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How does not getting enough sleep affect the developing brain?
Children who do not get enough sleep for one night can be cranky, groggy, or meltdown prone the next day.
Over time, though, insufficient sleep may impair neurodevelopment in ways that can be measured on brain scans and tests long term, a new study shows.
Research published in The Lancet Child & Adolescent Health found that 9- and 10-year-olds who do not get at least 9 hours of sleep most nights tend to have less gray matter and smaller areas of the brain responsible for attention, memory, and inhibition control, relative to children who do get enough sleep.
The researchers also found a relationship between insufficient sleep and disrupted connections between the basal ganglia and cortical regions of the brain. These disruptions appeared to be linked to depression, thought problems, and impairments in crystallized intelligence, a type of intelligence that depends on memory.
The overall patterns persisted 2 years later, even as those who got enough sleep at baseline gradually slept less over time, while those who were not getting enough sleep to begin with continued to sleep about the same amount, the researchers reported.
The results bolster the case for delaying school start times, as California recently did, according one researcher who was not involved in the study.
The ABCD Study
To examine how insufficient sleep affects children’s mental health, cognition, brain function, and brain structure over 2 years, Ze Wang, PhD, professor of diagnostic radiology and nuclear medicine at the University of Maryland, Baltimore, and colleagues analyzed data from the ongoing Adolescent Brain Cognitive Development (ABCD) Study. The ABCD Study is tracking the biologic and behavioral development of more than 11,000 children in the United States who were recruited for the study when they were 9 or 10 years old.
For their new analysis, Dr. Wang’s group focused on 6,042 participants: 3,021 children with insufficient sleep who were matched with an equal number of participants who were similar in many respects, including sex, socioeconomic status, and puberty status, except they got at least 9 hours of sleep. They also looked at outcomes 2 years later from 749 of the matched pairs who had results available.
The investigators determined sleep duration based on how parents answered the question: “How many hours of sleep does your child get on most nights in the past 6 months?” Possible answers included at least 9 hours, 8-9 hours, 7-8 hours, 5-7 hours, or less than 5 hours. They also looked at functional and structural MRI scans, test results, and responses to questionnaires.
Negative effects of inadequate sleep were spread over “several different domains including brain structure, function, cognition, behavior, and mental health,” Dr. Wang said.
The strength of the relationship between sleep duration and the various outcomes was “modest” and based on group averages, he said. So, a given child who does not sleep for 9 hours most nights won’t necessarily perform worse than a child who gets enough sleep.
Still, modest effects may accumulate and have lasting consequences, Dr. Wang said.
Crystallized intelligence
The researchers looked at 42 behavioral outcomes, 32 of which were significantly different between the groups. Four outcomes in particular – depression, thought problems, performance on a picture-vocabulary test, and crystallized intelligence – were areas where insufficient sleep seemed to have a larger negative effect.
Sleep duration’s relationship with crystallized intelligence was twice that for fluid intelligence, which does not depend on memory.
“Sleep affects memory,” Dr. Wang said. “Crystallized intelligence depends on learned skills and knowledge, which are memory. In this sense, sleep is related to crystallized intelligence.”
One limitation of the study is that some parents may not accurately report how much sleep their child gets, Dr. Wang acknowledged. Children may be awake when parents think they are asleep, for example.
And although the results show getting 9 hours of sleep may help neurocognitive development, it’s also possible that excessive amounts of sleep could be problematic, the study authors wrote.
Further experiments are needed to prove that insufficient sleep – and not some other, unaccounted for factor – causes the observed impairments in neurodevelopment.
To promote healthy sleep, parents should keep a strict routine for their children, such as a regular bedtime and no electronic devices in the bedroom, Dr. Wang suggested. More physical activity during the day also should help.
If children have high levels of stress and depression, “finding the source is critical,” he said. Likewise, clinicians should consider how mental health can affect their patients’ sleep.
More to healthy sleep than duration
“This study both aligns with and advances existing research on the importance of sufficient sleep for child well-being,” said Ariel A. Williamson, PhD, DBSM, a psychologist and pediatric sleep expert in the department of child and adolescent psychiatry and behavioral sciences at Children’s Hospital of Philadelphia and assistant professor of psychiatry and pediatrics at University of Pennsylvania, also in Philadelphia.
The researchers used rigorous propensity score matching, longitudinal data, and brain imaging, which are “innovative methods that provide more evidence on potential mechanisms linking insufficient sleep and child outcomes,” said Dr. Williamson, who was not involved in the study.
While the investigators focused on sleep duration, child sleep health is multidimensional and includes other elements like timing and perception of sleep quality, Dr. Williamson noted. “For example, some research shows that having a sleep schedule that varies night to night is linked to poor child outcomes.”
Dr. Williamson tells families and clinicians that “sleep is a pillar of health,” equal to diet and exercise. That said, sleep recommendations need to fit within a family’s life – taking into account after school activities and late-night homework sessions. But extending sleep by just “20-30 minutes can make a meaningful difference for daytime functioning,” Dr. Williamson said.
Start school later?
Researchers have only relatively recently begun to understand how insufficient sleep affects adolescent neurocognitive development long term, and this study provides “crucial evidence” about the consequences, Lydia Gabriela Speyer, PhD, said in an editorial published with the study. Dr. Speyer is affiliated with the department of psychology at the University of Cambridge (England).
“Given the novel finding that insufficient sleep is associated with changes in brain structure and connectivity that are long-lasting, early intervention is crucial because such neural changes are probably not reversible and might consequently affect adolescents’ development into adulthood,” Dr. Speyer wrote.
Delaying school start times could be one way to help kids get more sleep. The American Academy of Pediatrics and the American Academy of Sleep Medicine recommend that middle schools and high schools start no earlier than 8:30 a.m. to better align with students’ circadian rhythm, Dr. Speyer noted.
As it is in the United States, most schools start closer to 8 a.m. In California, though, a law that went into effect on July 1 prohibits high schools from starting before 8:30 a.m. Other states are weighing similar legislation.
The research was supported by the National Institutes of Health. Dr. Wang and his coauthors and Dr. Speyer had no conflict of interest disclosures. Dr. Williamson is a sleep expert for the Pediatric Sleep Council (www.babysleep.com), which provides free information about early childhood sleep, but she does not receive compensation for this role.
Children who do not get enough sleep for one night can be cranky, groggy, or meltdown prone the next day.
Over time, though, insufficient sleep may impair neurodevelopment in ways that can be measured on brain scans and tests long term, a new study shows.
Research published in The Lancet Child & Adolescent Health found that 9- and 10-year-olds who do not get at least 9 hours of sleep most nights tend to have less gray matter and smaller areas of the brain responsible for attention, memory, and inhibition control, relative to children who do get enough sleep.
The researchers also found a relationship between insufficient sleep and disrupted connections between the basal ganglia and cortical regions of the brain. These disruptions appeared to be linked to depression, thought problems, and impairments in crystallized intelligence, a type of intelligence that depends on memory.
The overall patterns persisted 2 years later, even as those who got enough sleep at baseline gradually slept less over time, while those who were not getting enough sleep to begin with continued to sleep about the same amount, the researchers reported.
The results bolster the case for delaying school start times, as California recently did, according one researcher who was not involved in the study.
The ABCD Study
To examine how insufficient sleep affects children’s mental health, cognition, brain function, and brain structure over 2 years, Ze Wang, PhD, professor of diagnostic radiology and nuclear medicine at the University of Maryland, Baltimore, and colleagues analyzed data from the ongoing Adolescent Brain Cognitive Development (ABCD) Study. The ABCD Study is tracking the biologic and behavioral development of more than 11,000 children in the United States who were recruited for the study when they were 9 or 10 years old.
For their new analysis, Dr. Wang’s group focused on 6,042 participants: 3,021 children with insufficient sleep who were matched with an equal number of participants who were similar in many respects, including sex, socioeconomic status, and puberty status, except they got at least 9 hours of sleep. They also looked at outcomes 2 years later from 749 of the matched pairs who had results available.
The investigators determined sleep duration based on how parents answered the question: “How many hours of sleep does your child get on most nights in the past 6 months?” Possible answers included at least 9 hours, 8-9 hours, 7-8 hours, 5-7 hours, or less than 5 hours. They also looked at functional and structural MRI scans, test results, and responses to questionnaires.
Negative effects of inadequate sleep were spread over “several different domains including brain structure, function, cognition, behavior, and mental health,” Dr. Wang said.
The strength of the relationship between sleep duration and the various outcomes was “modest” and based on group averages, he said. So, a given child who does not sleep for 9 hours most nights won’t necessarily perform worse than a child who gets enough sleep.
Still, modest effects may accumulate and have lasting consequences, Dr. Wang said.
Crystallized intelligence
The researchers looked at 42 behavioral outcomes, 32 of which were significantly different between the groups. Four outcomes in particular – depression, thought problems, performance on a picture-vocabulary test, and crystallized intelligence – were areas where insufficient sleep seemed to have a larger negative effect.
Sleep duration’s relationship with crystallized intelligence was twice that for fluid intelligence, which does not depend on memory.
“Sleep affects memory,” Dr. Wang said. “Crystallized intelligence depends on learned skills and knowledge, which are memory. In this sense, sleep is related to crystallized intelligence.”
One limitation of the study is that some parents may not accurately report how much sleep their child gets, Dr. Wang acknowledged. Children may be awake when parents think they are asleep, for example.
And although the results show getting 9 hours of sleep may help neurocognitive development, it’s also possible that excessive amounts of sleep could be problematic, the study authors wrote.
Further experiments are needed to prove that insufficient sleep – and not some other, unaccounted for factor – causes the observed impairments in neurodevelopment.
To promote healthy sleep, parents should keep a strict routine for their children, such as a regular bedtime and no electronic devices in the bedroom, Dr. Wang suggested. More physical activity during the day also should help.
If children have high levels of stress and depression, “finding the source is critical,” he said. Likewise, clinicians should consider how mental health can affect their patients’ sleep.
More to healthy sleep than duration
“This study both aligns with and advances existing research on the importance of sufficient sleep for child well-being,” said Ariel A. Williamson, PhD, DBSM, a psychologist and pediatric sleep expert in the department of child and adolescent psychiatry and behavioral sciences at Children’s Hospital of Philadelphia and assistant professor of psychiatry and pediatrics at University of Pennsylvania, also in Philadelphia.
The researchers used rigorous propensity score matching, longitudinal data, and brain imaging, which are “innovative methods that provide more evidence on potential mechanisms linking insufficient sleep and child outcomes,” said Dr. Williamson, who was not involved in the study.
While the investigators focused on sleep duration, child sleep health is multidimensional and includes other elements like timing and perception of sleep quality, Dr. Williamson noted. “For example, some research shows that having a sleep schedule that varies night to night is linked to poor child outcomes.”
Dr. Williamson tells families and clinicians that “sleep is a pillar of health,” equal to diet and exercise. That said, sleep recommendations need to fit within a family’s life – taking into account after school activities and late-night homework sessions. But extending sleep by just “20-30 minutes can make a meaningful difference for daytime functioning,” Dr. Williamson said.
Start school later?
Researchers have only relatively recently begun to understand how insufficient sleep affects adolescent neurocognitive development long term, and this study provides “crucial evidence” about the consequences, Lydia Gabriela Speyer, PhD, said in an editorial published with the study. Dr. Speyer is affiliated with the department of psychology at the University of Cambridge (England).
“Given the novel finding that insufficient sleep is associated with changes in brain structure and connectivity that are long-lasting, early intervention is crucial because such neural changes are probably not reversible and might consequently affect adolescents’ development into adulthood,” Dr. Speyer wrote.
Delaying school start times could be one way to help kids get more sleep. The American Academy of Pediatrics and the American Academy of Sleep Medicine recommend that middle schools and high schools start no earlier than 8:30 a.m. to better align with students’ circadian rhythm, Dr. Speyer noted.
As it is in the United States, most schools start closer to 8 a.m. In California, though, a law that went into effect on July 1 prohibits high schools from starting before 8:30 a.m. Other states are weighing similar legislation.
The research was supported by the National Institutes of Health. Dr. Wang and his coauthors and Dr. Speyer had no conflict of interest disclosures. Dr. Williamson is a sleep expert for the Pediatric Sleep Council (www.babysleep.com), which provides free information about early childhood sleep, but she does not receive compensation for this role.
Children who do not get enough sleep for one night can be cranky, groggy, or meltdown prone the next day.
Over time, though, insufficient sleep may impair neurodevelopment in ways that can be measured on brain scans and tests long term, a new study shows.
Research published in The Lancet Child & Adolescent Health found that 9- and 10-year-olds who do not get at least 9 hours of sleep most nights tend to have less gray matter and smaller areas of the brain responsible for attention, memory, and inhibition control, relative to children who do get enough sleep.
The researchers also found a relationship between insufficient sleep and disrupted connections between the basal ganglia and cortical regions of the brain. These disruptions appeared to be linked to depression, thought problems, and impairments in crystallized intelligence, a type of intelligence that depends on memory.
The overall patterns persisted 2 years later, even as those who got enough sleep at baseline gradually slept less over time, while those who were not getting enough sleep to begin with continued to sleep about the same amount, the researchers reported.
The results bolster the case for delaying school start times, as California recently did, according one researcher who was not involved in the study.
The ABCD Study
To examine how insufficient sleep affects children’s mental health, cognition, brain function, and brain structure over 2 years, Ze Wang, PhD, professor of diagnostic radiology and nuclear medicine at the University of Maryland, Baltimore, and colleagues analyzed data from the ongoing Adolescent Brain Cognitive Development (ABCD) Study. The ABCD Study is tracking the biologic and behavioral development of more than 11,000 children in the United States who were recruited for the study when they were 9 or 10 years old.
For their new analysis, Dr. Wang’s group focused on 6,042 participants: 3,021 children with insufficient sleep who were matched with an equal number of participants who were similar in many respects, including sex, socioeconomic status, and puberty status, except they got at least 9 hours of sleep. They also looked at outcomes 2 years later from 749 of the matched pairs who had results available.
The investigators determined sleep duration based on how parents answered the question: “How many hours of sleep does your child get on most nights in the past 6 months?” Possible answers included at least 9 hours, 8-9 hours, 7-8 hours, 5-7 hours, or less than 5 hours. They also looked at functional and structural MRI scans, test results, and responses to questionnaires.
Negative effects of inadequate sleep were spread over “several different domains including brain structure, function, cognition, behavior, and mental health,” Dr. Wang said.
The strength of the relationship between sleep duration and the various outcomes was “modest” and based on group averages, he said. So, a given child who does not sleep for 9 hours most nights won’t necessarily perform worse than a child who gets enough sleep.
Still, modest effects may accumulate and have lasting consequences, Dr. Wang said.
Crystallized intelligence
The researchers looked at 42 behavioral outcomes, 32 of which were significantly different between the groups. Four outcomes in particular – depression, thought problems, performance on a picture-vocabulary test, and crystallized intelligence – were areas where insufficient sleep seemed to have a larger negative effect.
Sleep duration’s relationship with crystallized intelligence was twice that for fluid intelligence, which does not depend on memory.
“Sleep affects memory,” Dr. Wang said. “Crystallized intelligence depends on learned skills and knowledge, which are memory. In this sense, sleep is related to crystallized intelligence.”
One limitation of the study is that some parents may not accurately report how much sleep their child gets, Dr. Wang acknowledged. Children may be awake when parents think they are asleep, for example.
And although the results show getting 9 hours of sleep may help neurocognitive development, it’s also possible that excessive amounts of sleep could be problematic, the study authors wrote.
Further experiments are needed to prove that insufficient sleep – and not some other, unaccounted for factor – causes the observed impairments in neurodevelopment.
To promote healthy sleep, parents should keep a strict routine for their children, such as a regular bedtime and no electronic devices in the bedroom, Dr. Wang suggested. More physical activity during the day also should help.
