient redness of the forehead.

Light “may compensate for the reduction in the visual sensory input of patients with dementia and stimulate specific neurons in the suprachiasmatic nucleus of the hypothalamus to regulate circadian rhythm,” the researchers suggested.

“As circadian rhythms are involved in optimal brain function, light supplementation may act on the synchronizing/phase-shifting effects of circadian rhythms to improve cognitive function,” they added.

They note that the light box is the “most commonly used device in phototherapy.” Light boxes provide full-spectrum bright light, usually greater than 2,500 lux. The duration is 30 minutes in the daytime, and treatment lasts 4-8 weeks.

The investigators cautioned that the light box should be placed 60 cm away from the patient or above the patient’s eye level. They said that a ceiling-mounted light is a “good choice” for providing whole-day phototherapy, since such lights do not interfere with the patient’s daily routine, reduce the demand on staff, and contribute to better adherence.

Phototherapy helmets and glasses are also available. These portable devices “allow for better control of light intensity and are ergonomic without interfering with patients’ normal activities.”

The researchers noted that “further well-designed studies are needed to explore the most effective clinical implementation conditions, including device type, duration, frequency, and time.”
 

Easy to use

Mariana Figueiro, PhD, professor and director of the Light and Health Research Center, department of population health medicine, Icahn School of Medicine at Mount Sinai, New York, said light is the “major stimulus for the circadian system, and a robust light-dark pattern daily (which can be given by light therapy during the day) improves sleep and behavior and reduces depression and agitation.”

Dr. Figueiro, who was not involved with the current study, noted that patients with dementia “have sleep issues, which can further affect their cognition; improvement in sleep leads to improvement in cognition,” and this may be an underlying mechanism associated with these results.

The clinical significance of the study “is that this is a nonpharmacological intervention and can be easily applied in the homes or controlled facilities, and it can be used with any other medication,” she pointed out.

“More importantly, sleep medications have negative side effects, so the use of nonpharmacological interventions improving sleep and cognition is great for clinical practice,” she added.

However, she took issue with the finding that phototherapy was not effective for depression and agitation, noting that there were “too few studies to say for sure that light therapy is ineffective at improving these outcomes.”

The research received no external funding. The authors and Dr. Figueiro disclosed no relevant financial relationships.

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

Disordered sleep is associated with a significantly increased risk for stroke, new research shows.

Results of a large international study show stroke risk was more than three times higher in those who slept too little, more than twice as high in those who sleep too much, and two to three times higher in those with symptoms of severe obstructive sleep apnea.

The study also showed that the greater the number of sleep disorder symptoms, the greater the stroke risk. The 11% of study participants with five or more symptoms of disordered sleep had a fivefold increased risk for stroke.

Jupiterimages/Thinkstock

More symptoms, more risk

Previous research shows severe OSA doubles the risk of stroke and increases the chance of recurrent stroke. A 2019 study showed that people with insomnia had a small increased risk of stroke.

“Both snoring and extremes of sleep duration have been previously associated with an increased risk of stroke in observational research, but less is known about other symptoms of sleep impairment, with less consistent findings,” Dr. McCarthy said.

Prior studies have also generally come from a single geographic region, which Dr. McCarthy noted could limit their generalizability.

For this effort, investigators used data from 4,496 participants in INTERSTROKE, an international case-control study of risk factors for a first acute stroke. About half of the participants had a history of stroke.

Using information collected from a survey of sleep habits, researchers found an elevated stroke risk in those who received less than 5 hours of sleep per night (odds ratio, 3.15; 95% confidence interval, 2.09-4.76) or more than 9 hours of sleep per night (OR, 2.67; 95% CI, 1.89-3.78), compared with those who slept 7 hours a night.

Participants who took unplanned naps or naps lasting an hour or more (OR, 2.46; 95% CI, 1.69-3.57) and participants who reported poor quality sleep (OR,1.52; 95% CI, 1.32-1.75) were also at an increased risk for stroke.

Symptoms of OSA were also strongly associated with increased stroke risk, including snoring (OR, 1.91; 95% CI, 1.62-2.24), snorting (OR, 2.64; 95% CI, 2.17-3.20), and breathing cessation (OR, 2.87; 95% CI, 2.28-2.60).

Stroke risk increased as the number of sleep disturbance symptoms rose, with the greatest risk in the 11% of participants who had five or more symptoms (OR, 5.38; 95% CI, 4.03-7.18).

“This study finds an association between a broad range of sleep impairment symptoms and stroke, and a graded association with increasing symptoms, in an international setting,” Dr. McCarthy said.

