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FDA fast-tracks lecanemab for Alzheimer’s disease
Lecanemab (formerly BAN2401) is a humanized monoclonal antibody that selectively binds to large, soluble aggregated Abeta protofibrils. The antibody was developed following the discovery of a mutation in amyloid precursor protein that leads to a form of Alzheimer’s disease that is marked by particularly high levels of Abeta protofibrils.
“As such, lecanemab may have the potential to have an effect on disease pathology and to slow down the progression of the disease,” Eisai and Biogen said in a joint news release.
The breakthrough therapy designation for lecanemab is based on results of a randomized, double-blind, phase 2b proof-of-concept study published April 17 in Alzheimer’s Research & Therapy.
The study enrolled 856 patients with mild cognitive impairment (MCI) due to Alzheimer’s disease and mild Alzheimer’s disease with confirmed presence of amyloid pathology.
At the highest doses, treatment with lecanemab led to a reduction in brain amyloid accompanied by a consistent reduction of clinical decline across several clinical and biomarker endpoints.
Phase 3 testing underway
In March, Eisai and Biogen completed enrollment in a phase 3 study designed to confirm the safety and efficacy of lecanemab in patients with symptomatic early Alzheimer’s disease.
The CLARITY AD study includes 1,795 patients with early Alzheimer’s disease, and initial results are expected by the end of September 2022. The core study will compare lecanemab against placebo on the change from baseline in the Clinical Dementia Rating-Sum of Boxes (CDR-SB) at 18 months. The study will also evaluate the long-term safety and tolerability of lecanemab in the extension phase and whether the long-term effects of lecanemab, as measured by the CDR-SB at the end of the core study, are maintained over time.
Additionally, the phase 3 AHEAD 3-45 clinical study is currently exploring lecanemab in adults with preclinical Alzheimer’s disease (clinically normal but with intermediate or elevated brain amyloid).
On June 7, the FDA – amid significant controversy – approved aducanumab (Aduhelm), the first anti-amyloid agent for the treatment Alzheimer’s disease, disregarding the recommendation by its own advisory panel not to approve the drug. Three members of the FDA’s Peripheral and Central Nervous System Drugs Advisory Committee subsequently resigned in protest following the agency’s approval of aducanumab.
In addition, the high-profile consumer advocacy group Public Citizen sent a letter to the secretary of the U.S. Department of Health & Human Services demanding the removal of three FDA officials, including acting FDA Commissioner Janet Woodcock, MD.
A version of this article first appeared on Medscape.com.
Lecanemab (formerly BAN2401) is a humanized monoclonal antibody that selectively binds to large, soluble aggregated Abeta protofibrils. The antibody was developed following the discovery of a mutation in amyloid precursor protein that leads to a form of Alzheimer’s disease that is marked by particularly high levels of Abeta protofibrils.
“As such, lecanemab may have the potential to have an effect on disease pathology and to slow down the progression of the disease,” Eisai and Biogen said in a joint news release.
The breakthrough therapy designation for lecanemab is based on results of a randomized, double-blind, phase 2b proof-of-concept study published April 17 in Alzheimer’s Research & Therapy.
The study enrolled 856 patients with mild cognitive impairment (MCI) due to Alzheimer’s disease and mild Alzheimer’s disease with confirmed presence of amyloid pathology.
At the highest doses, treatment with lecanemab led to a reduction in brain amyloid accompanied by a consistent reduction of clinical decline across several clinical and biomarker endpoints.
Phase 3 testing underway
In March, Eisai and Biogen completed enrollment in a phase 3 study designed to confirm the safety and efficacy of lecanemab in patients with symptomatic early Alzheimer’s disease.
The CLARITY AD study includes 1,795 patients with early Alzheimer’s disease, and initial results are expected by the end of September 2022. The core study will compare lecanemab against placebo on the change from baseline in the Clinical Dementia Rating-Sum of Boxes (CDR-SB) at 18 months. The study will also evaluate the long-term safety and tolerability of lecanemab in the extension phase and whether the long-term effects of lecanemab, as measured by the CDR-SB at the end of the core study, are maintained over time.
Additionally, the phase 3 AHEAD 3-45 clinical study is currently exploring lecanemab in adults with preclinical Alzheimer’s disease (clinically normal but with intermediate or elevated brain amyloid).
On June 7, the FDA – amid significant controversy – approved aducanumab (Aduhelm), the first anti-amyloid agent for the treatment Alzheimer’s disease, disregarding the recommendation by its own advisory panel not to approve the drug. Three members of the FDA’s Peripheral and Central Nervous System Drugs Advisory Committee subsequently resigned in protest following the agency’s approval of aducanumab.
In addition, the high-profile consumer advocacy group Public Citizen sent a letter to the secretary of the U.S. Department of Health & Human Services demanding the removal of three FDA officials, including acting FDA Commissioner Janet Woodcock, MD.
A version of this article first appeared on Medscape.com.
Lecanemab (formerly BAN2401) is a humanized monoclonal antibody that selectively binds to large, soluble aggregated Abeta protofibrils. The antibody was developed following the discovery of a mutation in amyloid precursor protein that leads to a form of Alzheimer’s disease that is marked by particularly high levels of Abeta protofibrils.
“As such, lecanemab may have the potential to have an effect on disease pathology and to slow down the progression of the disease,” Eisai and Biogen said in a joint news release.
The breakthrough therapy designation for lecanemab is based on results of a randomized, double-blind, phase 2b proof-of-concept study published April 17 in Alzheimer’s Research & Therapy.
The study enrolled 856 patients with mild cognitive impairment (MCI) due to Alzheimer’s disease and mild Alzheimer’s disease with confirmed presence of amyloid pathology.
At the highest doses, treatment with lecanemab led to a reduction in brain amyloid accompanied by a consistent reduction of clinical decline across several clinical and biomarker endpoints.
Phase 3 testing underway
In March, Eisai and Biogen completed enrollment in a phase 3 study designed to confirm the safety and efficacy of lecanemab in patients with symptomatic early Alzheimer’s disease.
The CLARITY AD study includes 1,795 patients with early Alzheimer’s disease, and initial results are expected by the end of September 2022. The core study will compare lecanemab against placebo on the change from baseline in the Clinical Dementia Rating-Sum of Boxes (CDR-SB) at 18 months. The study will also evaluate the long-term safety and tolerability of lecanemab in the extension phase and whether the long-term effects of lecanemab, as measured by the CDR-SB at the end of the core study, are maintained over time.
Additionally, the phase 3 AHEAD 3-45 clinical study is currently exploring lecanemab in adults with preclinical Alzheimer’s disease (clinically normal but with intermediate or elevated brain amyloid).
On June 7, the FDA – amid significant controversy – approved aducanumab (Aduhelm), the first anti-amyloid agent for the treatment Alzheimer’s disease, disregarding the recommendation by its own advisory panel not to approve the drug. Three members of the FDA’s Peripheral and Central Nervous System Drugs Advisory Committee subsequently resigned in protest following the agency’s approval of aducanumab.
In addition, the high-profile consumer advocacy group Public Citizen sent a letter to the secretary of the U.S. Department of Health & Human Services demanding the removal of three FDA officials, including acting FDA Commissioner Janet Woodcock, MD.
A version of this article first appeared on Medscape.com.
Profound brain changes found in patients who died of COVID-19
The most comprehensive molecular study to date of brain tissue from people who died of COVID-19 provides clear evidence that SARS-CoV-2 causes profound molecular changes in the brain, despite no molecular trace of the virus in brain tissue.
“The signature the virus leaves in the brain speaks of strong inflammation and disrupted brain circuits and resembles signatures the field has observed in Alzheimer’s or other neurodegenerative diseases,” senior author Tony Wyss-Coray, PhD, professor of neurology and neurological sciences, Stanford (Calif.) University, told this news organization.
The study was published online June 21 in Nature.
Signs of distress
“We know that up to a third of SARS-CoV-2-infected people show brain symptoms including brain fog, memory problems, and fatigue, and a growing number of people have such symptoms long after they [have] seemingly recovered from virus infection,” said Dr. Wyss-Coray.
“However, we have very little understanding of how the virus causes these symptoms and what its effects are on the brain at a molecular level,” he added.
Using single-cell RNA sequencing, the researchers profiled the transcriptomes of 65,309 nuclei isolated from frontal cortex and choroid plexus samples from eight patients who died of COVID-19 and 14 controls who died of other causes.
There was no molecular evidence of SARS-CoV-2 in brain tissue samples from the patients who died of COVID-19.
Yet, “we were very surprised to learn that no matter which type of cell we studied (different types of nerve cells, immune cells, or different support cells in the brain) there were prominent changes” compared with brain tissue samples from controls who died of other causes, said Dr. Wyss-Coray.
The changes in the COVID-19 brains showed signatures of inflammation, abnormal nerve cell communication, and chronic neurodegeneration.
“Across cell types, COVID-19 perturbations overlap with those in chronic brain disorders and reside in genetic variants associated with cognition, schizophrenia, and depression,” the researchers report.
“Viral infection appears to trigger inflammatory responses throughout the body that may cause inflammatory signaling across the blood–brain barrier, which in turn could ‘trip off’ neuroinflammation in the brain,” Dr. Wyss-Coray said.
The findings may help explain the brain fog, fatigue, and other neurological and psychiatric symptoms of long COVID.
“While we studied only brains from people who died of COVID-19, we believe it is likely that similar, but hopefully weaker, signs of inflammation and chronic neurodegeneration will be found in COVID-19 survivors, especially those with chronic brain symptoms,” Dr. Wyss-Coray said.
This research was funded by the Nomis Foundation, the National Institutes of Health, Nan Fung Life Sciences, the Wu Tsai Neurosciences Institute and the Stanford Alzheimer’s Disease Research Center. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The most comprehensive molecular study to date of brain tissue from people who died of COVID-19 provides clear evidence that SARS-CoV-2 causes profound molecular changes in the brain, despite no molecular trace of the virus in brain tissue.
“The signature the virus leaves in the brain speaks of strong inflammation and disrupted brain circuits and resembles signatures the field has observed in Alzheimer’s or other neurodegenerative diseases,” senior author Tony Wyss-Coray, PhD, professor of neurology and neurological sciences, Stanford (Calif.) University, told this news organization.
The study was published online June 21 in Nature.
Signs of distress
“We know that up to a third of SARS-CoV-2-infected people show brain symptoms including brain fog, memory problems, and fatigue, and a growing number of people have such symptoms long after they [have] seemingly recovered from virus infection,” said Dr. Wyss-Coray.
“However, we have very little understanding of how the virus causes these symptoms and what its effects are on the brain at a molecular level,” he added.
Using single-cell RNA sequencing, the researchers profiled the transcriptomes of 65,309 nuclei isolated from frontal cortex and choroid plexus samples from eight patients who died of COVID-19 and 14 controls who died of other causes.
There was no molecular evidence of SARS-CoV-2 in brain tissue samples from the patients who died of COVID-19.
Yet, “we were very surprised to learn that no matter which type of cell we studied (different types of nerve cells, immune cells, or different support cells in the brain) there were prominent changes” compared with brain tissue samples from controls who died of other causes, said Dr. Wyss-Coray.
The changes in the COVID-19 brains showed signatures of inflammation, abnormal nerve cell communication, and chronic neurodegeneration.
“Across cell types, COVID-19 perturbations overlap with those in chronic brain disorders and reside in genetic variants associated with cognition, schizophrenia, and depression,” the researchers report.
“Viral infection appears to trigger inflammatory responses throughout the body that may cause inflammatory signaling across the blood–brain barrier, which in turn could ‘trip off’ neuroinflammation in the brain,” Dr. Wyss-Coray said.
The findings may help explain the brain fog, fatigue, and other neurological and psychiatric symptoms of long COVID.
“While we studied only brains from people who died of COVID-19, we believe it is likely that similar, but hopefully weaker, signs of inflammation and chronic neurodegeneration will be found in COVID-19 survivors, especially those with chronic brain symptoms,” Dr. Wyss-Coray said.
This research was funded by the Nomis Foundation, the National Institutes of Health, Nan Fung Life Sciences, the Wu Tsai Neurosciences Institute and the Stanford Alzheimer’s Disease Research Center. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The most comprehensive molecular study to date of brain tissue from people who died of COVID-19 provides clear evidence that SARS-CoV-2 causes profound molecular changes in the brain, despite no molecular trace of the virus in brain tissue.
“The signature the virus leaves in the brain speaks of strong inflammation and disrupted brain circuits and resembles signatures the field has observed in Alzheimer’s or other neurodegenerative diseases,” senior author Tony Wyss-Coray, PhD, professor of neurology and neurological sciences, Stanford (Calif.) University, told this news organization.
The study was published online June 21 in Nature.
Signs of distress
“We know that up to a third of SARS-CoV-2-infected people show brain symptoms including brain fog, memory problems, and fatigue, and a growing number of people have such symptoms long after they [have] seemingly recovered from virus infection,” said Dr. Wyss-Coray.
“However, we have very little understanding of how the virus causes these symptoms and what its effects are on the brain at a molecular level,” he added.
Using single-cell RNA sequencing, the researchers profiled the transcriptomes of 65,309 nuclei isolated from frontal cortex and choroid plexus samples from eight patients who died of COVID-19 and 14 controls who died of other causes.
There was no molecular evidence of SARS-CoV-2 in brain tissue samples from the patients who died of COVID-19.
