Covid ICYMI

Epithelial and immune cells of the upper airways of children are preactivated and primed to detect SARS-CoV-2 infection, which may contribute to stronger early immune responses to SARS-CoV-2 infection than adults, new research suggests.

The findings may help to explain why children have a lower risk of developing severe COVID-19 illness or becoming infected with SARS-CoV-2 in the first place, the researchers say.

The study was published online Aug. 18 in Nature Biotechnology.
 

Primed for action

Children appear to be better able than adults to control SARS-CoV-2 infection, but, until now, the exact molecular mechanisms have been unclear.

A team of investigators from Germany did an in-depth analysis of nasal swab samples obtained from 24 children and 21 adults who tested positive for SARS-CoV-2, as well as a control group of 18 children and 23 adults who tested negative for SARS-CoV-2.

“We wanted to understand why viral defense appears to work so much better in children than in adults,” Irina Lehmann, PhD, head of the molecular epidemiology unit at the Berlin Institute of Health Charité – Universitätsmedizin Berlin, explained in a news release. 

Single-cell sequencing showed that children had higher baseline levels of certain RNA-sensing receptors that are relevant to SARS-CoV-2 detection, such as MDA5 and RIG-I, in the epithelial and immune cells of their noses.

This differential expression led to stronger early immune responses to SARS-CoV-2 infection in children than in adults.

Children were also more likely than adults to have distinct immune cell subpopulations, including KLRC1+ cytotoxic T cells, involved in fighting infection, and memory CD8+ T cells, associated with the development of long-lasting immunity.
 

‘Clear evidence’

The study provides “clear evidence” that upper-airway immune cells of children are “primed for virus sensing, resulting in a stronger early innate antiviral response to SARS-CoV-2 infection than in adults,” the investigators say.

Primed virus sensing and a preactivated innate immune response in children leads to efficient early production of interferons (IFNs) in the infected airways, likely mediating substantial antiviral effects, they note.

Ultimately, this may lead to lower viral replication and faster clearance in children. In fact, several studies have already shown that children eliminate the virus more quickly than adults, consistent with the concept that they shut down viral replication earlier, the study team says.

Weighing in on the findings for this news organization, John Wherry, PhD, director of the Institute for Immunology at the University of Pennsylvania, Philadelphia, said this “interesting study highlights potential differences in innate immunity and possibly geographic immunity in the upper respiratory tract in children versus adults.”

“We know there are differences in innate immunity over a lifespan, but exactly how these differences might relate to viral infection remains unclear,” said Dr. Wherry, who was not involved in the study.

“Children, of course, often have more respiratory infections than adults [but] whether this is due to exposure [i.e., daycare, schools, etc.] or susceptibility [lack of accumulated adaptive immunity over a greater number of years of exposure] is unclear,” Dr. Wherry noted.

“These data may help reveal what kinds of innate immune responses in the upper respiratory tract might help restrain SARS-CoV-2 and [perhaps partially] explain why children typically have milder COVID-19 disease,” he added.

The study was supported by the Berlin Institute of Health COVID-19 research program and fightCOVID@DKFZ initiative, European Commission, German Federal Ministry for Education and Research (BMBF), and German Research Foundation. Dr. Lehmann and Dr. Wherry have reported no relevant financial relationships.

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

Epithelial and immune cells of the upper airways of children are preactivated and primed to detect SARS-CoV-2 infection, which may contribute to stronger early immune responses to SARS-CoV-2 infection than adults, new research suggests.

The findings may help to explain why children have a lower risk of developing severe COVID-19 illness or becoming infected with SARS-CoV-2 in the first place, the researchers say.

The study was published online Aug. 18 in Nature Biotechnology.
 

Primed for action

Children appear to be better able than adults to control SARS-CoV-2 infection, but, until now, the exact molecular mechanisms have been unclear.

A team of investigators from Germany did an in-depth analysis of nasal swab samples obtained from 24 children and 21 adults who tested positive for SARS-CoV-2, as well as a control group of 18 children and 23 adults who tested negative for SARS-CoV-2.

“We wanted to understand why viral defense appears to work so much better in children than in adults,” Irina Lehmann, PhD, head of the molecular epidemiology unit at the Berlin Institute of Health Charité – Universitätsmedizin Berlin, explained in a news release. 

Single-cell sequencing showed that children had higher baseline levels of certain RNA-sensing receptors that are relevant to SARS-CoV-2 detection, such as MDA5 and RIG-I, in the epithelial and immune cells of their noses.

This differential expression led to stronger early immune responses to SARS-CoV-2 infection in children than in adults.

Children were also more likely than adults to have distinct immune cell subpopulations, including KLRC1+ cytotoxic T cells, involved in fighting infection, and memory CD8+ T cells, associated with the development of long-lasting immunity.
 

‘Clear evidence’

The study provides “clear evidence” that upper-airway immune cells of children are “primed for virus sensing, resulting in a stronger early innate antiviral response to SARS-CoV-2 infection than in adults,” the investigators say.

Primed virus sensing and a preactivated innate immune response in children leads to efficient early production of interferons (IFNs) in the infected airways, likely mediating substantial antiviral effects, they note.

Ultimately, this may lead to lower viral replication and faster clearance in children. In fact, several studies have already shown that children eliminate the virus more quickly than adults, consistent with the concept that they shut down viral replication earlier, the study team says.

Weighing in on the findings for this news organization, John Wherry, PhD, director of the Institute for Immunology at the University of Pennsylvania, Philadelphia, said this “interesting study highlights potential differences in innate immunity and possibly geographic immunity in the upper respiratory tract in children versus adults.”

“We know there are differences in innate immunity over a lifespan, but exactly how these differences might relate to viral infection remains unclear,” said Dr. Wherry, who was not involved in the study.

“Children, of course, often have more respiratory infections than adults [but] whether this is due to exposure [i.e., daycare, schools, etc.] or susceptibility [lack of accumulated adaptive immunity over a greater number of years of exposure] is unclear,” Dr. Wherry noted.

“These data may help reveal what kinds of innate immune responses in the upper respiratory tract might help restrain SARS-CoV-2 and [perhaps partially] explain why children typically have milder COVID-19 disease,” he added.

The study was supported by the Berlin Institute of Health COVID-19 research program and fightCOVID@DKFZ initiative, European Commission, German Federal Ministry for Education and Research (BMBF), and German Research Foundation. Dr. Lehmann and Dr. Wherry have reported no relevant financial relationships.

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

Epithelial and immune cells of the upper airways of children are preactivated and primed to detect SARS-CoV-2 infection, which may contribute to stronger early immune responses to SARS-CoV-2 infection than adults, new research suggests.

The findings may help to explain why children have a lower risk of developing severe COVID-19 illness or becoming infected with SARS-CoV-2 in the first place, the researchers say.

The study was published online Aug. 18 in Nature Biotechnology.
 

Primed for action

Children appear to be better able than adults to control SARS-CoV-2 infection, but, until now, the exact molecular mechanisms have been unclear.

A team of investigators from Germany did an in-depth analysis of nasal swab samples obtained from 24 children and 21 adults who tested positive for SARS-CoV-2, as well as a control group of 18 children and 23 adults who tested negative for SARS-CoV-2.

“We wanted to understand why viral defense appears to work so much better in children than in adults,” Irina Lehmann, PhD, head of the molecular epidemiology unit at the Berlin Institute of Health Charité – Universitätsmedizin Berlin, explained in a news release. 

Single-cell sequencing showed that children had higher baseline levels of certain RNA-sensing receptors that are relevant to SARS-CoV-2 detection, such as MDA5 and RIG-I, in the epithelial and immune cells of their noses.

This differential expression led to stronger early immune responses to SARS-CoV-2 infection in children than in adults.

Children were also more likely than adults to have distinct immune cell subpopulations, including KLRC1+ cytotoxic T cells, involved in fighting infection, and memory CD8+ T cells, associated with the development of long-lasting immunity.
 

‘Clear evidence’

The study provides “clear evidence” that upper-airway immune cells of children are “primed for virus sensing, resulting in a stronger early innate antiviral response to SARS-CoV-2 infection than in adults,” the investigators say.

Primed virus sensing and a preactivated innate immune response in children leads to efficient early production of interferons (IFNs) in the infected airways, likely mediating substantial antiviral effects, they note.

Ultimately, this may lead to lower viral replication and faster clearance in children. In fact, several studies have already shown that children eliminate the virus more quickly than adults, consistent with the concept that they shut down viral replication earlier, the study team says.

Weighing in on the findings for this news organization, John Wherry, PhD, director of the Institute for Immunology at the University of Pennsylvania, Philadelphia, said this “interesting study highlights potential differences in innate immunity and possibly geographic immunity in the upper respiratory tract in children versus adults.”

“We know there are differences in innate immunity over a lifespan, but exactly how these differences might relate to viral infection remains unclear,” said Dr. Wherry, who was not involved in the study.

“Children, of course, often have more respiratory infections than adults [but] whether this is due to exposure [i.e., daycare, schools, etc.] or susceptibility [lack of accumulated adaptive immunity over a greater number of years of exposure] is unclear,” Dr. Wherry noted.

“These data may help reveal what kinds of innate immune responses in the upper respiratory tract might help restrain SARS-CoV-2 and [perhaps partially] explain why children typically have milder COVID-19 disease,” he added.

The study was supported by the Berlin Institute of Health COVID-19 research program and fightCOVID@DKFZ initiative, European Commission, German Federal Ministry for Education and Research (BMBF), and German Research Foundation. Dr. Lehmann and Dr. Wherry have reported no relevant financial relationships.

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

A handful of studies have suggested that for newly infected COVID-19 patients, risk for serious illness may be reduced with a short course of fluvoxamine (Luvox), a decades-old pill typically prescribed for depression or obsessive-compulsive disorder (OCD). But those were small studies involving just a few hundred people.

This week, researchers reported promising data from a large, randomized phase 3 trial that enrolled COVID-19 patients from 11 sites in Brazil. In this study, in which 1,472 people were assigned to receive either a 10-day course of fluvoxamine or placebo pills, the antidepressant cut emergency department and hospital admissions by 29%.

Findings from the new study, which have not yet been peer reviewed, were published August 23 in MedRxiv.

Around the globe, particularly in countries without access to vaccines, “treatment options that are cheap and available and supported by good-quality evidence are the only hope we’ve got to reduce mortality within high-risk populations,” said Edward Mills, PhD, professor in the department of health research methods, evidence, and impact, McMaster University, Hamilton, Ont.

The new findings came from TOGETHER, a large platform trial coordinated by Dr. Mills and colleagues to evaluate the use of fluvoxamine and other repurposed drug candidates for symptomatic, high-risk, adult outpatients with confirmed cases of COVID-19.

The trial’s adaptive format allows multiple agents to be added and tested alongside placebo in a single master protocol – similar to the United Kingdom’s Recovery trial, which found that the common steroid dexamethasone could reduce deaths among hospitalized COVID-19 patients.

In platform trials, treatment arms can be dropped for futility, as was the case with hydroxychloroquine and lopinavir-ritonavir, neither of which did better than placebo at preventing hospitalization in an earlier TOGETHER trial analysis.
 

Study details

In the newly reported analysis, patients were randomly assigned to receive fluvoxamine or placebo between January and August 2021. Participants took fluvoxamine 100 mg twice daily for 10 days. By comparison, the U.S. Food and Drug Administration recommends a maximum daily dose of 300 mg of fluvoxamine for patients with OCD; full psychiatric benefits occur after 6 weeks.

For the primary outcome, the investigators assessed whether the conditions of patients with COVID worsened over a 28-day period so as to require either hospitalization or observation in the emergency department for more than 6 hours. In the placebo group, 108 of 733 patients’ conditions deteriorated to this extent (14.7%); by contrast, only 77 of 739 patients in the fluvoxamine group (10.4%) met these primary criteria – a relative risk reduction of 29%.

The treatment effect was greater (34%) in the per protocol analysis of participants who completed their course of pills.

The investigators also collected data on vital signs, including temperature and oxygen saturation, as well as adverse events reported at clinic visits or through video conferencing, phone calls, or social media applications. Side effects were mild, most commonly nausea and fatigue, and did not differ significantly between active treatment and control groups, Dr. Mills said in an interview.

Amid scores of studies evaluating repurposed drugs for COVID-19, the data on fluvoxamine are “looking much more favorable than anyone could have guessed – at least anyone in infectious disease,” said Paul Sax, MD, clinical director of the Division of Infectious Diseases at Brigham and Women’s Hospital and professor of medicine at Harvard Medical School, Boston.

The new TOGETHER trial results augment supportive data published in JAMA last November from a phase 2 randomized trial that was small but “very well done,” Dr. Sax told this news organization.

Those results got a boost from a subsequent study of 65 racetrack workers who chose to take fluvoxamine during a COVID-19 outbreak in the San Francisco Bay area. Forty-eight persons opted against taking the drug. In this small, nonrandomized study, “the people who chose to be treated with fluvoxamine were sicker [at baseline] than the people who didn’t go on it, and yet the [treated group] ended up better,” said Dr. Sax, who discussed accumulating data on the use of fluvoxamine for COVID-19 in a recent New England Journal of Medicine blog post.
 

Anti-inflammatory effect?

After reviewing the new findings, Frank Domino, MD, professor of family medicine and community health at the University of Massachusetts, Worcester, said he would encourage patients with high-risk COVID-19 to consider taking fluvoxamine to lower their risk of being hospitalized. “But I would make it clear this was not a ‘cure,’ “ he said, “and we are unsure how it helps.”

At this point, U.S. treatment guidelines do not recommend fluvoxamine as the standard of care for nonhospitalized COVID-19 patients, but the National Institutes of Health is “very aware of the data,” Dr. Sax told this news organization.

Fluvoxamine is a selective serotonin reuptake inhibitor (SSRI) – a class of drugs that includes the more commonly prescribed antidepressant fluoxetine (Prozac). If prescribed off-label to COVID-19 patients, fluvoxamine should not be used within 2 weeks of starting treatment with other SSRI or monoamine oxidase inhibitor antidepressants and should be used with caution with other QT-interval prolonging medications, Dr. Sax said.

In addition, fluvoxamine can enhance the effect of antiplatelet and anticoagulant drugs, potentially triggering bleeding.

On the basis of in vitro and mouse studies of fluvoxamine, “we think it has an anti-inflammatory effect,” said child psychiatrist Angela Reiersen, MD, of Washington University, St. Louis, who came up with the idea for testing fluvoxamine in last year’s phase 2 trial and coauthored a recent article describing the drug’s potential mechanisms of action in COVID-19.

She and other researchers believe fluvoxamine’s anti-inflammatory effects derive from the molecule’s binding to the sigma-1 receptor in the endoplasmic reticulum, which regulates cellular responses to stress and infection.

Fluvoxamine also inhibits the activation of platelets. “In COVID-19, there does seem to be a problem with hyperactivation of platelets and excessive blood clots forming, so it is possible this could be another mechanism where it might be helping,” Dr. Reiersen said.

If sigma-1 activation turns out to be the main mechanism underlying fluvoxamine’s benefits in COVID-19, other sigma-1 agonists, such as fluoxetine, may also help. In a retrospective analysis of thousands of adults hospitalized for COVID-19 in France early in the pandemic, those who were taking antidepressants had a 44% lower risk for intubation or death.

And in a study under review, researchers at Stanford (Calif.) University and the University of California, San Francisco, analyzed electronic health records to explore a potential link between fluoxetine use and COVID outcomes among more than 80,000 patients from over 80 institutions across the United States. Other research suggests that antipsychotics could also have protective effects for patients with COVID-19.
 

Long COVID, long-term challenges

On the basis of its potential mechanisms of action, fluvoxamine may be able to prevent or treat long COVID, Dr. Reiersen said. That possibility will be assessed among other secondary endpoints in two ongoing studies of repurposed drugs: the NIH’s ACTIV-6, and the University of Minnesota’s COVID-OUT, an at-home trial of ivermectin, metformin, and fluvoxamine.

Dr. Reiersen and Washington University colleagues are also analyzing longer-term outcomes of participants in their own phase 3 trial of fluvoxamine (Stop COVID 2), which was discontinued when enrollment slowed to a trickle during the U.S. vaccine rollout. Logistical hurdles and scant funding have greatly hampered efforts to test the use of off-patent drugs for COVID-19 outpatients during the pandemic.

U.S. efforts face other obstacles as well. Elsewhere in the world – including Brazil, where the TOGETHER trial was run – vaccines are scarce, and there are no monoclonal antibodies.

“People have a great sense of community duty, and they’re participating in the trials,” Dr. Mills said. “You’re in a much more political environment in the U.S. on these outpatient trials.”

The TOGETHER trial was funded by Fast Grants and the Rainwater Foundation. Dr. Reiersen is an inventor on a patent application related to methods of treating COVID-19, which was filed by Washington University, St. Louis. Dr. Mills, Dr. Domino, and Dr. Sax report no relevant financial relationships.

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

A handful of studies have suggested that for newly infected COVID-19 patients, risk for serious illness may be reduced with a short course of fluvoxamine (Luvox), a decades-old pill typically prescribed for depression or obsessive-compulsive disorder (OCD). But those were small studies involving just a few hundred people.

This week, researchers reported promising data from a large, randomized phase 3 trial that enrolled COVID-19 patients from 11 sites in Brazil. In this study, in which 1,472 people were assigned to receive either a 10-day course of fluvoxamine or placebo pills, the antidepressant cut emergency department and hospital admissions by 29%.

Findings from the new study, which have not yet been peer reviewed, were published August 23 in MedRxiv.

Around the globe, particularly in countries without access to vaccines, “treatment options that are cheap and available and supported by good-quality evidence are the only hope we’ve got to reduce mortality within high-risk populations,” said Edward Mills, PhD, professor in the department of health research methods, evidence, and impact, McMaster University, Hamilton, Ont.

The new findings came from TOGETHER, a large platform trial coordinated by Dr. Mills and colleagues to evaluate the use of fluvoxamine and other repurposed drug candidates for symptomatic, high-risk, adult outpatients with confirmed cases of COVID-19.