If children have high levels of stress and depression, “finding the source is critical,” he said. Likewise, clinicians should consider how mental health can affect their patients’ sleep.
More to healthy sleep than duration
“This study both aligns with and advances existing research on the importance of sufficient sleep for child well-being,” said Ariel A. Williamson, PhD, DBSM, a psychologist and pediatric sleep expert in the department of child and adolescent psychiatry and behavioral sciences at Children’s Hospital of Philadelphia and assistant professor of psychiatry and pediatrics at University of Pennsylvania, also in Philadelphia.
The researchers used rigorous propensity score matching, longitudinal data, and brain imaging, which are “innovative methods that provide more evidence on potential mechanisms linking insufficient sleep and child outcomes,” said Dr. Williamson, who was not involved in the study.
While the investigators focused on sleep duration, child sleep health is multidimensional and includes other elements like timing and perception of sleep quality, Dr. Williamson noted. “For example, some research shows that having a sleep schedule that varies night to night is linked to poor child outcomes.”
Dr. Williamson tells families and clinicians that “sleep is a pillar of health,” equal to diet and exercise. That said, sleep recommendations need to fit within a family’s life – taking into account after school activities and late-night homework sessions. But extending sleep by just “20-30 minutes can make a meaningful difference for daytime functioning,” Dr. Williamson said.
Start school later?
Researchers have only relatively recently begun to understand how insufficient sleep affects adolescent neurocognitive development long term, and this study provides “crucial evidence” about the consequences, Lydia Gabriela Speyer, PhD, said in an editorial published with the study. Dr. Speyer is affiliated with the department of psychology at the University of Cambridge (England).
“Given the novel finding that insufficient sleep is associated with changes in brain structure and connectivity that are long-lasting, early intervention is crucial because such neural changes are probably not reversible and might consequently affect adolescents’ development into adulthood,” Dr. Speyer wrote.
Delaying school start times could be one way to help kids get more sleep. The American Academy of Pediatrics and the American Academy of Sleep Medicine recommend that middle schools and high schools start no earlier than 8:30 a.m. to better align with students’ circadian rhythm, Dr. Speyer noted.
As it is in the United States, most schools start closer to 8 a.m. In California, though, a law that went into effect on July 1 prohibits high schools from starting before 8:30 a.m. Other states are weighing similar legislation.
The research was supported by the National Institutes of Health. Dr. Wang and his coauthors and Dr. Speyer had no conflict of interest disclosures. Dr. Williamson is a sleep expert for the Pediatric Sleep Council (www.babysleep.com), which provides free information about early childhood sleep, but she does not receive compensation for this role.
FROM THE LANCET CHILD & ADOLESCENT HEALTH
FDA clears new neurostimulation system for chronic pain
The “next generation” of its proprietary BurstDR stimulation, FlexBurst360 therapy, provides pain coverage across up to six areas of the trunk and limbs, with programming that can be adjusted as a patient’s individual therapeutic needs evolve, the manufacturer noted.
“Using FlexBurst360 therapy on the Proclaim Plus system, physicians can identify the lowest effective dose of stimulation for each patient and adapt it based on evolving pain needs,” the company said in a news release.
The system also has therapy settings accessed with a mobile device.
Through their mobile devices, patients can access the manufacturer’s NeuroSphere Virtual Clinic, which allows them to communicate with their providers and receive remote adjustments to their therapeutic settings as needed.
Game changer?
The newly approved system has a battery life of up to 10 years, akin to the company’s Proclaim XR neurostimulation system for chronic pain. As reported at the time by this news organization, that system was approved by the FDA in 2019.
More than 50 million people in the United States experience chronic pain and most have pain in more than one area of the body. Steven Falowski, MD, with Argires Marotti Neurosurgical Associates of Lancaster, Pa., noted in the release that spinal cord stimulation has provided “tremendous relief” for patients with chronic pain.
Dr. Falowski added that “with its ability to mimic natural patterns found in the brain, the Abbott BurstDR platform has been a game changer” for these patients.
“However, despite the many benefits of BurstDR, such as being effective as a low-energy stimulation therapy, some patients continue to be burdened ... because of multiple painful areas and evolving pain,” he said.
“Now, with Proclaim Plus and FlexBurst360, an already established platform has been improved to treat more patients who suffer from pain across different body parts and changing pain over time,” said Dr. Falowski.
A version of this article first appeared on Medscape.com.
The “next generation” of its proprietary BurstDR stimulation, FlexBurst360 therapy, provides pain coverage across up to six areas of the trunk and limbs, with programming that can be adjusted as a patient’s individual therapeutic needs evolve, the manufacturer noted.
“Using FlexBurst360 therapy on the Proclaim Plus system, physicians can identify the lowest effective dose of stimulation for each patient and adapt it based on evolving pain needs,” the company said in a news release.
The system also has therapy settings accessed with a mobile device.
Through their mobile devices, patients can access the manufacturer’s NeuroSphere Virtual Clinic, which allows them to communicate with their providers and receive remote adjustments to their therapeutic settings as needed.
Game changer?
The newly approved system has a battery life of up to 10 years, akin to the company’s Proclaim XR neurostimulation system for chronic pain. As reported at the time by this news organization, that system was approved by the FDA in 2019.
More than 50 million people in the United States experience chronic pain and most have pain in more than one area of the body. Steven Falowski, MD, with Argires Marotti Neurosurgical Associates of Lancaster, Pa., noted in the release that spinal cord stimulation has provided “tremendous relief” for patients with chronic pain.
Dr. Falowski added that “with its ability to mimic natural patterns found in the brain, the Abbott BurstDR platform has been a game changer” for these patients.
“However, despite the many benefits of BurstDR, such as being effective as a low-energy stimulation therapy, some patients continue to be burdened ... because of multiple painful areas and evolving pain,” he said.
“Now, with Proclaim Plus and FlexBurst360, an already established platform has been improved to treat more patients who suffer from pain across different body parts and changing pain over time,” said Dr. Falowski.
A version of this article first appeared on Medscape.com.
The “next generation” of its proprietary BurstDR stimulation, FlexBurst360 therapy, provides pain coverage across up to six areas of the trunk and limbs, with programming that can be adjusted as a patient’s individual therapeutic needs evolve, the manufacturer noted.
“Using FlexBurst360 therapy on the Proclaim Plus system, physicians can identify the lowest effective dose of stimulation for each patient and adapt it based on evolving pain needs,” the company said in a news release.
The system also has therapy settings accessed with a mobile device.
Through their mobile devices, patients can access the manufacturer’s NeuroSphere Virtual Clinic, which allows them to communicate with their providers and receive remote adjustments to their therapeutic settings as needed.
Game changer?
The newly approved system has a battery life of up to 10 years, akin to the company’s Proclaim XR neurostimulation system for chronic pain. As reported at the time by this news organization, that system was approved by the FDA in 2019.
More than 50 million people in the United States experience chronic pain and most have pain in more than one area of the body. Steven Falowski, MD, with Argires Marotti Neurosurgical Associates of Lancaster, Pa., noted in the release that spinal cord stimulation has provided “tremendous relief” for patients with chronic pain.
Dr. Falowski added that “with its ability to mimic natural patterns found in the brain, the Abbott BurstDR platform has been a game changer” for these patients.
“However, despite the many benefits of BurstDR, such as being effective as a low-energy stimulation therapy, some patients continue to be burdened ... because of multiple painful areas and evolving pain,” he said.
“Now, with Proclaim Plus and FlexBurst360, an already established platform has been improved to treat more patients who suffer from pain across different body parts and changing pain over time,” said Dr. Falowski.
A version of this article first appeared on Medscape.com.
Watching TV, using computer have opposite ties to dementia risk
The relationship to dementia with these activities remained strong no matter how much physical activity a person did, the authors wrote in Proceedings of the National Academy of Sciences.
Both watching TV and using a computer have been linked to increased risk of chronic disease and mortality, while exercise and physical activity (PA) have shown benefit in reducing cognitive decline, structural brain atrophy, and dementia risk in older adults, the authors wrote.
The authors said they wanted to try to understand the effects of watching TV and using computers on dementia risk, because people in the United States and Europe have been engaging in both of these activities more often.
They concluded that it’s not the sitting part of sedentary behavior (SB) that potentially has the effect on dementia but what people are doing while sitting.
Some of the results were surprising, lead author David Raichlen, PhD, professor of Human and Evolutionary Biology at University of Southern California, Los Angeles, said in an interview.
Previous literature on sedentary behaviors have documented their negative effects on a wide range of health outcomes, rather than finding positive associations, he explained.
More than 140,000 included in study
The researchers conducted their prospective cohort study using data from the United Kingdom Biobank. After excluding people younger than 60, those with prevalent dementia at the start of follow-up, and those without complete data, 146,651 participants were included.
The participants were followed from their baseline visit until they received a dementia diagnosis, died, were lost to follow-up, or were last admitted to the hospital.
TV-watching time was linked with an increased risk of incident dementia (HR [95% confidence interval] = 1.31 [1.23-1.40]), and computer use was linked with a reduced risk of incident dementia HR [95% CI] = 0.80 [0.76-0.85]).
TV’s link with higher dementia risk increased in those who had the highest use, compared with those who had the lowest use (HR [95% CI] = 1.28 [1.18-1.39].
Similarly, the link with risk reduction for dementia with computer use increased with more use.
Both medium and high computer time were associated with reduced risk of incident dementia (HR [95% CI] = 0.70 [0.64-0.76] and HR [95% CI] = 0.76 [0.70-0.83] respectively).
Dr. Raichlen pointed out that the high use of TV in this study was 4 or more hours a day and computer use – which included leisure use, not work use – had benefits on dementia risk after just half an hour.
These results remained significant after researchers adjusted for demographic, health, and lifestyle variables, including time spent on physical activity, sleeping, obesity, alcohol consumption, smoking status, diet scores, education level, body mass index, and employment type.
Physical is still better than sedentary activity
One potential reason for the different effects on dementia risk in the two activities studied, the authors write, is that sitting down to watch TV is associated with “uniquely low levels of muscle activity and energy expenditure, compared with sitting to use a computer.”
Andrew Budson, MD, chief of Cognitive & Behavioral Neurology and Associate Chief of Staff for Education for the VA Boston Healthcare System, Mass., who was not part of the study, said he thinks a more likely explanation for the study findings lies in the active versus passive tasks required in the two kinds of viewing that the authors reference.
“When we’re doing cognitive activity involving using the computer, we’re using large parts of our cortex to carry out that activity, whereas when we’re watching TV, there are probably relatively small amounts of our brain that are actually active,” Dr. Budson, author of Seven Steps to Managing Your Memory, explained in an interview.
“This is one of the first times I’ve been convinced that even when the computer activity isn’t completely new and novel, it may be beneficial,” Dr. Budson said.
It would be much better to do physical activity, but if the choice is sedentary activity, active cognitive activities, such as computer use, are better than TV watching, he continued.
The results of the current study are consistent with previous work showing that the type of sedentary behavior matters, according to the authors.
“Several studies have shown that TV time is associated with mortality and poor cardiometabolic biomarkers, whereas computer time is not,” they wrote.
A limitation of the study is that sedentary behaviors were self-reported via questionnaires, and there may be errors in recall.
“The use of objective methods for measuring both SB and PA are needed in future studies,” they write.
The authors receive support from the National Institutes of Health, the State of Arizona, the Arizona Department of Health Services, and the McKnight Brain Research Foundation. Neither the authors nor Dr. Budson declared relevant financial relationships.
The relationship to dementia with these activities remained strong no matter how much physical activity a person did, the authors wrote in Proceedings of the National Academy of Sciences.
Both watching TV and using a computer have been linked to increased risk of chronic disease and mortality, while exercise and physical activity (PA) have shown benefit in reducing cognitive decline, structural brain atrophy, and dementia risk in older adults, the authors wrote.
The authors said they wanted to try to understand the effects of watching TV and using computers on dementia risk, because people in the United States and Europe have been engaging in both of these activities more often.
They concluded that it’s not the sitting part of sedentary behavior (SB) that potentially has the effect on dementia but what people are doing while sitting.
Some of the results were surprising, lead author David Raichlen, PhD, professor of Human and Evolutionary Biology at University of Southern California, Los Angeles, said in an interview.
Previous literature on sedentary behaviors have documented their negative effects on a wide range of health outcomes, rather than finding positive associations, he explained.
More than 140,000 included in study
The researchers conducted their prospective cohort study using data from the United Kingdom Biobank. After excluding people younger than 60, those with prevalent dementia at the start of follow-up, and those without complete data, 146,651 participants were included.
The participants were followed from their baseline visit until they received a dementia diagnosis, died, were lost to follow-up, or were last admitted to the hospital.
TV-watching time was linked with an increased risk of incident dementia (HR [95% confidence interval] = 1.31 [1.23-1.40]), and computer use was linked with a reduced risk of incident dementia HR [95% CI] = 0.80 [0.76-0.85]).
TV’s link with higher dementia risk increased in those who had the highest use, compared with those who had the lowest use (HR [95% CI] = 1.28 [1.18-1.39].
Similarly, the link with risk reduction for dementia with computer use increased with more use.
Both medium and high computer time were associated with reduced risk of incident dementia (HR [95% CI] = 0.70 [0.64-0.76] and HR [95% CI] = 0.76 [0.70-0.83] respectively).
Dr. Raichlen pointed out that the high use of TV in this study was 4 or more hours a day and computer use – which included leisure use, not work use – had benefits on dementia risk after just half an hour.
These results remained significant after researchers adjusted for demographic, health, and lifestyle variables, including time spent on physical activity, sleeping, obesity, alcohol consumption, smoking status, diet scores, education level, body mass index, and employment type.
Physical is still better than sedentary activity
One potential reason for the different effects on dementia risk in the two activities studied, the authors write, is that sitting down to watch TV is associated with “uniquely low levels of muscle activity and energy expenditure, compared with sitting to use a computer.”
Andrew Budson, MD, chief of Cognitive & Behavioral Neurology and Associate Chief of Staff for Education for the VA Boston Healthcare System, Mass., who was not part of the study, said he thinks a more likely explanation for the study findings lies in the active versus passive tasks required in the two kinds of viewing that the authors reference.
“When we’re doing cognitive activity involving using the computer, we’re using large parts of our cortex to carry out that activity, whereas when we’re watching TV, there are probably relatively small amounts of our brain that are actually active,” Dr. Budson, author of Seven Steps to Managing Your Memory, explained in an interview.
“This is one of the first times I’ve been convinced that even when the computer activity isn’t completely new and novel, it may be beneficial,” Dr. Budson said.
It would be much better to do physical activity, but if the choice is sedentary activity, active cognitive activities, such as computer use, are better than TV watching, he continued.
The results of the current study are consistent with previous work showing that the type of sedentary behavior matters, according to the authors.
“Several studies have shown that TV time is associated with mortality and poor cardiometabolic biomarkers, whereas computer time is not,” they wrote.
A limitation of the study is that sedentary behaviors were self-reported via questionnaires, and there may be errors in recall.
“The use of objective methods for measuring both SB and PA are needed in future studies,” they write.
The authors receive support from the National Institutes of Health, the State of Arizona, the Arizona Department of Health Services, and the McKnight Brain Research Foundation. Neither the authors nor Dr. Budson declared relevant financial relationships.
The relationship to dementia with these activities remained strong no matter how much physical activity a person did, the authors wrote in Proceedings of the National Academy of Sciences.
Both watching TV and using a computer have been linked to increased risk of chronic disease and mortality, while exercise and physical activity (PA) have shown benefit in reducing cognitive decline, structural brain atrophy, and dementia risk in older adults, the authors wrote.
The authors said they wanted to try to understand the effects of watching TV and using computers on dementia risk, because people in the United States and Europe have been engaging in both of these activities more often.
They concluded that it’s not the sitting part of sedentary behavior (SB) that potentially has the effect on dementia but what people are doing while sitting.
