MDedge Psychiatry

Parents, teachers, children, and adolescents are facing stress and anxiety as K-12 school districts across the country debate whether to return to in-person instruction amid the COVID-19 pandemic. As we approach the opening of schools, the stress and anxiety seem to be heightening.

alexsokolov/Thinkstock

According to Education Week, which is tracking the reopening plans of public schools across the United States, 21 of the 25 largest school districts are opting to implement remote learning only as their model. I would like to see all of those districts adopt that model until we understand more about this illness, and can prevent and treat it.

Yes, it’s true – I am a psychiatrist – not an infectious disease specialist. And I realize that the American Academy of Pediatrics and the Centers for Disease Control and Prevention have taken nuanced positions on this issue. Their positions make it clear that it is within a child’s best interests – from an educational and social point of view – to attend school in person. Not only is the classroom experience important, but so is the socialization and the exercise. However, when I look at the science on children who have been exposed to the coronavirus, I worry.

For example, a study by Lael M. Yonker, MD, and associates on pediatric SARS-CoV-2 found that the children in days 0-2 of illness have far higher viral loads than adults who have been hospitalized for severe disease. “This study reveals that children may be a potential source of contagion in the SARS-CoV-2 pandemic in spite of milder disease or lack of symptoms, and immune dysregulation is implicated in severe post-infectious [multisystem inflammatory syndrome in children],” Dr. Yonker and associates wrote, referring to the illness associated with COVID-19 in children. Their study was published recently in the Journal of Pediatrics (2020 Aug 19. doi: 10.1016/j.jpeds.2020.08.037).

In my state, where positivity rates are fairly low, Gov. Andrew Cuomo admitted in an interview recently that sending children to school in New York City is a “tricky proposition.” At this point, New York City public schools are scheduled to open in mid-September using a hybrid mixture of in-person and remote learning.

And look at what happened several weeks ago in Israel, where schools reopened after the virus was beaten back. At one high school in Jerusalem, just days after the reopening, the virus spread so prolifically to students, teachers, and relatives that the schools had to be closed again. Other countries should not follow Israel’s example, Eli Weizmann, who chairs the team advising Israel’s National Security Council on the pandemic, reportedly told the New York Times. “It was a major failure.”

But I must be honest: I was worried about children returning to school before I heard about the study by Dr. Yonker and associates, Gov. Cuomo’s comments, and what happened in Israel. So far, here in the Northeast, particularly in New York, New Jersey, and Connecticut, we have managed to get COVID-19 under control. Perhaps, in this part of the country, opening classroom education might be feasible – with close monitoring and proper precautions.

But COVID-19 has taken the lives of hundreds of thousands of Americans – more than 176,000 as of this writing. A new model from the University of Washington’s Institute for Health Metrics and Evaluation projects that COVID-19 could lead to more than 300,000 U.S. deaths by Dec. 1. Thankfully, the number of COVID-19–positive children who have died has been low. But they could still pass on the virus to adults.

To get a better understanding of COVID-19, I spoke with Sheryl L. Wulkan, MD, an internist and expert in personal protective equipment (PPE) who has consulted for numerous health care agencies about these issues. Dr. Wulkan said that, in some areas with low infection rates, school openings might be appropriate. However, she said, without proper testing and contact tracing, we are at a loss of controlling the spread.
 

What we should tell patients, family, and friends

From a psychiatric point of view, how should we advise our patients, family, and friends about sending their children back to school? Is on-site learning better than remote learning? It is. Do our children need the socialization that a school brings? Yes, they do.

Socialization and relating to peers are, indeed, important, but today’s children socialize in many ways beyond attending school – and they have peer friendships and interactions with electronic devices at their disposal.

Can remote learning cause social isolation – an isolation so profound that school is necessary not only for learning but the psyche as well? A meta-analysis of 80 studies that looked at the impact of social isolation and loneliness on adolescents and children who were previously healthy found that the young people “are probably more likely to experience high rates of depression and probably anxiety during and after enforced isolation ends. This may increase as enforced isolation continues,” wrote Maria Elizabeth Loades, PhD, and associates (J Am Acad Child Adolesc Psychiatry. 2020 Jun 3. S0890-8567[20]30337-3).

I am concerned about young people who experience anxiety and depression, and agree with Dr. Loades that we mental health professionals need to be ready to intervene early and provide preventive support. To do this, we should encourage parents to keep us informed about how their children are doing.

So my advice is that, in the absence of a vaccine and an effective treatment like we have for influenza – such as Tamiflu – and effective testing, such the saliva-based test developed by Yale University researchers, if I had school-aged children, I would continue to keep them home from school. Ultimately, however, parents must look at the science and make their decisions based on that. My children are adults with their own children, and only they can make informed decisions about which options are best for their families.

Interestingly, Sanjay Gupta, MD, the neurosurgeon who works as chief medical correspondent of CNN, recently discussed the thought process he and his wife used to determine whether their daughters would return to the classroom. After weighing many factors, including the viral spread in Fulton County, Ga., where they live, the Guptas decided that, at this time, the risks of allowing the girls to return to the classroom outweigh the benefits. “This was not an easy decision, but one that we believe best respects the science, decreases the risk of further spread, and follows the task force criteria,” wrote Dr. Gupta, who is affiliated with Emory University in Atlanta. “After 2 weeks, we will reassess.”

I understand that parents worry about the social and psychological costs of remote learning. And I can only imagine the difficulty of those who must balance homeschooling with working. And frankly, remote learning is not an option for all students. For those less fortunate, substantial governmental aid is important to assist these people and to keep them safe and on their feet until this pandemic is done. Also, those who were under the care of a psychiatrist should continue to receive care during the pandemic. We must be prepared to step in with interventions that can address the suffering that is inevitable, such as the use of targeted cognitive-behavioral therapy.

Public TV as an educational tool

Families with Internet access and those without it could benefit from using public television as a tool.

I would advise educators and the entertainment industry to harness the wonder of TV to develop curricula that can be used to educate children. As we know, Sesame Street proved to be an effective early childhood intervention, particularly for boys (Am Econ J: Applied Economics. 2019;11[1]:318-50). I would like to see programming that goes beyond Sesame Street. Learning from watching this kind of programming would be no substitute for engaging with teachers in real, live classrooms, however.

Children and adolescents will be changed by learning remotely. They will miss their friends, teachers, and other staff members, but their lives will not be ruined. Mental health professionals should be prepared to intervene to address depression, anxiety, and other sequelae and problematic behaviors that could result from social isolation. Schools, businesses, and the economy will again flourish after we get the virus behind us but controlling and eliminating this pandemic need to come first. Let’s keep our children home – to the extent that we can – until we move beyond this pandemic.
 

Dr. London has been a practicing psychiatrist for 4 decades and a newspaper columnist for almost as long. He has a private practice in New York and is author of “Find Freedom Fast: Short-Term Therapy That Works” (New York: Kettlehole Publishing, 2019). Dr. London has no conflicts of interest.

Parents, teachers, children, and adolescents are facing stress and anxiety as K-12 school districts across the country debate whether to return to in-person instruction amid the COVID-19 pandemic. As we approach the opening of schools, the stress and anxiety seem to be heightening.

alexsokolov/Thinkstock

According to Education Week, which is tracking the reopening plans of public schools across the United States, 21 of the 25 largest school districts are opting to implement remote learning only as their model. I would like to see all of those districts adopt that model until we understand more about this illness, and can prevent and treat it.

Yes, it’s true – I am a psychiatrist – not an infectious disease specialist. And I realize that the American Academy of Pediatrics and the Centers for Disease Control and Prevention have taken nuanced positions on this issue. Their positions make it clear that it is within a child’s best interests – from an educational and social point of view – to attend school in person. Not only is the classroom experience important, but so is the socialization and the exercise. However, when I look at the science on children who have been exposed to the coronavirus, I worry.

For example, a study by Lael M. Yonker, MD, and associates on pediatric SARS-CoV-2 found that the children in days 0-2 of illness have far higher viral loads than adults who have been hospitalized for severe disease. “This study reveals that children may be a potential source of contagion in the SARS-CoV-2 pandemic in spite of milder disease or lack of symptoms, and immune dysregulation is implicated in severe post-infectious [multisystem inflammatory syndrome in children],” Dr. Yonker and associates wrote, referring to the illness associated with COVID-19 in children. Their study was published recently in the Journal of Pediatrics (2020 Aug 19. doi: 10.1016/j.jpeds.2020.08.037).

In my state, where positivity rates are fairly low, Gov. Andrew Cuomo admitted in an interview recently that sending children to school in New York City is a “tricky proposition.” At this point, New York City public schools are scheduled to open in mid-September using a hybrid mixture of in-person and remote learning.

And look at what happened several weeks ago in Israel, where schools reopened after the virus was beaten back. At one high school in Jerusalem, just days after the reopening, the virus spread so prolifically to students, teachers, and relatives that the schools had to be closed again. Other countries should not follow Israel’s example, Eli Weizmann, who chairs the team advising Israel’s National Security Council on the pandemic, reportedly told the New York Times. “It was a major failure.”

But I must be honest: I was worried about children returning to school before I heard about the study by Dr. Yonker and associates, Gov. Cuomo’s comments, and what happened in Israel. So far, here in the Northeast, particularly in New York, New Jersey, and Connecticut, we have managed to get COVID-19 under control. Perhaps, in this part of the country, opening classroom education might be feasible – with close monitoring and proper precautions.

But COVID-19 has taken the lives of hundreds of thousands of Americans – more than 176,000 as of this writing. A new model from the University of Washington’s Institute for Health Metrics and Evaluation projects that COVID-19 could lead to more than 300,000 U.S. deaths by Dec. 1. Thankfully, the number of COVID-19–positive children who have died has been low. But they could still pass on the virus to adults.

To get a better understanding of COVID-19, I spoke with Sheryl L. Wulkan, MD, an internist and expert in personal protective equipment (PPE) who has consulted for numerous health care agencies about these issues. Dr. Wulkan said that, in some areas with low infection rates, school openings might be appropriate. However, she said, without proper testing and contact tracing, we are at a loss of controlling the spread.
 

What we should tell patients, family, and friends

From a psychiatric point of view, how should we advise our patients, family, and friends about sending their children back to school? Is on-site learning better than remote learning? It is. Do our children need the socialization that a school brings? Yes, they do.

Socialization and relating to peers are, indeed, important, but today’s children socialize in many ways beyond attending school – and they have peer friendships and interactions with electronic devices at their disposal.

Can remote learning cause social isolation – an isolation so profound that school is necessary not only for learning but the psyche as well? A meta-analysis of 80 studies that looked at the impact of social isolation and loneliness on adolescents and children who were previously healthy found that the young people “are probably more likely to experience high rates of depression and probably anxiety during and after enforced isolation ends. This may increase as enforced isolation continues,” wrote Maria Elizabeth Loades, PhD, and associates (J Am Acad Child Adolesc Psychiatry. 2020 Jun 3. S0890-8567[20]30337-3).

I am concerned about young people who experience anxiety and depression, and agree with Dr. Loades that we mental health professionals need to be ready to intervene early and provide preventive support. To do this, we should encourage parents to keep us informed about how their children are doing.

So my advice is that, in the absence of a vaccine and an effective treatment like we have for influenza – such as Tamiflu – and effective testing, such the saliva-based test developed by Yale University researchers, if I had school-aged children, I would continue to keep them home from school. Ultimately, however, parents must look at the science and make their decisions based on that. My children are adults with their own children, and only they can make informed decisions about which options are best for their families.

Interestingly, Sanjay Gupta, MD, the neurosurgeon who works as chief medical correspondent of CNN, recently discussed the thought process he and his wife used to determine whether their daughters would return to the classroom. After weighing many factors, including the viral spread in Fulton County, Ga., where they live, the Guptas decided that, at this time, the risks of allowing the girls to return to the classroom outweigh the benefits. “This was not an easy decision, but one that we believe best respects the science, decreases the risk of further spread, and follows the task force criteria,” wrote Dr. Gupta, who is affiliated with Emory University in Atlanta. “After 2 weeks, we will reassess.”

I understand that parents worry about the social and psychological costs of remote learning. And I can only imagine the difficulty of those who must balance homeschooling with working. And frankly, remote learning is not an option for all students. For those less fortunate, substantial governmental aid is important to assist these people and to keep them safe and on their feet until this pandemic is done. Also, those who were under the care of a psychiatrist should continue to receive care during the pandemic. We must be prepared to step in with interventions that can address the suffering that is inevitable, such as the use of targeted cognitive-behavioral therapy.

Public TV as an educational tool

Families with Internet access and those without it could benefit from using public television as a tool.

I would advise educators and the entertainment industry to harness the wonder of TV to develop curricula that can be used to educate children. As we know, Sesame Street proved to be an effective early childhood intervention, particularly for boys (Am Econ J: Applied Economics. 2019;11[1]:318-50). I would like to see programming that goes beyond Sesame Street. Learning from watching this kind of programming would be no substitute for engaging with teachers in real, live classrooms, however.

Children and adolescents will be changed by learning remotely. They will miss their friends, teachers, and other staff members, but their lives will not be ruined. Mental health professionals should be prepared to intervene to address depression, anxiety, and other sequelae and problematic behaviors that could result from social isolation. Schools, businesses, and the economy will again flourish after we get the virus behind us but controlling and eliminating this pandemic need to come first. Let’s keep our children home – to the extent that we can – until we move beyond this pandemic.
 

Dr. London has been a practicing psychiatrist for 4 decades and a newspaper columnist for almost as long. He has a private practice in New York and is author of “Find Freedom Fast: Short-Term Therapy That Works” (New York: Kettlehole Publishing, 2019). Dr. London has no conflicts of interest.

Parents, teachers, children, and adolescents are facing stress and anxiety as K-12 school districts across the country debate whether to return to in-person instruction amid the COVID-19 pandemic. As we approach the opening of schools, the stress and anxiety seem to be heightening.

alexsokolov/Thinkstock

According to Education Week, which is tracking the reopening plans of public schools across the United States, 21 of the 25 largest school districts are opting to implement remote learning only as their model. I would like to see all of those districts adopt that model until we understand more about this illness, and can prevent and treat it.

Yes, it’s true – I am a psychiatrist – not an infectious disease specialist. And I realize that the American Academy of Pediatrics and the Centers for Disease Control and Prevention have taken nuanced positions on this issue. Their positions make it clear that it is within a child’s best interests – from an educational and social point of view – to attend school in person. Not only is the classroom experience important, but so is the socialization and the exercise. However, when I look at the science on children who have been exposed to the coronavirus, I worry.

For example, a study by Lael M. Yonker, MD, and associates on pediatric SARS-CoV-2 found that the children in days 0-2 of illness have far higher viral loads than adults who have been hospitalized for severe disease. “This study reveals that children may be a potential source of contagion in the SARS-CoV-2 pandemic in spite of milder disease or lack of symptoms, and immune dysregulation is implicated in severe post-infectious [multisystem inflammatory syndrome in children],” Dr. Yonker and associates wrote, referring to the illness associated with COVID-19 in children. Their study was published recently in the Journal of Pediatrics (2020 Aug 19. doi: 10.1016/j.jpeds.2020.08.037).

In my state, where positivity rates are fairly low, Gov. Andrew Cuomo admitted in an interview recently that sending children to school in New York City is a “tricky proposition.” At this point, New York City public schools are scheduled to open in mid-September using a hybrid mixture of in-person and remote learning.

And look at what happened several weeks ago in Israel, where schools reopened after the virus was beaten back. At one high school in Jerusalem, just days after the reopening, the virus spread so prolifically to students, teachers, and relatives that the schools had to be closed again. Other countries should not follow Israel’s example, Eli Weizmann, who chairs the team advising Israel’s National Security Council on the pandemic, reportedly told the New York Times. “It was a major failure.”

But I must be honest: I was worried about children returning to school before I heard about the study by Dr. Yonker and associates, Gov. Cuomo’s comments, and what happened in Israel. So far, here in the Northeast, particularly in New York, New Jersey, and Connecticut, we have managed to get COVID-19 under control. Perhaps, in this part of the country, opening classroom education might be feasible – with close monitoring and proper precautions.

But COVID-19 has taken the lives of hundreds of thousands of Americans – more than 176,000 as of this writing. A new model from the University of Washington’s Institute for Health Metrics and Evaluation projects that COVID-19 could lead to more than 300,000 U.S. deaths by Dec. 1. Thankfully, the number of COVID-19–positive children who have died has been low. But they could still pass on the virus to adults.

To get a better understanding of COVID-19, I spoke with Sheryl L. Wulkan, MD, an internist and expert in personal protective equipment (PPE) who has consulted for numerous health care agencies about these issues. Dr. Wulkan said that, in some areas with low infection rates, school openings might be appropriate. However, she said, without proper testing and contact tracing, we are at a loss of controlling the spread.
 

What we should tell patients, family, and friends

From a psychiatric point of view, how should we advise our patients, family, and friends about sending their children back to school? Is on-site learning better than remote learning? It is. Do our children need the socialization that a school brings? Yes, they do.

Socialization and relating to peers are, indeed, important, but today’s children socialize in many ways beyond attending school – and they have peer friendships and interactions with electronic devices at their disposal.

Can remote learning cause social isolation – an isolation so profound that school is necessary not only for learning but the psyche as well? A meta-analysis of 80 studies that looked at the impact of social isolation and loneliness on adolescents and children who were previously healthy found that the young people “are probably more likely to experience high rates of depression and probably anxiety during and after enforced isolation ends. This may increase as enforced isolation continues,” wrote Maria Elizabeth Loades, PhD, and associates (J Am Acad Child Adolesc Psychiatry. 2020 Jun 3. S0890-8567[20]30337-3).

I am concerned about young people who experience anxiety and depression, and agree with Dr. Loades that we mental health professionals need to be ready to intervene early and provide preventive support. To do this, we should encourage parents to keep us informed about how their children are doing.

So my advice is that, in the absence of a vaccine and an effective treatment like we have for influenza – such as Tamiflu – and effective testing, such the saliva-based test developed by Yale University researchers, if I had school-aged children, I would continue to keep them home from school. Ultimately, however, parents must look at the science and make their decisions based on that. My children are adults with their own children, and only they can make informed decisions about which options are best for their families.

