Clinical Psychiatry News

TOPLINE:

A blood test that measures biomarkers linked to manic symptoms can accurately identify patients with bipolar disorder (BD) who were previously misdiagnosed with major depressive disorder (MDD), new research shows. Investigators state that the test could identify up to 30% of patients with BD when used on its own and could be even more effective when combined with a standardized psychometric assessment.

METHODOLOGY:

• In the proof-of-concept study, investigators sought to identify biomarkers to accurately identify BD, which is frequently misdiagnosed as MDD because of overlapping symptoms and the lack of objective diagnostic tools.
• The study included 241 participants (70% female; mean age, 28 years) from the U.K.-based Delta Study who had been diagnosed with MDD within the past 5 years and had depressive symptoms as assessed with the Patient Health Questionnaire-9 (score ≥ 5).
• Participants completed an online questionnaire that included questions from the Mood Disorder Questionnaire and the Warwick-Edinburgh Mental Well-Being Scale and were asked to return a dried blood spot (DBS) fasting blood sample.
• Investigators analyzed the DBS samples for 630 metabolites and contacted participants by phone to establish diagnoses at 6 and 12 months using the World Health Organization World Mental Health Composite International Diagnostic Interview.

TAKEAWAY:

• Investigators used a panel of 17 biomarkers to correctly identify 67 (27.8%) participants with BD who had been previously misdiagnosed with MDD. They confirmed MDD in the remaining 174 patients.
• The biomarkers used in the test were correlated primarily with lifetime manic symptoms and were validated in a separate group of 30 patients.
• The identified biomarker panel provided a mean cross-validated area under the receiver operating characteristic curve of 0.71 (P < .001), with ceramide d18:0/24:1 emerging as the strongest biomarker.
• Combining biomarker readouts with patient-reported data significantly improved the performance of diagnostic models based on extensive demographic data and information from the Patient Health Questionnaire and Mood Disorder Questionnaire (P = .03 for all).

IN PRACTICE:

“The added value of biomarkers was particularly evident in scenarios where data on psychiatric symptoms were unavailable and at intermediate diagnostic thresholds, suggesting that biomarker tests may especially benefit patients who do not report their symptoms and whose diagnoses are uncertain,” the authors write.

SOURCE:

Jakub Tomasik, PhD, of the University of Cambridge (England), led the study, which was published online in JAMA Psychiatry. Stanley Medical Research Institute and Psyomics funded the study.

LIMITATIONS:

Data on confounding factors such as diet and blood pressure were missing. In addition, investigators noted that the sample mostly comprised White Internet users and was not representative of all individuals with BD.

Dr. Tomasik has a patent pending for DBS blood biomarkers. Other disclosures are noted in the original article.

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

TOPLINE:

A blood test that measures biomarkers linked to manic symptoms can accurately identify patients with bipolar disorder (BD) who were previously misdiagnosed with major depressive disorder (MDD), new research shows. Investigators state that the test could identify up to 30% of patients with BD when used on its own and could be even more effective when combined with a standardized psychometric assessment.

METHODOLOGY:

• In the proof-of-concept study, investigators sought to identify biomarkers to accurately identify BD, which is frequently misdiagnosed as MDD because of overlapping symptoms and the lack of objective diagnostic tools.
• The study included 241 participants (70% female; mean age, 28 years) from the U.K.-based Delta Study who had been diagnosed with MDD within the past 5 years and had depressive symptoms as assessed with the Patient Health Questionnaire-9 (score ≥ 5).
• Participants completed an online questionnaire that included questions from the Mood Disorder Questionnaire and the Warwick-Edinburgh Mental Well-Being Scale and were asked to return a dried blood spot (DBS) fasting blood sample.
• Investigators analyzed the DBS samples for 630 metabolites and contacted participants by phone to establish diagnoses at 6 and 12 months using the World Health Organization World Mental Health Composite International Diagnostic Interview.

TAKEAWAY:

• Investigators used a panel of 17 biomarkers to correctly identify 67 (27.8%) participants with BD who had been previously misdiagnosed with MDD. They confirmed MDD in the remaining 174 patients.
• The biomarkers used in the test were correlated primarily with lifetime manic symptoms and were validated in a separate group of 30 patients.
• The identified biomarker panel provided a mean cross-validated area under the receiver operating characteristic curve of 0.71 (P < .001), with ceramide d18:0/24:1 emerging as the strongest biomarker.
• Combining biomarker readouts with patient-reported data significantly improved the performance of diagnostic models based on extensive demographic data and information from the Patient Health Questionnaire and Mood Disorder Questionnaire (P = .03 for all).

IN PRACTICE:

“The added value of biomarkers was particularly evident in scenarios where data on psychiatric symptoms were unavailable and at intermediate diagnostic thresholds, suggesting that biomarker tests may especially benefit patients who do not report their symptoms and whose diagnoses are uncertain,” the authors write.

SOURCE:

Jakub Tomasik, PhD, of the University of Cambridge (England), led the study, which was published online in JAMA Psychiatry. Stanley Medical Research Institute and Psyomics funded the study.

LIMITATIONS:

Data on confounding factors such as diet and blood pressure were missing. In addition, investigators noted that the sample mostly comprised White Internet users and was not representative of all individuals with BD.

Dr. Tomasik has a patent pending for DBS blood biomarkers. Other disclosures are noted in the original article.

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

TOPLINE:

A blood test that measures biomarkers linked to manic symptoms can accurately identify patients with bipolar disorder (BD) who were previously misdiagnosed with major depressive disorder (MDD), new research shows. Investigators state that the test could identify up to 30% of patients with BD when used on its own and could be even more effective when combined with a standardized psychometric assessment.

METHODOLOGY:

• In the proof-of-concept study, investigators sought to identify biomarkers to accurately identify BD, which is frequently misdiagnosed as MDD because of overlapping symptoms and the lack of objective diagnostic tools.
• The study included 241 participants (70% female; mean age, 28 years) from the U.K.-based Delta Study who had been diagnosed with MDD within the past 5 years and had depressive symptoms as assessed with the Patient Health Questionnaire-9 (score ≥ 5).
• Participants completed an online questionnaire that included questions from the Mood Disorder Questionnaire and the Warwick-Edinburgh Mental Well-Being Scale and were asked to return a dried blood spot (DBS) fasting blood sample.
• Investigators analyzed the DBS samples for 630 metabolites and contacted participants by phone to establish diagnoses at 6 and 12 months using the World Health Organization World Mental Health Composite International Diagnostic Interview.

TAKEAWAY:

• Investigators used a panel of 17 biomarkers to correctly identify 67 (27.8%) participants with BD who had been previously misdiagnosed with MDD. They confirmed MDD in the remaining 174 patients.
• The biomarkers used in the test were correlated primarily with lifetime manic symptoms and were validated in a separate group of 30 patients.
• The identified biomarker panel provided a mean cross-validated area under the receiver operating characteristic curve of 0.71 (P < .001), with ceramide d18:0/24:1 emerging as the strongest biomarker.
• Combining biomarker readouts with patient-reported data significantly improved the performance of diagnostic models based on extensive demographic data and information from the Patient Health Questionnaire and Mood Disorder Questionnaire (P = .03 for all).

IN PRACTICE:

“The added value of biomarkers was particularly evident in scenarios where data on psychiatric symptoms were unavailable and at intermediate diagnostic thresholds, suggesting that biomarker tests may especially benefit patients who do not report their symptoms and whose diagnoses are uncertain,” the authors write.

SOURCE:

Jakub Tomasik, PhD, of the University of Cambridge (England), led the study, which was published online in JAMA Psychiatry. Stanley Medical Research Institute and Psyomics funded the study.

LIMITATIONS:

Data on confounding factors such as diet and blood pressure were missing. In addition, investigators noted that the sample mostly comprised White Internet users and was not representative of all individuals with BD.

Dr. Tomasik has a patent pending for DBS blood biomarkers. Other disclosures are noted in the original article.

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

BARCELONA – The typical lag between treatment initiation with selective serotonin reuptake inhibitors (SSRIs) for depression and enhanced mood may be because of the time it takes to increase brain synaptic density, new imaging data suggest.

In a double-blind study, more than 30 volunteers were randomly assigned to the SSRI escitalopram or placebo for 3-5 weeks. Using PET imaging, the investigators found that over time, synaptic density significantly increased significantly in the neocortex and hippocampus but only in patients taking the active drug.

The results point to two conclusions, said study investigator Gitta Moos Knudsen, MD, PhD, clinical professor and chief physician at the department of clinical medicine, neurology, psychiatry and sensory sciences at Copenhagen (Denmark) University Hospital.

First, they indicate that SSRIs increase synaptic density in brain areas critically involved in depression, a finding that would go some way to indicating that the synaptic density in the brain may be involved in how antidepressants function, “which would give us a target for developing novel drugs against depression,” said Dr. Knudsen.

“Secondly, our data suggest synapses build up over a period of weeks, which would explain why the effects of these drugs take time to kick in,” she added.

The findings were presented at the 36th European College of Neuropsychopharmacology (ECNP) Congress and simultaneously published online in Molecular Psychiatry.
 

Marked increase in synaptic density

SSRIs are widely used for depression as well as anxiety and obsessive-compulsive disorder. It is thought that they act via neuroplasticity and synaptic remodeling to improve cognition and emotion processing. However, the investigators note clinical evidence is lacking.

For the study, the researchers randomly assigned healthy individuals to either 20-mg escitalopram or placebo for 3-5 weeks.

They performed PET with the 11C-UCB-J tracer, which allows imaging of the synaptic vesicle glycoprotein 2A (SV2A) in the brain, synaptic density, as well as changes in density over time, in the hippocampus and neocortex.

Between May 2020 and October 2021, 17 individuals were assigned to escitalopram and 15 to placebo. There were no significant differences between two groups in terms of age, sex, and PET-related variables. Serum escitalopram measurements confirmed that all participants in the active drug group were compliant.

When synaptic density was assessed at a single time point, an average of 29 days after the intervention, there were no significant differences between the escitalopram and placebo groups in either the neocortex (P = .41) or in the hippocampus (P = .26).

However, when they performed a secondary analysis of the time-dependent effect on SV2A levels, they found a marked difference between the two study groups.

Compared with the placebo group, participants taking escitalopram had a marked increase in synaptic density in both the neocortex (rp value, 0.58; P = .003) and the hippocampus (rp value, 0.41; P = .048).

In contrast, there were no significant changes in synaptic density in either the neocortex (rp value, –0.01; P = .95) or the hippocampus (rp value, –0.06; P = .62) in the hippocampus.

“That is consistent with our clinical observation that it takes time to evolve synaptic density, along with clinical improvement. Does that mean that the increase in synaptic density is a precondition for improvement in symptoms? We don’t know,” said Dr. Knudsen.
 

Exciting but not conclusive

Session co-chair Oliver Howes, MD, PhD, professor of molecular psychiatry, King’s College London, agreed that the results do not prove the gradual increase in synaptic density the treatment response lag with SSRIs.

“We definitely don’t yet have all the data to know one way or the other,” he said in an interview.

Another potential hypothesis, he said, is that SSRIs are causing shifts in underlying brain circuits that lead to cognitive changes before there is a discernable improvement in mood.

Indeed, Dr. Howes suggested that increases in synaptic density and cognitive changes related to SSRI use are not necessarily dependent on each other and could even be unrelated.