Some of the results were surprising, lead author David Raichlen, PhD, professor of Human and Evolutionary Biology at University of Southern California, Los Angeles, said in an interview.
Previous literature on sedentary behaviors have documented their negative effects on a wide range of health outcomes, rather than finding positive associations, he explained.
More than 140,000 included in study
The researchers conducted their prospective cohort study using data from the United Kingdom Biobank. After excluding people younger than 60, those with prevalent dementia at the start of follow-up, and those without complete data, 146,651 participants were included.
The participants were followed from their baseline visit until they received a dementia diagnosis, died, were lost to follow-up, or were last admitted to the hospital.
TV-watching time was linked with an increased risk of incident dementia (HR [95% confidence interval] = 1.31 [1.23-1.40]), and computer use was linked with a reduced risk of incident dementia HR [95% CI] = 0.80 [0.76-0.85]).
TV’s link with higher dementia risk increased in those who had the highest use, compared with those who had the lowest use (HR [95% CI] = 1.28 [1.18-1.39].
Similarly, the link with risk reduction for dementia with computer use increased with more use.
Both medium and high computer time were associated with reduced risk of incident dementia (HR [95% CI] = 0.70 [0.64-0.76] and HR [95% CI] = 0.76 [0.70-0.83] respectively).
Dr. Raichlen pointed out that the high use of TV in this study was 4 or more hours a day and computer use – which included leisure use, not work use – had benefits on dementia risk after just half an hour.
These results remained significant after researchers adjusted for demographic, health, and lifestyle variables, including time spent on physical activity, sleeping, obesity, alcohol consumption, smoking status, diet scores, education level, body mass index, and employment type.
Physical is still better than sedentary activity
One potential reason for the different effects on dementia risk in the two activities studied, the authors write, is that sitting down to watch TV is associated with “uniquely low levels of muscle activity and energy expenditure, compared with sitting to use a computer.”
Andrew Budson, MD, chief of Cognitive & Behavioral Neurology and Associate Chief of Staff for Education for the VA Boston Healthcare System, Mass., who was not part of the study, said he thinks a more likely explanation for the study findings lies in the active versus passive tasks required in the two kinds of viewing that the authors reference.
“When we’re doing cognitive activity involving using the computer, we’re using large parts of our cortex to carry out that activity, whereas when we’re watching TV, there are probably relatively small amounts of our brain that are actually active,” Dr. Budson, author of Seven Steps to Managing Your Memory, explained in an interview.
“This is one of the first times I’ve been convinced that even when the computer activity isn’t completely new and novel, it may be beneficial,” Dr. Budson said.
It would be much better to do physical activity, but if the choice is sedentary activity, active cognitive activities, such as computer use, are better than TV watching, he continued.
The results of the current study are consistent with previous work showing that the type of sedentary behavior matters, according to the authors.
“Several studies have shown that TV time is associated with mortality and poor cardiometabolic biomarkers, whereas computer time is not,” they wrote.
A limitation of the study is that sedentary behaviors were self-reported via questionnaires, and there may be errors in recall.
“The use of objective methods for measuring both SB and PA are needed in future studies,” they write.
The authors receive support from the National Institutes of Health, the State of Arizona, the Arizona Department of Health Services, and the McKnight Brain Research Foundation. Neither the authors nor Dr. Budson declared relevant financial relationships.
FROM PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES
Atrial cardiopathy linked to 35% higher dementia risk
“We cautiously suggest that an understanding of this relationship might provide a basis for new interventional strategies to help thwart the development of dementia,” the authors write.
The research, led by Michelle C. Johansen, MD, department of neurology, Johns Hopkins University, Baltimore, was published online in the Journal of the American Heart Association.
Atrial cardiopathy, characterized by abnormal size and function of the left atrium, has been associated with an increased risk of stroke and atrial fibrillation (AFib), and because both stroke and AFib are associated with an increased dementia risk, the authors write, it was important to investigate whether atrial cardiopathy is linked to dementia.
If that’s the case, they reasoned, the next question was whether that link is independent of AFib and stroke, and their new research suggests that it is.
For this analysis, the researchers conducted a prospective cohort analysis of participants in the Atherosclerosis Risk in Communities (ARIC) study who were attending visit 5 (2011-2013). During their fifth, sixth, and seventh clinical visits, the ARIC participants were evaluated for cognitive decline indicating dementia.
They studied a diverse population of 5,078 older adults living in four U.S. communities: Washington County, Md.; Forsyth County, N.C.; the northwestern suburbs of Minneapolis; and Jackson, Miss.
Just more than a third (34%) had atrial cardiopathy (average age, 75 years; 59% female; 21% Black) and 763 participants developed dementia.
Investigators found that atrial cardiopathy was significantly associated with dementia (adjusted hazard ratio, 1.35 [95% confidence interval, 1.16-1.58]).
They considered ARIC participants to have atrial cardiopathy if they had at least one of the following: P-wave terminal force greater than 5,000 mV·ms in ECG lead V1; NTproBNP greater than 250 pg/mL; or left atrial volume index greater than or equal to 34 mL/m2 by transthoracic echocardiography.
The risk of dementia was even stronger when the researchers defined cardiopathy by at least two biomarkers instead of one (aHR, 1.54 [95% CI, 1.25-1.89]).
The authors point out, however, that this study is observational and cannot make a causal link.
Clifford Kavinsky, MD, PhD, head of the Comprehensive Stroke and Cardiology Clinic at Rush University Medical Center, Chicago, told this news organization that much more research would need to be done to show convincingly that atrial cardiopathy causes dementia.
He called the findings “provocative in trying to understand in a general sense how cardiac dysfunction leads to dementia.”
“We all know heart failure leads to dementia, but now we see there may be a relationship with just dysfunction of the upper chambers,” he said.
Unresolved questions
But it still not clear is what is mediating the connection, who is at risk, and how the increased risk can be prevented, he said.
He said he also wonders whether the results eliminated all patients with atrial fibrillation, a point the authors acknowledge as well.
Researchers list in the limitations that “asymptomatic AFib or silent cerebral infarction may have been missed by the ARIC adjudication process.”
There is broad understanding that preventing heart disease is important for a wide array of reasons, Dr. Kavinsky noted, and one of the reasons is cognitive deterioration.
He said this study helps identify that “even dysfunction of the upper chambers of the heart contributes to the evolution of dementia.”
The study amplifies the need to shift to prevention with heart disease in general, and more specifically in atrial dysfunction, Dr. Kavinsky said, noting a lot of atrial dysfunction is mediated by underlying hypertension and coronary disease.
Researchers evaluated cognitive decline in all participants with a comprehensive array of neuropsychological tests and interviewed some of the patients.
“A diagnosis of dementia was generated based on testing results by a computer diagnostic algorithm and then decided upon by an expert based on the Diagnostic and Statistical Manual of Mental Disorders and the criteria outlined by the National Institutes of Health and the National Institutes of Health,” they write.
Dr. Johansen reported funding from National Institute of Neurological Disorders and Stroke. Study coauthor disclosures are listed in the paper. Dr. Kavinsky has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
“We cautiously suggest that an understanding of this relationship might provide a basis for new interventional strategies to help thwart the development of dementia,” the authors write.
The research, led by Michelle C. Johansen, MD, department of neurology, Johns Hopkins University, Baltimore, was published online in the Journal of the American Heart Association.
Atrial cardiopathy, characterized by abnormal size and function of the left atrium, has been associated with an increased risk of stroke and atrial fibrillation (AFib), and because both stroke and AFib are associated with an increased dementia risk, the authors write, it was important to investigate whether atrial cardiopathy is linked to dementia.
If that’s the case, they reasoned, the next question was whether that link is independent of AFib and stroke, and their new research suggests that it is.
For this analysis, the researchers conducted a prospective cohort analysis of participants in the Atherosclerosis Risk in Communities (ARIC) study who were attending visit 5 (2011-2013). During their fifth, sixth, and seventh clinical visits, the ARIC participants were evaluated for cognitive decline indicating dementia.
They studied a diverse population of 5,078 older adults living in four U.S. communities: Washington County, Md.; Forsyth County, N.C.; the northwestern suburbs of Minneapolis; and Jackson, Miss.
Just more than a third (34%) had atrial cardiopathy (average age, 75 years; 59% female; 21% Black) and 763 participants developed dementia.
Investigators found that atrial cardiopathy was significantly associated with dementia (adjusted hazard ratio, 1.35 [95% confidence interval, 1.16-1.58]).
They considered ARIC participants to have atrial cardiopathy if they had at least one of the following: P-wave terminal force greater than 5,000 mV·ms in ECG lead V1; NTproBNP greater than 250 pg/mL; or left atrial volume index greater than or equal to 34 mL/m2 by transthoracic echocardiography.
The risk of dementia was even stronger when the researchers defined cardiopathy by at least two biomarkers instead of one (aHR, 1.54 [95% CI, 1.25-1.89]).
The authors point out, however, that this study is observational and cannot make a causal link.
Clifford Kavinsky, MD, PhD, head of the Comprehensive Stroke and Cardiology Clinic at Rush University Medical Center, Chicago, told this news organization that much more research would need to be done to show convincingly that atrial cardiopathy causes dementia.
He called the findings “provocative in trying to understand in a general sense how cardiac dysfunction leads to dementia.”
“We all know heart failure leads to dementia, but now we see there may be a relationship with just dysfunction of the upper chambers,” he said.
Unresolved questions
But it still not clear is what is mediating the connection, who is at risk, and how the increased risk can be prevented, he said.
He said he also wonders whether the results eliminated all patients with atrial fibrillation, a point the authors acknowledge as well.
Researchers list in the limitations that “asymptomatic AFib or silent cerebral infarction may have been missed by the ARIC adjudication process.”
There is broad understanding that preventing heart disease is important for a wide array of reasons, Dr. Kavinsky noted, and one of the reasons is cognitive deterioration.
He said this study helps identify that “even dysfunction of the upper chambers of the heart contributes to the evolution of dementia.”
The study amplifies the need to shift to prevention with heart disease in general, and more specifically in atrial dysfunction, Dr. Kavinsky said, noting a lot of atrial dysfunction is mediated by underlying hypertension and coronary disease.
Researchers evaluated cognitive decline in all participants with a comprehensive array of neuropsychological tests and interviewed some of the patients.
“A diagnosis of dementia was generated based on testing results by a computer diagnostic algorithm and then decided upon by an expert based on the Diagnostic and Statistical Manual of Mental Disorders and the criteria outlined by the National Institutes of Health and the National Institutes of Health,” they write.
Dr. Johansen reported funding from National Institute of Neurological Disorders and Stroke. Study coauthor disclosures are listed in the paper. Dr. Kavinsky has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
“We cautiously suggest that an understanding of this relationship might provide a basis for new interventional strategies to help thwart the development of dementia,” the authors write.
The research, led by Michelle C. Johansen, MD, department of neurology, Johns Hopkins University, Baltimore, was published online in the Journal of the American Heart Association.
Atrial cardiopathy, characterized by abnormal size and function of the left atrium, has been associated with an increased risk of stroke and atrial fibrillation (AFib), and because both stroke and AFib are associated with an increased dementia risk, the authors write, it was important to investigate whether atrial cardiopathy is linked to dementia.
If that’s the case, they reasoned, the next question was whether that link is independent of AFib and stroke, and their new research suggests that it is.
For this analysis, the researchers conducted a prospective cohort analysis of participants in the Atherosclerosis Risk in Communities (ARIC) study who were attending visit 5 (2011-2013). During their fifth, sixth, and seventh clinical visits, the ARIC participants were evaluated for cognitive decline indicating dementia.
They studied a diverse population of 5,078 older adults living in four U.S. communities: Washington County, Md.; Forsyth County, N.C.; the northwestern suburbs of Minneapolis; and Jackson, Miss.
Just more than a third (34%) had atrial cardiopathy (average age, 75 years; 59% female; 21% Black) and 763 participants developed dementia.
Investigators found that atrial cardiopathy was significantly associated with dementia (adjusted hazard ratio, 1.35 [95% confidence interval, 1.16-1.58]).
They considered ARIC participants to have atrial cardiopathy if they had at least one of the following: P-wave terminal force greater than 5,000 mV·ms in ECG lead V1; NTproBNP greater than 250 pg/mL; or left atrial volume index greater than or equal to 34 mL/m2 by transthoracic echocardiography.
The risk of dementia was even stronger when the researchers defined cardiopathy by at least two biomarkers instead of one (aHR, 1.54 [95% CI, 1.25-1.89]).
The authors point out, however, that this study is observational and cannot make a causal link.
Clifford Kavinsky, MD, PhD, head of the Comprehensive Stroke and Cardiology Clinic at Rush University Medical Center, Chicago, told this news organization that much more research would need to be done to show convincingly that atrial cardiopathy causes dementia.
He called the findings “provocative in trying to understand in a general sense how cardiac dysfunction leads to dementia.”
“We all know heart failure leads to dementia, but now we see there may be a relationship with just dysfunction of the upper chambers,” he said.
Unresolved questions
But it still not clear is what is mediating the connection, who is at risk, and how the increased risk can be prevented, he said.
He said he also wonders whether the results eliminated all patients with atrial fibrillation, a point the authors acknowledge as well.
Researchers list in the limitations that “asymptomatic AFib or silent cerebral infarction may have been missed by the ARIC adjudication process.”
There is broad understanding that preventing heart disease is important for a wide array of reasons, Dr. Kavinsky noted, and one of the reasons is cognitive deterioration.
He said this study helps identify that “even dysfunction of the upper chambers of the heart contributes to the evolution of dementia.”
The study amplifies the need to shift to prevention with heart disease in general, and more specifically in atrial dysfunction, Dr. Kavinsky said, noting a lot of atrial dysfunction is mediated by underlying hypertension and coronary disease.
Researchers evaluated cognitive decline in all participants with a comprehensive array of neuropsychological tests and interviewed some of the patients.
“A diagnosis of dementia was generated based on testing results by a computer diagnostic algorithm and then decided upon by an expert based on the Diagnostic and Statistical Manual of Mental Disorders and the criteria outlined by the National Institutes of Health and the National Institutes of Health,” they write.
Dr. Johansen reported funding from National Institute of Neurological Disorders and Stroke. Study coauthor disclosures are listed in the paper. Dr. Kavinsky has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Children born very prematurely at higher risk to struggle in secondary school
A new study of educational attainment among U.K. primary and secondary schoolchildren born prematurely now provides some reassurance about the longer-term outcomes for many of these children.
For the study, published in the open-access journal PLOS ONE, researchers from the University of Oxford with colleagues from the University of Leicester and City University, London, used data from 11,695 children in the population-based UK Millennium Cohort Study, which included children born in England from Sept. 1, 2000 to Aug. 31, 2001. They analyzed data on educational attainment in primary school, at age 11, for 6,950 pupils and in secondary school, at age 16, for 7,131 pupils.
Preterm birth is a known risk factor for developmental impairment, lower educational performance and reduced academic attainment, with the impact proportional to the degree of prematurity. Not every child born prematurely will experience learning or developmental challenges, but studies of children born before 34 weeks gestation have shown that they are more likely to have cognitive difficulties, particularly poorer reading and maths skills, at primary school, and to have special educational needs by the end of primary education.
Elevated risk of all preterm children in primary school
Until now, few studies have followed these children through secondary school or examined the full spectrum of gestational ages at birth. Yet as neonatal care advances and more premature babies now survive, an average primary class in the United Kingdom now includes two preterm children.
Among the primary school children overall, 17.7% had not achieved their expected level in English and mathematics at age 11. Children born very preterm, before 32 weeks or at 32-33 weeks gestation, were more than twice as likely as full term children to fail to meet these benchmarks, with adjusted relative risks of 2.06 and 2.13, respectively. Those born late preterm, at 34-36 weeks, or early term, at 37-38 weeks, were at lesser risk, with RRs of 1.18 and 1.21, respectively.