Interestingly, Sanjay Gupta, MD, the neurosurgeon who works as chief medical correspondent of CNN, recently discussed the thought process he and his wife used to determine whether their daughters would return to the classroom. After weighing many factors, including the viral spread in Fulton County, Ga., where they live, the Guptas decided that, at this time, the risks of allowing the girls to return to the classroom outweigh the benefits. “This was not an easy decision, but one that we believe best respects the science, decreases the risk of further spread, and follows the task force criteria,” wrote Dr. Gupta, who is affiliated with Emory University in Atlanta. “After 2 weeks, we will reassess.”

I understand that parents worry about the social and psychological costs of remote learning. And I can only imagine the difficulty of those who must balance homeschooling with working. And frankly, remote learning is not an option for all students. For those less fortunate, substantial governmental aid is important to assist these people and to keep them safe and on their feet until this pandemic is done. Also, those who were under the care of a psychiatrist should continue to receive care during the pandemic. We must be prepared to step in with interventions that can address the suffering that is inevitable, such as the use of targeted cognitive-behavioral therapy.

Public TV as an educational tool

Families with Internet access and those without it could benefit from using public television as a tool.

I would advise educators and the entertainment industry to harness the wonder of TV to develop curricula that can be used to educate children. As we know, Sesame Street proved to be an effective early childhood intervention, particularly for boys (Am Econ J: Applied Economics. 2019;11[1]:318-50). I would like to see programming that goes beyond Sesame Street. Learning from watching this kind of programming would be no substitute for engaging with teachers in real, live classrooms, however.

Children and adolescents will be changed by learning remotely. They will miss their friends, teachers, and other staff members, but their lives will not be ruined. Mental health professionals should be prepared to intervene to address depression, anxiety, and other sequelae and problematic behaviors that could result from social isolation. Schools, businesses, and the economy will again flourish after we get the virus behind us but controlling and eliminating this pandemic need to come first. Let’s keep our children home – to the extent that we can – until we move beyond this pandemic.
 

Dr. London has been a practicing psychiatrist for 4 decades and a newspaper columnist for almost as long. He has a private practice in New York and is author of “Find Freedom Fast: Short-Term Therapy That Works” (New York: Kettlehole Publishing, 2019). Dr. London has no conflicts of interest.

Alzheimer’s disease may have a causal effect on sleep patterns, but disturbed sleep does not appear to cause Alzheimer’s disease, new research suggests.

The causal association between disturbed sleep and Alzheimer’s disease that has been observed in previous studies may have resulted from reverse causation, the researchers noted. The current Mendelian randomization analysis also failed to find a causal relationship between Alzheimer’s disease and major depressive disorder. Future studies should examine the genetic heterogeneity of depression syndromes to test for causal relationships between subtypes of depression with distinct causes and Alzheimer’s disease.

Mendelian randomization compares individuals who have different genetic profiles for a given exposure. “Given that genetic variants are inherited at random, these two groups are comparable, and any differences are not likely to be due to other associated factors,” such as confounding bias, said corresponding author Abbas Dehghan, PhD, reader in cardiometabolic disease epidemiology at Imperial College London. “Moreover, given that genetic information is constant over the lifetime, the chances for reverse causation are small.”

The findings were published online August 19 in Neurology.

Causal questions

Many patients with late-life neurodegenerative disorders such as Alzheimer’s disease have comorbid depression, but whether these two disorders have a causal relationship or common risk factors has been unclear, the investigators noted. Abnormal sleep patterns are symptoms of both depression and Alzheimer’s disease. Abnormal sleep is also associated with cognitive decline and anxiety.

The researchers hypothesized that sleep causally affects major depressive disorder and Alzheimer’s disease but that there is no causal relationship between major depressive disorder and Alzheimer’s disease. They conducted a bidirectional, two-sample Mendelian randomization study to test these hypotheses.

The investigators conducted genomewide association studies (GWASs) using data from the prospective, population-based U.K. Biobank. Sleep phenotypes were measured by self-report or accelerometer. Genetic associations were derived from 403,195 patients for chronotype, 237,627 patients for insomnia, 446,118 people for sleep duration, and 85,670 people for accelerometer-derived phenotypes.

Two binary variables from sleep duration were derived: short sleep (duration of less than 7 hours) and long sleep (duration of 9 or more hours). A sleep episode was defined as a period of at least 5 minutes with a change on the dorsal-ventral axis of less than 5 degrees. The durations of all sleep episodes were added to calculate total sleep duration.

Major depressive disorder was diagnosed clinically in accordance with DSM-IV criteria. Genetic associations were derived from 9,240 case patients and 9,519 control participants. Alzheimer’s disease was diagnosed on the basis of physician examination or autopsy results. Genetic associations were obtained from a meta-analysis of GWAS on participants of European ancestry in the International Genomics of Alzheimer’s Project, which included 21,982 case patients and 41,944 control participants.

More risk factor research needed

Results showed no causal relationships between sleep-related phenotypes and major depressive disorder in either direction. Causal relationships between major depressive disorder and Alzheimer’s disease were found in both directions, but neither was statistically significant.

A genetically higher risk for Alzheimer’s disease was associated with being a “morning person,” being at decreased risk for insomnia, having shorter sleep duration on self-report and accelerometer, having decreased likelihood of reporting long sleep, having an earlier timing of the least active 5 hours, and having a smaller number of sleep episodes. However, no analysis supported a causal effect of sleep-related phenotypes on risk for Alzheimer’s disease.

Because APOE4 can influence disease processes that may contribute to Alzheimer’s disease risk, the investigators also conducted a sensitivity analysis that excluded APOE single-nucleotide polymorphisms. In this analysis, the causal associations of Alzheimer’s disease with self-reported and accelerometer-based sleep duration were not significant. The sensitivity analysis did support the other causal associations between Alzheimer’s disease and sleep phenotypes, however.

The causal associations between major depressive disorder and Alzheimer’s disease observed in other studies may have been the result of confounding, and the participants may have had other associated characteristics that put them at risk for the disease, said Dr. Dehghan. Furthermore, the previous studies considered various sleep phenotypes together, whereas in the current study, the investigators examined them separately.

The results suggest that preclinical and clinical Alzheimer’s disease may affect sleep phenotypes differently. Sleep management thus could be an important approach to improving quality of life for patients with Alzheimer’s disease, the researchers wrote.

“Our study indicates that depression and sleep disorders are not likely to be a causal factor for Alzheimer’s disease,” Dr. Dehghan said. “We need to search for other risk factors for the prevention of Alzheimer’s disease.”

Several strengths, lacks details

Walter A. Kukull, PhD, professor of epidemiology and director of the National Alzheimer’s Coordinating Center at the University of Washington, Seattle, noted that the investigators appear to have implemented their chosen methods of causal association analysis well. “They attempted to examine the direction of the causal arrow for risk factors … and that is a step usually not well examined in other studies.”

He added that the collection of objective measures, such as of sleep, is another strength of the study.

However, “the common weakness of the basic GWAS sample is that clinical symptomatology determined Alzheimer’s disease diagnosis. Thus, asymptomatic or very mildly symptomatic persons with Alzheimer’s disease pathology in their brains were likely included among normal controls,” said Dr. Kukull, who was not involved with the research.

Because of an apparent lack of biomarker data, patients who had been diagnosed with Alzheimer’s disease may in fact have had a different form of dementia. Given the nature of their data, the investigators could have done little to compensate for these possibilities, Dr. Kukull added. In addition, the article lacks details that would improve the interpretation of the results.

“Timing is everything with regard to potential associations between risk factor and outcome,” Dr. Kukull said. “With the exceptions of genes, it would be nice to know more about the timing of risk factors’ onset and Alzheimer’s disease onset.”

Still, the results indicate potential areas of future study, he noted. “Primarily, further research must address the question of pathological onset of disease and misclassification of diagnosis in both cases and controls due to lack of biomarker-confirmed diagnosis. Then research can also struggle with the timing of potential risk factors with respect to disease.”

The study was funded by the U.K. Dementia Research Institute. Dr. Dehghan and Dr. Kukull reported no relevant financial relationships.

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

Alzheimer’s disease may have a causal effect on sleep patterns, but disturbed sleep does not appear to cause Alzheimer’s disease, new research suggests.

The causal association between disturbed sleep and Alzheimer’s disease that has been observed in previous studies may have resulted from reverse causation, the researchers noted. The current Mendelian randomization analysis also failed to find a causal relationship between Alzheimer’s disease and major depressive disorder. Future studies should examine the genetic heterogeneity of depression syndromes to test for causal relationships between subtypes of depression with distinct causes and Alzheimer’s disease.

Mendelian randomization compares individuals who have different genetic profiles for a given exposure. “Given that genetic variants are inherited at random, these two groups are comparable, and any differences are not likely to be due to other associated factors,” such as confounding bias, said corresponding author Abbas Dehghan, PhD, reader in cardiometabolic disease epidemiology at Imperial College London. “Moreover, given that genetic information is constant over the lifetime, the chances for reverse causation are small.”

The findings were published online August 19 in Neurology.

Causal questions

Many patients with late-life neurodegenerative disorders such as Alzheimer’s disease have comorbid depression, but whether these two disorders have a causal relationship or common risk factors has been unclear, the investigators noted. Abnormal sleep patterns are symptoms of both depression and Alzheimer’s disease. Abnormal sleep is also associated with cognitive decline and anxiety.

The researchers hypothesized that sleep causally affects major depressive disorder and Alzheimer’s disease but that there is no causal relationship between major depressive disorder and Alzheimer’s disease. They conducted a bidirectional, two-sample Mendelian randomization study to test these hypotheses.

The investigators conducted genomewide association studies (GWASs) using data from the prospective, population-based U.K. Biobank. Sleep phenotypes were measured by self-report or accelerometer. Genetic associations were derived from 403,195 patients for chronotype, 237,627 patients for insomnia, 446,118 people for sleep duration, and 85,670 people for accelerometer-derived phenotypes.

Two binary variables from sleep duration were derived: short sleep (duration of less than 7 hours) and long sleep (duration of 9 or more hours). A sleep episode was defined as a period of at least 5 minutes with a change on the dorsal-ventral axis of less than 5 degrees. The durations of all sleep episodes were added to calculate total sleep duration.

Major depressive disorder was diagnosed clinically in accordance with DSM-IV criteria. Genetic associations were derived from 9,240 case patients and 9,519 control participants. Alzheimer’s disease was diagnosed on the basis of physician examination or autopsy results. Genetic associations were obtained from a meta-analysis of GWAS on participants of European ancestry in the International Genomics of Alzheimer’s Project, which included 21,982 case patients and 41,944 control participants.

More risk factor research needed

Results showed no causal relationships between sleep-related phenotypes and major depressive disorder in either direction. Causal relationships between major depressive disorder and Alzheimer’s disease were found in both directions, but neither was statistically significant.

A genetically higher risk for Alzheimer’s disease was associated with being a “morning person,” being at decreased risk for insomnia, having shorter sleep duration on self-report and accelerometer, having decreased likelihood of reporting long sleep, having an earlier timing of the least active 5 hours, and having a smaller number of sleep episodes. However, no analysis supported a causal effect of sleep-related phenotypes on risk for Alzheimer’s disease.

Because APOE4 can influence disease processes that may contribute to Alzheimer’s disease risk, the investigators also conducted a sensitivity analysis that excluded APOE single-nucleotide polymorphisms. In this analysis, the causal associations of Alzheimer’s disease with self-reported and accelerometer-based sleep duration were not significant. The sensitivity analysis did support the other causal associations between Alzheimer’s disease and sleep phenotypes, however.

The causal associations between major depressive disorder and Alzheimer’s disease observed in other studies may have been the result of confounding, and the participants may have had other associated characteristics that put them at risk for the disease, said Dr. Dehghan. Furthermore, the previous studies considered various sleep phenotypes together, whereas in the current study, the investigators examined them separately.

The results suggest that preclinical and clinical Alzheimer’s disease may affect sleep phenotypes differently. Sleep management thus could be an important approach to improving quality of life for patients with Alzheimer’s disease, the researchers wrote.

“Our study indicates that depression and sleep disorders are not likely to be a causal factor for Alzheimer’s disease,” Dr. Dehghan said. “We need to search for other risk factors for the prevention of Alzheimer’s disease.”

Several strengths, lacks details

Walter A. Kukull, PhD, professor of epidemiology and director of the National Alzheimer’s Coordinating Center at the University of Washington, Seattle, noted that the investigators appear to have implemented their chosen methods of causal association analysis well. “They attempted to examine the direction of the causal arrow for risk factors … and that is a step usually not well examined in other studies.”

He added that the collection of objective measures, such as of sleep, is another strength of the study.

However, “the common weakness of the basic GWAS sample is that clinical symptomatology determined Alzheimer’s disease diagnosis. Thus, asymptomatic or very mildly symptomatic persons with Alzheimer’s disease pathology in their brains were likely included among normal controls,” said Dr. Kukull, who was not involved with the research.

Because of an apparent lack of biomarker data, patients who had been diagnosed with Alzheimer’s disease may in fact have had a different form of dementia. Given the nature of their data, the investigators could have done little to compensate for these possibilities, Dr. Kukull added. In addition, the article lacks details that would improve the interpretation of the results.

“Timing is everything with regard to potential associations between risk factor and outcome,” Dr. Kukull said. “With the exceptions of genes, it would be nice to know more about the timing of risk factors’ onset and Alzheimer’s disease onset.”

Still, the results indicate potential areas of future study, he noted. “Primarily, further research must address the question of pathological onset of disease and misclassification of diagnosis in both cases and controls due to lack of biomarker-confirmed diagnosis. Then research can also struggle with the timing of potential risk factors with respect to disease.”

The study was funded by the U.K. Dementia Research Institute. Dr. Dehghan and Dr. Kukull reported no relevant financial relationships.

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

Alzheimer’s disease may have a causal effect on sleep patterns, but disturbed sleep does not appear to cause Alzheimer’s disease, new research suggests.

The causal association between disturbed sleep and Alzheimer’s disease that has been observed in previous studies may have resulted from reverse causation, the researchers noted. The current Mendelian randomization analysis also failed to find a causal relationship between Alzheimer’s disease and major depressive disorder. Future studies should examine the genetic heterogeneity of depression syndromes to test for causal relationships between subtypes of depression with distinct causes and Alzheimer’s disease.

Mendelian randomization compares individuals who have different genetic profiles for a given exposure. “Given that genetic variants are inherited at random, these two groups are comparable, and any differences are not likely to be due to other associated factors,” such as confounding bias, said corresponding author Abbas Dehghan, PhD, reader in cardiometabolic disease epidemiology at Imperial College London. “Moreover, given that genetic information is constant over the lifetime, the chances for reverse causation are small.”

The findings were published online August 19 in Neurology.

Causal questions

Many patients with late-life neurodegenerative disorders such as Alzheimer’s disease have comorbid depression, but whether these two disorders have a causal relationship or common risk factors has been unclear, the investigators noted. Abnormal sleep patterns are symptoms of both depression and Alzheimer’s disease. Abnormal sleep is also associated with cognitive decline and anxiety.

The researchers hypothesized that sleep causally affects major depressive disorder and Alzheimer’s disease but that there is no causal relationship between major depressive disorder and Alzheimer’s disease. They conducted a bidirectional, two-sample Mendelian randomization study to test these hypotheses.

The investigators conducted genomewide association studies (GWASs) using data from the prospective, population-based U.K. Biobank. Sleep phenotypes were measured by self-report or accelerometer. Genetic associations were derived from 403,195 patients for chronotype, 237,627 patients for insomnia, 446,118 people for sleep duration, and 85,670 people for accelerometer-derived phenotypes.

Two binary variables from sleep duration were derived: short sleep (duration of less than 7 hours) and long sleep (duration of 9 or more hours). A sleep episode was defined as a period of at least 5 minutes with a change on the dorsal-ventral axis of less than 5 degrees. The durations of all sleep episodes were added to calculate total sleep duration.

Major depressive disorder was diagnosed clinically in accordance with DSM-IV criteria. Genetic associations were derived from 9,240 case patients and 9,519 control participants. Alzheimer’s disease was diagnosed on the basis of physician examination or autopsy results. Genetic associations were obtained from a meta-analysis of GWAS on participants of European ancestry in the International Genomics of Alzheimer’s Project, which included 21,982 case patients and 41,944 control participants.

More risk factor research needed

Results showed no causal relationships between sleep-related phenotypes and major depressive disorder in either direction. Causal relationships between major depressive disorder and Alzheimer’s disease were found in both directions, but neither was statistically significant.

A genetically higher risk for Alzheimer’s disease was associated with being a “morning person,” being at decreased risk for insomnia, having shorter sleep duration on self-report and accelerometer, having decreased likelihood of reporting long sleep, having an earlier timing of the least active 5 hours, and having a smaller number of sleep episodes. However, no analysis supported a causal effect of sleep-related phenotypes on risk for Alzheimer’s disease.

Because APOE4 can influence disease processes that may contribute to Alzheimer’s disease risk, the investigators also conducted a sensitivity analysis that excluded APOE single-nucleotide polymorphisms. In this analysis, the causal associations of Alzheimer’s disease with self-reported and accelerometer-based sleep duration were not significant. The sensitivity analysis did support the other causal associations between Alzheimer’s disease and sleep phenotypes, however.

The causal associations between major depressive disorder and Alzheimer’s disease observed in other studies may have been the result of confounding, and the participants may have had other associated characteristics that put them at risk for the disease, said Dr. Dehghan. Furthermore, the previous studies considered various sleep phenotypes together, whereas in the current study, the investigators examined them separately.

The results suggest that preclinical and clinical Alzheimer’s disease may affect sleep phenotypes differently. Sleep management thus could be an important approach to improving quality of life for patients with Alzheimer’s disease, the researchers wrote.

“Our study indicates that depression and sleep disorders are not likely to be a causal factor for Alzheimer’s disease,” Dr. Dehghan said. “We need to search for other risk factors for the prevention of Alzheimer’s disease.”

Several strengths, lacks details

Walter A. Kukull, PhD, professor of epidemiology and director of the National Alzheimer’s Coordinating Center at the University of Washington, Seattle, noted that the investigators appear to have implemented their chosen methods of causal association analysis well. “They attempted to examine the direction of the causal arrow for risk factors … and that is a step usually not well examined in other studies.”

He added that the collection of objective measures, such as of sleep, is another strength of the study.

However, “the common weakness of the basic GWAS sample is that clinical symptomatology determined Alzheimer’s disease diagnosis. Thus, asymptomatic or very mildly symptomatic persons with Alzheimer’s disease pathology in their brains were likely included among normal controls,” said Dr. Kukull, who was not involved with the research.