Also commenting on the research, David Nutt, MD, PhD, Edmond J. Safra professor of neuropsychopharmacology at Imperial College London, said that the “delay in therapeutic action of antidepressants has been a puzzle to psychiatrists ever since they were first discerned over 50 years ago. So, these new data in humans, that use cutting edge brain imaging to demonstrate an increase in brain connections developing over the period that the depression lifts, are very exciting.”

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

BARCELONA – The typical lag between treatment initiation with selective serotonin reuptake inhibitors (SSRIs) for depression and enhanced mood may be because of the time it takes to increase brain synaptic density, new imaging data suggest.

In a double-blind study, more than 30 volunteers were randomly assigned to the SSRI escitalopram or placebo for 3-5 weeks. Using PET imaging, the investigators found that over time, synaptic density significantly increased significantly in the neocortex and hippocampus but only in patients taking the active drug.

The results point to two conclusions, said study investigator Gitta Moos Knudsen, MD, PhD, clinical professor and chief physician at the department of clinical medicine, neurology, psychiatry and sensory sciences at Copenhagen (Denmark) University Hospital.

First, they indicate that SSRIs increase synaptic density in brain areas critically involved in depression, a finding that would go some way to indicating that the synaptic density in the brain may be involved in how antidepressants function, “which would give us a target for developing novel drugs against depression,” said Dr. Knudsen.

“Secondly, our data suggest synapses build up over a period of weeks, which would explain why the effects of these drugs take time to kick in,” she added.

The findings were presented at the 36th European College of Neuropsychopharmacology (ECNP) Congress and simultaneously published online in Molecular Psychiatry.
 

Marked increase in synaptic density

SSRIs are widely used for depression as well as anxiety and obsessive-compulsive disorder. It is thought that they act via neuroplasticity and synaptic remodeling to improve cognition and emotion processing. However, the investigators note clinical evidence is lacking.

For the study, the researchers randomly assigned healthy individuals to either 20-mg escitalopram or placebo for 3-5 weeks.

They performed PET with the 11C-UCB-J tracer, which allows imaging of the synaptic vesicle glycoprotein 2A (SV2A) in the brain, synaptic density, as well as changes in density over time, in the hippocampus and neocortex.

Between May 2020 and October 2021, 17 individuals were assigned to escitalopram and 15 to placebo. There were no significant differences between two groups in terms of age, sex, and PET-related variables. Serum escitalopram measurements confirmed that all participants in the active drug group were compliant.

When synaptic density was assessed at a single time point, an average of 29 days after the intervention, there were no significant differences between the escitalopram and placebo groups in either the neocortex (P = .41) or in the hippocampus (P = .26).

However, when they performed a secondary analysis of the time-dependent effect on SV2A levels, they found a marked difference between the two study groups.

Compared with the placebo group, participants taking escitalopram had a marked increase in synaptic density in both the neocortex (rp value, 0.58; P = .003) and the hippocampus (rp value, 0.41; P = .048).

In contrast, there were no significant changes in synaptic density in either the neocortex (rp value, –0.01; P = .95) or the hippocampus (rp value, –0.06; P = .62) in the hippocampus.

“That is consistent with our clinical observation that it takes time to evolve synaptic density, along with clinical improvement. Does that mean that the increase in synaptic density is a precondition for improvement in symptoms? We don’t know,” said Dr. Knudsen.
 

Exciting but not conclusive

Session co-chair Oliver Howes, MD, PhD, professor of molecular psychiatry, King’s College London, agreed that the results do not prove the gradual increase in synaptic density the treatment response lag with SSRIs.

“We definitely don’t yet have all the data to know one way or the other,” he said in an interview.

Another potential hypothesis, he said, is that SSRIs are causing shifts in underlying brain circuits that lead to cognitive changes before there is a discernable improvement in mood.

Indeed, Dr. Howes suggested that increases in synaptic density and cognitive changes related to SSRI use are not necessarily dependent on each other and could even be unrelated.

Also commenting on the research, David Nutt, MD, PhD, Edmond J. Safra professor of neuropsychopharmacology at Imperial College London, said that the “delay in therapeutic action of antidepressants has been a puzzle to psychiatrists ever since they were first discerned over 50 years ago. So, these new data in humans, that use cutting edge brain imaging to demonstrate an increase in brain connections developing over the period that the depression lifts, are very exciting.”

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

BARCELONA – The typical lag between treatment initiation with selective serotonin reuptake inhibitors (SSRIs) for depression and enhanced mood may be because of the time it takes to increase brain synaptic density, new imaging data suggest.

In a double-blind study, more than 30 volunteers were randomly assigned to the SSRI escitalopram or placebo for 3-5 weeks. Using PET imaging, the investigators found that over time, synaptic density significantly increased significantly in the neocortex and hippocampus but only in patients taking the active drug.

The results point to two conclusions, said study investigator Gitta Moos Knudsen, MD, PhD, clinical professor and chief physician at the department of clinical medicine, neurology, psychiatry and sensory sciences at Copenhagen (Denmark) University Hospital.

First, they indicate that SSRIs increase synaptic density in brain areas critically involved in depression, a finding that would go some way to indicating that the synaptic density in the brain may be involved in how antidepressants function, “which would give us a target for developing novel drugs against depression,” said Dr. Knudsen.

“Secondly, our data suggest synapses build up over a period of weeks, which would explain why the effects of these drugs take time to kick in,” she added.

The findings were presented at the 36th European College of Neuropsychopharmacology (ECNP) Congress and simultaneously published online in Molecular Psychiatry.
 

Marked increase in synaptic density

SSRIs are widely used for depression as well as anxiety and obsessive-compulsive disorder. It is thought that they act via neuroplasticity and synaptic remodeling to improve cognition and emotion processing. However, the investigators note clinical evidence is lacking.

For the study, the researchers randomly assigned healthy individuals to either 20-mg escitalopram or placebo for 3-5 weeks.

They performed PET with the 11C-UCB-J tracer, which allows imaging of the synaptic vesicle glycoprotein 2A (SV2A) in the brain, synaptic density, as well as changes in density over time, in the hippocampus and neocortex.

Between May 2020 and October 2021, 17 individuals were assigned to escitalopram and 15 to placebo. There were no significant differences between two groups in terms of age, sex, and PET-related variables. Serum escitalopram measurements confirmed that all participants in the active drug group were compliant.

When synaptic density was assessed at a single time point, an average of 29 days after the intervention, there were no significant differences between the escitalopram and placebo groups in either the neocortex (P = .41) or in the hippocampus (P = .26).

However, when they performed a secondary analysis of the time-dependent effect on SV2A levels, they found a marked difference between the two study groups.

Compared with the placebo group, participants taking escitalopram had a marked increase in synaptic density in both the neocortex (rp value, 0.58; P = .003) and the hippocampus (rp value, 0.41; P = .048).

In contrast, there were no significant changes in synaptic density in either the neocortex (rp value, –0.01; P = .95) or the hippocampus (rp value, –0.06; P = .62) in the hippocampus.

“That is consistent with our clinical observation that it takes time to evolve synaptic density, along with clinical improvement. Does that mean that the increase in synaptic density is a precondition for improvement in symptoms? We don’t know,” said Dr. Knudsen.
 

Exciting but not conclusive

Session co-chair Oliver Howes, MD, PhD, professor of molecular psychiatry, King’s College London, agreed that the results do not prove the gradual increase in synaptic density the treatment response lag with SSRIs.

“We definitely don’t yet have all the data to know one way or the other,” he said in an interview.

Another potential hypothesis, he said, is that SSRIs are causing shifts in underlying brain circuits that lead to cognitive changes before there is a discernable improvement in mood.

Indeed, Dr. Howes suggested that increases in synaptic density and cognitive changes related to SSRI use are not necessarily dependent on each other and could even be unrelated.

Also commenting on the research, David Nutt, MD, PhD, Edmond J. Safra professor of neuropsychopharmacology at Imperial College London, said that the “delay in therapeutic action of antidepressants has been a puzzle to psychiatrists ever since they were first discerned over 50 years ago. So, these new data in humans, that use cutting edge brain imaging to demonstrate an increase in brain connections developing over the period that the depression lifts, are very exciting.”

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

TOPLINE:

Starting treatment with buprenorphine for opioid use disorder (OUD) via telehealth is associated with longer retention in treatment, compared with starting treatment in-person, new research suggests.

METHODOLOGY:

• Researchers analyzed Medicaid claims data from November 2019 through the end of 2020 in Kentucky and Ohio to investigate the impact of a policy change implemented during the COVID-19 pandemic that allowed the use of telehealth to prescribe buprenorphine for OUD.
• The two main outcomes of interest were retention in treatment after initiation (telehealth vs. traditional) and opioid-related nonfatal overdose after initiation.

TAKEAWAY:

• For both states combined, nearly 92,000 adults had a buprenorphine prescription in at least one quarter in 2020, with nearly 43,000 of those individuals starting treatment in 2020. 
• Sharp increases in telehealth delivery of buprenorphine were noted at the beginning of 2020 at the pandemic outset, and this was associated with greater retention in treatment (Kentucky adjusted odds ratio, 1.13; 95% confidence interval, 1.01-1.27 and Ohio aOR, 1.19; 95% CI, 1.06-1.32).
• Furthermore, 90-day retention rates were higher among those who started treatment via telehealth versus those who started treatment in nontelehealth settings in Kentucky (48% vs. 44%, respectively) and in Ohio (32% vs. 28%, respectively).
• There was no increased risk of nonfatal overdose with telehealth treatment, providing added evidence to suggest that patients were not harmed by having increased access to buprenorphine treatment via telehealth.

IN PRACTICE:

“These results offer important insights for states with a high burden of OUD looking to policies and methods to reduce barriers to treatment,” the authors write.

SOURCE:

The study, with first author Lindsey Hammerslag, PhD, with University of Kentucky College of Medicine, Lexington, was published online  in JAMA Network Open, with an invited commentary by Lindsey Allen, PhD, Northwestern University, Chicago, on navigating the path to effective, equitable, and evidence-based telehealth for OUD treatment.

LIMITATIONS:

The analysis was limited to Medicaid patients in two states over 1 year and there may have been unmeasured confounders, such as perceived patient stability, that influenced the findings. Because Medicaid data were not linked to emergency services or death records, this study considered only medically treated overdose.

DISCLOSURES:

The study was supported by the National Institute on Drug Abuse and carried out in partnership with the Substance Abuse and Mental Health Services Administration. The authors report no relevant financial relationships.

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

TOPLINE:

Starting treatment with buprenorphine for opioid use disorder (OUD) via telehealth is associated with longer retention in treatment, compared with starting treatment in-person, new research suggests.

METHODOLOGY:

• Researchers analyzed Medicaid claims data from November 2019 through the end of 2020 in Kentucky and Ohio to investigate the impact of a policy change implemented during the COVID-19 pandemic that allowed the use of telehealth to prescribe buprenorphine for OUD.
• The two main outcomes of interest were retention in treatment after initiation (telehealth vs. traditional) and opioid-related nonfatal overdose after initiation.