The trial’s adaptive format allows multiple agents to be added and tested alongside placebo in a single master protocol – similar to the United Kingdom’s Recovery trial, which found that the common steroid dexamethasone could reduce deaths among hospitalized COVID-19 patients.

In platform trials, treatment arms can be dropped for futility, as was the case with hydroxychloroquine and lopinavir-ritonavir, neither of which did better than placebo at preventing hospitalization in an earlier TOGETHER trial analysis.
 

Study details

In the newly reported analysis, patients were randomly assigned to receive fluvoxamine or placebo between January and August 2021. Participants took fluvoxamine 100 mg twice daily for 10 days. By comparison, the U.S. Food and Drug Administration recommends a maximum daily dose of 300 mg of fluvoxamine for patients with OCD; full psychiatric benefits occur after 6 weeks.

For the primary outcome, the investigators assessed whether the conditions of patients with COVID worsened over a 28-day period so as to require either hospitalization or observation in the emergency department for more than 6 hours. In the placebo group, 108 of 733 patients’ conditions deteriorated to this extent (14.7%); by contrast, only 77 of 739 patients in the fluvoxamine group (10.4%) met these primary criteria – a relative risk reduction of 29%.

The treatment effect was greater (34%) in the per protocol analysis of participants who completed their course of pills.

The investigators also collected data on vital signs, including temperature and oxygen saturation, as well as adverse events reported at clinic visits or through video conferencing, phone calls, or social media applications. Side effects were mild, most commonly nausea and fatigue, and did not differ significantly between active treatment and control groups, Dr. Mills said in an interview.

Amid scores of studies evaluating repurposed drugs for COVID-19, the data on fluvoxamine are “looking much more favorable than anyone could have guessed – at least anyone in infectious disease,” said Paul Sax, MD, clinical director of the Division of Infectious Diseases at Brigham and Women’s Hospital and professor of medicine at Harvard Medical School, Boston.

The new TOGETHER trial results augment supportive data published in JAMA last November from a phase 2 randomized trial that was small but “very well done,” Dr. Sax told this news organization.

Those results got a boost from a subsequent study of 65 racetrack workers who chose to take fluvoxamine during a COVID-19 outbreak in the San Francisco Bay area. Forty-eight persons opted against taking the drug. In this small, nonrandomized study, “the people who chose to be treated with fluvoxamine were sicker [at baseline] than the people who didn’t go on it, and yet the [treated group] ended up better,” said Dr. Sax, who discussed accumulating data on the use of fluvoxamine for COVID-19 in a recent New England Journal of Medicine blog post.
 

Anti-inflammatory effect?

After reviewing the new findings, Frank Domino, MD, professor of family medicine and community health at the University of Massachusetts, Worcester, said he would encourage patients with high-risk COVID-19 to consider taking fluvoxamine to lower their risk of being hospitalized. “But I would make it clear this was not a ‘cure,’ “ he said, “and we are unsure how it helps.”

At this point, U.S. treatment guidelines do not recommend fluvoxamine as the standard of care for nonhospitalized COVID-19 patients, but the National Institutes of Health is “very aware of the data,” Dr. Sax told this news organization.

Fluvoxamine is a selective serotonin reuptake inhibitor (SSRI) – a class of drugs that includes the more commonly prescribed antidepressant fluoxetine (Prozac). If prescribed off-label to COVID-19 patients, fluvoxamine should not be used within 2 weeks of starting treatment with other SSRI or monoamine oxidase inhibitor antidepressants and should be used with caution with other QT-interval prolonging medications, Dr. Sax said.

In addition, fluvoxamine can enhance the effect of antiplatelet and anticoagulant drugs, potentially triggering bleeding.

On the basis of in vitro and mouse studies of fluvoxamine, “we think it has an anti-inflammatory effect,” said child psychiatrist Angela Reiersen, MD, of Washington University, St. Louis, who came up with the idea for testing fluvoxamine in last year’s phase 2 trial and coauthored a recent article describing the drug’s potential mechanisms of action in COVID-19.

She and other researchers believe fluvoxamine’s anti-inflammatory effects derive from the molecule’s binding to the sigma-1 receptor in the endoplasmic reticulum, which regulates cellular responses to stress and infection.

Fluvoxamine also inhibits the activation of platelets. “In COVID-19, there does seem to be a problem with hyperactivation of platelets and excessive blood clots forming, so it is possible this could be another mechanism where it might be helping,” Dr. Reiersen said.

If sigma-1 activation turns out to be the main mechanism underlying fluvoxamine’s benefits in COVID-19, other sigma-1 agonists, such as fluoxetine, may also help. In a retrospective analysis of thousands of adults hospitalized for COVID-19 in France early in the pandemic, those who were taking antidepressants had a 44% lower risk for intubation or death.

And in a study under review, researchers at Stanford (Calif.) University and the University of California, San Francisco, analyzed electronic health records to explore a potential link between fluoxetine use and COVID outcomes among more than 80,000 patients from over 80 institutions across the United States. Other research suggests that antipsychotics could also have protective effects for patients with COVID-19.
 

Long COVID, long-term challenges

On the basis of its potential mechanisms of action, fluvoxamine may be able to prevent or treat long COVID, Dr. Reiersen said. That possibility will be assessed among other secondary endpoints in two ongoing studies of repurposed drugs: the NIH’s ACTIV-6, and the University of Minnesota’s COVID-OUT, an at-home trial of ivermectin, metformin, and fluvoxamine.

Dr. Reiersen and Washington University colleagues are also analyzing longer-term outcomes of participants in their own phase 3 trial of fluvoxamine (Stop COVID 2), which was discontinued when enrollment slowed to a trickle during the U.S. vaccine rollout. Logistical hurdles and scant funding have greatly hampered efforts to test the use of off-patent drugs for COVID-19 outpatients during the pandemic.

U.S. efforts face other obstacles as well. Elsewhere in the world – including Brazil, where the TOGETHER trial was run – vaccines are scarce, and there are no monoclonal antibodies.

“People have a great sense of community duty, and they’re participating in the trials,” Dr. Mills said. “You’re in a much more political environment in the U.S. on these outpatient trials.”

The TOGETHER trial was funded by Fast Grants and the Rainwater Foundation. Dr. Reiersen is an inventor on a patent application related to methods of treating COVID-19, which was filed by Washington University, St. Louis. Dr. Mills, Dr. Domino, and Dr. Sax report no relevant financial relationships.

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

A handful of studies have suggested that for newly infected COVID-19 patients, risk for serious illness may be reduced with a short course of fluvoxamine (Luvox), a decades-old pill typically prescribed for depression or obsessive-compulsive disorder (OCD). But those were small studies involving just a few hundred people.

This week, researchers reported promising data from a large, randomized phase 3 trial that enrolled COVID-19 patients from 11 sites in Brazil. In this study, in which 1,472 people were assigned to receive either a 10-day course of fluvoxamine or placebo pills, the antidepressant cut emergency department and hospital admissions by 29%.

Findings from the new study, which have not yet been peer reviewed, were published August 23 in MedRxiv.

Around the globe, particularly in countries without access to vaccines, “treatment options that are cheap and available and supported by good-quality evidence are the only hope we’ve got to reduce mortality within high-risk populations,” said Edward Mills, PhD, professor in the department of health research methods, evidence, and impact, McMaster University, Hamilton, Ont.

The new findings came from TOGETHER, a large platform trial coordinated by Dr. Mills and colleagues to evaluate the use of fluvoxamine and other repurposed drug candidates for symptomatic, high-risk, adult outpatients with confirmed cases of COVID-19.

The trial’s adaptive format allows multiple agents to be added and tested alongside placebo in a single master protocol – similar to the United Kingdom’s Recovery trial, which found that the common steroid dexamethasone could reduce deaths among hospitalized COVID-19 patients.

In platform trials, treatment arms can be dropped for futility, as was the case with hydroxychloroquine and lopinavir-ritonavir, neither of which did better than placebo at preventing hospitalization in an earlier TOGETHER trial analysis.
 

Study details

In the newly reported analysis, patients were randomly assigned to receive fluvoxamine or placebo between January and August 2021. Participants took fluvoxamine 100 mg twice daily for 10 days. By comparison, the U.S. Food and Drug Administration recommends a maximum daily dose of 300 mg of fluvoxamine for patients with OCD; full psychiatric benefits occur after 6 weeks.

For the primary outcome, the investigators assessed whether the conditions of patients with COVID worsened over a 28-day period so as to require either hospitalization or observation in the emergency department for more than 6 hours. In the placebo group, 108 of 733 patients’ conditions deteriorated to this extent (14.7%); by contrast, only 77 of 739 patients in the fluvoxamine group (10.4%) met these primary criteria – a relative risk reduction of 29%.

The treatment effect was greater (34%) in the per protocol analysis of participants who completed their course of pills.

The investigators also collected data on vital signs, including temperature and oxygen saturation, as well as adverse events reported at clinic visits or through video conferencing, phone calls, or social media applications. Side effects were mild, most commonly nausea and fatigue, and did not differ significantly between active treatment and control groups, Dr. Mills said in an interview.

Amid scores of studies evaluating repurposed drugs for COVID-19, the data on fluvoxamine are “looking much more favorable than anyone could have guessed – at least anyone in infectious disease,” said Paul Sax, MD, clinical director of the Division of Infectious Diseases at Brigham and Women’s Hospital and professor of medicine at Harvard Medical School, Boston.

The new TOGETHER trial results augment supportive data published in JAMA last November from a phase 2 randomized trial that was small but “very well done,” Dr. Sax told this news organization.

Those results got a boost from a subsequent study of 65 racetrack workers who chose to take fluvoxamine during a COVID-19 outbreak in the San Francisco Bay area. Forty-eight persons opted against taking the drug. In this small, nonrandomized study, “the people who chose to be treated with fluvoxamine were sicker [at baseline] than the people who didn’t go on it, and yet the [treated group] ended up better,” said Dr. Sax, who discussed accumulating data on the use of fluvoxamine for COVID-19 in a recent New England Journal of Medicine blog post.
 

Anti-inflammatory effect?

After reviewing the new findings, Frank Domino, MD, professor of family medicine and community health at the University of Massachusetts, Worcester, said he would encourage patients with high-risk COVID-19 to consider taking fluvoxamine to lower their risk of being hospitalized. “But I would make it clear this was not a ‘cure,’ “ he said, “and we are unsure how it helps.”

At this point, U.S. treatment guidelines do not recommend fluvoxamine as the standard of care for nonhospitalized COVID-19 patients, but the National Institutes of Health is “very aware of the data,” Dr. Sax told this news organization.

Fluvoxamine is a selective serotonin reuptake inhibitor (SSRI) – a class of drugs that includes the more commonly prescribed antidepressant fluoxetine (Prozac). If prescribed off-label to COVID-19 patients, fluvoxamine should not be used within 2 weeks of starting treatment with other SSRI or monoamine oxidase inhibitor antidepressants and should be used with caution with other QT-interval prolonging medications, Dr. Sax said.

In addition, fluvoxamine can enhance the effect of antiplatelet and anticoagulant drugs, potentially triggering bleeding.

On the basis of in vitro and mouse studies of fluvoxamine, “we think it has an anti-inflammatory effect,” said child psychiatrist Angela Reiersen, MD, of Washington University, St. Louis, who came up with the idea for testing fluvoxamine in last year’s phase 2 trial and coauthored a recent article describing the drug’s potential mechanisms of action in COVID-19.

She and other researchers believe fluvoxamine’s anti-inflammatory effects derive from the molecule’s binding to the sigma-1 receptor in the endoplasmic reticulum, which regulates cellular responses to stress and infection.

Fluvoxamine also inhibits the activation of platelets. “In COVID-19, there does seem to be a problem with hyperactivation of platelets and excessive blood clots forming, so it is possible this could be another mechanism where it might be helping,” Dr. Reiersen said.

If sigma-1 activation turns out to be the main mechanism underlying fluvoxamine’s benefits in COVID-19, other sigma-1 agonists, such as fluoxetine, may also help. In a retrospective analysis of thousands of adults hospitalized for COVID-19 in France early in the pandemic, those who were taking antidepressants had a 44% lower risk for intubation or death.

And in a study under review, researchers at Stanford (Calif.) University and the University of California, San Francisco, analyzed electronic health records to explore a potential link between fluoxetine use and COVID outcomes among more than 80,000 patients from over 80 institutions across the United States. Other research suggests that antipsychotics could also have protective effects for patients with COVID-19.
 

Long COVID, long-term challenges

On the basis of its potential mechanisms of action, fluvoxamine may be able to prevent or treat long COVID, Dr. Reiersen said. That possibility will be assessed among other secondary endpoints in two ongoing studies of repurposed drugs: the NIH’s ACTIV-6, and the University of Minnesota’s COVID-OUT, an at-home trial of ivermectin, metformin, and fluvoxamine.

Dr. Reiersen and Washington University colleagues are also analyzing longer-term outcomes of participants in their own phase 3 trial of fluvoxamine (Stop COVID 2), which was discontinued when enrollment slowed to a trickle during the U.S. vaccine rollout. Logistical hurdles and scant funding have greatly hampered efforts to test the use of off-patent drugs for COVID-19 outpatients during the pandemic.

U.S. efforts face other obstacles as well. Elsewhere in the world – including Brazil, where the TOGETHER trial was run – vaccines are scarce, and there are no monoclonal antibodies.

“People have a great sense of community duty, and they’re participating in the trials,” Dr. Mills said. “You’re in a much more political environment in the U.S. on these outpatient trials.”

The TOGETHER trial was funded by Fast Grants and the Rainwater Foundation. Dr. Reiersen is an inventor on a patent application related to methods of treating COVID-19, which was filed by Washington University, St. Louis. Dr. Mills, Dr. Domino, and Dr. Sax report no relevant financial relationships.

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

As governors and legislatures in states such as Texas, Florida, South Carolina, and Arkansas have banned schools and other entities from implementing mask mandates, disability rights advocates have pushed back. In federal civil rights lawsuits, they argue that bans on mask mandates violate antidiscrimination laws protecting people with disabilities.

OsakaWayne Studios/Moment

For unvaccinated and immunosuppressed individuals, masks can provide crucial protection from SARS-CoV-2.

People who are immunocompromised can harness the power of the Americans With Disabilities Act to fight against bans on mask mandates and protect themselves in their workplaces, argues Mical Raz, MD, PhD, a professor at the University of Rochester (N.Y.) and a physician at Strong Memorial Hospital, also in Rochester, New York, in an article published in JAMA with coauthor Doron Dorfman, LLB, JSD.

This news organization talked with Dr. Raz about approaching mask requirements as disability accommodation during the COVID-19 pandemic. The following interview was lightly edited for length and clarity.
 

How did you come to think about mask requirements as a form of disability accommodation?

I saw a tweet from a professor at a university who said they couldn’t ask students about their vaccination status or to wear a mask. All agency was removed from the professor to take care of and protect themselves. I thought, well, that can’t be right. And ostensibly, that would be particularly dangerous for somebody with immunosuppression for whom the vaccine is not adequately protective. So, I called my friend, Doron Dorfman, and asked him to help me think through the legal part of this. We fleshed it out and wrote the article that same night.
 

How novel is it to view accommodations for people who are immunosuppressed through the lens of disability accommodation?

I think there has not been enough focus during the pandemic on individuals with disabilities or on how disability law can be mobilized during this pandemic to help supplement the public health law. This framework should be used a lot more because it’s good for everybody, not just for individuals with disabilities.

For example, take what’s called the “curb effect.” If you expand sidewalks, yes, it helps individuals who use a wheelchair. But it also helps me as a mom with a stroller. It helps somebody with a shopping cart, or a kid with a bike. If we adopt policies that are inclusive to those who are disadvantaged, it’s good for everybody. We should always strive to be an inclusive society, not just because it’s the right thing to do but because it really makes our society better.
 

How can mask requirements be used as a form of disability accommodation, as you argue in the JAMA article?

The ADA requires employers to provide reasonable accommodations for disability. In this case, the disability is your immunosuppressive status. We have an abundance of evidence showing individuals who are immunocompromised and vaccinated are still inadequately protected from the SARS-CoV-2 virus. So, there is absolute data to show individuals with immunosuppression have a disability that requires accommodation.

The ADA has a mandate requiring employers to adjust or modify policies in order to accommodate a disability. There are certain situations in which you cannot or do not need to accommodate a disability, when it would fundamentally alter the kind of employment you offer or if it’s an undue burden or hardship. But given that we’ve been wearing masks and working remotely for a year now, arguing that somehow these accommodations are no longer possible seems disingenuous.

In that way, allowing a person who’s immunocompromised to require those around them to mask is a form of modified protective policies. And in this case, those policies line up with a public health good, masking in the face of the highly contagious Delta variant ravaging our country right now.
 

In your view, can this argument be used in the mask debates happening right now across the country?

This argument can and should be useful for a couple of different lawsuits that are now underway in different states. I hope our article will provide further support for those suits. And I hope in school board hearings, when parents and teachers are talking about their concerns, this could be one way to argue for why we should allow mask mandates in classes. I’ve received emails from parents who said they’re going to bring this article to their school board hearing.

I also hope this could shift the narrative around the pandemic. Instead of focusing on individual responsibility – I got my vaccine shot so I’m fine – let’s focus on how we create an inclusive environment where we protect everybody, including those who cannot be vaccinated because of age or disability, or those who are vaccinated but inadequately protected because of their underlying conditions.
 

In the JAMA article, you talk about how our pandemic response has focused on individual health and how that individual focus can be ableist. Can you explain that point?

I think this idea that we just make our choices – like whether to get vaccinated or wear a mask, or not – and live with it really perpetuates a highly individualistic and ableist mindset. It doesn’t consider the people I admit to the hospital who are vaccinated but have a heart transplant and didn’t mount the sufficient immune response. Or even the people who chose not to be vaccinated because they were exposed to hours and hours of misinformation on TV.

We like to individualize everything, focusing on personal responsibility and choices, but a pandemic is one of those moments where everybody’s choices affect everybody else. Laying responsibility at the doorstep of each person, rather than thinking about what steps we as a society could be taking, is cheap and politically expedient. There is no public health rationale behind the bans on mask requirements in states like Texas, Iowa, and Florida. These choices are about politics. And the price is always borne by the most disadvantaged among us.

