Feature

Moderna probably will not have clinical trial results anytime soon on how its COVID-19 vaccine affects children and adolescents, according to the company CEO and a federal official.

The Moderna vaccine was authorized for use in December and is now being given to people 18 and over. But children would receive lower doses, so new clinical trials must be done, Moderna CEO Stephane Bancel said at the JPMorgan virtual Health Care Conference on Monday.

Clinical trials on children 11 and younger “will take much longer, because we have to age deescalate and start at a lower dose. So we should not anticipate clinical data in 2021, but more in 2022,” Ms. Bancel said, according to Business Insider.

Moderna’s clinical trials for 12- to 17-year-olds started 4 weeks ago, but the company is having trouble getting enough participants, said Moncef Slaoui, PhD, the scientific head of Operation Warp Speed, the U.S. government’s vaccine effort. That could delay Food and Drug Administration approval, he said.

“It’s really very important for all of us, for all the population in America, to realize that we can’t have that indication unless adolescents aged 12-18 decide to participate,” Dr. Slaoui said, according to USA Today.

He said the adolescent trials are getting only about 800 volunteers a month, but need at least 3,000 volunteers to complete the study, USA Today reported. Parents interested in having their child participate can check eligibility and sign at this website.

The Pfizer/BioNTech vaccine won authorization for use in 16- to 17-year-olds as well as adults.

The coronavirus doesn’t appear to have as serious complications for children as for adults.

“At this time, it appears that severe illness due to COVID-19 is rare among children,” the American Association of Pediatrics says. “However, there is an urgent need to collect more data on longer-term impacts of the pandemic on children, including ways the virus may harm the long-term physical health of infected children, as well as its emotional and mental health effects.”

The association says 179 children had died of COVID-related reasons in 43 states and New York City as of Dec. 31, 2020. That’s about 0.06% of total COVID deaths, it says.

But children do get sick. As of Jan. 7, 2021, nearly 2.3 million children had tested positive for COVID-19 since the start of the pandemic, the association says.

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

Moderna probably will not have clinical trial results anytime soon on how its COVID-19 vaccine affects children and adolescents, according to the company CEO and a federal official.

The Moderna vaccine was authorized for use in December and is now being given to people 18 and over. But children would receive lower doses, so new clinical trials must be done, Moderna CEO Stephane Bancel said at the JPMorgan virtual Health Care Conference on Monday.

Clinical trials on children 11 and younger “will take much longer, because we have to age deescalate and start at a lower dose. So we should not anticipate clinical data in 2021, but more in 2022,” Ms. Bancel said, according to Business Insider.

Moderna’s clinical trials for 12- to 17-year-olds started 4 weeks ago, but the company is having trouble getting enough participants, said Moncef Slaoui, PhD, the scientific head of Operation Warp Speed, the U.S. government’s vaccine effort. That could delay Food and Drug Administration approval, he said.

“It’s really very important for all of us, for all the population in America, to realize that we can’t have that indication unless adolescents aged 12-18 decide to participate,” Dr. Slaoui said, according to USA Today.

He said the adolescent trials are getting only about 800 volunteers a month, but need at least 3,000 volunteers to complete the study, USA Today reported. Parents interested in having their child participate can check eligibility and sign at this website.

The Pfizer/BioNTech vaccine won authorization for use in 16- to 17-year-olds as well as adults.

The coronavirus doesn’t appear to have as serious complications for children as for adults.

“At this time, it appears that severe illness due to COVID-19 is rare among children,” the American Association of Pediatrics says. “However, there is an urgent need to collect more data on longer-term impacts of the pandemic on children, including ways the virus may harm the long-term physical health of infected children, as well as its emotional and mental health effects.”

The association says 179 children had died of COVID-related reasons in 43 states and New York City as of Dec. 31, 2020. That’s about 0.06% of total COVID deaths, it says.

But children do get sick. As of Jan. 7, 2021, nearly 2.3 million children had tested positive for COVID-19 since the start of the pandemic, the association says.

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

Moderna probably will not have clinical trial results anytime soon on how its COVID-19 vaccine affects children and adolescents, according to the company CEO and a federal official.

The Moderna vaccine was authorized for use in December and is now being given to people 18 and over. But children would receive lower doses, so new clinical trials must be done, Moderna CEO Stephane Bancel said at the JPMorgan virtual Health Care Conference on Monday.

Clinical trials on children 11 and younger “will take much longer, because we have to age deescalate and start at a lower dose. So we should not anticipate clinical data in 2021, but more in 2022,” Ms. Bancel said, according to Business Insider.

Moderna’s clinical trials for 12- to 17-year-olds started 4 weeks ago, but the company is having trouble getting enough participants, said Moncef Slaoui, PhD, the scientific head of Operation Warp Speed, the U.S. government’s vaccine effort. That could delay Food and Drug Administration approval, he said.

“It’s really very important for all of us, for all the population in America, to realize that we can’t have that indication unless adolescents aged 12-18 decide to participate,” Dr. Slaoui said, according to USA Today.

He said the adolescent trials are getting only about 800 volunteers a month, but need at least 3,000 volunteers to complete the study, USA Today reported. Parents interested in having their child participate can check eligibility and sign at this website.

The Pfizer/BioNTech vaccine won authorization for use in 16- to 17-year-olds as well as adults.

The coronavirus doesn’t appear to have as serious complications for children as for adults.

“At this time, it appears that severe illness due to COVID-19 is rare among children,” the American Association of Pediatrics says. “However, there is an urgent need to collect more data on longer-term impacts of the pandemic on children, including ways the virus may harm the long-term physical health of infected children, as well as its emotional and mental health effects.”

The association says 179 children had died of COVID-related reasons in 43 states and New York City as of Dec. 31, 2020. That’s about 0.06% of total COVID deaths, it says.