TAKEAWAY:

• For both states combined, nearly 92,000 adults had a buprenorphine prescription in at least one quarter in 2020, with nearly 43,000 of those individuals starting treatment in 2020. 
• Sharp increases in telehealth delivery of buprenorphine were noted at the beginning of 2020 at the pandemic outset, and this was associated with greater retention in treatment (Kentucky adjusted odds ratio, 1.13; 95% confidence interval, 1.01-1.27 and Ohio aOR, 1.19; 95% CI, 1.06-1.32).
• Furthermore, 90-day retention rates were higher among those who started treatment via telehealth versus those who started treatment in nontelehealth settings in Kentucky (48% vs. 44%, respectively) and in Ohio (32% vs. 28%, respectively).
• There was no increased risk of nonfatal overdose with telehealth treatment, providing added evidence to suggest that patients were not harmed by having increased access to buprenorphine treatment via telehealth.

IN PRACTICE:

“These results offer important insights for states with a high burden of OUD looking to policies and methods to reduce barriers to treatment,” the authors write.

SOURCE:

The study, with first author Lindsey Hammerslag, PhD, with University of Kentucky College of Medicine, Lexington, was published online  in JAMA Network Open, with an invited commentary by Lindsey Allen, PhD, Northwestern University, Chicago, on navigating the path to effective, equitable, and evidence-based telehealth for OUD treatment.

LIMITATIONS:

The analysis was limited to Medicaid patients in two states over 1 year and there may have been unmeasured confounders, such as perceived patient stability, that influenced the findings. Because Medicaid data were not linked to emergency services or death records, this study considered only medically treated overdose.

DISCLOSURES:

The study was supported by the National Institute on Drug Abuse and carried out in partnership with the Substance Abuse and Mental Health Services Administration. The authors report no relevant financial relationships.

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

TOPLINE:

Starting treatment with buprenorphine for opioid use disorder (OUD) via telehealth is associated with longer retention in treatment, compared with starting treatment in-person, new research suggests.

METHODOLOGY:

• Researchers analyzed Medicaid claims data from November 2019 through the end of 2020 in Kentucky and Ohio to investigate the impact of a policy change implemented during the COVID-19 pandemic that allowed the use of telehealth to prescribe buprenorphine for OUD.
• The two main outcomes of interest were retention in treatment after initiation (telehealth vs. traditional) and opioid-related nonfatal overdose after initiation.

TAKEAWAY:

• For both states combined, nearly 92,000 adults had a buprenorphine prescription in at least one quarter in 2020, with nearly 43,000 of those individuals starting treatment in 2020. 
• Sharp increases in telehealth delivery of buprenorphine were noted at the beginning of 2020 at the pandemic outset, and this was associated with greater retention in treatment (Kentucky adjusted odds ratio, 1.13; 95% confidence interval, 1.01-1.27 and Ohio aOR, 1.19; 95% CI, 1.06-1.32).
• Furthermore, 90-day retention rates were higher among those who started treatment via telehealth versus those who started treatment in nontelehealth settings in Kentucky (48% vs. 44%, respectively) and in Ohio (32% vs. 28%, respectively).
• There was no increased risk of nonfatal overdose with telehealth treatment, providing added evidence to suggest that patients were not harmed by having increased access to buprenorphine treatment via telehealth.

IN PRACTICE:

“These results offer important insights for states with a high burden of OUD looking to policies and methods to reduce barriers to treatment,” the authors write.

SOURCE:

The study, with first author Lindsey Hammerslag, PhD, with University of Kentucky College of Medicine, Lexington, was published online  in JAMA Network Open, with an invited commentary by Lindsey Allen, PhD, Northwestern University, Chicago, on navigating the path to effective, equitable, and evidence-based telehealth for OUD treatment.

LIMITATIONS:

The analysis was limited to Medicaid patients in two states over 1 year and there may have been unmeasured confounders, such as perceived patient stability, that influenced the findings. Because Medicaid data were not linked to emergency services or death records, this study considered only medically treated overdose.

DISCLOSURES:

The study was supported by the National Institute on Drug Abuse and carried out in partnership with the Substance Abuse and Mental Health Services Administration. The authors report no relevant financial relationships.

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

TOPLINE:

U.S. adults with psychiatric illness experienced fewer disruptions in receiving psychotherapy following the transition to virtual psychiatric care that accompanied the onset of the COVID-19 pandemic, a large study has shown.

METHODOLOGY:

• Retrospective study using electronic health records and insurance claims data from three large U.S. health systems.
• Sample included 110,089 patients with mental health conditions who attended at least two psychotherapy visits during the 9 months before and 9 months after the onset of COVID-19, defined in this study as March 14, 2020.
• Outcome was disruption in psychotherapy, defined as a gap of more than 45 days between visits.

TAKEAWAY:

• Before the pandemic, 96.9% of psychotherapy visits were in person and 35.4% were followed by a gap of more than 45 days.
• After the onset of the pandemic, more than half of visits (51.8%) were virtual, and only 17.9% were followed by a gap of more than 45 days.
• Prior to the pandemic, the median time between visits was 27 days, and after the pandemic, it dropped to 14 days, suggesting individuals were more likely to return for additional psychotherapy after the widespread shift to virtual care.
• Over the entire study period, individuals with depressive, anxiety, or bipolar disorders were more likely to maintain consistent psychotherapy visits, whereas those with schizophrenia, ADHD, autism, conduct or disruptive disorders, dementia, or personality disorders were more likely to have a disruption in their visits.

IN PRACTICE:

“These findings support continued use of virtual psychotherapy as an option for care when appropriate infrastructure is in place. In addition, these findings support the continuation of policies that provide access to and coverage for virtual psychotherapy,” the authors write.

SOURCE:

The study, led by Brian K. Ahmedani, PhD, with the Center for Health Policy and Health Services Research, Henry Ford Health, Detroit, was published online  in Psychiatric Services.

LIMITATIONS:

The study was conducted in three large health systems with virtual care infrastructure already in place. Researchers did not examine use of virtual care for medication management or for types of care other than psychotherapy, which may present different challenges.

DISCLOSURES:

The study was supported by the National Institute of Mental Health. The authors have no relevant disclosures.

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

TOPLINE:

U.S. adults with psychiatric illness experienced fewer disruptions in receiving psychotherapy following the transition to virtual psychiatric care that accompanied the onset of the COVID-19 pandemic, a large study has shown.

METHODOLOGY:

• Retrospective study using electronic health records and insurance claims data from three large U.S. health systems.
• Sample included 110,089 patients with mental health conditions who attended at least two psychotherapy visits during the 9 months before and 9 months after the onset of COVID-19, defined in this study as March 14, 2020.
• Outcome was disruption in psychotherapy, defined as a gap of more than 45 days between visits.

TAKEAWAY:

• Before the pandemic, 96.9% of psychotherapy visits were in person and 35.4% were followed by a gap of more than 45 days.
• After the onset of the pandemic, more than half of visits (51.8%) were virtual, and only 17.9% were followed by a gap of more than 45 days.
• Prior to the pandemic, the median time between visits was 27 days, and after the pandemic, it dropped to 14 days, suggesting individuals were more likely to return for additional psychotherapy after the widespread shift to virtual care.
• Over the entire study period, individuals with depressive, anxiety, or bipolar disorders were more likely to maintain consistent psychotherapy visits, whereas those with schizophrenia, ADHD, autism, conduct or disruptive disorders, dementia, or personality disorders were more likely to have a disruption in their visits.

IN PRACTICE:

“These findings support continued use of virtual psychotherapy as an option for care when appropriate infrastructure is in place. In addition, these findings support the continuation of policies that provide access to and coverage for virtual psychotherapy,” the authors write.

SOURCE:

The study, led by Brian K. Ahmedani, PhD, with the Center for Health Policy and Health Services Research, Henry Ford Health, Detroit, was published online  in Psychiatric Services.

LIMITATIONS:

The study was conducted in three large health systems with virtual care infrastructure already in place. Researchers did not examine use of virtual care for medication management or for types of care other than psychotherapy, which may present different challenges.

DISCLOSURES:

The study was supported by the National Institute of Mental Health. The authors have no relevant disclosures.

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

TOPLINE:

U.S. adults with psychiatric illness experienced fewer disruptions in receiving psychotherapy following the transition to virtual psychiatric care that accompanied the onset of the COVID-19 pandemic, a large study has shown.

METHODOLOGY:

• Retrospective study using electronic health records and insurance claims data from three large U.S. health systems.
• Sample included 110,089 patients with mental health conditions who attended at least two psychotherapy visits during the 9 months before and 9 months after the onset of COVID-19, defined in this study as March 14, 2020.
• Outcome was disruption in psychotherapy, defined as a gap of more than 45 days between visits.

TAKEAWAY:

• Before the pandemic, 96.9% of psychotherapy visits were in person and 35.4% were followed by a gap of more than 45 days.
• After the onset of the pandemic, more than half of visits (51.8%) were virtual, and only 17.9% were followed by a gap of more than 45 days.
• Prior to the pandemic, the median time between visits was 27 days, and after the pandemic, it dropped to 14 days, suggesting individuals were more likely to return for additional psychotherapy after the widespread shift to virtual care.
• Over the entire study period, individuals with depressive, anxiety, or bipolar disorders were more likely to maintain consistent psychotherapy visits, whereas those with schizophrenia, ADHD, autism, conduct or disruptive disorders, dementia, or personality disorders were more likely to have a disruption in their visits.

IN PRACTICE:

“These findings support continued use of virtual psychotherapy as an option for care when appropriate infrastructure is in place. In addition, these findings support the continuation of policies that provide access to and coverage for virtual psychotherapy,” the authors write.

SOURCE:

The study, led by Brian K. Ahmedani, PhD, with the Center for Health Policy and Health Services Research, Henry Ford Health, Detroit, was published online  in Psychiatric Services.

LIMITATIONS:

The study was conducted in three large health systems with virtual care infrastructure already in place. Researchers did not examine use of virtual care for medication management or for types of care other than psychotherapy, which may present different challenges.

DISCLOSURES:

The study was supported by the National Institute of Mental Health. The authors have no relevant disclosures.

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

Which conditions are caused by infection? Though it may seem like an amateur concern in the era of advanced microscopy, some culprits evade conventional methods of detection. Large medical databases hold the power to unlock answers. 

A recent study from Sweden and Denmark meticulously traced the lives and medical histories of nearly one million men and women in those countries who had received blood transfusions over nearly five decades. Some of these patients later experienced brain bleeds. The inescapable question: Could a virus found in some donor blood have caused the hemorrhages?

Traditionally, brain bleeds have been thought to strike at random. But the new study, published in JAMA, points toward an infection that causes or, at the very least, is linked to the condition. The researchers used a large databank to make the discovery. 

“As health data becomes more available and easier to analyze, we’ll see all kinds of cases like this,” said Jingcheng Zhao, MD, of the clinical epidemiology division of Sweden’s Karolinska Institutet in Solna and lead author of the study.

Scientists say the field of medical research is on the cusp of a revolution as immense health databases guide discovery and improve clinical care. 

“If you can aggregate data, you have the statistical power to identify associations,” said David R. Crosslin, PhD, professor in the division of biomedical informatics and genomics at Tulane University in New Orleans. “It opens up the world for understanding diseases.”

With access to the large database, Dr. Zhao and his team found that some blood donors later experienced brain bleeds. And it turned out that the recipients of blood from those same donors carried the highest risk of experiencing a brain bleed later in life. Meanwhile, patients whose donors remained bleed-free had the lowest risk.
 