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

As governors and legislatures in states such as Texas, Florida, South Carolina, and Arkansas have banned schools and other entities from implementing mask mandates, disability rights advocates have pushed back. In federal civil rights lawsuits, they argue that bans on mask mandates violate antidiscrimination laws protecting people with disabilities.

OsakaWayne Studios/Moment

For unvaccinated and immunosuppressed individuals, masks can provide crucial protection from SARS-CoV-2.

People who are immunocompromised can harness the power of the Americans With Disabilities Act to fight against bans on mask mandates and protect themselves in their workplaces, argues Mical Raz, MD, PhD, a professor at the University of Rochester (N.Y.) and a physician at Strong Memorial Hospital, also in Rochester, New York, in an article published in JAMA with coauthor Doron Dorfman, LLB, JSD.

This news organization talked with Dr. Raz about approaching mask requirements as disability accommodation during the COVID-19 pandemic. The following interview was lightly edited for length and clarity.
 

How did you come to think about mask requirements as a form of disability accommodation?

I saw a tweet from a professor at a university who said they couldn’t ask students about their vaccination status or to wear a mask. All agency was removed from the professor to take care of and protect themselves. I thought, well, that can’t be right. And ostensibly, that would be particularly dangerous for somebody with immunosuppression for whom the vaccine is not adequately protective. So, I called my friend, Doron Dorfman, and asked him to help me think through the legal part of this. We fleshed it out and wrote the article that same night.
 

How novel is it to view accommodations for people who are immunosuppressed through the lens of disability accommodation?

I think there has not been enough focus during the pandemic on individuals with disabilities or on how disability law can be mobilized during this pandemic to help supplement the public health law. This framework should be used a lot more because it’s good for everybody, not just for individuals with disabilities.

For example, take what’s called the “curb effect.” If you expand sidewalks, yes, it helps individuals who use a wheelchair. But it also helps me as a mom with a stroller. It helps somebody with a shopping cart, or a kid with a bike. If we adopt policies that are inclusive to those who are disadvantaged, it’s good for everybody. We should always strive to be an inclusive society, not just because it’s the right thing to do but because it really makes our society better.
 

How can mask requirements be used as a form of disability accommodation, as you argue in the JAMA article?

The ADA requires employers to provide reasonable accommodations for disability. In this case, the disability is your immunosuppressive status. We have an abundance of evidence showing individuals who are immunocompromised and vaccinated are still inadequately protected from the SARS-CoV-2 virus. So, there is absolute data to show individuals with immunosuppression have a disability that requires accommodation.

The ADA has a mandate requiring employers to adjust or modify policies in order to accommodate a disability. There are certain situations in which you cannot or do not need to accommodate a disability, when it would fundamentally alter the kind of employment you offer or if it’s an undue burden or hardship. But given that we’ve been wearing masks and working remotely for a year now, arguing that somehow these accommodations are no longer possible seems disingenuous.

In that way, allowing a person who’s immunocompromised to require those around them to mask is a form of modified protective policies. And in this case, those policies line up with a public health good, masking in the face of the highly contagious Delta variant ravaging our country right now.
 

In your view, can this argument be used in the mask debates happening right now across the country?

This argument can and should be useful for a couple of different lawsuits that are now underway in different states. I hope our article will provide further support for those suits. And I hope in school board hearings, when parents and teachers are talking about their concerns, this could be one way to argue for why we should allow mask mandates in classes. I’ve received emails from parents who said they’re going to bring this article to their school board hearing.

I also hope this could shift the narrative around the pandemic. Instead of focusing on individual responsibility – I got my vaccine shot so I’m fine – let’s focus on how we create an inclusive environment where we protect everybody, including those who cannot be vaccinated because of age or disability, or those who are vaccinated but inadequately protected because of their underlying conditions.
 

In the JAMA article, you talk about how our pandemic response has focused on individual health and how that individual focus can be ableist. Can you explain that point?

I think this idea that we just make our choices – like whether to get vaccinated or wear a mask, or not – and live with it really perpetuates a highly individualistic and ableist mindset. It doesn’t consider the people I admit to the hospital who are vaccinated but have a heart transplant and didn’t mount the sufficient immune response. Or even the people who chose not to be vaccinated because they were exposed to hours and hours of misinformation on TV.

We like to individualize everything, focusing on personal responsibility and choices, but a pandemic is one of those moments where everybody’s choices affect everybody else. Laying responsibility at the doorstep of each person, rather than thinking about what steps we as a society could be taking, is cheap and politically expedient. There is no public health rationale behind the bans on mask requirements in states like Texas, Iowa, and Florida. These choices are about politics. And the price is always borne by the most disadvantaged among us.

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

As governors and legislatures in states such as Texas, Florida, South Carolina, and Arkansas have banned schools and other entities from implementing mask mandates, disability rights advocates have pushed back. In federal civil rights lawsuits, they argue that bans on mask mandates violate antidiscrimination laws protecting people with disabilities.

OsakaWayne Studios/Moment

For unvaccinated and immunosuppressed individuals, masks can provide crucial protection from SARS-CoV-2.

People who are immunocompromised can harness the power of the Americans With Disabilities Act to fight against bans on mask mandates and protect themselves in their workplaces, argues Mical Raz, MD, PhD, a professor at the University of Rochester (N.Y.) and a physician at Strong Memorial Hospital, also in Rochester, New York, in an article published in JAMA with coauthor Doron Dorfman, LLB, JSD.

This news organization talked with Dr. Raz about approaching mask requirements as disability accommodation during the COVID-19 pandemic. The following interview was lightly edited for length and clarity.
 

How did you come to think about mask requirements as a form of disability accommodation?

I saw a tweet from a professor at a university who said they couldn’t ask students about their vaccination status or to wear a mask. All agency was removed from the professor to take care of and protect themselves. I thought, well, that can’t be right. And ostensibly, that would be particularly dangerous for somebody with immunosuppression for whom the vaccine is not adequately protective. So, I called my friend, Doron Dorfman, and asked him to help me think through the legal part of this. We fleshed it out and wrote the article that same night.
 

How novel is it to view accommodations for people who are immunosuppressed through the lens of disability accommodation?

I think there has not been enough focus during the pandemic on individuals with disabilities or on how disability law can be mobilized during this pandemic to help supplement the public health law. This framework should be used a lot more because it’s good for everybody, not just for individuals with disabilities.

For example, take what’s called the “curb effect.” If you expand sidewalks, yes, it helps individuals who use a wheelchair. But it also helps me as a mom with a stroller. It helps somebody with a shopping cart, or a kid with a bike. If we adopt policies that are inclusive to those who are disadvantaged, it’s good for everybody. We should always strive to be an inclusive society, not just because it’s the right thing to do but because it really makes our society better.
 

How can mask requirements be used as a form of disability accommodation, as you argue in the JAMA article?

The ADA requires employers to provide reasonable accommodations for disability. In this case, the disability is your immunosuppressive status. We have an abundance of evidence showing individuals who are immunocompromised and vaccinated are still inadequately protected from the SARS-CoV-2 virus. So, there is absolute data to show individuals with immunosuppression have a disability that requires accommodation.

The ADA has a mandate requiring employers to adjust or modify policies in order to accommodate a disability. There are certain situations in which you cannot or do not need to accommodate a disability, when it would fundamentally alter the kind of employment you offer or if it’s an undue burden or hardship. But given that we’ve been wearing masks and working remotely for a year now, arguing that somehow these accommodations are no longer possible seems disingenuous.

In that way, allowing a person who’s immunocompromised to require those around them to mask is a form of modified protective policies. And in this case, those policies line up with a public health good, masking in the face of the highly contagious Delta variant ravaging our country right now.
 

In your view, can this argument be used in the mask debates happening right now across the country?

This argument can and should be useful for a couple of different lawsuits that are now underway in different states. I hope our article will provide further support for those suits. And I hope in school board hearings, when parents and teachers are talking about their concerns, this could be one way to argue for why we should allow mask mandates in classes. I’ve received emails from parents who said they’re going to bring this article to their school board hearing.

I also hope this could shift the narrative around the pandemic. Instead of focusing on individual responsibility – I got my vaccine shot so I’m fine – let’s focus on how we create an inclusive environment where we protect everybody, including those who cannot be vaccinated because of age or disability, or those who are vaccinated but inadequately protected because of their underlying conditions.
 

In the JAMA article, you talk about how our pandemic response has focused on individual health and how that individual focus can be ableist. Can you explain that point?

I think this idea that we just make our choices – like whether to get vaccinated or wear a mask, or not – and live with it really perpetuates a highly individualistic and ableist mindset. It doesn’t consider the people I admit to the hospital who are vaccinated but have a heart transplant and didn’t mount the sufficient immune response. Or even the people who chose not to be vaccinated because they were exposed to hours and hours of misinformation on TV.

We like to individualize everything, focusing on personal responsibility and choices, but a pandemic is one of those moments where everybody’s choices affect everybody else. Laying responsibility at the doorstep of each person, rather than thinking about what steps we as a society could be taking, is cheap and politically expedient. There is no public health rationale behind the bans on mask requirements in states like Texas, Iowa, and Florida. These choices are about politics. And the price is always borne by the most disadvantaged among us.

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

Patients on immunosuppressive or immunomodulatory therapy should receive a third dose of either the Pfizer-BioNTech COVID-19 vaccine or the Moderna COVID-19 vaccine at least 28 days after the second dose of either of these two mRNA vaccines, according to updated recommendations from the American College of Rheumatology.

Mongkolchon Akesin/Getty Images

The update follows the Centers for Disease Control and Prevention’s recommendation that certain immunocompromised patients receive a third dose of an mRNA vaccine to reduce their risk of contracting COVID-19.

Individuals receiving the Pfizer vaccine must be aged 12 years and older, while those receiving the Moderna vaccine must be 18 years and older, the ACR emphasized.

“These statements were based upon a dearth of high-quality data and are not intended to replace clinical judgment,” the authors wrote. “Modifications made to treatment plans, particularly in complex rheumatic disease patients, are highly disease, patient, geography, and time specific and, therefore, must be individualized as part of a shared decision-making process.”

The task force recommended using the same mRNA vaccine booster as the patient received for their initial two-dose series when possible, but notes that either mRNA vaccine is acceptable, and recommends the mRNA vaccine for patients who have yet to receive any vaccine because of the availability of the booster. The task force emphasized that they achieved no consensus on recommending a booster mRNA vaccine to patients who received a single dose of Johnson & Johnson vaccine because the safety data are uncertain.

The updated guidance also identifies the Food and Drug Administration’s emergency use authorization in August for the use of REGEN-COV monoclonal antibody treatment for emergency postexposure prophylaxis for COVID-19 in adults and adolescents aged 12 years and older who weigh at least 40 kg and are at increased risk for severe COVID-19, which includes patients receiving immunosuppressive or immunomodulatory therapies other than hydroxychloroquine. Patients who have been exposed to an individual with COVID-19 should discuss this treatment with their health care provider as an added precaution; however, the guidance emphasized that the prophylactic treatment is not a substitute for COVID-19 vaccination.

The recommendations advise clinicians to counsel their patients to refrain from taking certain immunomodulatory or immunosuppressive medications for 1-2 weeks after booster vaccination if disease activity allows, with the exception of glucocorticoids and anticytokines such as tumor necrosis factor inhibitors and others including interleukin-17, IL-12/23, IL-23, IL-1R, IL-6R antagonists, for which the task force did not achieve a consensus recommendation.

The guidance notes that patients on rituximab or other anti-CD20 medications “should discuss the optimal timing [of the booster] with their rheumatology provider” and that some practitioners measure CD19 B cells as a tool with which to time the booster and subsequent rituximab dosing. For those who elect to dose without such information, or for whom such measurement is not available or feasible, provide the booster 2-4 weeks before next anticipated rituximab dose (e.g., at month 5.0 or 5.5 for patients on an every-6-month rituximab dosing schedule).”

There was strong consensus from the task force that health care providers “should not routinely order any lab testing (e.g., antibody tests for IgM and/or IgG to spike or nucleocapsid proteins) to assess immunity to COVID-19 post vaccination, nor to assess the need for vaccination in a yet-unvaccinated person.”

“The updated information from the ACR addresses not only booster vaccination but also other important and practical issues facing rheumatology providers and their patients related to the pandemic,” said task force chair Jeffrey R. Curtis, MD, of the University of Alabama at Birmingham, in an ACR statement announcing the updates.

“Although the guidance is issued in light of the best evidence available, the science regarding COVID-19 vaccination as it affects the practice of rheumatology is undergoing rapid evolution,” he noted. “We need direct evidence such as that from randomized trials to inform the best practices of what we can do to protect our patients from SARS-CoV-2.”

The update retains the current recommendations that rheumatology patients follow all public health guidelines regarding physical distancing and other preventive measures following vaccination, but the task force did not recommend exceeding current public health guidance. “The appropriateness for continued preventive measures (e.g., masking, physical distancing) should be discussed with patients as their rheumatology providers deem appropriate,” they wrote.

The full updated version of the ACR’s COVID-19 Vaccine Clinical Guidance for Patients with Rheumatic and Musculoskeletal Diseases will be published in Arthritis & Rheumatology. The summary was developed by the ACR COVID-19 Vaccine Clinical Guidance Task Force, which included 9 rheumatologists, 2 infectious disease specialists, and 2 public health experts with current or past employment history with the CDC.

The ACR encourages clinicians with questions or concerns to email [email protected] for support.

Patients on immunosuppressive or immunomodulatory therapy should receive a third dose of either the Pfizer-BioNTech COVID-19 vaccine or the Moderna COVID-19 vaccine at least 28 days after the second dose of either of these two mRNA vaccines, according to updated recommendations from the American College of Rheumatology.

Mongkolchon Akesin/Getty Images

The update follows the Centers for Disease Control and Prevention’s recommendation that certain immunocompromised patients receive a third dose of an mRNA vaccine to reduce their risk of contracting COVID-19.

Individuals receiving the Pfizer vaccine must be aged 12 years and older, while those receiving the Moderna vaccine must be 18 years and older, the ACR emphasized.

“These statements were based upon a dearth of high-quality data and are not intended to replace clinical judgment,” the authors wrote. “Modifications made to treatment plans, particularly in complex rheumatic disease patients, are highly disease, patient, geography, and time specific and, therefore, must be individualized as part of a shared decision-making process.”

The task force recommended using the same mRNA vaccine booster as the patient received for their initial two-dose series when possible, but notes that either mRNA vaccine is acceptable, and recommends the mRNA vaccine for patients who have yet to receive any vaccine because of the availability of the booster. The task force emphasized that they achieved no consensus on recommending a booster mRNA vaccine to patients who received a single dose of Johnson & Johnson vaccine because the safety data are uncertain.

The updated guidance also identifies the Food and Drug Administration’s emergency use authorization in August for the use of REGEN-COV monoclonal antibody treatment for emergency postexposure prophylaxis for COVID-19 in adults and adolescents aged 12 years and older who weigh at least 40 kg and are at increased risk for severe COVID-19, which includes patients receiving immunosuppressive or immunomodulatory therapies other than hydroxychloroquine. Patients who have been exposed to an individual with COVID-19 should discuss this treatment with their health care provider as an added precaution; however, the guidance emphasized that the prophylactic treatment is not a substitute for COVID-19 vaccination.

The recommendations advise clinicians to counsel their patients to refrain from taking certain immunomodulatory or immunosuppressive medications for 1-2 weeks after booster vaccination if disease activity allows, with the exception of glucocorticoids and anticytokines such as tumor necrosis factor inhibitors and others including interleukin-17, IL-12/23, IL-23, IL-1R, IL-6R antagonists, for which the task force did not achieve a consensus recommendation.

The guidance notes that patients on rituximab or other anti-CD20 medications “should discuss the optimal timing [of the booster] with their rheumatology provider” and that some practitioners measure CD19 B cells as a tool with which to time the booster and subsequent rituximab dosing. For those who elect to dose without such information, or for whom such measurement is not available or feasible, provide the booster 2-4 weeks before next anticipated rituximab dose (e.g., at month 5.0 or 5.5 for patients on an every-6-month rituximab dosing schedule).”

There was strong consensus from the task force that health care providers “should not routinely order any lab testing (e.g., antibody tests for IgM and/or IgG to spike or nucleocapsid proteins) to assess immunity to COVID-19 post vaccination, nor to assess the need for vaccination in a yet-unvaccinated person.”

“The updated information from the ACR addresses not only booster vaccination but also other important and practical issues facing rheumatology providers and their patients related to the pandemic,” said task force chair Jeffrey R. Curtis, MD, of the University of Alabama at Birmingham, in an ACR statement announcing the updates.

“Although the guidance is issued in light of the best evidence available, the science regarding COVID-19 vaccination as it affects the practice of rheumatology is undergoing rapid evolution,” he noted. “We need direct evidence such as that from randomized trials to inform the best practices of what we can do to protect our patients from SARS-CoV-2.”

The update retains the current recommendations that rheumatology patients follow all public health guidelines regarding physical distancing and other preventive measures following vaccination, but the task force did not recommend exceeding current public health guidance. “The appropriateness for continued preventive measures (e.g., masking, physical distancing) should be discussed with patients as their rheumatology providers deem appropriate,” they wrote.

The full updated version of the ACR’s COVID-19 Vaccine Clinical Guidance for Patients with Rheumatic and Musculoskeletal Diseases will be published in Arthritis & Rheumatology. The summary was developed by the ACR COVID-19 Vaccine Clinical Guidance Task Force, which included 9 rheumatologists, 2 infectious disease specialists, and 2 public health experts with current or past employment history with the CDC.

The ACR encourages clinicians with questions or concerns to email [email protected] for support.

Patients on immunosuppressive or immunomodulatory therapy should receive a third dose of either the Pfizer-BioNTech COVID-19 vaccine or the Moderna COVID-19 vaccine at least 28 days after the second dose of either of these two mRNA vaccines, according to updated recommendations from the American College of Rheumatology.

Mongkolchon Akesin/Getty Images

The update follows the Centers for Disease Control and Prevention’s recommendation that certain immunocompromised patients receive a third dose of an mRNA vaccine to reduce their risk of contracting COVID-19.