But children do get sick. As of Jan. 7, 2021, nearly 2.3 million children had tested positive for COVID-19 since the start of the pandemic, the association says.

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

New findings suggest that monoclonal antibodies used to treat RA could improve severe COVID-19 outcomes, including risk for death.

Given within 24 hours of critical illness, tocilizumab (Actemra) was associated with a median of 10 days free of respiratory and cardiovascular support up to day 21, the primary outcome. Similarly, sarilumab (Kevzara) was linked to a median of 11 days. In contrast, the usual care control group experienced zero such days in the hospital.

However, the Randomized, Embedded, Multifactorial Adaptive Platform Trial for Community-Acquired Pneumonia (REMAP-CAP) trial comes with a caveat. The preprint findings have not yet been peer reviewed and “should not be used to guide clinical practice,” the authors stated.

The results were published online Jan. 7 in MedRxiv.

Nevertheless, the trial also revealed a mortality benefit associated with the two interleukin-6 antagonists. The hospital mortality rate was 22% with sarilumab, 28% with tocilizumab, and almost 36% with usual care.

“That’s a big change in survival. They are both lifesaving drugs,” lead coinvestigator Anthony Gordon, an Imperial College London professor of anesthesia and critical care, commented in a recent  story by Reuters.
 

Consider the big picture

“What I think is important is ... this is one of many trials,” Paul Auwaerter, MD, MBA, said in an interview. Many other studies looking at monoclonal antibody therapy for people with COVID-19 were halted because they did not show improvement.

One exception is the EMPACTA trial, which suggested that tocilizumab was effective if given before a person becomes ill enough to be placed on a ventilator, said Dr. Auwaerter, clinical director of the division of infectious diseases at Johns Hopkins Medicine and a contributor to this news organization. “It appeared to reduce the need for mechanical ventilation or death.”

“These two trials are the first randomized, prospective trials that show a benefit on a background of others which have not,” Dr. Auwaerter added.
 

Interim findings

The REMAP-CAP investigators randomly assigned adults within 24 hours of critical care for COVID-19 to 8 mg/kg tocilizumab, 400 mg sarilumab, or usual care at 113 sites in six countries. There were 353 participants in the tocilizumab arm, 48 in the sarilumab group, and 402 in the control group.

Compared with the control group, the 10 days free of organ support in the tocilizumab cohort was associated with an adjusted odds ratio of 1.64 (95% confidence interval, 1.25-2.14). The 11 days free of organ support in the sarilumab cohort was likewise superior to control (adjusted odds ratio, 1.76; 95% CI, 1.17-2.91).

“All secondary outcomes and analyses supported efficacy of these IL-6 receptor antagonists,” the authors note. These endpoints included 90-day survival, time to intensive care unit discharge, and hospital discharge.
 

Cautious optimism?

“The results were quite impressive – having 10 or 11 fewer days in the ICU, compared to standard of care,” Deepa Gotur, MD, said in an interview. “Choosing the right patient population and providing the anti-IL-6 treatment at the right time would be the key here.”

In addition to not yet receiving peer review, an open-label design, a relatively short follow-up of 21 days, and steroids becoming standard of care about halfway through the trial are potential limitations, said Dr. Gotur, an intensivist at Houston Methodist Hospital and associate professor of clinical medicine at Weill Cornell Medicine, New York.

“This is an interesting study,” Carl J. Fichtenbaum, MD, professor of clinical medicine at the University of Cincinnati, said in a comment.

Additional detail on how many participants in each group received steroids is warranted, Dr. Fichtenbaum said. “The analysis did not carefully adjust for the use of steroids that might have influenced outcomes.”

Dr. Fichtenbaum said it’s important to look at what is distinctive about REMAP-CAP because “there are several other studies showing opposite results.”

Dr. Gotur was an investigator on a previous study evaluating tocilizumab for patients already on mechanical ventilation. “One of the key differences between this and other studies is that they included more of the ICU population,” she said. “They also included patients within 24 hours of requiring organ support, cardiac, as well as respiratory support.” Some other research included less-acute patients, including all comers into the ED who required oxygen and received tocilizumab.

The prior studies also evaluated cytokine or inflammatory markers. In contrast, REMAP-CAP researchers “looked at organ failure itself ... which I think makes sense,” Dr. Gotur said.

Cytokine release syndrome can cause organ damage or organ failure, she added, “but these markers are all over the place. I’ve seen patients who are very, very sick despite having a low [C-reactive protein] or IL-6 level.”
 

Backing from the British

Citing the combined 24% decrease in the risk for death associated with these agents in the REMAP-CAP trial, the U.K. government announced Jan. 7 it will work to make tocilizumab and sarilumab available to citizens with severe COVID-19.

Experts in the United Kingdom shared their perspectives on the REMAP-CAP interim findings through the U.K. Science Media Centre.

“There are few treatments for severe COVID-19,” said Robin Ferner, MD, honorary professor of clinical pharmacology at the University of Birmingham (England) and honorary consultant physician at City Hospital Birmingham. “If the published data from REMAP-CAP are supported by further studies, this suggests that two IL-6 receptor antagonists can reduce the death rate in the most severely ill patients.”

Dr. Ferner added that the findings are not a “magic cure,” however. He pointed out that of 401 patients given the drugs, 109 died, and with standard treatment, 144 out of 402 died.

Peter Horby, MD, PhD, was more optimistic. “It is great to see a positive result at a time that we really need good news and more tools to fight COVID. This is great achievement for REMAP-CAP,” he said.

“We hope to soon have results from RECOVERY on the effect of tocilizumab in less severely ill patients in the hospital,” said Dr. Horby, cochief investigator of the RECOVERY trial and professor of emerging infectious diseases at the Centre for Tropical Medicine and Global Health at the University of Oxford (England).