Because of an apparent lack of biomarker data, patients who had been diagnosed with Alzheimer’s disease may in fact have had a different form of dementia. Given the nature of their data, the investigators could have done little to compensate for these possibilities, Dr. Kukull added. In addition, the article lacks details that would improve the interpretation of the results.

“Timing is everything with regard to potential associations between risk factor and outcome,” Dr. Kukull said. “With the exceptions of genes, it would be nice to know more about the timing of risk factors’ onset and Alzheimer’s disease onset.”

Still, the results indicate potential areas of future study, he noted. “Primarily, further research must address the question of pathological onset of disease and misclassification of diagnosis in both cases and controls due to lack of biomarker-confirmed diagnosis. Then research can also struggle with the timing of potential risk factors with respect to disease.”

The study was funded by the U.K. Dementia Research Institute. Dr. Dehghan and Dr. Kukull reported no relevant financial relationships.

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

The US Food and Drug Administration has approved phase one clinical trials for a synthetic cannabinoid drug designed to treat acute respiratory distress syndrome (ARDS), a life-threatening lung condition which may occur in severe cases of the novel coronavirus, Forbes reported.

ARDS can be triggered by over-creation of cytokines, proteins which tell the body to produce more inflammation, Forbes said.

The drug going to clinical trials, ARDS-003, would “dampen the cytokine release” and prevent development of ARDS, Tetra Bio-Pharma company CEO and chief regulatory officer Guy Chamberland, MD, said in a news release.

Consequences of ARDS include scarring of the lungs and organ injury caused by the decrease in blood to the tissue, the release said.

“The FDA repeatedly stated that they want clinical trials for COVID-19 to begin as soon as possible, as long as they meet regulatory requirements,” the news release said. “The medical community is in urgent need of drugs that can reduce the strength and duration of the severe inflammation. It is anticipated that this type of new drug would favorably impact health care and possibly reduce the negative health outcomes post infection.”

ARDS-003 works by binding to CB2 receptors, one of two main receptors in the endocannabinoid system which modulate inflammation and cytokine activity, Forbes said. CB2 receptors don’t bring on a psychoactive high.

Phase one clinical trials would begin enrolling participants in December to determine if the drug is safe, Chamberland said, according to Forbes.

If phase one is successful, phase two would test the drug on a larger group in the second quarter of 2021 to assess safety and tolerability for people who have COVID-19. 

If phase two is successful, the company may seek emergency authorization through the FDA, Chamberland said.  Phase three would start at the end of 2021.

Tetra Bio-Pharma says it has already contracted with Dalton Pharma Services to manufacture the active pharmaceutical ingredient (API), HU-308, and the finished drug product ARDS-003.
 

This article first appeared on Medscape.com.

The US Food and Drug Administration has approved phase one clinical trials for a synthetic cannabinoid drug designed to treat acute respiratory distress syndrome (ARDS), a life-threatening lung condition which may occur in severe cases of the novel coronavirus, Forbes reported.

ARDS can be triggered by over-creation of cytokines, proteins which tell the body to produce more inflammation, Forbes said.

The drug going to clinical trials, ARDS-003, would “dampen the cytokine release” and prevent development of ARDS, Tetra Bio-Pharma company CEO and chief regulatory officer Guy Chamberland, MD, said in a news release.

Consequences of ARDS include scarring of the lungs and organ injury caused by the decrease in blood to the tissue, the release said.

“The FDA repeatedly stated that they want clinical trials for COVID-19 to begin as soon as possible, as long as they meet regulatory requirements,” the news release said. “The medical community is in urgent need of drugs that can reduce the strength and duration of the severe inflammation. It is anticipated that this type of new drug would favorably impact health care and possibly reduce the negative health outcomes post infection.”

ARDS-003 works by binding to CB2 receptors, one of two main receptors in the endocannabinoid system which modulate inflammation and cytokine activity, Forbes said. CB2 receptors don’t bring on a psychoactive high.

Phase one clinical trials would begin enrolling participants in December to determine if the drug is safe, Chamberland said, according to Forbes.

If phase one is successful, phase two would test the drug on a larger group in the second quarter of 2021 to assess safety and tolerability for people who have COVID-19. 

If phase two is successful, the company may seek emergency authorization through the FDA, Chamberland said.  Phase three would start at the end of 2021.

Tetra Bio-Pharma says it has already contracted with Dalton Pharma Services to manufacture the active pharmaceutical ingredient (API), HU-308, and the finished drug product ARDS-003.
 

This article first appeared on Medscape.com.

The US Food and Drug Administration has approved phase one clinical trials for a synthetic cannabinoid drug designed to treat acute respiratory distress syndrome (ARDS), a life-threatening lung condition which may occur in severe cases of the novel coronavirus, Forbes reported.

ARDS can be triggered by over-creation of cytokines, proteins which tell the body to produce more inflammation, Forbes said.

The drug going to clinical trials, ARDS-003, would “dampen the cytokine release” and prevent development of ARDS, Tetra Bio-Pharma company CEO and chief regulatory officer Guy Chamberland, MD, said in a news release.

Consequences of ARDS include scarring of the lungs and organ injury caused by the decrease in blood to the tissue, the release said.

“The FDA repeatedly stated that they want clinical trials for COVID-19 to begin as soon as possible, as long as they meet regulatory requirements,” the news release said. “The medical community is in urgent need of drugs that can reduce the strength and duration of the severe inflammation. It is anticipated that this type of new drug would favorably impact health care and possibly reduce the negative health outcomes post infection.”

ARDS-003 works by binding to CB2 receptors, one of two main receptors in the endocannabinoid system which modulate inflammation and cytokine activity, Forbes said. CB2 receptors don’t bring on a psychoactive high.

Phase one clinical trials would begin enrolling participants in December to determine if the drug is safe, Chamberland said, according to Forbes.

If phase one is successful, phase two would test the drug on a larger group in the second quarter of 2021 to assess safety and tolerability for people who have COVID-19. 

If phase two is successful, the company may seek emergency authorization through the FDA, Chamberland said.  Phase three would start at the end of 2021.

Tetra Bio-Pharma says it has already contracted with Dalton Pharma Services to manufacture the active pharmaceutical ingredient (API), HU-308, and the finished drug product ARDS-003.
 

This article first appeared on Medscape.com.

Researchers in Hong Kong say they’ve confirmed that a person can be infected with COVID-19 twice.

There have been sporadic accounts on social media sites of people who say they’ve gotten COVID-19 twice. But scientists have been skeptical about that possibility, saying there’s no evidence it happens.

The new proof comes from a 33-year-old man in Hong Kong who first caught COVID-19 in March. He was tested for the coronavirus after he developed a cough, sore throat, fever, and a headache for 3 days. He stayed in the hospital until he twice tested negative for the virus in mid-April.

On Aug. 15, the man returned to Hong Kong from a recent trip to Spain and the United Kingdom, areas that have recently seen a resurgence of COVID-19 cases. At the airport, he was screened for COVID-19 with a test that checks saliva for the virus. He tested positive, but this time, had no symptoms. He was taken to the hospital for monitoring. His viral load – the amount of virus he had in his body – went down over time, suggesting that his immune system was taking care of the intrusion on its own.

The special thing about his case is that each time he was hospitalized, doctors sequenced the genome of the virus that infected him. It was slightly different from one infection to the next, suggesting that the virus had mutated – or changed – in the 4 months between his infections. It also proves that it’s possible for this coronavirus to infect the same person twice.

Experts with the World Health Organization responded to the case at a news briefing.

“What we are learning about infection is that people do develop an immune response. What is not completely clear yet is how strong that immune response is and for how long that immune response lasts,” said Maria Van Kerkhove, PhD, an infectious disease epidemiologist with the World Health Organization in Geneva, Switzerland.

A study on the man’s case is being prepared for publication in the journal Clinical Infectious Diseases. Experts say the finding shouldn’t cause alarm, but it does have important implications for the development of herd immunity and efforts to come up with vaccines and treatments.

“This appears to be pretty clear-cut evidence of reinfection because of sequencing and isolation of two different viruses,” said Gregory Poland, MD, an expert on vaccine development and immunology at the Mayo Clinic in Rochester, Minn. “The big unknown is how often is this happening,” he said. More studies are needed to learn whether this was a rare case or something that is happening often.
 

Past experience guides present

Until we know more, Dr. Poland said, the possibility of getting COVID-19 twice shouldn’t make anyone worry.

This also happens with other kinds of coronaviruses – the ones that cause common colds. Those coronaviruses change slightly each year as they circle the globe, which allows them to keep spreading and causing their more run-of-the-mill kind of misery.

It also happens with seasonal flu. It is the reason people have to get vaccinated against the flu year after year, and why the flu vaccine has to change slightly each year in an effort to keep up with the ever-evolving influenza virus.

“We’ve been making flu vaccines for 80 years, and there are clinical trials happening as we speak to find new and better influenza vaccines,” Dr. Poland said.

There has been other evidence the virus that causes COVID-19 can change this way, too. Researchers at Howard Hughes Medical Center, at Rockefeller University in New York, recently used a key piece of the SARS-CoV-2 virus – the genetic instructions for its spike protein – to repeatedly infect human cells. Scientists watched as each new generation of the virus went on to infect a new batch of cells. Over time, as it copied itself, some of the copies changed their genes to allow them to survive after scientists attacked them with neutralizing antibodies. Those antibodies are among the main weapons used by the immune system to recognize and disable a virus.

Though that study is still a preprint, which means it hasn’t yet been reviewed by outside experts, the authors wrote that their findings suggest the virus can change in ways that help it evade our immune system. If true, they wrote in mid-July, it means reinfection is possible, especially in people who have a weak immune response to the virus the first time they encounter it.
 

Good news

That seems to be true in the case of the man from Hong Kong. When doctors tested his blood to look for antibodies to the virus, they didn’t find any. That could mean that he either had a weak immune response to the virus the first time around, or that the antibodies he made during his first infection diminished over time. But during his second infection, he quickly developed more antibodies, suggesting that the second infection acted a little bit like a booster to fire up his immune system. That’s probably the reason he didn’t have any symptoms the second time, too.

That’s good news, Dr. Poland said. It means our bodies can get better at fighting off the COVID-19 virus and that catching it once means the second time might not be so bad.

But the fact that the virus can change quickly this way does have some impact on the effort to come up with a vaccine that works well.

“I think a potential implication of this is that we will have to give booster doses. The question is how frequently,” Dr. Poland said. That will depend on how fast the virus is changing, and how often reinfection is happening in the real world.

“I’m a little surprised at 4½ months,” Dr. Poland said, referencing the time between the Hong Kong man’s infections. “I’m not surprised by, you know, I got infected last winter and I got infected again this winter,” he said.

It also suggests that immune-based therapies such as convalescent plasma and monoclonal antibodies may be of limited help over time, since the virus might be changing in ways that help it outsmart those treatments.

Convalescent plasma is essentially a concentrated dose of antibodies from people who have recovered from a COVID-19 infection. As the virus changes, the antibodies in that plasma may not work as well for future infections.

Drug companies have learned to harness the power of monoclonal antibodies as powerful treatments against cancer and other diseases. Monoclonal antibodies, which are mass-produced in a lab, mimic the body’s natural defenses against a pathogen. Just like the virus can become resistant to natural immunity, it can change in ways that help it outsmart lab-created treatments. Some drug companies that are developing monoclonal antibodies to fight COVID-19 have already prepared for that possibility by making antibody cocktails that are designed to disable the virus by locking onto it in different places, which may help prevent it from developing resistance to those therapies.

“We have a lot to learn,” Dr. Poland said. “Now that the proof of principle has been established, and I would say it has with this man, and with our knowledge of seasonal coronaviruses, we need to look more aggressively to define how often this occurs.”

A version of this article originally appeared on WebMD.com.

Researchers in Hong Kong say they’ve confirmed that a person can be infected with COVID-19 twice.

There have been sporadic accounts on social media sites of people who say they’ve gotten COVID-19 twice. But scientists have been skeptical about that possibility, saying there’s no evidence it happens.

The new proof comes from a 33-year-old man in Hong Kong who first caught COVID-19 in March. He was tested for the coronavirus after he developed a cough, sore throat, fever, and a headache for 3 days. He stayed in the hospital until he twice tested negative for the virus in mid-April.

On Aug. 15, the man returned to Hong Kong from a recent trip to Spain and the United Kingdom, areas that have recently seen a resurgence of COVID-19 cases. At the airport, he was screened for COVID-19 with a test that checks saliva for the virus. He tested positive, but this time, had no symptoms. He was taken to the hospital for monitoring. His viral load – the amount of virus he had in his body – went down over time, suggesting that his immune system was taking care of the intrusion on its own.

The special thing about his case is that each time he was hospitalized, doctors sequenced the genome of the virus that infected him. It was slightly different from one infection to the next, suggesting that the virus had mutated – or changed – in the 4 months between his infections. It also proves that it’s possible for this coronavirus to infect the same person twice.

Experts with the World Health Organization responded to the case at a news briefing.

“What we are learning about infection is that people do develop an immune response. What is not completely clear yet is how strong that immune response is and for how long that immune response lasts,” said Maria Van Kerkhove, PhD, an infectious disease epidemiologist with the World Health Organization in Geneva, Switzerland.

A study on the man’s case is being prepared for publication in the journal Clinical Infectious Diseases. Experts say the finding shouldn’t cause alarm, but it does have important implications for the development of herd immunity and efforts to come up with vaccines and treatments.

“This appears to be pretty clear-cut evidence of reinfection because of sequencing and isolation of two different viruses,” said Gregory Poland, MD, an expert on vaccine development and immunology at the Mayo Clinic in Rochester, Minn. “The big unknown is how often is this happening,” he said. More studies are needed to learn whether this was a rare case or something that is happening often.
 

Past experience guides present

Until we know more, Dr. Poland said, the possibility of getting COVID-19 twice shouldn’t make anyone worry.

This also happens with other kinds of coronaviruses – the ones that cause common colds. Those coronaviruses change slightly each year as they circle the globe, which allows them to keep spreading and causing their more run-of-the-mill kind of misery.

It also happens with seasonal flu. It is the reason people have to get vaccinated against the flu year after year, and why the flu vaccine has to change slightly each year in an effort to keep up with the ever-evolving influenza virus.

“We’ve been making flu vaccines for 80 years, and there are clinical trials happening as we speak to find new and better influenza vaccines,” Dr. Poland said.

There has been other evidence the virus that causes COVID-19 can change this way, too. Researchers at Howard Hughes Medical Center, at Rockefeller University in New York, recently used a key piece of the SARS-CoV-2 virus – the genetic instructions for its spike protein – to repeatedly infect human cells. Scientists watched as each new generation of the virus went on to infect a new batch of cells. Over time, as it copied itself, some of the copies changed their genes to allow them to survive after scientists attacked them with neutralizing antibodies. Those antibodies are among the main weapons used by the immune system to recognize and disable a virus.

Though that study is still a preprint, which means it hasn’t yet been reviewed by outside experts, the authors wrote that their findings suggest the virus can change in ways that help it evade our immune system. If true, they wrote in mid-July, it means reinfection is possible, especially in people who have a weak immune response to the virus the first time they encounter it.
 

Good news

That seems to be true in the case of the man from Hong Kong. When doctors tested his blood to look for antibodies to the virus, they didn’t find any. That could mean that he either had a weak immune response to the virus the first time around, or that the antibodies he made during his first infection diminished over time. But during his second infection, he quickly developed more antibodies, suggesting that the second infection acted a little bit like a booster to fire up his immune system. That’s probably the reason he didn’t have any symptoms the second time, too.

That’s good news, Dr. Poland said. It means our bodies can get better at fighting off the COVID-19 virus and that catching it once means the second time might not be so bad.

But the fact that the virus can change quickly this way does have some impact on the effort to come up with a vaccine that works well.

“I think a potential implication of this is that we will have to give booster doses. The question is how frequently,” Dr. Poland said. That will depend on how fast the virus is changing, and how often reinfection is happening in the real world.

“I’m a little surprised at 4½ months,” Dr. Poland said, referencing the time between the Hong Kong man’s infections. “I’m not surprised by, you know, I got infected last winter and I got infected again this winter,” he said.

It also suggests that immune-based therapies such as convalescent plasma and monoclonal antibodies may be of limited help over time, since the virus might be changing in ways that help it outsmart those treatments.

Convalescent plasma is essentially a concentrated dose of antibodies from people who have recovered from a COVID-19 infection. As the virus changes, the antibodies in that plasma may not work as well for future infections.

Drug companies have learned to harness the power of monoclonal antibodies as powerful treatments against cancer and other diseases. Monoclonal antibodies, which are mass-produced in a lab, mimic the body’s natural defenses against a pathogen. Just like the virus can become resistant to natural immunity, it can change in ways that help it outsmart lab-created treatments. Some drug companies that are developing monoclonal antibodies to fight COVID-19 have already prepared for that possibility by making antibody cocktails that are designed to disable the virus by locking onto it in different places, which may help prevent it from developing resistance to those therapies.

“We have a lot to learn,” Dr. Poland said. “Now that the proof of principle has been established, and I would say it has with this man, and with our knowledge of seasonal coronaviruses, we need to look more aggressively to define how often this occurs.”

A version of this article originally appeared on WebMD.com.

Researchers in Hong Kong say they’ve confirmed that a person can be infected with COVID-19 twice.

There have been sporadic accounts on social media sites of people who say they’ve gotten COVID-19 twice. But scientists have been skeptical about that possibility, saying there’s no evidence it happens.

The new proof comes from a 33-year-old man in Hong Kong who first caught COVID-19 in March. He was tested for the coronavirus after he developed a cough, sore throat, fever, and a headache for 3 days. He stayed in the hospital until he twice tested negative for the virus in mid-April.

On Aug. 15, the man returned to Hong Kong from a recent trip to Spain and the United Kingdom, areas that have recently seen a resurgence of COVID-19 cases. At the airport, he was screened for COVID-19 with a test that checks saliva for the virus. He tested positive, but this time, had no symptoms. He was taken to the hospital for monitoring. His viral load – the amount of virus he had in his body – went down over time, suggesting that his immune system was taking care of the intrusion on its own.

The special thing about his case is that each time he was hospitalized, doctors sequenced the genome of the virus that infected him. It was slightly different from one infection to the next, suggesting that the virus had mutated – or changed – in the 4 months between his infections. It also proves that it’s possible for this coronavirus to infect the same person twice.

Experts with the World Health Organization responded to the case at a news briefing.