Individuals receiving the Pfizer vaccine must be aged 12 years and older, while those receiving the Moderna vaccine must be 18 years and older, the ACR emphasized.

“These statements were based upon a dearth of high-quality data and are not intended to replace clinical judgment,” the authors wrote. “Modifications made to treatment plans, particularly in complex rheumatic disease patients, are highly disease, patient, geography, and time specific and, therefore, must be individualized as part of a shared decision-making process.”

The task force recommended using the same mRNA vaccine booster as the patient received for their initial two-dose series when possible, but notes that either mRNA vaccine is acceptable, and recommends the mRNA vaccine for patients who have yet to receive any vaccine because of the availability of the booster. The task force emphasized that they achieved no consensus on recommending a booster mRNA vaccine to patients who received a single dose of Johnson & Johnson vaccine because the safety data are uncertain.

The updated guidance also identifies the Food and Drug Administration’s emergency use authorization in August for the use of REGEN-COV monoclonal antibody treatment for emergency postexposure prophylaxis for COVID-19 in adults and adolescents aged 12 years and older who weigh at least 40 kg and are at increased risk for severe COVID-19, which includes patients receiving immunosuppressive or immunomodulatory therapies other than hydroxychloroquine. Patients who have been exposed to an individual with COVID-19 should discuss this treatment with their health care provider as an added precaution; however, the guidance emphasized that the prophylactic treatment is not a substitute for COVID-19 vaccination.

The recommendations advise clinicians to counsel their patients to refrain from taking certain immunomodulatory or immunosuppressive medications for 1-2 weeks after booster vaccination if disease activity allows, with the exception of glucocorticoids and anticytokines such as tumor necrosis factor inhibitors and others including interleukin-17, IL-12/23, IL-23, IL-1R, IL-6R antagonists, for which the task force did not achieve a consensus recommendation.

The guidance notes that patients on rituximab or other anti-CD20 medications “should discuss the optimal timing [of the booster] with their rheumatology provider” and that some practitioners measure CD19 B cells as a tool with which to time the booster and subsequent rituximab dosing. For those who elect to dose without such information, or for whom such measurement is not available or feasible, provide the booster 2-4 weeks before next anticipated rituximab dose (e.g., at month 5.0 or 5.5 for patients on an every-6-month rituximab dosing schedule).”

There was strong consensus from the task force that health care providers “should not routinely order any lab testing (e.g., antibody tests for IgM and/or IgG to spike or nucleocapsid proteins) to assess immunity to COVID-19 post vaccination, nor to assess the need for vaccination in a yet-unvaccinated person.”

“The updated information from the ACR addresses not only booster vaccination but also other important and practical issues facing rheumatology providers and their patients related to the pandemic,” said task force chair Jeffrey R. Curtis, MD, of the University of Alabama at Birmingham, in an ACR statement announcing the updates.

“Although the guidance is issued in light of the best evidence available, the science regarding COVID-19 vaccination as it affects the practice of rheumatology is undergoing rapid evolution,” he noted. “We need direct evidence such as that from randomized trials to inform the best practices of what we can do to protect our patients from SARS-CoV-2.”

The update retains the current recommendations that rheumatology patients follow all public health guidelines regarding physical distancing and other preventive measures following vaccination, but the task force did not recommend exceeding current public health guidance. “The appropriateness for continued preventive measures (e.g., masking, physical distancing) should be discussed with patients as their rheumatology providers deem appropriate,” they wrote.

The full updated version of the ACR’s COVID-19 Vaccine Clinical Guidance for Patients with Rheumatic and Musculoskeletal Diseases will be published in Arthritis & Rheumatology. The summary was developed by the ACR COVID-19 Vaccine Clinical Guidance Task Force, which included 9 rheumatologists, 2 infectious disease specialists, and 2 public health experts with current or past employment history with the CDC.

The ACR encourages clinicians with questions or concerns to email [email protected] for support.

In the wake of the Centers for Disease Control and Prevention’s recommendation for a third COVID-19 mRNA vaccine dose for immunocompromised people and the Food and Drug Administration’s authorization of the third dose, the National Institute of Allergy and Infectious Diseases has begun a phase 2 trial to assess the antibody response to a booster dose of the Pfizer-BioNTech, Moderna, or Janssen vaccine in people with autoimmune disease who did not respond to their original COVID-19 vaccine regimen, according to an announcement.

The investigators of the trial, called COVID‐19 Booster Vaccine in Autoimmune Disease Non‐Responders, also want to determine if pausing immunosuppressive therapy for autoimmune disease improves the antibody response to an extra dose of a COVID-19 vaccine.

The trial will specifically look at the effects of mycophenolate mofetil (MMF) or mycophenolic acid (MPA), and methotrexate (MTX), or receipt of B cell–depletion therapy such as rituximab within the past 12 months on immune response to a booster dose in people with systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, systemic sclerosis, or pemphigus. They have to have either no serologic response to their initial COVID-19 vaccine regimen or a suboptimal response, defined as a Roche Elecsys Anti-SARS-CoV-2 S (RBD) result greater than or equal to 50 U/mL.

The results of studies conducted in solid-organ transplant recipients who take immunosuppressants showed that an extra dose of vaccine could improve the immune response to the vaccine in many of the individuals, which suggests that the same approach might work in people with autoimmune disease who need treatment with immunosuppressive drugs. Improving the immune response of people with autoimmune disease to COVID-19 vaccines is important because higher rates of severe COVID-19 and death have been reported in this group of patients than in the general population, and it is unclear whether this is attributable to the autoimmune disease, the immunosuppressive medications taken to treat it, or both.

The open-label trial, conducted by the NIAID-funded Autoimmunity Centers of Excellence, aims to enroll 600 people aged 18 years and older with those conditions at 15-20 sites in the United States.

Because medications commonly taken by people with these conditions have been associated with poorer immune responses to vaccines, the trial will randomize the following two cohorts to stop or continue taking their immunosuppressive medication(s) or stop them before and after the booster according to protocol:

• Cohort 1 includes people who are taking MMF or MPA, without additional B cell–depleting medications or MTX.
• Cohort 2 includes people who are taking MTX without additional B cell–depleting medications or MMF/MPA.

A third, nonrandomized cohort consists of people who have received B cell–depletion therapy within the past 12 months regardless of whether they are also taking MMF/MPA or MTX.

Besides the cohort-specific exclusions, other rheumatic disease medications, including biologics, are allowed in the groups.

The primary outcome of the trial is the proportion of participants who have a protective antibody response at week 4. Secondary outcomes will examine various antibody responses at intervals, changes in disease activity across autoimmune diseases, adverse events, and SARS-CoV-2 infections out to 48 weeks.

Study participants will be followed for a total of 13 months. Preliminary results are expected in November 2021, according to the National Institutes of Health.

The trial is being led by Judith James, MD, PhD; Meggan Mackay, MD, MS; Dinesh Khanna, MBBS, MSc; and Amit Bar-Or, MD.

[email protected]

In the wake of the Centers for Disease Control and Prevention’s recommendation for a third COVID-19 mRNA vaccine dose for immunocompromised people and the Food and Drug Administration’s authorization of the third dose, the National Institute of Allergy and Infectious Diseases has begun a phase 2 trial to assess the antibody response to a booster dose of the Pfizer-BioNTech, Moderna, or Janssen vaccine in people with autoimmune disease who did not respond to their original COVID-19 vaccine regimen, according to an announcement.

The investigators of the trial, called COVID‐19 Booster Vaccine in Autoimmune Disease Non‐Responders, also want to determine if pausing immunosuppressive therapy for autoimmune disease improves the antibody response to an extra dose of a COVID-19 vaccine.

The trial will specifically look at the effects of mycophenolate mofetil (MMF) or mycophenolic acid (MPA), and methotrexate (MTX), or receipt of B cell–depletion therapy such as rituximab within the past 12 months on immune response to a booster dose in people with systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, systemic sclerosis, or pemphigus. They have to have either no serologic response to their initial COVID-19 vaccine regimen or a suboptimal response, defined as a Roche Elecsys Anti-SARS-CoV-2 S (RBD) result greater than or equal to 50 U/mL.

The results of studies conducted in solid-organ transplant recipients who take immunosuppressants showed that an extra dose of vaccine could improve the immune response to the vaccine in many of the individuals, which suggests that the same approach might work in people with autoimmune disease who need treatment with immunosuppressive drugs. Improving the immune response of people with autoimmune disease to COVID-19 vaccines is important because higher rates of severe COVID-19 and death have been reported in this group of patients than in the general population, and it is unclear whether this is attributable to the autoimmune disease, the immunosuppressive medications taken to treat it, or both.

The open-label trial, conducted by the NIAID-funded Autoimmunity Centers of Excellence, aims to enroll 600 people aged 18 years and older with those conditions at 15-20 sites in the United States.

Because medications commonly taken by people with these conditions have been associated with poorer immune responses to vaccines, the trial will randomize the following two cohorts to stop or continue taking their immunosuppressive medication(s) or stop them before and after the booster according to protocol:

• Cohort 1 includes people who are taking MMF or MPA, without additional B cell–depleting medications or MTX.
• Cohort 2 includes people who are taking MTX without additional B cell–depleting medications or MMF/MPA.

A third, nonrandomized cohort consists of people who have received B cell–depletion therapy within the past 12 months regardless of whether they are also taking MMF/MPA or MTX.

Besides the cohort-specific exclusions, other rheumatic disease medications, including biologics, are allowed in the groups.

The primary outcome of the trial is the proportion of participants who have a protective antibody response at week 4. Secondary outcomes will examine various antibody responses at intervals, changes in disease activity across autoimmune diseases, adverse events, and SARS-CoV-2 infections out to 48 weeks.

Study participants will be followed for a total of 13 months. Preliminary results are expected in November 2021, according to the National Institutes of Health.

The trial is being led by Judith James, MD, PhD; Meggan Mackay, MD, MS; Dinesh Khanna, MBBS, MSc; and Amit Bar-Or, MD.

[email protected]

In the wake of the Centers for Disease Control and Prevention’s recommendation for a third COVID-19 mRNA vaccine dose for immunocompromised people and the Food and Drug Administration’s authorization of the third dose, the National Institute of Allergy and Infectious Diseases has begun a phase 2 trial to assess the antibody response to a booster dose of the Pfizer-BioNTech, Moderna, or Janssen vaccine in people with autoimmune disease who did not respond to their original COVID-19 vaccine regimen, according to an announcement.

The investigators of the trial, called COVID‐19 Booster Vaccine in Autoimmune Disease Non‐Responders, also want to determine if pausing immunosuppressive therapy for autoimmune disease improves the antibody response to an extra dose of a COVID-19 vaccine.

The trial will specifically look at the effects of mycophenolate mofetil (MMF) or mycophenolic acid (MPA), and methotrexate (MTX), or receipt of B cell–depletion therapy such as rituximab within the past 12 months on immune response to a booster dose in people with systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, systemic sclerosis, or pemphigus. They have to have either no serologic response to their initial COVID-19 vaccine regimen or a suboptimal response, defined as a Roche Elecsys Anti-SARS-CoV-2 S (RBD) result greater than or equal to 50 U/mL.

The results of studies conducted in solid-organ transplant recipients who take immunosuppressants showed that an extra dose of vaccine could improve the immune response to the vaccine in many of the individuals, which suggests that the same approach might work in people with autoimmune disease who need treatment with immunosuppressive drugs. Improving the immune response of people with autoimmune disease to COVID-19 vaccines is important because higher rates of severe COVID-19 and death have been reported in this group of patients than in the general population, and it is unclear whether this is attributable to the autoimmune disease, the immunosuppressive medications taken to treat it, or both.

The open-label trial, conducted by the NIAID-funded Autoimmunity Centers of Excellence, aims to enroll 600 people aged 18 years and older with those conditions at 15-20 sites in the United States.

Because medications commonly taken by people with these conditions have been associated with poorer immune responses to vaccines, the trial will randomize the following two cohorts to stop or continue taking their immunosuppressive medication(s) or stop them before and after the booster according to protocol:

• Cohort 1 includes people who are taking MMF or MPA, without additional B cell–depleting medications or MTX.
• Cohort 2 includes people who are taking MTX without additional B cell–depleting medications or MMF/MPA.

A third, nonrandomized cohort consists of people who have received B cell–depletion therapy within the past 12 months regardless of whether they are also taking MMF/MPA or MTX.

Besides the cohort-specific exclusions, other rheumatic disease medications, including biologics, are allowed in the groups.

The primary outcome of the trial is the proportion of participants who have a protective antibody response at week 4. Secondary outcomes will examine various antibody responses at intervals, changes in disease activity across autoimmune diseases, adverse events, and SARS-CoV-2 infections out to 48 weeks.

Study participants will be followed for a total of 13 months. Preliminary results are expected in November 2021, according to the National Institutes of Health.

The trial is being led by Judith James, MD, PhD; Meggan Mackay, MD, MS; Dinesh Khanna, MBBS, MSc; and Amit Bar-Or, MD.

[email protected]

As politicians battle over masks and mandates, heated rhetoric has been used to describe the fourth heartbreaking surge in COVID as a “pandemic of the unvaccinated.”

While it may serve to further divide red and blue states, I disagree with the assertion that the current surge in cases is driven simply by the unvaccinated. Why? First, the premise would assume complete efficacy with our vaccinated population, which is statistically incorrect (at least 15 million of the U.S. population never completed a second round of injections), which means they were not considered “fully vaccinated.”

Alternately, we need to examine what has occurred in nations with significantly higher vaccination rates than ours (the United Kingdom and Israel) to realize that variants have overrun the dramatic success achieved in those countries as well. Israel, once considered to be the most vaccinated country in the world, is facing a brutal fourth wave of COVID that has sent the country spiraling into another heartbreaking lockdown.

The unvaccinated could hardly be blamed for what is happening in either of these highly vaccinated countries.
 

The concept of blame

So why use blame? It defeats the purpose of encouraging those who are hesitant or possibly misinformed or disenfranchised to move forward. It lacks compassion. It does not encompass the art and science of nursing (for example, the University of Southern Indiana), such as those that hospitals have used to frame optimal nursing care. I abhor the idea of labeling because it denies the prospect of future comprehension.

Labeling reminds me of one of the saddest cases in my career.
 

An unfortunate case

I was the nurse caring for a man from a motor vehicular accident where an entire family was brutally killed. My patient was alleged to be the cause, with a blood alcohol level of 0.40%+ post hydration, intubated and ventilated, with a flailed chest and multiple orthopedic injuries as well as blunt head trauma. He was secured to the bed with handcuffs, although that was unnecessary. Multiple times I was asked how I could possibly care for such an individual, by the police and even a few colleagues. But it was not my place to judge the man.

He was in pain, and he was dying. I comforted him for the 2 weeks it took his battered body to pass into the next realm. No one visited him except the police, eagerly waiting for the man to wake up to explain the tragic events that occurred. It was my job to ease what pain I could and protect him from labels. Did he deserve the labels? Who knew? I did not care. I cared about his writhing and his physical anguish.
 

The comparison

Blame did not help the situation then, nor does it help us move forward now. As nurses, we seek to work within a framework of understanding. As we tire of caring for thousands of COVID patients, we do not stop to ask if they “deserve” care or if they have taken precautions and lived reasonably prior to seeking assistance for disease. We would not be nurses if we did this.

Think about Gov. Greg Abbott, who has asked that Texans not be allowed to mandate masks for children returning to school. He has recently been diagnosed with COVID, despite assuring the public he is fully vaccinated. Politically, his diagnosis could be visualized as a fiasco for a purple state where he has been adamant in denying the efficacy of masks for children.

Yet, his diagnosis should not be fodder for the press. The first concern should be his health and well-being, similar for any man of his age and potential comorbidity.
 

Conclusion

We should be people first, human beings that remain interconnected by our need for care and survival, not conservatives, independents, or liberals, not “vaccinated or unvaccinated,” not seen as “breakthrough” infections, or the immunosuppressed possibly unable to mount a robust response to COVID.

Labels do not define the ability to effectively defeat coronavirus or variants, as highly vaccinated countries have demonstrated in recent months. We are in the midst of a global pandemic, and the battle is raging onward.

In fact, the longer this pandemic continues, the more likely it is we will need to live with this as an endemic disease, so we should stop blaming those who become ill and need support.

It could be any of us.

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

As politicians battle over masks and mandates, heated rhetoric has been used to describe the fourth heartbreaking surge in COVID as a “pandemic of the unvaccinated.”

While it may serve to further divide red and blue states, I disagree with the assertion that the current surge in cases is driven simply by the unvaccinated. Why? First, the premise would assume complete efficacy with our vaccinated population, which is statistically incorrect (at least 15 million of the U.S. population never completed a second round of injections), which means they were not considered “fully vaccinated.”

Alternately, we need to examine what has occurred in nations with significantly higher vaccination rates than ours (the United Kingdom and Israel) to realize that variants have overrun the dramatic success achieved in those countries as well. Israel, once considered to be the most vaccinated country in the world, is facing a brutal fourth wave of COVID that has sent the country spiraling into another heartbreaking lockdown.

The unvaccinated could hardly be blamed for what is happening in either of these highly vaccinated countries.
 

The concept of blame

So why use blame? It defeats the purpose of encouraging those who are hesitant or possibly misinformed or disenfranchised to move forward. It lacks compassion. It does not encompass the art and science of nursing (for example, the University of Southern Indiana), such as those that hospitals have used to frame optimal nursing care. I abhor the idea of labeling because it denies the prospect of future comprehension.

Labeling reminds me of one of the saddest cases in my career.
 

An unfortunate case

I was the nurse caring for a man from a motor vehicular accident where an entire family was brutally killed. My patient was alleged to be the cause, with a blood alcohol level of 0.40%+ post hydration, intubated and ventilated, with a flailed chest and multiple orthopedic injuries as well as blunt head trauma. He was secured to the bed with handcuffs, although that was unnecessary. Multiple times I was asked how I could possibly care for such an individual, by the police and even a few colleagues. But it was not my place to judge the man.