By the end of secondary school, 45.2% of pupils had not passed the benchmark of at least five General Certificate of Secondary Education (GCSE) examinations, including English and mathematics. The RR for children born very preterm, compared with full term children, was 1.26, with 60% of students in this group failing to achieve five GCSEs. However, children born at gestations between 32 and 38 weeks were not at elevated risk, compared with children born at full term.
Risk persists to secondary level only for very preterm children
A similar pattern was seen with English and mathematics analyzed separately, with no additional risk of not passing among children born at 32 weeks or above, but adjusted RRs of 1.33 for not passing English and 1.42 for not passing maths among pupils who had been born very preterm, compared with full term children.
“All children born before full term are more likely to have poorer attainment during primary school, compared with children born full term (39-41 weeks), but only children born very preterm (before 32 weeks) remain at risk of poor attainment at the end of secondary schooling,” the researchers concluded.
“Further studies are needed in order to confirm this result,” they acknowledge. They suggested their results could be explained by catch-up in academic attainment among children born moderately or late preterm or at early term. However, “very preterm children appear to be a high-risk group with persistent difficulties in terms of educational outcomes,” they said, noting that even this risk was of lower magnitude than the reduced attainment scores they found among pupils eligible for free school meals, meaning those from disadvantaged socioeconomic backgrounds.
Extra educational support needed
The researchers concluded: “Children born very preterm may benefit from screening for cognitive and language difficulties prior to school entry to guide the provision of additional support during schooling.” In addition, those born very preterm “may require additional educational support throughout compulsory schooling.”
Commenting on the study, Caroline Lee-Davey, chief executive of premature baby charity Bliss, told this news organization: “Every child who is born premature is unique, and their development and achievements will be individual to them. However, these new findings are significant and add to our understanding of how prematurity is related to longer-term educational attainment, particularly for children who were born very preterm.”
“Most importantly, they highlight the need for all children who were born premature – and particularly those who were born before 32 weeks – to have access to early support. This means ensuring all eligible babies receive a follow-up check at 2 and 4 years as recommended by NICE and for early years and educational professionals to be aware of the relationship between premature birth and development.”
“We know how concerning these findings might be for families with babies and very young children right now. That’s why Bliss has developed a suite of information to support families as they make choices about their child’s education.”
A version of this article first appeared on Medscape UK.
A new study of educational attainment among U.K. primary and secondary schoolchildren born prematurely now provides some reassurance about the longer-term outcomes for many of these children.
For the study, published in the open-access journal PLOS ONE, researchers from the University of Oxford with colleagues from the University of Leicester and City University, London, used data from 11,695 children in the population-based UK Millennium Cohort Study, which included children born in England from Sept. 1, 2000 to Aug. 31, 2001. They analyzed data on educational attainment in primary school, at age 11, for 6,950 pupils and in secondary school, at age 16, for 7,131 pupils.
Preterm birth is a known risk factor for developmental impairment, lower educational performance and reduced academic attainment, with the impact proportional to the degree of prematurity. Not every child born prematurely will experience learning or developmental challenges, but studies of children born before 34 weeks gestation have shown that they are more likely to have cognitive difficulties, particularly poorer reading and maths skills, at primary school, and to have special educational needs by the end of primary education.
Elevated risk of all preterm children in primary school
Until now, few studies have followed these children through secondary school or examined the full spectrum of gestational ages at birth. Yet as neonatal care advances and more premature babies now survive, an average primary class in the United Kingdom now includes two preterm children.
Among the primary school children overall, 17.7% had not achieved their expected level in English and mathematics at age 11. Children born very preterm, before 32 weeks or at 32-33 weeks gestation, were more than twice as likely as full term children to fail to meet these benchmarks, with adjusted relative risks of 2.06 and 2.13, respectively. Those born late preterm, at 34-36 weeks, or early term, at 37-38 weeks, were at lesser risk, with RRs of 1.18 and 1.21, respectively.
By the end of secondary school, 45.2% of pupils had not passed the benchmark of at least five General Certificate of Secondary Education (GCSE) examinations, including English and mathematics. The RR for children born very preterm, compared with full term children, was 1.26, with 60% of students in this group failing to achieve five GCSEs. However, children born at gestations between 32 and 38 weeks were not at elevated risk, compared with children born at full term.
Risk persists to secondary level only for very preterm children
A similar pattern was seen with English and mathematics analyzed separately, with no additional risk of not passing among children born at 32 weeks or above, but adjusted RRs of 1.33 for not passing English and 1.42 for not passing maths among pupils who had been born very preterm, compared with full term children.
“All children born before full term are more likely to have poorer attainment during primary school, compared with children born full term (39-41 weeks), but only children born very preterm (before 32 weeks) remain at risk of poor attainment at the end of secondary schooling,” the researchers concluded.
“Further studies are needed in order to confirm this result,” they acknowledge. They suggested their results could be explained by catch-up in academic attainment among children born moderately or late preterm or at early term. However, “very preterm children appear to be a high-risk group with persistent difficulties in terms of educational outcomes,” they said, noting that even this risk was of lower magnitude than the reduced attainment scores they found among pupils eligible for free school meals, meaning those from disadvantaged socioeconomic backgrounds.
Extra educational support needed
The researchers concluded: “Children born very preterm may benefit from screening for cognitive and language difficulties prior to school entry to guide the provision of additional support during schooling.” In addition, those born very preterm “may require additional educational support throughout compulsory schooling.”
Commenting on the study, Caroline Lee-Davey, chief executive of premature baby charity Bliss, told this news organization: “Every child who is born premature is unique, and their development and achievements will be individual to them. However, these new findings are significant and add to our understanding of how prematurity is related to longer-term educational attainment, particularly for children who were born very preterm.”
“Most importantly, they highlight the need for all children who were born premature – and particularly those who were born before 32 weeks – to have access to early support. This means ensuring all eligible babies receive a follow-up check at 2 and 4 years as recommended by NICE and for early years and educational professionals to be aware of the relationship between premature birth and development.”
“We know how concerning these findings might be for families with babies and very young children right now. That’s why Bliss has developed a suite of information to support families as they make choices about their child’s education.”
A version of this article first appeared on Medscape UK.
A new study of educational attainment among U.K. primary and secondary schoolchildren born prematurely now provides some reassurance about the longer-term outcomes for many of these children.
For the study, published in the open-access journal PLOS ONE, researchers from the University of Oxford with colleagues from the University of Leicester and City University, London, used data from 11,695 children in the population-based UK Millennium Cohort Study, which included children born in England from Sept. 1, 2000 to Aug. 31, 2001. They analyzed data on educational attainment in primary school, at age 11, for 6,950 pupils and in secondary school, at age 16, for 7,131 pupils.
Preterm birth is a known risk factor for developmental impairment, lower educational performance and reduced academic attainment, with the impact proportional to the degree of prematurity. Not every child born prematurely will experience learning or developmental challenges, but studies of children born before 34 weeks gestation have shown that they are more likely to have cognitive difficulties, particularly poorer reading and maths skills, at primary school, and to have special educational needs by the end of primary education.
Elevated risk of all preterm children in primary school
Until now, few studies have followed these children through secondary school or examined the full spectrum of gestational ages at birth. Yet as neonatal care advances and more premature babies now survive, an average primary class in the United Kingdom now includes two preterm children.
Among the primary school children overall, 17.7% had not achieved their expected level in English and mathematics at age 11. Children born very preterm, before 32 weeks or at 32-33 weeks gestation, were more than twice as likely as full term children to fail to meet these benchmarks, with adjusted relative risks of 2.06 and 2.13, respectively. Those born late preterm, at 34-36 weeks, or early term, at 37-38 weeks, were at lesser risk, with RRs of 1.18 and 1.21, respectively.
By the end of secondary school, 45.2% of pupils had not passed the benchmark of at least five General Certificate of Secondary Education (GCSE) examinations, including English and mathematics. The RR for children born very preterm, compared with full term children, was 1.26, with 60% of students in this group failing to achieve five GCSEs. However, children born at gestations between 32 and 38 weeks were not at elevated risk, compared with children born at full term.
Risk persists to secondary level only for very preterm children
A similar pattern was seen with English and mathematics analyzed separately, with no additional risk of not passing among children born at 32 weeks or above, but adjusted RRs of 1.33 for not passing English and 1.42 for not passing maths among pupils who had been born very preterm, compared with full term children.
“All children born before full term are more likely to have poorer attainment during primary school, compared with children born full term (39-41 weeks), but only children born very preterm (before 32 weeks) remain at risk of poor attainment at the end of secondary schooling,” the researchers concluded.
“Further studies are needed in order to confirm this result,” they acknowledge. They suggested their results could be explained by catch-up in academic attainment among children born moderately or late preterm or at early term. However, “very preterm children appear to be a high-risk group with persistent difficulties in terms of educational outcomes,” they said, noting that even this risk was of lower magnitude than the reduced attainment scores they found among pupils eligible for free school meals, meaning those from disadvantaged socioeconomic backgrounds.
Extra educational support needed
The researchers concluded: “Children born very preterm may benefit from screening for cognitive and language difficulties prior to school entry to guide the provision of additional support during schooling.” In addition, those born very preterm “may require additional educational support throughout compulsory schooling.”
Commenting on the study, Caroline Lee-Davey, chief executive of premature baby charity Bliss, told this news organization: “Every child who is born premature is unique, and their development and achievements will be individual to them. However, these new findings are significant and add to our understanding of how prematurity is related to longer-term educational attainment, particularly for children who were born very preterm.”
“Most importantly, they highlight the need for all children who were born premature – and particularly those who were born before 32 weeks – to have access to early support. This means ensuring all eligible babies receive a follow-up check at 2 and 4 years as recommended by NICE and for early years and educational professionals to be aware of the relationship between premature birth and development.”
“We know how concerning these findings might be for families with babies and very young children right now. That’s why Bliss has developed a suite of information to support families as they make choices about their child’s education.”
A version of this article first appeared on Medscape UK.
FROM PLOS ONE
Early dementia but no specialists: Reinforcements needed?
Patients in rural areas are also less likely to see psychologists and undergo neuropsychological testing, according to the study, published in JAMA Network Open.
Patients who forgo such specialist visits and testing may be missing information about their condition that could help them prepare for changes in job responsibilities and future care decisions, said Wendy Yi Xu, PhD, of The Ohio State University, Columbus, who led the research.
“A lot of them are still in the workforce,” Dr. Xu said. Patients in the study were an average age of 56 years, well before the conventional age of retirement.
Location, location, location
To examine rural versus urban differences in the use of diagnostic tests and health care visits for early onset Alzheimer’s disease and related dementias, Dr. Xu and colleagues analyzed commercial claims data from 2012-2018. They identified more than 71,000 patients aged 40-64 years with those conditions and focused on health care use by 7,311 patients in urban areas and 1,119 in rural areas within 90 days of a new dementia diagnosis.
The proportion who received neuropsychological testing was 19% among urban patients and 16% among rural patients. Psychological assessments, which are less specialized and detailed than neuropsychological testing, and brain imaging occurred at similar rates in both groups. Similar proportions of rural and urban patients visited neurologists (17.7% and 17.96%, respectively) and psychiatrists (6.02% and 6.47%).
But more urban patients than rural patients visited a psychologist, at 19% versus 15%, according to the researchers.
Approximately 18% of patients in rural areas saw a primary care provider without visiting other specialists, compared with 13% in urban areas.
The researchers found that rural patients were significantly less likely to undergo neuropsychological testing (odds ratio, 0.83; 95% confidence interval, 0.70-0.98) or see a psychologist (OR, 0.72; 95% CI, 0.60-0.85).
Similarly, rural patients had significantly higher odds of having only primary care providers involved in the diagnosis of dementia and symptom management (OR, 1.40; 95% CI, 1.19-1.66).
Addressing workforce deficiencies
More primary care training in dementia care and collaboration with specialist colleagues could help address differences in care, Dr. Xu’s group writes. Such efforts are already underway.
In 2018, the Alzheimer’s Association launched telementoring programs focused on dementia care using the Project ECHO (Extension for Community Healthcare Outcomes) model. Researchers originally developed Project ECHO at the University of New Mexico in 2003 to teach primary care clinicians in remote settings how to treat patients infected with the hepatitis C virus.
With the Alzheimer’s and Dementia Care ECHO Program for Clinicians, primary care clinicians can participate in interactive case-based video conferencing sessions to better understand dementia and how to provide high-quality care in community settings, according to the association.
The program covers guidelines for diagnosis, disclosure, and follow-up; the initiation of care planning; managing disease-related challenges; and resources for patients and caregivers.
Since 2018, nearly 100 primary care practices in the United States have completed training in dementia care using Project ECHO, said Morgan Daven, vice president of health systems for the Alzheimer’s Association. Many cases featured in the program are challenging, he added.
“With primary care being on the front lines, it is really important that primary care physicians are equipped to do what they can to detect or diagnose and know when to refer,” Mr. Daven said.
The association has compiled other resources for clinicians as well.
A 2020 report from the association examined the role that primary care physicians play in dementia care. One survey found that 82% of primary care physicians consider themselves on the front lines of providing care for patients with dementia.
Meanwhile, about half say medical professionals are not prepared to meet rising demands associated with Alzheimer’s disease and dementia care.
Mr. Daven said the geographic disparities Dr. Xu and colleagues found are unsurprising. More than half of primary care physicians who care for people with Alzheimer’s disease say dementia specialists in their communities cannot meet demand. The problem is more urgent in rural areas. Roughly half of nonmetropolitan counties in the United States lack a practicing psychologist, according to a 2018 study published in the American Journal of Preventive Medicine.
“We really need to approach this on both sides – build the capacity in primary care, but we also need to address the dementia care specialty shortages,” Mr. Daven said.
The lack of obvious differences in access to neurologists in the new study “was surprising, given the more than fourfold difference between urban and rural areas in the supply of neurologists,” the researchers note. Health plans may maintain more access to neurologists than psychologists because of relatively higher reimbursement for neurologists, they observed.
One of the study coauthors disclosed ties to Aveanna Healthcare, a company that delivers home health and hospice care.
A version of this article first appeared on Medscape.com.
Patients in rural areas are also less likely to see psychologists and undergo neuropsychological testing, according to the study, published in JAMA Network Open.
Patients who forgo such specialist visits and testing may be missing information about their condition that could help them prepare for changes in job responsibilities and future care decisions, said Wendy Yi Xu, PhD, of The Ohio State University, Columbus, who led the research.
“A lot of them are still in the workforce,” Dr. Xu said. Patients in the study were an average age of 56 years, well before the conventional age of retirement.
Location, location, location
To examine rural versus urban differences in the use of diagnostic tests and health care visits for early onset Alzheimer’s disease and related dementias, Dr. Xu and colleagues analyzed commercial claims data from 2012-2018. They identified more than 71,000 patients aged 40-64 years with those conditions and focused on health care use by 7,311 patients in urban areas and 1,119 in rural areas within 90 days of a new dementia diagnosis.
The proportion who received neuropsychological testing was 19% among urban patients and 16% among rural patients. Psychological assessments, which are less specialized and detailed than neuropsychological testing, and brain imaging occurred at similar rates in both groups. Similar proportions of rural and urban patients visited neurologists (17.7% and 17.96%, respectively) and psychiatrists (6.02% and 6.47%).
But more urban patients than rural patients visited a psychologist, at 19% versus 15%, according to the researchers.
Approximately 18% of patients in rural areas saw a primary care provider without visiting other specialists, compared with 13% in urban areas.
The researchers found that rural patients were significantly less likely to undergo neuropsychological testing (odds ratio, 0.83; 95% confidence interval, 0.70-0.98) or see a psychologist (OR, 0.72; 95% CI, 0.60-0.85).
Similarly, rural patients had significantly higher odds of having only primary care providers involved in the diagnosis of dementia and symptom management (OR, 1.40; 95% CI, 1.19-1.66).