Stephen Evans, BA, MSc, FRCP, professor of pharmacoepidemiology at the London School of Hygiene & Tropical Medicine, said, “This is a high-quality trial, and although published as a preprint, is of much higher quality than many non–peer-reviewed papers.”

Dr. Evans also noted the addition of steroid therapy for many participants. “Partway through the trial, the RECOVERY trial findings showed that the corticosteroid drug dexamethasone had notable mortality benefits. Consequently, quite a number of the patients in this trial had also received a corticosteroid.”

“It does look as though these drugs give some additional benefit beyond that given by dexamethasone,” he added.

Awaiting peer review

“We need to wait for the final results and ensure it was adequately powered with enough observations to make us confident in the results,” Dr. Fichtenbaum said.

“We in the United States have to step back and look at the entire set of studies and also, for this particular one, REMAP-CAP, to be in a peer-reviewed publication,” Dr. Auwaerter said. Preprints are often released “in the setting of the pandemic, where there may be important findings, especially if they impact mortality or severity of illness.”

“We need to make sure these findings, as outlined, hold up,” he said.

In the meantime, Dr. Auwaerter added, “Exactly how this will fit in is unclear. But it’s important to me as another potential drug that can help our critically ill patients.”

The REMAP-CAP study is ongoing and updated results will be provided online.

Dr. Auwaerter disclosed that he is a consultant for EMD Serono and a member of the data monitoring safety board for Humanigen. Dr. Gotur, Dr. Fichtenbaum, Dr. Ferner, and Dr. Evans disclosed no relevant financial relationships. Dr. Horby reported that Oxford University receives funding for the RECOVERY trial from U.K. Research and Innovation and the National Institute for Health Research. Roche Products and Sanofi supported REMAP-CAP through provision of tocilizumab and sarilumab in the United Kingdom.

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

New findings suggest that monoclonal antibodies used to treat RA could improve severe COVID-19 outcomes, including risk for death.

Given within 24 hours of critical illness, tocilizumab (Actemra) was associated with a median of 10 days free of respiratory and cardiovascular support up to day 21, the primary outcome. Similarly, sarilumab (Kevzara) was linked to a median of 11 days. In contrast, the usual care control group experienced zero such days in the hospital.

However, the Randomized, Embedded, Multifactorial Adaptive Platform Trial for Community-Acquired Pneumonia (REMAP-CAP) trial comes with a caveat. The preprint findings have not yet been peer reviewed and “should not be used to guide clinical practice,” the authors stated.

The results were published online Jan. 7 in MedRxiv.

Nevertheless, the trial also revealed a mortality benefit associated with the two interleukin-6 antagonists. The hospital mortality rate was 22% with sarilumab, 28% with tocilizumab, and almost 36% with usual care.

“That’s a big change in survival. They are both lifesaving drugs,” lead coinvestigator Anthony Gordon, an Imperial College London professor of anesthesia and critical care, commented in a recent  story by Reuters.
 

Consider the big picture

“What I think is important is ... this is one of many trials,” Paul Auwaerter, MD, MBA, said in an interview. Many other studies looking at monoclonal antibody therapy for people with COVID-19 were halted because they did not show improvement.

One exception is the EMPACTA trial, which suggested that tocilizumab was effective if given before a person becomes ill enough to be placed on a ventilator, said Dr. Auwaerter, clinical director of the division of infectious diseases at Johns Hopkins Medicine and a contributor to this news organization. “It appeared to reduce the need for mechanical ventilation or death.”

“These two trials are the first randomized, prospective trials that show a benefit on a background of others which have not,” Dr. Auwaerter added.
 

Interim findings

The REMAP-CAP investigators randomly assigned adults within 24 hours of critical care for COVID-19 to 8 mg/kg tocilizumab, 400 mg sarilumab, or usual care at 113 sites in six countries. There were 353 participants in the tocilizumab arm, 48 in the sarilumab group, and 402 in the control group.

Compared with the control group, the 10 days free of organ support in the tocilizumab cohort was associated with an adjusted odds ratio of 1.64 (95% confidence interval, 1.25-2.14). The 11 days free of organ support in the sarilumab cohort was likewise superior to control (adjusted odds ratio, 1.76; 95% CI, 1.17-2.91).

“All secondary outcomes and analyses supported efficacy of these IL-6 receptor antagonists,” the authors note. These endpoints included 90-day survival, time to intensive care unit discharge, and hospital discharge.
 

Cautious optimism?

“The results were quite impressive – having 10 or 11 fewer days in the ICU, compared to standard of care,” Deepa Gotur, MD, said in an interview. “Choosing the right patient population and providing the anti-IL-6 treatment at the right time would be the key here.”

In addition to not yet receiving peer review, an open-label design, a relatively short follow-up of 21 days, and steroids becoming standard of care about halfway through the trial are potential limitations, said Dr. Gotur, an intensivist at Houston Methodist Hospital and associate professor of clinical medicine at Weill Cornell Medicine, New York.

“This is an interesting study,” Carl J. Fichtenbaum, MD, professor of clinical medicine at the University of Cincinnati, said in a comment.

Additional detail on how many participants in each group received steroids is warranted, Dr. Fichtenbaum said. “The analysis did not carefully adjust for the use of steroids that might have influenced outcomes.”

Dr. Fichtenbaum said it’s important to look at what is distinctive about REMAP-CAP because “there are several other studies showing opposite results.”

Dr. Gotur was an investigator on a previous study evaluating tocilizumab for patients already on mechanical ventilation. “One of the key differences between this and other studies is that they included more of the ICU population,” she said. “They also included patients within 24 hours of requiring organ support, cardiac, as well as respiratory support.” Some other research included less-acute patients, including all comers into the ED who required oxygen and received tocilizumab.