Yet, “we were very surprised to learn that no matter which type of cell we studied (different types of nerve cells, immune cells, or different support cells in the brain) there were prominent changes” compared with brain tissue samples from controls who died of other causes, said Dr. Wyss-Coray.
The changes in the COVID-19 brains showed signatures of inflammation, abnormal nerve cell communication, and chronic neurodegeneration.
“Across cell types, COVID-19 perturbations overlap with those in chronic brain disorders and reside in genetic variants associated with cognition, schizophrenia, and depression,” the researchers report.
“Viral infection appears to trigger inflammatory responses throughout the body that may cause inflammatory signaling across the blood–brain barrier, which in turn could ‘trip off’ neuroinflammation in the brain,” Dr. Wyss-Coray said.
The findings may help explain the brain fog, fatigue, and other neurological and psychiatric symptoms of long COVID.
“While we studied only brains from people who died of COVID-19, we believe it is likely that similar, but hopefully weaker, signs of inflammation and chronic neurodegeneration will be found in COVID-19 survivors, especially those with chronic brain symptoms,” Dr. Wyss-Coray said.
This research was funded by the Nomis Foundation, the National Institutes of Health, Nan Fung Life Sciences, the Wu Tsai Neurosciences Institute and the Stanford Alzheimer’s Disease Research Center. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Key driver of fish oil’s antidepressant effects revealed
A key molecular mechanism underpinning the anti-inflammatory, antidepressant, and neuroprotective effects of omega-3 fatty acids has been identified. In findings that could lead to the development of new treatments for depression, the research provides the “first evidence” that hippocampal neurons are able to produce two key lipid metabolites of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) – lipoxygenase and cytochrome P450, lead investigator Alessandra Borsini, PhD, told this news organization.
This is how EPA and DHA exert their anti-inflammatory and neurogenic properties in vitro, as well as antidepressant properties in patients with depression, said Dr. Borsini, from King’s College London.
“Indeed, we found evidence for a correlation between increased levels of these metabolites and a decrease in severity of depressive symptoms in patients with major depressive disorder,” Dr. Borsini said.
The study was published online June 16 in Molecular Psychiatry.
‘Depression in a dish’
Despite the known role of inflammation in depression, there remains a lack of data showing anti-inflammatory strategies that are effective, safe for everyday use, and with a clear mechanism of action, the researchers note.
Dr. Borsini and colleagues tested the theory that when EPA and DHA are metabolized, some of their metabolites, or lipid mediators, can protect the brain from the harmful effects of inflammation. They used a validated “depression in a dish” in vitro human hippocampal cell model to test their theory.
They found that treating human hippocampal cells with EPA or DHA before exposing them to cytokines prevented increased cell death and decreased neurogenesis. Both these impacts had been previously observed in cells exposed to cytokines alone.
They confirmed that these effects were mediated by the formation of several key lipid mediators produced by EPA and DHA – namely hydroxyeicosapentaenoic acid, hydroxydocosahexaenoic acid, epoxyeicosatetraenoic acid (EpETE), and epoxydocosapentaenoic acid (EpDPA).
It’s the first time these lipid mediators were detected in human hippocampal neurons, the researchers say.
They also found that treating the neurons with an enzyme inhibitor increased the availability of two of these metabolites (EpETE and EpDPA), suggesting a possible way by which future treatments could be optimized.
The findings were replicated in 22 patients with major depression given either EPA (3 g/day) or DHA (1.4 g/day) for 12 weeks. In both groups, EPA or DHA treatment was associated with an increase in their respective metabolites and significant improvement in depressive symptoms.
The average reduction in symptom scores was 64% and 71% in the EPA and DHA groups, respectively, and there was some evidence that higher levels of the same metabolites correlated with less severe depressive symptoms.
“For some time we have known that omega-3 [polyunsaturated fatty acid (PUFA)] can induce antidepressant and anti-inflammatory effects, but, without further understanding of how this happens in the human brain, it has been difficult to develop treatments,” Dr. Borsini said in a news release.
“ which can inform the development of potential new treatments for depression using omega-3 PUFA,” Dr. Borsini added.
“We need to be cautious when interpreting data generated from the correlation between levels of metabolites and depressive symptoms as findings require further validation in a bigger sample of patients,” Dr. Borsini said.
“It is important to highlight that our research has not shown that by simply increasing omega-3 fatty acids in our diets or through taking nutritional supplements we can reduce inflammation or depression,” study author Carmine Pariante, MD, PhD, from King’s College London, said in the news release.
“The mechanisms behind the associations between depression and omega-3 PUFA are complicated and require further research and clinical trials to fully understand how they work and inform future therapeutic approaches,” Dr. Pariante said.
No clinical implications
Weighing in on this research in a Science Media Centre statement, Kevin McConway, emeritus professor of applied statistics, The Open University, Milton Keynes, United Kingdom, said, “The point of the study was to throw some light on the mechanisms in the body by which omega-3 fatty acids might work to reduce inflammation or depression.”
“The research mostly involved cells in laboratory dishes, but it also involved treating a small sample of patients with major depression by giving them supplements of one or other of the two omega-3 acids under investigation for 12 weeks,” he noted.
“The researchers found that the patients’ average scores on a standard set of questions, used to diagnose and measure depression, improved over that 12-week period, for each of the two fatty acids.
While depression symptoms improved over 12 weeks with omega-3 fatty acid treatment, “depression symptoms change over time anyway, for many reasons,” and depressive symptoms might have improved over 12 weeks even if the patients had not been given the omega-3 acids, Dr. McConway said.
“We just can’t tell since every patient got omega-3 fatty acids. So these results can hint that omega-3 fatty acids might help in depression, but it comes nowhere near showing that this is the case with a reasonable degree of certainty,” he cautioned.
“Indeed the researchers did not carry out this part of their study to see whether the omega-3 supplements help with depression – they did it to see whether the biochemical changes that they had seen in cell cultures in the lab might also occur in human bodies,” he noted.
This research was funded in part by grants to the investigators from the U.K. Medical Research Council, the European Commission Horizon 2020, and the National Institute for Health Research (NIHR), Maudsley Biomedical Research Centre (BRC) at South London and Maudsley NHS Foundation Trust and King’s College London. Dr. Borsini has received research funding from Johnson & Johnson for research on depression and inflammation. Dr. McConway is a trustee of the Science Media Centre and a member of its advisory committee.
A version of this article first appeared on Medscape.com.
A key molecular mechanism underpinning the anti-inflammatory, antidepressant, and neuroprotective effects of omega-3 fatty acids has been identified. In findings that could lead to the development of new treatments for depression, the research provides the “first evidence” that hippocampal neurons are able to produce two key lipid metabolites of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) – lipoxygenase and cytochrome P450, lead investigator Alessandra Borsini, PhD, told this news organization.
This is how EPA and DHA exert their anti-inflammatory and neurogenic properties in vitro, as well as antidepressant properties in patients with depression, said Dr. Borsini, from King’s College London.
“Indeed, we found evidence for a correlation between increased levels of these metabolites and a decrease in severity of depressive symptoms in patients with major depressive disorder,” Dr. Borsini said.
The study was published online June 16 in Molecular Psychiatry.
‘Depression in a dish’
Despite the known role of inflammation in depression, there remains a lack of data showing anti-inflammatory strategies that are effective, safe for everyday use, and with a clear mechanism of action, the researchers note.
Dr. Borsini and colleagues tested the theory that when EPA and DHA are metabolized, some of their metabolites, or lipid mediators, can protect the brain from the harmful effects of inflammation. They used a validated “depression in a dish” in vitro human hippocampal cell model to test their theory.
They found that treating human hippocampal cells with EPA or DHA before exposing them to cytokines prevented increased cell death and decreased neurogenesis. Both these impacts had been previously observed in cells exposed to cytokines alone.
They confirmed that these effects were mediated by the formation of several key lipid mediators produced by EPA and DHA – namely hydroxyeicosapentaenoic acid, hydroxydocosahexaenoic acid, epoxyeicosatetraenoic acid (EpETE), and epoxydocosapentaenoic acid (EpDPA).
It’s the first time these lipid mediators were detected in human hippocampal neurons, the researchers say.
They also found that treating the neurons with an enzyme inhibitor increased the availability of two of these metabolites (EpETE and EpDPA), suggesting a possible way by which future treatments could be optimized.
The findings were replicated in 22 patients with major depression given either EPA (3 g/day) or DHA (1.4 g/day) for 12 weeks. In both groups, EPA or DHA treatment was associated with an increase in their respective metabolites and significant improvement in depressive symptoms.
The average reduction in symptom scores was 64% and 71% in the EPA and DHA groups, respectively, and there was some evidence that higher levels of the same metabolites correlated with less severe depressive symptoms.
“For some time we have known that omega-3 [polyunsaturated fatty acid (PUFA)] can induce antidepressant and anti-inflammatory effects, but, without further understanding of how this happens in the human brain, it has been difficult to develop treatments,” Dr. Borsini said in a news release.
“ which can inform the development of potential new treatments for depression using omega-3 PUFA,” Dr. Borsini added.
“We need to be cautious when interpreting data generated from the correlation between levels of metabolites and depressive symptoms as findings require further validation in a bigger sample of patients,” Dr. Borsini said.
“It is important to highlight that our research has not shown that by simply increasing omega-3 fatty acids in our diets or through taking nutritional supplements we can reduce inflammation or depression,” study author Carmine Pariante, MD, PhD, from King’s College London, said in the news release.
“The mechanisms behind the associations between depression and omega-3 PUFA are complicated and require further research and clinical trials to fully understand how they work and inform future therapeutic approaches,” Dr. Pariante said.
No clinical implications
Weighing in on this research in a Science Media Centre statement, Kevin McConway, emeritus professor of applied statistics, The Open University, Milton Keynes, United Kingdom, said, “The point of the study was to throw some light on the mechanisms in the body by which omega-3 fatty acids might work to reduce inflammation or depression.”
“The research mostly involved cells in laboratory dishes, but it also involved treating a small sample of patients with major depression by giving them supplements of one or other of the two omega-3 acids under investigation for 12 weeks,” he noted.
“The researchers found that the patients’ average scores on a standard set of questions, used to diagnose and measure depression, improved over that 12-week period, for each of the two fatty acids.
While depression symptoms improved over 12 weeks with omega-3 fatty acid treatment, “depression symptoms change over time anyway, for many reasons,” and depressive symptoms might have improved over 12 weeks even if the patients had not been given the omega-3 acids, Dr. McConway said.
“We just can’t tell since every patient got omega-3 fatty acids. So these results can hint that omega-3 fatty acids might help in depression, but it comes nowhere near showing that this is the case with a reasonable degree of certainty,” he cautioned.
“Indeed the researchers did not carry out this part of their study to see whether the omega-3 supplements help with depression – they did it to see whether the biochemical changes that they had seen in cell cultures in the lab might also occur in human bodies,” he noted.
This research was funded in part by grants to the investigators from the U.K. Medical Research Council, the European Commission Horizon 2020, and the National Institute for Health Research (NIHR), Maudsley Biomedical Research Centre (BRC) at South London and Maudsley NHS Foundation Trust and King’s College London. Dr. Borsini has received research funding from Johnson & Johnson for research on depression and inflammation. Dr. McConway is a trustee of the Science Media Centre and a member of its advisory committee.
A version of this article first appeared on Medscape.com.
A key molecular mechanism underpinning the anti-inflammatory, antidepressant, and neuroprotective effects of omega-3 fatty acids has been identified. In findings that could lead to the development of new treatments for depression, the research provides the “first evidence” that hippocampal neurons are able to produce two key lipid metabolites of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) – lipoxygenase and cytochrome P450, lead investigator Alessandra Borsini, PhD, told this news organization.
This is how EPA and DHA exert their anti-inflammatory and neurogenic properties in vitro, as well as antidepressant properties in patients with depression, said Dr. Borsini, from King’s College London.
“Indeed, we found evidence for a correlation between increased levels of these metabolites and a decrease in severity of depressive symptoms in patients with major depressive disorder,” Dr. Borsini said.
The study was published online June 16 in Molecular Psychiatry.
‘Depression in a dish’
Despite the known role of inflammation in depression, there remains a lack of data showing anti-inflammatory strategies that are effective, safe for everyday use, and with a clear mechanism of action, the researchers note.
Dr. Borsini and colleagues tested the theory that when EPA and DHA are metabolized, some of their metabolites, or lipid mediators, can protect the brain from the harmful effects of inflammation. They used a validated “depression in a dish” in vitro human hippocampal cell model to test their theory.
They found that treating human hippocampal cells with EPA or DHA before exposing them to cytokines prevented increased cell death and decreased neurogenesis. Both these impacts had been previously observed in cells exposed to cytokines alone.
They confirmed that these effects were mediated by the formation of several key lipid mediators produced by EPA and DHA – namely hydroxyeicosapentaenoic acid, hydroxydocosahexaenoic acid, epoxyeicosatetraenoic acid (EpETE), and epoxydocosapentaenoic acid (EpDPA).
It’s the first time these lipid mediators were detected in human hippocampal neurons, the researchers say.
They also found that treating the neurons with an enzyme inhibitor increased the availability of two of these metabolites (EpETE and EpDPA), suggesting a possible way by which future treatments could be optimized.
The findings were replicated in 22 patients with major depression given either EPA (3 g/day) or DHA (1.4 g/day) for 12 weeks. In both groups, EPA or DHA treatment was associated with an increase in their respective metabolites and significant improvement in depressive symptoms.