Not so fast in the United States

In Nordic countries, all hospitals, clinics, and pharmacies report data on diagnoses and health care visits to the government, tracking that began with paper and pen in the 1960s. But the United States health care system is too fragmented to replicate such efforts, with several brands of electronic medical records operating across different systems. Data sharing across institutions is minimal. 

Most comparable health data in the United States comes from reimbursement information collected by the Centers for Medicare & Medicaid Services on government-sponsored insurance programs.

“We would need all the health care systems in the country to operate within the same IT system or use the same data model,” said Euan Ashley, MD, PhD, professor of genomics at Stanford (Calif.) University. “It’s an exciting prospect. But I think [the United States] is one of the last countries where it’ll happen.”

States, meanwhile, collect health data on specific areas like sexually transmitted infection cases and rates. Other states have registries, like the Connecticut Tumor Registry, which was established in 1941 and is the oldest population-based cancer registry in the world.

But all of these efforts are ad hoc, and no equivalent exists for heart disease and other conditions.

Health data companies have recently entered the U.S. data industry mainly through partnerships with health systems and insurance companies, using deidentified information from patient charts.

The large databases have yielded important findings that randomized clinical trials simply cannot, according to Dr. Ashley.

For instance, a study found that a heavily-lauded immunotherapy treatment did not provide meaningful outcomes for patients aged 75 years or older, but it did for younger patients.

This sort of analysis might enable clinicians to administer treatments based on how effective they are for patients with particular demographics, according to Cary Gross, MD, professor at Yale University in New Haven, Conn.

“From a bedside standpoint, these large databases can identify who benefits from what,” Dr. Gross said. “Precision medicine is not just about genetic tailoring.” These large datasets also provide insight into genetic and environmental variables that contribute to disease. 

For instance, the UK Biobank has more than 500,000 participants paired with their medical records and scans of their body and brain. Researchers perform cognitive tests on participants and extract DNA from blood samples over their lifetime, allowing examination of interactions between risk factors. 

A similar but much smaller-scale effort underway in the United States, called the All of Us Research Program, has enrolled more than 650,000 people, less than one-third the size of the UK Biobank by relative populations. The goal of the program is to provide insights into prevention and treatment of chronic disease among a diverse set of at least one million participants. The database includes information on sexual orientation, which is a fairly new datapoint collected by researchers in an effort to study health outcomes and inequities among the LGBTQ+ community.

Dr. Crosslin and his colleagues are writing a grant proposal to use the All of Us database to identify genetic risks for preeclampsia. People with certain genetic profiles may be predisposed to the life-threatening condition, and researchers may discover that lifestyle changes could decrease risk, Dr. Crosslin said. 
 

Changes in the United States

The COVID-19 pandemic exposed the lack of centralized data in the United States because a majority of research on the virus has been conducted abroad in countries with national health care systems and these large databases. 

The U.S. gap spurred a group of researchers to create the National Institutes of Health–funded National COVID Cohort Collaborative (N3C), a project that gathers medical records from millions of patients across health systems and provides access to research teams investigating a wide spectrum of topics, such as optimal timing for ventilator use.

But until government or private health systems develop a way to share and regulate health data ethically and efficiently, significant limits will persist on what large-scale databases can do, Dr. Gross said. 

“At the federal level, we need to ensure this health information is made available for public health researchers so we don’t create these private fiefdoms of data,” Dr. Gross said. “Things have to be transparent. I think our country needs to take a step back and think about what we’re doing with our health data and how we can make sure it’s being managed ethically.”

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

Which conditions are caused by infection? Though it may seem like an amateur concern in the era of advanced microscopy, some culprits evade conventional methods of detection. Large medical databases hold the power to unlock answers. 

A recent study from Sweden and Denmark meticulously traced the lives and medical histories of nearly one million men and women in those countries who had received blood transfusions over nearly five decades. Some of these patients later experienced brain bleeds. The inescapable question: Could a virus found in some donor blood have caused the hemorrhages?

Traditionally, brain bleeds have been thought to strike at random. But the new study, published in JAMA, points toward an infection that causes or, at the very least, is linked to the condition. The researchers used a large databank to make the discovery. 

“As health data becomes more available and easier to analyze, we’ll see all kinds of cases like this,” said Jingcheng Zhao, MD, of the clinical epidemiology division of Sweden’s Karolinska Institutet in Solna and lead author of the study.

Scientists say the field of medical research is on the cusp of a revolution as immense health databases guide discovery and improve clinical care. 

“If you can aggregate data, you have the statistical power to identify associations,” said David R. Crosslin, PhD, professor in the division of biomedical informatics and genomics at Tulane University in New Orleans. “It opens up the world for understanding diseases.”

With access to the large database, Dr. Zhao and his team found that some blood donors later experienced brain bleeds. And it turned out that the recipients of blood from those same donors carried the highest risk of experiencing a brain bleed later in life. Meanwhile, patients whose donors remained bleed-free had the lowest risk.
 

Not so fast in the United States

In Nordic countries, all hospitals, clinics, and pharmacies report data on diagnoses and health care visits to the government, tracking that began with paper and pen in the 1960s. But the United States health care system is too fragmented to replicate such efforts, with several brands of electronic medical records operating across different systems. Data sharing across institutions is minimal. 

Most comparable health data in the United States comes from reimbursement information collected by the Centers for Medicare & Medicaid Services on government-sponsored insurance programs.

“We would need all the health care systems in the country to operate within the same IT system or use the same data model,” said Euan Ashley, MD, PhD, professor of genomics at Stanford (Calif.) University. “It’s an exciting prospect. But I think [the United States] is one of the last countries where it’ll happen.”

States, meanwhile, collect health data on specific areas like sexually transmitted infection cases and rates. Other states have registries, like the Connecticut Tumor Registry, which was established in 1941 and is the oldest population-based cancer registry in the world.

But all of these efforts are ad hoc, and no equivalent exists for heart disease and other conditions.

Health data companies have recently entered the U.S. data industry mainly through partnerships with health systems and insurance companies, using deidentified information from patient charts.

The large databases have yielded important findings that randomized clinical trials simply cannot, according to Dr. Ashley.

For instance, a study found that a heavily-lauded immunotherapy treatment did not provide meaningful outcomes for patients aged 75 years or older, but it did for younger patients.

This sort of analysis might enable clinicians to administer treatments based on how effective they are for patients with particular demographics, according to Cary Gross, MD, professor at Yale University in New Haven, Conn.

“From a bedside standpoint, these large databases can identify who benefits from what,” Dr. Gross said. “Precision medicine is not just about genetic tailoring.” These large datasets also provide insight into genetic and environmental variables that contribute to disease. 

For instance, the UK Biobank has more than 500,000 participants paired with their medical records and scans of their body and brain. Researchers perform cognitive tests on participants and extract DNA from blood samples over their lifetime, allowing examination of interactions between risk factors. 

A similar but much smaller-scale effort underway in the United States, called the All of Us Research Program, has enrolled more than 650,000 people, less than one-third the size of the UK Biobank by relative populations. The goal of the program is to provide insights into prevention and treatment of chronic disease among a diverse set of at least one million participants. The database includes information on sexual orientation, which is a fairly new datapoint collected by researchers in an effort to study health outcomes and inequities among the LGBTQ+ community.

Dr. Crosslin and his colleagues are writing a grant proposal to use the All of Us database to identify genetic risks for preeclampsia. People with certain genetic profiles may be predisposed to the life-threatening condition, and researchers may discover that lifestyle changes could decrease risk, Dr. Crosslin said. 
 

Changes in the United States

The COVID-19 pandemic exposed the lack of centralized data in the United States because a majority of research on the virus has been conducted abroad in countries with national health care systems and these large databases. 

The U.S. gap spurred a group of researchers to create the National Institutes of Health–funded National COVID Cohort Collaborative (N3C), a project that gathers medical records from millions of patients across health systems and provides access to research teams investigating a wide spectrum of topics, such as optimal timing for ventilator use.

But until government or private health systems develop a way to share and regulate health data ethically and efficiently, significant limits will persist on what large-scale databases can do, Dr. Gross said. 

“At the federal level, we need to ensure this health information is made available for public health researchers so we don’t create these private fiefdoms of data,” Dr. Gross said. “Things have to be transparent. I think our country needs to take a step back and think about what we’re doing with our health data and how we can make sure it’s being managed ethically.”

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

Which conditions are caused by infection? Though it may seem like an amateur concern in the era of advanced microscopy, some culprits evade conventional methods of detection. Large medical databases hold the power to unlock answers. 

A recent study from Sweden and Denmark meticulously traced the lives and medical histories of nearly one million men and women in those countries who had received blood transfusions over nearly five decades. Some of these patients later experienced brain bleeds. The inescapable question: Could a virus found in some donor blood have caused the hemorrhages?

Traditionally, brain bleeds have been thought to strike at random. But the new study, published in JAMA, points toward an infection that causes or, at the very least, is linked to the condition. The researchers used a large databank to make the discovery. 

“As health data becomes more available and easier to analyze, we’ll see all kinds of cases like this,” said Jingcheng Zhao, MD, of the clinical epidemiology division of Sweden’s Karolinska Institutet in Solna and lead author of the study.

Scientists say the field of medical research is on the cusp of a revolution as immense health databases guide discovery and improve clinical care. 

“If you can aggregate data, you have the statistical power to identify associations,” said David R. Crosslin, PhD, professor in the division of biomedical informatics and genomics at Tulane University in New Orleans. “It opens up the world for understanding diseases.”

With access to the large database, Dr. Zhao and his team found that some blood donors later experienced brain bleeds. And it turned out that the recipients of blood from those same donors carried the highest risk of experiencing a brain bleed later in life. Meanwhile, patients whose donors remained bleed-free had the lowest risk.
 

Not so fast in the United States

In Nordic countries, all hospitals, clinics, and pharmacies report data on diagnoses and health care visits to the government, tracking that began with paper and pen in the 1960s. But the United States health care system is too fragmented to replicate such efforts, with several brands of electronic medical records operating across different systems. Data sharing across institutions is minimal. 

Most comparable health data in the United States comes from reimbursement information collected by the Centers for Medicare & Medicaid Services on government-sponsored insurance programs.

“We would need all the health care systems in the country to operate within the same IT system or use the same data model,” said Euan Ashley, MD, PhD, professor of genomics at Stanford (Calif.) University. “It’s an exciting prospect. But I think [the United States] is one of the last countries where it’ll happen.”

States, meanwhile, collect health data on specific areas like sexually transmitted infection cases and rates. Other states have registries, like the Connecticut Tumor Registry, which was established in 1941 and is the oldest population-based cancer registry in the world.

But all of these efforts are ad hoc, and no equivalent exists for heart disease and other conditions.

Health data companies have recently entered the U.S. data industry mainly through partnerships with health systems and insurance companies, using deidentified information from patient charts.

The large databases have yielded important findings that randomized clinical trials simply cannot, according to Dr. Ashley.

For instance, a study found that a heavily-lauded immunotherapy treatment did not provide meaningful outcomes for patients aged 75 years or older, but it did for younger patients.

This sort of analysis might enable clinicians to administer treatments based on how effective they are for patients with particular demographics, according to Cary Gross, MD, professor at Yale University in New Haven, Conn.