The prior studies also evaluated cytokine or inflammatory markers. In contrast, REMAP-CAP researchers “looked at organ failure itself ... which I think makes sense,” Dr. Gotur said.

Cytokine release syndrome can cause organ damage or organ failure, she added, “but these markers are all over the place. I’ve seen patients who are very, very sick despite having a low [C-reactive protein] or IL-6 level.”
 

Backing from the British

Citing the combined 24% decrease in the risk for death associated with these agents in the REMAP-CAP trial, the U.K. government announced Jan. 7 it will work to make tocilizumab and sarilumab available to citizens with severe COVID-19.

Experts in the United Kingdom shared their perspectives on the REMAP-CAP interim findings through the U.K. Science Media Centre.

“There are few treatments for severe COVID-19,” said Robin Ferner, MD, honorary professor of clinical pharmacology at the University of Birmingham (England) and honorary consultant physician at City Hospital Birmingham. “If the published data from REMAP-CAP are supported by further studies, this suggests that two IL-6 receptor antagonists can reduce the death rate in the most severely ill patients.”

Dr. Ferner added that the findings are not a “magic cure,” however. He pointed out that of 401 patients given the drugs, 109 died, and with standard treatment, 144 out of 402 died.

Peter Horby, MD, PhD, was more optimistic. “It is great to see a positive result at a time that we really need good news and more tools to fight COVID. This is great achievement for REMAP-CAP,” he said.

“We hope to soon have results from RECOVERY on the effect of tocilizumab in less severely ill patients in the hospital,” said Dr. Horby, cochief investigator of the RECOVERY trial and professor of emerging infectious diseases at the Centre for Tropical Medicine and Global Health at the University of Oxford (England).

Stephen Evans, BA, MSc, FRCP, professor of pharmacoepidemiology at the London School of Hygiene & Tropical Medicine, said, “This is a high-quality trial, and although published as a preprint, is of much higher quality than many non–peer-reviewed papers.”

Dr. Evans also noted the addition of steroid therapy for many participants. “Partway through the trial, the RECOVERY trial findings showed that the corticosteroid drug dexamethasone had notable mortality benefits. Consequently, quite a number of the patients in this trial had also received a corticosteroid.”

“It does look as though these drugs give some additional benefit beyond that given by dexamethasone,” he added.

Awaiting peer review

“We need to wait for the final results and ensure it was adequately powered with enough observations to make us confident in the results,” Dr. Fichtenbaum said.

“We in the United States have to step back and look at the entire set of studies and also, for this particular one, REMAP-CAP, to be in a peer-reviewed publication,” Dr. Auwaerter said. Preprints are often released “in the setting of the pandemic, where there may be important findings, especially if they impact mortality or severity of illness.”

“We need to make sure these findings, as outlined, hold up,” he said.

In the meantime, Dr. Auwaerter added, “Exactly how this will fit in is unclear. But it’s important to me as another potential drug that can help our critically ill patients.”

The REMAP-CAP study is ongoing and updated results will be provided online.

Dr. Auwaerter disclosed that he is a consultant for EMD Serono and a member of the data monitoring safety board for Humanigen. Dr. Gotur, Dr. Fichtenbaum, Dr. Ferner, and Dr. Evans disclosed no relevant financial relationships. Dr. Horby reported that Oxford University receives funding for the RECOVERY trial from U.K. Research and Innovation and the National Institute for Health Research. Roche Products and Sanofi supported REMAP-CAP through provision of tocilizumab and sarilumab in the United Kingdom.

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

New findings suggest that monoclonal antibodies used to treat RA could improve severe COVID-19 outcomes, including risk for death.

Given within 24 hours of critical illness, tocilizumab (Actemra) was associated with a median of 10 days free of respiratory and cardiovascular support up to day 21, the primary outcome. Similarly, sarilumab (Kevzara) was linked to a median of 11 days. In contrast, the usual care control group experienced zero such days in the hospital.

However, the Randomized, Embedded, Multifactorial Adaptive Platform Trial for Community-Acquired Pneumonia (REMAP-CAP) trial comes with a caveat. The preprint findings have not yet been peer reviewed and “should not be used to guide clinical practice,” the authors stated.

The results were published online Jan. 7 in MedRxiv.

Nevertheless, the trial also revealed a mortality benefit associated with the two interleukin-6 antagonists. The hospital mortality rate was 22% with sarilumab, 28% with tocilizumab, and almost 36% with usual care.

“That’s a big change in survival. They are both lifesaving drugs,” lead coinvestigator Anthony Gordon, an Imperial College London professor of anesthesia and critical care, commented in a recent  story by Reuters.
 

Consider the big picture

“What I think is important is ... this is one of many trials,” Paul Auwaerter, MD, MBA, said in an interview. Many other studies looking at monoclonal antibody therapy for people with COVID-19 were halted because they did not show improvement.

One exception is the EMPACTA trial, which suggested that tocilizumab was effective if given before a person becomes ill enough to be placed on a ventilator, said Dr. Auwaerter, clinical director of the division of infectious diseases at Johns Hopkins Medicine and a contributor to this news organization. “It appeared to reduce the need for mechanical ventilation or death.”

“These two trials are the first randomized, prospective trials that show a benefit on a background of others which have not,” Dr. Auwaerter added.
 

Interim findings

The REMAP-CAP investigators randomly assigned adults within 24 hours of critical care for COVID-19 to 8 mg/kg tocilizumab, 400 mg sarilumab, or usual care at 113 sites in six countries. There were 353 participants in the tocilizumab arm, 48 in the sarilumab group, and 402 in the control group.

