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Child assault tied to triple the risk for mental illness within 1 year
The greatest risk was found in the first year following the assault, increasing to three times the risk of being diagnosed with mental illness, compared with children not assaulted. Mood and anxiety disorders were the most common diagnoses.
“From a clinical and policy perspective, our study highlights that there is a critical opportunity for health care clinicians to support children in the first year following physical assault,” Natasha Saunders, MD, MSc, of the Hospital for Sick Children, Toronto, and colleagues wrote. “There is a need to develop and implement targeted mental illness prevention, screening, and treatment programs for assaulted children.”
The findings were published online in JAMA Network Open.
While it has been well established that children exposed to assault have an increased risk for subsequent mental illness, Dr. Saunders and coinvestigators noted that using an age-matched, population-based cohort study would enable them to obtain detailed information on the patterns and timing of subsequent psychiatric diagnoses.
To that end, the researchers used several medical databases in Ontario to find 5,487 children (infants to age 13 years) who required an ED visit or hospitalization for a physical assault in Ontario between 2006 and 2014.
These children were matched on a 1:4 basis with 21,948 children not exposed to physical assault. The children were followed until their 18th birthday or until the study ended in March 2019.
The researchers found that more than a third of the children (39%) who were exposed to assault received a mental health diagnosis, according to health records, compared with 23% of unexposed children.
Mood and anxiety disorders were the most common diagnoses among children exposed to assault (16.2% vs. 10.6%, respectively); followed by select childhood behavior disorders, such as ADHD, oppositional defiant disorder, or conduct disorder (9.9% vs. 5.2%); and substance use disorders (2.4% vs. 0.4%).
Triple risk of mental illness in first year
The researchers found that the children exposed to assault were nearly twice as likely to be diagnosed with a mental illness over a median follow-up of 7 years, compared with those not exposed to assault (adjusted hazard ratio, 1.96; 95% confidence interval, 1.85,2.08).
In the year following the assault, children exposed to assault bore three times the risk of being diagnosed with a mental illness, compared with unexposed children (aHR, 3.08; 95% CI, 2.68,3.54).
In addition, the children who had been assaulted were more likely to be diagnosed in an acute care setting than those who were not assaulted (14% vs. 2.8%).
The children who had been assaulted were an average age of 7 years and were more often boys (55% vs. 45%). Children who were assaulted were also more likely to have mothers with mental illness (35% vs. 19%).
The investigators noted that the study likely underestimated the number of children exposed to assault, as many do not end up in the ED.
In addition to highlighting the need for medical personnel to support children in the first year following assault, the investigators wrote that “our results also advocate for accessible mental health care outside of the acute setting and for care that addresses the social and health needs of mothers, who themselves have high social and health risks.”
This study received funding from the National Foundation to End Child Abuse and Neglect and the Ontario Ministry of Health and the Ministry of Long-Term Care. Dr. Saunders reported receiving personal fees from The BMJ Group, Archives of Diseases in Childhood outside the submitted work.
A version of this article first appeared on Medscape.com.
The greatest risk was found in the first year following the assault, increasing to three times the risk of being diagnosed with mental illness, compared with children not assaulted. Mood and anxiety disorders were the most common diagnoses.
“From a clinical and policy perspective, our study highlights that there is a critical opportunity for health care clinicians to support children in the first year following physical assault,” Natasha Saunders, MD, MSc, of the Hospital for Sick Children, Toronto, and colleagues wrote. “There is a need to develop and implement targeted mental illness prevention, screening, and treatment programs for assaulted children.”
The findings were published online in JAMA Network Open.
While it has been well established that children exposed to assault have an increased risk for subsequent mental illness, Dr. Saunders and coinvestigators noted that using an age-matched, population-based cohort study would enable them to obtain detailed information on the patterns and timing of subsequent psychiatric diagnoses.
To that end, the researchers used several medical databases in Ontario to find 5,487 children (infants to age 13 years) who required an ED visit or hospitalization for a physical assault in Ontario between 2006 and 2014.
These children were matched on a 1:4 basis with 21,948 children not exposed to physical assault. The children were followed until their 18th birthday or until the study ended in March 2019.
The researchers found that more than a third of the children (39%) who were exposed to assault received a mental health diagnosis, according to health records, compared with 23% of unexposed children.
Mood and anxiety disorders were the most common diagnoses among children exposed to assault (16.2% vs. 10.6%, respectively); followed by select childhood behavior disorders, such as ADHD, oppositional defiant disorder, or conduct disorder (9.9% vs. 5.2%); and substance use disorders (2.4% vs. 0.4%).
Triple risk of mental illness in first year
The researchers found that the children exposed to assault were nearly twice as likely to be diagnosed with a mental illness over a median follow-up of 7 years, compared with those not exposed to assault (adjusted hazard ratio, 1.96; 95% confidence interval, 1.85,2.08).
In the year following the assault, children exposed to assault bore three times the risk of being diagnosed with a mental illness, compared with unexposed children (aHR, 3.08; 95% CI, 2.68,3.54).
In addition, the children who had been assaulted were more likely to be diagnosed in an acute care setting than those who were not assaulted (14% vs. 2.8%).
The children who had been assaulted were an average age of 7 years and were more often boys (55% vs. 45%). Children who were assaulted were also more likely to have mothers with mental illness (35% vs. 19%).
The investigators noted that the study likely underestimated the number of children exposed to assault, as many do not end up in the ED.
In addition to highlighting the need for medical personnel to support children in the first year following assault, the investigators wrote that “our results also advocate for accessible mental health care outside of the acute setting and for care that addresses the social and health needs of mothers, who themselves have high social and health risks.”
This study received funding from the National Foundation to End Child Abuse and Neglect and the Ontario Ministry of Health and the Ministry of Long-Term Care. Dr. Saunders reported receiving personal fees from The BMJ Group, Archives of Diseases in Childhood outside the submitted work.
A version of this article first appeared on Medscape.com.
The greatest risk was found in the first year following the assault, increasing to three times the risk of being diagnosed with mental illness, compared with children not assaulted. Mood and anxiety disorders were the most common diagnoses.
“From a clinical and policy perspective, our study highlights that there is a critical opportunity for health care clinicians to support children in the first year following physical assault,” Natasha Saunders, MD, MSc, of the Hospital for Sick Children, Toronto, and colleagues wrote. “There is a need to develop and implement targeted mental illness prevention, screening, and treatment programs for assaulted children.”
The findings were published online in JAMA Network Open.
While it has been well established that children exposed to assault have an increased risk for subsequent mental illness, Dr. Saunders and coinvestigators noted that using an age-matched, population-based cohort study would enable them to obtain detailed information on the patterns and timing of subsequent psychiatric diagnoses.
To that end, the researchers used several medical databases in Ontario to find 5,487 children (infants to age 13 years) who required an ED visit or hospitalization for a physical assault in Ontario between 2006 and 2014.
These children were matched on a 1:4 basis with 21,948 children not exposed to physical assault. The children were followed until their 18th birthday or until the study ended in March 2019.
The researchers found that more than a third of the children (39%) who were exposed to assault received a mental health diagnosis, according to health records, compared with 23% of unexposed children.
Mood and anxiety disorders were the most common diagnoses among children exposed to assault (16.2% vs. 10.6%, respectively); followed by select childhood behavior disorders, such as ADHD, oppositional defiant disorder, or conduct disorder (9.9% vs. 5.2%); and substance use disorders (2.4% vs. 0.4%).
Triple risk of mental illness in first year
The researchers found that the children exposed to assault were nearly twice as likely to be diagnosed with a mental illness over a median follow-up of 7 years, compared with those not exposed to assault (adjusted hazard ratio, 1.96; 95% confidence interval, 1.85,2.08).
In the year following the assault, children exposed to assault bore three times the risk of being diagnosed with a mental illness, compared with unexposed children (aHR, 3.08; 95% CI, 2.68,3.54).
In addition, the children who had been assaulted were more likely to be diagnosed in an acute care setting than those who were not assaulted (14% vs. 2.8%).
The children who had been assaulted were an average age of 7 years and were more often boys (55% vs. 45%). Children who were assaulted were also more likely to have mothers with mental illness (35% vs. 19%).
The investigators noted that the study likely underestimated the number of children exposed to assault, as many do not end up in the ED.
In addition to highlighting the need for medical personnel to support children in the first year following assault, the investigators wrote that “our results also advocate for accessible mental health care outside of the acute setting and for care that addresses the social and health needs of mothers, who themselves have high social and health risks.”
This study received funding from the National Foundation to End Child Abuse and Neglect and the Ontario Ministry of Health and the Ministry of Long-Term Care. Dr. Saunders reported receiving personal fees from The BMJ Group, Archives of Diseases in Childhood outside the submitted work.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN
Bipolar disorder tied to a sixfold increased risk of early death
In addition, patients with BD are three times more likely to die prematurely of all causes, compared with the general population, with alcohol-related diseases contributing to more premature deaths than cardiovascular disease (CVD), diabetes, and cancer.
The study results emphasize the need for personalized approaches to risk prediction and prevention of premature cause-specific mortality over the life-course of individuals with BD, lead investigator Tapio Paljärvi, PhD, an epidemiologist at Niuvanniemi Hospital in Kuopio, Finland, told this news organization.
The findings were published online in BMJ Mental Health.
Alcohol a major contributor to early death
A number of studies have established that those with BD have twice the risk of dying prematurely, compared with those without the disorder.
To learn more about the factors contributing to early death in this patient population, the investigators analyzed data from nationwide Finnish medical and insurance registries. They identified and tracked the health of 47,000 patients, aged 15-64 years, with BD between 2004 and 2018.
The average age at the beginning of the monitoring period was 38 years, and 57% of the cohort were women.
To determine the excess deaths directly attributable to BD, the researchers compared the ratio of deaths observed over the monitoring period in those with BD to the number expected to die in the general population, also known as the standard mortality ratio.
Of the group with BD, 3,300 died during the monitoring period. The average age at death was 50, and almost two-thirds (65%, or 2,137) of those who died were men.
Investigators grouped excess deaths in BD patients into two categories – somatic and external.
Of those with BD who died from somatic or disease-related causes, alcohol caused the highest rate of death (29%). The second-leading cause was heart disease and stroke (27%), followed by cancer (22%), respiratory diseases (4%), and diabetes (2%).
Among the 595 patients with BD who died because of alcohol consumption, liver disease was the leading cause of death (48%). The second cause was accidental alcohol poisoning (28%), followed by alcohol dependence (10%).
The leading cause of death from external causes in BD patients was suicide (58%, or 740), nearly half of which (48%) were from an overdose with prescribed psychotropic medications.
Overall, 64%, or 2,104, of the deaths in BD patients from any cause were considered excess deaths, that is, the number of deaths above those expected for those without BD of comparable age and sex.
Most of the excess deaths from somatic illness were either from alcohol-related causes (40%) – a rate three times higher than that of the general population – CVD (26%), or cancer (10%).
High suicide rate
When the team examined excess deaths from external causes, they found that 61% (651) were attributable to suicide, a rate eight times higher than that of the general population.
“In terms of absolute numbers, somatic causes of death represented the majority of all deaths in BD, as also reported in previous research,” Dr. Paljärvi said.
“However, this finding reflects the fact that in many high-income countries most of the deaths are due to somatic causes; with CVD, cancers, and diseases of the nervous system as the leading causes of death in the older age groups,” he added.
Dr. Paljärvi advised that clinicians treating patients with BD balance therapeutic response with potentially serious long-term medication side effects, to prevent premature deaths.
A stronger emphasis on identifying and treating comorbid substance abuse is also warranted, he noted.
Dr. Paljärvi noted that the underlying causes of the excess somatic mortality in people with BD are not fully understood, but may result from the “complex interaction between various established risk factors, including tobacco use, alcohol abuse, physical inactivity, unhealthy diet, obesity, hypertension, etc.”
Regarding the generalizability of the findings, he said many previous studies have been based only on inpatient data and noted that the current study included individuals from various sources including inpatient and outpatient registries as well as social insurance registries.
“While the reported excess all-cause mortality rates are strikingly similar across populations globally, there is a paucity of more detailed cause-specific analyses of excess mortality in BD,” said Dr. Paljärvi, adding that these findings should be replicated in other countries, including the United States.
Chronic inflammation
Commenting on the findings, Benjamin Goldstein, MD, PhD, professor of psychiatry and pharmacology at the University of Toronto, noted that there are clear disparities in access to, and quality of care among, patients with BD and other serious mental illnesses.
“Taking heart disease as an example, disparities exist at virtually every point of contact, ranging from the point of preventive care to the time it takes to be assessed in the ER, to the likelihood of receiving cardiac catheterization, to the quality of postdischarge care,” said Dr. Goldstein.
He also noted that CVD occurs in patients with BD, on average, 10-15 years earlier than the general population. However, he added, “there is important evidence that when people with BD receive the same standard of care as those without BD their cardiovascular outcomes are similar.”
Dr. Goldstein also noted that inflammation, which is a driver of cardiovascular risk, is elevated among patients with BD, particularly during mania and depression.
“Given that the average person with BD has some degree of mood symptoms about 40% of the time, chronically elevated inflammation likely contributes in part to the excess risk of heart disease in bipolar disorder,” he said.
Dr. Goldstein’s team’s research focuses on microvessels. “We have found that microvessel function in both the heart and the brain, determined by MRI, is reduced among teens with BD,” he said.
His team has also found that endothelial function in fingertip microvessels, an indicator of future heart disease risk, varies according to mood states.
“Collectively, these findings suggest the microvascular problems may explain, in part, the extra risk of heart disease beyond traditional risk factors in BD,” he added.
The study was funded by a Wellcome Trust Senior Clinical Research Fellowship and by the Oxford Health Biomedical Research Centre. Dr. Paljärvi and Dr. Goldstein report no relevant financial relationships.
A version of this article appeared on Medscape.com.
In addition, patients with BD are three times more likely to die prematurely of all causes, compared with the general population, with alcohol-related diseases contributing to more premature deaths than cardiovascular disease (CVD), diabetes, and cancer.
The study results emphasize the need for personalized approaches to risk prediction and prevention of premature cause-specific mortality over the life-course of individuals with BD, lead investigator Tapio Paljärvi, PhD, an epidemiologist at Niuvanniemi Hospital in Kuopio, Finland, told this news organization.
The findings were published online in BMJ Mental Health.
Alcohol a major contributor to early death
A number of studies have established that those with BD have twice the risk of dying prematurely, compared with those without the disorder.
To learn more about the factors contributing to early death in this patient population, the investigators analyzed data from nationwide Finnish medical and insurance registries. They identified and tracked the health of 47,000 patients, aged 15-64 years, with BD between 2004 and 2018.
The average age at the beginning of the monitoring period was 38 years, and 57% of the cohort were women.
To determine the excess deaths directly attributable to BD, the researchers compared the ratio of deaths observed over the monitoring period in those with BD to the number expected to die in the general population, also known as the standard mortality ratio.
Of the group with BD, 3,300 died during the monitoring period. The average age at death was 50, and almost two-thirds (65%, or 2,137) of those who died were men.
Investigators grouped excess deaths in BD patients into two categories – somatic and external.
Of those with BD who died from somatic or disease-related causes, alcohol caused the highest rate of death (29%). The second-leading cause was heart disease and stroke (27%), followed by cancer (22%), respiratory diseases (4%), and diabetes (2%).