Addressing workforce deficiencies
More primary care training in dementia care and collaboration with specialist colleagues could help address differences in care, Dr. Xu’s group writes. Such efforts are already underway.
In 2018, the Alzheimer’s Association launched telementoring programs focused on dementia care using the Project ECHO (Extension for Community Healthcare Outcomes) model. Researchers originally developed Project ECHO at the University of New Mexico in 2003 to teach primary care clinicians in remote settings how to treat patients infected with the hepatitis C virus.
With the Alzheimer’s and Dementia Care ECHO Program for Clinicians, primary care clinicians can participate in interactive case-based video conferencing sessions to better understand dementia and how to provide high-quality care in community settings, according to the association.
The program covers guidelines for diagnosis, disclosure, and follow-up; the initiation of care planning; managing disease-related challenges; and resources for patients and caregivers.
Since 2018, nearly 100 primary care practices in the United States have completed training in dementia care using Project ECHO, said Morgan Daven, vice president of health systems for the Alzheimer’s Association. Many cases featured in the program are challenging, he added.
“With primary care being on the front lines, it is really important that primary care physicians are equipped to do what they can to detect or diagnose and know when to refer,” Mr. Daven said.
The association has compiled other resources for clinicians as well.
A 2020 report from the association examined the role that primary care physicians play in dementia care. One survey found that 82% of primary care physicians consider themselves on the front lines of providing care for patients with dementia.
Meanwhile, about half say medical professionals are not prepared to meet rising demands associated with Alzheimer’s disease and dementia care.
Mr. Daven said the geographic disparities Dr. Xu and colleagues found are unsurprising. More than half of primary care physicians who care for people with Alzheimer’s disease say dementia specialists in their communities cannot meet demand. The problem is more urgent in rural areas. Roughly half of nonmetropolitan counties in the United States lack a practicing psychologist, according to a 2018 study published in the American Journal of Preventive Medicine.
“We really need to approach this on both sides – build the capacity in primary care, but we also need to address the dementia care specialty shortages,” Mr. Daven said.
The lack of obvious differences in access to neurologists in the new study “was surprising, given the more than fourfold difference between urban and rural areas in the supply of neurologists,” the researchers note. Health plans may maintain more access to neurologists than psychologists because of relatively higher reimbursement for neurologists, they observed.
One of the study coauthors disclosed ties to Aveanna Healthcare, a company that delivers home health and hospice care.
A version of this article first appeared on Medscape.com.
Patients in rural areas are also less likely to see psychologists and undergo neuropsychological testing, according to the study, published in JAMA Network Open.
Patients who forgo such specialist visits and testing may be missing information about their condition that could help them prepare for changes in job responsibilities and future care decisions, said Wendy Yi Xu, PhD, of The Ohio State University, Columbus, who led the research.
“A lot of them are still in the workforce,” Dr. Xu said. Patients in the study were an average age of 56 years, well before the conventional age of retirement.
Location, location, location
To examine rural versus urban differences in the use of diagnostic tests and health care visits for early onset Alzheimer’s disease and related dementias, Dr. Xu and colleagues analyzed commercial claims data from 2012-2018. They identified more than 71,000 patients aged 40-64 years with those conditions and focused on health care use by 7,311 patients in urban areas and 1,119 in rural areas within 90 days of a new dementia diagnosis.
The proportion who received neuropsychological testing was 19% among urban patients and 16% among rural patients. Psychological assessments, which are less specialized and detailed than neuropsychological testing, and brain imaging occurred at similar rates in both groups. Similar proportions of rural and urban patients visited neurologists (17.7% and 17.96%, respectively) and psychiatrists (6.02% and 6.47%).
But more urban patients than rural patients visited a psychologist, at 19% versus 15%, according to the researchers.
Approximately 18% of patients in rural areas saw a primary care provider without visiting other specialists, compared with 13% in urban areas.
The researchers found that rural patients were significantly less likely to undergo neuropsychological testing (odds ratio, 0.83; 95% confidence interval, 0.70-0.98) or see a psychologist (OR, 0.72; 95% CI, 0.60-0.85).
Similarly, rural patients had significantly higher odds of having only primary care providers involved in the diagnosis of dementia and symptom management (OR, 1.40; 95% CI, 1.19-1.66).
Addressing workforce deficiencies
More primary care training in dementia care and collaboration with specialist colleagues could help address differences in care, Dr. Xu’s group writes. Such efforts are already underway.
In 2018, the Alzheimer’s Association launched telementoring programs focused on dementia care using the Project ECHO (Extension for Community Healthcare Outcomes) model. Researchers originally developed Project ECHO at the University of New Mexico in 2003 to teach primary care clinicians in remote settings how to treat patients infected with the hepatitis C virus.
With the Alzheimer’s and Dementia Care ECHO Program for Clinicians, primary care clinicians can participate in interactive case-based video conferencing sessions to better understand dementia and how to provide high-quality care in community settings, according to the association.
The program covers guidelines for diagnosis, disclosure, and follow-up; the initiation of care planning; managing disease-related challenges; and resources for patients and caregivers.
Since 2018, nearly 100 primary care practices in the United States have completed training in dementia care using Project ECHO, said Morgan Daven, vice president of health systems for the Alzheimer’s Association. Many cases featured in the program are challenging, he added.
“With primary care being on the front lines, it is really important that primary care physicians are equipped to do what they can to detect or diagnose and know when to refer,” Mr. Daven said.
The association has compiled other resources for clinicians as well.
A 2020 report from the association examined the role that primary care physicians play in dementia care. One survey found that 82% of primary care physicians consider themselves on the front lines of providing care for patients with dementia.
Meanwhile, about half say medical professionals are not prepared to meet rising demands associated with Alzheimer’s disease and dementia care.
Mr. Daven said the geographic disparities Dr. Xu and colleagues found are unsurprising. More than half of primary care physicians who care for people with Alzheimer’s disease say dementia specialists in their communities cannot meet demand. The problem is more urgent in rural areas. Roughly half of nonmetropolitan counties in the United States lack a practicing psychologist, according to a 2018 study published in the American Journal of Preventive Medicine.
“We really need to approach this on both sides – build the capacity in primary care, but we also need to address the dementia care specialty shortages,” Mr. Daven said.
The lack of obvious differences in access to neurologists in the new study “was surprising, given the more than fourfold difference between urban and rural areas in the supply of neurologists,” the researchers note. Health plans may maintain more access to neurologists than psychologists because of relatively higher reimbursement for neurologists, they observed.
One of the study coauthors disclosed ties to Aveanna Healthcare, a company that delivers home health and hospice care.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN
Primary care now offering physicians the 26.7-hour day
Taking ‘not enough hours in the day’ to new heights
It’s no secret that there’s a big doctor shortage in the United States. Going through medical school is long, expensive, and stressful, and it’s not like those long, stressful hours stop once you finally do get that degree. There is, however, an excellent reason to take that dive into doctorhood: You’ll gain mastery over time itself.
A study from the University of Chicago, Johns Hopkins University, and Imperial College London has revealed the truth. By using data pulled from the National Health and Nutrition Examination Survey, the researchers found that primary care physicians who see an average number of patients and follow all the current national guidelines for preventive care, chronic disease care, and acute care – plus administrative tasks – must work 26.7 hours a day. That works out to 14.1 hours of preventive care, 7.2 hours of chronic disease care, 2.2 hours of acute care, and 3.2 hours of documentation and inbox management.
Astute readers may note that this is a bit more than the traditional 8-hour workday. It is, in fact, more hours than there actually are in a day. As it turns out, Doctor Strange is more of a documentary than …
Hang on, we’re receiving word that doctors are not in fact wizards who can bend time and space to their will, nor are they sitting on a stash of Time-Turners they saved from the Ministry of Magic before Voldemort destroyed them all. They are, according to the study, overworked and overburdened with too many things and too little time. This is why outcomes haven’t improved despite technological advances and why burnout is so common. We’d be burned out too, having to work temporally impossible hours.
The study authors suggested a team-based approach to medicine that would spread the workload out to nurses, physician assistants, dietitians, etc., estimating that about two-thirds of what a primary care physician does can be handled by someone else. A team-based approach would reduce the physician’s required hours down to 9.3 hours a day, which is at least physically possible. It’s either that or we make the day longer, which sounds like the plot of an episode of Futurama. Swap overwork for global warming and a longer day for a longer year and it is actually the plot of an episode of Futurama.
After a hard day of thinking, brains need their rest
Do you ever feel like you have no more capacity to think or make any more decisions after a long day at work? Do you need a few extra cups of coffee to even make it through the day, even though you’re mostly just sitting around talking and typing? Have we got the research for you: Mental exhaustion is an actual thing. Imagine that double whammy of having a job that’s physically and mentally demanding.
A recent study in Current Biology explained why we feel so exhausted after doing something mentally demanding for several hours. Over that time, glutamate builds up in synapses of the prefrontal cortex, which affects our decision making and leads to cognitive lethargy. Your brain eventually becomes more interested in tasks that are less mentally fatiguing, and that’s probably why you’re reading this LOTME right now instead of getting back to work.
“Our findings show that cognitive work results in a true functional alteration – accumulation of noxious substances – so fatigue would indeed be a signal that makes us stop working but for a different purpose: to preserve the integrity of brain functioning,” senior author Mathias Pessiglione of Pitié-Salpêtrière University, Paris, said in a written statement.
The group of researchers conducted studies by using magnetic resonance spectroscopy to look at two groups of people over the course of a workday: One group had mentally tasking jobs and one didn’t. Those who had to think harder for their jobs had more signs of fatigue, such as reduced pupil dilation and glutamate in synapses of the prefrontal cortex. They also looked for more rewards that required less thinking.
For those whose mentally exhausting jobs probably won’t get better or change, the researchers suggest getting as much rest as possible. Those who don’t have that option will have to continue drinking those 7 cups of coffee a day. ... and reading LOTME.
Hmm, might be a new tagline for us in there somewhere. LOTME: Tired brains love us? When you’re too tired to think, think of LOTME? You can’t spell mental exhaustion without L-O-T-M-E?
Testosterone shows its warm and fuzzy side
Stereotypically, men are loud, knuckle-dragging Neanderthals. The hair coming out of our faces is kind of a dead giveaway, right? We grunt, we scratch, we start wars, we watch sports on TV. But why? It’s the testosterone. Everyone knows that. Testosterone makes men aggressive … or does it?
Since this sort of research generally isn’t done with actual men, investigators at Emory University used Mongolian gerbils. The advantage being that males exhibit cuddling behavior after females become pregnant and they don’t watch a lot of sports on TV. They introduced a male and female gerbil, who then formed a pair bond and the female became pregnant. When the male started displaying cuddling behaviors, the researchers injected him with testosterone, expecting to see his antisocial side.
“Instead, we were surprised that a male gerbil became even more cuddly and prosocial with his partner. He became like ‘super partner,’ ” lead author Aubrey Kelly, PhD, said in a written statement from the university.
For the next experiment, the female was removed and another male was introduced to a male who had already received a testosterone injection. That male was surprisingly unaggressive toward the intruder, at least initially. Then he received a second injection of testosterone. “It was like they suddenly woke up and realized they weren’t supposed to be friendly in that context,” Dr. Kelly said.
The testosterone seemed to influence the activity of oxytocin, the so-called “love hormone,” the investigators suggested. “It’s surprising because normally we think of testosterone as increasing sexual behaviors and aggression. But we’ve shown that it can have more nuanced effects, depending on the social context.”
The researchers were not as surprised when their use of the phrase “super partner” led to a bidding war between DC and Marvel. Then came the contact from the Department of Defense, wondering about weaponized testosterone: Would it be possible for some sort of bomb to turn Vlad “the Impaler” Putin into Vlad “the Cuddler” Putin?
Are instruments spreading the sounds of COVID?
COVID restrictions are practically a thing of the past now. With more people laxed on being in close proximity to each other and the CDC not even recommending social distancing anymore, live concerts and events are back in full swing. But with new variants on the rise and people being a little more cautious, should we be worried about musical instruments spreading COVID?
Yes and no.
A study published in Physics of Fluids looked at wind instruments specifically and how much aerosol is produced and dispersed when playing them. For the study, the investigators measured fog particles with a laser and aerosol concentration with a particle counter to see how fast these particles decay in the air from the distance of the instrument.
Musicians in an orchestra typically would sit close together to produce the best sound, but with COVID that became an issue, senior author Paulo Arratia of the University of Pennsylvania, Philadelphia, noted in a separate written statement. By looking at the distance traveled by the particles coming from a single instrument and how quickly they decayed, they could determine if sitting in close proximity is an actual threat.
Well, the threat was no greater than talking to someone face to face. Particle exit speeds were lower than for a cough or a sneeze, and the maximum decay length was 2 meters from the instrument’s opening.
But that’s just one instrument: What kind of impact does a whole orchestra have on a space? The researchers are looking into that too, but for now they suggest that musicians continue to stay 6 feet away from each other.
So, yeah, there is a threat, but it’s probably safer for you to see that orchestra than have someone sneeze on you.
Music to our ears.
Taking ‘not enough hours in the day’ to new heights
It’s no secret that there’s a big doctor shortage in the United States. Going through medical school is long, expensive, and stressful, and it’s not like those long, stressful hours stop once you finally do get that degree. There is, however, an excellent reason to take that dive into doctorhood: You’ll gain mastery over time itself.
A study from the University of Chicago, Johns Hopkins University, and Imperial College London has revealed the truth. By using data pulled from the National Health and Nutrition Examination Survey, the researchers found that primary care physicians who see an average number of patients and follow all the current national guidelines for preventive care, chronic disease care, and acute care – plus administrative tasks – must work 26.7 hours a day. That works out to 14.1 hours of preventive care, 7.2 hours of chronic disease care, 2.2 hours of acute care, and 3.2 hours of documentation and inbox management.
Astute readers may note that this is a bit more than the traditional 8-hour workday. It is, in fact, more hours than there actually are in a day. As it turns out, Doctor Strange is more of a documentary than …
Hang on, we’re receiving word that doctors are not in fact wizards who can bend time and space to their will, nor are they sitting on a stash of Time-Turners they saved from the Ministry of Magic before Voldemort destroyed them all. They are, according to the study, overworked and overburdened with too many things and too little time. This is why outcomes haven’t improved despite technological advances and why burnout is so common. We’d be burned out too, having to work temporally impossible hours.
The study authors suggested a team-based approach to medicine that would spread the workload out to nurses, physician assistants, dietitians, etc., estimating that about two-thirds of what a primary care physician does can be handled by someone else. A team-based approach would reduce the physician’s required hours down to 9.3 hours a day, which is at least physically possible. It’s either that or we make the day longer, which sounds like the plot of an episode of Futurama. Swap overwork for global warming and a longer day for a longer year and it is actually the plot of an episode of Futurama.
After a hard day of thinking, brains need their rest
Do you ever feel like you have no more capacity to think or make any more decisions after a long day at work? Do you need a few extra cups of coffee to even make it through the day, even though you’re mostly just sitting around talking and typing? Have we got the research for you: Mental exhaustion is an actual thing. Imagine that double whammy of having a job that’s physically and mentally demanding.
A recent study in Current Biology explained why we feel so exhausted after doing something mentally demanding for several hours. Over that time, glutamate builds up in synapses of the prefrontal cortex, which affects our decision making and leads to cognitive lethargy. Your brain eventually becomes more interested in tasks that are less mentally fatiguing, and that’s probably why you’re reading this LOTME right now instead of getting back to work.
“Our findings show that cognitive work results in a true functional alteration – accumulation of noxious substances – so fatigue would indeed be a signal that makes us stop working but for a different purpose: to preserve the integrity of brain functioning,” senior author Mathias Pessiglione of Pitié-Salpêtrière University, Paris, said in a written statement.