Compared with the control group, the 10 days free of organ support in the tocilizumab cohort was associated with an adjusted odds ratio of 1.64 (95% confidence interval, 1.25-2.14). The 11 days free of organ support in the sarilumab cohort was likewise superior to control (adjusted odds ratio, 1.76; 95% CI, 1.17-2.91).

“All secondary outcomes and analyses supported efficacy of these IL-6 receptor antagonists,” the authors note. These endpoints included 90-day survival, time to intensive care unit discharge, and hospital discharge.
 

Cautious optimism?

“The results were quite impressive – having 10 or 11 fewer days in the ICU, compared to standard of care,” Deepa Gotur, MD, said in an interview. “Choosing the right patient population and providing the anti-IL-6 treatment at the right time would be the key here.”

In addition to not yet receiving peer review, an open-label design, a relatively short follow-up of 21 days, and steroids becoming standard of care about halfway through the trial are potential limitations, said Dr. Gotur, an intensivist at Houston Methodist Hospital and associate professor of clinical medicine at Weill Cornell Medicine, New York.

“This is an interesting study,” Carl J. Fichtenbaum, MD, professor of clinical medicine at the University of Cincinnati, said in a comment.

Additional detail on how many participants in each group received steroids is warranted, Dr. Fichtenbaum said. “The analysis did not carefully adjust for the use of steroids that might have influenced outcomes.”

Dr. Fichtenbaum said it’s important to look at what is distinctive about REMAP-CAP because “there are several other studies showing opposite results.”

Dr. Gotur was an investigator on a previous study evaluating tocilizumab for patients already on mechanical ventilation. “One of the key differences between this and other studies is that they included more of the ICU population,” she said. “They also included patients within 24 hours of requiring organ support, cardiac, as well as respiratory support.” Some other research included less-acute patients, including all comers into the ED who required oxygen and received tocilizumab.

The prior studies also evaluated cytokine or inflammatory markers. In contrast, REMAP-CAP researchers “looked at organ failure itself ... which I think makes sense,” Dr. Gotur said.

Cytokine release syndrome can cause organ damage or organ failure, she added, “but these markers are all over the place. I’ve seen patients who are very, very sick despite having a low [C-reactive protein] or IL-6 level.”
 

Backing from the British

Citing the combined 24% decrease in the risk for death associated with these agents in the REMAP-CAP trial, the U.K. government announced Jan. 7 it will work to make tocilizumab and sarilumab available to citizens with severe COVID-19.

Experts in the United Kingdom shared their perspectives on the REMAP-CAP interim findings through the U.K. Science Media Centre.

“There are few treatments for severe COVID-19,” said Robin Ferner, MD, honorary professor of clinical pharmacology at the University of Birmingham (England) and honorary consultant physician at City Hospital Birmingham. “If the published data from REMAP-CAP are supported by further studies, this suggests that two IL-6 receptor antagonists can reduce the death rate in the most severely ill patients.”

Dr. Ferner added that the findings are not a “magic cure,” however. He pointed out that of 401 patients given the drugs, 109 died, and with standard treatment, 144 out of 402 died.

Peter Horby, MD, PhD, was more optimistic. “It is great to see a positive result at a time that we really need good news and more tools to fight COVID. This is great achievement for REMAP-CAP,” he said.

“We hope to soon have results from RECOVERY on the effect of tocilizumab in less severely ill patients in the hospital,” said Dr. Horby, cochief investigator of the RECOVERY trial and professor of emerging infectious diseases at the Centre for Tropical Medicine and Global Health at the University of Oxford (England).

Stephen Evans, BA, MSc, FRCP, professor of pharmacoepidemiology at the London School of Hygiene & Tropical Medicine, said, “This is a high-quality trial, and although published as a preprint, is of much higher quality than many non–peer-reviewed papers.”

Dr. Evans also noted the addition of steroid therapy for many participants. “Partway through the trial, the RECOVERY trial findings showed that the corticosteroid drug dexamethasone had notable mortality benefits. Consequently, quite a number of the patients in this trial had also received a corticosteroid.”

“It does look as though these drugs give some additional benefit beyond that given by dexamethasone,” he added.

Awaiting peer review

“We need to wait for the final results and ensure it was adequately powered with enough observations to make us confident in the results,” Dr. Fichtenbaum said.

“We in the United States have to step back and look at the entire set of studies and also, for this particular one, REMAP-CAP, to be in a peer-reviewed publication,” Dr. Auwaerter said. Preprints are often released “in the setting of the pandemic, where there may be important findings, especially if they impact mortality or severity of illness.”

“We need to make sure these findings, as outlined, hold up,” he said.

In the meantime, Dr. Auwaerter added, “Exactly how this will fit in is unclear. But it’s important to me as another potential drug that can help our critically ill patients.”

The REMAP-CAP study is ongoing and updated results will be provided online.

Dr. Auwaerter disclosed that he is a consultant for EMD Serono and a member of the data monitoring safety board for Humanigen. Dr. Gotur, Dr. Fichtenbaum, Dr. Ferner, and Dr. Evans disclosed no relevant financial relationships. Dr. Horby reported that Oxford University receives funding for the RECOVERY trial from U.K. Research and Innovation and the National Institute for Health Research. Roche Products and Sanofi supported REMAP-CAP through provision of tocilizumab and sarilumab in the United Kingdom.

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

When Margot Gage-Witvliet began feeling run down after her family returned from a trip to the Netherlands in late February 2020, she initially chalked up her symptoms to jet lag. Three days later, however, her situation went from concerning to alarming as she struggled to breathe. “It felt like there was an elephant sitting on my chest,” she said.

Her husband and daughters also became ill with COVID-19, but Ms. Gage-Witvliet was the only one in her family who didn’t get better. After an early improvement, a rare coronavirus-induced tonic-clonic seizure in early April sent her spiraling back down. Ms. Gage-Witvliet spent the next several weeks in bed with the curtains drawn, unable to tolerate light or sound.