Among the 595 patients with BD who died because of alcohol consumption, liver disease was the leading cause of death (48%). The second cause was accidental alcohol poisoning (28%), followed by alcohol dependence (10%).
The leading cause of death from external causes in BD patients was suicide (58%, or 740), nearly half of which (48%) were from an overdose with prescribed psychotropic medications.
Overall, 64%, or 2,104, of the deaths in BD patients from any cause were considered excess deaths, that is, the number of deaths above those expected for those without BD of comparable age and sex.
Most of the excess deaths from somatic illness were either from alcohol-related causes (40%) – a rate three times higher than that of the general population – CVD (26%), or cancer (10%).
High suicide rate
When the team examined excess deaths from external causes, they found that 61% (651) were attributable to suicide, a rate eight times higher than that of the general population.
“In terms of absolute numbers, somatic causes of death represented the majority of all deaths in BD, as also reported in previous research,” Dr. Paljärvi said.
“However, this finding reflects the fact that in many high-income countries most of the deaths are due to somatic causes; with CVD, cancers, and diseases of the nervous system as the leading causes of death in the older age groups,” he added.
Dr. Paljärvi advised that clinicians treating patients with BD balance therapeutic response with potentially serious long-term medication side effects, to prevent premature deaths.
A stronger emphasis on identifying and treating comorbid substance abuse is also warranted, he noted.
Dr. Paljärvi noted that the underlying causes of the excess somatic mortality in people with BD are not fully understood, but may result from the “complex interaction between various established risk factors, including tobacco use, alcohol abuse, physical inactivity, unhealthy diet, obesity, hypertension, etc.”
Regarding the generalizability of the findings, he said many previous studies have been based only on inpatient data and noted that the current study included individuals from various sources including inpatient and outpatient registries as well as social insurance registries.
“While the reported excess all-cause mortality rates are strikingly similar across populations globally, there is a paucity of more detailed cause-specific analyses of excess mortality in BD,” said Dr. Paljärvi, adding that these findings should be replicated in other countries, including the United States.
Chronic inflammation
Commenting on the findings, Benjamin Goldstein, MD, PhD, professor of psychiatry and pharmacology at the University of Toronto, noted that there are clear disparities in access to, and quality of care among, patients with BD and other serious mental illnesses.
“Taking heart disease as an example, disparities exist at virtually every point of contact, ranging from the point of preventive care to the time it takes to be assessed in the ER, to the likelihood of receiving cardiac catheterization, to the quality of postdischarge care,” said Dr. Goldstein.
He also noted that CVD occurs in patients with BD, on average, 10-15 years earlier than the general population. However, he added, “there is important evidence that when people with BD receive the same standard of care as those without BD their cardiovascular outcomes are similar.”
Dr. Goldstein also noted that inflammation, which is a driver of cardiovascular risk, is elevated among patients with BD, particularly during mania and depression.
“Given that the average person with BD has some degree of mood symptoms about 40% of the time, chronically elevated inflammation likely contributes in part to the excess risk of heart disease in bipolar disorder,” he said.
Dr. Goldstein’s team’s research focuses on microvessels. “We have found that microvessel function in both the heart and the brain, determined by MRI, is reduced among teens with BD,” he said.
His team has also found that endothelial function in fingertip microvessels, an indicator of future heart disease risk, varies according to mood states.
“Collectively, these findings suggest the microvascular problems may explain, in part, the extra risk of heart disease beyond traditional risk factors in BD,” he added.
The study was funded by a Wellcome Trust Senior Clinical Research Fellowship and by the Oxford Health Biomedical Research Centre. Dr. Paljärvi and Dr. Goldstein report no relevant financial relationships.
A version of this article appeared on Medscape.com.
In addition, patients with BD are three times more likely to die prematurely of all causes, compared with the general population, with alcohol-related diseases contributing to more premature deaths than cardiovascular disease (CVD), diabetes, and cancer.
The study results emphasize the need for personalized approaches to risk prediction and prevention of premature cause-specific mortality over the life-course of individuals with BD, lead investigator Tapio Paljärvi, PhD, an epidemiologist at Niuvanniemi Hospital in Kuopio, Finland, told this news organization.
The findings were published online in BMJ Mental Health.
Alcohol a major contributor to early death
A number of studies have established that those with BD have twice the risk of dying prematurely, compared with those without the disorder.
To learn more about the factors contributing to early death in this patient population, the investigators analyzed data from nationwide Finnish medical and insurance registries. They identified and tracked the health of 47,000 patients, aged 15-64 years, with BD between 2004 and 2018.
The average age at the beginning of the monitoring period was 38 years, and 57% of the cohort were women.
To determine the excess deaths directly attributable to BD, the researchers compared the ratio of deaths observed over the monitoring period in those with BD to the number expected to die in the general population, also known as the standard mortality ratio.
Of the group with BD, 3,300 died during the monitoring period. The average age at death was 50, and almost two-thirds (65%, or 2,137) of those who died were men.
Investigators grouped excess deaths in BD patients into two categories – somatic and external.
Of those with BD who died from somatic or disease-related causes, alcohol caused the highest rate of death (29%). The second-leading cause was heart disease and stroke (27%), followed by cancer (22%), respiratory diseases (4%), and diabetes (2%).
Among the 595 patients with BD who died because of alcohol consumption, liver disease was the leading cause of death (48%). The second cause was accidental alcohol poisoning (28%), followed by alcohol dependence (10%).
The leading cause of death from external causes in BD patients was suicide (58%, or 740), nearly half of which (48%) were from an overdose with prescribed psychotropic medications.
Overall, 64%, or 2,104, of the deaths in BD patients from any cause were considered excess deaths, that is, the number of deaths above those expected for those without BD of comparable age and sex.
Most of the excess deaths from somatic illness were either from alcohol-related causes (40%) – a rate three times higher than that of the general population – CVD (26%), or cancer (10%).
High suicide rate
When the team examined excess deaths from external causes, they found that 61% (651) were attributable to suicide, a rate eight times higher than that of the general population.
“In terms of absolute numbers, somatic causes of death represented the majority of all deaths in BD, as also reported in previous research,” Dr. Paljärvi said.
“However, this finding reflects the fact that in many high-income countries most of the deaths are due to somatic causes; with CVD, cancers, and diseases of the nervous system as the leading causes of death in the older age groups,” he added.
Dr. Paljärvi advised that clinicians treating patients with BD balance therapeutic response with potentially serious long-term medication side effects, to prevent premature deaths.
A stronger emphasis on identifying and treating comorbid substance abuse is also warranted, he noted.
Dr. Paljärvi noted that the underlying causes of the excess somatic mortality in people with BD are not fully understood, but may result from the “complex interaction between various established risk factors, including tobacco use, alcohol abuse, physical inactivity, unhealthy diet, obesity, hypertension, etc.”
Regarding the generalizability of the findings, he said many previous studies have been based only on inpatient data and noted that the current study included individuals from various sources including inpatient and outpatient registries as well as social insurance registries.
“While the reported excess all-cause mortality rates are strikingly similar across populations globally, there is a paucity of more detailed cause-specific analyses of excess mortality in BD,” said Dr. Paljärvi, adding that these findings should be replicated in other countries, including the United States.
Chronic inflammation
Commenting on the findings, Benjamin Goldstein, MD, PhD, professor of psychiatry and pharmacology at the University of Toronto, noted that there are clear disparities in access to, and quality of care among, patients with BD and other serious mental illnesses.
“Taking heart disease as an example, disparities exist at virtually every point of contact, ranging from the point of preventive care to the time it takes to be assessed in the ER, to the likelihood of receiving cardiac catheterization, to the quality of postdischarge care,” said Dr. Goldstein.
He also noted that CVD occurs in patients with BD, on average, 10-15 years earlier than the general population. However, he added, “there is important evidence that when people with BD receive the same standard of care as those without BD their cardiovascular outcomes are similar.”
Dr. Goldstein also noted that inflammation, which is a driver of cardiovascular risk, is elevated among patients with BD, particularly during mania and depression.
“Given that the average person with BD has some degree of mood symptoms about 40% of the time, chronically elevated inflammation likely contributes in part to the excess risk of heart disease in bipolar disorder,” he said.
Dr. Goldstein’s team’s research focuses on microvessels. “We have found that microvessel function in both the heart and the brain, determined by MRI, is reduced among teens with BD,” he said.
His team has also found that endothelial function in fingertip microvessels, an indicator of future heart disease risk, varies according to mood states.
“Collectively, these findings suggest the microvascular problems may explain, in part, the extra risk of heart disease beyond traditional risk factors in BD,” he added.
The study was funded by a Wellcome Trust Senior Clinical Research Fellowship and by the Oxford Health Biomedical Research Centre. Dr. Paljärvi and Dr. Goldstein report no relevant financial relationships.
A version of this article appeared on Medscape.com.
FROM BMJ MENTAL HEALTH
Reassuring data on stimulants for ADHD in kids and later substance abuse
“Throughout rigorous analyses, and after accounting for more than 70 variables in this longitudinal sample of children with ADHD taking stimulants, we did not find an association with later substance use,” lead investigator Brooke Molina, PhD, director of the youth and family research program at the University of Pittsburgh, said in an interview.
The findings were published online in JAMA Psychiatry.
Protective effect?
Owing to symptoms of impulsivity inherent to ADHD, the disorder itself carries a risk for elevated substance use, the investigators note.
They speculate that this may be why some previous research suggests prescription stimulants reduce the risk of subsequent substance use disorder. However, other studies have found no such protective link.
To shed more light on the issue, the investigators used data from the Multimodal Treatment Study of ADHD, a multicenter, 14-month randomized clinical trial of medication and behavioral therapy for children with ADHD. However, for the purposes of the present study, investigators focused only on stimulant use in children.
At the time of recruitment, the children were aged 7-9 and had been diagnosed with ADHD between 1994 and 1996.
Investigators assessed the participants prior to randomization, at months 3 and 9, and at the end of treatment. They were then followed for 16 years and were assessed at years 2, 3, 6, 8, 10, 12, 14, and 16 until a mean age of 25.
During 12-, 14-, and 16-year follow-up, participants completed a questionnaire on their use of alcohol, marijuana, cigarettes, and several illicit and prescription drugs.
Investigators collected information on participants’ stimulant treatment via the Services for Children and Adolescents Parent Interview until they reached age 18. After that, participants reported their own stimulant treatment.
A total of 579 participants were included in the analysis. Of these, 61% were White, 20% were Black, and 8% were Hispanic.
Decline in stimulant use over time
The analysis showed that stimulant use declined “precipitously” over time – from 60% at the 2- and 3-year assessments to an average of 7% during early adulthood.
The investigators also found that for some participants, substance use increased steadily through adolescence and remained stable through early adulthood. For instance, 36.5% of the adolescents in the total cohort reported smoking tobacco daily, and 29.6% reported using marijuana every week.
In addition, approximately 21% of the participants indulged in heavy drinking at least once a week, and 6% reported “other” substance use, which included sedative misuse, heroin, inhalants, hallucinogens, or other substances taken to “get high.”
After accounting for developmental trends in substance use in the sample through adolescence into early adulthood with several rigorous statistical models, the researchers found no association between current or prior stimulant treatment and cigarette, marijuana, alcohol, or other substance use, with one exception.
While cumulative stimulant treatment was associated with increased heavy drinking, the effect size of this association was small. Each additional year of cumulative stimulant use was estimated to increase participants’ likelihood of any binge drinking/drunkenness vs. none in the past year by 4% (95% confidence interval, 0.01-0.08; P =.03).
When the investigators used a causal analytic method to account for age and other time-varying characteristics, including household income, behavior problems, and parental support, there was no evidence that current (B range, –0.62-0.34) or prior stimulant treatment (B range, –0.06-0.70) or their interaction (B range, –0.49-0.86) was associated with substance use in adulthood.
Dr. Molina noted that although participants were recruited from multiple sites, the sample may not be generalizable because children and parents who present for an intensive treatment study such as this are not necessarily representative of the general ADHD population.
Reassuring findings
In a comment, Julie Schweitzer, PhD, professor of psychiatry and behavioral sciences at the University of California, Davis, said she hopes the study findings will quell the stigma surrounding stimulant use by children with ADHD.
“Parents’ fears that stimulant use will lead to a substance use disorder inhibits them from bringing their children for an ADHD evaluation, thus reducing the likelihood that they will receive timely treatment,” Dr. Schweitzer said.
“While stimulant medication is the first-line treatment most often recommended for most persons with ADHD, by not following through on evaluations, parents also miss the opportunity to learn about nonpharmacological strategies that might also be helpful to help cope with ADHD symptoms and its potential co-occurring challenges,” she added.
Dr. Schweitzer also noted that many parents hope their children will outgrow the symptoms without realizing that by not obtaining an evaluation and treatment for their child, there is an associated cost, including less than optimal academic performance, social relationships, and emotional health.
The Multimodal Treatment Study of Children with ADHD was a National Institute of Mental Health cooperative agreement randomized clinical trial, continued under an NIMH contract as a follow-up study and under a National Institute on Drug Abuse contract followed by a data analysis grant. Dr. Molina reported grants from the NIMH and the National Institute on Drug Abuse during the conduct of the study.
A version of this article first appeared on Medscape.com.
“Throughout rigorous analyses, and after accounting for more than 70 variables in this longitudinal sample of children with ADHD taking stimulants, we did not find an association with later substance use,” lead investigator Brooke Molina, PhD, director of the youth and family research program at the University of Pittsburgh, said in an interview.
The findings were published online in JAMA Psychiatry.
Protective effect?
Owing to symptoms of impulsivity inherent to ADHD, the disorder itself carries a risk for elevated substance use, the investigators note.
They speculate that this may be why some previous research suggests prescription stimulants reduce the risk of subsequent substance use disorder. However, other studies have found no such protective link.
To shed more light on the issue, the investigators used data from the Multimodal Treatment Study of ADHD, a multicenter, 14-month randomized clinical trial of medication and behavioral therapy for children with ADHD. However, for the purposes of the present study, investigators focused only on stimulant use in children.
At the time of recruitment, the children were aged 7-9 and had been diagnosed with ADHD between 1994 and 1996.
Investigators assessed the participants prior to randomization, at months 3 and 9, and at the end of treatment. They were then followed for 16 years and were assessed at years 2, 3, 6, 8, 10, 12, 14, and 16 until a mean age of 25.
During 12-, 14-, and 16-year follow-up, participants completed a questionnaire on their use of alcohol, marijuana, cigarettes, and several illicit and prescription drugs.
Investigators collected information on participants’ stimulant treatment via the Services for Children and Adolescents Parent Interview until they reached age 18. After that, participants reported their own stimulant treatment.
A total of 579 participants were included in the analysis. Of these, 61% were White, 20% were Black, and 8% were Hispanic.
Decline in stimulant use over time
The analysis showed that stimulant use declined “precipitously” over time – from 60% at the 2- and 3-year assessments to an average of 7% during early adulthood.
The investigators also found that for some participants, substance use increased steadily through adolescence and remained stable through early adulthood. For instance, 36.5% of the adolescents in the total cohort reported smoking tobacco daily, and 29.6% reported using marijuana every week.