“What we are learning about infection is that people do develop an immune response. What is not completely clear yet is how strong that immune response is and for how long that immune response lasts,” said Maria Van Kerkhove, PhD, an infectious disease epidemiologist with the World Health Organization in Geneva, Switzerland.

A study on the man’s case is being prepared for publication in the journal Clinical Infectious Diseases. Experts say the finding shouldn’t cause alarm, but it does have important implications for the development of herd immunity and efforts to come up with vaccines and treatments.

“This appears to be pretty clear-cut evidence of reinfection because of sequencing and isolation of two different viruses,” said Gregory Poland, MD, an expert on vaccine development and immunology at the Mayo Clinic in Rochester, Minn. “The big unknown is how often is this happening,” he said. More studies are needed to learn whether this was a rare case or something that is happening often.
 

Past experience guides present

Until we know more, Dr. Poland said, the possibility of getting COVID-19 twice shouldn’t make anyone worry.

This also happens with other kinds of coronaviruses – the ones that cause common colds. Those coronaviruses change slightly each year as they circle the globe, which allows them to keep spreading and causing their more run-of-the-mill kind of misery.

It also happens with seasonal flu. It is the reason people have to get vaccinated against the flu year after year, and why the flu vaccine has to change slightly each year in an effort to keep up with the ever-evolving influenza virus.

“We’ve been making flu vaccines for 80 years, and there are clinical trials happening as we speak to find new and better influenza vaccines,” Dr. Poland said.

There has been other evidence the virus that causes COVID-19 can change this way, too. Researchers at Howard Hughes Medical Center, at Rockefeller University in New York, recently used a key piece of the SARS-CoV-2 virus – the genetic instructions for its spike protein – to repeatedly infect human cells. Scientists watched as each new generation of the virus went on to infect a new batch of cells. Over time, as it copied itself, some of the copies changed their genes to allow them to survive after scientists attacked them with neutralizing antibodies. Those antibodies are among the main weapons used by the immune system to recognize and disable a virus.

Though that study is still a preprint, which means it hasn’t yet been reviewed by outside experts, the authors wrote that their findings suggest the virus can change in ways that help it evade our immune system. If true, they wrote in mid-July, it means reinfection is possible, especially in people who have a weak immune response to the virus the first time they encounter it.
 

Good news

That seems to be true in the case of the man from Hong Kong. When doctors tested his blood to look for antibodies to the virus, they didn’t find any. That could mean that he either had a weak immune response to the virus the first time around, or that the antibodies he made during his first infection diminished over time. But during his second infection, he quickly developed more antibodies, suggesting that the second infection acted a little bit like a booster to fire up his immune system. That’s probably the reason he didn’t have any symptoms the second time, too.

That’s good news, Dr. Poland said. It means our bodies can get better at fighting off the COVID-19 virus and that catching it once means the second time might not be so bad.

But the fact that the virus can change quickly this way does have some impact on the effort to come up with a vaccine that works well.

“I think a potential implication of this is that we will have to give booster doses. The question is how frequently,” Dr. Poland said. That will depend on how fast the virus is changing, and how often reinfection is happening in the real world.

“I’m a little surprised at 4½ months,” Dr. Poland said, referencing the time between the Hong Kong man’s infections. “I’m not surprised by, you know, I got infected last winter and I got infected again this winter,” he said.

It also suggests that immune-based therapies such as convalescent plasma and monoclonal antibodies may be of limited help over time, since the virus might be changing in ways that help it outsmart those treatments.

Convalescent plasma is essentially a concentrated dose of antibodies from people who have recovered from a COVID-19 infection. As the virus changes, the antibodies in that plasma may not work as well for future infections.

Drug companies have learned to harness the power of monoclonal antibodies as powerful treatments against cancer and other diseases. Monoclonal antibodies, which are mass-produced in a lab, mimic the body’s natural defenses against a pathogen. Just like the virus can become resistant to natural immunity, it can change in ways that help it outsmart lab-created treatments. Some drug companies that are developing monoclonal antibodies to fight COVID-19 have already prepared for that possibility by making antibody cocktails that are designed to disable the virus by locking onto it in different places, which may help prevent it from developing resistance to those therapies.

“We have a lot to learn,” Dr. Poland said. “Now that the proof of principle has been established, and I would say it has with this man, and with our knowledge of seasonal coronaviruses, we need to look more aggressively to define how often this occurs.”

A version of this article originally appeared on WebMD.com.

The persistence of long-term symptoms in some individuals with COVID-19 illness has opened up a new line of research into the mechanisms underlying myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and other chronic postviral illnesses.

Some patients who had COVID-19 continue to have symptoms weeks to months later, even after they no longer test positive for the virus. In two recent reports – one published in JAMA in July and another published in Morbidity and Mortality Weekly Report in August – chronic fatigue was listed as the top symptom among individuals still feeling unwell beyond 2 weeks after COVID-19 onset.

Although some of the reported persistent symptoms appear specific to SARS-CoV-2 – such as cough, chest pain, and dyspnea – others overlap with the diagnostic criteria for ME/CFS, which is defined by substantial, profound fatigue for at least 6 months, postexertional malaise, unrefreshing sleep, and one or both of orthostatic intolerance and/or cognitive impairment. Although the etiology of ME/CFS is unclear, the condition commonly arises following a viral illness.

At the virtual meeting of the International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis August 21, the opening session was devoted to research documenting the extent to which COVID-19 survivors subsequently meet ME/CFS criteria, and to exploring underlying mechanisms.

“It offers a lot of opportunities for us to study potentially early ME/CFS and how it develops, but in addition, a lot of the research that has been done on ME/CFS may also provide answers for COVID-19,” IACFS/ME vice president Lily Chu, MD, said in an interview.
 

A hint from the SARS outbreak

This isn’t the first time researchers have seen a possible link between a coronavirus and ME/CFS, Harvey Moldofsky, MD, told attendees. To illustrate that point, Dr. Moldofsky, of the department of psychiatry (emeritus) at the University of Toronto, reviewed data from a previously published case-controlled study, which included 22 health care workers who had been infected in 2003 with SARS-CoV-1 and continued to report chronic fatigue, musculoskeletal pain, and disturbed and unrefreshing sleep with EEG-documented sleep disturbances 1-3 years following the illness. None had been able to return to work by 1 year.

“We’re looking at similar symptoms now” among survivors of COVID-19, Dr. Moldofsky said. “[T]he key issue is that we have no idea of its prevalence. … We need epidemiologic studies.”
 

Distinguishing ME/CFS from other post–COVID-19 symptoms

Not everyone who has persistent symptoms after COVID-19 will develop ME/CFS, and distinguishing between cases may be important.

Clinically, Dr. Chu said, one way to assess whether a patient with persistent COVID-19 symptoms might be progressing to ME/CFS is to ask him or her specifically about the level of fatigue following physical exertion and the timing of any fatigue. With ME/CFS, postexertional malaise often involves a dramatic exacerbation of symptoms such as fatigue, pain, and cognitive impairment a day or 2 after exertion rather than immediately following it. In contrast, shortness of breath during exertion isn’t typical of ME/CFS.

Objective measures of ME/CFS include low natural killer cell function (the test can be ordered from commercial labs but requires rapid transport of the blood sample), and autonomic dysfunction assessed by a tilt-table test.

While there is currently no cure for ME/CFS, diagnosing it allows for the patient to be taught “pacing” in which the person conserves his or her energy by balancing activity with rest. “That type of behavioral technique is valuable for everyone who suffers from a chronic disease with fatigue. It can help them be more functional,” Dr. Chu said.

If a patient appears to be exhibiting signs of ME/CFS, “don’t wait until they hit the 6-month mark to start helping them manage their symptoms,” she said. “Teaching pacing to COVID-19 patients who have a lot of fatigue isn’t going to harm them. As they get better they’re going to just naturally do more. But if they do have ME/CFS, [pacing] stresses their system less, since the data seem to be pointing to deficiencies in producing energy.”
 

Will COVID-19 unleash a new wave of ME/CFS patients?

Much of the session at the virtual meeting was devoted to ongoing studies. For example, Leonard Jason, PhD, of the Center for Community Research at DePaul University, Chicago, described a prospective study launched in 2014 that looked at risk factors for developing ME/CFS in college students who contracted infectious mononucleosis as a result of Epstein-Barr virus. Now, his team is also following students from the same cohort who develop COVID-19.

Because the study included collection of baseline biological samples, the results could help reveal predisposing factors associated with long-term illness from either virus.

Another project, funded by the Open Medicine Foundation, will follow patients who are discharged from the ICU following severe COVID-19 illness. Blood, urine, and cerebrospinal fluid will be collected from those with persistent symptoms at 6 months, along with questionnaire data. At 18-24 months, those who continue to report symptoms will undergo more intensive evaluation using genomics, metabolomics, and proteomics.

“We’re taking advantage of this horrible situation, hoping to understand how a serious viral infection might lead to ME/CFS,” said lead investigator Ronald Tompkins, MD, ScD, chief medical officer at the Open Medicine Foundation and a faculty member at Harvard Medical School, Boston. The results, he said, “might give us insight into potential drug targets or biomarkers useful for prevention and treatment strategies.”

Meanwhile, Sadie Whittaker, PhD, head of the Solve ME/CFS initiative, described her organization’s new plan to use their registry to prospectively track the impact of COVID-19 on people with ME/CFS. 

She noted that they’ve also teamed up with “long-COVID” communities including Body Politic. “Our goal is to form a coalition to study together or at least harmonize data … and understand what’s going on through the power of bigger sample sizes,” Dr. Whittaker said.

None of the speakers disclosed relevant financial relationships.

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

The persistence of long-term symptoms in some individuals with COVID-19 illness has opened up a new line of research into the mechanisms underlying myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and other chronic postviral illnesses.

Some patients who had COVID-19 continue to have symptoms weeks to months later, even after they no longer test positive for the virus. In two recent reports – one published in JAMA in July and another published in Morbidity and Mortality Weekly Report in August – chronic fatigue was listed as the top symptom among individuals still feeling unwell beyond 2 weeks after COVID-19 onset.

Although some of the reported persistent symptoms appear specific to SARS-CoV-2 – such as cough, chest pain, and dyspnea – others overlap with the diagnostic criteria for ME/CFS, which is defined by substantial, profound fatigue for at least 6 months, postexertional malaise, unrefreshing sleep, and one or both of orthostatic intolerance and/or cognitive impairment. Although the etiology of ME/CFS is unclear, the condition commonly arises following a viral illness.

At the virtual meeting of the International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis August 21, the opening session was devoted to research documenting the extent to which COVID-19 survivors subsequently meet ME/CFS criteria, and to exploring underlying mechanisms.

“It offers a lot of opportunities for us to study potentially early ME/CFS and how it develops, but in addition, a lot of the research that has been done on ME/CFS may also provide answers for COVID-19,” IACFS/ME vice president Lily Chu, MD, said in an interview.
 

A hint from the SARS outbreak

This isn’t the first time researchers have seen a possible link between a coronavirus and ME/CFS, Harvey Moldofsky, MD, told attendees. To illustrate that point, Dr. Moldofsky, of the department of psychiatry (emeritus) at the University of Toronto, reviewed data from a previously published case-controlled study, which included 22 health care workers who had been infected in 2003 with SARS-CoV-1 and continued to report chronic fatigue, musculoskeletal pain, and disturbed and unrefreshing sleep with EEG-documented sleep disturbances 1-3 years following the illness. None had been able to return to work by 1 year.

“We’re looking at similar symptoms now” among survivors of COVID-19, Dr. Moldofsky said. “[T]he key issue is that we have no idea of its prevalence. … We need epidemiologic studies.”
 

Distinguishing ME/CFS from other post–COVID-19 symptoms

Not everyone who has persistent symptoms after COVID-19 will develop ME/CFS, and distinguishing between cases may be important.

Clinically, Dr. Chu said, one way to assess whether a patient with persistent COVID-19 symptoms might be progressing to ME/CFS is to ask him or her specifically about the level of fatigue following physical exertion and the timing of any fatigue. With ME/CFS, postexertional malaise often involves a dramatic exacerbation of symptoms such as fatigue, pain, and cognitive impairment a day or 2 after exertion rather than immediately following it. In contrast, shortness of breath during exertion isn’t typical of ME/CFS.

Objective measures of ME/CFS include low natural killer cell function (the test can be ordered from commercial labs but requires rapid transport of the blood sample), and autonomic dysfunction assessed by a tilt-table test.

While there is currently no cure for ME/CFS, diagnosing it allows for the patient to be taught “pacing” in which the person conserves his or her energy by balancing activity with rest. “That type of behavioral technique is valuable for everyone who suffers from a chronic disease with fatigue. It can help them be more functional,” Dr. Chu said.

If a patient appears to be exhibiting signs of ME/CFS, “don’t wait until they hit the 6-month mark to start helping them manage their symptoms,” she said. “Teaching pacing to COVID-19 patients who have a lot of fatigue isn’t going to harm them. As they get better they’re going to just naturally do more. But if they do have ME/CFS, [pacing] stresses their system less, since the data seem to be pointing to deficiencies in producing energy.”
 

Will COVID-19 unleash a new wave of ME/CFS patients?

Much of the session at the virtual meeting was devoted to ongoing studies. For example, Leonard Jason, PhD, of the Center for Community Research at DePaul University, Chicago, described a prospective study launched in 2014 that looked at risk factors for developing ME/CFS in college students who contracted infectious mononucleosis as a result of Epstein-Barr virus. Now, his team is also following students from the same cohort who develop COVID-19.

Because the study included collection of baseline biological samples, the results could help reveal predisposing factors associated with long-term illness from either virus.

Another project, funded by the Open Medicine Foundation, will follow patients who are discharged from the ICU following severe COVID-19 illness. Blood, urine, and cerebrospinal fluid will be collected from those with persistent symptoms at 6 months, along with questionnaire data. At 18-24 months, those who continue to report symptoms will undergo more intensive evaluation using genomics, metabolomics, and proteomics.

“We’re taking advantage of this horrible situation, hoping to understand how a serious viral infection might lead to ME/CFS,” said lead investigator Ronald Tompkins, MD, ScD, chief medical officer at the Open Medicine Foundation and a faculty member at Harvard Medical School, Boston. The results, he said, “might give us insight into potential drug targets or biomarkers useful for prevention and treatment strategies.”

Meanwhile, Sadie Whittaker, PhD, head of the Solve ME/CFS initiative, described her organization’s new plan to use their registry to prospectively track the impact of COVID-19 on people with ME/CFS. 

She noted that they’ve also teamed up with “long-COVID” communities including Body Politic. “Our goal is to form a coalition to study together or at least harmonize data … and understand what’s going on through the power of bigger sample sizes,” Dr. Whittaker said.

None of the speakers disclosed relevant financial relationships.

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

The persistence of long-term symptoms in some individuals with COVID-19 illness has opened up a new line of research into the mechanisms underlying myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and other chronic postviral illnesses.

Some patients who had COVID-19 continue to have symptoms weeks to months later, even after they no longer test positive for the virus. In two recent reports – one published in JAMA in July and another published in Morbidity and Mortality Weekly Report in August – chronic fatigue was listed as the top symptom among individuals still feeling unwell beyond 2 weeks after COVID-19 onset.

Although some of the reported persistent symptoms appear specific to SARS-CoV-2 – such as cough, chest pain, and dyspnea – others overlap with the diagnostic criteria for ME/CFS, which is defined by substantial, profound fatigue for at least 6 months, postexertional malaise, unrefreshing sleep, and one or both of orthostatic intolerance and/or cognitive impairment. Although the etiology of ME/CFS is unclear, the condition commonly arises following a viral illness.

At the virtual meeting of the International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis August 21, the opening session was devoted to research documenting the extent to which COVID-19 survivors subsequently meet ME/CFS criteria, and to exploring underlying mechanisms.

“It offers a lot of opportunities for us to study potentially early ME/CFS and how it develops, but in addition, a lot of the research that has been done on ME/CFS may also provide answers for COVID-19,” IACFS/ME vice president Lily Chu, MD, said in an interview.
 

A hint from the SARS outbreak

This isn’t the first time researchers have seen a possible link between a coronavirus and ME/CFS, Harvey Moldofsky, MD, told attendees. To illustrate that point, Dr. Moldofsky, of the department of psychiatry (emeritus) at the University of Toronto, reviewed data from a previously published case-controlled study, which included 22 health care workers who had been infected in 2003 with SARS-CoV-1 and continued to report chronic fatigue, musculoskeletal pain, and disturbed and unrefreshing sleep with EEG-documented sleep disturbances 1-3 years following the illness. None had been able to return to work by 1 year.

“We’re looking at similar symptoms now” among survivors of COVID-19, Dr. Moldofsky said. “[T]he key issue is that we have no idea of its prevalence. … We need epidemiologic studies.”
 

Distinguishing ME/CFS from other post–COVID-19 symptoms

Not everyone who has persistent symptoms after COVID-19 will develop ME/CFS, and distinguishing between cases may be important.

Clinically, Dr. Chu said, one way to assess whether a patient with persistent COVID-19 symptoms might be progressing to ME/CFS is to ask him or her specifically about the level of fatigue following physical exertion and the timing of any fatigue. With ME/CFS, postexertional malaise often involves a dramatic exacerbation of symptoms such as fatigue, pain, and cognitive impairment a day or 2 after exertion rather than immediately following it. In contrast, shortness of breath during exertion isn’t typical of ME/CFS.

Objective measures of ME/CFS include low natural killer cell function (the test can be ordered from commercial labs but requires rapid transport of the blood sample), and autonomic dysfunction assessed by a tilt-table test.

While there is currently no cure for ME/CFS, diagnosing it allows for the patient to be taught “pacing” in which the person conserves his or her energy by balancing activity with rest. “That type of behavioral technique is valuable for everyone who suffers from a chronic disease with fatigue. It can help them be more functional,” Dr. Chu said.

If a patient appears to be exhibiting signs of ME/CFS, “don’t wait until they hit the 6-month mark to start helping them manage their symptoms,” she said. “Teaching pacing to COVID-19 patients who have a lot of fatigue isn’t going to harm them. As they get better they’re going to just naturally do more. But if they do have ME/CFS, [pacing] stresses their system less, since the data seem to be pointing to deficiencies in producing energy.”
 

Will COVID-19 unleash a new wave of ME/CFS patients?