He was in pain, and he was dying. I comforted him for the 2 weeks it took his battered body to pass into the next realm. No one visited him except the police, eagerly waiting for the man to wake up to explain the tragic events that occurred. It was my job to ease what pain I could and protect him from labels. Did he deserve the labels? Who knew? I did not care. I cared about his writhing and his physical anguish.
 

The comparison

Blame did not help the situation then, nor does it help us move forward now. As nurses, we seek to work within a framework of understanding. As we tire of caring for thousands of COVID patients, we do not stop to ask if they “deserve” care or if they have taken precautions and lived reasonably prior to seeking assistance for disease. We would not be nurses if we did this.

Think about Gov. Greg Abbott, who has asked that Texans not be allowed to mandate masks for children returning to school. He has recently been diagnosed with COVID, despite assuring the public he is fully vaccinated. Politically, his diagnosis could be visualized as a fiasco for a purple state where he has been adamant in denying the efficacy of masks for children.

Yet, his diagnosis should not be fodder for the press. The first concern should be his health and well-being, similar for any man of his age and potential comorbidity.
 

Conclusion

We should be people first, human beings that remain interconnected by our need for care and survival, not conservatives, independents, or liberals, not “vaccinated or unvaccinated,” not seen as “breakthrough” infections, or the immunosuppressed possibly unable to mount a robust response to COVID.

Labels do not define the ability to effectively defeat coronavirus or variants, as highly vaccinated countries have demonstrated in recent months. We are in the midst of a global pandemic, and the battle is raging onward.

In fact, the longer this pandemic continues, the more likely it is we will need to live with this as an endemic disease, so we should stop blaming those who become ill and need support.

It could be any of us.

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

As politicians battle over masks and mandates, heated rhetoric has been used to describe the fourth heartbreaking surge in COVID as a “pandemic of the unvaccinated.”

While it may serve to further divide red and blue states, I disagree with the assertion that the current surge in cases is driven simply by the unvaccinated. Why? First, the premise would assume complete efficacy with our vaccinated population, which is statistically incorrect (at least 15 million of the U.S. population never completed a second round of injections), which means they were not considered “fully vaccinated.”

Alternately, we need to examine what has occurred in nations with significantly higher vaccination rates than ours (the United Kingdom and Israel) to realize that variants have overrun the dramatic success achieved in those countries as well. Israel, once considered to be the most vaccinated country in the world, is facing a brutal fourth wave of COVID that has sent the country spiraling into another heartbreaking lockdown.

The unvaccinated could hardly be blamed for what is happening in either of these highly vaccinated countries.
 

The concept of blame

So why use blame? It defeats the purpose of encouraging those who are hesitant or possibly misinformed or disenfranchised to move forward. It lacks compassion. It does not encompass the art and science of nursing (for example, the University of Southern Indiana), such as those that hospitals have used to frame optimal nursing care. I abhor the idea of labeling because it denies the prospect of future comprehension.

Labeling reminds me of one of the saddest cases in my career.
 

An unfortunate case

I was the nurse caring for a man from a motor vehicular accident where an entire family was brutally killed. My patient was alleged to be the cause, with a blood alcohol level of 0.40%+ post hydration, intubated and ventilated, with a flailed chest and multiple orthopedic injuries as well as blunt head trauma. He was secured to the bed with handcuffs, although that was unnecessary. Multiple times I was asked how I could possibly care for such an individual, by the police and even a few colleagues. But it was not my place to judge the man.

He was in pain, and he was dying. I comforted him for the 2 weeks it took his battered body to pass into the next realm. No one visited him except the police, eagerly waiting for the man to wake up to explain the tragic events that occurred. It was my job to ease what pain I could and protect him from labels. Did he deserve the labels? Who knew? I did not care. I cared about his writhing and his physical anguish.
 

The comparison

Blame did not help the situation then, nor does it help us move forward now. As nurses, we seek to work within a framework of understanding. As we tire of caring for thousands of COVID patients, we do not stop to ask if they “deserve” care or if they have taken precautions and lived reasonably prior to seeking assistance for disease. We would not be nurses if we did this.

Think about Gov. Greg Abbott, who has asked that Texans not be allowed to mandate masks for children returning to school. He has recently been diagnosed with COVID, despite assuring the public he is fully vaccinated. Politically, his diagnosis could be visualized as a fiasco for a purple state where he has been adamant in denying the efficacy of masks for children.

Yet, his diagnosis should not be fodder for the press. The first concern should be his health and well-being, similar for any man of his age and potential comorbidity.
 

Conclusion

We should be people first, human beings that remain interconnected by our need for care and survival, not conservatives, independents, or liberals, not “vaccinated or unvaccinated,” not seen as “breakthrough” infections, or the immunosuppressed possibly unable to mount a robust response to COVID.

Labels do not define the ability to effectively defeat coronavirus or variants, as highly vaccinated countries have demonstrated in recent months. We are in the midst of a global pandemic, and the battle is raging onward.

In fact, the longer this pandemic continues, the more likely it is we will need to live with this as an endemic disease, so we should stop blaming those who become ill and need support.

It could be any of us.

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

Death from COVID-19 was not more likely among patients with inflammatory bowel disease (IBD) who had COVID-19 who developed new GI symptoms after becoming infected, according to international registry data from nearly 3,000 adults.

Although GI symptoms may arise in the general population of COVID-19 patients, data on the association between GI symptoms and COVID-19 in patients with IBD are limited, as are data on the association of GI symptoms and COVID-19 outcomes in this population, Ryan C. Ungaro, MD, of the Icahn School of Medicine at Mount Sinai, New York, and colleagues wrote.

In a study published in Inflammatory Bowel Diseases, the researchers identified 2,917 adults with IBD who developed COVID-19 using the Surveillance Epidemiology of Coronavirus Under Research Exclusion in Inflammatory Bowel Disease (SECURE-IBD) database, a global registry created to understand COVID-19 outcomes in IBD patients.

The researchers recorded all new GI symptoms experienced by the patients while they were infected with COVID-19. Overall, 764 (26.2%) experienced new GI symptoms and 2,153 did not. The most common symptom was diarrhea, reported by 80% of the patients, followed by abdominal pain in 34%. Nausea and vomiting were reported by 24% and 12%, respectively, of all patients.

The average age of the patients was 43 years for those with no new GI symptoms and 40 for those without new GI symptoms; overall, approximately half were women and approximately three-quarters were White. Overall, 50% of those with new GI symptoms were in remission, as was the case for 58.4% of those without.

IBD patients who developed new GI symptoms were significantly more likely to be women, of Asian race, older, or have at least one comorbidity.

The researchers found no difference in new GI symptoms in patients with Crohn’s disease and ulcerative colitis. “Patients on any medication – but in particular [tumor necrosis factor] antagonist monotherapy – were less likely to report new GI symptoms.” they wrote.

Although IBD patients with new GI symptoms were significantly more likely than were those without new GI symptoms to be hospitalized for COVID-19 in bivariate analyses (31.4% vs. 19.2%; P < .001), they were not more likely to need a ventilator or intensive care (5.8% vs. 4.6%; P < .18). In a multivariate analysis, IBD patients with new GI symptoms had no greater risk of death from COVID-19 than did those without new GI symptoms (adjusted odds ratio, 0.72; 95% confidence interval, 0.38-1.36).

The new-onset GI symptoms common to IBD patients with COVID-19 are not likely caused by underlying disease activity, given the number of patients in remission who reported new GI symptoms, the researchers wrote.

The study findings were limited by several factors including the retrospective design, potential reporting bias, and reliance on physician global assessment for disease assessment, the researchers noted. However, the results were strengthened by the large sample size, by the ability to assess GI symptoms before and after COVID-19, and by the evaluation of GI symptoms and COVID-19 outcomes.

“In summary, new GI symptoms are common in IBD patients with COVID-19 and are not associated with an increased risk of death due to COVID-19,” the researchers concluded. “Our findings suggest that an increase in GI symptoms in IBD patients should prompt consideration of a COVID-19 diagnosis.”
 

Data to guide clinical care

“There are several potential causes for common GI symptoms, such as diarrhea and abdominal pain, among patients with IBD,” Shirley Cohen-Mekelburg, MD, of the University of Michigan, Ann Arbor, said in an interview. “These can be the initial presentation of an IBD flare, a noninflammatory cause such as irritable bowel syndrome, small intestinal bacterial overgrowth, or an infection such as Clostridioides difficile or SARS-CoV-2. Each of these diagnoses require different treatments. An IBD flare may require escalation of immunosuppressive medications such as biologics or corticosteroids, which can cause harm in the context of an untreated infection. Therefore, any guidance that will increase health care providers’ awareness of the possible causes of similar GI symptoms is important in caring for our patients with IBD. This is especially true in context of a newer entity such as COVID-19 with which we are overall less familiar.”

Dr. Cohen-Meckelburg said the lack of association between GI symptoms and death in IBD is reassuring. “It is interesting to note that GI symptoms, and particularly new diarrhea, were very common among patients with IBD and COVID-19,” she added.

“Every study has its limitations, which need to be considered in interpreting findings,” Dr. Cohen-Meckelburg noted . “SECURE-IBD has provided great insight into COVID-19 infections among patients with IBD. However, the registry relies on individuals reporting cases, so there is the potential for underreporting, particularly with less symptomatic or subclinical cases.”

“Health care providers who treat patients with IBD should have a high-index of suspicion for SARS-CoV-2 infections when patients with IBD present with GI symptoms,” said Dr. Cohen-Meckelburg. “The data from the current study may help us to consider standard testing to rule out COVID-19 as an alternative diagnosis when considering whether to treat patients with IBD who develop new GI symptoms for an IBD flare. This would be similar to how we currently test for C. difficile and other enteric infections before treating IBD flares.

“This approach – considering the possibility of COVID-19 in the context of new GI symptoms – is consistent with the AGA’s published guidelines and best practices,” said David Leiman, MD, MSHP, of Duke University, Durham, N.C., and Chair of the AGA’s Quality Committee. “Clinicians should also be aware of the possibility for variation in implementation of this approach, with some patients potentially at risk for disparate testing practices.” As outlined by the AGA’s Quality Committee, tracking adherence to this clinical approach through ongoing quality improvement may limit the development of such gaps in care.

The study was supported in part by the Helmsley Charitable Trust with additional funding provided by Pfizer, Takeda, Janssen, AbbVie, Lilly, Genentech, Boehringer Ingelheim, Bristol-Myers Squibb, Celtrion, and Arenapharm. Lead author Dr. Ungaro disclosed serving as an advisory board member or consultant for AbbVie, Bristol-Myers Squibb, Janssen, Eli Lilly, Pfizer, and Takeda and research support from AbbVie, Boehringer Ingelheim, and Pfizer. Other coauthors disclosed similar relationships with other pharmaceutical companies. Dr. Cohen-Mekelburg and Dr. Leiman had no financial conflicts to disclose.

Death from COVID-19 was not more likely among patients with inflammatory bowel disease (IBD) who had COVID-19 who developed new GI symptoms after becoming infected, according to international registry data from nearly 3,000 adults.

Although GI symptoms may arise in the general population of COVID-19 patients, data on the association between GI symptoms and COVID-19 in patients with IBD are limited, as are data on the association of GI symptoms and COVID-19 outcomes in this population, Ryan C. Ungaro, MD, of the Icahn School of Medicine at Mount Sinai, New York, and colleagues wrote.

In a study published in Inflammatory Bowel Diseases, the researchers identified 2,917 adults with IBD who developed COVID-19 using the Surveillance Epidemiology of Coronavirus Under Research Exclusion in Inflammatory Bowel Disease (SECURE-IBD) database, a global registry created to understand COVID-19 outcomes in IBD patients.

The researchers recorded all new GI symptoms experienced by the patients while they were infected with COVID-19. Overall, 764 (26.2%) experienced new GI symptoms and 2,153 did not. The most common symptom was diarrhea, reported by 80% of the patients, followed by abdominal pain in 34%. Nausea and vomiting were reported by 24% and 12%, respectively, of all patients.

The average age of the patients was 43 years for those with no new GI symptoms and 40 for those without new GI symptoms; overall, approximately half were women and approximately three-quarters were White. Overall, 50% of those with new GI symptoms were in remission, as was the case for 58.4% of those without.

IBD patients who developed new GI symptoms were significantly more likely to be women, of Asian race, older, or have at least one comorbidity.

The researchers found no difference in new GI symptoms in patients with Crohn’s disease and ulcerative colitis. “Patients on any medication – but in particular [tumor necrosis factor] antagonist monotherapy – were less likely to report new GI symptoms.” they wrote.

Although IBD patients with new GI symptoms were significantly more likely than were those without new GI symptoms to be hospitalized for COVID-19 in bivariate analyses (31.4% vs. 19.2%; P < .001), they were not more likely to need a ventilator or intensive care (5.8% vs. 4.6%; P < .18). In a multivariate analysis, IBD patients with new GI symptoms had no greater risk of death from COVID-19 than did those without new GI symptoms (adjusted odds ratio, 0.72; 95% confidence interval, 0.38-1.36).

The new-onset GI symptoms common to IBD patients with COVID-19 are not likely caused by underlying disease activity, given the number of patients in remission who reported new GI symptoms, the researchers wrote.

The study findings were limited by several factors including the retrospective design, potential reporting bias, and reliance on physician global assessment for disease assessment, the researchers noted. However, the results were strengthened by the large sample size, by the ability to assess GI symptoms before and after COVID-19, and by the evaluation of GI symptoms and COVID-19 outcomes.

“In summary, new GI symptoms are common in IBD patients with COVID-19 and are not associated with an increased risk of death due to COVID-19,” the researchers concluded. “Our findings suggest that an increase in GI symptoms in IBD patients should prompt consideration of a COVID-19 diagnosis.”
 

Data to guide clinical care

“There are several potential causes for common GI symptoms, such as diarrhea and abdominal pain, among patients with IBD,” Shirley Cohen-Mekelburg, MD, of the University of Michigan, Ann Arbor, said in an interview. “These can be the initial presentation of an IBD flare, a noninflammatory cause such as irritable bowel syndrome, small intestinal bacterial overgrowth, or an infection such as Clostridioides difficile or SARS-CoV-2. Each of these diagnoses require different treatments. An IBD flare may require escalation of immunosuppressive medications such as biologics or corticosteroids, which can cause harm in the context of an untreated infection. Therefore, any guidance that will increase health care providers’ awareness of the possible causes of similar GI symptoms is important in caring for our patients with IBD. This is especially true in context of a newer entity such as COVID-19 with which we are overall less familiar.”

Dr. Cohen-Meckelburg said the lack of association between GI symptoms and death in IBD is reassuring. “It is interesting to note that GI symptoms, and particularly new diarrhea, were very common among patients with IBD and COVID-19,” she added.

“Every study has its limitations, which need to be considered in interpreting findings,” Dr. Cohen-Meckelburg noted . “SECURE-IBD has provided great insight into COVID-19 infections among patients with IBD. However, the registry relies on individuals reporting cases, so there is the potential for underreporting, particularly with less symptomatic or subclinical cases.”

“Health care providers who treat patients with IBD should have a high-index of suspicion for SARS-CoV-2 infections when patients with IBD present with GI symptoms,” said Dr. Cohen-Meckelburg. “The data from the current study may help us to consider standard testing to rule out COVID-19 as an alternative diagnosis when considering whether to treat patients with IBD who develop new GI symptoms for an IBD flare. This would be similar to how we currently test for C. difficile and other enteric infections before treating IBD flares.

“This approach – considering the possibility of COVID-19 in the context of new GI symptoms – is consistent with the AGA’s published guidelines and best practices,” said David Leiman, MD, MSHP, of Duke University, Durham, N.C., and Chair of the AGA’s Quality Committee. “Clinicians should also be aware of the possibility for variation in implementation of this approach, with some patients potentially at risk for disparate testing practices.” As outlined by the AGA’s Quality Committee, tracking adherence to this clinical approach through ongoing quality improvement may limit the development of such gaps in care.

The study was supported in part by the Helmsley Charitable Trust with additional funding provided by Pfizer, Takeda, Janssen, AbbVie, Lilly, Genentech, Boehringer Ingelheim, Bristol-Myers Squibb, Celtrion, and Arenapharm. Lead author Dr. Ungaro disclosed serving as an advisory board member or consultant for AbbVie, Bristol-Myers Squibb, Janssen, Eli Lilly, Pfizer, and Takeda and research support from AbbVie, Boehringer Ingelheim, and Pfizer. Other coauthors disclosed similar relationships with other pharmaceutical companies. Dr. Cohen-Mekelburg and Dr. Leiman had no financial conflicts to disclose.

Death from COVID-19 was not more likely among patients with inflammatory bowel disease (IBD) who had COVID-19 who developed new GI symptoms after becoming infected, according to international registry data from nearly 3,000 adults.

Although GI symptoms may arise in the general population of COVID-19 patients, data on the association between GI symptoms and COVID-19 in patients with IBD are limited, as are data on the association of GI symptoms and COVID-19 outcomes in this population, Ryan C. Ungaro, MD, of the Icahn School of Medicine at Mount Sinai, New York, and colleagues wrote.

In a study published in Inflammatory Bowel Diseases, the researchers identified 2,917 adults with IBD who developed COVID-19 using the Surveillance Epidemiology of Coronavirus Under Research Exclusion in Inflammatory Bowel Disease (SECURE-IBD) database, a global registry created to understand COVID-19 outcomes in IBD patients.

The researchers recorded all new GI symptoms experienced by the patients while they were infected with COVID-19. Overall, 764 (26.2%) experienced new GI symptoms and 2,153 did not. The most common symptom was diarrhea, reported by 80% of the patients, followed by abdominal pain in 34%. Nausea and vomiting were reported by 24% and 12%, respectively, of all patients.

The average age of the patients was 43 years for those with no new GI symptoms and 40 for those without new GI symptoms; overall, approximately half were women and approximately three-quarters were White. Overall, 50% of those with new GI symptoms were in remission, as was the case for 58.4% of those without.

IBD patients who developed new GI symptoms were significantly more likely to be women, of Asian race, older, or have at least one comorbidity.

The researchers found no difference in new GI symptoms in patients with Crohn’s disease and ulcerative colitis. “Patients on any medication – but in particular [tumor necrosis factor] antagonist monotherapy – were less likely to report new GI symptoms.” they wrote.