In addition, approximately 21% of the participants indulged in heavy drinking at least once a week, and 6% reported “other” substance use, which included sedative misuse, heroin, inhalants, hallucinogens, or other substances taken to “get high.”
After accounting for developmental trends in substance use in the sample through adolescence into early adulthood with several rigorous statistical models, the researchers found no association between current or prior stimulant treatment and cigarette, marijuana, alcohol, or other substance use, with one exception.
While cumulative stimulant treatment was associated with increased heavy drinking, the effect size of this association was small. Each additional year of cumulative stimulant use was estimated to increase participants’ likelihood of any binge drinking/drunkenness vs. none in the past year by 4% (95% confidence interval, 0.01-0.08; P =.03).
When the investigators used a causal analytic method to account for age and other time-varying characteristics, including household income, behavior problems, and parental support, there was no evidence that current (B range, –0.62-0.34) or prior stimulant treatment (B range, –0.06-0.70) or their interaction (B range, –0.49-0.86) was associated with substance use in adulthood.
Dr. Molina noted that although participants were recruited from multiple sites, the sample may not be generalizable because children and parents who present for an intensive treatment study such as this are not necessarily representative of the general ADHD population.
Reassuring findings
In a comment, Julie Schweitzer, PhD, professor of psychiatry and behavioral sciences at the University of California, Davis, said she hopes the study findings will quell the stigma surrounding stimulant use by children with ADHD.
“Parents’ fears that stimulant use will lead to a substance use disorder inhibits them from bringing their children for an ADHD evaluation, thus reducing the likelihood that they will receive timely treatment,” Dr. Schweitzer said.
“While stimulant medication is the first-line treatment most often recommended for most persons with ADHD, by not following through on evaluations, parents also miss the opportunity to learn about nonpharmacological strategies that might also be helpful to help cope with ADHD symptoms and its potential co-occurring challenges,” she added.
Dr. Schweitzer also noted that many parents hope their children will outgrow the symptoms without realizing that by not obtaining an evaluation and treatment for their child, there is an associated cost, including less than optimal academic performance, social relationships, and emotional health.
The Multimodal Treatment Study of Children with ADHD was a National Institute of Mental Health cooperative agreement randomized clinical trial, continued under an NIMH contract as a follow-up study and under a National Institute on Drug Abuse contract followed by a data analysis grant. Dr. Molina reported grants from the NIMH and the National Institute on Drug Abuse during the conduct of the study.
A version of this article first appeared on Medscape.com.
“Throughout rigorous analyses, and after accounting for more than 70 variables in this longitudinal sample of children with ADHD taking stimulants, we did not find an association with later substance use,” lead investigator Brooke Molina, PhD, director of the youth and family research program at the University of Pittsburgh, said in an interview.
The findings were published online in JAMA Psychiatry.
Protective effect?
Owing to symptoms of impulsivity inherent to ADHD, the disorder itself carries a risk for elevated substance use, the investigators note.
They speculate that this may be why some previous research suggests prescription stimulants reduce the risk of subsequent substance use disorder. However, other studies have found no such protective link.
To shed more light on the issue, the investigators used data from the Multimodal Treatment Study of ADHD, a multicenter, 14-month randomized clinical trial of medication and behavioral therapy for children with ADHD. However, for the purposes of the present study, investigators focused only on stimulant use in children.
At the time of recruitment, the children were aged 7-9 and had been diagnosed with ADHD between 1994 and 1996.
Investigators assessed the participants prior to randomization, at months 3 and 9, and at the end of treatment. They were then followed for 16 years and were assessed at years 2, 3, 6, 8, 10, 12, 14, and 16 until a mean age of 25.
During 12-, 14-, and 16-year follow-up, participants completed a questionnaire on their use of alcohol, marijuana, cigarettes, and several illicit and prescription drugs.
Investigators collected information on participants’ stimulant treatment via the Services for Children and Adolescents Parent Interview until they reached age 18. After that, participants reported their own stimulant treatment.
A total of 579 participants were included in the analysis. Of these, 61% were White, 20% were Black, and 8% were Hispanic.
Decline in stimulant use over time
The analysis showed that stimulant use declined “precipitously” over time – from 60% at the 2- and 3-year assessments to an average of 7% during early adulthood.
The investigators also found that for some participants, substance use increased steadily through adolescence and remained stable through early adulthood. For instance, 36.5% of the adolescents in the total cohort reported smoking tobacco daily, and 29.6% reported using marijuana every week.
In addition, approximately 21% of the participants indulged in heavy drinking at least once a week, and 6% reported “other” substance use, which included sedative misuse, heroin, inhalants, hallucinogens, or other substances taken to “get high.”
After accounting for developmental trends in substance use in the sample through adolescence into early adulthood with several rigorous statistical models, the researchers found no association between current or prior stimulant treatment and cigarette, marijuana, alcohol, or other substance use, with one exception.
While cumulative stimulant treatment was associated with increased heavy drinking, the effect size of this association was small. Each additional year of cumulative stimulant use was estimated to increase participants’ likelihood of any binge drinking/drunkenness vs. none in the past year by 4% (95% confidence interval, 0.01-0.08; P =.03).
When the investigators used a causal analytic method to account for age and other time-varying characteristics, including household income, behavior problems, and parental support, there was no evidence that current (B range, –0.62-0.34) or prior stimulant treatment (B range, –0.06-0.70) or their interaction (B range, –0.49-0.86) was associated with substance use in adulthood.
Dr. Molina noted that although participants were recruited from multiple sites, the sample may not be generalizable because children and parents who present for an intensive treatment study such as this are not necessarily representative of the general ADHD population.
Reassuring findings
In a comment, Julie Schweitzer, PhD, professor of psychiatry and behavioral sciences at the University of California, Davis, said she hopes the study findings will quell the stigma surrounding stimulant use by children with ADHD.
“Parents’ fears that stimulant use will lead to a substance use disorder inhibits them from bringing their children for an ADHD evaluation, thus reducing the likelihood that they will receive timely treatment,” Dr. Schweitzer said.
“While stimulant medication is the first-line treatment most often recommended for most persons with ADHD, by not following through on evaluations, parents also miss the opportunity to learn about nonpharmacological strategies that might also be helpful to help cope with ADHD symptoms and its potential co-occurring challenges,” she added.
Dr. Schweitzer also noted that many parents hope their children will outgrow the symptoms without realizing that by not obtaining an evaluation and treatment for their child, there is an associated cost, including less than optimal academic performance, social relationships, and emotional health.
The Multimodal Treatment Study of Children with ADHD was a National Institute of Mental Health cooperative agreement randomized clinical trial, continued under an NIMH contract as a follow-up study and under a National Institute on Drug Abuse contract followed by a data analysis grant. Dr. Molina reported grants from the NIMH and the National Institute on Drug Abuse during the conduct of the study.
A version of this article first appeared on Medscape.com.
FROM JAMA PSYCHIATRY
Tooth loss, gum disease tied to hippocampal atrophy
Gum disease and tooth loss are linked to hippocampal atrophy and may have a more negative impact on the brain than aging, new research suggests.
Investigators found that in a late middle-aged and older cohort, among patients with mild periodontitis, having fewer teeth was linked to a faster rate of left hippocampal atrophy. For those with severe gum disease, each additional lost tooth was associated with a faster rate of brain shrinkage, equivalent to 1.3 years of brain aging.
“Tooth loss and gum disease, which is inflammation of the tissue around the teeth that can cause shrinkage of the gums and loosening of the teeth, are very common, so evaluating a potential link with dementia is incredibly important,” study investigator Satoshi Yamaguchi, PhD, DDS, of Tohoku University, in Sendai, Japan, said in a release.
“Our study found that these conditions may play a role in the health of the brain area that controls thinking and memory, giving people another reason to take better care of their teeth,” Dr. Yamaguchi noted.
The findings were published online in Neurology.
Greater effect than aging
Although previous research suggests that tooth loss and periodontitis are risk factors for Alzheimer’s disease, longitudinal research has not shown a significant correlation between these conditions and hippocampal atrophy.
To clarify this association, the investigators followed 172 men and women (average age, 67 years) who had undergone two MRI brain scans 4 years apart and had had a dental examination. None of the participants had any signs of cognitive decline at baseline.
At study outset, information on cerebrovascular and cardiovascular disease, alcohol consumption, smoking, depression history, and cognitive function was gathered. The Mini Mental State Exam and dental exams were administered at baseline and at 4-year follow-up.
For each participant, the number of teeth was counted, and all participants were assessed for gum disease via periodontal probing depth (PD).
Healthy gums typically measure between 1 and 3 mm in depth. Mild gum disease is signified by measurements of 3-4 mm in several areas. Severe gum disease involves measurements of 5-6 mm and is accompanied by greater bone loss, leading to potential tooth loss.
Multiple regression analysis was performed, with the annual symmetric percentage change (SPC) of hippocampal volume as the dependent variable. The analysis included an interaction term between the number of teeth present (NTP) and mean PD.
Over the 4-year study period, the investigators found that the qualitative interaction between NTP and mean PD was significant for the annual SPC in the left hippocampus.
Among those with mild periodontitis, having fewer teeth correlated with more rapid atrophy of the left hippocampus, such that every tooth lost was equivalent to nearly 1 year of brain aging.
In contrast, having more teeth was associated with a faster rate of left hippocampal atrophy among those with severe periodontitis and was equivalent to 1.3 years of brain aging.
For those with severe gum disease, each additional lost tooth corresponded to a faster rate of brain shrinkage, equivalent to 1.3 years of brain aging.
“This finding indicates that periodontitis may have a greater association with left hippocampal atrophy than the association exhibited by age. Furthermore, in cases of mild periodontitis, fewer teeth may be associated with a subsequent decline in cognitive function,” the investigators write.
The study’s results, they add, highlight the importance of preserving oral health, not just the retaining of teeth. “These findings suggest that retaining teeth with severe gum disease is associated with brain atrophy,” said Dr. Yamaguchi.
“Controlling the progression of gum disease through regular dental visits is crucial, and teeth with severe gum disease may need to be extracted and replaced with appropriate prosthetic devices,” he added.
The researchers note that further studies are needed to confirm these findings.
The study was supported the Japanese Ministry of Education, Culture, Sports, Science, and Technology; Kelo University; Japan Arteriosclerosis Prevention Fund; Japanese Ministry of Health, Labor, and Welfare; Teiko University; Pfizer Japan; Bayer Yakuhin; Chugai Pharmaceutical; Daiichi Sankyo; Astrellas Pharma; Takeda Pharmaceutical; the Health Care Science Institute; the Health Science Center; and the Takeda Science Foundation. The investigators reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Gum disease and tooth loss are linked to hippocampal atrophy and may have a more negative impact on the brain than aging, new research suggests.
Investigators found that in a late middle-aged and older cohort, among patients with mild periodontitis, having fewer teeth was linked to a faster rate of left hippocampal atrophy. For those with severe gum disease, each additional lost tooth was associated with a faster rate of brain shrinkage, equivalent to 1.3 years of brain aging.
“Tooth loss and gum disease, which is inflammation of the tissue around the teeth that can cause shrinkage of the gums and loosening of the teeth, are very common, so evaluating a potential link with dementia is incredibly important,” study investigator Satoshi Yamaguchi, PhD, DDS, of Tohoku University, in Sendai, Japan, said in a release.
“Our study found that these conditions may play a role in the health of the brain area that controls thinking and memory, giving people another reason to take better care of their teeth,” Dr. Yamaguchi noted.
The findings were published online in Neurology.
Greater effect than aging
Although previous research suggests that tooth loss and periodontitis are risk factors for Alzheimer’s disease, longitudinal research has not shown a significant correlation between these conditions and hippocampal atrophy.
To clarify this association, the investigators followed 172 men and women (average age, 67 years) who had undergone two MRI brain scans 4 years apart and had had a dental examination. None of the participants had any signs of cognitive decline at baseline.
At study outset, information on cerebrovascular and cardiovascular disease, alcohol consumption, smoking, depression history, and cognitive function was gathered. The Mini Mental State Exam and dental exams were administered at baseline and at 4-year follow-up.
For each participant, the number of teeth was counted, and all participants were assessed for gum disease via periodontal probing depth (PD).
Healthy gums typically measure between 1 and 3 mm in depth. Mild gum disease is signified by measurements of 3-4 mm in several areas. Severe gum disease involves measurements of 5-6 mm and is accompanied by greater bone loss, leading to potential tooth loss.
Multiple regression analysis was performed, with the annual symmetric percentage change (SPC) of hippocampal volume as the dependent variable. The analysis included an interaction term between the number of teeth present (NTP) and mean PD.
Over the 4-year study period, the investigators found that the qualitative interaction between NTP and mean PD was significant for the annual SPC in the left hippocampus.
Among those with mild periodontitis, having fewer teeth correlated with more rapid atrophy of the left hippocampus, such that every tooth lost was equivalent to nearly 1 year of brain aging.
In contrast, having more teeth was associated with a faster rate of left hippocampal atrophy among those with severe periodontitis and was equivalent to 1.3 years of brain aging.
For those with severe gum disease, each additional lost tooth corresponded to a faster rate of brain shrinkage, equivalent to 1.3 years of brain aging.
“This finding indicates that periodontitis may have a greater association with left hippocampal atrophy than the association exhibited by age. Furthermore, in cases of mild periodontitis, fewer teeth may be associated with a subsequent decline in cognitive function,” the investigators write.
The study’s results, they add, highlight the importance of preserving oral health, not just the retaining of teeth. “These findings suggest that retaining teeth with severe gum disease is associated with brain atrophy,” said Dr. Yamaguchi.
“Controlling the progression of gum disease through regular dental visits is crucial, and teeth with severe gum disease may need to be extracted and replaced with appropriate prosthetic devices,” he added.
The researchers note that further studies are needed to confirm these findings.
The study was supported the Japanese Ministry of Education, Culture, Sports, Science, and Technology; Kelo University; Japan Arteriosclerosis Prevention Fund; Japanese Ministry of Health, Labor, and Welfare; Teiko University; Pfizer Japan; Bayer Yakuhin; Chugai Pharmaceutical; Daiichi Sankyo; Astrellas Pharma; Takeda Pharmaceutical; the Health Care Science Institute; the Health Science Center; and the Takeda Science Foundation. The investigators reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Gum disease and tooth loss are linked to hippocampal atrophy and may have a more negative impact on the brain than aging, new research suggests.
Investigators found that in a late middle-aged and older cohort, among patients with mild periodontitis, having fewer teeth was linked to a faster rate of left hippocampal atrophy. For those with severe gum disease, each additional lost tooth was associated with a faster rate of brain shrinkage, equivalent to 1.3 years of brain aging.
“Tooth loss and gum disease, which is inflammation of the tissue around the teeth that can cause shrinkage of the gums and loosening of the teeth, are very common, so evaluating a potential link with dementia is incredibly important,” study investigator Satoshi Yamaguchi, PhD, DDS, of Tohoku University, in Sendai, Japan, said in a release.
“Our study found that these conditions may play a role in the health of the brain area that controls thinking and memory, giving people another reason to take better care of their teeth,” Dr. Yamaguchi noted.
The findings were published online in Neurology.
Greater effect than aging
Although previous research suggests that tooth loss and periodontitis are risk factors for Alzheimer’s disease, longitudinal research has not shown a significant correlation between these conditions and hippocampal atrophy.