Much of the session at the virtual meeting was devoted to ongoing studies. For example, Leonard Jason, PhD, of the Center for Community Research at DePaul University, Chicago, described a prospective study launched in 2014 that looked at risk factors for developing ME/CFS in college students who contracted infectious mononucleosis as a result of Epstein-Barr virus. Now, his team is also following students from the same cohort who develop COVID-19.

Because the study included collection of baseline biological samples, the results could help reveal predisposing factors associated with long-term illness from either virus.

Another project, funded by the Open Medicine Foundation, will follow patients who are discharged from the ICU following severe COVID-19 illness. Blood, urine, and cerebrospinal fluid will be collected from those with persistent symptoms at 6 months, along with questionnaire data. At 18-24 months, those who continue to report symptoms will undergo more intensive evaluation using genomics, metabolomics, and proteomics.

“We’re taking advantage of this horrible situation, hoping to understand how a serious viral infection might lead to ME/CFS,” said lead investigator Ronald Tompkins, MD, ScD, chief medical officer at the Open Medicine Foundation and a faculty member at Harvard Medical School, Boston. The results, he said, “might give us insight into potential drug targets or biomarkers useful for prevention and treatment strategies.”

Meanwhile, Sadie Whittaker, PhD, head of the Solve ME/CFS initiative, described her organization’s new plan to use their registry to prospectively track the impact of COVID-19 on people with ME/CFS. 

She noted that they’ve also teamed up with “long-COVID” communities including Body Politic. “Our goal is to form a coalition to study together or at least harmonize data … and understand what’s going on through the power of bigger sample sizes,” Dr. Whittaker said.

None of the speakers disclosed relevant financial relationships.

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

The Food and Drug Administration has granted marketing approval for the BrainsWay deep transcranial magnetic stimulation (TMS) system to help adult smokers kick tobacco.

This is the company’s third FDA-approved indication for its deep TMS system and the first FDA approval for any TMS device for addiction, the company said in a press release.

As previously reported, the system has already been approved by the FDA as a treatment for patients suffering from obsessive-compulsive disorder and major depressive disorder.

The BrainsWay deep TMS system with H4-coil is designed to target addiction-related brain circuits.

It was evaluated as an aid to short-term smoking cessation in a prospective, double-blind, randomized, sham-controlled, multicenter study that involved 262 adults who had a history of smoking an average of more than 26 years and had attempted to quit multiple times but failed.

Active and sham treatments were performed daily 5 days a week for 3 weeks, followed by an additional three sessions once weekly for 3 weeks, for a total of 18 sessions over 6 weeks.

In the full intention-to-treat population (all 262 participants), the 4-week continuous quit rate (CQR, the primary endpoint) was higher in the active deep TMS group than in the sham TMS group (17.1% vs. 7.9%; P = .0238).

Among participants who completed the study, that is, those who underwent treatment for 4 weeks, who kept daily records, and for whom confirmatory urine samples were available, the CQR was 28.4% in the active deep TMS group, compared with 11.7% in the sham treatment group (P = .0063).

The average number of cigarettes smoked per day, as determined on the basis of daily records (secondary endpoint), was statistically significantly lower in the active deep TMS group, compared with the sham treatment group (P = .0311).

No patient suffered a seizure. The most common adverse event was headache, for which there was no statistical difference between the active and sham treatment groups. Other side effects included application site discomfort, back pain, muscle twitching, and discomfort.

“This FDA clearance represents a significant milestone for BrainsWay and our deep TMS platform technology,” Christopher von Jako, PhD, president and CEO of the company, said in the release.

“While other therapies are currently available, a substantial medical need continues to exist for treatments that can increase the continuous quit rate among smokers,” Dr. von Jako noted.

“Based on the compelling data from our large, randomized pivotal study of 262 subjects, we are confident that our deep TMS technology can play an important role in treating cigarette smokers who seek to quit,” he added.

The company plans a “controlled” U.S. market release of the system for this indication early next year.
 

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

The Food and Drug Administration has granted marketing approval for the BrainsWay deep transcranial magnetic stimulation (TMS) system to help adult smokers kick tobacco.

This is the company’s third FDA-approved indication for its deep TMS system and the first FDA approval for any TMS device for addiction, the company said in a press release.

As previously reported, the system has already been approved by the FDA as a treatment for patients suffering from obsessive-compulsive disorder and major depressive disorder.

The BrainsWay deep TMS system with H4-coil is designed to target addiction-related brain circuits.

It was evaluated as an aid to short-term smoking cessation in a prospective, double-blind, randomized, sham-controlled, multicenter study that involved 262 adults who had a history of smoking an average of more than 26 years and had attempted to quit multiple times but failed.

Active and sham treatments were performed daily 5 days a week for 3 weeks, followed by an additional three sessions once weekly for 3 weeks, for a total of 18 sessions over 6 weeks.

In the full intention-to-treat population (all 262 participants), the 4-week continuous quit rate (CQR, the primary endpoint) was higher in the active deep TMS group than in the sham TMS group (17.1% vs. 7.9%; P = .0238).

Among participants who completed the study, that is, those who underwent treatment for 4 weeks, who kept daily records, and for whom confirmatory urine samples were available, the CQR was 28.4% in the active deep TMS group, compared with 11.7% in the sham treatment group (P = .0063).

The average number of cigarettes smoked per day, as determined on the basis of daily records (secondary endpoint), was statistically significantly lower in the active deep TMS group, compared with the sham treatment group (P = .0311).

No patient suffered a seizure. The most common adverse event was headache, for which there was no statistical difference between the active and sham treatment groups. Other side effects included application site discomfort, back pain, muscle twitching, and discomfort.

“This FDA clearance represents a significant milestone for BrainsWay and our deep TMS platform technology,” Christopher von Jako, PhD, president and CEO of the company, said in the release.

“While other therapies are currently available, a substantial medical need continues to exist for treatments that can increase the continuous quit rate among smokers,” Dr. von Jako noted.

“Based on the compelling data from our large, randomized pivotal study of 262 subjects, we are confident that our deep TMS technology can play an important role in treating cigarette smokers who seek to quit,” he added.

The company plans a “controlled” U.S. market release of the system for this indication early next year.
 

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

The Food and Drug Administration has granted marketing approval for the BrainsWay deep transcranial magnetic stimulation (TMS) system to help adult smokers kick tobacco.

This is the company’s third FDA-approved indication for its deep TMS system and the first FDA approval for any TMS device for addiction, the company said in a press release.

As previously reported, the system has already been approved by the FDA as a treatment for patients suffering from obsessive-compulsive disorder and major depressive disorder.

The BrainsWay deep TMS system with H4-coil is designed to target addiction-related brain circuits.

It was evaluated as an aid to short-term smoking cessation in a prospective, double-blind, randomized, sham-controlled, multicenter study that involved 262 adults who had a history of smoking an average of more than 26 years and had attempted to quit multiple times but failed.

Active and sham treatments were performed daily 5 days a week for 3 weeks, followed by an additional three sessions once weekly for 3 weeks, for a total of 18 sessions over 6 weeks.

In the full intention-to-treat population (all 262 participants), the 4-week continuous quit rate (CQR, the primary endpoint) was higher in the active deep TMS group than in the sham TMS group (17.1% vs. 7.9%; P = .0238).

Among participants who completed the study, that is, those who underwent treatment for 4 weeks, who kept daily records, and for whom confirmatory urine samples were available, the CQR was 28.4% in the active deep TMS group, compared with 11.7% in the sham treatment group (P = .0063).

The average number of cigarettes smoked per day, as determined on the basis of daily records (secondary endpoint), was statistically significantly lower in the active deep TMS group, compared with the sham treatment group (P = .0311).

No patient suffered a seizure. The most common adverse event was headache, for which there was no statistical difference between the active and sham treatment groups. Other side effects included application site discomfort, back pain, muscle twitching, and discomfort.

“This FDA clearance represents a significant milestone for BrainsWay and our deep TMS platform technology,” Christopher von Jako, PhD, president and CEO of the company, said in the release.

“While other therapies are currently available, a substantial medical need continues to exist for treatments that can increase the continuous quit rate among smokers,” Dr. von Jako noted.

“Based on the compelling data from our large, randomized pivotal study of 262 subjects, we are confident that our deep TMS technology can play an important role in treating cigarette smokers who seek to quit,” he added.

The company plans a “controlled” U.S. market release of the system for this indication early next year.
 

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

The Food and Drug Administration issued an emergency use authorization for convalescent plasma on Aug. 23, opening up more access for hospitalized COVID-19 patients.

Convalescent plasma contains antibodies from the blood of recovered COVID-19 patients, which can be used to treat people with severe infections. Convalescent plasma has been used to treat patients for other infectious diseases. The authorization allows the plasma to be distributed in the United States and administered by health care providers.

“COVID-19 convalescent plasma is safe and shows promising efficacy,” Stephen Hahn, MD, commissioner of the FDA, said during a press briefing with President Donald Trump.

In April, the FDA approved a program to test convalescent plasma in COVID-19 patients at the Mayo Clinic, followed by other institutions. More than 90,000 patients have enrolled in the program, and 70,000 have received the treatment, Dr. Hahn said.

The data indicate that the plasma can reduce mortality in patients by 35%, particularly if patients are treated within 3 days of being diagnosed. Those who have benefited the most were under age 80 and not on artificial respiration, Alex Azar, the secretary for the Department of Health & Human Services, said during the briefing.

“We dream, in drug development, of something like a 35% mortality reduction,” he said.

But top scientists pushed back against the announcement.

Eric Topol, MD, director of the Scripps Research Translational Institute, professor of molecular medicine, and executive vice president of Scripps Research, said the data the FDA are relying on did not come from the rigorous randomized, double-blind placebo trials that best determine if a treatment is successful.

Still, convalescent plasma is “one more tool added to the arsenal” of combating COVID-19, Mr. Azar said. The FDA will continue to study convalescent plasma as a COVID-19 treatment, Dr. Hahn added.

“We’re waiting for more data. We’re going to continue to gather data,” Dr. Hahn said during the briefing, but the current results meet FDA criteria for issuing an emergency use authorization.

Convalescent plasma “may be effective in lessening the severity or shortening the length of COVID-19 illness in some hospitalized patients,” according to the FDA announcement. Potential side effects include allergic reactions, transfusion-transmitted infections, and transfusion-associated lung injury.

“We’ve seen a great deal of demand for this from doctors around the country,” Dr. Hahn said during the briefing. “The EUA … allows us to continue that and meet that demand.”

Dr. Topol, however, said it appears Trump and the FDA are playing politics with science.

“There’s no evidence to support any survival benefit,” Dr. Topol said on Twitter. “Two days ago [the] FDA’s website stated there was no evidence for an EUA.”

The American Red Cross and other blood centers put out a national call for blood donors in July, especially for patients who have recovered from COVID-19. Mr. Azar and Dr. Hahn emphasized the need for blood donors during the press briefing.

“If you donate plasma, you could save a life,” Mr. Azar said.

The study has not been peer reviewed and did not include a placebo group for comparison, STAT reported.

Last week several health officials warned that the scientific data were too weak to warrant an emergency authorization, the New York Times reported.

A version of this originally appeared on WebMD.com.

The Food and Drug Administration issued an emergency use authorization for convalescent plasma on Aug. 23, opening up more access for hospitalized COVID-19 patients.

Convalescent plasma contains antibodies from the blood of recovered COVID-19 patients, which can be used to treat people with severe infections. Convalescent plasma has been used to treat patients for other infectious diseases. The authorization allows the plasma to be distributed in the United States and administered by health care providers.

“COVID-19 convalescent plasma is safe and shows promising efficacy,” Stephen Hahn, MD, commissioner of the FDA, said during a press briefing with President Donald Trump.

In April, the FDA approved a program to test convalescent plasma in COVID-19 patients at the Mayo Clinic, followed by other institutions. More than 90,000 patients have enrolled in the program, and 70,000 have received the treatment, Dr. Hahn said.

The data indicate that the plasma can reduce mortality in patients by 35%, particularly if patients are treated within 3 days of being diagnosed. Those who have benefited the most were under age 80 and not on artificial respiration, Alex Azar, the secretary for the Department of Health & Human Services, said during the briefing.

“We dream, in drug development, of something like a 35% mortality reduction,” he said.

But top scientists pushed back against the announcement.

Eric Topol, MD, director of the Scripps Research Translational Institute, professor of molecular medicine, and executive vice president of Scripps Research, said the data the FDA are relying on did not come from the rigorous randomized, double-blind placebo trials that best determine if a treatment is successful.

Still, convalescent plasma is “one more tool added to the arsenal” of combating COVID-19, Mr. Azar said. The FDA will continue to study convalescent plasma as a COVID-19 treatment, Dr. Hahn added.

“We’re waiting for more data. We’re going to continue to gather data,” Dr. Hahn said during the briefing, but the current results meet FDA criteria for issuing an emergency use authorization.

Convalescent plasma “may be effective in lessening the severity or shortening the length of COVID-19 illness in some hospitalized patients,” according to the FDA announcement. Potential side effects include allergic reactions, transfusion-transmitted infections, and transfusion-associated lung injury.

“We’ve seen a great deal of demand for this from doctors around the country,” Dr. Hahn said during the briefing. “The EUA … allows us to continue that and meet that demand.”

Dr. Topol, however, said it appears Trump and the FDA are playing politics with science.

“There’s no evidence to support any survival benefit,” Dr. Topol said on Twitter. “Two days ago [the] FDA’s website stated there was no evidence for an EUA.”

The American Red Cross and other blood centers put out a national call for blood donors in July, especially for patients who have recovered from COVID-19. Mr. Azar and Dr. Hahn emphasized the need for blood donors during the press briefing.

“If you donate plasma, you could save a life,” Mr. Azar said.

The study has not been peer reviewed and did not include a placebo group for comparison, STAT reported.

Last week several health officials warned that the scientific data were too weak to warrant an emergency authorization, the New York Times reported.

A version of this originally appeared on WebMD.com.

The Food and Drug Administration issued an emergency use authorization for convalescent plasma on Aug. 23, opening up more access for hospitalized COVID-19 patients.

Convalescent plasma contains antibodies from the blood of recovered COVID-19 patients, which can be used to treat people with severe infections. Convalescent plasma has been used to treat patients for other infectious diseases. The authorization allows the plasma to be distributed in the United States and administered by health care providers.

“COVID-19 convalescent plasma is safe and shows promising efficacy,” Stephen Hahn, MD, commissioner of the FDA, said during a press briefing with President Donald Trump.

In April, the FDA approved a program to test convalescent plasma in COVID-19 patients at the Mayo Clinic, followed by other institutions. More than 90,000 patients have enrolled in the program, and 70,000 have received the treatment, Dr. Hahn said.

The data indicate that the plasma can reduce mortality in patients by 35%, particularly if patients are treated within 3 days of being diagnosed. Those who have benefited the most were under age 80 and not on artificial respiration, Alex Azar, the secretary for the Department of Health & Human Services, said during the briefing.

“We dream, in drug development, of something like a 35% mortality reduction,” he said.

But top scientists pushed back against the announcement.

Eric Topol, MD, director of the Scripps Research Translational Institute, professor of molecular medicine, and executive vice president of Scripps Research, said the data the FDA are relying on did not come from the rigorous randomized, double-blind placebo trials that best determine if a treatment is successful.

Still, convalescent plasma is “one more tool added to the arsenal” of combating COVID-19, Mr. Azar said. The FDA will continue to study convalescent plasma as a COVID-19 treatment, Dr. Hahn added.

“We’re waiting for more data. We’re going to continue to gather data,” Dr. Hahn said during the briefing, but the current results meet FDA criteria for issuing an emergency use authorization.

Convalescent plasma “may be effective in lessening the severity or shortening the length of COVID-19 illness in some hospitalized patients,” according to the FDA announcement. Potential side effects include allergic reactions, transfusion-transmitted infections, and transfusion-associated lung injury.

“We’ve seen a great deal of demand for this from doctors around the country,” Dr. Hahn said during the briefing. “The EUA … allows us to continue that and meet that demand.”

Dr. Topol, however, said it appears Trump and the FDA are playing politics with science.

“There’s no evidence to support any survival benefit,” Dr. Topol said on Twitter. “Two days ago [the] FDA’s website stated there was no evidence for an EUA.”

The American Red Cross and other blood centers put out a national call for blood donors in July, especially for patients who have recovered from COVID-19. Mr. Azar and Dr. Hahn emphasized the need for blood donors during the press briefing.

“If you donate plasma, you could save a life,” Mr. Azar said.

The study has not been peer reviewed and did not include a placebo group for comparison, STAT reported.

Last week several health officials warned that the scientific data were too weak to warrant an emergency authorization, the New York Times reported.

A version of this originally appeared on WebMD.com.

Suicide by hanging results in many deaths, and half of those survivors who are admitted later die from cardiac arrest.

Although hanging is a common form of suicide, studies of the clinical outcomes of near-hanging injury are rare. To address this void, Louise de Charentenay, MD, of the Medical-Surgical Intensive Care Unit, Centre Hospitalier de Versailles (France) and colleagues examined the vital and functional outcomes of more than 800 patients with suicidal near-hanging injury over 2 decades. Despite the high in-hospital mortality rate among survivors, those who do survive have an excellent chance of a full neurocognitive recovery. The investigators published their findings in Chest.
 

New data on near-hanging injuries

Near hanging refers to strangulation or hanging that doesn’t immediately lead to death. Little data have been available on this subject, particularly on the morbidity and mortality of patients admitted to the ICU following near-hanging injuries. In a retrospective analysis spanning 23 years (1992-2014), researchers looked at outcomes and early predictors of hospital deaths in patients with this injury. The study included 886 adult patients who were admitted to 31 university or university-affiliated ICUs in France and Belgium following successful resuscitation of suicidal near-hanging injury.

Investigators used logistic multivariate regression to report vital and functional outcomes at hospital discharge as a primary objective. They also aimed to identify predictors of hospital mortality in these patients. 

Among all patients, 450 (50.8%) had hanging-induced cardiac arrest and of these, 371 (95.4%) eventually died. Although the rate of crude hospital deaths decreased over the 23-year period, hanging-induced cardiac arrest emerged as the strongest predictor of hospital mortality, followed by high blood lactate and hyperglycemia at ICU admission. “Hanging-induced cardiac arrest and worse consciousness impairment at ICU admission are directly related to the hanging, whereas higher glycemia and lactate levels at ICU admission represent biochemical markers of physiologic perturbation and injury severity that may suggest avenues for improvement in prehospital care,” wrote the investigators.

More than 56% of the patients survived to discharge, with a majority achieving favorable outcomes (a Glasgow Outcome Scale scores of 4 or 5 at discharge).
 