Although IBD patients with new GI symptoms were significantly more likely than were those without new GI symptoms to be hospitalized for COVID-19 in bivariate analyses (31.4% vs. 19.2%; P < .001), they were not more likely to need a ventilator or intensive care (5.8% vs. 4.6%; P < .18). In a multivariate analysis, IBD patients with new GI symptoms had no greater risk of death from COVID-19 than did those without new GI symptoms (adjusted odds ratio, 0.72; 95% confidence interval, 0.38-1.36).

The new-onset GI symptoms common to IBD patients with COVID-19 are not likely caused by underlying disease activity, given the number of patients in remission who reported new GI symptoms, the researchers wrote.

The study findings were limited by several factors including the retrospective design, potential reporting bias, and reliance on physician global assessment for disease assessment, the researchers noted. However, the results were strengthened by the large sample size, by the ability to assess GI symptoms before and after COVID-19, and by the evaluation of GI symptoms and COVID-19 outcomes.

“In summary, new GI symptoms are common in IBD patients with COVID-19 and are not associated with an increased risk of death due to COVID-19,” the researchers concluded. “Our findings suggest that an increase in GI symptoms in IBD patients should prompt consideration of a COVID-19 diagnosis.”
 

Data to guide clinical care

“There are several potential causes for common GI symptoms, such as diarrhea and abdominal pain, among patients with IBD,” Shirley Cohen-Mekelburg, MD, of the University of Michigan, Ann Arbor, said in an interview. “These can be the initial presentation of an IBD flare, a noninflammatory cause such as irritable bowel syndrome, small intestinal bacterial overgrowth, or an infection such as Clostridioides difficile or SARS-CoV-2. Each of these diagnoses require different treatments. An IBD flare may require escalation of immunosuppressive medications such as biologics or corticosteroids, which can cause harm in the context of an untreated infection. Therefore, any guidance that will increase health care providers’ awareness of the possible causes of similar GI symptoms is important in caring for our patients with IBD. This is especially true in context of a newer entity such as COVID-19 with which we are overall less familiar.”

Dr. Cohen-Meckelburg said the lack of association between GI symptoms and death in IBD is reassuring. “It is interesting to note that GI symptoms, and particularly new diarrhea, were very common among patients with IBD and COVID-19,” she added.

“Every study has its limitations, which need to be considered in interpreting findings,” Dr. Cohen-Meckelburg noted . “SECURE-IBD has provided great insight into COVID-19 infections among patients with IBD. However, the registry relies on individuals reporting cases, so there is the potential for underreporting, particularly with less symptomatic or subclinical cases.”

“Health care providers who treat patients with IBD should have a high-index of suspicion for SARS-CoV-2 infections when patients with IBD present with GI symptoms,” said Dr. Cohen-Meckelburg. “The data from the current study may help us to consider standard testing to rule out COVID-19 as an alternative diagnosis when considering whether to treat patients with IBD who develop new GI symptoms for an IBD flare. This would be similar to how we currently test for C. difficile and other enteric infections before treating IBD flares.

“This approach – considering the possibility of COVID-19 in the context of new GI symptoms – is consistent with the AGA’s published guidelines and best practices,” said David Leiman, MD, MSHP, of Duke University, Durham, N.C., and Chair of the AGA’s Quality Committee. “Clinicians should also be aware of the possibility for variation in implementation of this approach, with some patients potentially at risk for disparate testing practices.” As outlined by the AGA’s Quality Committee, tracking adherence to this clinical approach through ongoing quality improvement may limit the development of such gaps in care.

The study was supported in part by the Helmsley Charitable Trust with additional funding provided by Pfizer, Takeda, Janssen, AbbVie, Lilly, Genentech, Boehringer Ingelheim, Bristol-Myers Squibb, Celtrion, and Arenapharm. Lead author Dr. Ungaro disclosed serving as an advisory board member or consultant for AbbVie, Bristol-Myers Squibb, Janssen, Eli Lilly, Pfizer, and Takeda and research support from AbbVie, Boehringer Ingelheim, and Pfizer. Other coauthors disclosed similar relationships with other pharmaceutical companies. Dr. Cohen-Mekelburg and Dr. Leiman had no financial conflicts to disclose.

The same genetic variations may boost susceptibility to both severe COVID-19 and cannabis use disorder (CUD), a new study suggests. The research does not confirm a genetic link, but the lead author said the signs of an association are still “troubling.”

“Reducing cannabis use among heavy users may potentially provide protection against severe COVID-19 presentations,” Alexander S. Hatoum, PhD, a postdoctoral scholar at Washington University, St. Louis, said in an interview. “Outside of individual risk, these data also have important implications for policy regarding vaccination as well as treatment prioritization in an overly taxed medical system.”

The study was published in the journal Biological Psychiatry Global Open Science.

Dr. Hatoum and colleagues launched the study to gain insight into whether CUD might be a risk factor for severe COVID-19 presentations.

As defined by the DSM-5, people with CUD suffer from impairment or distress because of their cannabis use and meet at least 2 of 11 criteria over a 12-month period, such as cravings, cannabis tolerance, and withdrawal symptoms. According to a 2020 study that examined 2008-2016 data, 2.72% of children aged 12-17 showed signs of CUD, as did 1.23% of those aged over 26.

The primary reasons for hospitalization and death related to COVID-19 are respiratory symptoms. “And we have observed that genetic vulnerability to CUD is shared with respiratory disease, even after tobacco use is considered,” Dr. Hatoum said.

He and his colleagues examined data from genomewide association studies and searched for genetic correlations between CUD (14,080 cases, 343,726 controls) and COVID-19 hospitalization (9,373 cases, 1,197,256 controls). “Genetic vulnerability to COVID-19 was correlated with genetic liability to CUD (P = 1.33e^–6),” the researchers wrote. “This association remained when accounting for genetic liability to related risk factors and covariates (P = .012-.049).”

According to Dr. Hatoum, the researchers found inconclusive evidence that CUD might worsen COVID-19 cases. “We applied statistical causal models, which found an effect consistent with causality, but it was nonsignificant,” he said.

Despite the absence of causality, the study findings could prove useful for clinicians and policy makers.

“Those struggling with CUD may be prioritized for vaccination and vaccination boosters to mitigate their higher likelihood of a severe COVID-19 presentation,” Dr. Hatoum said. “When testing positive for COVID-19, they may also be prioritized for earlier treatment.”

The study authors also added that the findings “urge caution” in regard to the wave of U.S. states legalizing cannabis. “Our data suggest that heavy cannabis use, but not lifetime cannabis use, represents a risk factor for severe COVID-19 presentations,” Dr. Hatoum said.

In an interview, Danielle Dick, PhD, who was not involved with the study, said it applies “cutting-edge methods to an important research question” and offers a “hint” of a genetic risk factor that makes some people more likely to be hospitalized for COVID-19. However, “the study does not tell us what those underlying genetically influenced processes might be,” added Dr. Dick, professor of psychology, and human and molecular genetics at Virginia Commonwealth University, Richmond. “And it’s an important caveat to point out that the results from this study are limited in that they are based on data from people from European descent – so they can’t necessarily be applied to address the harm experienced by so many people of color from the COVID pandemic. That’s an unfortunate limitation.”

As for the idea that the study findings should prompt caution about marijuana legalization, Dr. Dick said it’s true that increased acceptability of drug use “increases the likelihood that individuals who are genetically vulnerable will develop problems. There is robust evidence of this.”

However, Dr. Dick said, “the legalization of marijuana is a complex topic because the health consequences aren’t the only consideration when it comes to legalization. The other side of the coin is the huge harm that has been caused to communities of color through marijuana criminalization. Legalization will hopefully lead to decreased harm on that front. So it’s a double-edged sword.”

Dr. Hatoum, his colleagues, and Dr. Dick reported no relevant disclosures.

The same genetic variations may boost susceptibility to both severe COVID-19 and cannabis use disorder (CUD), a new study suggests. The research does not confirm a genetic link, but the lead author said the signs of an association are still “troubling.”

“Reducing cannabis use among heavy users may potentially provide protection against severe COVID-19 presentations,” Alexander S. Hatoum, PhD, a postdoctoral scholar at Washington University, St. Louis, said in an interview. “Outside of individual risk, these data also have important implications for policy regarding vaccination as well as treatment prioritization in an overly taxed medical system.”

The study was published in the journal Biological Psychiatry Global Open Science.

Dr. Hatoum and colleagues launched the study to gain insight into whether CUD might be a risk factor for severe COVID-19 presentations.

As defined by the DSM-5, people with CUD suffer from impairment or distress because of their cannabis use and meet at least 2 of 11 criteria over a 12-month period, such as cravings, cannabis tolerance, and withdrawal symptoms. According to a 2020 study that examined 2008-2016 data, 2.72% of children aged 12-17 showed signs of CUD, as did 1.23% of those aged over 26.

The primary reasons for hospitalization and death related to COVID-19 are respiratory symptoms. “And we have observed that genetic vulnerability to CUD is shared with respiratory disease, even after tobacco use is considered,” Dr. Hatoum said.

He and his colleagues examined data from genomewide association studies and searched for genetic correlations between CUD (14,080 cases, 343,726 controls) and COVID-19 hospitalization (9,373 cases, 1,197,256 controls). “Genetic vulnerability to COVID-19 was correlated with genetic liability to CUD (P = 1.33e^–6),” the researchers wrote. “This association remained when accounting for genetic liability to related risk factors and covariates (P = .012-.049).”

According to Dr. Hatoum, the researchers found inconclusive evidence that CUD might worsen COVID-19 cases. “We applied statistical causal models, which found an effect consistent with causality, but it was nonsignificant,” he said.

Despite the absence of causality, the study findings could prove useful for clinicians and policy makers.

“Those struggling with CUD may be prioritized for vaccination and vaccination boosters to mitigate their higher likelihood of a severe COVID-19 presentation,” Dr. Hatoum said. “When testing positive for COVID-19, they may also be prioritized for earlier treatment.”

The study authors also added that the findings “urge caution” in regard to the wave of U.S. states legalizing cannabis. “Our data suggest that heavy cannabis use, but not lifetime cannabis use, represents a risk factor for severe COVID-19 presentations,” Dr. Hatoum said.

In an interview, Danielle Dick, PhD, who was not involved with the study, said it applies “cutting-edge methods to an important research question” and offers a “hint” of a genetic risk factor that makes some people more likely to be hospitalized for COVID-19. However, “the study does not tell us what those underlying genetically influenced processes might be,” added Dr. Dick, professor of psychology, and human and molecular genetics at Virginia Commonwealth University, Richmond. “And it’s an important caveat to point out that the results from this study are limited in that they are based on data from people from European descent – so they can’t necessarily be applied to address the harm experienced by so many people of color from the COVID pandemic. That’s an unfortunate limitation.”

As for the idea that the study findings should prompt caution about marijuana legalization, Dr. Dick said it’s true that increased acceptability of drug use “increases the likelihood that individuals who are genetically vulnerable will develop problems. There is robust evidence of this.”

However, Dr. Dick said, “the legalization of marijuana is a complex topic because the health consequences aren’t the only consideration when it comes to legalization. The other side of the coin is the huge harm that has been caused to communities of color through marijuana criminalization. Legalization will hopefully lead to decreased harm on that front. So it’s a double-edged sword.”

Dr. Hatoum, his colleagues, and Dr. Dick reported no relevant disclosures.

The same genetic variations may boost susceptibility to both severe COVID-19 and cannabis use disorder (CUD), a new study suggests. The research does not confirm a genetic link, but the lead author said the signs of an association are still “troubling.”

“Reducing cannabis use among heavy users may potentially provide protection against severe COVID-19 presentations,” Alexander S. Hatoum, PhD, a postdoctoral scholar at Washington University, St. Louis, said in an interview. “Outside of individual risk, these data also have important implications for policy regarding vaccination as well as treatment prioritization in an overly taxed medical system.”

The study was published in the journal Biological Psychiatry Global Open Science.

Dr. Hatoum and colleagues launched the study to gain insight into whether CUD might be a risk factor for severe COVID-19 presentations.

As defined by the DSM-5, people with CUD suffer from impairment or distress because of their cannabis use and meet at least 2 of 11 criteria over a 12-month period, such as cravings, cannabis tolerance, and withdrawal symptoms. According to a 2020 study that examined 2008-2016 data, 2.72% of children aged 12-17 showed signs of CUD, as did 1.23% of those aged over 26.

The primary reasons for hospitalization and death related to COVID-19 are respiratory symptoms. “And we have observed that genetic vulnerability to CUD is shared with respiratory disease, even after tobacco use is considered,” Dr. Hatoum said.

He and his colleagues examined data from genomewide association studies and searched for genetic correlations between CUD (14,080 cases, 343,726 controls) and COVID-19 hospitalization (9,373 cases, 1,197,256 controls). “Genetic vulnerability to COVID-19 was correlated with genetic liability to CUD (P = 1.33e^–6),” the researchers wrote. “This association remained when accounting for genetic liability to related risk factors and covariates (P = .012-.049).”

According to Dr. Hatoum, the researchers found inconclusive evidence that CUD might worsen COVID-19 cases. “We applied statistical causal models, which found an effect consistent with causality, but it was nonsignificant,” he said.

Despite the absence of causality, the study findings could prove useful for clinicians and policy makers.

“Those struggling with CUD may be prioritized for vaccination and vaccination boosters to mitigate their higher likelihood of a severe COVID-19 presentation,” Dr. Hatoum said. “When testing positive for COVID-19, they may also be prioritized for earlier treatment.”

The study authors also added that the findings “urge caution” in regard to the wave of U.S. states legalizing cannabis. “Our data suggest that heavy cannabis use, but not lifetime cannabis use, represents a risk factor for severe COVID-19 presentations,” Dr. Hatoum said.

In an interview, Danielle Dick, PhD, who was not involved with the study, said it applies “cutting-edge methods to an important research question” and offers a “hint” of a genetic risk factor that makes some people more likely to be hospitalized for COVID-19. However, “the study does not tell us what those underlying genetically influenced processes might be,” added Dr. Dick, professor of psychology, and human and molecular genetics at Virginia Commonwealth University, Richmond. “And it’s an important caveat to point out that the results from this study are limited in that they are based on data from people from European descent – so they can’t necessarily be applied to address the harm experienced by so many people of color from the COVID pandemic. That’s an unfortunate limitation.”

As for the idea that the study findings should prompt caution about marijuana legalization, Dr. Dick said it’s true that increased acceptability of drug use “increases the likelihood that individuals who are genetically vulnerable will develop problems. There is robust evidence of this.”

However, Dr. Dick said, “the legalization of marijuana is a complex topic because the health consequences aren’t the only consideration when it comes to legalization. The other side of the coin is the huge harm that has been caused to communities of color through marijuana criminalization. Legalization will hopefully lead to decreased harm on that front. So it’s a double-edged sword.”

Dr. Hatoum, his colleagues, and Dr. Dick reported no relevant disclosures.

This story is a collaboration between KHN and “Science Friday.” 

Rafiah Maxie has been a licensed clinical social worker in the Chicago area for a decade. Throughout that time, she’d viewed suicide as a problem most prevalent among middle-aged white men.

Until May 27, 2020.

That day, Maxie’s 19-year-old son, Jamal Clay – who loved playing the trumpet and participating in theater, who would help her unload groceries from the car and raise funds for the March of the Dimes – killed himself in their garage.

“Now I cannot blink without seeing my son hanging,” said Maxie, who is Black.

Clay’s death, along with the suicides of more than 100 other Black residents in Illinois last year, has led locals to call for new prevention efforts focused on Black communities. In 2020, during the pandemic’s first year, suicides among White residents decreased compared with previous years, while they increased among Black residents, according to state data.

But this is not a local problem. Nor is it limited to the pandemic.

Interviews with a dozen suicide researchers, data collected from states across the country, and a review of decades of research revealed that suicide is a growing crisis for communities of color – one that plagued them well before the pandemic and has only been exacerbated since.

Overall suicide rates in the U.S. decreased in 2019 and 2020. National and local studies attribute the trend to a drop among White Americans, who make up the majority of suicide deaths. Meanwhile, rates for Black, Hispanic, and Asian Americans – though lower than those of their white peers – continued to climb in many states. (Suicide rates have been consistently high for Native Americans.)

“COVID created more transparency regarding what we already knew was happening,” said Sonyia Richardson, a licensed clinical social worker who focuses on serving people of color, and assistant professor at the University of North Carolina–Charlotte, where she researches suicide. When you put the suicide rates of all communities in one bucket, “that bucket says it’s getting better and what we’re doing is working,” she said. “But that’s not the case for communities of color.”
 

Losing generations

Although the suicide rate is highest among middle-aged White men, young people of color are emerging as particularly at risk.

Research shows Black kids younger than 13 die by suicide at nearly twice the rate of White kids and, over time, their suicide rates have grown even as rates have decreased for White children. Among teenagers and young adults, suicide deaths have increased more than 45% for Black Americans and about 40% for Asian Americans in the 7 years ending in 2019. Other concerning trends in suicide attempts date to the ’90s.

“We’re losing generations,” said Sean Joe, a national expert on Black suicide and a professor at Washington University in St. Louis. “We have to pay attention now because if you’re out of the first decade of life and think life is not worth pursuing, that’s a signal to say something is going really wrong.”

These statistics also refute traditional ideas that suicide doesn’t happen in certain ethnic or minority populations because they’re “protected” and “resilient” or the “model minority,” said Kiara Alvarez, a researcher and psychologist at Massachusetts General Hospital who focuses on suicide among Hispanic and immigrant populations.

Although these groups may have had low suicide rates historically, that’s changing, she said.

Paul Chin lost his 17-year-old brother, Chris, to suicide in 2009. A poem Chris wrote in high school about his heritage has left Chin, 8 years his senior, wondering if his brother struggled to feel accepted in the U.S., despite being born and raised in New York.

Growing up, Asian Americans weren’t represented in lessons at school or in pop culture, said Chin, now 37. Even in clinical research on suicide as well as other health topics, kids like Chris are underrepresented, with less than 1% of federal research funding focused on Asian Americans.