“From a bedside standpoint, these large databases can identify who benefits from what,” Dr. Gross said. “Precision medicine is not just about genetic tailoring.” These large datasets also provide insight into genetic and environmental variables that contribute to disease. 

For instance, the UK Biobank has more than 500,000 participants paired with their medical records and scans of their body and brain. Researchers perform cognitive tests on participants and extract DNA from blood samples over their lifetime, allowing examination of interactions between risk factors. 

A similar but much smaller-scale effort underway in the United States, called the All of Us Research Program, has enrolled more than 650,000 people, less than one-third the size of the UK Biobank by relative populations. The goal of the program is to provide insights into prevention and treatment of chronic disease among a diverse set of at least one million participants. The database includes information on sexual orientation, which is a fairly new datapoint collected by researchers in an effort to study health outcomes and inequities among the LGBTQ+ community.

Dr. Crosslin and his colleagues are writing a grant proposal to use the All of Us database to identify genetic risks for preeclampsia. People with certain genetic profiles may be predisposed to the life-threatening condition, and researchers may discover that lifestyle changes could decrease risk, Dr. Crosslin said. 
 

Changes in the United States

The COVID-19 pandemic exposed the lack of centralized data in the United States because a majority of research on the virus has been conducted abroad in countries with national health care systems and these large databases. 

The U.S. gap spurred a group of researchers to create the National Institutes of Health–funded National COVID Cohort Collaborative (N3C), a project that gathers medical records from millions of patients across health systems and provides access to research teams investigating a wide spectrum of topics, such as optimal timing for ventilator use.

But until government or private health systems develop a way to share and regulate health data ethically and efficiently, significant limits will persist on what large-scale databases can do, Dr. Gross said. 

“At the federal level, we need to ensure this health information is made available for public health researchers so we don’t create these private fiefdoms of data,” Dr. Gross said. “Things have to be transparent. I think our country needs to take a step back and think about what we’re doing with our health data and how we can make sure it’s being managed ethically.”

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

A Canadian systematic review of 28 observational studies has identified 10 strong predictors of fatal and nonfatal prescription opioid overdose.

Published in CMAJ, the analysis found the risk of fatal and nonfatal opioid overdose was notably tied to such factors as high-dose and fentanyl prescriptions, multiple opioid prescribers or pharmacies, and several mental health issues. High-certainty evidence from 14 studies involving more than a million patients showed a linear dose-response relationship with opioid overdose.

“Our findings suggest that awareness of, and attention to, several patient and prescription characteristics may help reduce the risk of opioid overdose among people living with chronic pain,” wrote a research team led by Li Wang, PhD, a researcher at the Michael G. DeGroote Institute for Pain Research and Care and the department of anesthesia at McMaster University, Hamilton, Ont.
 

Predictors of fatal and nonfatal overdose

Reporting on studies of 103 possible predictors in a pooled cohort of almost 24 million patients, the review found moderate- to high-certainty evidence for large relative associations with the following 10 criteria:

• A history of overdose (odds ratio, 5.85; 95% confidence interval, 3.78-9.04).
• A higher opioid dosage (OR, 2.57; 95% CI, 2.08-3.18 per 90-mg increment).
• Three or more prescribers (OR, 4.68; 95% CI, 3.57-6.12).
• Four or more dispensing pharmacies (OR, 4.92; 95% CI, 4.35-5.57).
• Prescription for fentanyl (OR, 2.80; 95% CI, 2.30-3.41).
• Current substance use disorder (OR, 2.62; 95% CI, 2.09-3.27).
• Any mental health diagnosis (OR, 2.12; 95% CI, 1.73-2.61).
• Depression (OR, 2.22; 95% CI, 1.57-314).
• Bipolar disorder (OR, 2.07; 95% CI, 1.77-2.41).
• Pancreatitis (OR, 2.00; 95% CI,1.52-2.64).

Absolute risks in patients with the predictor ranged from 2 to 6 per 1,000 for fatal overdose and 4 to 12 per 1,000 for nonfatal overdose.

The authors noted that chronic pain affects 20% of the world’s population worldwide, and a 2021 meta-analysis of 60 observational studies revealed that opioids are prescribed for 27% of adults living with chronic pain, with a higher prevalence of prescribing in North America than in Europe.
 

International review

A total of 28 observational studies comprising 23,963,716 patients (52% female) with mean age of 52 years were enrolled. All used administrative databases. Twenty-four studies were conducted in the United States, three in Canada, and one in the United Kingdom. Twenty-one studies included only patients with noncancer chronic pain, while seven included patients with either cancer-related or noncancer chronic pain. Twenty-two studies accepted patients with previous or current substance use disorder and three excluded patients with comorbid substance use disorder. Twenty-three studies included patients with comorbid mental illness and five exclusively recruited veterans.

The median sample size was 43,885. As a limitation, 25 studies (89%) were at high risk of bias for at least one criterion, the authors acknowledged. Moderate-certainty evidence showed the pooled prevalence of fatal opioid overdose after prescription for chronic pain was 1.3 per 1,000 (95% CI, 0.6-2.3 per 1,000) for fatal overdose and 3.2 per 1,000 (95% CI, 2.0-4.7 per 1,000) for nonfatal overdose.

“Awareness of these predictors may facilitate shared decision-making regarding prescribing opioids for chronic pain and may inform harm-reduction strategies,” Dr. Wang and associates wrote.

This study was supported by a grant from Health Canada’s Substance Use and Addictions Program. Coauthor Dr. Corey Hayes was supported by Veterans Affairs Health Services Research and Development and the National Institute on Drug Abuse Clinical Trials Network. Dr. Jason Busse is supported by the Canadian Institutes of Health Research. Dr. David Juurlink has received travel support for presentations from the CIHR, Stanford University, and Texas Tech University Health Sciences Center.

A Canadian systematic review of 28 observational studies has identified 10 strong predictors of fatal and nonfatal prescription opioid overdose.

Published in CMAJ, the analysis found the risk of fatal and nonfatal opioid overdose was notably tied to such factors as high-dose and fentanyl prescriptions, multiple opioid prescribers or pharmacies, and several mental health issues. High-certainty evidence from 14 studies involving more than a million patients showed a linear dose-response relationship with opioid overdose.

“Our findings suggest that awareness of, and attention to, several patient and prescription characteristics may help reduce the risk of opioid overdose among people living with chronic pain,” wrote a research team led by Li Wang, PhD, a researcher at the Michael G. DeGroote Institute for Pain Research and Care and the department of anesthesia at McMaster University, Hamilton, Ont.
 

Predictors of fatal and nonfatal overdose

Reporting on studies of 103 possible predictors in a pooled cohort of almost 24 million patients, the review found moderate- to high-certainty evidence for large relative associations with the following 10 criteria:

• A history of overdose (odds ratio, 5.85; 95% confidence interval, 3.78-9.04).
• A higher opioid dosage (OR, 2.57; 95% CI, 2.08-3.18 per 90-mg increment).
• Three or more prescribers (OR, 4.68; 95% CI, 3.57-6.12).
• Four or more dispensing pharmacies (OR, 4.92; 95% CI, 4.35-5.57).
• Prescription for fentanyl (OR, 2.80; 95% CI, 2.30-3.41).
• Current substance use disorder (OR, 2.62; 95% CI, 2.09-3.27).
• Any mental health diagnosis (OR, 2.12; 95% CI, 1.73-2.61).
• Depression (OR, 2.22; 95% CI, 1.57-314).
• Bipolar disorder (OR, 2.07; 95% CI, 1.77-2.41).
• Pancreatitis (OR, 2.00; 95% CI,1.52-2.64).

Absolute risks in patients with the predictor ranged from 2 to 6 per 1,000 for fatal overdose and 4 to 12 per 1,000 for nonfatal overdose.

The authors noted that chronic pain affects 20% of the world’s population worldwide, and a 2021 meta-analysis of 60 observational studies revealed that opioids are prescribed for 27% of adults living with chronic pain, with a higher prevalence of prescribing in North America than in Europe.
 

International review

A total of 28 observational studies comprising 23,963,716 patients (52% female) with mean age of 52 years were enrolled. All used administrative databases. Twenty-four studies were conducted in the United States, three in Canada, and one in the United Kingdom. Twenty-one studies included only patients with noncancer chronic pain, while seven included patients with either cancer-related or noncancer chronic pain. Twenty-two studies accepted patients with previous or current substance use disorder and three excluded patients with comorbid substance use disorder. Twenty-three studies included patients with comorbid mental illness and five exclusively recruited veterans.

The median sample size was 43,885. As a limitation, 25 studies (89%) were at high risk of bias for at least one criterion, the authors acknowledged. Moderate-certainty evidence showed the pooled prevalence of fatal opioid overdose after prescription for chronic pain was 1.3 per 1,000 (95% CI, 0.6-2.3 per 1,000) for fatal overdose and 3.2 per 1,000 (95% CI, 2.0-4.7 per 1,000) for nonfatal overdose.

“Awareness of these predictors may facilitate shared decision-making regarding prescribing opioids for chronic pain and may inform harm-reduction strategies,” Dr. Wang and associates wrote.

This study was supported by a grant from Health Canada’s Substance Use and Addictions Program. Coauthor Dr. Corey Hayes was supported by Veterans Affairs Health Services Research and Development and the National Institute on Drug Abuse Clinical Trials Network. Dr. Jason Busse is supported by the Canadian Institutes of Health Research. Dr. David Juurlink has received travel support for presentations from the CIHR, Stanford University, and Texas Tech University Health Sciences Center.

A Canadian systematic review of 28 observational studies has identified 10 strong predictors of fatal and nonfatal prescription opioid overdose.

Published in CMAJ, the analysis found the risk of fatal and nonfatal opioid overdose was notably tied to such factors as high-dose and fentanyl prescriptions, multiple opioid prescribers or pharmacies, and several mental health issues. High-certainty evidence from 14 studies involving more than a million patients showed a linear dose-response relationship with opioid overdose.

“Our findings suggest that awareness of, and attention to, several patient and prescription characteristics may help reduce the risk of opioid overdose among people living with chronic pain,” wrote a research team led by Li Wang, PhD, a researcher at the Michael G. DeGroote Institute for Pain Research and Care and the department of anesthesia at McMaster University, Hamilton, Ont.
 

Predictors of fatal and nonfatal overdose

Reporting on studies of 103 possible predictors in a pooled cohort of almost 24 million patients, the review found moderate- to high-certainty evidence for large relative associations with the following 10 criteria:

• A history of overdose (odds ratio, 5.85; 95% confidence interval, 3.78-9.04).
• A higher opioid dosage (OR, 2.57; 95% CI, 2.08-3.18 per 90-mg increment).
• Three or more prescribers (OR, 4.68; 95% CI, 3.57-6.12).
• Four or more dispensing pharmacies (OR, 4.92; 95% CI, 4.35-5.57).
• Prescription for fentanyl (OR, 2.80; 95% CI, 2.30-3.41).
• Current substance use disorder (OR, 2.62; 95% CI, 2.09-3.27).
• Any mental health diagnosis (OR, 2.12; 95% CI, 1.73-2.61).
• Depression (OR, 2.22; 95% CI, 1.57-314).
• Bipolar disorder (OR, 2.07; 95% CI, 1.77-2.41).
• Pancreatitis (OR, 2.00; 95% CI,1.52-2.64).