Today, Ms. Gage-Witvliet’s life looks nothing like it did 6 months ago when she first got sick. As one of COVID-19’s so called long-haulers, she continues to struggle with crushing fatigue, brain fog, and headaches – symptoms that worsen when she pushes herself to do more. Across the country, as many as 1 in 10 COVID-19 patients are reporting illnesses that continue for weeks and months after their initial diagnosis. Nearly all report neurologic issues like Ms. Gage-Witvliet, as well as shortness of breath and psychiatric concerns.

For Avindra Nath, MD, a neurologist at the National Institutes of Health, the experience of these long-haul COVID-19 patients feels familiar and reminds him of myalgic encephalomyelitis, also known as chronic fatigue syndrome.

Dr. Nath has long been interested in the lingering neurologic issues connected to chronic fatigue. An estimated three-quarters of all patients with chronic fatigue syndrome report that their symptoms started after a viral infection, and they suffer unrelenting exhaustion, difficulties regulating pulse and blood pressure, aches and pains, and brain fog. When Dr. Nath first read about the novel coronavirus, he began to worry that the virus would trigger symptoms in a subset of those infected. Hearing about the experiences of long-haulers like Ms. Gage-Witvliet raised his suspicions even more.

Unlike COVID-19 long-haulers, however, many patients with chronic fatigue syndrome go at least a year with these symptoms before receiving a diagnosis, according to a British survey. That means researchers have had few opportunities to study the early stages of the syndrome. “When we see patients with myalgic encephalomyelitis, whatever infection they might have had occurred in the remote past, so there’s no way for us to know how they got infected with it, what the infection was, or what the effects of it were in that early phase. We’re seeing them 2 years afterward,” Dr. Nath said.

Dr. Nath quickly realized that studying patients like Ms. Gage-Witvliet would give physicians and scientists a unique opportunity to understand not only long-term outcomes of COVID-19 infections, but also other postviral syndromes, including chronic fatigue syndrome at their earliest stages. It’s why Dr. Nath has spent the past several months scrambling to launch two NIH studies to examine the phenomenon.

Although Dr. Nath said that the parallels between COVID-19 long-haulers and those with chronic fatigue syndrome are obvious, he cautions against assuming that they are the same phenomenon. Some long-haulers might simply be taking a much slower path to recovery, or they might have a condition that looks similar on the surface but differs from chronic fatigue syndrome on a molecular level. But even if Dr. Nath fails to see links to chronic fatigue syndrome, with more than 92.5 million documented cases of COVID-19 around the world, the work will be relevant to the substantial number of infected individuals who don’t recover quickly.

“With so many people having exposure to the same virus over a similar time period, we really have the opportunity to look at these manifestations and at the very least to understand postviral syndromes,” said Mady Hornig, MD, a psychiatrist at Columbia University, New York.

The origins of chronic fatigue syndrome date back to 1985, when the Centers for Disease Control and Prevention received a request from two physicians – Paul Cheney, MD, and Daniel Peterson, MD – to investigate a mysterious disease outbreak in Nevada. In November 1984, residents in and around the idyllic vacation spot of Incline Village, a small town tucked into the north shore of Lake Tahoe, had begun reporting flu-like symptoms that persisted for weeks, even months. The doctors had searched high and low for a cause, but they couldn’t figure out what was making their patients sick.

They reported a range of symptoms – including muscle aches and pains, low-grade fevers, sore throats, and headaches – but everyone said that crippling fatigue was the most debilitating issue. This wasn’t the kind of fatigue that could be cured by a nap or even a long holiday. No matter how much their patients slept – and some were almost completely bedbound – their fatigue didn’t abate. What’s more, the fatigue got worse whenever they tried to push themselves to do more. Puzzled, the CDC sent two epidemic intelligence service (EIS) officers to try to get to the bottom of what might be happening.


 

Muscle aches and pains with crippling fatigue

After their visit to Incline Village, however, the CDC was just as perplexed as Dr. Cheney and Dr. Peterson. Many of the people with the condition reported flu-like symptoms right around the time they first got sick, and the physicians’ leading hypothesis was that the outbreak and its lasting symptoms were caused by chronic Epstein-Barr virus infection. But neither the CDC nor anyone else could identify the infection or any other microbial cause. The two EIS officers duly wrote up a report for the CDC’s flagship publication, Morbidity and Mortality Weekly ReportI, titled “Chronic Fatigue Possibly Related to Epstein-Barr Virus – Nevada”.

That investigators focused on the fatigue aspect made sense, says Leonard A. Jason, PhD, professor of psychology at DePaul University and director of the Center for Community Research, both in Chicago, because it was one of the few symptoms shared by all the individuals studied and it was also the most debilitating. But that focus – and the name “chronic fatigue syndrome” – led to broad public dismissal of the condition’s severity, as did an editorial note in MMWR urging physicians to look for “more definable, and possibly treatable, conditions.” Subsequent research failed to confirm a specific link to the Epstein-Barr virus, which only added to the condition’s phony reputation. Rather than being considered a potentially disabling illness, it was disregarded as a “yuppie flu” or a fancy name for malingering.

“It’s not a surprise that patients are being dismissed because there’s already this sort of grandfathered-in sense that fatigue is not real,” said Jennifer Frankovich, MD, a pediatric rheumatologist at Stanford (Calif.) University’s Lucile Packard Children’s Hospital in Palo Alto. “I’m sure that’s frustrating for them to be tired and then to have the clinician not believe them or dismiss them or think they’re making it up. It would be more helpful to the families to say: ‘You know what, we don’t know, we do not have the answer, and we believe you.’ ”
 

A syndrome’s shame

As time passed, patient advocacy groups began pushing back against the negative way the condition was being perceived. This criticism came as organizations like the CDC worked to develop a set of diagnostic criteria that researchers and clinicians dealing with chronic fatigue syndrome could use. With such a heterogeneous group of patients and symptoms, the task was no small challenge. The discussions, which took place over nearly 2 decades, played a key role in helping scientists home in on the single factor that was central to chronic fatigue: postexertional malaise.