The group of researchers conducted studies by using magnetic resonance spectroscopy to look at two groups of people over the course of a workday: One group had mentally tasking jobs and one didn’t. Those who had to think harder for their jobs had more signs of fatigue, such as reduced pupil dilation and glutamate in synapses of the prefrontal cortex. They also looked for more rewards that required less thinking.
For those whose mentally exhausting jobs probably won’t get better or change, the researchers suggest getting as much rest as possible. Those who don’t have that option will have to continue drinking those 7 cups of coffee a day. ... and reading LOTME.
Hmm, might be a new tagline for us in there somewhere. LOTME: Tired brains love us? When you’re too tired to think, think of LOTME? You can’t spell mental exhaustion without L-O-T-M-E?
Testosterone shows its warm and fuzzy side
Stereotypically, men are loud, knuckle-dragging Neanderthals. The hair coming out of our faces is kind of a dead giveaway, right? We grunt, we scratch, we start wars, we watch sports on TV. But why? It’s the testosterone. Everyone knows that. Testosterone makes men aggressive … or does it?
Since this sort of research generally isn’t done with actual men, investigators at Emory University used Mongolian gerbils. The advantage being that males exhibit cuddling behavior after females become pregnant and they don’t watch a lot of sports on TV. They introduced a male and female gerbil, who then formed a pair bond and the female became pregnant. When the male started displaying cuddling behaviors, the researchers injected him with testosterone, expecting to see his antisocial side.
“Instead, we were surprised that a male gerbil became even more cuddly and prosocial with his partner. He became like ‘super partner,’ ” lead author Aubrey Kelly, PhD, said in a written statement from the university.
For the next experiment, the female was removed and another male was introduced to a male who had already received a testosterone injection. That male was surprisingly unaggressive toward the intruder, at least initially. Then he received a second injection of testosterone. “It was like they suddenly woke up and realized they weren’t supposed to be friendly in that context,” Dr. Kelly said.
The testosterone seemed to influence the activity of oxytocin, the so-called “love hormone,” the investigators suggested. “It’s surprising because normally we think of testosterone as increasing sexual behaviors and aggression. But we’ve shown that it can have more nuanced effects, depending on the social context.”
The researchers were not as surprised when their use of the phrase “super partner” led to a bidding war between DC and Marvel. Then came the contact from the Department of Defense, wondering about weaponized testosterone: Would it be possible for some sort of bomb to turn Vlad “the Impaler” Putin into Vlad “the Cuddler” Putin?
Are instruments spreading the sounds of COVID?
COVID restrictions are practically a thing of the past now. With more people laxed on being in close proximity to each other and the CDC not even recommending social distancing anymore, live concerts and events are back in full swing. But with new variants on the rise and people being a little more cautious, should we be worried about musical instruments spreading COVID?
Yes and no.
A study published in Physics of Fluids looked at wind instruments specifically and how much aerosol is produced and dispersed when playing them. For the study, the investigators measured fog particles with a laser and aerosol concentration with a particle counter to see how fast these particles decay in the air from the distance of the instrument.
Musicians in an orchestra typically would sit close together to produce the best sound, but with COVID that became an issue, senior author Paulo Arratia of the University of Pennsylvania, Philadelphia, noted in a separate written statement. By looking at the distance traveled by the particles coming from a single instrument and how quickly they decayed, they could determine if sitting in close proximity is an actual threat.
Well, the threat was no greater than talking to someone face to face. Particle exit speeds were lower than for a cough or a sneeze, and the maximum decay length was 2 meters from the instrument’s opening.
But that’s just one instrument: What kind of impact does a whole orchestra have on a space? The researchers are looking into that too, but for now they suggest that musicians continue to stay 6 feet away from each other.
So, yeah, there is a threat, but it’s probably safer for you to see that orchestra than have someone sneeze on you.
Music to our ears.
Taking ‘not enough hours in the day’ to new heights
It’s no secret that there’s a big doctor shortage in the United States. Going through medical school is long, expensive, and stressful, and it’s not like those long, stressful hours stop once you finally do get that degree. There is, however, an excellent reason to take that dive into doctorhood: You’ll gain mastery over time itself.
A study from the University of Chicago, Johns Hopkins University, and Imperial College London has revealed the truth. By using data pulled from the National Health and Nutrition Examination Survey, the researchers found that primary care physicians who see an average number of patients and follow all the current national guidelines for preventive care, chronic disease care, and acute care – plus administrative tasks – must work 26.7 hours a day. That works out to 14.1 hours of preventive care, 7.2 hours of chronic disease care, 2.2 hours of acute care, and 3.2 hours of documentation and inbox management.
Astute readers may note that this is a bit more than the traditional 8-hour workday. It is, in fact, more hours than there actually are in a day. As it turns out, Doctor Strange is more of a documentary than …
Hang on, we’re receiving word that doctors are not in fact wizards who can bend time and space to their will, nor are they sitting on a stash of Time-Turners they saved from the Ministry of Magic before Voldemort destroyed them all. They are, according to the study, overworked and overburdened with too many things and too little time. This is why outcomes haven’t improved despite technological advances and why burnout is so common. We’d be burned out too, having to work temporally impossible hours.
The study authors suggested a team-based approach to medicine that would spread the workload out to nurses, physician assistants, dietitians, etc., estimating that about two-thirds of what a primary care physician does can be handled by someone else. A team-based approach would reduce the physician’s required hours down to 9.3 hours a day, which is at least physically possible. It’s either that or we make the day longer, which sounds like the plot of an episode of Futurama. Swap overwork for global warming and a longer day for a longer year and it is actually the plot of an episode of Futurama.
After a hard day of thinking, brains need their rest
Do you ever feel like you have no more capacity to think or make any more decisions after a long day at work? Do you need a few extra cups of coffee to even make it through the day, even though you’re mostly just sitting around talking and typing? Have we got the research for you: Mental exhaustion is an actual thing. Imagine that double whammy of having a job that’s physically and mentally demanding.
A recent study in Current Biology explained why we feel so exhausted after doing something mentally demanding for several hours. Over that time, glutamate builds up in synapses of the prefrontal cortex, which affects our decision making and leads to cognitive lethargy. Your brain eventually becomes more interested in tasks that are less mentally fatiguing, and that’s probably why you’re reading this LOTME right now instead of getting back to work.
“Our findings show that cognitive work results in a true functional alteration – accumulation of noxious substances – so fatigue would indeed be a signal that makes us stop working but for a different purpose: to preserve the integrity of brain functioning,” senior author Mathias Pessiglione of Pitié-Salpêtrière University, Paris, said in a written statement.
The group of researchers conducted studies by using magnetic resonance spectroscopy to look at two groups of people over the course of a workday: One group had mentally tasking jobs and one didn’t. Those who had to think harder for their jobs had more signs of fatigue, such as reduced pupil dilation and glutamate in synapses of the prefrontal cortex. They also looked for more rewards that required less thinking.
For those whose mentally exhausting jobs probably won’t get better or change, the researchers suggest getting as much rest as possible. Those who don’t have that option will have to continue drinking those 7 cups of coffee a day. ... and reading LOTME.
Hmm, might be a new tagline for us in there somewhere. LOTME: Tired brains love us? When you’re too tired to think, think of LOTME? You can’t spell mental exhaustion without L-O-T-M-E?
Testosterone shows its warm and fuzzy side
Stereotypically, men are loud, knuckle-dragging Neanderthals. The hair coming out of our faces is kind of a dead giveaway, right? We grunt, we scratch, we start wars, we watch sports on TV. But why? It’s the testosterone. Everyone knows that. Testosterone makes men aggressive … or does it?
Since this sort of research generally isn’t done with actual men, investigators at Emory University used Mongolian gerbils. The advantage being that males exhibit cuddling behavior after females become pregnant and they don’t watch a lot of sports on TV. They introduced a male and female gerbil, who then formed a pair bond and the female became pregnant. When the male started displaying cuddling behaviors, the researchers injected him with testosterone, expecting to see his antisocial side.
“Instead, we were surprised that a male gerbil became even more cuddly and prosocial with his partner. He became like ‘super partner,’ ” lead author Aubrey Kelly, PhD, said in a written statement from the university.
For the next experiment, the female was removed and another male was introduced to a male who had already received a testosterone injection. That male was surprisingly unaggressive toward the intruder, at least initially. Then he received a second injection of testosterone. “It was like they suddenly woke up and realized they weren’t supposed to be friendly in that context,” Dr. Kelly said.
The testosterone seemed to influence the activity of oxytocin, the so-called “love hormone,” the investigators suggested. “It’s surprising because normally we think of testosterone as increasing sexual behaviors and aggression. But we’ve shown that it can have more nuanced effects, depending on the social context.”
The researchers were not as surprised when their use of the phrase “super partner” led to a bidding war between DC and Marvel. Then came the contact from the Department of Defense, wondering about weaponized testosterone: Would it be possible for some sort of bomb to turn Vlad “the Impaler” Putin into Vlad “the Cuddler” Putin?
Are instruments spreading the sounds of COVID?
COVID restrictions are practically a thing of the past now. With more people laxed on being in close proximity to each other and the CDC not even recommending social distancing anymore, live concerts and events are back in full swing. But with new variants on the rise and people being a little more cautious, should we be worried about musical instruments spreading COVID?
Yes and no.
A study published in Physics of Fluids looked at wind instruments specifically and how much aerosol is produced and dispersed when playing them. For the study, the investigators measured fog particles with a laser and aerosol concentration with a particle counter to see how fast these particles decay in the air from the distance of the instrument.
Musicians in an orchestra typically would sit close together to produce the best sound, but with COVID that became an issue, senior author Paulo Arratia of the University of Pennsylvania, Philadelphia, noted in a separate written statement. By looking at the distance traveled by the particles coming from a single instrument and how quickly they decayed, they could determine if sitting in close proximity is an actual threat.
Well, the threat was no greater than talking to someone face to face. Particle exit speeds were lower than for a cough or a sneeze, and the maximum decay length was 2 meters from the instrument’s opening.
But that’s just one instrument: What kind of impact does a whole orchestra have on a space? The researchers are looking into that too, but for now they suggest that musicians continue to stay 6 feet away from each other.
So, yeah, there is a threat, but it’s probably safer for you to see that orchestra than have someone sneeze on you.
Music to our ears.
Mechanistic link between herpes virus, Alzheimer’s revealed?
, new research suggests.
“Our results suggest one pathway to Alzheimer’s disease, caused by a VZV infection which creates inflammatory triggers that awaken HSV in the brain,” lead author Dana Cairns, PhD, research associate, department of biomedical engineering at Tufts University, Boston, said in a news release.
The findings were published online in Journal of Alzheimer’s Disease.
‘One-two punch’
Previous research has suggested a correlation between HSV-1 and AD and involvement of VZV. However, the sequence of events that the viruses create to set the disease in motion has been unclear.
“We think we now have evidence of those events,” co–senior author David Kaplan, PhD, chair of the department of biomedical engineering at Tufts, said in the release.
Working with co–senior author Ruth Itzhaki, PhD, University of Oxford, United Kingdom, the researchers infected human-induced neural stem cells (hiNSCs) and 3D brain tissue models with HSV-1 and/or VZV. Dr. Itzhaki was one of the first to hypothesize a connection between herpes virus and AD.
The investigators found that HSV-1 infection of hiNSCs induces amyloid-beta and P-tau accumulation: the main components of AD plaques and neurofibrillary tangles, respectively.
On the other hand, VZV infection of cultured hiNSCs did not lead to amyloid-beta and P-tau accumulation but instead resulted in gliosis and increased levels of proinflammatory cytokines.
“Strikingly,” VZV infection of cells quiescently infected with HSV-1 caused reactivation of HSV-1, leading to AD-like changes, including amyloid-beta and P-tau accumulation, the investigators report.
This suggests that VZV is unlikely to be a direct cause of AD but rather acts indirectly via reactivation of HSV-1, they add.
Similar findings emerged in similar experiments using 3D human brain tissue models.
“It’s a one-two punch of two viruses that are very common and usually harmless, but the lab studies suggest that if a new exposure to VZV wakes up dormant HSV-1, they could cause trouble,” Dr. Cairns said.
The researchers note that vaccination against VZV has been shown previously to reduce risk for dementia. It is possible, they add, that the vaccine is helping to stop the cycle of viral reactivation, inflammation, and neuronal damage.
‘A first step’
Heather M. Snyder, PhD, vice president of Medical & Scientific Relations at the Alzheimer’s Association, said that the study “is using artificial systems with the goal of more clearly and more deeply understanding” the assessed associations.
She added that although it is a first step, it may provide valuable direction for follow-up research.
“This is preliminary work that first needs replication, validation, and further development to understand if any association that is uncovered between viruses and Alzheimer’s/dementia has a mechanistic link,” said Dr. Snyder.
She noted that several past studies have sought to help the research field better understand the links between different viruses and Alzheimer’s and other forms of dementia.
“There have been some challenges in evaluating these associations in our current model systems or in individuals for a number of reasons,” said Dr. Snyder.
However, “the COVID-19 pandemic has created an opportunity to examine and investigate the relationships between different viruses and Alzheimer’s and other dementias by following individuals in more common and well-established ways,” she added.
She reported that her organization is “leading and working with a large global network of studies and investigators to address some of these questions” from during and after the COVID pandemic.
“The lessons we learn and share may inform our understanding of how other viruses are, or are not, connected to Alzheimer’s and other dementia,” Dr. Snyder said.
More information on the Alzheimer’s Association International Cohort Study of Chronic Neurological Sequelae of SARS-CoV-2 is available online.
The study was funded by the National Institutes of Health. Dr. Cairns, Dr. Kaplan, Dr. Itzhaki, and Dr. Snyder have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, new research suggests.
“Our results suggest one pathway to Alzheimer’s disease, caused by a VZV infection which creates inflammatory triggers that awaken HSV in the brain,” lead author Dana Cairns, PhD, research associate, department of biomedical engineering at Tufts University, Boston, said in a news release.
The findings were published online in Journal of Alzheimer’s Disease.
‘One-two punch’
Previous research has suggested a correlation between HSV-1 and AD and involvement of VZV. However, the sequence of events that the viruses create to set the disease in motion has been unclear.
“We think we now have evidence of those events,” co–senior author David Kaplan, PhD, chair of the department of biomedical engineering at Tufts, said in the release.
Working with co–senior author Ruth Itzhaki, PhD, University of Oxford, United Kingdom, the researchers infected human-induced neural stem cells (hiNSCs) and 3D brain tissue models with HSV-1 and/or VZV. Dr. Itzhaki was one of the first to hypothesize a connection between herpes virus and AD.
The investigators found that HSV-1 infection of hiNSCs induces amyloid-beta and P-tau accumulation: the main components of AD plaques and neurofibrillary tangles, respectively.
On the other hand, VZV infection of cultured hiNSCs did not lead to amyloid-beta and P-tau accumulation but instead resulted in gliosis and increased levels of proinflammatory cytokines.
“Strikingly,” VZV infection of cells quiescently infected with HSV-1 caused reactivation of HSV-1, leading to AD-like changes, including amyloid-beta and P-tau accumulation, the investigators report.
This suggests that VZV is unlikely to be a direct cause of AD but rather acts indirectly via reactivation of HSV-1, they add.
Similar findings emerged in similar experiments using 3D human brain tissue models.
“It’s a one-two punch of two viruses that are very common and usually harmless, but the lab studies suggest that if a new exposure to VZV wakes up dormant HSV-1, they could cause trouble,” Dr. Cairns said.
The researchers note that vaccination against VZV has been shown previously to reduce risk for dementia. It is possible, they add, that the vaccine is helping to stop the cycle of viral reactivation, inflammation, and neuronal damage.
‘A first step’
Heather M. Snyder, PhD, vice president of Medical & Scientific Relations at the Alzheimer’s Association, said that the study “is using artificial systems with the goal of more clearly and more deeply understanding” the assessed associations.
She added that although it is a first step, it may provide valuable direction for follow-up research.