Researchers aren’t sure what’s driving the higher stroke risk among people with sleep disturbances. Although the study did control for potential confounders, it wasn’t designed to get at what’s driving the association.

“Sleep disturbance may also have a bi-directional relationship with many stroke risk factors; for example, sleep disturbance may be a symptom of disease and exacerbate disease,” Dr. McCarthy said. “Future interventional studies are required to determine the true direction of the relationship.”
 

A marker of stroke risk

Daniel Lackland, DrPH, professor of neurology at the Medical University of South Carolina, Charleston, said the findings provide additional evidence of the link between sleep and stroke risk.

“The results confirm sleep disorders as a potential marker and part of the risk profile,” he said.

Collecting information about sleep using a validated assessment tool is an important piece of clinical care, Dr. Lackland said, especially among patients with other stroke risk factors.

One limitation of the study was that data on sleep was collected only at one point, and participants were not followed over time to see if changes in sleep affected stroke risk.

“This is an important point and should be a focus for future studies, as it is critical in the design of interventions,” Dr. Lackland said.

The INTERSTROKE study is funded by the Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, Canadian Stroke Network, Swedish Research Council, Swedish Heart and Lung Foundation, The Health & Medical Care Committee of the Regional Executive Board, Region Västra Götaland, Astra Zeneca, Boehringer Ingelheim (Canada), Pfizer (Canada), MERCK, Sharp and Dohme, Swedish Heart and Lung Foundation, U.K. Chest, and U.K. Heart and Stroke. Dr. McCarthy and Lackland report no relevant financial relationships.

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

Disordered sleep is associated with a significantly increased risk for stroke, new research shows.

Results of a large international study show stroke risk was more than three times higher in those who slept too little, more than twice as high in those who sleep too much, and two to three times higher in those with symptoms of severe obstructive sleep apnea.

The study also showed that the greater the number of sleep disorder symptoms, the greater the stroke risk. The 11% of study participants with five or more symptoms of disordered sleep had a fivefold increased risk for stroke.

Jupiterimages/Thinkstock

More symptoms, more risk

Previous research shows severe OSA doubles the risk of stroke and increases the chance of recurrent stroke. A 2019 study showed that people with insomnia had a small increased risk of stroke.

“Both snoring and extremes of sleep duration have been previously associated with an increased risk of stroke in observational research, but less is known about other symptoms of sleep impairment, with less consistent findings,” Dr. McCarthy said.

Prior studies have also generally come from a single geographic region, which Dr. McCarthy noted could limit their generalizability.

For this effort, investigators used data from 4,496 participants in INTERSTROKE, an international case-control study of risk factors for a first acute stroke. About half of the participants had a history of stroke.

Using information collected from a survey of sleep habits, researchers found an elevated stroke risk in those who received less than 5 hours of sleep per night (odds ratio, 3.15; 95% confidence interval, 2.09-4.76) or more than 9 hours of sleep per night (OR, 2.67; 95% CI, 1.89-3.78), compared with those who slept 7 hours a night.

Participants who took unplanned naps or naps lasting an hour or more (OR, 2.46; 95% CI, 1.69-3.57) and participants who reported poor quality sleep (OR,1.52; 95% CI, 1.32-1.75) were also at an increased risk for stroke.

Symptoms of OSA were also strongly associated with increased stroke risk, including snoring (OR, 1.91; 95% CI, 1.62-2.24), snorting (OR, 2.64; 95% CI, 2.17-3.20), and breathing cessation (OR, 2.87; 95% CI, 2.28-2.60).

Stroke risk increased as the number of sleep disturbance symptoms rose, with the greatest risk in the 11% of participants who had five or more symptoms (OR, 5.38; 95% CI, 4.03-7.18).

“This study finds an association between a broad range of sleep impairment symptoms and stroke, and a graded association with increasing symptoms, in an international setting,” Dr. McCarthy said.

Researchers aren’t sure what’s driving the higher stroke risk among people with sleep disturbances. Although the study did control for potential confounders, it wasn’t designed to get at what’s driving the association.

“Sleep disturbance may also have a bi-directional relationship with many stroke risk factors; for example, sleep disturbance may be a symptom of disease and exacerbate disease,” Dr. McCarthy said. “Future interventional studies are required to determine the true direction of the relationship.”
 

A marker of stroke risk

Daniel Lackland, DrPH, professor of neurology at the Medical University of South Carolina, Charleston, said the findings provide additional evidence of the link between sleep and stroke risk.

“The results confirm sleep disorders as a potential marker and part of the risk profile,” he said.

Collecting information about sleep using a validated assessment tool is an important piece of clinical care, Dr. Lackland said, especially among patients with other stroke risk factors.