To clarify this association, the investigators followed 172 men and women (average age, 67 years) who had undergone two MRI brain scans 4 years apart and had had a dental examination. None of the participants had any signs of cognitive decline at baseline.
At study outset, information on cerebrovascular and cardiovascular disease, alcohol consumption, smoking, depression history, and cognitive function was gathered. The Mini Mental State Exam and dental exams were administered at baseline and at 4-year follow-up.
For each participant, the number of teeth was counted, and all participants were assessed for gum disease via periodontal probing depth (PD).
Healthy gums typically measure between 1 and 3 mm in depth. Mild gum disease is signified by measurements of 3-4 mm in several areas. Severe gum disease involves measurements of 5-6 mm and is accompanied by greater bone loss, leading to potential tooth loss.
Multiple regression analysis was performed, with the annual symmetric percentage change (SPC) of hippocampal volume as the dependent variable. The analysis included an interaction term between the number of teeth present (NTP) and mean PD.
Over the 4-year study period, the investigators found that the qualitative interaction between NTP and mean PD was significant for the annual SPC in the left hippocampus.
Among those with mild periodontitis, having fewer teeth correlated with more rapid atrophy of the left hippocampus, such that every tooth lost was equivalent to nearly 1 year of brain aging.
In contrast, having more teeth was associated with a faster rate of left hippocampal atrophy among those with severe periodontitis and was equivalent to 1.3 years of brain aging.
For those with severe gum disease, each additional lost tooth corresponded to a faster rate of brain shrinkage, equivalent to 1.3 years of brain aging.
“This finding indicates that periodontitis may have a greater association with left hippocampal atrophy than the association exhibited by age. Furthermore, in cases of mild periodontitis, fewer teeth may be associated with a subsequent decline in cognitive function,” the investigators write.
The study’s results, they add, highlight the importance of preserving oral health, not just the retaining of teeth. “These findings suggest that retaining teeth with severe gum disease is associated with brain atrophy,” said Dr. Yamaguchi.
“Controlling the progression of gum disease through regular dental visits is crucial, and teeth with severe gum disease may need to be extracted and replaced with appropriate prosthetic devices,” he added.
The researchers note that further studies are needed to confirm these findings.
The study was supported the Japanese Ministry of Education, Culture, Sports, Science, and Technology; Kelo University; Japan Arteriosclerosis Prevention Fund; Japanese Ministry of Health, Labor, and Welfare; Teiko University; Pfizer Japan; Bayer Yakuhin; Chugai Pharmaceutical; Daiichi Sankyo; Astrellas Pharma; Takeda Pharmaceutical; the Health Care Science Institute; the Health Science Center; and the Takeda Science Foundation. The investigators reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM NEUROLOGY
Social isolation linked to lower brain volume
Further, the association between social isolation and reduced brain volume appears to be at least partly mediated by depressive symptoms.
“We believe that efforts should be made to reduce social isolation among the elderly as much as possible,” investigator Toshiharu Ninomiya, MD, PhD, professor of epidemiology and public health at Kyushu University in Fukuoka, Japan, said in an interview.
The study was published online in Neurology.
A dementia prevention strategy
Dr. Ninomiya noted there have been several studies suggesting that social interaction is beneficial in preventing cognitive decline and the onset of dementia.
In addition, recent epidemiological studies have shown social isolation is associated with a risk for cognitive decline and dementia.
Although the investigators note that very little is known about the link between the two, some studies have shown that social isolation is linked with depressive symptoms in older adults, and late-life depression has been associated with brain atrophy.
To explore the potential link between social isolation and brain atrophy, as well as the role of depression as a potential mediator, the investigators studied nearly 9,000 citizens aged 65 and older as part of the Japan Prospective Studies Collaboration for Aging and Dementia (JPSC-AD), an ongoing, community-based nationwide cohort study of dementia in Japan.
Participants were recruited from eight research sites across Japan, and each had a baseline MRI scan between 2016 and 2018. The investigators excluded those with a dementia diagnosis at baseline. Self-reported frequency of social contact was categorized as every day, several times a week, several times a month, or seldom.
Participants also answered questions about medical history and treatment, antihypertensive or antidiabetic medications, exercise, current alcohol intake, and smoking habits. Depressive symptoms were assessed with the Geriatric Depression Scale. Of the participants, 57% were women, and the mean age was 73 years.
Lower brain volume
Total brain volume was lower in those with the lowest frequency of social contact vs. those with the highest frequency (67.3% vs. 67.8%). Less social contact was also linked to smaller temporal lobe, occipital lobe, cingulum, hippocampus, and amygdala volumes.
White matter lesion volume increased with fewer social interactions, from 0.26% in the most social group to 0.30% in the least.
Cognitive function was higher in participants who had daily social contact, compared with those who had the least contact (28 vs. 27 on the Mini-Mental State Examination; P < .001). Scores between 25 and 30 are considered normal.
Depressive symptoms were lower in the daily contact group, compared with the seldom-contact group (P < .001).
The team also found that lower frequency of social contact was significantly associated with the smaller superior, middle, or inferior temporal gyrus; and a smaller fusiform gyrus, transverse temporal gyrus, temporal pole, and entorhinal cortex, among other subregions.
Mediation analyses indicated that depressive symptoms accounted for only 15%-29% of the associations of lower frequency of social contact with each regional volume.
Worse physical health
The results also showed that socially isolated participants were more likely to have diabetes, to have hypertension, to smoke, and to be physically inactive.
“Cardiovascular risk factors have been reported to cause endothelial dysfunction in the brain, which could in turn lead to problems in maintaining microcirculation and blood-brain barrier function,” the investigators write.
Some epidemiological studies have associated cardiovascular risk factors with brain atrophy, they noted, which could have been one of the underlying mechanisms.
Another possibility is that reduced cognitive stimulation due to social isolation may cause brain atrophy, they add.
“Ultimately,” Dr. Ninomiya said, “the detailed mechanism of the relationship between social isolation and brain volume is not yet clear.”
He also said more research is needed to know whether the findings would apply to people in other countries.
In an accompanying editorial, Alexa Walter, PhD, and Danielle Sandsmark, MD, PhD, from the University of Pennsylvania, Philadelphia, note that isolation has been associated with many adverse health outcomes, including increased risk of heart disease, stroke, and premature death.
“Given these findings, future work considering social health factors in the context of neurological disease is an important area of research to consider. Additionally, leveraging other existing longitudinal studies could provide us with an opportunity to better understand these relationships within populations and inform public policy to address these issues,” Dr. Walter and Dr. Sandsmark write.
The study was funded by the Japan Agency for Medical Research and Development and Suntory Holdings Limited. Dr. Ninomiya reports receiving grants from Suntory Holdings Limited.
A version of this article first appeared on Medscape.com.
Further, the association between social isolation and reduced brain volume appears to be at least partly mediated by depressive symptoms.
“We believe that efforts should be made to reduce social isolation among the elderly as much as possible,” investigator Toshiharu Ninomiya, MD, PhD, professor of epidemiology and public health at Kyushu University in Fukuoka, Japan, said in an interview.
The study was published online in Neurology.
A dementia prevention strategy
Dr. Ninomiya noted there have been several studies suggesting that social interaction is beneficial in preventing cognitive decline and the onset of dementia.
In addition, recent epidemiological studies have shown social isolation is associated with a risk for cognitive decline and dementia.
Although the investigators note that very little is known about the link between the two, some studies have shown that social isolation is linked with depressive symptoms in older adults, and late-life depression has been associated with brain atrophy.
To explore the potential link between social isolation and brain atrophy, as well as the role of depression as a potential mediator, the investigators studied nearly 9,000 citizens aged 65 and older as part of the Japan Prospective Studies Collaboration for Aging and Dementia (JPSC-AD), an ongoing, community-based nationwide cohort study of dementia in Japan.
Participants were recruited from eight research sites across Japan, and each had a baseline MRI scan between 2016 and 2018. The investigators excluded those with a dementia diagnosis at baseline. Self-reported frequency of social contact was categorized as every day, several times a week, several times a month, or seldom.
Participants also answered questions about medical history and treatment, antihypertensive or antidiabetic medications, exercise, current alcohol intake, and smoking habits. Depressive symptoms were assessed with the Geriatric Depression Scale. Of the participants, 57% were women, and the mean age was 73 years.
Lower brain volume
Total brain volume was lower in those with the lowest frequency of social contact vs. those with the highest frequency (67.3% vs. 67.8%). Less social contact was also linked to smaller temporal lobe, occipital lobe, cingulum, hippocampus, and amygdala volumes.
White matter lesion volume increased with fewer social interactions, from 0.26% in the most social group to 0.30% in the least.
Cognitive function was higher in participants who had daily social contact, compared with those who had the least contact (28 vs. 27 on the Mini-Mental State Examination; P < .001). Scores between 25 and 30 are considered normal.
Depressive symptoms were lower in the daily contact group, compared with the seldom-contact group (P < .001).
The team also found that lower frequency of social contact was significantly associated with the smaller superior, middle, or inferior temporal gyrus; and a smaller fusiform gyrus, transverse temporal gyrus, temporal pole, and entorhinal cortex, among other subregions.
Mediation analyses indicated that depressive symptoms accounted for only 15%-29% of the associations of lower frequency of social contact with each regional volume.
Worse physical health
The results also showed that socially isolated participants were more likely to have diabetes, to have hypertension, to smoke, and to be physically inactive.
“Cardiovascular risk factors have been reported to cause endothelial dysfunction in the brain, which could in turn lead to problems in maintaining microcirculation and blood-brain barrier function,” the investigators write.
Some epidemiological studies have associated cardiovascular risk factors with brain atrophy, they noted, which could have been one of the underlying mechanisms.
Another possibility is that reduced cognitive stimulation due to social isolation may cause brain atrophy, they add.
“Ultimately,” Dr. Ninomiya said, “the detailed mechanism of the relationship between social isolation and brain volume is not yet clear.”
He also said more research is needed to know whether the findings would apply to people in other countries.
In an accompanying editorial, Alexa Walter, PhD, and Danielle Sandsmark, MD, PhD, from the University of Pennsylvania, Philadelphia, note that isolation has been associated with many adverse health outcomes, including increased risk of heart disease, stroke, and premature death.
“Given these findings, future work considering social health factors in the context of neurological disease is an important area of research to consider. Additionally, leveraging other existing longitudinal studies could provide us with an opportunity to better understand these relationships within populations and inform public policy to address these issues,” Dr. Walter and Dr. Sandsmark write.
The study was funded by the Japan Agency for Medical Research and Development and Suntory Holdings Limited. Dr. Ninomiya reports receiving grants from Suntory Holdings Limited.
A version of this article first appeared on Medscape.com.
Further, the association between social isolation and reduced brain volume appears to be at least partly mediated by depressive symptoms.
“We believe that efforts should be made to reduce social isolation among the elderly as much as possible,” investigator Toshiharu Ninomiya, MD, PhD, professor of epidemiology and public health at Kyushu University in Fukuoka, Japan, said in an interview.
The study was published online in Neurology.
A dementia prevention strategy
Dr. Ninomiya noted there have been several studies suggesting that social interaction is beneficial in preventing cognitive decline and the onset of dementia.
In addition, recent epidemiological studies have shown social isolation is associated with a risk for cognitive decline and dementia.
Although the investigators note that very little is known about the link between the two, some studies have shown that social isolation is linked with depressive symptoms in older adults, and late-life depression has been associated with brain atrophy.
To explore the potential link between social isolation and brain atrophy, as well as the role of depression as a potential mediator, the investigators studied nearly 9,000 citizens aged 65 and older as part of the Japan Prospective Studies Collaboration for Aging and Dementia (JPSC-AD), an ongoing, community-based nationwide cohort study of dementia in Japan.
Participants were recruited from eight research sites across Japan, and each had a baseline MRI scan between 2016 and 2018. The investigators excluded those with a dementia diagnosis at baseline. Self-reported frequency of social contact was categorized as every day, several times a week, several times a month, or seldom.
Participants also answered questions about medical history and treatment, antihypertensive or antidiabetic medications, exercise, current alcohol intake, and smoking habits. Depressive symptoms were assessed with the Geriatric Depression Scale. Of the participants, 57% were women, and the mean age was 73 years.
Lower brain volume
Total brain volume was lower in those with the lowest frequency of social contact vs. those with the highest frequency (67.3% vs. 67.8%). Less social contact was also linked to smaller temporal lobe, occipital lobe, cingulum, hippocampus, and amygdala volumes.
White matter lesion volume increased with fewer social interactions, from 0.26% in the most social group to 0.30% in the least.
Cognitive function was higher in participants who had daily social contact, compared with those who had the least contact (28 vs. 27 on the Mini-Mental State Examination; P < .001). Scores between 25 and 30 are considered normal.
Depressive symptoms were lower in the daily contact group, compared with the seldom-contact group (P < .001).
The team also found that lower frequency of social contact was significantly associated with the smaller superior, middle, or inferior temporal gyrus; and a smaller fusiform gyrus, transverse temporal gyrus, temporal pole, and entorhinal cortex, among other subregions.
Mediation analyses indicated that depressive symptoms accounted for only 15%-29% of the associations of lower frequency of social contact with each regional volume.
Worse physical health
The results also showed that socially isolated participants were more likely to have diabetes, to have hypertension, to smoke, and to be physically inactive.
“Cardiovascular risk factors have been reported to cause endothelial dysfunction in the brain, which could in turn lead to problems in maintaining microcirculation and blood-brain barrier function,” the investigators write.
Some epidemiological studies have associated cardiovascular risk factors with brain atrophy, they noted, which could have been one of the underlying mechanisms.
Another possibility is that reduced cognitive stimulation due to social isolation may cause brain atrophy, they add.
“Ultimately,” Dr. Ninomiya said, “the detailed mechanism of the relationship between social isolation and brain volume is not yet clear.”
He also said more research is needed to know whether the findings would apply to people in other countries.
In an accompanying editorial, Alexa Walter, PhD, and Danielle Sandsmark, MD, PhD, from the University of Pennsylvania, Philadelphia, note that isolation has been associated with many adverse health outcomes, including increased risk of heart disease, stroke, and premature death.
“Given these findings, future work considering social health factors in the context of neurological disease is an important area of research to consider. Additionally, leveraging other existing longitudinal studies could provide us with an opportunity to better understand these relationships within populations and inform public policy to address these issues,” Dr. Walter and Dr. Sandsmark write.
The study was funded by the Japan Agency for Medical Research and Development and Suntory Holdings Limited. Dr. Ninomiya reports receiving grants from Suntory Holdings Limited.
A version of this article first appeared on Medscape.com.
FROM NEUROLOGY
HT, even short-term use, linked to dementia risk in women
Short-term and cyclical use of estrogen and progestin therapy for menopausal symptoms is linked to an increased risk of dementia, results of a large observational study show.
(AD) 20 years later, compared with those who didn’t use HT. The risk was present even in women who used HT for brief periods at menopause onset.
However, both the investigators and experts not involved in the research caution that further studies are needed to explore whether the increased risk of dementia stems from HT use or whether women in need of HT have other underlying dementia risk factors.