The average reduction in symptom scores was 64% and 71% in the EPA and DHA groups, respectively, and there was some evidence that higher levels of the same metabolites correlated with less severe depressive symptoms.
“For some time we have known that omega-3 [polyunsaturated fatty acid (PUFA)] can induce antidepressant and anti-inflammatory effects, but, without further understanding of how this happens in the human brain, it has been difficult to develop treatments,” Dr. Borsini said in a news release.
“ which can inform the development of potential new treatments for depression using omega-3 PUFA,” Dr. Borsini added.
“We need to be cautious when interpreting data generated from the correlation between levels of metabolites and depressive symptoms as findings require further validation in a bigger sample of patients,” Dr. Borsini said.
“It is important to highlight that our research has not shown that by simply increasing omega-3 fatty acids in our diets or through taking nutritional supplements we can reduce inflammation or depression,” study author Carmine Pariante, MD, PhD, from King’s College London, said in the news release.
“The mechanisms behind the associations between depression and omega-3 PUFA are complicated and require further research and clinical trials to fully understand how they work and inform future therapeutic approaches,” Dr. Pariante said.
No clinical implications
Weighing in on this research in a Science Media Centre statement, Kevin McConway, emeritus professor of applied statistics, The Open University, Milton Keynes, United Kingdom, said, “The point of the study was to throw some light on the mechanisms in the body by which omega-3 fatty acids might work to reduce inflammation or depression.”
“The research mostly involved cells in laboratory dishes, but it also involved treating a small sample of patients with major depression by giving them supplements of one or other of the two omega-3 acids under investigation for 12 weeks,” he noted.
“The researchers found that the patients’ average scores on a standard set of questions, used to diagnose and measure depression, improved over that 12-week period, for each of the two fatty acids.
While depression symptoms improved over 12 weeks with omega-3 fatty acid treatment, “depression symptoms change over time anyway, for many reasons,” and depressive symptoms might have improved over 12 weeks even if the patients had not been given the omega-3 acids, Dr. McConway said.
“We just can’t tell since every patient got omega-3 fatty acids. So these results can hint that omega-3 fatty acids might help in depression, but it comes nowhere near showing that this is the case with a reasonable degree of certainty,” he cautioned.
“Indeed the researchers did not carry out this part of their study to see whether the omega-3 supplements help with depression – they did it to see whether the biochemical changes that they had seen in cell cultures in the lab might also occur in human bodies,” he noted.
This research was funded in part by grants to the investigators from the U.K. Medical Research Council, the European Commission Horizon 2020, and the National Institute for Health Research (NIHR), Maudsley Biomedical Research Centre (BRC) at South London and Maudsley NHS Foundation Trust and King’s College London. Dr. Borsini has received research funding from Johnson & Johnson for research on depression and inflammation. Dr. McConway is a trustee of the Science Media Centre and a member of its advisory committee.
A version of this article first appeared on Medscape.com.
Does vitamin D deficiency play a role in opioid addiction?
Vitamin D deficiency amplifies the craving for, and the effects of, opioids, potentially raising the risk for opioid dependence and addiction, new research suggests. However, some experts are urging caution in interpreting the findings.
The study, which also linked vitamin D deficiency to sun-seeking behavior, points to the potential of vitamin D supplementation to help address the opioid epidemic, the investigators note.
“Even modest rescue of vitamin D deficiency could be beneficial in the prevention and treatment of opioid addiction, especially considering that vitamin D is generally inexpensive, accessible, and safe,” they write.
The study was published online June 11 in Science Advances.
Endorphin rush
In earlier work, researchers led by David Fisher, MD, PhD, with the Massachusetts General Hospital (MGH) and Harvard Medical School, Boston, found that exposure to ultraviolet rays causes the skin to produce the hormone endorphin, which is chemically related to morphine, heroin, and other opioids.
They also observed that UV exposure raises endorphin levels in mice, which leads the animals to display behavior consistent with opioid addiction.
In their latest research, they conducted a series of animal and human studies designed to better understand the relationship between vitamin D and UV-seeking and opioid-seeking behavior.
They first compared normal laboratory mice with vitamin D–deficient mice.
“We found that modulating vitamin D levels changes multiple addictive behaviors to both UV and opioids,” lead author Lajos Kemény, MD, PhD, a postdoctoral research fellow in dermatology at MGH, said in a statement.
When the mice were conditioned with modest doses of morphine, those deficient in vitamin D continued seeking out the drug. This behavior was less common in the normal mice. When morphine was withdrawn, the vitamin D–deficient mice were far more likely to show withdrawal symptoms.
Morphine also appeared to work more effectively as a pain reliever in the vitamin D–deficient mice, suggesting that response to the opioid was exaggerated in the setting of low vitamin D.
“When we corrected vitamin D levels in the deficient mice, their opioid responses reversed and returned to normal,” Dr. Fisher said in the statement.
The animal data that suggest vitamin D deficiency increases addictive behavior was supported by several analyses using National Health and Nutrition Examination Survey data and MGH patient health records.
The results show an increase in the prevalence of vitamin D deficiency among patients diagnosed with opioid use disorder (OUD) and an inverse and dose-dependent association of vitamin D levels with self-reported opioid use.
, whereas patients who were severely vitamin D deficient were 90% more likely to use opioids, the researchers report.
“Our results imply that vitamin D–deficient individuals may be at risk for developing tolerance and physiologic opioid dependence more rapidly, experiencing more significant withdrawal and experiencing greater reward from opioid exposure,” they note.
“Vitamin D supplementation might have a preventative benefit by decreasing opioid reward and possibly diminishing the risk of OUD. Vitamin D supplementation may also improve the beneficial effects of medications for OUD,” they add.
Interpret with caution
Weighing in on this research for this news organization, Richard Saitz, MD, MPH, professor, Boston University Schools of Medicine and Public Health, urged caution in interpreting the results.
“The human studies are cross-sectional and subject to many biases and may show that opioid use and disorder are associated with vitamin D deficiency (which is not news) and does not at all show deficiency causes disorder or use,” said Dr. Saitz.
“All in all, the studies are interesting and could generate hypotheses to be tested in well-designed prospective studies of vitamin D deficiency as a risk factor and vitamin D as a treatment,” he added.
However, he cautioned that it’s “going way beyond the data” to conclude that vitamin D causes or exacerbates opioid addiction in people, “but suggesting clinical studies be done is certainly reasonable.”
Also weighing in on this research, Kenneth Stoller, MD, director of the Johns Hopkins Broadway Center for Addiction and associate professor of psychiatry and behavioral sciences at Johns Hopkins University, Baltimore, noted that “95% of patients with co-occurring disorders coming to the inpatient unit are vitamin D deficient, so it’s very common in the population.
“It’s hard to know, but I really think that it’s unlikely that vitamin D deficiency is a common pathway for development of addiction – that is, that they developed an addiction specifically because of the vitamin D deficiency,” Dr. Stoller said.
“However, it does make me think that for my patients who are experiencing maybe a partial but not a full response to medications for opioid use disorder, maybe I’ll be more likely to check the vitamin D level, and if it’s really off, try them on some supplementation,” said Dr. Stoller.
He pointed to a recent study that showed some benefit of vitamin D supplementation on cognitive function and some mental health parameters for people on methadone, “but I don’t think this is necessarily a silver bullet.”
The work was supported by a grant from the National Institutes of Health and the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation. Dr. Fisher, Dr. Saitz, and Dr. Stoller have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Vitamin D deficiency amplifies the craving for, and the effects of, opioids, potentially raising the risk for opioid dependence and addiction, new research suggests. However, some experts are urging caution in interpreting the findings.
The study, which also linked vitamin D deficiency to sun-seeking behavior, points to the potential of vitamin D supplementation to help address the opioid epidemic, the investigators note.
“Even modest rescue of vitamin D deficiency could be beneficial in the prevention and treatment of opioid addiction, especially considering that vitamin D is generally inexpensive, accessible, and safe,” they write.
The study was published online June 11 in Science Advances.
Endorphin rush
In earlier work, researchers led by David Fisher, MD, PhD, with the Massachusetts General Hospital (MGH) and Harvard Medical School, Boston, found that exposure to ultraviolet rays causes the skin to produce the hormone endorphin, which is chemically related to morphine, heroin, and other opioids.
They also observed that UV exposure raises endorphin levels in mice, which leads the animals to display behavior consistent with opioid addiction.
In their latest research, they conducted a series of animal and human studies designed to better understand the relationship between vitamin D and UV-seeking and opioid-seeking behavior.
They first compared normal laboratory mice with vitamin D–deficient mice.
“We found that modulating vitamin D levels changes multiple addictive behaviors to both UV and opioids,” lead author Lajos Kemény, MD, PhD, a postdoctoral research fellow in dermatology at MGH, said in a statement.
When the mice were conditioned with modest doses of morphine, those deficient in vitamin D continued seeking out the drug. This behavior was less common in the normal mice. When morphine was withdrawn, the vitamin D–deficient mice were far more likely to show withdrawal symptoms.
Morphine also appeared to work more effectively as a pain reliever in the vitamin D–deficient mice, suggesting that response to the opioid was exaggerated in the setting of low vitamin D.
“When we corrected vitamin D levels in the deficient mice, their opioid responses reversed and returned to normal,” Dr. Fisher said in the statement.
The animal data that suggest vitamin D deficiency increases addictive behavior was supported by several analyses using National Health and Nutrition Examination Survey data and MGH patient health records.
The results show an increase in the prevalence of vitamin D deficiency among patients diagnosed with opioid use disorder (OUD) and an inverse and dose-dependent association of vitamin D levels with self-reported opioid use.
, whereas patients who were severely vitamin D deficient were 90% more likely to use opioids, the researchers report.
“Our results imply that vitamin D–deficient individuals may be at risk for developing tolerance and physiologic opioid dependence more rapidly, experiencing more significant withdrawal and experiencing greater reward from opioid exposure,” they note.
“Vitamin D supplementation might have a preventative benefit by decreasing opioid reward and possibly diminishing the risk of OUD. Vitamin D supplementation may also improve the beneficial effects of medications for OUD,” they add.
Interpret with caution
Weighing in on this research for this news organization, Richard Saitz, MD, MPH, professor, Boston University Schools of Medicine and Public Health, urged caution in interpreting the results.
“The human studies are cross-sectional and subject to many biases and may show that opioid use and disorder are associated with vitamin D deficiency (which is not news) and does not at all show deficiency causes disorder or use,” said Dr. Saitz.
“All in all, the studies are interesting and could generate hypotheses to be tested in well-designed prospective studies of vitamin D deficiency as a risk factor and vitamin D as a treatment,” he added.
However, he cautioned that it’s “going way beyond the data” to conclude that vitamin D causes or exacerbates opioid addiction in people, “but suggesting clinical studies be done is certainly reasonable.”
Also weighing in on this research, Kenneth Stoller, MD, director of the Johns Hopkins Broadway Center for Addiction and associate professor of psychiatry and behavioral sciences at Johns Hopkins University, Baltimore, noted that “95% of patients with co-occurring disorders coming to the inpatient unit are vitamin D deficient, so it’s very common in the population.
“It’s hard to know, but I really think that it’s unlikely that vitamin D deficiency is a common pathway for development of addiction – that is, that they developed an addiction specifically because of the vitamin D deficiency,” Dr. Stoller said.
“However, it does make me think that for my patients who are experiencing maybe a partial but not a full response to medications for opioid use disorder, maybe I’ll be more likely to check the vitamin D level, and if it’s really off, try them on some supplementation,” said Dr. Stoller.
He pointed to a recent study that showed some benefit of vitamin D supplementation on cognitive function and some mental health parameters for people on methadone, “but I don’t think this is necessarily a silver bullet.”
The work was supported by a grant from the National Institutes of Health and the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation. Dr. Fisher, Dr. Saitz, and Dr. Stoller have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Vitamin D deficiency amplifies the craving for, and the effects of, opioids, potentially raising the risk for opioid dependence and addiction, new research suggests. However, some experts are urging caution in interpreting the findings.
The study, which also linked vitamin D deficiency to sun-seeking behavior, points to the potential of vitamin D supplementation to help address the opioid epidemic, the investigators note.
“Even modest rescue of vitamin D deficiency could be beneficial in the prevention and treatment of opioid addiction, especially considering that vitamin D is generally inexpensive, accessible, and safe,” they write.
The study was published online June 11 in Science Advances.
Endorphin rush
In earlier work, researchers led by David Fisher, MD, PhD, with the Massachusetts General Hospital (MGH) and Harvard Medical School, Boston, found that exposure to ultraviolet rays causes the skin to produce the hormone endorphin, which is chemically related to morphine, heroin, and other opioids.
They also observed that UV exposure raises endorphin levels in mice, which leads the animals to display behavior consistent with opioid addiction.
In their latest research, they conducted a series of animal and human studies designed to better understand the relationship between vitamin D and UV-seeking and opioid-seeking behavior.
They first compared normal laboratory mice with vitamin D–deficient mice.
“We found that modulating vitamin D levels changes multiple addictive behaviors to both UV and opioids,” lead author Lajos Kemény, MD, PhD, a postdoctoral research fellow in dermatology at MGH, said in a statement.
When the mice were conditioned with modest doses of morphine, those deficient in vitamin D continued seeking out the drug. This behavior was less common in the normal mice. When morphine was withdrawn, the vitamin D–deficient mice were far more likely to show withdrawal symptoms.