“This is quite unique for chronic fatigue syndrome. With other diseases, yes, you may have fatigue as one of the components of the disease, but postexertional fatigue is very specific,” said Alain Moreau, PhD, a molecular biologist at the University of Montreal.

Of course, plenty of people have pushed themselves too hard physically and paid the price the next day. But those with chronic fatigue syndrome weren’t running marathons. To them, exertion could be anything from getting the mail to reading a book. Nor could the resulting exhaustion be resolved by an afternoon on the couch or a long vacation.

“If they do these activities, they can crash for weeks, even months,” Dr. Moreau said. It was deep, persistent, and – for 40% of those with chronic fatigue syndrome – disabling. In 2015, a study group from the Institute of Medicine proposed renaming chronic fatigue to “systemic exercise intolerance disease” because of the centrality of this symptom. Although that effort mostly stalled, their report did bring the condition out of its historic place as a scientific backwater. What resulted was an uptick in research on chronic fatigue syndrome, which helped define some of the physiological issues that either contribute to or result from the condition.

Researchers had long known about the link between infection and fatigue, said Dr. Frankovich. Work included mysterious outbreaks like the one in Lake Tahoe and well-documented issues like the wave of encephalitis lethargica (a condition that leaves patients in an almost vegetative state) that followed the 1918 H1N1 influenza pandemic.

“As a clinician, when you see someone who comes in with a chronic infection, they’re tired. I think that’s why, in the chronic-fatigue world, people are desperately looking for the infection so we can treat it, and maybe these poor suffering people will feel better,” Dr. Frankovich added. Then the pandemic struck, giving him yet another opportunity to study postviral syndromes.
 

Immunologic symptoms

Given the close link between a nonspecific viral illness and the onset of symptoms in chronic fatigue syndrome, scientists like Dr. Hornig opted to focus on immunologic symptoms. In a 2015 analysis published in Science, Dr. Hornig and colleagues showed that immune problems can be found in the earliest stages of chronic fatigue syndrome, and that they change as the illness progresses. Patients who had been sick for less than 3 years showed significant increases in levels of both pro- and anti-inflammatory cytokines, and the factor most strongly correlated to this inability to regulate cytokine levels was the duration of symptoms, not their severity. A series of other studies also revealed problems with regulation of the immune system, although no one could show what might have set these problems in motion.

Other researchers found signs of mitochondrial dysfunction in those with chronic fatigue syndrome. Because mitochondria make energy for cells, it wasn’t an intellectual stretch to believe that glitches in this process could contribute to fatigue. As early as 1991, scientists had discovered signs of mitochondrial degeneration in muscle biopsies from people with chronic fatigue syndrome. Subsequent studies showed that those affected by chronic fatigue were missing segments of mitochondrial DNA and had significantly reduced levels of mitochondrial activity. Although exercise normally improves mitochondrial functioning, the opposite appears to happen in chronic fatigue.

To Dr. Nath, these dual hypotheses aren’t necessarily mutually exclusive. Some studies have hinted that infection with the common human herpesvirus–6 (HHV-6) can lead to an autoimmune condition in which the body makes antibodies against the mitochondria. Mitochondria also play a key role in the ability of the innate immune system to produce interferon and other proinflammatory cytokines. It might also be that the link between immune and mitochondrial problems is more convoluted than originally thought, or that the two systems are affected independent of one another, Dr. Nath said.

Finding answers, especially those that could lead to potential treatments, wouldn’t be easy, however. In 2016, the NIH launched an in-depth study of a small number of individuals with chronic fatigue, hoping to find clues about what the condition was and how it might be treated.

For scientists like Dr. Nath, the NIH study provided a way to get at the underlying biology of chronic fatigue syndrome. Then the pandemic struck, giving him yet another opportunity to study postviral syndromes.
 

Chronic post-SARS syndrome

In March 2020, retired physician Harvey Moldofsky, MD, began receiving inquiries about a 2011 study he and his colleague, John Patcai, MD, had published in BMC Neurology about something they dubbed “chronic post-SARS syndrome.” The small case-control study, which involved mainly health care workers in Toronto, received little attention when it was first published, but with COVID-19, it was suddenly relevant.

Early clusters of similar cases in Miami made local physicians desperate for Dr. Moldofsky’s expertise. Luckily, he was nearby; he had fled the frigid Canadian winter for the warmth of Sarasota, Fla.

“I had people from various countries around the world writing to me and asking what they should do. And of course I don’t have any answers,” he said. But the study contained one of the world’s only references to the syndrome.

In 2003, a woman arrived in Toronto from Hong Kong. She didn’t know it at the time, but her preairport stay at the Hotel Metropole had infected her with the first SARS (severe acute respiratory syndrome) coronavirus. Her subsequent hospitalization in Toronto sparked a city-wide outbreak of SARS in which 273 people became ill and 44 died. Many of those affected were health care workers, including nurses and respiratory therapists. Although most eventually returned to work, a subset couldn’t. They complained of energy-sapping fatigue, poor sleep, brain fog, and assorted body aches and pains that persisted for more than 18 months. The aches and pains brought them to the attention of Dr. Moldofsky, then director of the Centre for the Study of Pain at the University of Toronto.