“We cannot guarantee that our findings illustrate a causal relationship or if they represent underlying disposition to dementia in women in need of [HT],” lead investigator Nelsan Pourhadi, MD, from the Danish Dementia Research Centre at Copenhagen University Hospital Rigshospitalet, told this news organization.
Still, he added, the findings supported evidence from the Women’s Health Initiative Memory Study (WHIMS), the largest randomized trial on menopausal hormone therapy and dementia.
The findings were published online in BMJ.
Conflicting findings
Before WHIMS was published in 2003, HT was widely prescribed to relieve menopausal symptoms. However, WHIMS, which included more than 4,000 women aged 65 years or older, revealed that HT was associated with a twofold increased risk of dementia.
Studies published since then have yielded mixed results, adding to the controversy surrounding the safety of HT.
To discover whether age of initiation or length of duration of HT affects health outcomes, Dr. Pourhadi and his team undertook the observational study.
Between 2000 and 2018, the researchers tracked more than 60,000 Danish women aged 50-60 years using diagnosis and prescription information from Denmark’s National Registry of Patients.
The registry records showed that nearly 5,600 women developed dementia and 56,000 did not develop dementia. Of the 5,600 women with dementia, 1,460 had a diagnosis of AD.
Nearly 18,000 participants in the study sample received HT – 1,790 (29%) in the dementia group and 16,150 (32%) in the control group. Half started treatment before age 53 years and half stopped within 4 years. Roughly 90% used oral medications, which included a combination of estrogen and progestin.
The median age at which participants started HT was 53 years for both cases and controls, and the median duration of use was 4 years.
Longer use equals greater risk
Compared with those who did not use HT, those who used estrogen-progestin therapy had a 24% increased risk of developing all-cause dementia (hazard ratio, 1.24; 95% confidence interval, 1.17-1.44).
The increased dementia risk was similar between continuous (estrogen and progestin taken daily) and cyclic (daily estrogen with progestin taken 10-14 days a month) treatment regimens.
Longer durations of HT use were associated with increased risk, ranging from a 21% increased risk (HR, 1.21; 95% CI, 1.09-1.35) for those who used it for 1 year or less to a 74% increased risk (HR, 1.74; 95% CI, 1.45-2.10) for use lasting 12 years or more.
Women who started HT between the age of 45 and 50 had a 26% increased risk of developing all-cause dementia (HR, 1.26; 95% CI, 1.13-1.41) while women who initiated HT between age 51 and 60 had a 21% greater risk (HR, 1.21; 95% CI, 1.12-1.29).
Progestin-only or vaginal-estrogen-only therapy was not associated with the development of dementia.
The investigators noted that because this is an observational study, “further studies are warranted to explore if the observed association in this study between menopausal hormone therapy use and increased risk of dementia illustrates a causal effect.”
No causal relationship
In an accompanying editorial, Kejal Kantarci, MD, a professor of radiology at the Mayo Clinic, Rochester, Minn., noted that three clinical trials, including the WHIMS of Younger Women (WHIMS-Y) in 2013, did not show a link between cognitive function and HT.
“Although [Dr.] Pourhadi and colleagues’ study was done carefully using national registries, the observed associations could be artefactual and should not be used to infer a causal relationship between hormone therapy and dementia risk. These findings cannot inform shared decision-making about use of hormone therapy for menopausal symptoms,” she states in the editorial.
Also commenting on the findings, Amanda Heslegrave, PhD, a senior research fellow at the U.K. Dementia Research Institute, London, said in a release from the U.K.’s Science Media Centre that while the study “may cause alarm for women taking [HT], it highlights just how much we still don’t know about the effects of hormones on women’s brain health, and with promising treatments on the horizon, it should be a call to action to make this a priority area of research.”
There was no specific funding for the study. Dr. Kantarci reported working on an unpaid educational activity on Alzheimer’s disease for Biogen and is the PI on a study of a PET imaging ligand for Alzheimer’s disease, to which Eli Lilly and Avid Radiopharmaceuticals donated supplies.
A version of this article originally appeared on Medscape.com.
Short-term and cyclical use of estrogen and progestin therapy for menopausal symptoms is linked to an increased risk of dementia, results of a large observational study show.
(AD) 20 years later, compared with those who didn’t use HT. The risk was present even in women who used HT for brief periods at menopause onset.
However, both the investigators and experts not involved in the research caution that further studies are needed to explore whether the increased risk of dementia stems from HT use or whether women in need of HT have other underlying dementia risk factors.
“We cannot guarantee that our findings illustrate a causal relationship or if they represent underlying disposition to dementia in women in need of [HT],” lead investigator Nelsan Pourhadi, MD, from the Danish Dementia Research Centre at Copenhagen University Hospital Rigshospitalet, told this news organization.
Still, he added, the findings supported evidence from the Women’s Health Initiative Memory Study (WHIMS), the largest randomized trial on menopausal hormone therapy and dementia.
The findings were published online in BMJ.
Conflicting findings
Before WHIMS was published in 2003, HT was widely prescribed to relieve menopausal symptoms. However, WHIMS, which included more than 4,000 women aged 65 years or older, revealed that HT was associated with a twofold increased risk of dementia.
Studies published since then have yielded mixed results, adding to the controversy surrounding the safety of HT.
To discover whether age of initiation or length of duration of HT affects health outcomes, Dr. Pourhadi and his team undertook the observational study.
Between 2000 and 2018, the researchers tracked more than 60,000 Danish women aged 50-60 years using diagnosis and prescription information from Denmark’s National Registry of Patients.
The registry records showed that nearly 5,600 women developed dementia and 56,000 did not develop dementia. Of the 5,600 women with dementia, 1,460 had a diagnosis of AD.
Nearly 18,000 participants in the study sample received HT – 1,790 (29%) in the dementia group and 16,150 (32%) in the control group. Half started treatment before age 53 years and half stopped within 4 years. Roughly 90% used oral medications, which included a combination of estrogen and progestin.
The median age at which participants started HT was 53 years for both cases and controls, and the median duration of use was 4 years.
Longer use equals greater risk
Compared with those who did not use HT, those who used estrogen-progestin therapy had a 24% increased risk of developing all-cause dementia (hazard ratio, 1.24; 95% confidence interval, 1.17-1.44).
The increased dementia risk was similar between continuous (estrogen and progestin taken daily) and cyclic (daily estrogen with progestin taken 10-14 days a month) treatment regimens.
Longer durations of HT use were associated with increased risk, ranging from a 21% increased risk (HR, 1.21; 95% CI, 1.09-1.35) for those who used it for 1 year or less to a 74% increased risk (HR, 1.74; 95% CI, 1.45-2.10) for use lasting 12 years or more.
Women who started HT between the age of 45 and 50 had a 26% increased risk of developing all-cause dementia (HR, 1.26; 95% CI, 1.13-1.41) while women who initiated HT between age 51 and 60 had a 21% greater risk (HR, 1.21; 95% CI, 1.12-1.29).
Progestin-only or vaginal-estrogen-only therapy was not associated with the development of dementia.
The investigators noted that because this is an observational study, “further studies are warranted to explore if the observed association in this study between menopausal hormone therapy use and increased risk of dementia illustrates a causal effect.”
No causal relationship
In an accompanying editorial, Kejal Kantarci, MD, a professor of radiology at the Mayo Clinic, Rochester, Minn., noted that three clinical trials, including the WHIMS of Younger Women (WHIMS-Y) in 2013, did not show a link between cognitive function and HT.
“Although [Dr.] Pourhadi and colleagues’ study was done carefully using national registries, the observed associations could be artefactual and should not be used to infer a causal relationship between hormone therapy and dementia risk. These findings cannot inform shared decision-making about use of hormone therapy for menopausal symptoms,” she states in the editorial.
Also commenting on the findings, Amanda Heslegrave, PhD, a senior research fellow at the U.K. Dementia Research Institute, London, said in a release from the U.K.’s Science Media Centre that while the study “may cause alarm for women taking [HT], it highlights just how much we still don’t know about the effects of hormones on women’s brain health, and with promising treatments on the horizon, it should be a call to action to make this a priority area of research.”
There was no specific funding for the study. Dr. Kantarci reported working on an unpaid educational activity on Alzheimer’s disease for Biogen and is the PI on a study of a PET imaging ligand for Alzheimer’s disease, to which Eli Lilly and Avid Radiopharmaceuticals donated supplies.
A version of this article originally appeared on Medscape.com.
Short-term and cyclical use of estrogen and progestin therapy for menopausal symptoms is linked to an increased risk of dementia, results of a large observational study show.
(AD) 20 years later, compared with those who didn’t use HT. The risk was present even in women who used HT for brief periods at menopause onset.
However, both the investigators and experts not involved in the research caution that further studies are needed to explore whether the increased risk of dementia stems from HT use or whether women in need of HT have other underlying dementia risk factors.
“We cannot guarantee that our findings illustrate a causal relationship or if they represent underlying disposition to dementia in women in need of [HT],” lead investigator Nelsan Pourhadi, MD, from the Danish Dementia Research Centre at Copenhagen University Hospital Rigshospitalet, told this news organization.
Still, he added, the findings supported evidence from the Women’s Health Initiative Memory Study (WHIMS), the largest randomized trial on menopausal hormone therapy and dementia.
The findings were published online in BMJ.
Conflicting findings
Before WHIMS was published in 2003, HT was widely prescribed to relieve menopausal symptoms. However, WHIMS, which included more than 4,000 women aged 65 years or older, revealed that HT was associated with a twofold increased risk of dementia.
Studies published since then have yielded mixed results, adding to the controversy surrounding the safety of HT.
To discover whether age of initiation or length of duration of HT affects health outcomes, Dr. Pourhadi and his team undertook the observational study.
Between 2000 and 2018, the researchers tracked more than 60,000 Danish women aged 50-60 years using diagnosis and prescription information from Denmark’s National Registry of Patients.
The registry records showed that nearly 5,600 women developed dementia and 56,000 did not develop dementia. Of the 5,600 women with dementia, 1,460 had a diagnosis of AD.
Nearly 18,000 participants in the study sample received HT – 1,790 (29%) in the dementia group and 16,150 (32%) in the control group. Half started treatment before age 53 years and half stopped within 4 years. Roughly 90% used oral medications, which included a combination of estrogen and progestin.
The median age at which participants started HT was 53 years for both cases and controls, and the median duration of use was 4 years.
Longer use equals greater risk
Compared with those who did not use HT, those who used estrogen-progestin therapy had a 24% increased risk of developing all-cause dementia (hazard ratio, 1.24; 95% confidence interval, 1.17-1.44).
The increased dementia risk was similar between continuous (estrogen and progestin taken daily) and cyclic (daily estrogen with progestin taken 10-14 days a month) treatment regimens.
Longer durations of HT use were associated with increased risk, ranging from a 21% increased risk (HR, 1.21; 95% CI, 1.09-1.35) for those who used it for 1 year or less to a 74% increased risk (HR, 1.74; 95% CI, 1.45-2.10) for use lasting 12 years or more.
Women who started HT between the age of 45 and 50 had a 26% increased risk of developing all-cause dementia (HR, 1.26; 95% CI, 1.13-1.41) while women who initiated HT between age 51 and 60 had a 21% greater risk (HR, 1.21; 95% CI, 1.12-1.29).
Progestin-only or vaginal-estrogen-only therapy was not associated with the development of dementia.
The investigators noted that because this is an observational study, “further studies are warranted to explore if the observed association in this study between menopausal hormone therapy use and increased risk of dementia illustrates a causal effect.”
No causal relationship
In an accompanying editorial, Kejal Kantarci, MD, a professor of radiology at the Mayo Clinic, Rochester, Minn., noted that three clinical trials, including the WHIMS of Younger Women (WHIMS-Y) in 2013, did not show a link between cognitive function and HT.
“Although [Dr.] Pourhadi and colleagues’ study was done carefully using national registries, the observed associations could be artefactual and should not be used to infer a causal relationship between hormone therapy and dementia risk. These findings cannot inform shared decision-making about use of hormone therapy for menopausal symptoms,” she states in the editorial.
Also commenting on the findings, Amanda Heslegrave, PhD, a senior research fellow at the U.K. Dementia Research Institute, London, said in a release from the U.K.’s Science Media Centre that while the study “may cause alarm for women taking [HT], it highlights just how much we still don’t know about the effects of hormones on women’s brain health, and with promising treatments on the horizon, it should be a call to action to make this a priority area of research.”
There was no specific funding for the study. Dr. Kantarci reported working on an unpaid educational activity on Alzheimer’s disease for Biogen and is the PI on a study of a PET imaging ligand for Alzheimer’s disease, to which Eli Lilly and Avid Radiopharmaceuticals donated supplies.
A version of this article originally appeared on Medscape.com.
AI model interprets EEGs with near-perfect accuracy
An automated artificial intelligence (AI) model trained to read electroencephalograms (EEGs) in patients with suspected epilepsy is just as accurate as trained neurologists, new data suggest.
Known as SCORE-AI, the technology distinguishes between abnormal and normal EEG recordings and classifies irregular recordings into specific categories crucial for patient decision-making.
“SCORE-AI can be used in place of experts in underprivileged areas, where expertise is missing, or to help physicians to preselect or prescore recordings in areas where the workload is high – we can all benefit from AI,” study investigator Sándor Beniczky, MD, PhD, said in a JAMA Neurology podcast.
Dr. Beniczky is professor of clinical neurophysiology at Aarhus University in Denmark.
The findings were published online in JAMA Neurology.
Gaining a foothold
Increasingly, AI is gaining a foothold in medicine by credibly addressing patient queries and aiding radiologists.
To bring AI to EEG interpretation, the researchers developed and validated an AI model that was able to assess routine, clinical EEGs in patients with suspected epilepsy.
Beyond using AI to distinguish abnormal from normal EEG recordings, the researchers wanted to train the new system to classify abnormal recordings into the major categories that are most relevant for clinical decision-making in patients who may have epilepsy. The categories included epileptiform-focal, epileptiform-generalized, nonepileptiform-focal, and nonepileptiform-diffuse abnormalities.
The researchers trained the learning model using Standardized Computer-based Organized Reporting of EEG (SCORE) software.
In the development phase, the model was trained using more than 30,490 anonymized and highly annotated EEG recordings from 14,100 men (median age, 25 years) from a single center. The recordings had an average duration of 31 minutes and were interpreted by 17 neurologists using standardized criteria. If an EEG recording was abnormal, the physicians had to specify which abnormal features were present.
SCORE-AI then performed an analysis of the recordings based on input from the experts.
To validate the findings, investigators used two independent test datasets. The first dataset consisted of 100 representative routine EEGs from 61 men (median age, 26 years), evaluated by 11 neurologists from different centers.
The consensus of these evaluations served as the reference standard. The second dataset comprised nearly 10,000 EEGs from a single center (5,170 men; median age, 35 years), independently assessed by 14 neurologists.
Near-perfect accuracy
When compared with the experts, SCORE-AI had near-perfect accuracy with an area under the receiver operating characteristic (AUROC) curve for differentiating normal from abnormal EEG recordings of 0.95.
SCORE-AI also performed well at identifying generalized epileptiform abnormalities (AUROC, 0.96), focal epileptiform abnormalities (AUROC, 0.91), focal nonepileptiform abnormalities (AUROC, 0.89), and diffuse nonepileptiform abnormalities (AUROC, 0.93).