Morphine also appeared to work more effectively as a pain reliever in the vitamin D–deficient mice, suggesting that response to the opioid was exaggerated in the setting of low vitamin D.
“When we corrected vitamin D levels in the deficient mice, their opioid responses reversed and returned to normal,” Dr. Fisher said in the statement.
The animal data that suggest vitamin D deficiency increases addictive behavior was supported by several analyses using National Health and Nutrition Examination Survey data and MGH patient health records.
The results show an increase in the prevalence of vitamin D deficiency among patients diagnosed with opioid use disorder (OUD) and an inverse and dose-dependent association of vitamin D levels with self-reported opioid use.
, whereas patients who were severely vitamin D deficient were 90% more likely to use opioids, the researchers report.
“Our results imply that vitamin D–deficient individuals may be at risk for developing tolerance and physiologic opioid dependence more rapidly, experiencing more significant withdrawal and experiencing greater reward from opioid exposure,” they note.
“Vitamin D supplementation might have a preventative benefit by decreasing opioid reward and possibly diminishing the risk of OUD. Vitamin D supplementation may also improve the beneficial effects of medications for OUD,” they add.
Interpret with caution
Weighing in on this research for this news organization, Richard Saitz, MD, MPH, professor, Boston University Schools of Medicine and Public Health, urged caution in interpreting the results.
“The human studies are cross-sectional and subject to many biases and may show that opioid use and disorder are associated with vitamin D deficiency (which is not news) and does not at all show deficiency causes disorder or use,” said Dr. Saitz.
“All in all, the studies are interesting and could generate hypotheses to be tested in well-designed prospective studies of vitamin D deficiency as a risk factor and vitamin D as a treatment,” he added.
However, he cautioned that it’s “going way beyond the data” to conclude that vitamin D causes or exacerbates opioid addiction in people, “but suggesting clinical studies be done is certainly reasonable.”
Also weighing in on this research, Kenneth Stoller, MD, director of the Johns Hopkins Broadway Center for Addiction and associate professor of psychiatry and behavioral sciences at Johns Hopkins University, Baltimore, noted that “95% of patients with co-occurring disorders coming to the inpatient unit are vitamin D deficient, so it’s very common in the population.
“It’s hard to know, but I really think that it’s unlikely that vitamin D deficiency is a common pathway for development of addiction – that is, that they developed an addiction specifically because of the vitamin D deficiency,” Dr. Stoller said.
“However, it does make me think that for my patients who are experiencing maybe a partial but not a full response to medications for opioid use disorder, maybe I’ll be more likely to check the vitamin D level, and if it’s really off, try them on some supplementation,” said Dr. Stoller.
He pointed to a recent study that showed some benefit of vitamin D supplementation on cognitive function and some mental health parameters for people on methadone, “but I don’t think this is necessarily a silver bullet.”
The work was supported by a grant from the National Institutes of Health and the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation. Dr. Fisher, Dr. Saitz, and Dr. Stoller have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Treating sleep apnea lowers MI and stroke risk
particularly for patients with moderate to severe OSA and those who are more adherent to CPAP therapy, a new study suggests.
“Most clinical trials on the effect of CPAP on CV diseases to date have focused on secondary CV prevention. This study contributes another piece of evidence about the role of CPAP therapy to prevent CV diseases,” said Diego R. Mazzotti, PhD, an assistant professor at the University of Kansas Medical Center, Kansas City.
“Our study, while observational, suggests that clinical trials focused on understanding how to sustain long-term CPAP adherence in obstructive sleep apnea patients are necessary and could be critical for optimizing comorbidity risk reduction,” Dr. Mazzotti said.
The study was presented at the virtual annual meeting of the Associated Professional Sleep Societies.
Good adherence important
The researchers analyzed the electronic health records of adults referred for a sleep study through the Kaiser Permanente Southern California health system. The sample included 11,145 adults without OSA, 13,898 with OSA who used CPAP, and 20,884 adults with OSA who did not use CPAP. None of them had CV disease at baseline. Median follow-up was 262 days.
The primary outcome was first occurrence of myocardial infarction, stroke, unstable angina, heart failure, or death caused by CV disease.
In adjusted models, adults with moderate to severe OSA (apnea-hypopnea index ≥15) who did not use CPAP were 71% more likely than those without OSA to have a first CV event (hazard ratio, 1.71; 95% CI, 1.11-2.64). However, the risk for a CV event during follow-up was 32% lower among OSA patients with any CPAP use (HR, 0.68; 95% CI, 0.50-0.93; P = .016).
The effect was mostly driven by those who used CPAP for at least 4 hours per night (HR, 0.60; 95% CI, 0.39-0.95). This association was stronger for those with moderate to severe OSA (HR, 0.56; 95% CI, 0.39-0.81).
“This study highlights the importance of long-term management of CPAP therapy in patients with moderate-severe OSA,” Dr. Mazzotti said in an interview.
“It suggests that maintaining good CPAP adherence might be beneficial for cardiovascular health, besides the already established benefits on quality of life, sleepiness, and other cardiometabolic functions,” he said.
Dr. Mazzotti said several mechanisms might explain the association between CPAP use and lower risk for CV events. “CPAP treats OSA by preventing respiratory pauses that occur during sleep, therefore preventing arousals, sleep fragmentation, and decreases in blood oxygen. These improved cardiorespiratory functions can be beneficial to avoid certain molecular changes that are known to contribute to cardiovascular risk, such as oxidative stress and inflammation,” he explained.
“However, specific studies fully understanding these mechanisms are necessary,” Dr. Mazzotti added.
In a comment, Nitun Verma, MD, a spokesperson for the American Academy of Sleep Medicine, said that “the frequent decreases in oxygen levels and fragmented sleep from apnea are associated with cardiovascular disorders. We know this from multiple studies. This, however, was a large study and strengthens the association between improving apnea and reduced serious cardiovascular events.”
Funding for the study was provided by the American Academy of Sleep Medicine Foundation and the American Heart Association. Dr. Mazzotti and Dr. Verma disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
particularly for patients with moderate to severe OSA and those who are more adherent to CPAP therapy, a new study suggests.
“Most clinical trials on the effect of CPAP on CV diseases to date have focused on secondary CV prevention. This study contributes another piece of evidence about the role of CPAP therapy to prevent CV diseases,” said Diego R. Mazzotti, PhD, an assistant professor at the University of Kansas Medical Center, Kansas City.
“Our study, while observational, suggests that clinical trials focused on understanding how to sustain long-term CPAP adherence in obstructive sleep apnea patients are necessary and could be critical for optimizing comorbidity risk reduction,” Dr. Mazzotti said.
The study was presented at the virtual annual meeting of the Associated Professional Sleep Societies.
Good adherence important
The researchers analyzed the electronic health records of adults referred for a sleep study through the Kaiser Permanente Southern California health system. The sample included 11,145 adults without OSA, 13,898 with OSA who used CPAP, and 20,884 adults with OSA who did not use CPAP. None of them had CV disease at baseline. Median follow-up was 262 days.
The primary outcome was first occurrence of myocardial infarction, stroke, unstable angina, heart failure, or death caused by CV disease.
In adjusted models, adults with moderate to severe OSA (apnea-hypopnea index ≥15) who did not use CPAP were 71% more likely than those without OSA to have a first CV event (hazard ratio, 1.71; 95% CI, 1.11-2.64). However, the risk for a CV event during follow-up was 32% lower among OSA patients with any CPAP use (HR, 0.68; 95% CI, 0.50-0.93; P = .016).
The effect was mostly driven by those who used CPAP for at least 4 hours per night (HR, 0.60; 95% CI, 0.39-0.95). This association was stronger for those with moderate to severe OSA (HR, 0.56; 95% CI, 0.39-0.81).
“This study highlights the importance of long-term management of CPAP therapy in patients with moderate-severe OSA,” Dr. Mazzotti said in an interview.
“It suggests that maintaining good CPAP adherence might be beneficial for cardiovascular health, besides the already established benefits on quality of life, sleepiness, and other cardiometabolic functions,” he said.
Dr. Mazzotti said several mechanisms might explain the association between CPAP use and lower risk for CV events. “CPAP treats OSA by preventing respiratory pauses that occur during sleep, therefore preventing arousals, sleep fragmentation, and decreases in blood oxygen. These improved cardiorespiratory functions can be beneficial to avoid certain molecular changes that are known to contribute to cardiovascular risk, such as oxidative stress and inflammation,” he explained.
“However, specific studies fully understanding these mechanisms are necessary,” Dr. Mazzotti added.
In a comment, Nitun Verma, MD, a spokesperson for the American Academy of Sleep Medicine, said that “the frequent decreases in oxygen levels and fragmented sleep from apnea are associated with cardiovascular disorders. We know this from multiple studies. This, however, was a large study and strengthens the association between improving apnea and reduced serious cardiovascular events.”
Funding for the study was provided by the American Academy of Sleep Medicine Foundation and the American Heart Association. Dr. Mazzotti and Dr. Verma disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
particularly for patients with moderate to severe OSA and those who are more adherent to CPAP therapy, a new study suggests.
“Most clinical trials on the effect of CPAP on CV diseases to date have focused on secondary CV prevention. This study contributes another piece of evidence about the role of CPAP therapy to prevent CV diseases,” said Diego R. Mazzotti, PhD, an assistant professor at the University of Kansas Medical Center, Kansas City.
“Our study, while observational, suggests that clinical trials focused on understanding how to sustain long-term CPAP adherence in obstructive sleep apnea patients are necessary and could be critical for optimizing comorbidity risk reduction,” Dr. Mazzotti said.
The study was presented at the virtual annual meeting of the Associated Professional Sleep Societies.
Good adherence important
The researchers analyzed the electronic health records of adults referred for a sleep study through the Kaiser Permanente Southern California health system. The sample included 11,145 adults without OSA, 13,898 with OSA who used CPAP, and 20,884 adults with OSA who did not use CPAP. None of them had CV disease at baseline. Median follow-up was 262 days.
The primary outcome was first occurrence of myocardial infarction, stroke, unstable angina, heart failure, or death caused by CV disease.
In adjusted models, adults with moderate to severe OSA (apnea-hypopnea index ≥15) who did not use CPAP were 71% more likely than those without OSA to have a first CV event (hazard ratio, 1.71; 95% CI, 1.11-2.64). However, the risk for a CV event during follow-up was 32% lower among OSA patients with any CPAP use (HR, 0.68; 95% CI, 0.50-0.93; P = .016).
The effect was mostly driven by those who used CPAP for at least 4 hours per night (HR, 0.60; 95% CI, 0.39-0.95). This association was stronger for those with moderate to severe OSA (HR, 0.56; 95% CI, 0.39-0.81).
“This study highlights the importance of long-term management of CPAP therapy in patients with moderate-severe OSA,” Dr. Mazzotti said in an interview.
“It suggests that maintaining good CPAP adherence might be beneficial for cardiovascular health, besides the already established benefits on quality of life, sleepiness, and other cardiometabolic functions,” he said.
Dr. Mazzotti said several mechanisms might explain the association between CPAP use and lower risk for CV events. “CPAP treats OSA by preventing respiratory pauses that occur during sleep, therefore preventing arousals, sleep fragmentation, and decreases in blood oxygen. These improved cardiorespiratory functions can be beneficial to avoid certain molecular changes that are known to contribute to cardiovascular risk, such as oxidative stress and inflammation,” he explained.
“However, specific studies fully understanding these mechanisms are necessary,” Dr. Mazzotti added.
In a comment, Nitun Verma, MD, a spokesperson for the American Academy of Sleep Medicine, said that “the frequent decreases in oxygen levels and fragmented sleep from apnea are associated with cardiovascular disorders. We know this from multiple studies. This, however, was a large study and strengthens the association between improving apnea and reduced serious cardiovascular events.”
Funding for the study was provided by the American Academy of Sleep Medicine Foundation and the American Heart Association. Dr. Mazzotti and Dr. Verma disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM SLEEP 2021
Potential first-in-class, targeted therapy for myasthenia gravis
(gMG), new research suggests. Results from the phase 3, randomized, placebo-controlled ADAPT trial showed that reduction in disease burden and improvement in strength and quality of life in patients with gMG were consistent across four MG-specific scales for those receiving the novel treatment. In addition, these benefits were observed early and were reproducible and durable, the researchers noted.
Efgartigimod is a “very rapidly acting drug relative to other treatments that may take 4, 6, sometimes 10 months before they start to work, and the side effect profile is much like placebo,” said principal investigator James Howard, Jr., MD, Distinguished Professor of Neuromuscular Disease, department of neurology, University of North Carolina at Chapel Hill.
The ADAPT results are “important for the MG community, and I am hopeful efgartigimod will provide a first-in-class targeted therapy that can be dosed in an individual way for people living with this chronic autoimmune disease,” Dr. Howard added in a news release.
The findings were published online June 17 in Lancet Neurology.
Targeted molecular therapy
The rare and chronic autoimmune neuromuscular disorder of gMG causes debilitating and potentially life-threatening muscle weakness and significantly impaired independence and quality of life. Most patients with gMG have immunoglobulin G (IgG) antibodies, which are most often directed against skeletal muscle nicotinic acetylcholine receptors.
Efgartigimod is an investigational antibody fragment designed to reduce pathogenic IgG antibodies and block the IgG recycling process in patients with gMG.
The novel agent binds to the neonatal Fc receptor (FcRn), which is widely expressed throughout the body and plays a central role in rescuing IgG antibodies from degradation. Blocking FcRn reduces IgG antibody levels.