‘COVID-lateral’ damage and ICU management

Casey D. Bryant, MD, of the department of anesthesiology and the department of emergency medicine at Wake Forest Baptist Health, Winston-Salem, N.C., has treated these patients in the ICU and is prepared to see more of them in light of the current situation. He said in an interview, “The “COVID-lateral” damage being unleashed on the population as a result of increased isolation, lack of access to resources, higher unemployment, and increased substance abuse was detailed recently in an article by one of my colleagues, Dr. Seth Hawkins (Emerg Med News. 2020 Jun;42[6]:1,31-2). According to the Centers for Disease Control and Prevention, hanging is the second leading cause of suicide in the United States, and one can only assume that with increased mental health crises there will also be an increased number of hanging attempts.”

Dr. Bryant suggested that the first task of doctors who learn that a near-hanging patient has been admitted is to “recover from the gut-punch you feel when you learn that a fellow human has tried to take their own life.” Once one is composed, he said, the first order of business is to come up with a treatment plan, one that typically begins with the airway. “These patients are at a high risk for cervical vertebrae injury (e.g., hangman’s fracture), spinal cord injury, tracheal injury, and neck vessel injury or dissection, so care must be taken to maintain in-line stabilization and limit movement of the neck during intubation while also being prepared for all manner of airway disasters. After airway management, addressing traumatic injuries, and initial stabilization, the focus then shifts to ‘bread and butter’ critical care, including optimization of ventilator management, titration of analgosedation, providing adequate nutrition, and strict avoidance of hypoxia, hypotension, fever, and either hyper- or hypoglycemia.”

Dr. Bryant noted that targeted temperature management prescriptions remain an area of debate in those with comatose state after hanging, but fever should absolutely be avoided. He added: “As the path to recovery begins to be forged, the full gamut of mental health resources should be provided to the patients in order to give them the best chance for success once they leave the ICU, and ultimately the hospital.”

The different hospitals seemed to have varying degrees of success in saving these patients, which is surprising, Mangala Narasimhan, DO, FCCP, regional director of critical care, director of the acute lung injury/ECMO center at Northwell and a professor of medicine at the Hofstra/Northwell School of Medicine, New York, said in an interview. “Usually, the death rate for cardiac arrest is high and the death rate for hanging is high. But here, it was high in some places and low in others.” Different time frames from presenting from hanging and different treatments may explain this, said Dr. Narasimhan.
 

Patient characteristics

Consistent with previous research, near-hanging patients are predominantly male, have at least one psychiatric diagnosis and a previous suicidal attempt (rarely by hanging), and abuse substances such as an alcohol, Stéphane Legriel, MD, PhD, the study’s corresponding author, said in an interview. Overall, 67.7% of the patients had a diagnosed mental illness and 30% had previously attempted suicide. Most of the hangings took place at home (79%), while some took place in a hospital ward (6%), a correctional facility (7%), or outside (5%).

The study had several limitations: It applied only to near-hanging patients admitted to the ICU, and its long duration may have resulted in heterogeneity of the population and therapeutic interventions, and in some missing data. “However, the multivariate analysis was adjusted for the time period and we carried out a sensitivity analysis after multiple imputation for missing data by means of chained equations, which reinforces confidence in our findings,” Dr. Legriel said. Next steps are to conduct a prospective data collection.
 

Postdischarge recovery and psychiatric follow-up

Those left to treat survivors of near-hangings are psychiatrists and other mental health clinicians, Eric M. Plakun, MD, said in an interview.

“Some of these survivors will regret they survived and remain high suicide risks. Some will feel their lives are transformed or at least no longer as intensely drawn to suicide as a solution to a life filled with the impact of adversity, trauma, comorbidity, and other struggles – but even these individuals will still have to face the often complex underlying issues that led them to choose suicide as a solution,” said Dr. Plakun, medical director and CEO of the Austen Riggs Center in Stockbridge, Mass.

Patients with medically serious suicide attempts are seen a lot at Austen Riggs, he said, because acute inpatient settings are designed for brief, crisis-focused treatment of those for whom safety is an issue. After the crisis has been stabilized, patients are discharged, and then must begin to achieve recovery as outpatients, he said.

John Kruse, MD, PhD, a psychiatrist who practices in San Francisco, praised the size and the breath of the study. “One limitation was the reliance on hospital records, without an opportunity to directly evaluate or interview the patients involved.”

The authors disclosed no conflicts of interest. The study received grant support from the French public funding agency, Délégation la Recherche Clinique et de l’Innovation in Versailles, France.

SOURCE: de Charentenay L et al. 2020 Aug 3. doi: 10.1016/j.chest.2020.07.064

Suicide by hanging results in many deaths, and half of those survivors who are admitted later die from cardiac arrest.

Although hanging is a common form of suicide, studies of the clinical outcomes of near-hanging injury are rare. To address this void, Louise de Charentenay, MD, of the Medical-Surgical Intensive Care Unit, Centre Hospitalier de Versailles (France) and colleagues examined the vital and functional outcomes of more than 800 patients with suicidal near-hanging injury over 2 decades. Despite the high in-hospital mortality rate among survivors, those who do survive have an excellent chance of a full neurocognitive recovery. The investigators published their findings in Chest.
 

New data on near-hanging injuries

Near hanging refers to strangulation or hanging that doesn’t immediately lead to death. Little data have been available on this subject, particularly on the morbidity and mortality of patients admitted to the ICU following near-hanging injuries. In a retrospective analysis spanning 23 years (1992-2014), researchers looked at outcomes and early predictors of hospital deaths in patients with this injury. The study included 886 adult patients who were admitted to 31 university or university-affiliated ICUs in France and Belgium following successful resuscitation of suicidal near-hanging injury.

Investigators used logistic multivariate regression to report vital and functional outcomes at hospital discharge as a primary objective. They also aimed to identify predictors of hospital mortality in these patients. 

Among all patients, 450 (50.8%) had hanging-induced cardiac arrest and of these, 371 (95.4%) eventually died. Although the rate of crude hospital deaths decreased over the 23-year period, hanging-induced cardiac arrest emerged as the strongest predictor of hospital mortality, followed by high blood lactate and hyperglycemia at ICU admission. “Hanging-induced cardiac arrest and worse consciousness impairment at ICU admission are directly related to the hanging, whereas higher glycemia and lactate levels at ICU admission represent biochemical markers of physiologic perturbation and injury severity that may suggest avenues for improvement in prehospital care,” wrote the investigators.

More than 56% of the patients survived to discharge, with a majority achieving favorable outcomes (a Glasgow Outcome Scale scores of 4 or 5 at discharge).
 

‘COVID-lateral’ damage and ICU management

Casey D. Bryant, MD, of the department of anesthesiology and the department of emergency medicine at Wake Forest Baptist Health, Winston-Salem, N.C., has treated these patients in the ICU and is prepared to see more of them in light of the current situation. He said in an interview, “The “COVID-lateral” damage being unleashed on the population as a result of increased isolation, lack of access to resources, higher unemployment, and increased substance abuse was detailed recently in an article by one of my colleagues, Dr. Seth Hawkins (Emerg Med News. 2020 Jun;42[6]:1,31-2). According to the Centers for Disease Control and Prevention, hanging is the second leading cause of suicide in the United States, and one can only assume that with increased mental health crises there will also be an increased number of hanging attempts.”

Dr. Bryant suggested that the first task of doctors who learn that a near-hanging patient has been admitted is to “recover from the gut-punch you feel when you learn that a fellow human has tried to take their own life.” Once one is composed, he said, the first order of business is to come up with a treatment plan, one that typically begins with the airway. “These patients are at a high risk for cervical vertebrae injury (e.g., hangman’s fracture), spinal cord injury, tracheal injury, and neck vessel injury or dissection, so care must be taken to maintain in-line stabilization and limit movement of the neck during intubation while also being prepared for all manner of airway disasters. After airway management, addressing traumatic injuries, and initial stabilization, the focus then shifts to ‘bread and butter’ critical care, including optimization of ventilator management, titration of analgosedation, providing adequate nutrition, and strict avoidance of hypoxia, hypotension, fever, and either hyper- or hypoglycemia.”

Dr. Bryant noted that targeted temperature management prescriptions remain an area of debate in those with comatose state after hanging, but fever should absolutely be avoided. He added: “As the path to recovery begins to be forged, the full gamut of mental health resources should be provided to the patients in order to give them the best chance for success once they leave the ICU, and ultimately the hospital.”

The different hospitals seemed to have varying degrees of success in saving these patients, which is surprising, Mangala Narasimhan, DO, FCCP, regional director of critical care, director of the acute lung injury/ECMO center at Northwell and a professor of medicine at the Hofstra/Northwell School of Medicine, New York, said in an interview. “Usually, the death rate for cardiac arrest is high and the death rate for hanging is high. But here, it was high in some places and low in others.” Different time frames from presenting from hanging and different treatments may explain this, said Dr. Narasimhan.
 

Patient characteristics

Consistent with previous research, near-hanging patients are predominantly male, have at least one psychiatric diagnosis and a previous suicidal attempt (rarely by hanging), and abuse substances such as an alcohol, Stéphane Legriel, MD, PhD, the study’s corresponding author, said in an interview. Overall, 67.7% of the patients had a diagnosed mental illness and 30% had previously attempted suicide. Most of the hangings took place at home (79%), while some took place in a hospital ward (6%), a correctional facility (7%), or outside (5%).

The study had several limitations: It applied only to near-hanging patients admitted to the ICU, and its long duration may have resulted in heterogeneity of the population and therapeutic interventions, and in some missing data. “However, the multivariate analysis was adjusted for the time period and we carried out a sensitivity analysis after multiple imputation for missing data by means of chained equations, which reinforces confidence in our findings,” Dr. Legriel said. Next steps are to conduct a prospective data collection.
 

Postdischarge recovery and psychiatric follow-up

Those left to treat survivors of near-hangings are psychiatrists and other mental health clinicians, Eric M. Plakun, MD, said in an interview.

“Some of these survivors will regret they survived and remain high suicide risks. Some will feel their lives are transformed or at least no longer as intensely drawn to suicide as a solution to a life filled with the impact of adversity, trauma, comorbidity, and other struggles – but even these individuals will still have to face the often complex underlying issues that led them to choose suicide as a solution,” said Dr. Plakun, medical director and CEO of the Austen Riggs Center in Stockbridge, Mass.

Patients with medically serious suicide attempts are seen a lot at Austen Riggs, he said, because acute inpatient settings are designed for brief, crisis-focused treatment of those for whom safety is an issue. After the crisis has been stabilized, patients are discharged, and then must begin to achieve recovery as outpatients, he said.

John Kruse, MD, PhD, a psychiatrist who practices in San Francisco, praised the size and the breath of the study. “One limitation was the reliance on hospital records, without an opportunity to directly evaluate or interview the patients involved.”

The authors disclosed no conflicts of interest. The study received grant support from the French public funding agency, Délégation la Recherche Clinique et de l’Innovation in Versailles, France.

SOURCE: de Charentenay L et al. 2020 Aug 3. doi: 10.1016/j.chest.2020.07.064

Suicide by hanging results in many deaths, and half of those survivors who are admitted later die from cardiac arrest.

Although hanging is a common form of suicide, studies of the clinical outcomes of near-hanging injury are rare. To address this void, Louise de Charentenay, MD, of the Medical-Surgical Intensive Care Unit, Centre Hospitalier de Versailles (France) and colleagues examined the vital and functional outcomes of more than 800 patients with suicidal near-hanging injury over 2 decades. Despite the high in-hospital mortality rate among survivors, those who do survive have an excellent chance of a full neurocognitive recovery. The investigators published their findings in Chest.
 

New data on near-hanging injuries

Near hanging refers to strangulation or hanging that doesn’t immediately lead to death. Little data have been available on this subject, particularly on the morbidity and mortality of patients admitted to the ICU following near-hanging injuries. In a retrospective analysis spanning 23 years (1992-2014), researchers looked at outcomes and early predictors of hospital deaths in patients with this injury. The study included 886 adult patients who were admitted to 31 university or university-affiliated ICUs in France and Belgium following successful resuscitation of suicidal near-hanging injury.

Investigators used logistic multivariate regression to report vital and functional outcomes at hospital discharge as a primary objective. They also aimed to identify predictors of hospital mortality in these patients. 

Among all patients, 450 (50.8%) had hanging-induced cardiac arrest and of these, 371 (95.4%) eventually died. Although the rate of crude hospital deaths decreased over the 23-year period, hanging-induced cardiac arrest emerged as the strongest predictor of hospital mortality, followed by high blood lactate and hyperglycemia at ICU admission. “Hanging-induced cardiac arrest and worse consciousness impairment at ICU admission are directly related to the hanging, whereas higher glycemia and lactate levels at ICU admission represent biochemical markers of physiologic perturbation and injury severity that may suggest avenues for improvement in prehospital care,” wrote the investigators.

More than 56% of the patients survived to discharge, with a majority achieving favorable outcomes (a Glasgow Outcome Scale scores of 4 or 5 at discharge).
 

‘COVID-lateral’ damage and ICU management

Casey D. Bryant, MD, of the department of anesthesiology and the department of emergency medicine at Wake Forest Baptist Health, Winston-Salem, N.C., has treated these patients in the ICU and is prepared to see more of them in light of the current situation. He said in an interview, “The “COVID-lateral” damage being unleashed on the population as a result of increased isolation, lack of access to resources, higher unemployment, and increased substance abuse was detailed recently in an article by one of my colleagues, Dr. Seth Hawkins (Emerg Med News. 2020 Jun;42[6]:1,31-2). According to the Centers for Disease Control and Prevention, hanging is the second leading cause of suicide in the United States, and one can only assume that with increased mental health crises there will also be an increased number of hanging attempts.”

Dr. Bryant suggested that the first task of doctors who learn that a near-hanging patient has been admitted is to “recover from the gut-punch you feel when you learn that a fellow human has tried to take their own life.” Once one is composed, he said, the first order of business is to come up with a treatment plan, one that typically begins with the airway. “These patients are at a high risk for cervical vertebrae injury (e.g., hangman’s fracture), spinal cord injury, tracheal injury, and neck vessel injury or dissection, so care must be taken to maintain in-line stabilization and limit movement of the neck during intubation while also being prepared for all manner of airway disasters. After airway management, addressing traumatic injuries, and initial stabilization, the focus then shifts to ‘bread and butter’ critical care, including optimization of ventilator management, titration of analgosedation, providing adequate nutrition, and strict avoidance of hypoxia, hypotension, fever, and either hyper- or hypoglycemia.”

Dr. Bryant noted that targeted temperature management prescriptions remain an area of debate in those with comatose state after hanging, but fever should absolutely be avoided. He added: “As the path to recovery begins to be forged, the full gamut of mental health resources should be provided to the patients in order to give them the best chance for success once they leave the ICU, and ultimately the hospital.”

The different hospitals seemed to have varying degrees of success in saving these patients, which is surprising, Mangala Narasimhan, DO, FCCP, regional director of critical care, director of the acute lung injury/ECMO center at Northwell and a professor of medicine at the Hofstra/Northwell School of Medicine, New York, said in an interview. “Usually, the death rate for cardiac arrest is high and the death rate for hanging is high. But here, it was high in some places and low in others.” Different time frames from presenting from hanging and different treatments may explain this, said Dr. Narasimhan.
 

Patient characteristics

Consistent with previous research, near-hanging patients are predominantly male, have at least one psychiatric diagnosis and a previous suicidal attempt (rarely by hanging), and abuse substances such as an alcohol, Stéphane Legriel, MD, PhD, the study’s corresponding author, said in an interview. Overall, 67.7% of the patients had a diagnosed mental illness and 30% had previously attempted suicide. Most of the hangings took place at home (79%), while some took place in a hospital ward (6%), a correctional facility (7%), or outside (5%).

The study had several limitations: It applied only to near-hanging patients admitted to the ICU, and its long duration may have resulted in heterogeneity of the population and therapeutic interventions, and in some missing data. “However, the multivariate analysis was adjusted for the time period and we carried out a sensitivity analysis after multiple imputation for missing data by means of chained equations, which reinforces confidence in our findings,” Dr. Legriel said. Next steps are to conduct a prospective data collection.
 

Postdischarge recovery and psychiatric follow-up

Those left to treat survivors of near-hangings are psychiatrists and other mental health clinicians, Eric M. Plakun, MD, said in an interview.

“Some of these survivors will regret they survived and remain high suicide risks. Some will feel their lives are transformed or at least no longer as intensely drawn to suicide as a solution to a life filled with the impact of adversity, trauma, comorbidity, and other struggles – but even these individuals will still have to face the often complex underlying issues that led them to choose suicide as a solution,” said Dr. Plakun, medical director and CEO of the Austen Riggs Center in Stockbridge, Mass.

Patients with medically serious suicide attempts are seen a lot at Austen Riggs, he said, because acute inpatient settings are designed for brief, crisis-focused treatment of those for whom safety is an issue. After the crisis has been stabilized, patients are discharged, and then must begin to achieve recovery as outpatients, he said.

John Kruse, MD, PhD, a psychiatrist who practices in San Francisco, praised the size and the breath of the study. “One limitation was the reliance on hospital records, without an opportunity to directly evaluate or interview the patients involved.”

The authors disclosed no conflicts of interest. The study received grant support from the French public funding agency, Délégation la Recherche Clinique et de l’Innovation in Versailles, France.

SOURCE: de Charentenay L et al. 2020 Aug 3. doi: 10.1016/j.chest.2020.07.064

Spirituality and religion remain central to the worldview of millions of Americans. According to the Pew Research Center, almost 75% of Americans identify as Christian, Jewish, Muslim, Buddhist, or Hindu.¹ As is the case with many Americans,² the lens of spirituality³ and religion shaped my own worldview since childhood.

j-wildman/Getty Images

Growing up in a Christian household, many of my family’s discussions centered on bolstering our spiritual health. I grew to internalize the notion that spiritual health relates to a sense of self, a sense of purpose, and a connection to God, nature, and others. Religious texts such as the Bible, Quran, and Torah share principles aimed at developing believers’ spiritual health. However, the intricacies of mental health remain entirely foreign within many faith communities. In these communities, unfamiliarity with mental health topics seemingly leads to the conflation of spiritual health and mental health.⁴

Within faith communities, I often hear the phrase, “You can’t worry and pray at the same time.” This commonly used expression encourages people of faith to lean on their spiritual health in times of uncertainty. The perceived dichotomy between worry and prayer represents the theology of sole reliance on spiritual coping skills, such as prayer, when feelings of anxiety and other psychological stressors arise. Because of “pray it away” doctrines and ongoing stigma related to mental health, many of our spiritually minded patients are more likely to seek counsel from religious leaders than they are from mental health clinicians in times of psychological distress.^5,6

About 54% of U.S. adults identify as religious, and 75% think of themselves as spiritual.⁷ This intrapersonal conflict between religious/spiritual health and mental health raises an important question: How can psychiatrists more actively collaborate with religious communities to ease the perceived tensions between spiritual health and mental health for our patients?
 