In addition, SCORE-AI had excellent agreement with clinicians – and sometimes agreed with individual experts more than the experts agreed with one another.
When Dr. Beniczky and team tested SCORE-AI against three previously published AI models, SCORE-AI demonstrated greater specificity than those models (90% vs. 3%-63%) but was not as sensitive (86.7%) as two of the models (96.7% and 100%).
One of the study’s limitations was the fact that SCORE-AI was developed and validated on routine EEGs that excluded neonates and critically ill patients.
In the future, Dr. Beniczky said on the podcast, the team would like to train SCORE-AI to read EEGs with more granularity, and eventually use only one single channel to record EEGs. At present, SCORE-AI is being integrated with Natus Neuro, a widely used EEG equipment system, the investigators note.
In an accompanying editorial, Jonathan Kleen, MD, PhD, and Elan Guterman, MD, said, “The overall approach taken ... in developing and validating SCORE-AI sets a standard for this work going forward.”
Dr. Kleen and Dr. Guterman note that the technological gains brought about by SCORE-AI technology “could offer an exciting prospect to improve EEG availability and clinical care for the 50 million people with epilepsy worldwide.”
A version of this article originally appeared on Medscape.com.
An automated artificial intelligence (AI) model trained to read electroencephalograms (EEGs) in patients with suspected epilepsy is just as accurate as trained neurologists, new data suggest.
Known as SCORE-AI, the technology distinguishes between abnormal and normal EEG recordings and classifies irregular recordings into specific categories crucial for patient decision-making.
“SCORE-AI can be used in place of experts in underprivileged areas, where expertise is missing, or to help physicians to preselect or prescore recordings in areas where the workload is high – we can all benefit from AI,” study investigator Sándor Beniczky, MD, PhD, said in a JAMA Neurology podcast.
Dr. Beniczky is professor of clinical neurophysiology at Aarhus University in Denmark.
The findings were published online in JAMA Neurology.
Gaining a foothold
Increasingly, AI is gaining a foothold in medicine by credibly addressing patient queries and aiding radiologists.
To bring AI to EEG interpretation, the researchers developed and validated an AI model that was able to assess routine, clinical EEGs in patients with suspected epilepsy.
Beyond using AI to distinguish abnormal from normal EEG recordings, the researchers wanted to train the new system to classify abnormal recordings into the major categories that are most relevant for clinical decision-making in patients who may have epilepsy. The categories included epileptiform-focal, epileptiform-generalized, nonepileptiform-focal, and nonepileptiform-diffuse abnormalities.
The researchers trained the learning model using Standardized Computer-based Organized Reporting of EEG (SCORE) software.
In the development phase, the model was trained using more than 30,490 anonymized and highly annotated EEG recordings from 14,100 men (median age, 25 years) from a single center. The recordings had an average duration of 31 minutes and were interpreted by 17 neurologists using standardized criteria. If an EEG recording was abnormal, the physicians had to specify which abnormal features were present.
SCORE-AI then performed an analysis of the recordings based on input from the experts.
To validate the findings, investigators used two independent test datasets. The first dataset consisted of 100 representative routine EEGs from 61 men (median age, 26 years), evaluated by 11 neurologists from different centers.
The consensus of these evaluations served as the reference standard. The second dataset comprised nearly 10,000 EEGs from a single center (5,170 men; median age, 35 years), independently assessed by 14 neurologists.
Near-perfect accuracy
When compared with the experts, SCORE-AI had near-perfect accuracy with an area under the receiver operating characteristic (AUROC) curve for differentiating normal from abnormal EEG recordings of 0.95.
SCORE-AI also performed well at identifying generalized epileptiform abnormalities (AUROC, 0.96), focal epileptiform abnormalities (AUROC, 0.91), focal nonepileptiform abnormalities (AUROC, 0.89), and diffuse nonepileptiform abnormalities (AUROC, 0.93).
In addition, SCORE-AI had excellent agreement with clinicians – and sometimes agreed with individual experts more than the experts agreed with one another.
When Dr. Beniczky and team tested SCORE-AI against three previously published AI models, SCORE-AI demonstrated greater specificity than those models (90% vs. 3%-63%) but was not as sensitive (86.7%) as two of the models (96.7% and 100%).
One of the study’s limitations was the fact that SCORE-AI was developed and validated on routine EEGs that excluded neonates and critically ill patients.
In the future, Dr. Beniczky said on the podcast, the team would like to train SCORE-AI to read EEGs with more granularity, and eventually use only one single channel to record EEGs. At present, SCORE-AI is being integrated with Natus Neuro, a widely used EEG equipment system, the investigators note.
In an accompanying editorial, Jonathan Kleen, MD, PhD, and Elan Guterman, MD, said, “The overall approach taken ... in developing and validating SCORE-AI sets a standard for this work going forward.”
Dr. Kleen and Dr. Guterman note that the technological gains brought about by SCORE-AI technology “could offer an exciting prospect to improve EEG availability and clinical care for the 50 million people with epilepsy worldwide.”
A version of this article originally appeared on Medscape.com.
An automated artificial intelligence (AI) model trained to read electroencephalograms (EEGs) in patients with suspected epilepsy is just as accurate as trained neurologists, new data suggest.
Known as SCORE-AI, the technology distinguishes between abnormal and normal EEG recordings and classifies irregular recordings into specific categories crucial for patient decision-making.
“SCORE-AI can be used in place of experts in underprivileged areas, where expertise is missing, or to help physicians to preselect or prescore recordings in areas where the workload is high – we can all benefit from AI,” study investigator Sándor Beniczky, MD, PhD, said in a JAMA Neurology podcast.
Dr. Beniczky is professor of clinical neurophysiology at Aarhus University in Denmark.
The findings were published online in JAMA Neurology.
Gaining a foothold
Increasingly, AI is gaining a foothold in medicine by credibly addressing patient queries and aiding radiologists.
To bring AI to EEG interpretation, the researchers developed and validated an AI model that was able to assess routine, clinical EEGs in patients with suspected epilepsy.
Beyond using AI to distinguish abnormal from normal EEG recordings, the researchers wanted to train the new system to classify abnormal recordings into the major categories that are most relevant for clinical decision-making in patients who may have epilepsy. The categories included epileptiform-focal, epileptiform-generalized, nonepileptiform-focal, and nonepileptiform-diffuse abnormalities.
The researchers trained the learning model using Standardized Computer-based Organized Reporting of EEG (SCORE) software.
In the development phase, the model was trained using more than 30,490 anonymized and highly annotated EEG recordings from 14,100 men (median age, 25 years) from a single center. The recordings had an average duration of 31 minutes and were interpreted by 17 neurologists using standardized criteria. If an EEG recording was abnormal, the physicians had to specify which abnormal features were present.
SCORE-AI then performed an analysis of the recordings based on input from the experts.
To validate the findings, investigators used two independent test datasets. The first dataset consisted of 100 representative routine EEGs from 61 men (median age, 26 years), evaluated by 11 neurologists from different centers.
The consensus of these evaluations served as the reference standard. The second dataset comprised nearly 10,000 EEGs from a single center (5,170 men; median age, 35 years), independently assessed by 14 neurologists.
Near-perfect accuracy
When compared with the experts, SCORE-AI had near-perfect accuracy with an area under the receiver operating characteristic (AUROC) curve for differentiating normal from abnormal EEG recordings of 0.95.
SCORE-AI also performed well at identifying generalized epileptiform abnormalities (AUROC, 0.96), focal epileptiform abnormalities (AUROC, 0.91), focal nonepileptiform abnormalities (AUROC, 0.89), and diffuse nonepileptiform abnormalities (AUROC, 0.93).
In addition, SCORE-AI had excellent agreement with clinicians – and sometimes agreed with individual experts more than the experts agreed with one another.
When Dr. Beniczky and team tested SCORE-AI against three previously published AI models, SCORE-AI demonstrated greater specificity than those models (90% vs. 3%-63%) but was not as sensitive (86.7%) as two of the models (96.7% and 100%).
One of the study’s limitations was the fact that SCORE-AI was developed and validated on routine EEGs that excluded neonates and critically ill patients.
In the future, Dr. Beniczky said on the podcast, the team would like to train SCORE-AI to read EEGs with more granularity, and eventually use only one single channel to record EEGs. At present, SCORE-AI is being integrated with Natus Neuro, a widely used EEG equipment system, the investigators note.
In an accompanying editorial, Jonathan Kleen, MD, PhD, and Elan Guterman, MD, said, “The overall approach taken ... in developing and validating SCORE-AI sets a standard for this work going forward.”
Dr. Kleen and Dr. Guterman note that the technological gains brought about by SCORE-AI technology “could offer an exciting prospect to improve EEG availability and clinical care for the 50 million people with epilepsy worldwide.”
A version of this article originally appeared on Medscape.com.
Regular napping linked to greater brain volume
Investigators at University College London, and the University of the Republic of Uruguay, Montevideo, found individuals genetically predisposed to regular napping had larger total brain volume, a surrogate of better cognitive health.
“Our results suggest that napping may improve brain health,” first author Valentina Paz, MSc, a PhD candidate at the University of the Republic of Uruguay said in an interview. “Specifically, our work revealed a 15.8 cubic cm increase in total brain volume with more frequent daytime napping,” she said.
The findings were published online in Sleep Health.
Higher brain volume
Previous studies examining the potential link between napping and cognition in older adults have yielded conflicting results.
To clarify this association, Ms. Paz and colleagues used Mendelian randomization to study DNA samples, cognitive outcomes, and functional magnetic resonance imaging data in participants from the ongoing UK Biobank Study.
Starting with data from 378,932 study participants (mean age 57), investigators compared measures of brain health and cognition of those who are more genetically programmed to nap with people who did not have these genetic variations.
More specifically, the investigators examined 97 sections of genetic code previously linked to the likelihood of regular napping and correlated these results with fMRI and cognitive outcomes between those genetically predisposed to take regular naps and those who weren’t.
Study outcomes included total brain volume, hippocampal volume, reaction time, and visual memory.
The final study sample included 35,080 with neuroimaging, cognitive assessment, and genotype data.
The researchers estimated that the average difference in brain volume between individuals genetically programmed to be habitual nappers and those who were not was equivalent to 15.8 cubic cm, or 2.6-6.5 years of aging.
However, there was no difference in the other three outcomes – hippocampal volume, reaction time, and visual processing – between the two study groups.
Since investigators did not have information on the length of time participants napped, Ms. Paz suggested that “taking a short nap in the early afternoon may help cognition in those needing it.”
However, she added, the study’s findings need to be replicated before any firm conclusions can be made.
“More work is needed to examine the associations between napping and cognition, and the replication of these findings using other datasets and methods,” she said.
The investigators note that the study’s findings augment the knowledge of the “impact of habitual daytime napping on brain health, which is essential to understanding cognitive impairment in the aging population. The lack of evidence for an association between napping and hippocampal volume and cognitive outcomes (for example, alertness) may be affected by habitual daytime napping and should be studied in the future.”
Strengths, limitations
Tara Spires-Jones, PhD, president of the British Neuroscience Association and group leader at the UK Dementia Research Institute, said, “the study shows a small but significant increase in brain volume in people who have a genetic signature associated with taking daytime naps.”
Dr. Spires-Jones, who was not involved in the research, noted that while the study is well-conducted, it has limitations. Because Mendelian randomization uses a genetic signature, she noted, outcomes depend on the accuracy of the signature.
“The napping habits of UK Biobank participants were self-reported, which might not be entirely accurate, and the ‘napping’ signature overlapped substantially with the signature for cognitive outcomes in the study, which makes the causal link weaker,” she said.
“Even with those limitations, this study is interesting because it adds to the data indicating that sleep is important for brain health,” said Dr. Spires-Jones.
The study was supported by Diabetes UK, the British Heart Foundation, and the Diabetes Research and Wellness Foundation. In Uruguay, it was supported by Programa de Desarrollo de las Ciencias Básicas, Agencia Nacional de Investigación e Innovación, Comisión Sectorial de Investigación Científica, and Comisión Académica de Posgrado. In the United States it was supported by the National Heart, Lung, and Blood Institute. There were no disclosures reported.
A version of this article first appeared on Medscape.com.
Investigators at University College London, and the University of the Republic of Uruguay, Montevideo, found individuals genetically predisposed to regular napping had larger total brain volume, a surrogate of better cognitive health.
“Our results suggest that napping may improve brain health,” first author Valentina Paz, MSc, a PhD candidate at the University of the Republic of Uruguay said in an interview. “Specifically, our work revealed a 15.8 cubic cm increase in total brain volume with more frequent daytime napping,” she said.
The findings were published online in Sleep Health.
Higher brain volume
Previous studies examining the potential link between napping and cognition in older adults have yielded conflicting results.
To clarify this association, Ms. Paz and colleagues used Mendelian randomization to study DNA samples, cognitive outcomes, and functional magnetic resonance imaging data in participants from the ongoing UK Biobank Study.
Starting with data from 378,932 study participants (mean age 57), investigators compared measures of brain health and cognition of those who are more genetically programmed to nap with people who did not have these genetic variations.
More specifically, the investigators examined 97 sections of genetic code previously linked to the likelihood of regular napping and correlated these results with fMRI and cognitive outcomes between those genetically predisposed to take regular naps and those who weren’t.
Study outcomes included total brain volume, hippocampal volume, reaction time, and visual memory.
The final study sample included 35,080 with neuroimaging, cognitive assessment, and genotype data.
The researchers estimated that the average difference in brain volume between individuals genetically programmed to be habitual nappers and those who were not was equivalent to 15.8 cubic cm, or 2.6-6.5 years of aging.
However, there was no difference in the other three outcomes – hippocampal volume, reaction time, and visual processing – between the two study groups.
Since investigators did not have information on the length of time participants napped, Ms. Paz suggested that “taking a short nap in the early afternoon may help cognition in those needing it.”
However, she added, the study’s findings need to be replicated before any firm conclusions can be made.
“More work is needed to examine the associations between napping and cognition, and the replication of these findings using other datasets and methods,” she said.
The investigators note that the study’s findings augment the knowledge of the “impact of habitual daytime napping on brain health, which is essential to understanding cognitive impairment in the aging population. The lack of evidence for an association between napping and hippocampal volume and cognitive outcomes (for example, alertness) may be affected by habitual daytime napping and should be studied in the future.”
Strengths, limitations
Tara Spires-Jones, PhD, president of the British Neuroscience Association and group leader at the UK Dementia Research Institute, said, “the study shows a small but significant increase in brain volume in people who have a genetic signature associated with taking daytime naps.”
Dr. Spires-Jones, who was not involved in the research, noted that while the study is well-conducted, it has limitations. Because Mendelian randomization uses a genetic signature, she noted, outcomes depend on the accuracy of the signature.
“The napping habits of UK Biobank participants were self-reported, which might not be entirely accurate, and the ‘napping’ signature overlapped substantially with the signature for cognitive outcomes in the study, which makes the causal link weaker,” she said.
“Even with those limitations, this study is interesting because it adds to the data indicating that sleep is important for brain health,” said Dr. Spires-Jones.
The study was supported by Diabetes UK, the British Heart Foundation, and the Diabetes Research and Wellness Foundation. In Uruguay, it was supported by Programa de Desarrollo de las Ciencias Básicas, Agencia Nacional de Investigación e Innovación, Comisión Sectorial de Investigación Científica, and Comisión Académica de Posgrado. In the United States it was supported by the National Heart, Lung, and Blood Institute. There were no disclosures reported.