The ADAPT trial was conducted at 56 neuromuscular academic and community centers in 15 countries in North America, Europe, and Japan. The study included 167 adults with gMG, regardless of acetylcholine receptor antibody status. All had a Myasthenia Gravis Activities of Daily Living (MG-ADL) score of at least 5 (greater than 50% non-ocular) on a background of a stable dose of at least one MG drug.
For 26 weeks, 84 patients were randomly assigned to receive efgartigimod 10 mg/kg and 83 to receive matching placebo. Both treatments were administered as four infusions per cycle at one infusion per week. The process was repeated as needed depending on clinical response no sooner than 8 weeks after initiation of the previous cycle.
ADAPT was designed to allow an individualized treatment approach with an initial treatment cycle followed by a variable number of subsequent treatment cycles, the investigators noted.
Primary endpoint met
The primary efficacy endpoint was number of acetylcholine receptor antibody-positive (AChR-Ab+) patients who achieved a clinically meaningful response on the MG-ADL score. This was defined as at least a 2-point improvement from baseline for 4 or more consecutive weeks. Forty-four (68%) of 65 AChR-Ab+ patients treated with efgartigimod met this endpoint versus 19 (30%) of 64 patients treated with placebo (odds ratio, 4.95; 95% confidence interval, 2.21-11.53; P < .0001).
Many of the patients treated with efgartigimod showed improvement “beyond the clinically meaningful threshold, achieving up to 9-point reductions in MG-ADL,” the investigators reported. In addition, 40% of the efgartigimod group attained an MG-ADL score of 0 or 1 (minimal symptom expression) in cycle 1 versus 11% of the placebo group (P < .0001).
Nearly two-thirds (63%) of AChR-Ab+ patients responded to the first cycle of efgartigimod, and most of these patients (83%) responded to treatment within the first 2 weeks. Among the AChR-Ab+ participants who responded to efgartigimod in cycle 1, the duration of responder status was 6 to 7 weeks in 32% of patients, 8 to 11 weeks in 23% of patients, and 12 weeks or more in 34% of patients.
Safety profile
“Some patients never required retreatment over the 26-week period that they were under observation,” Dr. Howard said. “Patients want to be individuals. They don’t want to be assigned to a regimented therapy, and I think these results show that this therapy can be tailored to the individual patient, rather than simply giving it to them in a cookbook fashion,” he added.
The safety profile of efgartigimod was comparable to placebo. Most adverse events were mild or moderate in severity. The most commonly reported adverse events were headache, nasopharyngitis, nausea, diarrhea, upper respiratory tract infection, and urinary tract infection.
Four (5%) efgartigimod-treated patients had a serious adverse event, which included thrombocytosis, rectal adenocarcinoma, worsening MG, and depression.
The novel agent is currently under review with the U.S. Food and Drug Administration for the treatment of gMG, with a Prescription Drug User Fee Act target action date of Dec. 17. If approved, it would become the first FDA-approved FcRn antagonist.
Expanding therapeutic landscape
In a linked commentary, Shigeaki Suzuki, MD, PhD, department of neurology, Keio University School of Medicine, Tokyo, noted that the therapeutic landscape for patients with MG is “expanding year by year,” with several additional complement inhibitors and FcRn antagonists now in phase 3 testing.
“Biological drugs should be preferentially used as the treatment for patients with refractory myasthenia gravis, although the definition of refractory myasthenia gravis is different depending on the criteria used,” Dr. Suzuki wrote.
He noted that when “cost-effectiveness is not taken into account, targeted molecular therapy might be used widely” in patients with MG.
“Risks of myasthenic exacerbation and crises should be substantially decreased, particularly in patients with refractory myasthenia gravis,” Dr. Suzuki added.
The ADAPT study was supported by argenx. Dr. Howard has reported receiving research support from argenx, Alexion Pharmaceuticals, the Centers for Disease Control and Prevention, the Muscular Dystrophy Association, the National Institutes of Health, Patient-Centered Outcomes Research Institute, and Ra Pharmaceuticals; honoraria from argenx, Alexion, Immunovant, Ra, Regeneron Pharmaceuticals, and Viela Bio; and nonfinancial support from argenx, Alexion, Ra, and Toleranzia. Disclosures for the other investigators are listed in the original article. Dr. Suzuki has reported relationships with Alexion Pharmaceuticals, Japan Blood Products Organization, and Asahi Kasei Medical.
A version of this article first appeared on Medscape.com.
(gMG), new research suggests. Results from the phase 3, randomized, placebo-controlled ADAPT trial showed that reduction in disease burden and improvement in strength and quality of life in patients with gMG were consistent across four MG-specific scales for those receiving the novel treatment. In addition, these benefits were observed early and were reproducible and durable, the researchers noted.
Efgartigimod is a “very rapidly acting drug relative to other treatments that may take 4, 6, sometimes 10 months before they start to work, and the side effect profile is much like placebo,” said principal investigator James Howard, Jr., MD, Distinguished Professor of Neuromuscular Disease, department of neurology, University of North Carolina at Chapel Hill.
The ADAPT results are “important for the MG community, and I am hopeful efgartigimod will provide a first-in-class targeted therapy that can be dosed in an individual way for people living with this chronic autoimmune disease,” Dr. Howard added in a news release.
The findings were published online June 17 in Lancet Neurology.
Targeted molecular therapy
The rare and chronic autoimmune neuromuscular disorder of gMG causes debilitating and potentially life-threatening muscle weakness and significantly impaired independence and quality of life. Most patients with gMG have immunoglobulin G (IgG) antibodies, which are most often directed against skeletal muscle nicotinic acetylcholine receptors.
Efgartigimod is an investigational antibody fragment designed to reduce pathogenic IgG antibodies and block the IgG recycling process in patients with gMG.
The novel agent binds to the neonatal Fc receptor (FcRn), which is widely expressed throughout the body and plays a central role in rescuing IgG antibodies from degradation. Blocking FcRn reduces IgG antibody levels.
The ADAPT trial was conducted at 56 neuromuscular academic and community centers in 15 countries in North America, Europe, and Japan. The study included 167 adults with gMG, regardless of acetylcholine receptor antibody status. All had a Myasthenia Gravis Activities of Daily Living (MG-ADL) score of at least 5 (greater than 50% non-ocular) on a background of a stable dose of at least one MG drug.
For 26 weeks, 84 patients were randomly assigned to receive efgartigimod 10 mg/kg and 83 to receive matching placebo. Both treatments were administered as four infusions per cycle at one infusion per week. The process was repeated as needed depending on clinical response no sooner than 8 weeks after initiation of the previous cycle.
ADAPT was designed to allow an individualized treatment approach with an initial treatment cycle followed by a variable number of subsequent treatment cycles, the investigators noted.
Primary endpoint met
The primary efficacy endpoint was number of acetylcholine receptor antibody-positive (AChR-Ab+) patients who achieved a clinically meaningful response on the MG-ADL score. This was defined as at least a 2-point improvement from baseline for 4 or more consecutive weeks. Forty-four (68%) of 65 AChR-Ab+ patients treated with efgartigimod met this endpoint versus 19 (30%) of 64 patients treated with placebo (odds ratio, 4.95; 95% confidence interval, 2.21-11.53; P < .0001).
Many of the patients treated with efgartigimod showed improvement “beyond the clinically meaningful threshold, achieving up to 9-point reductions in MG-ADL,” the investigators reported. In addition, 40% of the efgartigimod group attained an MG-ADL score of 0 or 1 (minimal symptom expression) in cycle 1 versus 11% of the placebo group (P < .0001).
Nearly two-thirds (63%) of AChR-Ab+ patients responded to the first cycle of efgartigimod, and most of these patients (83%) responded to treatment within the first 2 weeks. Among the AChR-Ab+ participants who responded to efgartigimod in cycle 1, the duration of responder status was 6 to 7 weeks in 32% of patients, 8 to 11 weeks in 23% of patients, and 12 weeks or more in 34% of patients.
Safety profile
“Some patients never required retreatment over the 26-week period that they were under observation,” Dr. Howard said. “Patients want to be individuals. They don’t want to be assigned to a regimented therapy, and I think these results show that this therapy can be tailored to the individual patient, rather than simply giving it to them in a cookbook fashion,” he added.
The safety profile of efgartigimod was comparable to placebo. Most adverse events were mild or moderate in severity. The most commonly reported adverse events were headache, nasopharyngitis, nausea, diarrhea, upper respiratory tract infection, and urinary tract infection.
Four (5%) efgartigimod-treated patients had a serious adverse event, which included thrombocytosis, rectal adenocarcinoma, worsening MG, and depression.
The novel agent is currently under review with the U.S. Food and Drug Administration for the treatment of gMG, with a Prescription Drug User Fee Act target action date of Dec. 17. If approved, it would become the first FDA-approved FcRn antagonist.
Expanding therapeutic landscape
In a linked commentary, Shigeaki Suzuki, MD, PhD, department of neurology, Keio University School of Medicine, Tokyo, noted that the therapeutic landscape for patients with MG is “expanding year by year,” with several additional complement inhibitors and FcRn antagonists now in phase 3 testing.
“Biological drugs should be preferentially used as the treatment for patients with refractory myasthenia gravis, although the definition of refractory myasthenia gravis is different depending on the criteria used,” Dr. Suzuki wrote.
He noted that when “cost-effectiveness is not taken into account, targeted molecular therapy might be used widely” in patients with MG.
“Risks of myasthenic exacerbation and crises should be substantially decreased, particularly in patients with refractory myasthenia gravis,” Dr. Suzuki added.
The ADAPT study was supported by argenx. Dr. Howard has reported receiving research support from argenx, Alexion Pharmaceuticals, the Centers for Disease Control and Prevention, the Muscular Dystrophy Association, the National Institutes of Health, Patient-Centered Outcomes Research Institute, and Ra Pharmaceuticals; honoraria from argenx, Alexion, Immunovant, Ra, Regeneron Pharmaceuticals, and Viela Bio; and nonfinancial support from argenx, Alexion, Ra, and Toleranzia. Disclosures for the other investigators are listed in the original article. Dr. Suzuki has reported relationships with Alexion Pharmaceuticals, Japan Blood Products Organization, and Asahi Kasei Medical.
A version of this article first appeared on Medscape.com.
(gMG), new research suggests. Results from the phase 3, randomized, placebo-controlled ADAPT trial showed that reduction in disease burden and improvement in strength and quality of life in patients with gMG were consistent across four MG-specific scales for those receiving the novel treatment. In addition, these benefits were observed early and were reproducible and durable, the researchers noted.
Efgartigimod is a “very rapidly acting drug relative to other treatments that may take 4, 6, sometimes 10 months before they start to work, and the side effect profile is much like placebo,” said principal investigator James Howard, Jr., MD, Distinguished Professor of Neuromuscular Disease, department of neurology, University of North Carolina at Chapel Hill.
The ADAPT results are “important for the MG community, and I am hopeful efgartigimod will provide a first-in-class targeted therapy that can be dosed in an individual way for people living with this chronic autoimmune disease,” Dr. Howard added in a news release.
The findings were published online June 17 in Lancet Neurology.
Targeted molecular therapy
The rare and chronic autoimmune neuromuscular disorder of gMG causes debilitating and potentially life-threatening muscle weakness and significantly impaired independence and quality of life. Most patients with gMG have immunoglobulin G (IgG) antibodies, which are most often directed against skeletal muscle nicotinic acetylcholine receptors.
Efgartigimod is an investigational antibody fragment designed to reduce pathogenic IgG antibodies and block the IgG recycling process in patients with gMG.
The novel agent binds to the neonatal Fc receptor (FcRn), which is widely expressed throughout the body and plays a central role in rescuing IgG antibodies from degradation. Blocking FcRn reduces IgG antibody levels.
The ADAPT trial was conducted at 56 neuromuscular academic and community centers in 15 countries in North America, Europe, and Japan. The study included 167 adults with gMG, regardless of acetylcholine receptor antibody status. All had a Myasthenia Gravis Activities of Daily Living (MG-ADL) score of at least 5 (greater than 50% non-ocular) on a background of a stable dose of at least one MG drug.
For 26 weeks, 84 patients were randomly assigned to receive efgartigimod 10 mg/kg and 83 to receive matching placebo. Both treatments were administered as four infusions per cycle at one infusion per week. The process was repeated as needed depending on clinical response no sooner than 8 weeks after initiation of the previous cycle.
ADAPT was designed to allow an individualized treatment approach with an initial treatment cycle followed by a variable number of subsequent treatment cycles, the investigators noted.
Primary endpoint met
The primary efficacy endpoint was number of acetylcholine receptor antibody-positive (AChR-Ab+) patients who achieved a clinically meaningful response on the MG-ADL score. This was defined as at least a 2-point improvement from baseline for 4 or more consecutive weeks. Forty-four (68%) of 65 AChR-Ab+ patients treated with efgartigimod met this endpoint versus 19 (30%) of 64 patients treated with placebo (odds ratio, 4.95; 95% confidence interval, 2.21-11.53; P < .0001).
Many of the patients treated with efgartigimod showed improvement “beyond the clinically meaningful threshold, achieving up to 9-point reductions in MG-ADL,” the investigators reported. In addition, 40% of the efgartigimod group attained an MG-ADL score of 0 or 1 (minimal symptom expression) in cycle 1 versus 11% of the placebo group (P < .0001).