“This is preliminary work that first needs replication, validation, and further development to understand if any association that is uncovered between viruses and Alzheimer’s/dementia has a mechanistic link,” said Dr. Snyder.
She noted that several past studies have sought to help the research field better understand the links between different viruses and Alzheimer’s and other forms of dementia.
“There have been some challenges in evaluating these associations in our current model systems or in individuals for a number of reasons,” said Dr. Snyder.
However, “the COVID-19 pandemic has created an opportunity to examine and investigate the relationships between different viruses and Alzheimer’s and other dementias by following individuals in more common and well-established ways,” she added.
She reported that her organization is “leading and working with a large global network of studies and investigators to address some of these questions” from during and after the COVID pandemic.
“The lessons we learn and share may inform our understanding of how other viruses are, or are not, connected to Alzheimer’s and other dementia,” Dr. Snyder said.
More information on the Alzheimer’s Association International Cohort Study of Chronic Neurological Sequelae of SARS-CoV-2 is available online.
The study was funded by the National Institutes of Health. Dr. Cairns, Dr. Kaplan, Dr. Itzhaki, and Dr. Snyder have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, new research suggests.
“Our results suggest one pathway to Alzheimer’s disease, caused by a VZV infection which creates inflammatory triggers that awaken HSV in the brain,” lead author Dana Cairns, PhD, research associate, department of biomedical engineering at Tufts University, Boston, said in a news release.
The findings were published online in Journal of Alzheimer’s Disease.
‘One-two punch’
Previous research has suggested a correlation between HSV-1 and AD and involvement of VZV. However, the sequence of events that the viruses create to set the disease in motion has been unclear.
“We think we now have evidence of those events,” co–senior author David Kaplan, PhD, chair of the department of biomedical engineering at Tufts, said in the release.
Working with co–senior author Ruth Itzhaki, PhD, University of Oxford, United Kingdom, the researchers infected human-induced neural stem cells (hiNSCs) and 3D brain tissue models with HSV-1 and/or VZV. Dr. Itzhaki was one of the first to hypothesize a connection between herpes virus and AD.
The investigators found that HSV-1 infection of hiNSCs induces amyloid-beta and P-tau accumulation: the main components of AD plaques and neurofibrillary tangles, respectively.
On the other hand, VZV infection of cultured hiNSCs did not lead to amyloid-beta and P-tau accumulation but instead resulted in gliosis and increased levels of proinflammatory cytokines.
“Strikingly,” VZV infection of cells quiescently infected with HSV-1 caused reactivation of HSV-1, leading to AD-like changes, including amyloid-beta and P-tau accumulation, the investigators report.
This suggests that VZV is unlikely to be a direct cause of AD but rather acts indirectly via reactivation of HSV-1, they add.
Similar findings emerged in similar experiments using 3D human brain tissue models.
“It’s a one-two punch of two viruses that are very common and usually harmless, but the lab studies suggest that if a new exposure to VZV wakes up dormant HSV-1, they could cause trouble,” Dr. Cairns said.
The researchers note that vaccination against VZV has been shown previously to reduce risk for dementia. It is possible, they add, that the vaccine is helping to stop the cycle of viral reactivation, inflammation, and neuronal damage.
‘A first step’
Heather M. Snyder, PhD, vice president of Medical & Scientific Relations at the Alzheimer’s Association, said that the study “is using artificial systems with the goal of more clearly and more deeply understanding” the assessed associations.
She added that although it is a first step, it may provide valuable direction for follow-up research.
“This is preliminary work that first needs replication, validation, and further development to understand if any association that is uncovered between viruses and Alzheimer’s/dementia has a mechanistic link,” said Dr. Snyder.
She noted that several past studies have sought to help the research field better understand the links between different viruses and Alzheimer’s and other forms of dementia.
“There have been some challenges in evaluating these associations in our current model systems or in individuals for a number of reasons,” said Dr. Snyder.
However, “the COVID-19 pandemic has created an opportunity to examine and investigate the relationships between different viruses and Alzheimer’s and other dementias by following individuals in more common and well-established ways,” she added.
She reported that her organization is “leading and working with a large global network of studies and investigators to address some of these questions” from during and after the COVID pandemic.
“The lessons we learn and share may inform our understanding of how other viruses are, or are not, connected to Alzheimer’s and other dementia,” Dr. Snyder said.
More information on the Alzheimer’s Association International Cohort Study of Chronic Neurological Sequelae of SARS-CoV-2 is available online.
The study was funded by the National Institutes of Health. Dr. Cairns, Dr. Kaplan, Dr. Itzhaki, and Dr. Snyder have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF ALZHEIMER’S DISEASE
Why our brains wear out at the end of the day
The transcript has been edited for clarity.
Welcome to Impact Factor, your weekly dose of commentary on a new medical study. I’m Dr. F. Perry Wilson of the Yale School of Medicine.
Once again, we’re doing an informal journal club to talk about a really interesting study, “A Neuro-metabolic Account of Why Daylong Cognitive Work Alters the Control of Economic Decisions,” that just came out. It tries to answer the question of why our brains wear out. I’m going to put myself in the corner here. Let’s walk through this study, which appears in Current Biology, by lead author Antonius Wiehler from Paris.
The big question is what’s going on with cognitive fatigue. If you look at chess players who are exerting a lot of cognitive effort, it’s well documented that over hours of play, they get worse and make more mistakes. It takes them longer to make decisions. The question is, why?
Why does your brain get tired?
To date, it’s been a little bit hard to tease that out. Now, there is some suggestion of what is responsible for this. The cognitive control center of the brain is probably somewhere in the left lateral prefrontal cortex (LLPC).
The prefrontal cortex is responsible for higher-level thinking. It’s what causes you to be inhibited. It gets shut off by alcohol and leads to impulsive behaviors. The LLPC, according to functional MRI studies, has reduced activity as people become more and more cognitively fatigued. The LLPC helps you think through choices. As you become more fatigued, this area of the brain isn’t working as well. But why would it not work as well? What is going on in that particular part of the brain? It doesn’t seem to be something simple, like glucose levels; that’s been investigated and glucose levels are pretty constant throughout the brain, regardless of cognitive task. This paper seeks to tease out what is actually going on in the LLPC when you are becoming cognitively tired.
They did an experiment where they induced cognitive fatigue, and it sounds like a painful experiment. For more than 6 hours, volunteers completed sessions during which they had to perform cognitive switching tasks. Investigators showed participants a letter, in either red or green, and the participant would respond with whether it was a vowel or a consonant or whether it was a capital or lowercase letter, based on the color. If it’s red, say whether it’s a consonant or vowel. If it’s green, say whether it’s upper- or lowercase.
It’s hard, and doing it for 6 hours is likely to induce a lot of cognitive fatigue. They had a control group as well, which is really important here. The control group also did a task like this for 6 hours, but for them, investigators didn’t change the color as often – perhaps only once per session. For the study group, they were switching colors back and forth quite a lot. They also incorporated a memory challenge that worked in a similar way.
So, what are the readouts of this study? They had a group who went through the hard cognitive challenge and a group who went through the easy cognitive challenge. They looked at a variety of metrics. I’ll describe a few.
The first is performance decrement. Did they get it wrong? What percentage of the time did the participant say “consonant” when they should have said “lowercase?”
You can see here that the hard group did a little bit worse overall. It was harder, so they don’t do as well. That makes sense. But both groups kind of waned over time a little bit. It’s not as though the hard group declines much more. The slopes of those lines are pretty similar. So, not very robust findings there.
What about subjective fatigue? They asked the participants how exhausted they were from doing the tasks.
Both groups were worn out. It was a long day. There was a suggestion that the hard group became worn out a little bit sooner, but I don’t think this achieves statistical significance. Everyone was getting tired by hour 6 here.
What about response time? How quickly could the participant say “consonant,” “vowel,” “lowercase,” or “uppercase?”
The hard group took longer to respond because it was a harder task. But over time, the response times were pretty flat.
So far there isn’t a robust readout that would make us say, oh, yeah, that is a good marker of cognitive fatigue. That’s how you measure cognitive fatigue. It’s not what people say. It’s not how quick they are. It’s not even how accurate they are.
But then the investigators got a little bit clever. Participants were asked to play a “would you rather” game, a reward game. Here are two examples.
Would you rather:
- Have a 25% chance of earning $50 OR a 95% chance of earning $17.30?
- Earn $50, but your next task session will be hard or earn $40 and your next task session will be easy?
Participants had to figure out the better odds – what should they be choosing here? They had to tease out whether they preferred lower cost lower-risk choices – when they are cognitively fatigued, which has been shown in prior studies.
This showed a pretty dramatic difference between the groups in terms of the low-cost bias – how much more likely they were to pick the low-cost, easier choice as they became more and more cognitively fatigued. The hard group participants were more likely to pick the easy thing rather than the potentially more lucrative thing, which is really interesting when we think about how our own cognitive fatigue happens at the end of a difficult workday, how you may just be likely to go with the flow and do something easy because you just don’t have that much decision-making power left.
It would be nice to have some objective physiologic measurements for this, and they do. This is pupil dilation.
When you’re paying attention to something, your pupils dilate a little bit. They were able to show that as the hard group became more and more fatigued, pupil dilation sort of went away. In fact, if anything, their pupils constricted a little bit. But basically there was a significant difference here. The easy group’s pupils were still fine; they were still dilating. The hard group’s pupils got more sluggish. This is a physiologic correlate of what’s going on.
But again, these are all downstream of whatever is happening in the LLPC. So the real meat of this study is a functional MRI analysis, and the way they did this is pretty clever. They were looking for metabolites in the various parts of the brain using a labeled hydrogen MRI, which is even fancier than a functional MRI. It’s like MRI spectroscopy, and it can measure the levels of certain chemicals in the brain. They hypothesized that if there is a chemical that builds up when you are tired, it should build up preferentially in the LLPC.
Whereas in the rest of the brain, there shouldn’t be that much difference because we know the action is happening in the LLPC. The control part of the brain is a section called V1. They looked at a variety of metabolites, but the only one that behaved the way they expected was glutamate and glutamic acid (glutamate metabolites). In the hard group, the glutamate is building up over time, so there is a higher concentration of glutamate in the LLPC but not the rest of the brain. There is also a greater diffusion of glutamate from the intracellular to the extracellular space, which suggests that it’s kind of leaking out of the cells.
So the signal here is that the thing that’s impacting that part of the brain is this buildup of glutamate. To tie this together, they showed in the scatterplot the relationship between the increase in glutamate and the low-cost bias from the decision fatigue example.
It’s not the strongest correlation, but it is statistically significant that the more glutamate in your LLPC, the more likely you are to just take the easy decision as opposed to really thinking things through. That is pretty powerful. It’s telling us that your brain making you fatigued, and making you less likely to continue to use your LLPC, may be a self-defense mechanism against a buildup of glutamate, which may be neurotoxic. And that’s a fascinating bit of homeostasis.
Of course, it makes you wonder how we might adjust glutamate levels in the brain, although maybe we should let the brain be tired if the brain wants to be tired. It reminds me of that old Far Side cartoon where the guy is raising his hand and asking: “Can I be excused? My brain is full.” That is essentially what’s happening. This part of your brain is becoming taxed and building up glutamate. There’s some kind of negative feedback loop. The authors don’t know what the receptor pathway is that down-regulates that part of the brain based on the glutamate buildup, but some kind of negative feedback loop is saying, okay, give this part of the brain a rest. Things have gone on too far here.
It’s a fascinating study, although it’s not clear what we can do with this information. It’s not clear whether we can manipulate glutamate levels in this particular part of the brain or not. But it’s nice to see some biologic correlates of a psychological phenomenon that is incredibly well described – the phenomenon of decision fatigue. I think we all feel it at the end of a hard workday. If you’ve been doing a lot of cognitively intensive tasks, you just don’t have it in you anymore. And maybe the act of a good night’s sleep is clearing out some of that glutamate in the LLPC, which lets you start over and make some good decisions again. So I hope you all make some good decisions and keep your glutamate levels low. And I’ll see you next time.
For Medscape, I’m Perry Wilson.
Dr. Wilson is an associate professor of medicine and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
The transcript has been edited for clarity.
Welcome to Impact Factor, your weekly dose of commentary on a new medical study. I’m Dr. F. Perry Wilson of the Yale School of Medicine.
Once again, we’re doing an informal journal club to talk about a really interesting study, “A Neuro-metabolic Account of Why Daylong Cognitive Work Alters the Control of Economic Decisions,” that just came out. It tries to answer the question of why our brains wear out. I’m going to put myself in the corner here. Let’s walk through this study, which appears in Current Biology, by lead author Antonius Wiehler from Paris.
The big question is what’s going on with cognitive fatigue. If you look at chess players who are exerting a lot of cognitive effort, it’s well documented that over hours of play, they get worse and make more mistakes. It takes them longer to make decisions. The question is, why?
Why does your brain get tired?
To date, it’s been a little bit hard to tease that out. Now, there is some suggestion of what is responsible for this. The cognitive control center of the brain is probably somewhere in the left lateral prefrontal cortex (LLPC).
The prefrontal cortex is responsible for higher-level thinking. It’s what causes you to be inhibited. It gets shut off by alcohol and leads to impulsive behaviors. The LLPC, according to functional MRI studies, has reduced activity as people become more and more cognitively fatigued. The LLPC helps you think through choices. As you become more fatigued, this area of the brain isn’t working as well. But why would it not work as well? What is going on in that particular part of the brain? It doesn’t seem to be something simple, like glucose levels; that’s been investigated and glucose levels are pretty constant throughout the brain, regardless of cognitive task. This paper seeks to tease out what is actually going on in the LLPC when you are becoming cognitively tired.
They did an experiment where they induced cognitive fatigue, and it sounds like a painful experiment. For more than 6 hours, volunteers completed sessions during which they had to perform cognitive switching tasks. Investigators showed participants a letter, in either red or green, and the participant would respond with whether it was a vowel or a consonant or whether it was a capital or lowercase letter, based on the color. If it’s red, say whether it’s a consonant or vowel. If it’s green, say whether it’s upper- or lowercase.
It’s hard, and doing it for 6 hours is likely to induce a lot of cognitive fatigue. They had a control group as well, which is really important here. The control group also did a task like this for 6 hours, but for them, investigators didn’t change the color as often – perhaps only once per session. For the study group, they were switching colors back and forth quite a lot. They also incorporated a memory challenge that worked in a similar way.
So, what are the readouts of this study? They had a group who went through the hard cognitive challenge and a group who went through the easy cognitive challenge. They looked at a variety of metrics. I’ll describe a few.
The first is performance decrement. Did they get it wrong? What percentage of the time did the participant say “consonant” when they should have said “lowercase?”
You can see here that the hard group did a little bit worse overall. It was harder, so they don’t do as well. That makes sense. But both groups kind of waned over time a little bit. It’s not as though the hard group declines much more. The slopes of those lines are pretty similar. So, not very robust findings there.
What about subjective fatigue? They asked the participants how exhausted they were from doing the tasks.
Both groups were worn out. It was a long day. There was a suggestion that the hard group became worn out a little bit sooner, but I don’t think this achieves statistical significance. Everyone was getting tired by hour 6 here.
What about response time? How quickly could the participant say “consonant,” “vowel,” “lowercase,” or “uppercase?”
The hard group took longer to respond because it was a harder task. But over time, the response times were pretty flat.
So far there isn’t a robust readout that would make us say, oh, yeah, that is a good marker of cognitive fatigue. That’s how you measure cognitive fatigue. It’s not what people say. It’s not how quick they are. It’s not even how accurate they are.
But then the investigators got a little bit clever. Participants were asked to play a “would you rather” game, a reward game. Here are two examples.
Would you rather:
- Have a 25% chance of earning $50 OR a 95% chance of earning $17.30?
- Earn $50, but your next task session will be hard or earn $40 and your next task session will be easy?