Absolute risks in patients with the predictor ranged from 2 to 6 per 1,000 for fatal overdose and 4 to 12 per 1,000 for nonfatal overdose.

The authors noted that chronic pain affects 20% of the world’s population worldwide, and a 2021 meta-analysis of 60 observational studies revealed that opioids are prescribed for 27% of adults living with chronic pain, with a higher prevalence of prescribing in North America than in Europe.
 

International review

A total of 28 observational studies comprising 23,963,716 patients (52% female) with mean age of 52 years were enrolled. All used administrative databases. Twenty-four studies were conducted in the United States, three in Canada, and one in the United Kingdom. Twenty-one studies included only patients with noncancer chronic pain, while seven included patients with either cancer-related or noncancer chronic pain. Twenty-two studies accepted patients with previous or current substance use disorder and three excluded patients with comorbid substance use disorder. Twenty-three studies included patients with comorbid mental illness and five exclusively recruited veterans.

The median sample size was 43,885. As a limitation, 25 studies (89%) were at high risk of bias for at least one criterion, the authors acknowledged. Moderate-certainty evidence showed the pooled prevalence of fatal opioid overdose after prescription for chronic pain was 1.3 per 1,000 (95% CI, 0.6-2.3 per 1,000) for fatal overdose and 3.2 per 1,000 (95% CI, 2.0-4.7 per 1,000) for nonfatal overdose.

“Awareness of these predictors may facilitate shared decision-making regarding prescribing opioids for chronic pain and may inform harm-reduction strategies,” Dr. Wang and associates wrote.

This study was supported by a grant from Health Canada’s Substance Use and Addictions Program. Coauthor Dr. Corey Hayes was supported by Veterans Affairs Health Services Research and Development and the National Institute on Drug Abuse Clinical Trials Network. Dr. Jason Busse is supported by the Canadian Institutes of Health Research. Dr. David Juurlink has received travel support for presentations from the CIHR, Stanford University, and Texas Tech University Health Sciences Center.

TOPLINE:

New Canadian guidelines for the management of high-risk drinking and alcohol use disorder (AUD) include 15 recommendations on screening, diagnosis, withdrawal management, and ongoing treatment including psychosocial interventions, drug therapies, and community-based programs.

METHODOLOGY:

• The Canadian Research Initiative in Substance Misuse convened a 36-member committee of clinicians, researchers, people with personal experience of alcohol use, and Indigenous or Métis individuals to develop the guidelines, using the Appraisal of Guidelines for Research and Evaluation Instrument.
• Risk assessment was based on Alcohol Use Disorders Identification Test-Consumption scores.
• The definition of AUD was based on patients experiencing “clinically significant impairment or distress” from their alcohol use, with severity being mild, moderate, or severe.

TAKEAWAY:

• All adult and youth patients at moderate or high risk for AUD should be screened annually for alcohol use, and those screening positive should receive a diagnostic interview for AUD and an individualized treatment plan.
• Assessment of severe alcohol withdrawal complications should include clinical parameters such as past seizures or delirium tremens and the Prediction of Alcohol Withdrawal Severity Scale, with treatment including nonbenzodiazepine medications for low-risk patients and a short-term benzodiazepine prescription for high-risk patients, ideally in an inpatient setting.
• All patients with AUD should be referred for psychosocial treatment, and those with moderate to severe AUD should be offered naltrexone, acamprosate, topiramate, or gabapentin, depending on contraindications and effectiveness.
• Antipsychotics or SSRI antidepressants have little benefit and may worsen outcomes and should not be prescribed for AUD.

IN PRACTICE:

The authors noted that more than half of people aged 15 years or older in Canada drink more than the recommended amount, and about 18% meet the definition for AUD. “The aim of this guideline is to support primary care providers and services to offer more effective treatments routinely to patients with AUD as the standard of practice, with resulting improvements in health as well as potential for considerable cost savings in health and social systems,” the investigators write. They also note that policy makers can substantially improve standards of care by promoting adoption of the guideline and its recommendations.

SOURCE:

The article was written by Evan Wood, MD, PhD, professor of medicine, University of British Columbia, Vancouver, and colleagues. It was published online in the Canadian Medical Association Journal.

LIMITATIONS:

The guideline was published more than 3 years after the initial literature search in September 2020 and did not include comprehensive guidance for AUD with co-occurring substance use disorders or with severe mental health conditions. Certain groups, including immigrant and refugee populations, were not represented.

DISCLOSURES:

Development of the guideline received support from Health Canada’s Substance Use and Addictions Program, Canadian Institutes of Health Research, and BC Centre on Substance Use. No committee members disclosed direct monetary or nonmonetary support from alcohol or pharmaceutical industry sources within the past 5 years, or that their clinical revenue would be influenced by the guideline recommendations.

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

TOPLINE:

New Canadian guidelines for the management of high-risk drinking and alcohol use disorder (AUD) include 15 recommendations on screening, diagnosis, withdrawal management, and ongoing treatment including psychosocial interventions, drug therapies, and community-based programs.

METHODOLOGY:

• The Canadian Research Initiative in Substance Misuse convened a 36-member committee of clinicians, researchers, people with personal experience of alcohol use, and Indigenous or Métis individuals to develop the guidelines, using the Appraisal of Guidelines for Research and Evaluation Instrument.
• Risk assessment was based on Alcohol Use Disorders Identification Test-Consumption scores.
• The definition of AUD was based on patients experiencing “clinically significant impairment or distress” from their alcohol use, with severity being mild, moderate, or severe.

TAKEAWAY:

• All adult and youth patients at moderate or high risk for AUD should be screened annually for alcohol use, and those screening positive should receive a diagnostic interview for AUD and an individualized treatment plan.
• Assessment of severe alcohol withdrawal complications should include clinical parameters such as past seizures or delirium tremens and the Prediction of Alcohol Withdrawal Severity Scale, with treatment including nonbenzodiazepine medications for low-risk patients and a short-term benzodiazepine prescription for high-risk patients, ideally in an inpatient setting.
• All patients with AUD should be referred for psychosocial treatment, and those with moderate to severe AUD should be offered naltrexone, acamprosate, topiramate, or gabapentin, depending on contraindications and effectiveness.
• Antipsychotics or SSRI antidepressants have little benefit and may worsen outcomes and should not be prescribed for AUD.

IN PRACTICE:

The authors noted that more than half of people aged 15 years or older in Canada drink more than the recommended amount, and about 18% meet the definition for AUD. “The aim of this guideline is to support primary care providers and services to offer more effective treatments routinely to patients with AUD as the standard of practice, with resulting improvements in health as well as potential for considerable cost savings in health and social systems,” the investigators write. They also note that policy makers can substantially improve standards of care by promoting adoption of the guideline and its recommendations.

SOURCE:

The article was written by Evan Wood, MD, PhD, professor of medicine, University of British Columbia, Vancouver, and colleagues. It was published online in the Canadian Medical Association Journal.

LIMITATIONS:

The guideline was published more than 3 years after the initial literature search in September 2020 and did not include comprehensive guidance for AUD with co-occurring substance use disorders or with severe mental health conditions. Certain groups, including immigrant and refugee populations, were not represented.

DISCLOSURES:

Development of the guideline received support from Health Canada’s Substance Use and Addictions Program, Canadian Institutes of Health Research, and BC Centre on Substance Use. No committee members disclosed direct monetary or nonmonetary support from alcohol or pharmaceutical industry sources within the past 5 years, or that their clinical revenue would be influenced by the guideline recommendations.

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

TOPLINE:

New Canadian guidelines for the management of high-risk drinking and alcohol use disorder (AUD) include 15 recommendations on screening, diagnosis, withdrawal management, and ongoing treatment including psychosocial interventions, drug therapies, and community-based programs.

METHODOLOGY:

• The Canadian Research Initiative in Substance Misuse convened a 36-member committee of clinicians, researchers, people with personal experience of alcohol use, and Indigenous or Métis individuals to develop the guidelines, using the Appraisal of Guidelines for Research and Evaluation Instrument.
• Risk assessment was based on Alcohol Use Disorders Identification Test-Consumption scores.
• The definition of AUD was based on patients experiencing “clinically significant impairment or distress” from their alcohol use, with severity being mild, moderate, or severe.

TAKEAWAY:

• All adult and youth patients at moderate or high risk for AUD should be screened annually for alcohol use, and those screening positive should receive a diagnostic interview for AUD and an individualized treatment plan.
• Assessment of severe alcohol withdrawal complications should include clinical parameters such as past seizures or delirium tremens and the Prediction of Alcohol Withdrawal Severity Scale, with treatment including nonbenzodiazepine medications for low-risk patients and a short-term benzodiazepine prescription for high-risk patients, ideally in an inpatient setting.
• All patients with AUD should be referred for psychosocial treatment, and those with moderate to severe AUD should be offered naltrexone, acamprosate, topiramate, or gabapentin, depending on contraindications and effectiveness.
• Antipsychotics or SSRI antidepressants have little benefit and may worsen outcomes and should not be prescribed for AUD.

IN PRACTICE:

The authors noted that more than half of people aged 15 years or older in Canada drink more than the recommended amount, and about 18% meet the definition for AUD. “The aim of this guideline is to support primary care providers and services to offer more effective treatments routinely to patients with AUD as the standard of practice, with resulting improvements in health as well as potential for considerable cost savings in health and social systems,” the investigators write. They also note that policy makers can substantially improve standards of care by promoting adoption of the guideline and its recommendations.

SOURCE:

The article was written by Evan Wood, MD, PhD, professor of medicine, University of British Columbia, Vancouver, and colleagues. It was published online in the Canadian Medical Association Journal.

LIMITATIONS:

The guideline was published more than 3 years after the initial literature search in September 2020 and did not include comprehensive guidance for AUD with co-occurring substance use disorders or with severe mental health conditions. Certain groups, including immigrant and refugee populations, were not represented.

DISCLOSURES:

Development of the guideline received support from Health Canada’s Substance Use and Addictions Program, Canadian Institutes of Health Research, and BC Centre on Substance Use. No committee members disclosed direct monetary or nonmonetary support from alcohol or pharmaceutical industry sources within the past 5 years, or that their clinical revenue would be influenced by the guideline recommendations.

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

TOPLINE:

Challenging conventional wisdom, new research suggests that hitting the snooze button does not lead to cognitive impairment on waking and may actually provide cognitive benefits.

METHODOLOGY:

• Researchers did two studies to determine why intermittent morning alarms are used and how they affect sleep, cognition, cortisol, and mood.
• Study 1 was a survey of 1,732 healthy adults (mean age 34 years; 66% women) designed to elucidate the characteristics of people who snooze and why they choose to delay their waking in this way.
• Study 2 was a within-subject polysomnography study of 31 healthy habitual snoozers (mean age 27 years; 18 women) designed to explore the acute effects of snoozing on sleep architecture, sleepiness, cognitive ability, mood, and cortisol awakening response.

TAKEAWAY:

• Overall, 69% reported using the snooze button or setting multiple alarms at least sometimes, most often on workdays (71%), with an average snooze time per morning of 22 minutes.
• Sleep quality did not differ between snoozers and nonsnoozers, but snoozers were more likely to feel mentally drowsy on waking (odds ratio, 3.0; P < .001) and had slightly shorter sleep time on workdays (13 minutes).
• In the polysomnography study, compared with waking up abruptly, 30 minutes of snoozing in the morning improved or did not affect performance on standard cognitive tests completed directly on final awakening.
• Snoozing resulted in about 6 minutes of lost sleep, but it prevented awakening from slow-wave sleep and had no clear effects on the cortisol awakening response, morning sleepiness, mood, or overnight sleep architecture.