Nearly two-thirds (63%) of AChR-Ab+ patients responded to the first cycle of efgartigimod, and most of these patients (83%) responded to treatment within the first 2 weeks. Among the AChR-Ab+ participants who responded to efgartigimod in cycle 1, the duration of responder status was 6 to 7 weeks in 32% of patients, 8 to 11 weeks in 23% of patients, and 12 weeks or more in 34% of patients.
Safety profile
“Some patients never required retreatment over the 26-week period that they were under observation,” Dr. Howard said. “Patients want to be individuals. They don’t want to be assigned to a regimented therapy, and I think these results show that this therapy can be tailored to the individual patient, rather than simply giving it to them in a cookbook fashion,” he added.
The safety profile of efgartigimod was comparable to placebo. Most adverse events were mild or moderate in severity. The most commonly reported adverse events were headache, nasopharyngitis, nausea, diarrhea, upper respiratory tract infection, and urinary tract infection.
Four (5%) efgartigimod-treated patients had a serious adverse event, which included thrombocytosis, rectal adenocarcinoma, worsening MG, and depression.
The novel agent is currently under review with the U.S. Food and Drug Administration for the treatment of gMG, with a Prescription Drug User Fee Act target action date of Dec. 17. If approved, it would become the first FDA-approved FcRn antagonist.
Expanding therapeutic landscape
In a linked commentary, Shigeaki Suzuki, MD, PhD, department of neurology, Keio University School of Medicine, Tokyo, noted that the therapeutic landscape for patients with MG is “expanding year by year,” with several additional complement inhibitors and FcRn antagonists now in phase 3 testing.
“Biological drugs should be preferentially used as the treatment for patients with refractory myasthenia gravis, although the definition of refractory myasthenia gravis is different depending on the criteria used,” Dr. Suzuki wrote.
He noted that when “cost-effectiveness is not taken into account, targeted molecular therapy might be used widely” in patients with MG.
“Risks of myasthenic exacerbation and crises should be substantially decreased, particularly in patients with refractory myasthenia gravis,” Dr. Suzuki added.
The ADAPT study was supported by argenx. Dr. Howard has reported receiving research support from argenx, Alexion Pharmaceuticals, the Centers for Disease Control and Prevention, the Muscular Dystrophy Association, the National Institutes of Health, Patient-Centered Outcomes Research Institute, and Ra Pharmaceuticals; honoraria from argenx, Alexion, Immunovant, Ra, Regeneron Pharmaceuticals, and Viela Bio; and nonfinancial support from argenx, Alexion, Ra, and Toleranzia. Disclosures for the other investigators are listed in the original article. Dr. Suzuki has reported relationships with Alexion Pharmaceuticals, Japan Blood Products Organization, and Asahi Kasei Medical.
A version of this article first appeared on Medscape.com.
From Lancet Neurology
Is trouble falling asleep a modifiable risk factor for dementia?
, new research suggests.
Trouble falling asleep “may be a modifiable risk factor for later-life cognitive impairment and dementia,” said lead author Afsara Zaheed, a PhD candidate in clinical science, department of psychology, University of Michigan, Ann Arbor.
“Patients should also be aware of the importance of insomnia on cognitive functioning so that they can bring up these concerns with their providers early,” she said.
The findings were presented at Virtual SLEEP 2021, the 35th Annual Meeting of the Associated Professional Sleep Societies.
Poor sleep common with age
As many as one-half of older adults report having poor sleep quality and insomnia, and growing evidence suggests that insomnia may be a unique risk factor for cognitive decline in later life, Ms. Zaheed explained.
To investigate further, the researchers analyzed data on 2,496 adults aged 51 years and older who were participants in the Health and Retirement Study, a longitudinal study of aging in a nationally representative population of older adults.
In 2002, participants were asked how often they had trouble falling asleep, woke up during the night, woke up too early, and were not able to fall asleep again and how often they felt really rested when they woke up in the morning.
In 2016, participants’ cognition was assessed using a battery of neuropsychological tests that gauged episodic memory, executive function, language, visuospatial/construction, and processing speed.
Analyses controlled for sociodemographics, baseline global cognitive performance, and the influence of depressive symptoms and vascular disease.
Compared with other insomnia symptoms, having difficulty falling asleep in 2002 was the main insomnia symptom that was predictive of cognitive impairment 14 years later, in 2016.
More frequent trouble falling asleep was predictive of poorer episodic memory, executive function, language, processing speed, and visuospatial performance.
The associations between sleep initiation and later cognitive impairment were partially explained by depressive symptoms and vascular disease burden for all domains except episodic memory, which was only partially explained by depressive symptoms.
Unclear mechanism
Ms. Zaheed said research is needed to uncover neurophysiologic mechanisms underlying the observed associations. “It may be that chronic difficulty with falling asleep is associated with inflammatory or metabolic processes that negatively affect brain structure and function over time,” she said.
“Insomnia has also been linked with higher accumulation of protein aggregates in the brain that disrupt cell communication and are characteristic of late-life disorders such as Alzheimer’s disease,” she added.
“While our project did not directly investigate these potential causal pathways between insomnia and cognition, our results suggest that investigating these potential mechanisms is an important area for future research,” Ms. Zaheed said.
“While additional intervention research is needed to determine whether targeting insomnia in older patients can have lasting cognitive benefits, results from this study suggest that discussing insomnia symptoms at the primary care level may be beneficial for both doctors and patients,” she added.
“By targeting insomnia – for example, through an evidence-based cognitive–behavioral therapy approach – individuals may improve various mental and physical health outcomes in addition to improving their sleep quality,” Ms. Zaheed said.
Reached for comment, Shaheen E. Lakhan, MD, PhD, neurologist in Newton, Massachusetts, said, “There is a strong link between chronic sleep disturbances and cognitive impairment, including dementia.”
“This study further supports this link and specifically calls out initiating sleep (as opposed to staying asleep) as the culprit. It also raises the hypothesis that the link is primarily mediated by depression and vascular disease; however, the verdict is still out,” said Dr. Lakhan.
The study was funded by the National Institute on Aging. Ms. Zaheed and Dr. Lakhan have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, new research suggests.
Trouble falling asleep “may be a modifiable risk factor for later-life cognitive impairment and dementia,” said lead author Afsara Zaheed, a PhD candidate in clinical science, department of psychology, University of Michigan, Ann Arbor.
“Patients should also be aware of the importance of insomnia on cognitive functioning so that they can bring up these concerns with their providers early,” she said.
The findings were presented at Virtual SLEEP 2021, the 35th Annual Meeting of the Associated Professional Sleep Societies.
Poor sleep common with age
As many as one-half of older adults report having poor sleep quality and insomnia, and growing evidence suggests that insomnia may be a unique risk factor for cognitive decline in later life, Ms. Zaheed explained.
To investigate further, the researchers analyzed data on 2,496 adults aged 51 years and older who were participants in the Health and Retirement Study, a longitudinal study of aging in a nationally representative population of older adults.
In 2002, participants were asked how often they had trouble falling asleep, woke up during the night, woke up too early, and were not able to fall asleep again and how often they felt really rested when they woke up in the morning.
In 2016, participants’ cognition was assessed using a battery of neuropsychological tests that gauged episodic memory, executive function, language, visuospatial/construction, and processing speed.
Analyses controlled for sociodemographics, baseline global cognitive performance, and the influence of depressive symptoms and vascular disease.
Compared with other insomnia symptoms, having difficulty falling asleep in 2002 was the main insomnia symptom that was predictive of cognitive impairment 14 years later, in 2016.
More frequent trouble falling asleep was predictive of poorer episodic memory, executive function, language, processing speed, and visuospatial performance.
The associations between sleep initiation and later cognitive impairment were partially explained by depressive symptoms and vascular disease burden for all domains except episodic memory, which was only partially explained by depressive symptoms.
Unclear mechanism
Ms. Zaheed said research is needed to uncover neurophysiologic mechanisms underlying the observed associations. “It may be that chronic difficulty with falling asleep is associated with inflammatory or metabolic processes that negatively affect brain structure and function over time,” she said.
“Insomnia has also been linked with higher accumulation of protein aggregates in the brain that disrupt cell communication and are characteristic of late-life disorders such as Alzheimer’s disease,” she added.
“While our project did not directly investigate these potential causal pathways between insomnia and cognition, our results suggest that investigating these potential mechanisms is an important area for future research,” Ms. Zaheed said.
“While additional intervention research is needed to determine whether targeting insomnia in older patients can have lasting cognitive benefits, results from this study suggest that discussing insomnia symptoms at the primary care level may be beneficial for both doctors and patients,” she added.
“By targeting insomnia – for example, through an evidence-based cognitive–behavioral therapy approach – individuals may improve various mental and physical health outcomes in addition to improving their sleep quality,” Ms. Zaheed said.
Reached for comment, Shaheen E. Lakhan, MD, PhD, neurologist in Newton, Massachusetts, said, “There is a strong link between chronic sleep disturbances and cognitive impairment, including dementia.”
“This study further supports this link and specifically calls out initiating sleep (as opposed to staying asleep) as the culprit. It also raises the hypothesis that the link is primarily mediated by depression and vascular disease; however, the verdict is still out,” said Dr. Lakhan.
The study was funded by the National Institute on Aging. Ms. Zaheed and Dr. Lakhan have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, new research suggests.
Trouble falling asleep “may be a modifiable risk factor for later-life cognitive impairment and dementia,” said lead author Afsara Zaheed, a PhD candidate in clinical science, department of psychology, University of Michigan, Ann Arbor.
“Patients should also be aware of the importance of insomnia on cognitive functioning so that they can bring up these concerns with their providers early,” she said.
The findings were presented at Virtual SLEEP 2021, the 35th Annual Meeting of the Associated Professional Sleep Societies.
Poor sleep common with age
As many as one-half of older adults report having poor sleep quality and insomnia, and growing evidence suggests that insomnia may be a unique risk factor for cognitive decline in later life, Ms. Zaheed explained.
To investigate further, the researchers analyzed data on 2,496 adults aged 51 years and older who were participants in the Health and Retirement Study, a longitudinal study of aging in a nationally representative population of older adults.
In 2002, participants were asked how often they had trouble falling asleep, woke up during the night, woke up too early, and were not able to fall asleep again and how often they felt really rested when they woke up in the morning.
In 2016, participants’ cognition was assessed using a battery of neuropsychological tests that gauged episodic memory, executive function, language, visuospatial/construction, and processing speed.
Analyses controlled for sociodemographics, baseline global cognitive performance, and the influence of depressive symptoms and vascular disease.
Compared with other insomnia symptoms, having difficulty falling asleep in 2002 was the main insomnia symptom that was predictive of cognitive impairment 14 years later, in 2016.
More frequent trouble falling asleep was predictive of poorer episodic memory, executive function, language, processing speed, and visuospatial performance.
The associations between sleep initiation and later cognitive impairment were partially explained by depressive symptoms and vascular disease burden for all domains except episodic memory, which was only partially explained by depressive symptoms.
Unclear mechanism
Ms. Zaheed said research is needed to uncover neurophysiologic mechanisms underlying the observed associations. “It may be that chronic difficulty with falling asleep is associated with inflammatory or metabolic processes that negatively affect brain structure and function over time,” she said.
“Insomnia has also been linked with higher accumulation of protein aggregates in the brain that disrupt cell communication and are characteristic of late-life disorders such as Alzheimer’s disease,” she added.
“While our project did not directly investigate these potential causal pathways between insomnia and cognition, our results suggest that investigating these potential mechanisms is an important area for future research,” Ms. Zaheed said.
“While additional intervention research is needed to determine whether targeting insomnia in older patients can have lasting cognitive benefits, results from this study suggest that discussing insomnia symptoms at the primary care level may be beneficial for both doctors and patients,” she added.
“By targeting insomnia – for example, through an evidence-based cognitive–behavioral therapy approach – individuals may improve various mental and physical health outcomes in addition to improving their sleep quality,” Ms. Zaheed said.
Reached for comment, Shaheen E. Lakhan, MD, PhD, neurologist in Newton, Massachusetts, said, “There is a strong link between chronic sleep disturbances and cognitive impairment, including dementia.”
“This study further supports this link and specifically calls out initiating sleep (as opposed to staying asleep) as the culprit. It also raises the hypothesis that the link is primarily mediated by depression and vascular disease; however, the verdict is still out,” said Dr. Lakhan.
The study was funded by the National Institute on Aging. Ms. Zaheed and Dr. Lakhan have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Insomnia in children tied to mood and anxiety disorders in adulthood
, new research indicates. However, insomnia symptoms in childhood that remit in the transition to adolescence do not confer increased risk of mood or anxiety disorders later on, the study found.
“As insomnia symptoms may precipitate or maintain internalizing disorders, our findings further reinforce the need for early sleep interventions to prevent future mental health disorders,” said lead investigator Julio Fernandez-Mendoza, PhD, associate professor at Penn State University, Hershey.
He presented his research at Virtual SLEEP 2021, the 35th annual meeting of the Associated Professional Sleep Societies.
Results ‘very clear’
The findings are based on data from the Penn State Child Cohort, a longitudinal, population-based sample of 700 children with a median age of 9 years, including 421 who were followed up 8 years later as adolescents (median age, 16 years) and 502 who were followed up 15 years later as young adults (median age, 24 years).
The data are “very clear that the risk of having internalizing disorders in young adulthood associated with having persistent insomnia symptoms, since childhood through adolescence into young adulthood,” Dr. Fernandez-Mendoza said in his presentation.