It wasn’t until the pandemic, and the concurrent rise in hate crimes against Asian Americans, that Chin saw national attention on the community’s mental health. He hopes the interest is not short-lived.

Suicide is the leading cause of death for Asian Americans ages 15 to 24, yet “that doesn’t get enough attention,” Chin said. “It’s important to continue to share these stories.”

Kathy Williams, who is Black, has been on a similar mission since her 15-year-old son, Torian Graves, died by suicide in 1996. People didn’t talk about suicide in the Black community then, she said. So she started raising the topic at her church in Durham, N.C., and in local schools. She wanted Black families to know the warning signs and society at large to recognize the seriousness of the problem.

The pandemic may have highlighted this, Williams said, but “it has always happened. Always.”
 

Pandemic sheds light on the triggers

Pinpointing the root causes of rising suicide within communities of color has proved difficult. How much stems from mental illness? How much from socioeconomic changes like job losses or social isolation? Now, COVID-19 may offer some clues.

Recent decades have been marked by growing economic instability, a widening racial wealth gap, and more public attention on police killings of unarmed Black and Brown people, said Michael Lindsey, executive director of the New York University McSilver Institute for Poverty Policy and Research.

With social media, youths face racism on more fronts than their parents did, said Leslie Adams, assistant professor in the department of mental health at Johns Hopkins Bloomberg School of Public Health.

Each of these factors has been shown to affect suicide risk. For example, experiencing racism and sexism together is linked to a threefold increase in suicidal thoughts for Asian American women, said Brian Keum, assistant professor at UCLA, based on preliminary research findings.

COVID-19 intensified these hardships among communities of color, with disproportionate numbers of lost loved ones, lost jobs, and lost housing. The murder of George Floyd prompted widespread racial unrest, and Asian Americans saw an increase in hate crimes.

At the same time, studies in Connecticut and Maryland found that suicide rates rose within these populations and dropped for their White counterparts.

“It’s not just a problem within the person, but societal issues that need to be addressed,” said Shari Jager-Hyman, assistant professor of psychiatry at the University of Pennsylvania.
 

Lessons from Texas

In Texas, COVID-19 hit Hispanics especially hard. As of July 2021, they accounted for 45% of all COVID-19 deaths and disproportionately lost jobs. Individuals living in the U.S. without authorization were generally not eligible for unemployment benefits or federal stimulus checks.

During this time, suicide deaths among Hispanic Texans climbed from 847 deaths in 2019 to 962 deaths in 2020, according to preliminary state data. Suicide deaths rose for Black Texans and residents classified as “other” races or ethnicities, but decreased for White Texans.

The numbers didn’t surprise Marc Mendiola. The 20-year-old grew up in a majority-Hispanic community on the south side of San Antonio. Even before the pandemic, he often heard classmates say they were suicidal. Many faced dire finances at home, sometimes living without electricity, food, or water. Those who sought mental health treatment often found services prohibitively expensive or inaccessible because they weren’t offered in Spanish.

“These are conditions the community has always been in,” Mendiola said. “But with the pandemic, it’s even worse.”

Four years ago, Mendiola and his classmates at South San High School began advocating for mental health services. In late 2019, just months before COVID-19 struck, their vision became reality. Six community agencies partnered to offer free services to students and their families across three school districts.

Richard Davidson, chief operating officer of Family Service, one of the groups in the collaborative, said the number of students discussing economic stressors has been on the rise since April 2020. More than 90% of the students who received services in the first half of 2021 were Hispanic, and nearly 10% reported thoughts of suicide or self-harm, program data show. None died by suicide.

Many students are so worried about what’s for dinner the next day that they’re not able to see a future beyond that, Davidson said. That’s when suicide can feel like a viable option.

“One of the things we do is help them see … that despite this situation now, you can create a vision for your future,” Davidson said.
 

A good future

Researchers say the promise of a good future is often overlooked in suicide prevention, perhaps because achieving it is so challenging. It requires economic and social growth and breaking systemic barriers.

Tevis Simon works to address all those fronts. As a child in West Baltimore, Simon, who is Black, faced poverty and trauma. As an adult, she attempted suicide three times. But now she shares her story with youths across the city to inspire them to overcome challenges. She also talks to politicians, law enforcement agencies, and public policy officials about their responsibilities.

“We can’t not talk about race,” said Simon, 43. “We can’t not talk about systematic oppression. We cannot not talk about these conditions that affect our mental well-being and our feeling and desire to live.”

For Jamal Clay in Illinois, the systemic barriers started early. Before his suicide last year, he had tried to harm himself when he was 12 and the victim of bullies. At that time, he was hospitalized for a few days and told to follow up with outpatient therapy, said his mother, Maxie.

But it was difficult to find therapists who accepted Medicaid, she said. When Maxie finally found one, there was a 60-day wait. Other therapists canceled appointments, she said.

“So we worked on our own,” Maxie said, relying on church and community. Her son seemed to improve. “We thought we closed that chapter in our lives.”

But when the pandemic hit, everything got worse, she said. Clay came home from college and worked at an Amazon warehouse. On drives to and from work, he was frequently pulled over by police. He stopped wearing hats so officers would consider him less intimidating, Maxie said.

“He felt uncomfortable being out in the street,” she said.

Maxie is still trying to make sense of what happened the day Clay died. But she’s found meaning in starting a nonprofit called Soul Survivors of Chicago. Through the organization, she provides education, scholarships and shoes – including Jamal’s old ones – to those impacted by violence, suicide, and trauma.

“My son won’t be able to have a first interview in [those] shoes. He won’t be able to have a nice jump shot or go to church or even meet his wife,” Maxie said.

But she hopes his shoes will carry someone else to a good future.

[Editor’s note: For the purposes of this story, “people of color” or “communities of color” refers to any racial or ethnic populations whose members do not identify as White, including those who are multiracial. Hispanics can be of any race or combination of races.]

KHN senior correspondent JoNel Aleccia contributed to this report. KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.

This story is a collaboration between KHN and “Science Friday.” 

Rafiah Maxie has been a licensed clinical social worker in the Chicago area for a decade. Throughout that time, she’d viewed suicide as a problem most prevalent among middle-aged white men.

Until May 27, 2020.

That day, Maxie’s 19-year-old son, Jamal Clay – who loved playing the trumpet and participating in theater, who would help her unload groceries from the car and raise funds for the March of the Dimes – killed himself in their garage.

“Now I cannot blink without seeing my son hanging,” said Maxie, who is Black.

Clay’s death, along with the suicides of more than 100 other Black residents in Illinois last year, has led locals to call for new prevention efforts focused on Black communities. In 2020, during the pandemic’s first year, suicides among White residents decreased compared with previous years, while they increased among Black residents, according to state data.

But this is not a local problem. Nor is it limited to the pandemic.

Interviews with a dozen suicide researchers, data collected from states across the country, and a review of decades of research revealed that suicide is a growing crisis for communities of color – one that plagued them well before the pandemic and has only been exacerbated since.

Overall suicide rates in the U.S. decreased in 2019 and 2020. National and local studies attribute the trend to a drop among White Americans, who make up the majority of suicide deaths. Meanwhile, rates for Black, Hispanic, and Asian Americans – though lower than those of their white peers – continued to climb in many states. (Suicide rates have been consistently high for Native Americans.)

“COVID created more transparency regarding what we already knew was happening,” said Sonyia Richardson, a licensed clinical social worker who focuses on serving people of color, and assistant professor at the University of North Carolina–Charlotte, where she researches suicide. When you put the suicide rates of all communities in one bucket, “that bucket says it’s getting better and what we’re doing is working,” she said. “But that’s not the case for communities of color.”
 

Losing generations

Although the suicide rate is highest among middle-aged White men, young people of color are emerging as particularly at risk.

Research shows Black kids younger than 13 die by suicide at nearly twice the rate of White kids and, over time, their suicide rates have grown even as rates have decreased for White children. Among teenagers and young adults, suicide deaths have increased more than 45% for Black Americans and about 40% for Asian Americans in the 7 years ending in 2019. Other concerning trends in suicide attempts date to the ’90s.

“We’re losing generations,” said Sean Joe, a national expert on Black suicide and a professor at Washington University in St. Louis. “We have to pay attention now because if you’re out of the first decade of life and think life is not worth pursuing, that’s a signal to say something is going really wrong.”

These statistics also refute traditional ideas that suicide doesn’t happen in certain ethnic or minority populations because they’re “protected” and “resilient” or the “model minority,” said Kiara Alvarez, a researcher and psychologist at Massachusetts General Hospital who focuses on suicide among Hispanic and immigrant populations.

Although these groups may have had low suicide rates historically, that’s changing, she said.

Paul Chin lost his 17-year-old brother, Chris, to suicide in 2009. A poem Chris wrote in high school about his heritage has left Chin, 8 years his senior, wondering if his brother struggled to feel accepted in the U.S., despite being born and raised in New York.

Growing up, Asian Americans weren’t represented in lessons at school or in pop culture, said Chin, now 37. Even in clinical research on suicide as well as other health topics, kids like Chris are underrepresented, with less than 1% of federal research funding focused on Asian Americans.

It wasn’t until the pandemic, and the concurrent rise in hate crimes against Asian Americans, that Chin saw national attention on the community’s mental health. He hopes the interest is not short-lived.

Suicide is the leading cause of death for Asian Americans ages 15 to 24, yet “that doesn’t get enough attention,” Chin said. “It’s important to continue to share these stories.”

Kathy Williams, who is Black, has been on a similar mission since her 15-year-old son, Torian Graves, died by suicide in 1996. People didn’t talk about suicide in the Black community then, she said. So she started raising the topic at her church in Durham, N.C., and in local schools. She wanted Black families to know the warning signs and society at large to recognize the seriousness of the problem.

The pandemic may have highlighted this, Williams said, but “it has always happened. Always.”
 

Pandemic sheds light on the triggers

Pinpointing the root causes of rising suicide within communities of color has proved difficult. How much stems from mental illness? How much from socioeconomic changes like job losses or social isolation? Now, COVID-19 may offer some clues.

Recent decades have been marked by growing economic instability, a widening racial wealth gap, and more public attention on police killings of unarmed Black and Brown people, said Michael Lindsey, executive director of the New York University McSilver Institute for Poverty Policy and Research.

With social media, youths face racism on more fronts than their parents did, said Leslie Adams, assistant professor in the department of mental health at Johns Hopkins Bloomberg School of Public Health.

Each of these factors has been shown to affect suicide risk. For example, experiencing racism and sexism together is linked to a threefold increase in suicidal thoughts for Asian American women, said Brian Keum, assistant professor at UCLA, based on preliminary research findings.

COVID-19 intensified these hardships among communities of color, with disproportionate numbers of lost loved ones, lost jobs, and lost housing. The murder of George Floyd prompted widespread racial unrest, and Asian Americans saw an increase in hate crimes.

At the same time, studies in Connecticut and Maryland found that suicide rates rose within these populations and dropped for their White counterparts.

“It’s not just a problem within the person, but societal issues that need to be addressed,” said Shari Jager-Hyman, assistant professor of psychiatry at the University of Pennsylvania.
 

Lessons from Texas

In Texas, COVID-19 hit Hispanics especially hard. As of July 2021, they accounted for 45% of all COVID-19 deaths and disproportionately lost jobs. Individuals living in the U.S. without authorization were generally not eligible for unemployment benefits or federal stimulus checks.

During this time, suicide deaths among Hispanic Texans climbed from 847 deaths in 2019 to 962 deaths in 2020, according to preliminary state data. Suicide deaths rose for Black Texans and residents classified as “other” races or ethnicities, but decreased for White Texans.

The numbers didn’t surprise Marc Mendiola. The 20-year-old grew up in a majority-Hispanic community on the south side of San Antonio. Even before the pandemic, he often heard classmates say they were suicidal. Many faced dire finances at home, sometimes living without electricity, food, or water. Those who sought mental health treatment often found services prohibitively expensive or inaccessible because they weren’t offered in Spanish.

“These are conditions the community has always been in,” Mendiola said. “But with the pandemic, it’s even worse.”

Four years ago, Mendiola and his classmates at South San High School began advocating for mental health services. In late 2019, just months before COVID-19 struck, their vision became reality. Six community agencies partnered to offer free services to students and their families across three school districts.

Richard Davidson, chief operating officer of Family Service, one of the groups in the collaborative, said the number of students discussing economic stressors has been on the rise since April 2020. More than 90% of the students who received services in the first half of 2021 were Hispanic, and nearly 10% reported thoughts of suicide or self-harm, program data show. None died by suicide.

Many students are so worried about what’s for dinner the next day that they’re not able to see a future beyond that, Davidson said. That’s when suicide can feel like a viable option.

“One of the things we do is help them see … that despite this situation now, you can create a vision for your future,” Davidson said.
 

A good future

Researchers say the promise of a good future is often overlooked in suicide prevention, perhaps because achieving it is so challenging. It requires economic and social growth and breaking systemic barriers.

Tevis Simon works to address all those fronts. As a child in West Baltimore, Simon, who is Black, faced poverty and trauma. As an adult, she attempted suicide three times. But now she shares her story with youths across the city to inspire them to overcome challenges. She also talks to politicians, law enforcement agencies, and public policy officials about their responsibilities.

“We can’t not talk about race,” said Simon, 43. “We can’t not talk about systematic oppression. We cannot not talk about these conditions that affect our mental well-being and our feeling and desire to live.”

For Jamal Clay in Illinois, the systemic barriers started early. Before his suicide last year, he had tried to harm himself when he was 12 and the victim of bullies. At that time, he was hospitalized for a few days and told to follow up with outpatient therapy, said his mother, Maxie.

But it was difficult to find therapists who accepted Medicaid, she said. When Maxie finally found one, there was a 60-day wait. Other therapists canceled appointments, she said.

“So we worked on our own,” Maxie said, relying on church and community. Her son seemed to improve. “We thought we closed that chapter in our lives.”

But when the pandemic hit, everything got worse, she said. Clay came home from college and worked at an Amazon warehouse. On drives to and from work, he was frequently pulled over by police. He stopped wearing hats so officers would consider him less intimidating, Maxie said.

“He felt uncomfortable being out in the street,” she said.

Maxie is still trying to make sense of what happened the day Clay died. But she’s found meaning in starting a nonprofit called Soul Survivors of Chicago. Through the organization, she provides education, scholarships and shoes – including Jamal’s old ones – to those impacted by violence, suicide, and trauma.

“My son won’t be able to have a first interview in [those] shoes. He won’t be able to have a nice jump shot or go to church or even meet his wife,” Maxie said.

But she hopes his shoes will carry someone else to a good future.

[Editor’s note: For the purposes of this story, “people of color” or “communities of color” refers to any racial or ethnic populations whose members do not identify as White, including those who are multiracial. Hispanics can be of any race or combination of races.]

KHN senior correspondent JoNel Aleccia contributed to this report. KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.

This story is a collaboration between KHN and “Science Friday.” 

Rafiah Maxie has been a licensed clinical social worker in the Chicago area for a decade. Throughout that time, she’d viewed suicide as a problem most prevalent among middle-aged white men.

Until May 27, 2020.

That day, Maxie’s 19-year-old son, Jamal Clay – who loved playing the trumpet and participating in theater, who would help her unload groceries from the car and raise funds for the March of the Dimes – killed himself in their garage.

“Now I cannot blink without seeing my son hanging,” said Maxie, who is Black.

Clay’s death, along with the suicides of more than 100 other Black residents in Illinois last year, has led locals to call for new prevention efforts focused on Black communities. In 2020, during the pandemic’s first year, suicides among White residents decreased compared with previous years, while they increased among Black residents, according to state data.

But this is not a local problem. Nor is it limited to the pandemic.

Interviews with a dozen suicide researchers, data collected from states across the country, and a review of decades of research revealed that suicide is a growing crisis for communities of color – one that plagued them well before the pandemic and has only been exacerbated since.

Overall suicide rates in the U.S. decreased in 2019 and 2020. National and local studies attribute the trend to a drop among White Americans, who make up the majority of suicide deaths. Meanwhile, rates for Black, Hispanic, and Asian Americans – though lower than those of their white peers – continued to climb in many states. (Suicide rates have been consistently high for Native Americans.)

“COVID created more transparency regarding what we already knew was happening,” said Sonyia Richardson, a licensed clinical social worker who focuses on serving people of color, and assistant professor at the University of North Carolina–Charlotte, where she researches suicide. When you put the suicide rates of all communities in one bucket, “that bucket says it’s getting better and what we’re doing is working,” she said. “But that’s not the case for communities of color.”
 

Losing generations

Although the suicide rate is highest among middle-aged White men, young people of color are emerging as particularly at risk.

Research shows Black kids younger than 13 die by suicide at nearly twice the rate of White kids and, over time, their suicide rates have grown even as rates have decreased for White children. Among teenagers and young adults, suicide deaths have increased more than 45% for Black Americans and about 40% for Asian Americans in the 7 years ending in 2019. Other concerning trends in suicide attempts date to the ’90s.

“We’re losing generations,” said Sean Joe, a national expert on Black suicide and a professor at Washington University in St. Louis. “We have to pay attention now because if you’re out of the first decade of life and think life is not worth pursuing, that’s a signal to say something is going really wrong.”

These statistics also refute traditional ideas that suicide doesn’t happen in certain ethnic or minority populations because they’re “protected” and “resilient” or the “model minority,” said Kiara Alvarez, a researcher and psychologist at Massachusetts General Hospital who focuses on suicide among Hispanic and immigrant populations.

Although these groups may have had low suicide rates historically, that’s changing, she said.

Paul Chin lost his 17-year-old brother, Chris, to suicide in 2009. A poem Chris wrote in high school about his heritage has left Chin, 8 years his senior, wondering if his brother struggled to feel accepted in the U.S., despite being born and raised in New York.

Growing up, Asian Americans weren’t represented in lessons at school or in pop culture, said Chin, now 37. Even in clinical research on suicide as well as other health topics, kids like Chris are underrepresented, with less than 1% of federal research funding focused on Asian Americans.

It wasn’t until the pandemic, and the concurrent rise in hate crimes against Asian Americans, that Chin saw national attention on the community’s mental health. He hopes the interest is not short-lived.