Engaging with the community

In a recent virtual talk titled, “Dealing with Depression: Faith, Meds, and Therapy,” I openly discussed varying aspects of mental health and mental illness with approximately 70 women at my church in Philadelphia. Before this presentation, there had never been a leadership-sponsored conversation within the church to discuss spiritual health and mental health as separate but highly interconnected entities.

Throughout the nearly 2-hour session, I used biblical and biological principles to explain the differences between spiritual health and mental health, strategies to recognize signs and symptoms of depression, and treatment options for depression. After the formal presentation, a 45-minute question-and-answer session followed in which some members shared their own experiences with mental illness.

Two major themes emerged as central points of discussion during our time of open dialogue. First, several women shared the spiritual and clinical avenues they used to access support in times of psychological distress. There was a general tone of agreement among attendees that spiritual health and mental health are, in fact, different. Second, the presentation opened the door for attendees, previously unfamiliar with mental health services, to ask questions about connecting with the appropriate resources to receive mental health treatment. The subject of seeking psychiatric care for mental health challenges was, at least in part, demystified and brought to the forefront of the attendees’ minds.

Studies show that many faith-based communities are more likely to seek counsel for psychological distress from religious leaders than from mental health professionals. In this vein, my recent community engagement highlighted to me ways that we can readily reach spiritually and religiously minded patients who otherwise would not receive the psychiatric care that they need. Psychiatrists can play an integral role in bridging the gap in psychiatric care for faith-based persons through outreach to and collaboration with religious communities.
 

Opportunities for collaboration

In collaboration with religious leaders, psychiatrists can actively support the mental health of spiritually and religiously minded patients through several low-effort, but potentially high-yield, initiatives. Notably, many of my suggested interventions do not require significant, if any, infrastructural changes to the health care system or worship communities. As psychiatrists, we can collaborate with faith leaders as follows:

1. More regularly assess the role of religion and spirituality in our patients’ daily lives to better meet their spiritual and mental health needs.

2. Better use existing chaplain services to provide spiritual support for hospitalized patients.

3. Present information about mental health – in-person, virtually, or in written form – to religious communities through talks, discussions, popular religious publications, social media platforms, and webinars.

4. Amplify existing mental health guides for faith leaders (i.e., the American Psychiatric Association’s guidebook Mental Health: A Guide for Faith Leaders),⁸ thereby encouraging church leaders and staff to become better informed about common mental health conditions.

5. Collaborate with places of worship to offer psychiatric and psychological services to their members.

This sort of engagement with religious communities is the collective role of community-oriented psychiatrists, not just psychiatrists who ascribe to religious or spiritual beliefs. We ought to remain mindful of the spiritual distress that many spiritual and religious patients feel when they experience mental illness,⁹ particularly in light of the distress caused by the coronavirus pandemic.¹⁰ But first, we must become comfortable with asking our patients about their religious or spiritual affiliations using tools such as the Cultural Formulation Interview.¹¹ The more we recognize the role of spirituality in our patients’ lives, the better equipped we become to help patients identify and seek treatment for mental illness without the distress of their feeling spiritually deficient.
 

Dr. Jordan is a psychiatry resident physician in Philadelphia. She has no conflicts of interest.

References

1. Religious Landscape Study. pewforum.org.

2. U.S. Religion Census Census: Religious Congregations and Membership Study. Association of Religion Data Archives. 2010. doi: 10.17605/OSF.IO/9AMDJ.

3. J Med Ethics Hist Med. 2018 Apr 9;11:3.

4. The Dimensions of Health: Conceptual Models. Sudbury, Mass.: Jones & Bartlett, 2010.

5. J Res Christ Educ. 2014;23(2):176-86.

6. Health Serv Res. 2003 Apr;38(2):647-73.

7. “More Americans say they’re spiritual but not religious.” pewresearch.org. 2017 Sep 6.

8. Mental Health: A Guide for Faith Leaders. Washington: American Psychiatric Association Foundation, 2018.

9. Mental Health by the Numbers. NAMI: National Alliance on Mental Illness. 2019.

10. “Most Americans say coronavirus outbreak has impacted their lives. Pew Research Center. pewsocialtrends.org. 2020 Mar 30.

11. DSM-5 Handbook on the Cultural Formulation Interview. Washington: American Psychiatric Association Publishing, 2016.

Spirituality and religion remain central to the worldview of millions of Americans. According to the Pew Research Center, almost 75% of Americans identify as Christian, Jewish, Muslim, Buddhist, or Hindu.¹ As is the case with many Americans,² the lens of spirituality³ and religion shaped my own worldview since childhood.

j-wildman/Getty Images

Growing up in a Christian household, many of my family’s discussions centered on bolstering our spiritual health. I grew to internalize the notion that spiritual health relates to a sense of self, a sense of purpose, and a connection to God, nature, and others. Religious texts such as the Bible, Quran, and Torah share principles aimed at developing believers’ spiritual health. However, the intricacies of mental health remain entirely foreign within many faith communities. In these communities, unfamiliarity with mental health topics seemingly leads to the conflation of spiritual health and mental health.⁴

Within faith communities, I often hear the phrase, “You can’t worry and pray at the same time.” This commonly used expression encourages people of faith to lean on their spiritual health in times of uncertainty. The perceived dichotomy between worry and prayer represents the theology of sole reliance on spiritual coping skills, such as prayer, when feelings of anxiety and other psychological stressors arise. Because of “pray it away” doctrines and ongoing stigma related to mental health, many of our spiritually minded patients are more likely to seek counsel from religious leaders than they are from mental health clinicians in times of psychological distress.^5,6

About 54% of U.S. adults identify as religious, and 75% think of themselves as spiritual.⁷ This intrapersonal conflict between religious/spiritual health and mental health raises an important question: How can psychiatrists more actively collaborate with religious communities to ease the perceived tensions between spiritual health and mental health for our patients?
 

Engaging with the community

In a recent virtual talk titled, “Dealing with Depression: Faith, Meds, and Therapy,” I openly discussed varying aspects of mental health and mental illness with approximately 70 women at my church in Philadelphia. Before this presentation, there had never been a leadership-sponsored conversation within the church to discuss spiritual health and mental health as separate but highly interconnected entities.

Throughout the nearly 2-hour session, I used biblical and biological principles to explain the differences between spiritual health and mental health, strategies to recognize signs and symptoms of depression, and treatment options for depression. After the formal presentation, a 45-minute question-and-answer session followed in which some members shared their own experiences with mental illness.

Two major themes emerged as central points of discussion during our time of open dialogue. First, several women shared the spiritual and clinical avenues they used to access support in times of psychological distress. There was a general tone of agreement among attendees that spiritual health and mental health are, in fact, different. Second, the presentation opened the door for attendees, previously unfamiliar with mental health services, to ask questions about connecting with the appropriate resources to receive mental health treatment. The subject of seeking psychiatric care for mental health challenges was, at least in part, demystified and brought to the forefront of the attendees’ minds.

Studies show that many faith-based communities are more likely to seek counsel for psychological distress from religious leaders than from mental health professionals. In this vein, my recent community engagement highlighted to me ways that we can readily reach spiritually and religiously minded patients who otherwise would not receive the psychiatric care that they need. Psychiatrists can play an integral role in bridging the gap in psychiatric care for faith-based persons through outreach to and collaboration with religious communities.
 

Opportunities for collaboration

In collaboration with religious leaders, psychiatrists can actively support the mental health of spiritually and religiously minded patients through several low-effort, but potentially high-yield, initiatives. Notably, many of my suggested interventions do not require significant, if any, infrastructural changes to the health care system or worship communities. As psychiatrists, we can collaborate with faith leaders as follows:

1. More regularly assess the role of religion and spirituality in our patients’ daily lives to better meet their spiritual and mental health needs.

2. Better use existing chaplain services to provide spiritual support for hospitalized patients.

3. Present information about mental health – in-person, virtually, or in written form – to religious communities through talks, discussions, popular religious publications, social media platforms, and webinars.

4. Amplify existing mental health guides for faith leaders (i.e., the American Psychiatric Association’s guidebook Mental Health: A Guide for Faith Leaders),⁸ thereby encouraging church leaders and staff to become better informed about common mental health conditions.

5. Collaborate with places of worship to offer psychiatric and psychological services to their members.

This sort of engagement with religious communities is the collective role of community-oriented psychiatrists, not just psychiatrists who ascribe to religious or spiritual beliefs. We ought to remain mindful of the spiritual distress that many spiritual and religious patients feel when they experience mental illness,⁹ particularly in light of the distress caused by the coronavirus pandemic.¹⁰ But first, we must become comfortable with asking our patients about their religious or spiritual affiliations using tools such as the Cultural Formulation Interview.¹¹ The more we recognize the role of spirituality in our patients’ lives, the better equipped we become to help patients identify and seek treatment for mental illness without the distress of their feeling spiritually deficient.
 

Dr. Jordan is a psychiatry resident physician in Philadelphia. She has no conflicts of interest.

References

1. Religious Landscape Study. pewforum.org.

2. U.S. Religion Census Census: Religious Congregations and Membership Study. Association of Religion Data Archives. 2010. doi: 10.17605/OSF.IO/9AMDJ.

3. J Med Ethics Hist Med. 2018 Apr 9;11:3.

4. The Dimensions of Health: Conceptual Models. Sudbury, Mass.: Jones & Bartlett, 2010.

5. J Res Christ Educ. 2014;23(2):176-86.

6. Health Serv Res. 2003 Apr;38(2):647-73.

7. “More Americans say they’re spiritual but not religious.” pewresearch.org. 2017 Sep 6.

8. Mental Health: A Guide for Faith Leaders. Washington: American Psychiatric Association Foundation, 2018.

9. Mental Health by the Numbers. NAMI: National Alliance on Mental Illness. 2019.

10. “Most Americans say coronavirus outbreak has impacted their lives. Pew Research Center. pewsocialtrends.org. 2020 Mar 30.

11. DSM-5 Handbook on the Cultural Formulation Interview. Washington: American Psychiatric Association Publishing, 2016.

Spirituality and religion remain central to the worldview of millions of Americans. According to the Pew Research Center, almost 75% of Americans identify as Christian, Jewish, Muslim, Buddhist, or Hindu.¹ As is the case with many Americans,² the lens of spirituality³ and religion shaped my own worldview since childhood.

j-wildman/Getty Images

Growing up in a Christian household, many of my family’s discussions centered on bolstering our spiritual health. I grew to internalize the notion that spiritual health relates to a sense of self, a sense of purpose, and a connection to God, nature, and others. Religious texts such as the Bible, Quran, and Torah share principles aimed at developing believers’ spiritual health. However, the intricacies of mental health remain entirely foreign within many faith communities. In these communities, unfamiliarity with mental health topics seemingly leads to the conflation of spiritual health and mental health.⁴

Within faith communities, I often hear the phrase, “You can’t worry and pray at the same time.” This commonly used expression encourages people of faith to lean on their spiritual health in times of uncertainty. The perceived dichotomy between worry and prayer represents the theology of sole reliance on spiritual coping skills, such as prayer, when feelings of anxiety and other psychological stressors arise. Because of “pray it away” doctrines and ongoing stigma related to mental health, many of our spiritually minded patients are more likely to seek counsel from religious leaders than they are from mental health clinicians in times of psychological distress.^5,6

About 54% of U.S. adults identify as religious, and 75% think of themselves as spiritual.⁷ This intrapersonal conflict between religious/spiritual health and mental health raises an important question: How can psychiatrists more actively collaborate with religious communities to ease the perceived tensions between spiritual health and mental health for our patients?
 

Engaging with the community

In a recent virtual talk titled, “Dealing with Depression: Faith, Meds, and Therapy,” I openly discussed varying aspects of mental health and mental illness with approximately 70 women at my church in Philadelphia. Before this presentation, there had never been a leadership-sponsored conversation within the church to discuss spiritual health and mental health as separate but highly interconnected entities.

Throughout the nearly 2-hour session, I used biblical and biological principles to explain the differences between spiritual health and mental health, strategies to recognize signs and symptoms of depression, and treatment options for depression. After the formal presentation, a 45-minute question-and-answer session followed in which some members shared their own experiences with mental illness.

Two major themes emerged as central points of discussion during our time of open dialogue. First, several women shared the spiritual and clinical avenues they used to access support in times of psychological distress. There was a general tone of agreement among attendees that spiritual health and mental health are, in fact, different. Second, the presentation opened the door for attendees, previously unfamiliar with mental health services, to ask questions about connecting with the appropriate resources to receive mental health treatment. The subject of seeking psychiatric care for mental health challenges was, at least in part, demystified and brought to the forefront of the attendees’ minds.

Studies show that many faith-based communities are more likely to seek counsel for psychological distress from religious leaders than from mental health professionals. In this vein, my recent community engagement highlighted to me ways that we can readily reach spiritually and religiously minded patients who otherwise would not receive the psychiatric care that they need. Psychiatrists can play an integral role in bridging the gap in psychiatric care for faith-based persons through outreach to and collaboration with religious communities.
 

Opportunities for collaboration

In collaboration with religious leaders, psychiatrists can actively support the mental health of spiritually and religiously minded patients through several low-effort, but potentially high-yield, initiatives. Notably, many of my suggested interventions do not require significant, if any, infrastructural changes to the health care system or worship communities. As psychiatrists, we can collaborate with faith leaders as follows:

1. More regularly assess the role of religion and spirituality in our patients’ daily lives to better meet their spiritual and mental health needs.

2. Better use existing chaplain services to provide spiritual support for hospitalized patients.

3. Present information about mental health – in-person, virtually, or in written form – to religious communities through talks, discussions, popular religious publications, social media platforms, and webinars.

4. Amplify existing mental health guides for faith leaders (i.e., the American Psychiatric Association’s guidebook Mental Health: A Guide for Faith Leaders),⁸ thereby encouraging church leaders and staff to become better informed about common mental health conditions.

5. Collaborate with places of worship to offer psychiatric and psychological services to their members.

This sort of engagement with religious communities is the collective role of community-oriented psychiatrists, not just psychiatrists who ascribe to religious or spiritual beliefs. We ought to remain mindful of the spiritual distress that many spiritual and religious patients feel when they experience mental illness,⁹ particularly in light of the distress caused by the coronavirus pandemic.¹⁰ But first, we must become comfortable with asking our patients about their religious or spiritual affiliations using tools such as the Cultural Formulation Interview.¹¹ The more we recognize the role of spirituality in our patients’ lives, the better equipped we become to help patients identify and seek treatment for mental illness without the distress of their feeling spiritually deficient.
 

Dr. Jordan is a psychiatry resident physician in Philadelphia. She has no conflicts of interest.

References

1. Religious Landscape Study. pewforum.org.

2. U.S. Religion Census Census: Religious Congregations and Membership Study. Association of Religion Data Archives. 2010. doi: 10.17605/OSF.IO/9AMDJ.

3. J Med Ethics Hist Med. 2018 Apr 9;11:3.

4. The Dimensions of Health: Conceptual Models. Sudbury, Mass.: Jones & Bartlett, 2010.

5. J Res Christ Educ. 2014;23(2):176-86.

6. Health Serv Res. 2003 Apr;38(2):647-73.

7. “More Americans say they’re spiritual but not religious.” pewresearch.org. 2017 Sep 6.

8. Mental Health: A Guide for Faith Leaders. Washington: American Psychiatric Association Foundation, 2018.

9. Mental Health by the Numbers. NAMI: National Alliance on Mental Illness. 2019.

10. “Most Americans say coronavirus outbreak has impacted their lives. Pew Research Center. pewsocialtrends.org. 2020 Mar 30.

11. DSM-5 Handbook on the Cultural Formulation Interview. Washington: American Psychiatric Association Publishing, 2016.

Aggression in individuals is influenced by genetic and environmental factors, but can be reduced with treatment, according to Emil F. Coccaro, MD.

“It actually is a complex triad of emotion, cognition, and behavior. The emotion is anger, the cognition is hostility, and the behavior is aggression. And they sort of go in that order,” Dr. Coccaro said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

Although aggression can be thought of in a numerous ways, premeditated and impulsive aggression are most relevant to behavioral studies in psychiatry, Dr. Coccaro explained. Premeditated aggression is goal oriented, while impulsive aggression comes from frustration or a response to a threat. Impulsive aggression is “typically social or frustrative in nature, and studies that we’ve done that show that individuals move toward a threat while nonaggressives move away it,” he said. Both types of aggression can be seen in the same individuals at different times.

Aggression also can be considered using a threshold model. Calm individuals, for example, might have a low baseline of aggression and a high threshold before they act out. An aggressive person, on the other hand, has a lower threshold and a higher baseline level. “Their delta to get to the point where they’re going to explode is much shorter, much lower than it is in someone who is healthy,” Dr. Coccaro said.

“What we think is that the threshold to explode is probably regulated by various neurobiological features. The baseline state of aggression also may be related to baseline neurobiological features, but also what’s going on in the environment, because the neurobiological features that send someone to exploding aggression are there all the time,” he explained.

Individuals with secondary aggression are likely to have an underlying condition, such as a primary disease of the brain, systemic or metabolic disorder, or a psychiatric disorder such as schizophrenia. “If someone’s schizophrenic and they’ve got voices telling them to hurt somebody, or delusions that someone’s going to hurt them, that’s not primary aggression, that’s secondary to the psychosis,” Dr. Coccaro noted.

An individual with primary aggression is likely to have intermittent explosive disorder (IED). IED is not a new diagnosis and has been listed in the DSM since the DSM-I as “passive-aggressive personality.” It was relisted in the DSM-II as “explosive personality,” then changed to IED in the DSM-3 as a diagnosis of exclusion that was poorly operationalized, according to Dr. Coccaro. The criteria for IED under the DSM-III did not define the number of recurrent outbursts needed, what they looked like, the time frame, and excluded people who were generally impulsive.