A persistent developmental trajectory was associated with a threefold increased risk of adult internalizing disorder (hazard ratio, 3.19).
The risk of having an internalizing disorder in young adulthood associated with newly developing (incident) insomnia symptoms is about twofold higher (HR, 1.94), whereas the risk associated with the waxing and waning pattern of insomnia is 1.5-fold (HR, 1.53) higher and only marginally significant, he reported.
An equally important finding, said Dr. Fernandez-Mendoza, is that those who had remitted insomnia symptoms in the transition to adolescence and throughout young adulthood were not at increased risk of having an internalizing disorder in young adulthood.
“Insomnia symptoms in a persistent manner associated with long-term adverse mental health outcomes, but remission of those insomnia symptoms associated with a good prognosis,” he said.
It’s also important to note, he said, that about 40% of children do not outgrow their insomnia symptoms in the transition to adolescence and are at risk of developing mental health disorders later on during early adulthood.
Reached for comment, Nitun Verma, MD, a spokesperson for the American Academy of Sleep Medicine, said: “There is a connection with mood and anxiety disorders with sleep, especially insomnia. This is a good reminder that reviewing someone’s sleep habits should always be a part of assessing someone’s mental health.”
A version of this article first appeared on Medscape.com.
, new research indicates. However, insomnia symptoms in childhood that remit in the transition to adolescence do not confer increased risk of mood or anxiety disorders later on, the study found.
“As insomnia symptoms may precipitate or maintain internalizing disorders, our findings further reinforce the need for early sleep interventions to prevent future mental health disorders,” said lead investigator Julio Fernandez-Mendoza, PhD, associate professor at Penn State University, Hershey.
He presented his research at Virtual SLEEP 2021, the 35th annual meeting of the Associated Professional Sleep Societies.
Results ‘very clear’
The findings are based on data from the Penn State Child Cohort, a longitudinal, population-based sample of 700 children with a median age of 9 years, including 421 who were followed up 8 years later as adolescents (median age, 16 years) and 502 who were followed up 15 years later as young adults (median age, 24 years).
The data are “very clear that the risk of having internalizing disorders in young adulthood associated with having persistent insomnia symptoms, since childhood through adolescence into young adulthood,” Dr. Fernandez-Mendoza said in his presentation.
A persistent developmental trajectory was associated with a threefold increased risk of adult internalizing disorder (hazard ratio, 3.19).
The risk of having an internalizing disorder in young adulthood associated with newly developing (incident) insomnia symptoms is about twofold higher (HR, 1.94), whereas the risk associated with the waxing and waning pattern of insomnia is 1.5-fold (HR, 1.53) higher and only marginally significant, he reported.
An equally important finding, said Dr. Fernandez-Mendoza, is that those who had remitted insomnia symptoms in the transition to adolescence and throughout young adulthood were not at increased risk of having an internalizing disorder in young adulthood.
“Insomnia symptoms in a persistent manner associated with long-term adverse mental health outcomes, but remission of those insomnia symptoms associated with a good prognosis,” he said.
It’s also important to note, he said, that about 40% of children do not outgrow their insomnia symptoms in the transition to adolescence and are at risk of developing mental health disorders later on during early adulthood.
Reached for comment, Nitun Verma, MD, a spokesperson for the American Academy of Sleep Medicine, said: “There is a connection with mood and anxiety disorders with sleep, especially insomnia. This is a good reminder that reviewing someone’s sleep habits should always be a part of assessing someone’s mental health.”
A version of this article first appeared on Medscape.com.
, new research indicates. However, insomnia symptoms in childhood that remit in the transition to adolescence do not confer increased risk of mood or anxiety disorders later on, the study found.
“As insomnia symptoms may precipitate or maintain internalizing disorders, our findings further reinforce the need for early sleep interventions to prevent future mental health disorders,” said lead investigator Julio Fernandez-Mendoza, PhD, associate professor at Penn State University, Hershey.
He presented his research at Virtual SLEEP 2021, the 35th annual meeting of the Associated Professional Sleep Societies.
Results ‘very clear’
The findings are based on data from the Penn State Child Cohort, a longitudinal, population-based sample of 700 children with a median age of 9 years, including 421 who were followed up 8 years later as adolescents (median age, 16 years) and 502 who were followed up 15 years later as young adults (median age, 24 years).
The data are “very clear that the risk of having internalizing disorders in young adulthood associated with having persistent insomnia symptoms, since childhood through adolescence into young adulthood,” Dr. Fernandez-Mendoza said in his presentation.
A persistent developmental trajectory was associated with a threefold increased risk of adult internalizing disorder (hazard ratio, 3.19).
The risk of having an internalizing disorder in young adulthood associated with newly developing (incident) insomnia symptoms is about twofold higher (HR, 1.94), whereas the risk associated with the waxing and waning pattern of insomnia is 1.5-fold (HR, 1.53) higher and only marginally significant, he reported.
An equally important finding, said Dr. Fernandez-Mendoza, is that those who had remitted insomnia symptoms in the transition to adolescence and throughout young adulthood were not at increased risk of having an internalizing disorder in young adulthood.
“Insomnia symptoms in a persistent manner associated with long-term adverse mental health outcomes, but remission of those insomnia symptoms associated with a good prognosis,” he said.
It’s also important to note, he said, that about 40% of children do not outgrow their insomnia symptoms in the transition to adolescence and are at risk of developing mental health disorders later on during early adulthood.
Reached for comment, Nitun Verma, MD, a spokesperson for the American Academy of Sleep Medicine, said: “There is a connection with mood and anxiety disorders with sleep, especially insomnia. This is a good reminder that reviewing someone’s sleep habits should always be a part of assessing someone’s mental health.”
A version of this article first appeared on Medscape.com.
AHA: Don’t delay COVID shot while CDC reviews myocarditis cases
While the investigation into cases of myocarditis possibly associated with COVID vaccines proceeds, the American Heart Association/American Stroke Association (ASA) continue to urge everyone who is eligible for the vaccine to get it without delay.
“We remain confident that the benefits of vaccination far exceed the very unusual risks,” the leadership of the AHA/ASA said in a statement issued June 12.
“The risks of COVID-19 infection include its potentially fatal consequences and the potential long-term health effects that are still revealing themselves, including lingering consequences affecting the heart, brain, vascular system, and other organs after infection,” they point out.
Late last week, the Centers for Disease Control and Prevention alerted health care providers that the COVID-19 Vaccine Safety Technical Work Group (VaST) of the Advisory Committee on Immunization Practices (ACIP) will meet June 18 to review cases of myocarditis reported in adolescents and young adults after they received a COVID-19 vaccine manufactured by Pfizer-BioNTech or Moderna.
The CDC is monitoring the Vaccine Adverse Events Reporting System (VAERS) and the Vaccine Safety Datalink (VSD) for cases of myocarditis that have been associated with the mRNA vaccines against SARS-CoV-2 from Pfizer and Moderna.
These cases may occur more often in males than females and more frequently after the second dose than the first dose of either mRNA vaccine. Symptoms typically occur in the 3 days after administration.
“The CDC’s ongoing investigation into cases of suspected myocarditis reflects a strong and steadfast commitment to transparency and the importance of scientific rigor on all fronts. We applaud the CDC’s unwavering efforts to lead our nation’s scientific and public health efforts, including ensuring the continued safety of the COVID-19 vaccines,” the AHA/ASA states.
They emphasize that vaccinations should continue, and say it’s important to consider the details of the suspected myocarditis cases being investigated by the CDC.
As of June 11, more than 306 million doses of COVID-19 vaccines have been administered in the United States (since Dec. 14, 2020) and nearly 43% of Americans – more than 142 million people – are now fully vaccinated.
According to the June 10 CDC VAERS report detailing adverse events through May 31:
- 789 cases of suspected myocarditis have been reported, with 475 involving people younger than 30 years; 79 cases reported were in patients 16 or 17 years old.
- The vast majority (81%) of the 270 patients younger than 30 years who were discharged from care after suspected myocarditis related to COVID-19 vaccination have recovered fully; the remaining 19% of patients report ongoing symptoms or complete data are missing.
- 196 cases of suspected myocarditis after a COVID-19 vaccine were reported in young adults 18 to 24 years of age, which is higher than expected for this age group.
As of May 31, only about 9% of the COVID-19 vaccine doses administered were to people 16 to 24 years of age, which is why this “higher-than-normal rate of possible myocarditis cases” warrants investigation, the AHA/ASA says.
They note that these suspected myocarditis cases were reported to VAERS because of their proximity to COVID-19 vaccine administration.
It remains to be determined which cases meet the clinical criteria for a diagnosis of myocarditis and whether they have any direct connection to the COVID-19 vaccine, the AHA/ASA says.
They urge all health care professionals to be aware of “very rare” adverse events that could be related to a COVID-19 vaccine, including myocarditis, blood clots, low platelets, and symptoms of severe inflammation.
They advise asking patients who present with symptoms related to these conditions about the timing of recent COVID vaccinations, as needed, to confirm the diagnosis and provide appropriate treatment quickly.
The AHA will be at the CDC’s June 18 meeting to review the latest evidence on cases of suspected myocarditis after the COVID-19 vaccine, the statement adds.
The statement notes that it reflects the views of the AHA/ASA and its scientific leadership, including current president Mitchel S.V. Elkind, MD, PhD; immediate past-president Robert A. Harrington, MD; president-elect Donald M. Lloyd-Jones, MD; AHA/ASA chief science and medical officer Mariell Jessup, MD; and chief medical officer for prevention Eduardo Sanchez, MD, MPH.
A version of this article first appeared on Medscape.com.
While the investigation into cases of myocarditis possibly associated with COVID vaccines proceeds, the American Heart Association/American Stroke Association (ASA) continue to urge everyone who is eligible for the vaccine to get it without delay.
“We remain confident that the benefits of vaccination far exceed the very unusual risks,” the leadership of the AHA/ASA said in a statement issued June 12.
“The risks of COVID-19 infection include its potentially fatal consequences and the potential long-term health effects that are still revealing themselves, including lingering consequences affecting the heart, brain, vascular system, and other organs after infection,” they point out.
Late last week, the Centers for Disease Control and Prevention alerted health care providers that the COVID-19 Vaccine Safety Technical Work Group (VaST) of the Advisory Committee on Immunization Practices (ACIP) will meet June 18 to review cases of myocarditis reported in adolescents and young adults after they received a COVID-19 vaccine manufactured by Pfizer-BioNTech or Moderna.
The CDC is monitoring the Vaccine Adverse Events Reporting System (VAERS) and the Vaccine Safety Datalink (VSD) for cases of myocarditis that have been associated with the mRNA vaccines against SARS-CoV-2 from Pfizer and Moderna.
These cases may occur more often in males than females and more frequently after the second dose than the first dose of either mRNA vaccine. Symptoms typically occur in the 3 days after administration.
“The CDC’s ongoing investigation into cases of suspected myocarditis reflects a strong and steadfast commitment to transparency and the importance of scientific rigor on all fronts. We applaud the CDC’s unwavering efforts to lead our nation’s scientific and public health efforts, including ensuring the continued safety of the COVID-19 vaccines,” the AHA/ASA states.
They emphasize that vaccinations should continue, and say it’s important to consider the details of the suspected myocarditis cases being investigated by the CDC.
As of June 11, more than 306 million doses of COVID-19 vaccines have been administered in the United States (since Dec. 14, 2020) and nearly 43% of Americans – more than 142 million people – are now fully vaccinated.
According to the June 10 CDC VAERS report detailing adverse events through May 31:
- 789 cases of suspected myocarditis have been reported, with 475 involving people younger than 30 years; 79 cases reported were in patients 16 or 17 years old.
- The vast majority (81%) of the 270 patients younger than 30 years who were discharged from care after suspected myocarditis related to COVID-19 vaccination have recovered fully; the remaining 19% of patients report ongoing symptoms or complete data are missing.
- 196 cases of suspected myocarditis after a COVID-19 vaccine were reported in young adults 18 to 24 years of age, which is higher than expected for this age group.
As of May 31, only about 9% of the COVID-19 vaccine doses administered were to people 16 to 24 years of age, which is why this “higher-than-normal rate of possible myocarditis cases” warrants investigation, the AHA/ASA says.
They note that these suspected myocarditis cases were reported to VAERS because of their proximity to COVID-19 vaccine administration.
It remains to be determined which cases meet the clinical criteria for a diagnosis of myocarditis and whether they have any direct connection to the COVID-19 vaccine, the AHA/ASA says.
They urge all health care professionals to be aware of “very rare” adverse events that could be related to a COVID-19 vaccine, including myocarditis, blood clots, low platelets, and symptoms of severe inflammation.
They advise asking patients who present with symptoms related to these conditions about the timing of recent COVID vaccinations, as needed, to confirm the diagnosis and provide appropriate treatment quickly.
The AHA will be at the CDC’s June 18 meeting to review the latest evidence on cases of suspected myocarditis after the COVID-19 vaccine, the statement adds.
The statement notes that it reflects the views of the AHA/ASA and its scientific leadership, including current president Mitchel S.V. Elkind, MD, PhD; immediate past-president Robert A. Harrington, MD; president-elect Donald M. Lloyd-Jones, MD; AHA/ASA chief science and medical officer Mariell Jessup, MD; and chief medical officer for prevention Eduardo Sanchez, MD, MPH.
A version of this article first appeared on Medscape.com.