IN PRACTICE:

“The findings indicate that there is no reason to stop snoozing in the morning if you enjoy it, at least not for snooze times around 30 minutes. In fact, it may even help those with morning drowsiness to be slightly more awake once they get up,” corresponding author Tina Sundelin, PhD, of Stockholm University, said in a statement.

SOURCE:

The study was published online in the Journal of Sleep Research.

LIMITATIONS:

Study 1 focused on waking preferences in a convenience sample of adults. Study 2 included only habitual snoozers making it difficult to generalize the findings to people who don’t usually snooze. The study investigated only the effect of 30 minutes of snoozing on the studied parameters. It’s possible that shorter or longer snooze times have different cognitive effects.

DISCLOSURES:

Support for the study was provided by the Stress Research Institute, Stockholm University, and a grant from Vetenskapsrådet. The authors disclosed no relevant conflicts of interest.

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

TOPLINE:

Challenging conventional wisdom, new research suggests that hitting the snooze button does not lead to cognitive impairment on waking and may actually provide cognitive benefits.

METHODOLOGY:

• Researchers did two studies to determine why intermittent morning alarms are used and how they affect sleep, cognition, cortisol, and mood.
• Study 1 was a survey of 1,732 healthy adults (mean age 34 years; 66% women) designed to elucidate the characteristics of people who snooze and why they choose to delay their waking in this way.
• Study 2 was a within-subject polysomnography study of 31 healthy habitual snoozers (mean age 27 years; 18 women) designed to explore the acute effects of snoozing on sleep architecture, sleepiness, cognitive ability, mood, and cortisol awakening response.

TAKEAWAY:

• Overall, 69% reported using the snooze button or setting multiple alarms at least sometimes, most often on workdays (71%), with an average snooze time per morning of 22 minutes.
• Sleep quality did not differ between snoozers and nonsnoozers, but snoozers were more likely to feel mentally drowsy on waking (odds ratio, 3.0; P < .001) and had slightly shorter sleep time on workdays (13 minutes).
• In the polysomnography study, compared with waking up abruptly, 30 minutes of snoozing in the morning improved or did not affect performance on standard cognitive tests completed directly on final awakening.
• Snoozing resulted in about 6 minutes of lost sleep, but it prevented awakening from slow-wave sleep and had no clear effects on the cortisol awakening response, morning sleepiness, mood, or overnight sleep architecture.

IN PRACTICE:

“The findings indicate that there is no reason to stop snoozing in the morning if you enjoy it, at least not for snooze times around 30 minutes. In fact, it may even help those with morning drowsiness to be slightly more awake once they get up,” corresponding author Tina Sundelin, PhD, of Stockholm University, said in a statement.

SOURCE:

The study was published online in the Journal of Sleep Research.

LIMITATIONS:

Study 1 focused on waking preferences in a convenience sample of adults. Study 2 included only habitual snoozers making it difficult to generalize the findings to people who don’t usually snooze. The study investigated only the effect of 30 minutes of snoozing on the studied parameters. It’s possible that shorter or longer snooze times have different cognitive effects.

DISCLOSURES:

Support for the study was provided by the Stress Research Institute, Stockholm University, and a grant from Vetenskapsrådet. The authors disclosed no relevant conflicts of interest.

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

TOPLINE:

Challenging conventional wisdom, new research suggests that hitting the snooze button does not lead to cognitive impairment on waking and may actually provide cognitive benefits.

METHODOLOGY:

• Researchers did two studies to determine why intermittent morning alarms are used and how they affect sleep, cognition, cortisol, and mood.
• Study 1 was a survey of 1,732 healthy adults (mean age 34 years; 66% women) designed to elucidate the characteristics of people who snooze and why they choose to delay their waking in this way.
• Study 2 was a within-subject polysomnography study of 31 healthy habitual snoozers (mean age 27 years; 18 women) designed to explore the acute effects of snoozing on sleep architecture, sleepiness, cognitive ability, mood, and cortisol awakening response.

TAKEAWAY:

• Overall, 69% reported using the snooze button or setting multiple alarms at least sometimes, most often on workdays (71%), with an average snooze time per morning of 22 minutes.
• Sleep quality did not differ between snoozers and nonsnoozers, but snoozers were more likely to feel mentally drowsy on waking (odds ratio, 3.0; P < .001) and had slightly shorter sleep time on workdays (13 minutes).
• In the polysomnography study, compared with waking up abruptly, 30 minutes of snoozing in the morning improved or did not affect performance on standard cognitive tests completed directly on final awakening.
• Snoozing resulted in about 6 minutes of lost sleep, but it prevented awakening from slow-wave sleep and had no clear effects on the cortisol awakening response, morning sleepiness, mood, or overnight sleep architecture.

IN PRACTICE:

“The findings indicate that there is no reason to stop snoozing in the morning if you enjoy it, at least not for snooze times around 30 minutes. In fact, it may even help those with morning drowsiness to be slightly more awake once they get up,” corresponding author Tina Sundelin, PhD, of Stockholm University, said in a statement.

SOURCE:

The study was published online in the Journal of Sleep Research.

LIMITATIONS:

Study 1 focused on waking preferences in a convenience sample of adults. Study 2 included only habitual snoozers making it difficult to generalize the findings to people who don’t usually snooze. The study investigated only the effect of 30 minutes of snoozing on the studied parameters. It’s possible that shorter or longer snooze times have different cognitive effects.

DISCLOSURES:

Support for the study was provided by the Stress Research Institute, Stockholm University, and a grant from Vetenskapsrådet. The authors disclosed no relevant conflicts of interest.

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

TOPLINE:

More physical activity in late childhood is associated with an increase in brain volume in regions involved in cognition, emotion, learning, and psychiatric illness.

METHODOLOGY:

• Investigators used data on 1,088 children (52% girls) in the Generation R Study, a 4-year longitudinal population-based cohort study in Rotterdam, the Netherlands.
• At age 10 years, children and their caregivers reported on children’s level of physical activity and sports involvement.
• Investigators measured changes in participants’ brain volume via MRI at ages 10 and 14 years.

TAKEAWAY:

• Every 1 additional hour per week in sports participation was associated with a 64.0-mm³ larger volume change in subcortical gray matter (P = .04).
• Every 1 additional hour per week in total physical activity was associated with a 154.0-mm³ larger volume change in total white matter (P = .02).
• Total physical activity reported by any source (P = .03) and child reports of outdoor play (P = .01) were associated with increased amygdala volume over time.
• Total physical activity reported by the children was associated with hippocampal volume increases (P = .02).

IN PRACTICE:

“Physical activity is one of the most promising environmental exposures favorably influencing health across the lifespan,” the authors write. “This study adds to prior literature by highlighting the neurodevelopmental benefits physical activity may have on the architecture of the amygdala and hippocampus.”

SOURCE:

The study was led by Fernando Estévez-López, PhD, of the Harvard T.H. Chan School of Public Health, Boston, the SPORT Research Group and CERNEP Research Center at the University of Almería (Spain), and Erasmus MC University Medical Centre, Rotterdam, the Netherlands. It was published online on in JAMA Network Open.

LIMITATIONS:

The study only accounted for confounders at baseline, does not establish causation, and utilized unvalidated questionnaires to gather information on physical activity.

DISCLOSURES:

Individual authors report receiving financial support, but there was no specific funding for this study. Dr. Estévez-López reports no relevant financial conflicts. Full disclosures are available in the original article.

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

TOPLINE:

More physical activity in late childhood is associated with an increase in brain volume in regions involved in cognition, emotion, learning, and psychiatric illness.

METHODOLOGY:

• Investigators used data on 1,088 children (52% girls) in the Generation R Study, a 4-year longitudinal population-based cohort study in Rotterdam, the Netherlands.
• At age 10 years, children and their caregivers reported on children’s level of physical activity and sports involvement.
• Investigators measured changes in participants’ brain volume via MRI at ages 10 and 14 years.

TAKEAWAY:

• Every 1 additional hour per week in sports participation was associated with a 64.0-mm³ larger volume change in subcortical gray matter (P = .04).
• Every 1 additional hour per week in total physical activity was associated with a 154.0-mm³ larger volume change in total white matter (P = .02).
• Total physical activity reported by any source (P = .03) and child reports of outdoor play (P = .01) were associated with increased amygdala volume over time.
• Total physical activity reported by the children was associated with hippocampal volume increases (P = .02).

IN PRACTICE:

“Physical activity is one of the most promising environmental exposures favorably influencing health across the lifespan,” the authors write. “This study adds to prior literature by highlighting the neurodevelopmental benefits physical activity may have on the architecture of the amygdala and hippocampus.”

SOURCE:

The study was led by Fernando Estévez-López, PhD, of the Harvard T.H. Chan School of Public Health, Boston, the SPORT Research Group and CERNEP Research Center at the University of Almería (Spain), and Erasmus MC University Medical Centre, Rotterdam, the Netherlands. It was published online on in JAMA Network Open.

LIMITATIONS:

The study only accounted for confounders at baseline, does not establish causation, and utilized unvalidated questionnaires to gather information on physical activity.

DISCLOSURES:

Individual authors report receiving financial support, but there was no specific funding for this study. Dr. Estévez-López reports no relevant financial conflicts. Full disclosures are available in the original article.

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

TOPLINE:

More physical activity in late childhood is associated with an increase in brain volume in regions involved in cognition, emotion, learning, and psychiatric illness.

METHODOLOGY:

• Investigators used data on 1,088 children (52% girls) in the Generation R Study, a 4-year longitudinal population-based cohort study in Rotterdam, the Netherlands.
• At age 10 years, children and their caregivers reported on children’s level of physical activity and sports involvement.
• Investigators measured changes in participants’ brain volume via MRI at ages 10 and 14 years.

TAKEAWAY:

• Every 1 additional hour per week in sports participation was associated with a 64.0-mm³ larger volume change in subcortical gray matter (P = .04).
• Every 1 additional hour per week in total physical activity was associated with a 154.0-mm³ larger volume change in total white matter (P = .02).
• Total physical activity reported by any source (P = .03) and child reports of outdoor play (P = .01) were associated with increased amygdala volume over time.
• Total physical activity reported by the children was associated with hippocampal volume increases (P = .02).

IN PRACTICE:

“Physical activity is one of the most promising environmental exposures favorably influencing health across the lifespan,” the authors write. “This study adds to prior literature by highlighting the neurodevelopmental benefits physical activity may have on the architecture of the amygdala and hippocampus.”

SOURCE:

The study was led by Fernando Estévez-López, PhD, of the Harvard T.H. Chan School of Public Health, Boston, the SPORT Research Group and CERNEP Research Center at the University of Almería (Spain), and Erasmus MC University Medical Centre, Rotterdam, the Netherlands. It was published online on in JAMA Network Open.

LIMITATIONS:

The study only accounted for confounders at baseline, does not establish causation, and utilized unvalidated questionnaires to gather information on physical activity.