“That’s not really what these people look like and it’s not what impulsive aggression looks like,” he said. Although the DSM-IV removed the exclusion criteria for general impulsivity and aggression, “it was still purely operational.”

The DSM-5 criteria define IED as “verbal and physical aggression without destruction or assault, twice equally on average for 3 months, or three or more episodes of physical destruction/assault over a 1-year period. These individuals have outbursts “grossly out of proportion to provocation,” the aggression is generally impulsive, and it causes stress and impairment with an age of onset at older than 6 years.

“It’s not better accounted for a whole variety of things, but we actually made some of those exclusion criteria a little less stringent,” compared with criteria in the DSM-IV, Dr. Coccaro said. “That’s because it turns out that it doesn’t really matter much of the time what the comorbidity is. If you have this aggressiveness in the absence of those other conditions, it’s IED.”

According to a reanalysis of the National Comorbidity Survey, 11.7% of adolescents displayed aggressiveness within the last year and 17.3% over a lifetime, compared with 5.1% of adults within the last year and 8.0% within a lifetime. Under DSM-5 criteria, 6.4% of adolescents within the last year and 8.9% over a lifetime currently have IED, compared with 2.6% of adults within the last year and 4.0% over a lifetime, but “could go as high” as the percentage of individuals diagnosed with aggressiveness, Dr. Coccaro noted.

“People who are not called IED many times are not called IED because we didn’t have all the information we needed to actually make the diagnosis,” he said.

Individuals with DSM-5 IED can have as many as 30 episodes in 1 year, compared with those who are nonaggressive and are also more likely to damage property. “These are the big episodes, not simply the episodes where people are getting irritable and snapping at people. These are the big ones, where they’re really destroying objects and pushing or hitting people,” Dr. Coccaro said. About one-fourth of individuals with IED hurt victims badly enough that they require medical attention, one-fifth exhibit aggression toward a partner, and one-fourth receive aggression from their own partner.

In terms of comorbidity with other psychiatric disorders, “IEDs don’t have more comorbidity in general than other disorders,” Dr. Coccaro noted. Personality disorders such as paranoid, antisocial, borderline narcissistic, and obsessive-compulsive disorders are more common in individuals with IED. Aggression in these people present differently depending on the personality disorder. “Someone who’s paranoid might blow up at you if you get in their face. For an antisocial, they’ll blow up at you if you’re preventing them from doing what they want to do. Borderlines, you reject them or you abandon them, they’re going to blow up. Narcissists will blow up when you reject. OCD will also blow up when you mess around with their sense of order,” Dr. Coccaro said.

Genetics also play a role in whether a person may have IED. There is a “clear signal” in families, with about one-fourth of individuals with IED having a relative with IED, compared with 8% of nonaggressive individuals. These percentages were consistent, regardless of whether the individual had a comorbid condition, history of alcohol or drug use, or history of suicide, he said. Other factors that influence likelihood of IED are environment, behaviors such as smoking, and conditions such as traumatic brain injury. Experiencing aggression as a child is another factor.

“IED is the categorical expression of impulsive aggression, and it’s far more common than once thought,” Dr. Coccaro said. “And IED is totally unrecognized in its role in societal violence.”
 

Treatment can suppress, but not cure aggression

Medications used to treat aggression and impulsive aggression include lithium, SSRIs, mood stabilizers, neuroleptics, and beta-blockers. However, the treatments are not a “magic bullet,” Dr. Coccaro noted. “The meds tend to suppress aggressiveness, but not cure it.”

Timing of treatment is also a factor for medication. In studies of patients taking lithium for aggression, for example, “when they gave the drug to people who liked being aggressive, they didn’t like being on these drugs because it made them feel unprotected. It just was at odds with who they thought they were,” Dr. Coccaro said. “The people who took the drug and did well and really liked being on the drug with people who didn’t like that they were aggressive.”

Neurorehabilitation and cognitive-behavioral therapy specific to aggression, called cognitive relaxation and coping skills therapy, are nonpsychotropic approaches to treating aggression. “These therapeutic approaches are working not only to reduce progression, but also to reduce the social information processing problems that aggressive individuals have,” Dr. Coccaro said.

Another approach, known as interpretation bias training, teaches individuals with aggression to judge slightly angry-looking photos of people as not being angry. After 7-14 days of training, aggressive behavior in adolescents has been shown to be reduced. The changes were also visible on functional MRI.

“What they found was that when you treated them, the change in the amygdala went down when you looked at the angry faces and in the left lateral, post training, they became happier,” Dr. Coccaro said.

Global Academy and this news organization are owned by the same parent company. Dr. Coccaro reported serving as a consultant for Avanir, Azevan, and Bracket. He also reported receiving research grants from the National Institute of Mental Health, the National Institute on Alcohol Abuse and Alcoholism, and the Pritzker Pucker Family Foundation.

Aggression in individuals is influenced by genetic and environmental factors, but can be reduced with treatment, according to Emil F. Coccaro, MD.

“It actually is a complex triad of emotion, cognition, and behavior. The emotion is anger, the cognition is hostility, and the behavior is aggression. And they sort of go in that order,” Dr. Coccaro said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

Although aggression can be thought of in a numerous ways, premeditated and impulsive aggression are most relevant to behavioral studies in psychiatry, Dr. Coccaro explained. Premeditated aggression is goal oriented, while impulsive aggression comes from frustration or a response to a threat. Impulsive aggression is “typically social or frustrative in nature, and studies that we’ve done that show that individuals move toward a threat while nonaggressives move away it,” he said. Both types of aggression can be seen in the same individuals at different times.

Aggression also can be considered using a threshold model. Calm individuals, for example, might have a low baseline of aggression and a high threshold before they act out. An aggressive person, on the other hand, has a lower threshold and a higher baseline level. “Their delta to get to the point where they’re going to explode is much shorter, much lower than it is in someone who is healthy,” Dr. Coccaro said.

“What we think is that the threshold to explode is probably regulated by various neurobiological features. The baseline state of aggression also may be related to baseline neurobiological features, but also what’s going on in the environment, because the neurobiological features that send someone to exploding aggression are there all the time,” he explained.

Individuals with secondary aggression are likely to have an underlying condition, such as a primary disease of the brain, systemic or metabolic disorder, or a psychiatric disorder such as schizophrenia. “If someone’s schizophrenic and they’ve got voices telling them to hurt somebody, or delusions that someone’s going to hurt them, that’s not primary aggression, that’s secondary to the psychosis,” Dr. Coccaro noted.

An individual with primary aggression is likely to have intermittent explosive disorder (IED). IED is not a new diagnosis and has been listed in the DSM since the DSM-I as “passive-aggressive personality.” It was relisted in the DSM-II as “explosive personality,” then changed to IED in the DSM-3 as a diagnosis of exclusion that was poorly operationalized, according to Dr. Coccaro. The criteria for IED under the DSM-III did not define the number of recurrent outbursts needed, what they looked like, the time frame, and excluded people who were generally impulsive.

“That’s not really what these people look like and it’s not what impulsive aggression looks like,” he said. Although the DSM-IV removed the exclusion criteria for general impulsivity and aggression, “it was still purely operational.”

The DSM-5 criteria define IED as “verbal and physical aggression without destruction or assault, twice equally on average for 3 months, or three or more episodes of physical destruction/assault over a 1-year period. These individuals have outbursts “grossly out of proportion to provocation,” the aggression is generally impulsive, and it causes stress and impairment with an age of onset at older than 6 years.

“It’s not better accounted for a whole variety of things, but we actually made some of those exclusion criteria a little less stringent,” compared with criteria in the DSM-IV, Dr. Coccaro said. “That’s because it turns out that it doesn’t really matter much of the time what the comorbidity is. If you have this aggressiveness in the absence of those other conditions, it’s IED.”

According to a reanalysis of the National Comorbidity Survey, 11.7% of adolescents displayed aggressiveness within the last year and 17.3% over a lifetime, compared with 5.1% of adults within the last year and 8.0% within a lifetime. Under DSM-5 criteria, 6.4% of adolescents within the last year and 8.9% over a lifetime currently have IED, compared with 2.6% of adults within the last year and 4.0% over a lifetime, but “could go as high” as the percentage of individuals diagnosed with aggressiveness, Dr. Coccaro noted.

“People who are not called IED many times are not called IED because we didn’t have all the information we needed to actually make the diagnosis,” he said.

Individuals with DSM-5 IED can have as many as 30 episodes in 1 year, compared with those who are nonaggressive and are also more likely to damage property. “These are the big episodes, not simply the episodes where people are getting irritable and snapping at people. These are the big ones, where they’re really destroying objects and pushing or hitting people,” Dr. Coccaro said. About one-fourth of individuals with IED hurt victims badly enough that they require medical attention, one-fifth exhibit aggression toward a partner, and one-fourth receive aggression from their own partner.

In terms of comorbidity with other psychiatric disorders, “IEDs don’t have more comorbidity in general than other disorders,” Dr. Coccaro noted. Personality disorders such as paranoid, antisocial, borderline narcissistic, and obsessive-compulsive disorders are more common in individuals with IED. Aggression in these people present differently depending on the personality disorder. “Someone who’s paranoid might blow up at you if you get in their face. For an antisocial, they’ll blow up at you if you’re preventing them from doing what they want to do. Borderlines, you reject them or you abandon them, they’re going to blow up. Narcissists will blow up when you reject. OCD will also blow up when you mess around with their sense of order,” Dr. Coccaro said.

Genetics also play a role in whether a person may have IED. There is a “clear signal” in families, with about one-fourth of individuals with IED having a relative with IED, compared with 8% of nonaggressive individuals. These percentages were consistent, regardless of whether the individual had a comorbid condition, history of alcohol or drug use, or history of suicide, he said. Other factors that influence likelihood of IED are environment, behaviors such as smoking, and conditions such as traumatic brain injury. Experiencing aggression as a child is another factor.

“IED is the categorical expression of impulsive aggression, and it’s far more common than once thought,” Dr. Coccaro said. “And IED is totally unrecognized in its role in societal violence.”
 

Treatment can suppress, but not cure aggression

Medications used to treat aggression and impulsive aggression include lithium, SSRIs, mood stabilizers, neuroleptics, and beta-blockers. However, the treatments are not a “magic bullet,” Dr. Coccaro noted. “The meds tend to suppress aggressiveness, but not cure it.”

Timing of treatment is also a factor for medication. In studies of patients taking lithium for aggression, for example, “when they gave the drug to people who liked being aggressive, they didn’t like being on these drugs because it made them feel unprotected. It just was at odds with who they thought they were,” Dr. Coccaro said. “The people who took the drug and did well and really liked being on the drug with people who didn’t like that they were aggressive.”

Neurorehabilitation and cognitive-behavioral therapy specific to aggression, called cognitive relaxation and coping skills therapy, are nonpsychotropic approaches to treating aggression. “These therapeutic approaches are working not only to reduce progression, but also to reduce the social information processing problems that aggressive individuals have,” Dr. Coccaro said.

Another approach, known as interpretation bias training, teaches individuals with aggression to judge slightly angry-looking photos of people as not being angry. After 7-14 days of training, aggressive behavior in adolescents has been shown to be reduced. The changes were also visible on functional MRI.

“What they found was that when you treated them, the change in the amygdala went down when you looked at the angry faces and in the left lateral, post training, they became happier,” Dr. Coccaro said.

Global Academy and this news organization are owned by the same parent company. Dr. Coccaro reported serving as a consultant for Avanir, Azevan, and Bracket. He also reported receiving research grants from the National Institute of Mental Health, the National Institute on Alcohol Abuse and Alcoholism, and the Pritzker Pucker Family Foundation.

Aggression in individuals is influenced by genetic and environmental factors, but can be reduced with treatment, according to Emil F. Coccaro, MD.

“It actually is a complex triad of emotion, cognition, and behavior. The emotion is anger, the cognition is hostility, and the behavior is aggression. And they sort of go in that order,” Dr. Coccaro said at Focus on Neuropsychiatry presented by Current Psychiatry and the American Academy of Clinical Psychiatrists.

Although aggression can be thought of in a numerous ways, premeditated and impulsive aggression are most relevant to behavioral studies in psychiatry, Dr. Coccaro explained. Premeditated aggression is goal oriented, while impulsive aggression comes from frustration or a response to a threat. Impulsive aggression is “typically social or frustrative in nature, and studies that we’ve done that show that individuals move toward a threat while nonaggressives move away it,” he said. Both types of aggression can be seen in the same individuals at different times.

Aggression also can be considered using a threshold model. Calm individuals, for example, might have a low baseline of aggression and a high threshold before they act out. An aggressive person, on the other hand, has a lower threshold and a higher baseline level. “Their delta to get to the point where they’re going to explode is much shorter, much lower than it is in someone who is healthy,” Dr. Coccaro said.

“What we think is that the threshold to explode is probably regulated by various neurobiological features. The baseline state of aggression also may be related to baseline neurobiological features, but also what’s going on in the environment, because the neurobiological features that send someone to exploding aggression are there all the time,” he explained.

Individuals with secondary aggression are likely to have an underlying condition, such as a primary disease of the brain, systemic or metabolic disorder, or a psychiatric disorder such as schizophrenia. “If someone’s schizophrenic and they’ve got voices telling them to hurt somebody, or delusions that someone’s going to hurt them, that’s not primary aggression, that’s secondary to the psychosis,” Dr. Coccaro noted.

An individual with primary aggression is likely to have intermittent explosive disorder (IED). IED is not a new diagnosis and has been listed in the DSM since the DSM-I as “passive-aggressive personality.” It was relisted in the DSM-II as “explosive personality,” then changed to IED in the DSM-3 as a diagnosis of exclusion that was poorly operationalized, according to Dr. Coccaro. The criteria for IED under the DSM-III did not define the number of recurrent outbursts needed, what they looked like, the time frame, and excluded people who were generally impulsive.

“That’s not really what these people look like and it’s not what impulsive aggression looks like,” he said. Although the DSM-IV removed the exclusion criteria for general impulsivity and aggression, “it was still purely operational.”

The DSM-5 criteria define IED as “verbal and physical aggression without destruction or assault, twice equally on average for 3 months, or three or more episodes of physical destruction/assault over a 1-year period. These individuals have outbursts “grossly out of proportion to provocation,” the aggression is generally impulsive, and it causes stress and impairment with an age of onset at older than 6 years.

“It’s not better accounted for a whole variety of things, but we actually made some of those exclusion criteria a little less stringent,” compared with criteria in the DSM-IV, Dr. Coccaro said. “That’s because it turns out that it doesn’t really matter much of the time what the comorbidity is. If you have this aggressiveness in the absence of those other conditions, it’s IED.”

According to a reanalysis of the National Comorbidity Survey, 11.7% of adolescents displayed aggressiveness within the last year and 17.3% over a lifetime, compared with 5.1% of adults within the last year and 8.0% within a lifetime. Under DSM-5 criteria, 6.4% of adolescents within the last year and 8.9% over a lifetime currently have IED, compared with 2.6% of adults within the last year and 4.0% over a lifetime, but “could go as high” as the percentage of individuals diagnosed with aggressiveness, Dr. Coccaro noted.

“People who are not called IED many times are not called IED because we didn’t have all the information we needed to actually make the diagnosis,” he said.

Individuals with DSM-5 IED can have as many as 30 episodes in 1 year, compared with those who are nonaggressive and are also more likely to damage property. “These are the big episodes, not simply the episodes where people are getting irritable and snapping at people. These are the big ones, where they’re really destroying objects and pushing or hitting people,” Dr. Coccaro said. About one-fourth of individuals with IED hurt victims badly enough that they require medical attention, one-fifth exhibit aggression toward a partner, and one-fourth receive aggression from their own partner.

In terms of comorbidity with other psychiatric disorders, “IEDs don’t have more comorbidity in general than other disorders,” Dr. Coccaro noted. Personality disorders such as paranoid, antisocial, borderline narcissistic, and obsessive-compulsive disorders are more common in individuals with IED. Aggression in these people present differently depending on the personality disorder. “Someone who’s paranoid might blow up at you if you get in their face. For an antisocial, they’ll blow up at you if you’re preventing them from doing what they want to do. Borderlines, you reject them or you abandon them, they’re going to blow up. Narcissists will blow up when you reject. OCD will also blow up when you mess around with their sense of order,” Dr. Coccaro said.

Genetics also play a role in whether a person may have IED. There is a “clear signal” in families, with about one-fourth of individuals with IED having a relative with IED, compared with 8% of nonaggressive individuals. These percentages were consistent, regardless of whether the individual had a comorbid condition, history of alcohol or drug use, or history of suicide, he said. Other factors that influence likelihood of IED are environment, behaviors such as smoking, and conditions such as traumatic brain injury. Experiencing aggression as a child is another factor.

“IED is the categorical expression of impulsive aggression, and it’s far more common than once thought,” Dr. Coccaro said. “And IED is totally unrecognized in its role in societal violence.”
 

Treatment can suppress, but not cure aggression

Medications used to treat aggression and impulsive aggression include lithium, SSRIs, mood stabilizers, neuroleptics, and beta-blockers. However, the treatments are not a “magic bullet,” Dr. Coccaro noted. “The meds tend to suppress aggressiveness, but not cure it.”

Timing of treatment is also a factor for medication. In studies of patients taking lithium for aggression, for example, “when they gave the drug to people who liked being aggressive, they didn’t like being on these drugs because it made them feel unprotected. It just was at odds with who they thought they were,” Dr. Coccaro said. “The people who took the drug and did well and really liked being on the drug with people who didn’t like that they were aggressive.”

Neurorehabilitation and cognitive-behavioral therapy specific to aggression, called cognitive relaxation and coping skills therapy, are nonpsychotropic approaches to treating aggression. “These therapeutic approaches are working not only to reduce progression, but also to reduce the social information processing problems that aggressive individuals have,” Dr. Coccaro said.

Another approach, known as interpretation bias training, teaches individuals with aggression to judge slightly angry-looking photos of people as not being angry. After 7-14 days of training, aggressive behavior in adolescents has been shown to be reduced. The changes were also visible on functional MRI.

“What they found was that when you treated them, the change in the amygdala went down when you looked at the angry faces and in the left lateral, post training, they became happier,” Dr. Coccaro said.

Global Academy and this news organization are owned by the same parent company. Dr. Coccaro reported serving as a consultant for Avanir, Azevan, and Bracket. He also reported receiving research grants from the National Institute of Mental Health, the National Institute on Alcohol Abuse and Alcoholism, and the Pritzker Pucker Family Foundation.