One limitation of the study was that data on sleep was collected only at one point, and participants were not followed over time to see if changes in sleep affected stroke risk.

“This is an important point and should be a focus for future studies, as it is critical in the design of interventions,” Dr. Lackland said.

The INTERSTROKE study is funded by the Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, Canadian Stroke Network, Swedish Research Council, Swedish Heart and Lung Foundation, The Health & Medical Care Committee of the Regional Executive Board, Region Västra Götaland, Astra Zeneca, Boehringer Ingelheim (Canada), Pfizer (Canada), MERCK, Sharp and Dohme, Swedish Heart and Lung Foundation, U.K. Chest, and U.K. Heart and Stroke. Dr. McCarthy and Lackland report no relevant financial relationships.

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

Disordered sleep is associated with a significantly increased risk for stroke, new research shows.

Results of a large international study show stroke risk was more than three times higher in those who slept too little, more than twice as high in those who sleep too much, and two to three times higher in those with symptoms of severe obstructive sleep apnea.

The study also showed that the greater the number of sleep disorder symptoms, the greater the stroke risk. The 11% of study participants with five or more symptoms of disordered sleep had a fivefold increased risk for stroke.

Jupiterimages/Thinkstock

More symptoms, more risk

Previous research shows severe OSA doubles the risk of stroke and increases the chance of recurrent stroke. A 2019 study showed that people with insomnia had a small increased risk of stroke.

“Both snoring and extremes of sleep duration have been previously associated with an increased risk of stroke in observational research, but less is known about other symptoms of sleep impairment, with less consistent findings,” Dr. McCarthy said.

Prior studies have also generally come from a single geographic region, which Dr. McCarthy noted could limit their generalizability.

For this effort, investigators used data from 4,496 participants in INTERSTROKE, an international case-control study of risk factors for a first acute stroke. About half of the participants had a history of stroke.

Using information collected from a survey of sleep habits, researchers found an elevated stroke risk in those who received less than 5 hours of sleep per night (odds ratio, 3.15; 95% confidence interval, 2.09-4.76) or more than 9 hours of sleep per night (OR, 2.67; 95% CI, 1.89-3.78), compared with those who slept 7 hours a night.

Participants who took unplanned naps or naps lasting an hour or more (OR, 2.46; 95% CI, 1.69-3.57) and participants who reported poor quality sleep (OR,1.52; 95% CI, 1.32-1.75) were also at an increased risk for stroke.

Symptoms of OSA were also strongly associated with increased stroke risk, including snoring (OR, 1.91; 95% CI, 1.62-2.24), snorting (OR, 2.64; 95% CI, 2.17-3.20), and breathing cessation (OR, 2.87; 95% CI, 2.28-2.60).

Stroke risk increased as the number of sleep disturbance symptoms rose, with the greatest risk in the 11% of participants who had five or more symptoms (OR, 5.38; 95% CI, 4.03-7.18).

“This study finds an association between a broad range of sleep impairment symptoms and stroke, and a graded association with increasing symptoms, in an international setting,” Dr. McCarthy said.

Researchers aren’t sure what’s driving the higher stroke risk among people with sleep disturbances. Although the study did control for potential confounders, it wasn’t designed to get at what’s driving the association.

“Sleep disturbance may also have a bi-directional relationship with many stroke risk factors; for example, sleep disturbance may be a symptom of disease and exacerbate disease,” Dr. McCarthy said. “Future interventional studies are required to determine the true direction of the relationship.”
 

A marker of stroke risk

Daniel Lackland, DrPH, professor of neurology at the Medical University of South Carolina, Charleston, said the findings provide additional evidence of the link between sleep and stroke risk.

“The results confirm sleep disorders as a potential marker and part of the risk profile,” he said.

Collecting information about sleep using a validated assessment tool is an important piece of clinical care, Dr. Lackland said, especially among patients with other stroke risk factors.

One limitation of the study was that data on sleep was collected only at one point, and participants were not followed over time to see if changes in sleep affected stroke risk.

“This is an important point and should be a focus for future studies, as it is critical in the design of interventions,” Dr. Lackland said.

The INTERSTROKE study is funded by the Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, Canadian Stroke Network, Swedish Research Council, Swedish Heart and Lung Foundation, The Health & Medical Care Committee of the Regional Executive Board, Region Västra Götaland, Astra Zeneca, Boehringer Ingelheim (Canada), Pfizer (Canada), MERCK, Sharp and Dohme, Swedish Heart and Lung Foundation, U.K. Chest, and U.K. Heart and Stroke. Dr. McCarthy and Lackland report no relevant financial relationships.

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