A version of this article first appeared on Medscape.com.
Investigators at University College London, and the University of the Republic of Uruguay, Montevideo, found individuals genetically predisposed to regular napping had larger total brain volume, a surrogate of better cognitive health.
“Our results suggest that napping may improve brain health,” first author Valentina Paz, MSc, a PhD candidate at the University of the Republic of Uruguay said in an interview. “Specifically, our work revealed a 15.8 cubic cm increase in total brain volume with more frequent daytime napping,” she said.
The findings were published online in Sleep Health.
Higher brain volume
Previous studies examining the potential link between napping and cognition in older adults have yielded conflicting results.
To clarify this association, Ms. Paz and colleagues used Mendelian randomization to study DNA samples, cognitive outcomes, and functional magnetic resonance imaging data in participants from the ongoing UK Biobank Study.
Starting with data from 378,932 study participants (mean age 57), investigators compared measures of brain health and cognition of those who are more genetically programmed to nap with people who did not have these genetic variations.
More specifically, the investigators examined 97 sections of genetic code previously linked to the likelihood of regular napping and correlated these results with fMRI and cognitive outcomes between those genetically predisposed to take regular naps and those who weren’t.
Study outcomes included total brain volume, hippocampal volume, reaction time, and visual memory.
The final study sample included 35,080 with neuroimaging, cognitive assessment, and genotype data.
The researchers estimated that the average difference in brain volume between individuals genetically programmed to be habitual nappers and those who were not was equivalent to 15.8 cubic cm, or 2.6-6.5 years of aging.
However, there was no difference in the other three outcomes – hippocampal volume, reaction time, and visual processing – between the two study groups.
Since investigators did not have information on the length of time participants napped, Ms. Paz suggested that “taking a short nap in the early afternoon may help cognition in those needing it.”
However, she added, the study’s findings need to be replicated before any firm conclusions can be made.
“More work is needed to examine the associations between napping and cognition, and the replication of these findings using other datasets and methods,” she said.
The investigators note that the study’s findings augment the knowledge of the “impact of habitual daytime napping on brain health, which is essential to understanding cognitive impairment in the aging population. The lack of evidence for an association between napping and hippocampal volume and cognitive outcomes (for example, alertness) may be affected by habitual daytime napping and should be studied in the future.”
Strengths, limitations
Tara Spires-Jones, PhD, president of the British Neuroscience Association and group leader at the UK Dementia Research Institute, said, “the study shows a small but significant increase in brain volume in people who have a genetic signature associated with taking daytime naps.”
Dr. Spires-Jones, who was not involved in the research, noted that while the study is well-conducted, it has limitations. Because Mendelian randomization uses a genetic signature, she noted, outcomes depend on the accuracy of the signature.
“The napping habits of UK Biobank participants were self-reported, which might not be entirely accurate, and the ‘napping’ signature overlapped substantially with the signature for cognitive outcomes in the study, which makes the causal link weaker,” she said.
“Even with those limitations, this study is interesting because it adds to the data indicating that sleep is important for brain health,” said Dr. Spires-Jones.
The study was supported by Diabetes UK, the British Heart Foundation, and the Diabetes Research and Wellness Foundation. In Uruguay, it was supported by Programa de Desarrollo de las Ciencias Básicas, Agencia Nacional de Investigación e Innovación, Comisión Sectorial de Investigación Científica, and Comisión Académica de Posgrado. In the United States it was supported by the National Heart, Lung, and Blood Institute. There were no disclosures reported.
A version of this article first appeared on Medscape.com.
FROM SLEEP HEALTH
Probiotics an effective adjunct to antidepressants for major depression
By the end of the 8-week pilot study, participants who had an incomplete response to antidepressants prior to taking probiotics scored better on measures of anxiety and depression versus placebo.
“This was a pilot study, designed as an initial exploration of whether improving gut health with probiotics could act as a new pathway for supporting mood and mental health,” study investigator Viktoriya Nikolova, PhD, Institute of Psychiatry, Psychology and Neuroscience at King’s College London, said in an interview.
“While very promising and exciting, our findings are only the first step, and larger trials are needed,” she noted.
The findings were published online in JAMA Psychiatry.
Gut-brain axis
It is estimated that up to 60% of people taking antidepressants for major depressive disorder (MDD) do not achieve full response.
With an eye on the so-called gut-brain axis as a treatment target for depression, the researchers conducted a meta-analysis of seven randomized controlled trials (RCT) in 2021 and found that probiotics appeared effective in reducing depressive symptoms when taken alongside antidepressants. The studies in this meta-analysis either reported poor adherence rates or did not investigate how well study participants tolerated probiotics.
To further investigate, Dr. Nikolova and team launched a pilot RCT by recruiting study participants from primary and secondary health care services, and through general advertising in London. Data were collected from September 2019 to May 2022.
They included 49 adults diagnosed with MDD with an incomplete antidepressant response, indicated by a score of greater than 13 on the Hamilton Depression Rating Scale-17 (HAMD-17).
Half of the participants were randomly assigned to receive a widely available, proprietary, 14-strain blend probiotic supplement, and half received placebo. Both groups took their study drug four times per day during the 8-week trial.
At baseline, 4 weeks, and 8 weeks, investigators assessed the participants for depression with the HAMD-17, the Inventory of Depressive Symptomatology (IDS) Self-Report, and anxiety with the Hamilton Anxiety Rating Scale (HAMA).
The majority of participants (80%) were female with a mean age of 32 years. Adherence was high, with 97% of the doses taken as required, and no adverse events were reported.
Standardized effect sizes from linear mixed models demonstrated that, when compared with the placebo group, the probiotic group had more improvement in depressive symptoms according to the HAMD-17 (week 4: SES, 0.70; 95% confidence interval, 0.01-0.98) and IDS Self Report (week 8: SES, 0.64; 95% CI, 0.03-0.87).
When compared with the placebo group, the probiotic group also experienced greater improvements in anxiety symptoms according to the HAMA (week 4: SES, 0.67; 95% CI, 0-0.95; week 8: SES, 0.79; 95% CI, 0.06-1.05).
Dr. Nikolova said a large follow-up trial is planned to further confirm the results.
Nutritional psychiatrist Drew Ramsey, MD, author of Eat to Beat Depression and Anxiety and assistant clinical professor of psychiatry at Columbia University, New York, said in an interview: “This randomized clinical trial adds to the considerable evidence that food choices impact depression outcomes.”
He further noted that, “in nutritional psychiatry, we recommend eating fermented foods as they have been shown to improve microbiome diversity and decrease markers of inflammation.”
Dr. Ramsey noted that the RCT used the equivalent colony-forming unit of a “single serving of kombucha.”
“In our clinical group and our nutritional psychiatry course for clinicians, we recommend fermented foods over probiotics as this is the most sustainable, evidence-based way to improve microbiome diversity,” said Dr. Ramsey, citing recent research by Gardner and colleagues at Stanford (Calif.) University.
“This is an industry-funded trial that adds to the evidence base but should be interpreted by patients and clinicians as promoting consumption of more kefir, kimchi, and kombucha, not that patients should take probiotics,” he said.
A key place for probiotics in mental health
Commenting on the study, Uma Naidoo, MD, said: “As I shared throughout my first book, This is Your Brain on Food, there is a real place for the use of probiotics in mental health, including the importance of the gut-brain connection.”
Dr. Naidoo is the director of nutritional and metabolic psychiatry at Massachusetts General Hospital and of nutritional psychiatry at the MGH Academy, both in Boston.
She noted that, when a person stops using a probiotic after trying it out, the positive changes in the gut are reversed, so “remaining consistent in taking the probiotic is important if you have found it helpful for your mood.”
Dr. Naidoo added that “each person’s gut microbiome is so unique that it is likely not every human being will have the same reaction to a probiotic.”
“Eating foods with live probiotics may also benefit gut health and, therefore, mood,” she said. The same goes with eating fermented foods with live active cultures.”
The study was funded by a Medical Research Council Industrial CASE PhD Studentship with ADM Protexin (supplier of the probiotics) as the industry partner and additional support from Freya Green. Dr. Nikolova has received grants from the Medical Research Council and ADM Protexin during the conduct of the study as well as personal fees from Janssen outside the submitted work.
A version of this article first appeared on Medscape.com.
By the end of the 8-week pilot study, participants who had an incomplete response to antidepressants prior to taking probiotics scored better on measures of anxiety and depression versus placebo.
“This was a pilot study, designed as an initial exploration of whether improving gut health with probiotics could act as a new pathway for supporting mood and mental health,” study investigator Viktoriya Nikolova, PhD, Institute of Psychiatry, Psychology and Neuroscience at King’s College London, said in an interview.
“While very promising and exciting, our findings are only the first step, and larger trials are needed,” she noted.
The findings were published online in JAMA Psychiatry.
Gut-brain axis
It is estimated that up to 60% of people taking antidepressants for major depressive disorder (MDD) do not achieve full response.
With an eye on the so-called gut-brain axis as a treatment target for depression, the researchers conducted a meta-analysis of seven randomized controlled trials (RCT) in 2021 and found that probiotics appeared effective in reducing depressive symptoms when taken alongside antidepressants. The studies in this meta-analysis either reported poor adherence rates or did not investigate how well study participants tolerated probiotics.
To further investigate, Dr. Nikolova and team launched a pilot RCT by recruiting study participants from primary and secondary health care services, and through general advertising in London. Data were collected from September 2019 to May 2022.
They included 49 adults diagnosed with MDD with an incomplete antidepressant response, indicated by a score of greater than 13 on the Hamilton Depression Rating Scale-17 (HAMD-17).
Half of the participants were randomly assigned to receive a widely available, proprietary, 14-strain blend probiotic supplement, and half received placebo. Both groups took their study drug four times per day during the 8-week trial.
At baseline, 4 weeks, and 8 weeks, investigators assessed the participants for depression with the HAMD-17, the Inventory of Depressive Symptomatology (IDS) Self-Report, and anxiety with the Hamilton Anxiety Rating Scale (HAMA).
The majority of participants (80%) were female with a mean age of 32 years. Adherence was high, with 97% of the doses taken as required, and no adverse events were reported.
Standardized effect sizes from linear mixed models demonstrated that, when compared with the placebo group, the probiotic group had more improvement in depressive symptoms according to the HAMD-17 (week 4: SES, 0.70; 95% confidence interval, 0.01-0.98) and IDS Self Report (week 8: SES, 0.64; 95% CI, 0.03-0.87).
When compared with the placebo group, the probiotic group also experienced greater improvements in anxiety symptoms according to the HAMA (week 4: SES, 0.67; 95% CI, 0-0.95; week 8: SES, 0.79; 95% CI, 0.06-1.05).
Dr. Nikolova said a large follow-up trial is planned to further confirm the results.
Nutritional psychiatrist Drew Ramsey, MD, author of Eat to Beat Depression and Anxiety and assistant clinical professor of psychiatry at Columbia University, New York, said in an interview: “This randomized clinical trial adds to the considerable evidence that food choices impact depression outcomes.”
He further noted that, “in nutritional psychiatry, we recommend eating fermented foods as they have been shown to improve microbiome diversity and decrease markers of inflammation.”
Dr. Ramsey noted that the RCT used the equivalent colony-forming unit of a “single serving of kombucha.”
“In our clinical group and our nutritional psychiatry course for clinicians, we recommend fermented foods over probiotics as this is the most sustainable, evidence-based way to improve microbiome diversity,” said Dr. Ramsey, citing recent research by Gardner and colleagues at Stanford (Calif.) University.
“This is an industry-funded trial that adds to the evidence base but should be interpreted by patients and clinicians as promoting consumption of more kefir, kimchi, and kombucha, not that patients should take probiotics,” he said.
A key place for probiotics in mental health
Commenting on the study, Uma Naidoo, MD, said: “As I shared throughout my first book, This is Your Brain on Food, there is a real place for the use of probiotics in mental health, including the importance of the gut-brain connection.”
Dr. Naidoo is the director of nutritional and metabolic psychiatry at Massachusetts General Hospital and of nutritional psychiatry at the MGH Academy, both in Boston.
She noted that, when a person stops using a probiotic after trying it out, the positive changes in the gut are reversed, so “remaining consistent in taking the probiotic is important if you have found it helpful for your mood.”
Dr. Naidoo added that “each person’s gut microbiome is so unique that it is likely not every human being will have the same reaction to a probiotic.”
“Eating foods with live probiotics may also benefit gut health and, therefore, mood,” she said. The same goes with eating fermented foods with live active cultures.”
The study was funded by a Medical Research Council Industrial CASE PhD Studentship with ADM Protexin (supplier of the probiotics) as the industry partner and additional support from Freya Green. Dr. Nikolova has received grants from the Medical Research Council and ADM Protexin during the conduct of the study as well as personal fees from Janssen outside the submitted work.
A version of this article first appeared on Medscape.com.
By the end of the 8-week pilot study, participants who had an incomplete response to antidepressants prior to taking probiotics scored better on measures of anxiety and depression versus placebo.
“This was a pilot study, designed as an initial exploration of whether improving gut health with probiotics could act as a new pathway for supporting mood and mental health,” study investigator Viktoriya Nikolova, PhD, Institute of Psychiatry, Psychology and Neuroscience at King’s College London, said in an interview.
“While very promising and exciting, our findings are only the first step, and larger trials are needed,” she noted.
The findings were published online in JAMA Psychiatry.
Gut-brain axis
It is estimated that up to 60% of people taking antidepressants for major depressive disorder (MDD) do not achieve full response.
With an eye on the so-called gut-brain axis as a treatment target for depression, the researchers conducted a meta-analysis of seven randomized controlled trials (RCT) in 2021 and found that probiotics appeared effective in reducing depressive symptoms when taken alongside antidepressants. The studies in this meta-analysis either reported poor adherence rates or did not investigate how well study participants tolerated probiotics.
To further investigate, Dr. Nikolova and team launched a pilot RCT by recruiting study participants from primary and secondary health care services, and through general advertising in London. Data were collected from September 2019 to May 2022.
They included 49 adults diagnosed with MDD with an incomplete antidepressant response, indicated by a score of greater than 13 on the Hamilton Depression Rating Scale-17 (HAMD-17).
Half of the participants were randomly assigned to receive a widely available, proprietary, 14-strain blend probiotic supplement, and half received placebo. Both groups took their study drug four times per day during the 8-week trial.
At baseline, 4 weeks, and 8 weeks, investigators assessed the participants for depression with the HAMD-17, the Inventory of Depressive Symptomatology (IDS) Self-Report, and anxiety with the Hamilton Anxiety Rating Scale (HAMA).
The majority of participants (80%) were female with a mean age of 32 years. Adherence was high, with 97% of the doses taken as required, and no adverse events were reported.
Standardized effect sizes from linear mixed models demonstrated that, when compared with the placebo group, the probiotic group had more improvement in depressive symptoms according to the HAMD-17 (week 4: SES, 0.70; 95% confidence interval, 0.01-0.98) and IDS Self Report (week 8: SES, 0.64; 95% CI, 0.03-0.87).