Participants had to figure out the better odds – what should they be choosing here? They had to tease out whether they preferred lower cost lower-risk choices – when they are cognitively fatigued, which has been shown in prior studies.
This showed a pretty dramatic difference between the groups in terms of the low-cost bias – how much more likely they were to pick the low-cost, easier choice as they became more and more cognitively fatigued. The hard group participants were more likely to pick the easy thing rather than the potentially more lucrative thing, which is really interesting when we think about how our own cognitive fatigue happens at the end of a difficult workday, how you may just be likely to go with the flow and do something easy because you just don’t have that much decision-making power left.
It would be nice to have some objective physiologic measurements for this, and they do. This is pupil dilation.
When you’re paying attention to something, your pupils dilate a little bit. They were able to show that as the hard group became more and more fatigued, pupil dilation sort of went away. In fact, if anything, their pupils constricted a little bit. But basically there was a significant difference here. The easy group’s pupils were still fine; they were still dilating. The hard group’s pupils got more sluggish. This is a physiologic correlate of what’s going on.
But again, these are all downstream of whatever is happening in the LLPC. So the real meat of this study is a functional MRI analysis, and the way they did this is pretty clever. They were looking for metabolites in the various parts of the brain using a labeled hydrogen MRI, which is even fancier than a functional MRI. It’s like MRI spectroscopy, and it can measure the levels of certain chemicals in the brain. They hypothesized that if there is a chemical that builds up when you are tired, it should build up preferentially in the LLPC.
Whereas in the rest of the brain, there shouldn’t be that much difference because we know the action is happening in the LLPC. The control part of the brain is a section called V1. They looked at a variety of metabolites, but the only one that behaved the way they expected was glutamate and glutamic acid (glutamate metabolites). In the hard group, the glutamate is building up over time, so there is a higher concentration of glutamate in the LLPC but not the rest of the brain. There is also a greater diffusion of glutamate from the intracellular to the extracellular space, which suggests that it’s kind of leaking out of the cells.
So the signal here is that the thing that’s impacting that part of the brain is this buildup of glutamate. To tie this together, they showed in the scatterplot the relationship between the increase in glutamate and the low-cost bias from the decision fatigue example.
It’s not the strongest correlation, but it is statistically significant that the more glutamate in your LLPC, the more likely you are to just take the easy decision as opposed to really thinking things through. That is pretty powerful. It’s telling us that your brain making you fatigued, and making you less likely to continue to use your LLPC, may be a self-defense mechanism against a buildup of glutamate, which may be neurotoxic. And that’s a fascinating bit of homeostasis.
Of course, it makes you wonder how we might adjust glutamate levels in the brain, although maybe we should let the brain be tired if the brain wants to be tired. It reminds me of that old Far Side cartoon where the guy is raising his hand and asking: “Can I be excused? My brain is full.” That is essentially what’s happening. This part of your brain is becoming taxed and building up glutamate. There’s some kind of negative feedback loop. The authors don’t know what the receptor pathway is that down-regulates that part of the brain based on the glutamate buildup, but some kind of negative feedback loop is saying, okay, give this part of the brain a rest. Things have gone on too far here.
It’s a fascinating study, although it’s not clear what we can do with this information. It’s not clear whether we can manipulate glutamate levels in this particular part of the brain or not. But it’s nice to see some biologic correlates of a psychological phenomenon that is incredibly well described – the phenomenon of decision fatigue. I think we all feel it at the end of a hard workday. If you’ve been doing a lot of cognitively intensive tasks, you just don’t have it in you anymore. And maybe the act of a good night’s sleep is clearing out some of that glutamate in the LLPC, which lets you start over and make some good decisions again. So I hope you all make some good decisions and keep your glutamate levels low. And I’ll see you next time.
For Medscape, I’m Perry Wilson.
Dr. Wilson is an associate professor of medicine and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
The transcript has been edited for clarity.
Welcome to Impact Factor, your weekly dose of commentary on a new medical study. I’m Dr. F. Perry Wilson of the Yale School of Medicine.
Once again, we’re doing an informal journal club to talk about a really interesting study, “A Neuro-metabolic Account of Why Daylong Cognitive Work Alters the Control of Economic Decisions,” that just came out. It tries to answer the question of why our brains wear out. I’m going to put myself in the corner here. Let’s walk through this study, which appears in Current Biology, by lead author Antonius Wiehler from Paris.
The big question is what’s going on with cognitive fatigue. If you look at chess players who are exerting a lot of cognitive effort, it’s well documented that over hours of play, they get worse and make more mistakes. It takes them longer to make decisions. The question is, why?
Why does your brain get tired?
To date, it’s been a little bit hard to tease that out. Now, there is some suggestion of what is responsible for this. The cognitive control center of the brain is probably somewhere in the left lateral prefrontal cortex (LLPC).
The prefrontal cortex is responsible for higher-level thinking. It’s what causes you to be inhibited. It gets shut off by alcohol and leads to impulsive behaviors. The LLPC, according to functional MRI studies, has reduced activity as people become more and more cognitively fatigued. The LLPC helps you think through choices. As you become more fatigued, this area of the brain isn’t working as well. But why would it not work as well? What is going on in that particular part of the brain? It doesn’t seem to be something simple, like glucose levels; that’s been investigated and glucose levels are pretty constant throughout the brain, regardless of cognitive task. This paper seeks to tease out what is actually going on in the LLPC when you are becoming cognitively tired.
They did an experiment where they induced cognitive fatigue, and it sounds like a painful experiment. For more than 6 hours, volunteers completed sessions during which they had to perform cognitive switching tasks. Investigators showed participants a letter, in either red or green, and the participant would respond with whether it was a vowel or a consonant or whether it was a capital or lowercase letter, based on the color. If it’s red, say whether it’s a consonant or vowel. If it’s green, say whether it’s upper- or lowercase.
It’s hard, and doing it for 6 hours is likely to induce a lot of cognitive fatigue. They had a control group as well, which is really important here. The control group also did a task like this for 6 hours, but for them, investigators didn’t change the color as often – perhaps only once per session. For the study group, they were switching colors back and forth quite a lot. They also incorporated a memory challenge that worked in a similar way.
So, what are the readouts of this study? They had a group who went through the hard cognitive challenge and a group who went through the easy cognitive challenge. They looked at a variety of metrics. I’ll describe a few.
The first is performance decrement. Did they get it wrong? What percentage of the time did the participant say “consonant” when they should have said “lowercase?”
You can see here that the hard group did a little bit worse overall. It was harder, so they don’t do as well. That makes sense. But both groups kind of waned over time a little bit. It’s not as though the hard group declines much more. The slopes of those lines are pretty similar. So, not very robust findings there.
What about subjective fatigue? They asked the participants how exhausted they were from doing the tasks.
Both groups were worn out. It was a long day. There was a suggestion that the hard group became worn out a little bit sooner, but I don’t think this achieves statistical significance. Everyone was getting tired by hour 6 here.
What about response time? How quickly could the participant say “consonant,” “vowel,” “lowercase,” or “uppercase?”
The hard group took longer to respond because it was a harder task. But over time, the response times were pretty flat.
So far there isn’t a robust readout that would make us say, oh, yeah, that is a good marker of cognitive fatigue. That’s how you measure cognitive fatigue. It’s not what people say. It’s not how quick they are. It’s not even how accurate they are.
But then the investigators got a little bit clever. Participants were asked to play a “would you rather” game, a reward game. Here are two examples.
Would you rather:
- Have a 25% chance of earning $50 OR a 95% chance of earning $17.30?
- Earn $50, but your next task session will be hard or earn $40 and your next task session will be easy?
Participants had to figure out the better odds – what should they be choosing here? They had to tease out whether they preferred lower cost lower-risk choices – when they are cognitively fatigued, which has been shown in prior studies.
This showed a pretty dramatic difference between the groups in terms of the low-cost bias – how much more likely they were to pick the low-cost, easier choice as they became more and more cognitively fatigued. The hard group participants were more likely to pick the easy thing rather than the potentially more lucrative thing, which is really interesting when we think about how our own cognitive fatigue happens at the end of a difficult workday, how you may just be likely to go with the flow and do something easy because you just don’t have that much decision-making power left.
It would be nice to have some objective physiologic measurements for this, and they do. This is pupil dilation.
When you’re paying attention to something, your pupils dilate a little bit. They were able to show that as the hard group became more and more fatigued, pupil dilation sort of went away. In fact, if anything, their pupils constricted a little bit. But basically there was a significant difference here. The easy group’s pupils were still fine; they were still dilating. The hard group’s pupils got more sluggish. This is a physiologic correlate of what’s going on.
But again, these are all downstream of whatever is happening in the LLPC. So the real meat of this study is a functional MRI analysis, and the way they did this is pretty clever. They were looking for metabolites in the various parts of the brain using a labeled hydrogen MRI, which is even fancier than a functional MRI. It’s like MRI spectroscopy, and it can measure the levels of certain chemicals in the brain. They hypothesized that if there is a chemical that builds up when you are tired, it should build up preferentially in the LLPC.
Whereas in the rest of the brain, there shouldn’t be that much difference because we know the action is happening in the LLPC. The control part of the brain is a section called V1. They looked at a variety of metabolites, but the only one that behaved the way they expected was glutamate and glutamic acid (glutamate metabolites). In the hard group, the glutamate is building up over time, so there is a higher concentration of glutamate in the LLPC but not the rest of the brain. There is also a greater diffusion of glutamate from the intracellular to the extracellular space, which suggests that it’s kind of leaking out of the cells.
So the signal here is that the thing that’s impacting that part of the brain is this buildup of glutamate. To tie this together, they showed in the scatterplot the relationship between the increase in glutamate and the low-cost bias from the decision fatigue example.
It’s not the strongest correlation, but it is statistically significant that the more glutamate in your LLPC, the more likely you are to just take the easy decision as opposed to really thinking things through. That is pretty powerful. It’s telling us that your brain making you fatigued, and making you less likely to continue to use your LLPC, may be a self-defense mechanism against a buildup of glutamate, which may be neurotoxic. And that’s a fascinating bit of homeostasis.
Of course, it makes you wonder how we might adjust glutamate levels in the brain, although maybe we should let the brain be tired if the brain wants to be tired. It reminds me of that old Far Side cartoon where the guy is raising his hand and asking: “Can I be excused? My brain is full.” That is essentially what’s happening. This part of your brain is becoming taxed and building up glutamate. There’s some kind of negative feedback loop. The authors don’t know what the receptor pathway is that down-regulates that part of the brain based on the glutamate buildup, but some kind of negative feedback loop is saying, okay, give this part of the brain a rest. Things have gone on too far here.
It’s a fascinating study, although it’s not clear what we can do with this information. It’s not clear whether we can manipulate glutamate levels in this particular part of the brain or not. But it’s nice to see some biologic correlates of a psychological phenomenon that is incredibly well described – the phenomenon of decision fatigue. I think we all feel it at the end of a hard workday. If you’ve been doing a lot of cognitively intensive tasks, you just don’t have it in you anymore. And maybe the act of a good night’s sleep is clearing out some of that glutamate in the LLPC, which lets you start over and make some good decisions again. So I hope you all make some good decisions and keep your glutamate levels low. And I’ll see you next time.
For Medscape, I’m Perry Wilson.
Dr. Wilson is an associate professor of medicine and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
Hearing aids available in October without a prescription
The White House announced today that the Food and Drug Administration will move forward with plans to make hearing aids available over the counter in pharmacies, other retail locations, and online.
This major milestone aims to make hearing aids easier to buy and more affordable, potentially saving families thousands of dollars.
An estimated 28.8 million U.S. adults could benefit from using hearing aids, according to numbers from the National Institute on Deafness and Other Communication Disorders. But only about 16% of people aged 20-69 years who could be helped by hearing aids have ever used them.
The risk for hearing loss increases with age. Among Americans ages 70 and older, only 30% who could hear better with these devices have ever used them, the institute reports.
Once the FDA final rule takes effect, Americans with mild to moderate hearing loss will be able to buy a hearing aid without a doctor’s exam, prescription, or fitting adjustment.
President Joe Biden announced in 2021 he intended to allow hearing aids to be sold over the counter without a prescription to increase competition among manufacturers. Congress also passed bipartisan legislation in 2017 requiring the FDA to create a new category for hearing aids sold directly to consumers. Some devices intended for minors or people with severe hearing loss will remain available only with a prescription.
“This action makes good on my commitment to lower costs for American families, delivering nearly $3,000 in savings to American families for a pair of hearing aids and giving people more choices to improve their health and wellbeing,” the president said in a statement announcing the news.
The new over-the-counter hearing aids will be considered medical devices. To avoid confusion, the FDA explains the differences between hearing aids and personal sound amplification products (PSAPs). For example, PSAPs are considered electronic devices designed for people with normal hearing to use in certain situations, like birdwatching or hunting.
A version of this article first appeared on WebMD.com.
The White House announced today that the Food and Drug Administration will move forward with plans to make hearing aids available over the counter in pharmacies, other retail locations, and online.
This major milestone aims to make hearing aids easier to buy and more affordable, potentially saving families thousands of dollars.
An estimated 28.8 million U.S. adults could benefit from using hearing aids, according to numbers from the National Institute on Deafness and Other Communication Disorders. But only about 16% of people aged 20-69 years who could be helped by hearing aids have ever used them.
The risk for hearing loss increases with age. Among Americans ages 70 and older, only 30% who could hear better with these devices have ever used them, the institute reports.
Once the FDA final rule takes effect, Americans with mild to moderate hearing loss will be able to buy a hearing aid without a doctor’s exam, prescription, or fitting adjustment.
President Joe Biden announced in 2021 he intended to allow hearing aids to be sold over the counter without a prescription to increase competition among manufacturers. Congress also passed bipartisan legislation in 2017 requiring the FDA to create a new category for hearing aids sold directly to consumers. Some devices intended for minors or people with severe hearing loss will remain available only with a prescription.
“This action makes good on my commitment to lower costs for American families, delivering nearly $3,000 in savings to American families for a pair of hearing aids and giving people more choices to improve their health and wellbeing,” the president said in a statement announcing the news.
The new over-the-counter hearing aids will be considered medical devices. To avoid confusion, the FDA explains the differences between hearing aids and personal sound amplification products (PSAPs). For example, PSAPs are considered electronic devices designed for people with normal hearing to use in certain situations, like birdwatching or hunting.
A version of this article first appeared on WebMD.com.
The White House announced today that the Food and Drug Administration will move forward with plans to make hearing aids available over the counter in pharmacies, other retail locations, and online.
This major milestone aims to make hearing aids easier to buy and more affordable, potentially saving families thousands of dollars.
An estimated 28.8 million U.S. adults could benefit from using hearing aids, according to numbers from the National Institute on Deafness and Other Communication Disorders. But only about 16% of people aged 20-69 years who could be helped by hearing aids have ever used them.
The risk for hearing loss increases with age. Among Americans ages 70 and older, only 30% who could hear better with these devices have ever used them, the institute reports.
Once the FDA final rule takes effect, Americans with mild to moderate hearing loss will be able to buy a hearing aid without a doctor’s exam, prescription, or fitting adjustment.
President Joe Biden announced in 2021 he intended to allow hearing aids to be sold over the counter without a prescription to increase competition among manufacturers. Congress also passed bipartisan legislation in 2017 requiring the FDA to create a new category for hearing aids sold directly to consumers. Some devices intended for minors or people with severe hearing loss will remain available only with a prescription.
“This action makes good on my commitment to lower costs for American families, delivering nearly $3,000 in savings to American families for a pair of hearing aids and giving people more choices to improve their health and wellbeing,” the president said in a statement announcing the news.
The new over-the-counter hearing aids will be considered medical devices. To avoid confusion, the FDA explains the differences between hearing aids and personal sound amplification products (PSAPs). For example, PSAPs are considered electronic devices designed for people with normal hearing to use in certain situations, like birdwatching or hunting.
A version of this article first appeared on WebMD.com.