Suicide is the leading cause of death for Asian Americans ages 15 to 24, yet “that doesn’t get enough attention,” Chin said. “It’s important to continue to share these stories.”

Kathy Williams, who is Black, has been on a similar mission since her 15-year-old son, Torian Graves, died by suicide in 1996. People didn’t talk about suicide in the Black community then, she said. So she started raising the topic at her church in Durham, N.C., and in local schools. She wanted Black families to know the warning signs and society at large to recognize the seriousness of the problem.

The pandemic may have highlighted this, Williams said, but “it has always happened. Always.”
 

Pandemic sheds light on the triggers

Pinpointing the root causes of rising suicide within communities of color has proved difficult. How much stems from mental illness? How much from socioeconomic changes like job losses or social isolation? Now, COVID-19 may offer some clues.

Recent decades have been marked by growing economic instability, a widening racial wealth gap, and more public attention on police killings of unarmed Black and Brown people, said Michael Lindsey, executive director of the New York University McSilver Institute for Poverty Policy and Research.

With social media, youths face racism on more fronts than their parents did, said Leslie Adams, assistant professor in the department of mental health at Johns Hopkins Bloomberg School of Public Health.

Each of these factors has been shown to affect suicide risk. For example, experiencing racism and sexism together is linked to a threefold increase in suicidal thoughts for Asian American women, said Brian Keum, assistant professor at UCLA, based on preliminary research findings.

COVID-19 intensified these hardships among communities of color, with disproportionate numbers of lost loved ones, lost jobs, and lost housing. The murder of George Floyd prompted widespread racial unrest, and Asian Americans saw an increase in hate crimes.

At the same time, studies in Connecticut and Maryland found that suicide rates rose within these populations and dropped for their White counterparts.

“It’s not just a problem within the person, but societal issues that need to be addressed,” said Shari Jager-Hyman, assistant professor of psychiatry at the University of Pennsylvania.
 

Lessons from Texas

In Texas, COVID-19 hit Hispanics especially hard. As of July 2021, they accounted for 45% of all COVID-19 deaths and disproportionately lost jobs. Individuals living in the U.S. without authorization were generally not eligible for unemployment benefits or federal stimulus checks.

During this time, suicide deaths among Hispanic Texans climbed from 847 deaths in 2019 to 962 deaths in 2020, according to preliminary state data. Suicide deaths rose for Black Texans and residents classified as “other” races or ethnicities, but decreased for White Texans.

The numbers didn’t surprise Marc Mendiola. The 20-year-old grew up in a majority-Hispanic community on the south side of San Antonio. Even before the pandemic, he often heard classmates say they were suicidal. Many faced dire finances at home, sometimes living without electricity, food, or water. Those who sought mental health treatment often found services prohibitively expensive or inaccessible because they weren’t offered in Spanish.

“These are conditions the community has always been in,” Mendiola said. “But with the pandemic, it’s even worse.”

Four years ago, Mendiola and his classmates at South San High School began advocating for mental health services. In late 2019, just months before COVID-19 struck, their vision became reality. Six community agencies partnered to offer free services to students and their families across three school districts.

Richard Davidson, chief operating officer of Family Service, one of the groups in the collaborative, said the number of students discussing economic stressors has been on the rise since April 2020. More than 90% of the students who received services in the first half of 2021 were Hispanic, and nearly 10% reported thoughts of suicide or self-harm, program data show. None died by suicide.

Many students are so worried about what’s for dinner the next day that they’re not able to see a future beyond that, Davidson said. That’s when suicide can feel like a viable option.

“One of the things we do is help them see … that despite this situation now, you can create a vision for your future,” Davidson said.
 

A good future

Researchers say the promise of a good future is often overlooked in suicide prevention, perhaps because achieving it is so challenging. It requires economic and social growth and breaking systemic barriers.

Tevis Simon works to address all those fronts. As a child in West Baltimore, Simon, who is Black, faced poverty and trauma. As an adult, she attempted suicide three times. But now she shares her story with youths across the city to inspire them to overcome challenges. She also talks to politicians, law enforcement agencies, and public policy officials about their responsibilities.

“We can’t not talk about race,” said Simon, 43. “We can’t not talk about systematic oppression. We cannot not talk about these conditions that affect our mental well-being and our feeling and desire to live.”

For Jamal Clay in Illinois, the systemic barriers started early. Before his suicide last year, he had tried to harm himself when he was 12 and the victim of bullies. At that time, he was hospitalized for a few days and told to follow up with outpatient therapy, said his mother, Maxie.

But it was difficult to find therapists who accepted Medicaid, she said. When Maxie finally found one, there was a 60-day wait. Other therapists canceled appointments, she said.

“So we worked on our own,” Maxie said, relying on church and community. Her son seemed to improve. “We thought we closed that chapter in our lives.”

But when the pandemic hit, everything got worse, she said. Clay came home from college and worked at an Amazon warehouse. On drives to and from work, he was frequently pulled over by police. He stopped wearing hats so officers would consider him less intimidating, Maxie said.

“He felt uncomfortable being out in the street,” she said.

Maxie is still trying to make sense of what happened the day Clay died. But she’s found meaning in starting a nonprofit called Soul Survivors of Chicago. Through the organization, she provides education, scholarships and shoes – including Jamal’s old ones – to those impacted by violence, suicide, and trauma.

“My son won’t be able to have a first interview in [those] shoes. He won’t be able to have a nice jump shot or go to church or even meet his wife,” Maxie said.

But she hopes his shoes will carry someone else to a good future.

[Editor’s note: For the purposes of this story, “people of color” or “communities of color” refers to any racial or ethnic populations whose members do not identify as White, including those who are multiracial. Hispanics can be of any race or combination of races.]

KHN senior correspondent JoNel Aleccia contributed to this report. KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. Together with Policy Analysis and Polling, KHN is one of the three major operating programs at KFF (Kaiser Family Foundation). KFF is an endowed nonprofit organization providing information on health issues to the nation.

About one-third of the U.S. population had been infected with SARS-CoV-2 by the end of 2020, according to a modeling study published Aug. 26 online in Nature.

Jeffrey Shaman, PhD, professor in the department of environmental health sciences and director of the climate and health program at the Columbia University Mailman School of Public Health, New York City, and colleagues developed a model to simulate how SARS-CoV-2 was transmitted within and between all 3,142 counties in the United States.

In their model, the researchers considered migration data between counties, the observed case numbers, and estimates of infections based on the number of people who test positive for SARS-CoV-2 antibodies.

The United States had the highest number of confirmed COVID-19 cases and deaths in the world during 2020. More than 19.6 million cases were reported by the end of the year.

But the authors point out that “69% of the population remained susceptible to viral infection.”

The researchers also studied the ascertainment rate, or the ratio of detected cases to the number of confirmed cases. Nationally, that value increased from 11.3% in March 2020 to 24.5% in December 2020.

That’s one of the biggest pandemic lessons from the data, Dr. Shaman said: “It is vitally important when there is an outbreak and you’re counting cases that there are many more people infected in your community who are contagious than reported cases. Each individual is infectious for multiple days, and there are many more unreported cases.”

That applies now with the Delta variant, he said.

“Vaccinated people who get infected with the Delta variant are part of the transmission chain,” he said.
 

Fatality rates dropped

Some of the data were very positive, Dr. Shaman told this news organization. The infection fatality rate fell from 0.77% in April to 0.31% in December. The authors suggest that that may be because of improvements in diagnosis and treatment, patient care, and reduced disease severity.

However, the fatality rate was still nearly four times as high as the estimated fatality rate for seasonal influenza (0.08%) and the 2009 influenza pandemic (0.0076%), the authors point out.

Joe K. Gerald, MD, PhD, associate professor and program director of public health policy and management at the University of Arizona, Tucson, told this news organization that this article helps confirm that COVID is much deadlier than the flu and that the intensity of the response has been appropriate.

“We should be willing to invest a lot more in mitigating COVID-19 than seasonal influenza because it has much greater consequences,” he said.

The numbers emphasize that testing must improve.

“We didn’t have enough tests available, and they weren’t easily accessible. For much of the year we were flying in the dark,” Dr. Gerald said.

The number of tests has increased this year, he acknowledged, but testing still lags. “We just can’t miss this many infections or diagnoses and hope to gain control,” he said.

The study also points out the huge variation by state and by county in infections and deaths, and that variation continues. Gerald noted that the varied numbers make it difficult for some regions to accept broader mandates, because the threat from COVID-19 appears very different where they are.

“We have to think about regions, how many people are susceptible, and what the testing capacity is,” he said. “States and even counties should have some leeway to make some important public health decisions, because local conditions are going to differ at different points in time.”
 

‘We have not turned the corner’

Jill Foster, MD, a pediatric infectious disease physician at the University of Minnesota Medical School, Minneapolis, said in an interview that the study adds evidence: “We have not turned the corner on COVID-19 and are nowhere near herd immunity – if it exists for SARS-CoV-2.”

She said the numbers presented are particularly concerning in regard to how many people were susceptible and were actively able to infect others: “Much higher than most people imagined and very much higher than their comparison, influenza.

“There are still more people susceptible than we had believed,” Dr. Foster added. “If the pattern continues where the Delta variant infects a significant portion of those vaccinated, the number of people susceptible rises even higher than was predicted.”

She said that it is reassuring that the analysis shows a decrease in case fatality and said the finding supports the common opinion that medicine is better able to fight the disease.

“However,” she said, “the optimism is tempered by acknowledging that in order to benefit from these advances, we must not overwhelm the facilities where patients are cared for so that optimal care can be delivered.”

Dr. Foster said these numbers represent a warning that COVID should be treated as a continuing threat.

“We need to acknowledge that there is COVID-19 infection simmering and periodically erupting throughout the country,” she said. “It is not monolithic and varies by geography and seasons in ways that are difficult to predict other than at any given time there is likely more infection present than we are identifying and more people susceptible to infection than we have calculated.”

The authors and Dr. Gerald have disclosed no relevant financial relationships. Dr. Foster has received clinical trials funding from Moderna.

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

About one-third of the U.S. population had been infected with SARS-CoV-2 by the end of 2020, according to a modeling study published Aug. 26 online in Nature.

Jeffrey Shaman, PhD, professor in the department of environmental health sciences and director of the climate and health program at the Columbia University Mailman School of Public Health, New York City, and colleagues developed a model to simulate how SARS-CoV-2 was transmitted within and between all 3,142 counties in the United States.

In their model, the researchers considered migration data between counties, the observed case numbers, and estimates of infections based on the number of people who test positive for SARS-CoV-2 antibodies.

The United States had the highest number of confirmed COVID-19 cases and deaths in the world during 2020. More than 19.6 million cases were reported by the end of the year.

But the authors point out that “69% of the population remained susceptible to viral infection.”

The researchers also studied the ascertainment rate, or the ratio of detected cases to the number of confirmed cases. Nationally, that value increased from 11.3% in March 2020 to 24.5% in December 2020.

That’s one of the biggest pandemic lessons from the data, Dr. Shaman said: “It is vitally important when there is an outbreak and you’re counting cases that there are many more people infected in your community who are contagious than reported cases. Each individual is infectious for multiple days, and there are many more unreported cases.”

That applies now with the Delta variant, he said.

“Vaccinated people who get infected with the Delta variant are part of the transmission chain,” he said.
 

Fatality rates dropped

Some of the data were very positive, Dr. Shaman told this news organization. The infection fatality rate fell from 0.77% in April to 0.31% in December. The authors suggest that that may be because of improvements in diagnosis and treatment, patient care, and reduced disease severity.

However, the fatality rate was still nearly four times as high as the estimated fatality rate for seasonal influenza (0.08%) and the 2009 influenza pandemic (0.0076%), the authors point out.

Joe K. Gerald, MD, PhD, associate professor and program director of public health policy and management at the University of Arizona, Tucson, told this news organization that this article helps confirm that COVID is much deadlier than the flu and that the intensity of the response has been appropriate.

“We should be willing to invest a lot more in mitigating COVID-19 than seasonal influenza because it has much greater consequences,” he said.

The numbers emphasize that testing must improve.

“We didn’t have enough tests available, and they weren’t easily accessible. For much of the year we were flying in the dark,” Dr. Gerald said.

The number of tests has increased this year, he acknowledged, but testing still lags. “We just can’t miss this many infections or diagnoses and hope to gain control,” he said.

The study also points out the huge variation by state and by county in infections and deaths, and that variation continues. Gerald noted that the varied numbers make it difficult for some regions to accept broader mandates, because the threat from COVID-19 appears very different where they are.

“We have to think about regions, how many people are susceptible, and what the testing capacity is,” he said. “States and even counties should have some leeway to make some important public health decisions, because local conditions are going to differ at different points in time.”
 

‘We have not turned the corner’

Jill Foster, MD, a pediatric infectious disease physician at the University of Minnesota Medical School, Minneapolis, said in an interview that the study adds evidence: “We have not turned the corner on COVID-19 and are nowhere near herd immunity – if it exists for SARS-CoV-2.”

She said the numbers presented are particularly concerning in regard to how many people were susceptible and were actively able to infect others: “Much higher than most people imagined and very much higher than their comparison, influenza.

“There are still more people susceptible than we had believed,” Dr. Foster added. “If the pattern continues where the Delta variant infects a significant portion of those vaccinated, the number of people susceptible rises even higher than was predicted.”

She said that it is reassuring that the analysis shows a decrease in case fatality and said the finding supports the common opinion that medicine is better able to fight the disease.

“However,” she said, “the optimism is tempered by acknowledging that in order to benefit from these advances, we must not overwhelm the facilities where patients are cared for so that optimal care can be delivered.”

Dr. Foster said these numbers represent a warning that COVID should be treated as a continuing threat.

“We need to acknowledge that there is COVID-19 infection simmering and periodically erupting throughout the country,” she said. “It is not monolithic and varies by geography and seasons in ways that are difficult to predict other than at any given time there is likely more infection present than we are identifying and more people susceptible to infection than we have calculated.”

The authors and Dr. Gerald have disclosed no relevant financial relationships. Dr. Foster has received clinical trials funding from Moderna.

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

About one-third of the U.S. population had been infected with SARS-CoV-2 by the end of 2020, according to a modeling study published Aug. 26 online in Nature.

Jeffrey Shaman, PhD, professor in the department of environmental health sciences and director of the climate and health program at the Columbia University Mailman School of Public Health, New York City, and colleagues developed a model to simulate how SARS-CoV-2 was transmitted within and between all 3,142 counties in the United States.

In their model, the researchers considered migration data between counties, the observed case numbers, and estimates of infections based on the number of people who test positive for SARS-CoV-2 antibodies.

The United States had the highest number of confirmed COVID-19 cases and deaths in the world during 2020. More than 19.6 million cases were reported by the end of the year.

But the authors point out that “69% of the population remained susceptible to viral infection.”

The researchers also studied the ascertainment rate, or the ratio of detected cases to the number of confirmed cases. Nationally, that value increased from 11.3% in March 2020 to 24.5% in December 2020.

That’s one of the biggest pandemic lessons from the data, Dr. Shaman said: “It is vitally important when there is an outbreak and you’re counting cases that there are many more people infected in your community who are contagious than reported cases. Each individual is infectious for multiple days, and there are many more unreported cases.”

That applies now with the Delta variant, he said.

“Vaccinated people who get infected with the Delta variant are part of the transmission chain,” he said.
 

Fatality rates dropped

Some of the data were very positive, Dr. Shaman told this news organization. The infection fatality rate fell from 0.77% in April to 0.31% in December. The authors suggest that that may be because of improvements in diagnosis and treatment, patient care, and reduced disease severity.

However, the fatality rate was still nearly four times as high as the estimated fatality rate for seasonal influenza (0.08%) and the 2009 influenza pandemic (0.0076%), the authors point out.

Joe K. Gerald, MD, PhD, associate professor and program director of public health policy and management at the University of Arizona, Tucson, told this news organization that this article helps confirm that COVID is much deadlier than the flu and that the intensity of the response has been appropriate.

“We should be willing to invest a lot more in mitigating COVID-19 than seasonal influenza because it has much greater consequences,” he said.

The numbers emphasize that testing must improve.

“We didn’t have enough tests available, and they weren’t easily accessible. For much of the year we were flying in the dark,” Dr. Gerald said.

The number of tests has increased this year, he acknowledged, but testing still lags. “We just can’t miss this many infections or diagnoses and hope to gain control,” he said.

The study also points out the huge variation by state and by county in infections and deaths, and that variation continues. Gerald noted that the varied numbers make it difficult for some regions to accept broader mandates, because the threat from COVID-19 appears very different where they are.

“We have to think about regions, how many people are susceptible, and what the testing capacity is,” he said. “States and even counties should have some leeway to make some important public health decisions, because local conditions are going to differ at different points in time.”
 

‘We have not turned the corner’

Jill Foster, MD, a pediatric infectious disease physician at the University of Minnesota Medical School, Minneapolis, said in an interview that the study adds evidence: “We have not turned the corner on COVID-19 and are nowhere near herd immunity – if it exists for SARS-CoV-2.”

She said the numbers presented are particularly concerning in regard to how many people were susceptible and were actively able to infect others: “Much higher than most people imagined and very much higher than their comparison, influenza.

“There are still more people susceptible than we had believed,” Dr. Foster added. “If the pattern continues where the Delta variant infects a significant portion of those vaccinated, the number of people susceptible rises even higher than was predicted.”

She said that it is reassuring that the analysis shows a decrease in case fatality and said the finding supports the common opinion that medicine is better able to fight the disease.

“However,” she said, “the optimism is tempered by acknowledging that in order to benefit from these advances, we must not overwhelm the facilities where patients are cared for so that optimal care can be delivered.”

Dr. Foster said these numbers represent a warning that COVID should be treated as a continuing threat.

“We need to acknowledge that there is COVID-19 infection simmering and periodically erupting throughout the country,” she said. “It is not monolithic and varies by geography and seasons in ways that are difficult to predict other than at any given time there is likely more infection present than we are identifying and more people susceptible to infection than we have calculated.”

The authors and Dr. Gerald have disclosed no relevant financial relationships. Dr. Foster has received clinical trials funding from Moderna.

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