While the investigation into cases of myocarditis possibly associated with COVID vaccines proceeds, the American Heart Association/American Stroke Association (ASA) continue to urge everyone who is eligible for the vaccine to get it without delay.
“We remain confident that the benefits of vaccination far exceed the very unusual risks,” the leadership of the AHA/ASA said in a statement issued June 12.
“The risks of COVID-19 infection include its potentially fatal consequences and the potential long-term health effects that are still revealing themselves, including lingering consequences affecting the heart, brain, vascular system, and other organs after infection,” they point out.
Late last week, the Centers for Disease Control and Prevention alerted health care providers that the COVID-19 Vaccine Safety Technical Work Group (VaST) of the Advisory Committee on Immunization Practices (ACIP) will meet June 18 to review cases of myocarditis reported in adolescents and young adults after they received a COVID-19 vaccine manufactured by Pfizer-BioNTech or Moderna.
The CDC is monitoring the Vaccine Adverse Events Reporting System (VAERS) and the Vaccine Safety Datalink (VSD) for cases of myocarditis that have been associated with the mRNA vaccines against SARS-CoV-2 from Pfizer and Moderna.
These cases may occur more often in males than females and more frequently after the second dose than the first dose of either mRNA vaccine. Symptoms typically occur in the 3 days after administration.
“The CDC’s ongoing investigation into cases of suspected myocarditis reflects a strong and steadfast commitment to transparency and the importance of scientific rigor on all fronts. We applaud the CDC’s unwavering efforts to lead our nation’s scientific and public health efforts, including ensuring the continued safety of the COVID-19 vaccines,” the AHA/ASA states.
They emphasize that vaccinations should continue, and say it’s important to consider the details of the suspected myocarditis cases being investigated by the CDC.
As of June 11, more than 306 million doses of COVID-19 vaccines have been administered in the United States (since Dec. 14, 2020) and nearly 43% of Americans – more than 142 million people – are now fully vaccinated.
According to the June 10 CDC VAERS report detailing adverse events through May 31:
- 789 cases of suspected myocarditis have been reported, with 475 involving people younger than 30 years; 79 cases reported were in patients 16 or 17 years old.
- The vast majority (81%) of the 270 patients younger than 30 years who were discharged from care after suspected myocarditis related to COVID-19 vaccination have recovered fully; the remaining 19% of patients report ongoing symptoms or complete data are missing.
- 196 cases of suspected myocarditis after a COVID-19 vaccine were reported in young adults 18 to 24 years of age, which is higher than expected for this age group.
As of May 31, only about 9% of the COVID-19 vaccine doses administered were to people 16 to 24 years of age, which is why this “higher-than-normal rate of possible myocarditis cases” warrants investigation, the AHA/ASA says.
They note that these suspected myocarditis cases were reported to VAERS because of their proximity to COVID-19 vaccine administration.
It remains to be determined which cases meet the clinical criteria for a diagnosis of myocarditis and whether they have any direct connection to the COVID-19 vaccine, the AHA/ASA says.
They urge all health care professionals to be aware of “very rare” adverse events that could be related to a COVID-19 vaccine, including myocarditis, blood clots, low platelets, and symptoms of severe inflammation.
They advise asking patients who present with symptoms related to these conditions about the timing of recent COVID vaccinations, as needed, to confirm the diagnosis and provide appropriate treatment quickly.
The AHA will be at the CDC’s June 18 meeting to review the latest evidence on cases of suspected myocarditis after the COVID-19 vaccine, the statement adds.
The statement notes that it reflects the views of the AHA/ASA and its scientific leadership, including current president Mitchel S.V. Elkind, MD, PhD; immediate past-president Robert A. Harrington, MD; president-elect Donald M. Lloyd-Jones, MD; AHA/ASA chief science and medical officer Mariell Jessup, MD; and chief medical officer for prevention Eduardo Sanchez, MD, MPH.
A version of this article first appeared on Medscape.com.
COVID-19 tied to spike in suspected suicide attempts by girls
Suspected suicide attempts by teenage girls have increased significantly during the COVID-19 pandemic, according to data released today by the U.S. Centers for Disease Control and Prevention.
Among children and adolescents aged 12-17 years, the average weekly number of emergency department visits for suspected suicide attempts was 22.3% higher during summer 2020 and 39.1% higher during winter 2021 than during the corresponding periods in 2019.
The increase was most evident among young girls.
Between Feb. 21 and March 20, 2021, the number of ED visits for suspected suicide attempts was about 51% higher among girls aged 12-17 years than during the same period in 2019. Among boys aged 12-17 years, ED visits for suspected suicide attempts increased 4%, the CDC reports.
“Young persons might represent a group at high risk because they might have been particularly affected by mitigation measures, such as physical distancing (including a lack of connectedness to schools, teachers, and peers); barriers to mental health treatment; increases in substance use; and anxiety about family health and economic problems, which are all risk factors for suicide,” write the authors, led by Ellen Yard, PhD, with the CDC’s National Center for Injury Prevention and Control.
In addition, the findings from this study suggest there has been “more severe distress among young females than has been identified in previous reports during the pandemic, reinforcing the need for increased attention to, and prevention for, this population,” they point out.
The results were published June 11 in Morbidity and Mortality Weekly Report.
The findings are based on data for ED visits for suspected suicide from the National Syndromic Surveillance Program, which includes about 71% of the nation’s EDs in 49 states (all except Hawaii) and the District of Columbia.
Earlier data reported by the CDC showed that the proportion of mental health–related ED visits among children and adolescents aged 12-17 years increased by 31% during 2020, compared with 2019.
‘Time for action is now’
These new findings underscore the “enormous impact the COVID-19 pandemic is having on our country’s overall emotional wellbeing, especially among young people,” the National Action Alliance for Suicide Prevention (Action Alliance) Media Messaging Work Group said in a statement responding to the newly released data.
“Just as we have taken steps to protect our physical health throughout the pandemic, we must also take steps to protect our mental and emotional health,” the group says.
The data, the group says, specifically speak to the importance of improving suicide care both during and after ED visits by scaling up the adoption of best practices, such as the Recommended Standard Care for People with Suicide Risk: Making Health Care Suicide Safe and Best Practices in Care Transitions for Individuals with Suicide Risk: Inpatient Care to Outpatient Care.
“These and other evidence-based best practices must be adopted by health care systems nationwide to ensure safe, effective suicide care for all,” the group says.
“However, health care systems cannot address this issue alone. Suicide is a complex public health issue that also requires a comprehensive, community-based approach to addressing it. We must ensure suicide prevention is infused into a variety of community-based settings – such as schools, workplaces, and places of worship – to ensure people are connected with prevention activities and resources before a crisis occurs,” the group says.
It also highlights the crucial role of social connectedness as a protective factor against suicide.
“Research indicates that a sense of belonging and social connectedness improves physical, mental, and emotional wellbeing. Everyone can play a role in being there for each other and helping to build resiliency. Having real, honest conversations about our own mental health opens the door for connection and social support,” the group says.
It calls on leaders from all sectors and industries to make suicide prevention “a national priority by becoming engaged in the issue and bringing resources to bear. The time for action is now.”
A version of this article first appeared on Medscape.com.
Suspected suicide attempts by teenage girls have increased significantly during the COVID-19 pandemic, according to data released today by the U.S. Centers for Disease Control and Prevention.
Among children and adolescents aged 12-17 years, the average weekly number of emergency department visits for suspected suicide attempts was 22.3% higher during summer 2020 and 39.1% higher during winter 2021 than during the corresponding periods in 2019.
The increase was most evident among young girls.
Between Feb. 21 and March 20, 2021, the number of ED visits for suspected suicide attempts was about 51% higher among girls aged 12-17 years than during the same period in 2019. Among boys aged 12-17 years, ED visits for suspected suicide attempts increased 4%, the CDC reports.
“Young persons might represent a group at high risk because they might have been particularly affected by mitigation measures, such as physical distancing (including a lack of connectedness to schools, teachers, and peers); barriers to mental health treatment; increases in substance use; and anxiety about family health and economic problems, which are all risk factors for suicide,” write the authors, led by Ellen Yard, PhD, with the CDC’s National Center for Injury Prevention and Control.
In addition, the findings from this study suggest there has been “more severe distress among young females than has been identified in previous reports during the pandemic, reinforcing the need for increased attention to, and prevention for, this population,” they point out.
The results were published June 11 in Morbidity and Mortality Weekly Report.
The findings are based on data for ED visits for suspected suicide from the National Syndromic Surveillance Program, which includes about 71% of the nation’s EDs in 49 states (all except Hawaii) and the District of Columbia.
Earlier data reported by the CDC showed that the proportion of mental health–related ED visits among children and adolescents aged 12-17 years increased by 31% during 2020, compared with 2019.
‘Time for action is now’
These new findings underscore the “enormous impact the COVID-19 pandemic is having on our country’s overall emotional wellbeing, especially among young people,” the National Action Alliance for Suicide Prevention (Action Alliance) Media Messaging Work Group said in a statement responding to the newly released data.
“Just as we have taken steps to protect our physical health throughout the pandemic, we must also take steps to protect our mental and emotional health,” the group says.
The data, the group says, specifically speak to the importance of improving suicide care both during and after ED visits by scaling up the adoption of best practices, such as the Recommended Standard Care for People with Suicide Risk: Making Health Care Suicide Safe and Best Practices in Care Transitions for Individuals with Suicide Risk: Inpatient Care to Outpatient Care.
“These and other evidence-based best practices must be adopted by health care systems nationwide to ensure safe, effective suicide care for all,” the group says.
“However, health care systems cannot address this issue alone. Suicide is a complex public health issue that also requires a comprehensive, community-based approach to addressing it. We must ensure suicide prevention is infused into a variety of community-based settings – such as schools, workplaces, and places of worship – to ensure people are connected with prevention activities and resources before a crisis occurs,” the group says.
It also highlights the crucial role of social connectedness as a protective factor against suicide.
“Research indicates that a sense of belonging and social connectedness improves physical, mental, and emotional wellbeing. Everyone can play a role in being there for each other and helping to build resiliency. Having real, honest conversations about our own mental health opens the door for connection and social support,” the group says.
It calls on leaders from all sectors and industries to make suicide prevention “a national priority by becoming engaged in the issue and bringing resources to bear. The time for action is now.”
A version of this article first appeared on Medscape.com.
Suspected suicide attempts by teenage girls have increased significantly during the COVID-19 pandemic, according to data released today by the U.S. Centers for Disease Control and Prevention.
Among children and adolescents aged 12-17 years, the average weekly number of emergency department visits for suspected suicide attempts was 22.3% higher during summer 2020 and 39.1% higher during winter 2021 than during the corresponding periods in 2019.
The increase was most evident among young girls.
Between Feb. 21 and March 20, 2021, the number of ED visits for suspected suicide attempts was about 51% higher among girls aged 12-17 years than during the same period in 2019. Among boys aged 12-17 years, ED visits for suspected suicide attempts increased 4%, the CDC reports.
“Young persons might represent a group at high risk because they might have been particularly affected by mitigation measures, such as physical distancing (including a lack of connectedness to schools, teachers, and peers); barriers to mental health treatment; increases in substance use; and anxiety about family health and economic problems, which are all risk factors for suicide,” write the authors, led by Ellen Yard, PhD, with the CDC’s National Center for Injury Prevention and Control.
In addition, the findings from this study suggest there has been “more severe distress among young females than has been identified in previous reports during the pandemic, reinforcing the need for increased attention to, and prevention for, this population,” they point out.
The results were published June 11 in Morbidity and Mortality Weekly Report.
The findings are based on data for ED visits for suspected suicide from the National Syndromic Surveillance Program, which includes about 71% of the nation’s EDs in 49 states (all except Hawaii) and the District of Columbia.
Earlier data reported by the CDC showed that the proportion of mental health–related ED visits among children and adolescents aged 12-17 years increased by 31% during 2020, compared with 2019.
‘Time for action is now’
These new findings underscore the “enormous impact the COVID-19 pandemic is having on our country’s overall emotional wellbeing, especially among young people,” the National Action Alliance for Suicide Prevention (Action Alliance) Media Messaging Work Group said in a statement responding to the newly released data.
“Just as we have taken steps to protect our physical health throughout the pandemic, we must also take steps to protect our mental and emotional health,” the group says.
The data, the group says, specifically speak to the importance of improving suicide care both during and after ED visits by scaling up the adoption of best practices, such as the Recommended Standard Care for People with Suicide Risk: Making Health Care Suicide Safe and Best Practices in Care Transitions for Individuals with Suicide Risk: Inpatient Care to Outpatient Care.
“These and other evidence-based best practices must be adopted by health care systems nationwide to ensure safe, effective suicide care for all,” the group says.
“However, health care systems cannot address this issue alone. Suicide is a complex public health issue that also requires a comprehensive, community-based approach to addressing it. We must ensure suicide prevention is infused into a variety of community-based settings – such as schools, workplaces, and places of worship – to ensure people are connected with prevention activities and resources before a crisis occurs,” the group says.
It also highlights the crucial role of social connectedness as a protective factor against suicide.
“Research indicates that a sense of belonging and social connectedness improves physical, mental, and emotional wellbeing. Everyone can play a role in being there for each other and helping to build resiliency. Having real, honest conversations about our own mental health opens the door for connection and social support,” the group says.
It calls on leaders from all sectors and industries to make suicide prevention “a national priority by becoming engaged in the issue and bringing resources to bear. The time for action is now.”
A version of this article first appeared on Medscape.com.