When compared with the placebo group, the probiotic group also experienced greater improvements in anxiety symptoms according to the HAMA (week 4: SES, 0.67; 95% CI, 0-0.95; week 8: SES, 0.79; 95% CI, 0.06-1.05).
Dr. Nikolova said a large follow-up trial is planned to further confirm the results.
Nutritional psychiatrist Drew Ramsey, MD, author of Eat to Beat Depression and Anxiety and assistant clinical professor of psychiatry at Columbia University, New York, said in an interview: “This randomized clinical trial adds to the considerable evidence that food choices impact depression outcomes.”
He further noted that, “in nutritional psychiatry, we recommend eating fermented foods as they have been shown to improve microbiome diversity and decrease markers of inflammation.”
Dr. Ramsey noted that the RCT used the equivalent colony-forming unit of a “single serving of kombucha.”
“In our clinical group and our nutritional psychiatry course for clinicians, we recommend fermented foods over probiotics as this is the most sustainable, evidence-based way to improve microbiome diversity,” said Dr. Ramsey, citing recent research by Gardner and colleagues at Stanford (Calif.) University.
“This is an industry-funded trial that adds to the evidence base but should be interpreted by patients and clinicians as promoting consumption of more kefir, kimchi, and kombucha, not that patients should take probiotics,” he said.
A key place for probiotics in mental health
Commenting on the study, Uma Naidoo, MD, said: “As I shared throughout my first book, This is Your Brain on Food, there is a real place for the use of probiotics in mental health, including the importance of the gut-brain connection.”
Dr. Naidoo is the director of nutritional and metabolic psychiatry at Massachusetts General Hospital and of nutritional psychiatry at the MGH Academy, both in Boston.
She noted that, when a person stops using a probiotic after trying it out, the positive changes in the gut are reversed, so “remaining consistent in taking the probiotic is important if you have found it helpful for your mood.”
Dr. Naidoo added that “each person’s gut microbiome is so unique that it is likely not every human being will have the same reaction to a probiotic.”
“Eating foods with live probiotics may also benefit gut health and, therefore, mood,” she said. The same goes with eating fermented foods with live active cultures.”
The study was funded by a Medical Research Council Industrial CASE PhD Studentship with ADM Protexin (supplier of the probiotics) as the industry partner and additional support from Freya Green. Dr. Nikolova has received grants from the Medical Research Council and ADM Protexin during the conduct of the study as well as personal fees from Janssen outside the submitted work.
A version of this article first appeared on Medscape.com.
FROM JAMA PSYCHIATRY
‘Impressive’ results for intranasal ketamine in chronic, refractory migraine
Half of the study participants who used IN ketamine for chronic, treatment-refractory migraine in a new retrospective cohort study reported it as “very effective” and over one-third said it boosted their quality of life.
“In our study, we showed that with even a few uses per day, intranasal ketamine can still improve patients’ quality of life,” lead investigator Hsiangkuo Yuan, MD, PhD, said in an interview. Dr. Yuan is associate professor of neurology at Thomas Jefferson University, Philadelphia, and director of clinical research at the Jefferson Headache Center.
He added that “multiple medications failed these patients, and the majority of patients were having daily headaches. So, if anything works, even partially and shortly, it may still give patients some relief to get through the day.”
The findings were published online in Regional Anesthesia & Pain Medicine.
Daily migraine, failed medications
Use of IN ketamine has not been studied for the treatment of chronic, treatment-refractory migraine – although it has been studied in patients with cluster headache and migraine, the investigators note.
Ketamine is not yet approved by the Food and Drug Administration to treat migraine.
To further explore ketamine’s effect in those with chronic, treatment-refractory migraine, the investigators retrospectively analyzed electronic health records of patients at the Jefferson Headache Center who had received IN ketamine for the treatment of migraine between January 2019 and February 2020.
Of 242 patients who had received IN ketamine, Dr. Yuan’s team followed up with 169 who agreed to be part of the study.
The majority (67%) had daily migraine, and 85% had tried more than three classes of preventive medications for migraine. They currently used a median of two medications, the most common of which was a CGRP monoclonal antibody.
On average, patients used six sprays per day for a median 10 days per month. Median pain relief onset was 52 minutes after dosage.
Almost three-quarters of patients reported at least one side effect from the ketamine, most commonly fatigue (22%), double/blurred vision (21%), and confusion/dissociation (21%). These effects were mostly temporary, the researchers report.
The most common reasons for initiating IN ketamine included an incomplete response to prior acute medications (59%), incomplete response to prior preventive medications (31%), and prior benefit from IV ketamine (23%).
Study investigators noted that ketamine has the potential to become addictive and indicated that “clinicians should only consider the use of a potentially addictive medication such as ketamine for significantly disabled patients with migraine.”
About half of the participants who used IN ketamine found it “very effective,” and 40% found it “somewhat effective.” Within the same group, 36% and 43% found the overall impact of IN ketamine on their quality of life was much better and somewhat better, respectively.
Among those still using ketamine during study follow-up, 82% reported that ketamine was very effective.
Compared with other acute headache medications, IN ketamine was considered much better (43%) or somewhat better (30%).
Nearly 75% of participants reported using fewer pain relievers when using IN ketamine.
Dr. Yuan said that future research might focus on finding predictors for IN ketamine response or determining the optimal effective and safe dose for the drug in those with chronic, treatment-refractory migraine.
“We still need a prospective, randomized controlled trial to assess the efficacy and tolerability of intranasal ketamine,” he added.
‘Impressive result’
Commenting on the findings for this article, Richard Lipton, MD, professor of neurology, psychiatry and behavioral sciences and director of the Montefiore Headache Center at Albert Einstein College of Medicine, New York, said that “in this refractory population with multiple treatment failures, this is a very impressive, open-label result.”
“This real-world data suggests that ketamine is an effective option for people with medically intractable chronic migraine,” said Dr. Lipton, who was not part of the study. “In these very difficult to treat patients, 65% of those who started on ketamine persisted. Of those who remained on ketamine, 82% found it very effective.”
“This study makes me more confident that intranasal ketamine is a helpful treatment option, and I plan to use it more often in the future,” he added.
Like Dr. Yuan, Dr. Lipton highlighted the need for “well-designed placebo-controlled trials” and “rigorous comparative effectiveness studies.”
The study was funded by Miles for Migraine. Dr. Yuan has received institutional support for serving as an investigator from Teva and AbbVie, and royalties from Cambridge University Press and MedLink. Dr. Lipton has received compensation for consultation from Alder/Lumbeck, Axsome, Supernus, Theranica, Upsher-Smith, and Satsuma. He has participated in speaker bureaus for Eli Lilly and Amgen/Novartis and has received institutional support for serving as principal investigator from Teva, GammaCore, and Allergan/AbbVie. He has received payments for authorship or royalties from Demos Medical, Cambridge University Press, and MedLink.
A version of this article originally appeared on Medscape.com.
Half of the study participants who used IN ketamine for chronic, treatment-refractory migraine in a new retrospective cohort study reported it as “very effective” and over one-third said it boosted their quality of life.
“In our study, we showed that with even a few uses per day, intranasal ketamine can still improve patients’ quality of life,” lead investigator Hsiangkuo Yuan, MD, PhD, said in an interview. Dr. Yuan is associate professor of neurology at Thomas Jefferson University, Philadelphia, and director of clinical research at the Jefferson Headache Center.
He added that “multiple medications failed these patients, and the majority of patients were having daily headaches. So, if anything works, even partially and shortly, it may still give patients some relief to get through the day.”
The findings were published online in Regional Anesthesia & Pain Medicine.
Daily migraine, failed medications
Use of IN ketamine has not been studied for the treatment of chronic, treatment-refractory migraine – although it has been studied in patients with cluster headache and migraine, the investigators note.
Ketamine is not yet approved by the Food and Drug Administration to treat migraine.
To further explore ketamine’s effect in those with chronic, treatment-refractory migraine, the investigators retrospectively analyzed electronic health records of patients at the Jefferson Headache Center who had received IN ketamine for the treatment of migraine between January 2019 and February 2020.
Of 242 patients who had received IN ketamine, Dr. Yuan’s team followed up with 169 who agreed to be part of the study.
The majority (67%) had daily migraine, and 85% had tried more than three classes of preventive medications for migraine. They currently used a median of two medications, the most common of which was a CGRP monoclonal antibody.
On average, patients used six sprays per day for a median 10 days per month. Median pain relief onset was 52 minutes after dosage.
Almost three-quarters of patients reported at least one side effect from the ketamine, most commonly fatigue (22%), double/blurred vision (21%), and confusion/dissociation (21%). These effects were mostly temporary, the researchers report.
The most common reasons for initiating IN ketamine included an incomplete response to prior acute medications (59%), incomplete response to prior preventive medications (31%), and prior benefit from IV ketamine (23%).
Study investigators noted that ketamine has the potential to become addictive and indicated that “clinicians should only consider the use of a potentially addictive medication such as ketamine for significantly disabled patients with migraine.”
About half of the participants who used IN ketamine found it “very effective,” and 40% found it “somewhat effective.” Within the same group, 36% and 43% found the overall impact of IN ketamine on their quality of life was much better and somewhat better, respectively.
Among those still using ketamine during study follow-up, 82% reported that ketamine was very effective.
Compared with other acute headache medications, IN ketamine was considered much better (43%) or somewhat better (30%).
Nearly 75% of participants reported using fewer pain relievers when using IN ketamine.
Dr. Yuan said that future research might focus on finding predictors for IN ketamine response or determining the optimal effective and safe dose for the drug in those with chronic, treatment-refractory migraine.
“We still need a prospective, randomized controlled trial to assess the efficacy and tolerability of intranasal ketamine,” he added.
‘Impressive result’
Commenting on the findings for this article, Richard Lipton, MD, professor of neurology, psychiatry and behavioral sciences and director of the Montefiore Headache Center at Albert Einstein College of Medicine, New York, said that “in this refractory population with multiple treatment failures, this is a very impressive, open-label result.”
“This real-world data suggests that ketamine is an effective option for people with medically intractable chronic migraine,” said Dr. Lipton, who was not part of the study. “In these very difficult to treat patients, 65% of those who started on ketamine persisted. Of those who remained on ketamine, 82% found it very effective.”
“This study makes me more confident that intranasal ketamine is a helpful treatment option, and I plan to use it more often in the future,” he added.
Like Dr. Yuan, Dr. Lipton highlighted the need for “well-designed placebo-controlled trials” and “rigorous comparative effectiveness studies.”
The study was funded by Miles for Migraine. Dr. Yuan has received institutional support for serving as an investigator from Teva and AbbVie, and royalties from Cambridge University Press and MedLink. Dr. Lipton has received compensation for consultation from Alder/Lumbeck, Axsome, Supernus, Theranica, Upsher-Smith, and Satsuma. He has participated in speaker bureaus for Eli Lilly and Amgen/Novartis and has received institutional support for serving as principal investigator from Teva, GammaCore, and Allergan/AbbVie. He has received payments for authorship or royalties from Demos Medical, Cambridge University Press, and MedLink.
A version of this article originally appeared on Medscape.com.
Half of the study participants who used IN ketamine for chronic, treatment-refractory migraine in a new retrospective cohort study reported it as “very effective” and over one-third said it boosted their quality of life.
“In our study, we showed that with even a few uses per day, intranasal ketamine can still improve patients’ quality of life,” lead investigator Hsiangkuo Yuan, MD, PhD, said in an interview. Dr. Yuan is associate professor of neurology at Thomas Jefferson University, Philadelphia, and director of clinical research at the Jefferson Headache Center.
He added that “multiple medications failed these patients, and the majority of patients were having daily headaches. So, if anything works, even partially and shortly, it may still give patients some relief to get through the day.”
The findings were published online in Regional Anesthesia & Pain Medicine.
Daily migraine, failed medications
Use of IN ketamine has not been studied for the treatment of chronic, treatment-refractory migraine – although it has been studied in patients with cluster headache and migraine, the investigators note.
Ketamine is not yet approved by the Food and Drug Administration to treat migraine.
To further explore ketamine’s effect in those with chronic, treatment-refractory migraine, the investigators retrospectively analyzed electronic health records of patients at the Jefferson Headache Center who had received IN ketamine for the treatment of migraine between January 2019 and February 2020.
Of 242 patients who had received IN ketamine, Dr. Yuan’s team followed up with 169 who agreed to be part of the study.
The majority (67%) had daily migraine, and 85% had tried more than three classes of preventive medications for migraine. They currently used a median of two medications, the most common of which was a CGRP monoclonal antibody.
On average, patients used six sprays per day for a median 10 days per month. Median pain relief onset was 52 minutes after dosage.
Almost three-quarters of patients reported at least one side effect from the ketamine, most commonly fatigue (22%), double/blurred vision (21%), and confusion/dissociation (21%). These effects were mostly temporary, the researchers report.
The most common reasons for initiating IN ketamine included an incomplete response to prior acute medications (59%), incomplete response to prior preventive medications (31%), and prior benefit from IV ketamine (23%).
Study investigators noted that ketamine has the potential to become addictive and indicated that “clinicians should only consider the use of a potentially addictive medication such as ketamine for significantly disabled patients with migraine.”
About half of the participants who used IN ketamine found it “very effective,” and 40% found it “somewhat effective.” Within the same group, 36% and 43% found the overall impact of IN ketamine on their quality of life was much better and somewhat better, respectively.
Among those still using ketamine during study follow-up, 82% reported that ketamine was very effective.
Compared with other acute headache medications, IN ketamine was considered much better (43%) or somewhat better (30%).
Nearly 75% of participants reported using fewer pain relievers when using IN ketamine.
Dr. Yuan said that future research might focus on finding predictors for IN ketamine response or determining the optimal effective and safe dose for the drug in those with chronic, treatment-refractory migraine.
“We still need a prospective, randomized controlled trial to assess the efficacy and tolerability of intranasal ketamine,” he added.
‘Impressive result’
Commenting on the findings for this article, Richard Lipton, MD, professor of neurology, psychiatry and behavioral sciences and director of the Montefiore Headache Center at Albert Einstein College of Medicine, New York, said that “in this refractory population with multiple treatment failures, this is a very impressive, open-label result.”
“This real-world data suggests that ketamine is an effective option for people with medically intractable chronic migraine,” said Dr. Lipton, who was not part of the study. “In these very difficult to treat patients, 65% of those who started on ketamine persisted. Of those who remained on ketamine, 82% found it very effective.”
“This study makes me more confident that intranasal ketamine is a helpful treatment option, and I plan to use it more often in the future,” he added.
Like Dr. Yuan, Dr. Lipton highlighted the need for “well-designed placebo-controlled trials” and “rigorous comparative effectiveness studies.”
The study was funded by Miles for Migraine. Dr. Yuan has received institutional support for serving as an investigator from Teva and AbbVie, and royalties from Cambridge University Press and MedLink. Dr. Lipton has received compensation for consultation from Alder/Lumbeck, Axsome, Supernus, Theranica, Upsher-Smith, and Satsuma. He has participated in speaker bureaus for Eli Lilly and Amgen/Novartis and has received institutional support for serving as principal investigator from Teva, GammaCore, and Allergan/AbbVie. He has received payments for authorship or royalties from Demos Medical, Cambridge University Press, and MedLink.
A version of this article originally appeared on Medscape.com.
FROM REGIONAL ANESTHESIA & PAIN MEDICINE