DISCLOSURES:

Individual authors report receiving financial support, but there was no specific funding for this study. Dr. Estévez-López reports no relevant financial conflicts. Full disclosures are available in the original article.

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

PHILADELPHIA – Acute stress in peri- and postmenopausal women is associated with more depressive symptoms, while chronic stress showed greater association with memory and concentration problems, according to research presented at the annual meeting of the Menopause Society (formerly the North American Menopause Society).

“This work suggests that markers of hypothalamic-pituitary-axis activation that capture total cortisol secretion over multiple months, [such as] hair cortisol, strongly correlate with cognitive performance on attention and working memory tasks, whereas measures of more acute cortisol, [such as] salivary cortisol, may be more strongly associated with depression symptom severity and verbal learning,” Christina Metcalf, PhD, an assistant professor of psychiatry in the Colorado Center for Women’s Behavioral Health and Wellness at the University of Colorado at Denver, Aurora, told attendees. “Given the associations with chronic stress, there’s a lot of potential here to increase our knowledge about how women are doing and managing stress and life stressors during this life transition,” she said.

Measuring hair cortisol more feasible

The study was conducted remotely, with participants using video conferencing to communicate with the study personnel and then completing study procedures at home, including 2 days of cognitive testing with the California Verbal Learning Test – Third Edition and the n-back and continuous performance tasks. The participants also completed the Center for Epidemiologic Studies Depression Scale (CES-D).

Participants with higher levels of hair cortisol and salivary cortisol also had more severe depression symptoms (P < .001). Hair cortisol was also significantly associated with attention and working memory: Women with higher levels had fewer correct answers on the 0-back and 1-back trials (P < .01) and made more mistakes on the 2-back trial (P < .001). They also scored with less specificity on the continuous performance tasks (P = .022).

Although no association existed between hair cortisol levels and verbal learning or verbal memory (P > .05), participants with higher hair cortisol did score worse on the immediate recall trials (P = .034). Salivary cortisol levels, on the other hand, showed no association with memory recall trials, attention or working memory (P > .05).

Measuring cortisol from hair samples is more feasible than using saliva samples and may offer valuable insights regarding hypothalamic-pituitary-axis activity “to consider alongside the cognitive and mental health of late peri-/early postmenopausal women,” Dr. Metcalf told attendees. The next step is to find out whether the hypothalamic-pituitary-axis axis is a modifiable biomarker that can be used to improve executive function.

The study was limited by its small population, its cross-sectional design, and the lack of covariates in the current analyses.
 

Monitor symptoms in midlife

Hadine Joffe, MD, MSc, a professor of psychiatry and executive director of the Mary Horrigan Connors Center for Women’s Health and Gender Biology at Brigham and Women’s Hospital and Harvard Medical School, both in Boston, said the study findings were not surprising given how common the complaints of stress and depressive symptoms are.

“Mood changes are linked with acute, immediate cortisol levels at the same point in time, and cognitive symptoms were linked to more chronically elevated cortisol levels,” Dr. Joffe said in an interview. “Women and their providers should monitor for these challenging brain symptoms in midlife as they affect performance and quality of life and are linked with changes in the HPA axis as stress biomarkers.”

Because the study is small and has a cross-sectional design, it’s not possible to determine the direction of the associations or to make any inferences about causation, Dr. Joffe said.

“We cannot make the conclusion that stress is adversely affecting mood and cognitive performance given the design limitations. It is possible that mood and cognitive issues contributed to these stress markers,” Dr. Joffe said.“However, it is known that the experience of stress is linked with vulnerability to mood and cognitive symptoms, and also that mood and cognitive symptoms induce significant stress.”

The research was funded by the Menopause Society, Colorado University, the Ludeman Family Center for Women’s Health Research, the National Institute of Mental Health, and the National Institute of Aging. Dr. Metcalf had no disclosures. Dr. Joffe has received grant support from Merck, Pfizer and Sage, and has been a consultant or advisor for Bayer, Merck and Hello Therapeutics.

PHILADELPHIA – Acute stress in peri- and postmenopausal women is associated with more depressive symptoms, while chronic stress showed greater association with memory and concentration problems, according to research presented at the annual meeting of the Menopause Society (formerly the North American Menopause Society).

“This work suggests that markers of hypothalamic-pituitary-axis activation that capture total cortisol secretion over multiple months, [such as] hair cortisol, strongly correlate with cognitive performance on attention and working memory tasks, whereas measures of more acute cortisol, [such as] salivary cortisol, may be more strongly associated with depression symptom severity and verbal learning,” Christina Metcalf, PhD, an assistant professor of psychiatry in the Colorado Center for Women’s Behavioral Health and Wellness at the University of Colorado at Denver, Aurora, told attendees. “Given the associations with chronic stress, there’s a lot of potential here to increase our knowledge about how women are doing and managing stress and life stressors during this life transition,” she said.

Measuring hair cortisol more feasible

The study was conducted remotely, with participants using video conferencing to communicate with the study personnel and then completing study procedures at home, including 2 days of cognitive testing with the California Verbal Learning Test – Third Edition and the n-back and continuous performance tasks. The participants also completed the Center for Epidemiologic Studies Depression Scale (CES-D).

Participants with higher levels of hair cortisol and salivary cortisol also had more severe depression symptoms (P < .001). Hair cortisol was also significantly associated with attention and working memory: Women with higher levels had fewer correct answers on the 0-back and 1-back trials (P < .01) and made more mistakes on the 2-back trial (P < .001). They also scored with less specificity on the continuous performance tasks (P = .022).

Although no association existed between hair cortisol levels and verbal learning or verbal memory (P > .05), participants with higher hair cortisol did score worse on the immediate recall trials (P = .034). Salivary cortisol levels, on the other hand, showed no association with memory recall trials, attention or working memory (P > .05).

Measuring cortisol from hair samples is more feasible than using saliva samples and may offer valuable insights regarding hypothalamic-pituitary-axis activity “to consider alongside the cognitive and mental health of late peri-/early postmenopausal women,” Dr. Metcalf told attendees. The next step is to find out whether the hypothalamic-pituitary-axis axis is a modifiable biomarker that can be used to improve executive function.

The study was limited by its small population, its cross-sectional design, and the lack of covariates in the current analyses.
 

Monitor symptoms in midlife

Hadine Joffe, MD, MSc, a professor of psychiatry and executive director of the Mary Horrigan Connors Center for Women’s Health and Gender Biology at Brigham and Women’s Hospital and Harvard Medical School, both in Boston, said the study findings were not surprising given how common the complaints of stress and depressive symptoms are.

“Mood changes are linked with acute, immediate cortisol levels at the same point in time, and cognitive symptoms were linked to more chronically elevated cortisol levels,” Dr. Joffe said in an interview. “Women and their providers should monitor for these challenging brain symptoms in midlife as they affect performance and quality of life and are linked with changes in the HPA axis as stress biomarkers.”

Because the study is small and has a cross-sectional design, it’s not possible to determine the direction of the associations or to make any inferences about causation, Dr. Joffe said.

“We cannot make the conclusion that stress is adversely affecting mood and cognitive performance given the design limitations. It is possible that mood and cognitive issues contributed to these stress markers,” Dr. Joffe said.“However, it is known that the experience of stress is linked with vulnerability to mood and cognitive symptoms, and also that mood and cognitive symptoms induce significant stress.”

The research was funded by the Menopause Society, Colorado University, the Ludeman Family Center for Women’s Health Research, the National Institute of Mental Health, and the National Institute of Aging. Dr. Metcalf had no disclosures. Dr. Joffe has received grant support from Merck, Pfizer and Sage, and has been a consultant or advisor for Bayer, Merck and Hello Therapeutics.

PHILADELPHIA – Acute stress in peri- and postmenopausal women is associated with more depressive symptoms, while chronic stress showed greater association with memory and concentration problems, according to research presented at the annual meeting of the Menopause Society (formerly the North American Menopause Society).

“This work suggests that markers of hypothalamic-pituitary-axis activation that capture total cortisol secretion over multiple months, [such as] hair cortisol, strongly correlate with cognitive performance on attention and working memory tasks, whereas measures of more acute cortisol, [such as] salivary cortisol, may be more strongly associated with depression symptom severity and verbal learning,” Christina Metcalf, PhD, an assistant professor of psychiatry in the Colorado Center for Women’s Behavioral Health and Wellness at the University of Colorado at Denver, Aurora, told attendees. “Given the associations with chronic stress, there’s a lot of potential here to increase our knowledge about how women are doing and managing stress and life stressors during this life transition,” she said.

Measuring hair cortisol more feasible

The study was conducted remotely, with participants using video conferencing to communicate with the study personnel and then completing study procedures at home, including 2 days of cognitive testing with the California Verbal Learning Test – Third Edition and the n-back and continuous performance tasks. The participants also completed the Center for Epidemiologic Studies Depression Scale (CES-D).

Participants with higher levels of hair cortisol and salivary cortisol also had more severe depression symptoms (P < .001). Hair cortisol was also significantly associated with attention and working memory: Women with higher levels had fewer correct answers on the 0-back and 1-back trials (P < .01) and made more mistakes on the 2-back trial (P < .001). They also scored with less specificity on the continuous performance tasks (P = .022).

Although no association existed between hair cortisol levels and verbal learning or verbal memory (P > .05), participants with higher hair cortisol did score worse on the immediate recall trials (P = .034). Salivary cortisol levels, on the other hand, showed no association with memory recall trials, attention or working memory (P > .05).

Measuring cortisol from hair samples is more feasible than using saliva samples and may offer valuable insights regarding hypothalamic-pituitary-axis activity “to consider alongside the cognitive and mental health of late peri-/early postmenopausal women,” Dr. Metcalf told attendees. The next step is to find out whether the hypothalamic-pituitary-axis axis is a modifiable biomarker that can be used to improve executive function.

The study was limited by its small population, its cross-sectional design, and the lack of covariates in the current analyses.
 

Monitor symptoms in midlife

Hadine Joffe, MD, MSc, a professor of psychiatry and executive director of the Mary Horrigan Connors Center for Women’s Health and Gender Biology at Brigham and Women’s Hospital and Harvard Medical School, both in Boston, said the study findings were not surprising given how common the complaints of stress and depressive symptoms are.

“Mood changes are linked with acute, immediate cortisol levels at the same point in time, and cognitive symptoms were linked to more chronically elevated cortisol levels,” Dr. Joffe said in an interview. “Women and their providers should monitor for these challenging brain symptoms in midlife as they affect performance and quality of life and are linked with changes in the HPA axis as stress biomarkers.”

Because the study is small and has a cross-sectional design, it’s not possible to determine the direction of the associations or to make any inferences about causation, Dr. Joffe said.

“We cannot make the conclusion that stress is adversely affecting mood and cognitive performance given the design limitations. It is possible that mood and cognitive issues contributed to these stress markers,” Dr. Joffe said.“However, it is known that the experience of stress is linked with vulnerability to mood and cognitive symptoms, and also that mood and cognitive symptoms induce significant stress.”

The research was funded by the Menopause Society, Colorado University, the Ludeman Family Center for Women’s Health Research, the National Institute of Mental Health, and the National Institute of Aging. Dr. Metcalf had no disclosures. Dr. Joffe has received grant support from Merck, Pfizer and Sage, and has been a consultant or advisor for Bayer, Merck and Hello Therapeutics.