His primary interest at the time was fibromyalgia, which caused symptoms similar to those reported by the original SARS long-haulers. Intrigued, Dr. Moldofsky agreed to take a look. Their chest x-rays were clear and the nurses showed no signs of lingering viral infection. Dr. Moldofsky could see that the nurses were ill and suffering, but no lab tests or anything else could identify what was causing their symptoms.

In 2011, Dr. Moldofsky and Dr. Patcai found a strong overlap between chronic SARS, fibromyalgia, and chronic fatigue syndrome when they compared 22 patients with long-term SARS issues with 21 who had fibromyalgia. “Their problems are exactly the same. They have strange symptoms and nobody can figure out what they’re about. And these symptoms are aches and pains, and they have trouble thinking and concentrating,” Dr. Moldofsky said. Reports of COVID-19 long-haulers didn’t surprise Dr. Moldofsky, and he immediately recognized that Nath’s intention to follow these patients could provide insights into both fibromyalgia and chronic fatigue syndrome.

That’s exactly what Dr. Nath is proposing with the two NIH studies. One will focus solely on the neurologic impacts of COVID-19, including stroke, loss of taste and smell, and brain fog. The other will bring patients who have had COVID-19 symptoms for at least 6 months to the NIH Clinical Center for an inpatient stay during which they will undergo detailed physiologic tests.

Scientists around the world are launching their own post–COVID-19 studies. Dr. Moreau’s group in Montreal has laid the groundwork for such an endeavor, and the CoroNerve group in the United Kingdom is monitoring neurologic complications from the coronavirus. Many of them have the same goals as the NIH studies: Leverage the large number of COVID-19 long-haulers to better understand the earliest stages of postviral syndrome.

“At this juncture, after all the reports that we’ve seen so far, I think it’s very unlikely that there will be no relationship whatsoever between COVID-19 and chronic fatigue syndrome,” Dr. Hornig said. “I think there certainly will be some, but again, what’s the scope, what’s the size? And then, of course, even more importantly, if it is happening, what is the mechanism and how is it happening?”

For people like Ms. Gage-Witvliet, the answers can’t come soon enough. For the first time in more than a decade, the full-time professor of epidemiology didn’t prepare to teach this year because she simply can’t. It’s too taxing for her brain to deal with impromptu student questions. Ms. Gage-Witvliet hopes that, by sharing her own experiences with post COVID-19, she can help others.

“In my work, I use data to give a voice to people who don’t have a voice,” she said. “Now, I am one of those people.”

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

When Margot Gage-Witvliet began feeling run down after her family returned from a trip to the Netherlands in late February 2020, she initially chalked up her symptoms to jet lag. Three days later, however, her situation went from concerning to alarming as she struggled to breathe. “It felt like there was an elephant sitting on my chest,” she said.

Her husband and daughters also became ill with COVID-19, but Ms. Gage-Witvliet was the only one in her family who didn’t get better. After an early improvement, a rare coronavirus-induced tonic-clonic seizure in early April sent her spiraling back down. Ms. Gage-Witvliet spent the next several weeks in bed with the curtains drawn, unable to tolerate light or sound.

Today, Ms. Gage-Witvliet’s life looks nothing like it did 6 months ago when she first got sick. As one of COVID-19’s so called long-haulers, she continues to struggle with crushing fatigue, brain fog, and headaches – symptoms that worsen when she pushes herself to do more. Across the country, as many as 1 in 10 COVID-19 patients are reporting illnesses that continue for weeks and months after their initial diagnosis. Nearly all report neurologic issues like Ms. Gage-Witvliet, as well as shortness of breath and psychiatric concerns.

For Avindra Nath, MD, a neurologist at the National Institutes of Health, the experience of these long-haul COVID-19 patients feels familiar and reminds him of myalgic encephalomyelitis, also known as chronic fatigue syndrome.

Dr. Nath has long been interested in the lingering neurologic issues connected to chronic fatigue. An estimated three-quarters of all patients with chronic fatigue syndrome report that their symptoms started after a viral infection, and they suffer unrelenting exhaustion, difficulties regulating pulse and blood pressure, aches and pains, and brain fog. When Dr. Nath first read about the novel coronavirus, he began to worry that the virus would trigger symptoms in a subset of those infected. Hearing about the experiences of long-haulers like Ms. Gage-Witvliet raised his suspicions even more.

Unlike COVID-19 long-haulers, however, many patients with chronic fatigue syndrome go at least a year with these symptoms before receiving a diagnosis, according to a British survey. That means researchers have had few opportunities to study the early stages of the syndrome. “When we see patients with myalgic encephalomyelitis, whatever infection they might have had occurred in the remote past, so there’s no way for us to know how they got infected with it, what the infection was, or what the effects of it were in that early phase. We’re seeing them 2 years afterward,” Dr. Nath said.

Dr. Nath quickly realized that studying patients like Ms. Gage-Witvliet would give physicians and scientists a unique opportunity to understand not only long-term outcomes of COVID-19 infections, but also other postviral syndromes, including chronic fatigue syndrome at their earliest stages. It’s why Dr. Nath has spent the past several months scrambling to launch two NIH studies to examine the phenomenon.

Although Dr. Nath said that the parallels between COVID-19 long-haulers and those with chronic fatigue syndrome are obvious, he cautions against assuming that they are the same phenomenon. Some long-haulers might simply be taking a much slower path to recovery, or they might have a condition that looks similar on the surface but differs from chronic fatigue syndrome on a molecular level. But even if Dr. Nath fails to see links to chronic fatigue syndrome, with more than 92.5 million documented cases of COVID-19 around the world, the work will be relevant to the substantial number of infected individuals who don’t recover quickly.

“With so many people having exposure to the same virus over a similar time period, we really have the opportunity to look at these manifestations and at the very least to understand postviral syndromes,” said Mady Hornig, MD, a psychiatrist at Columbia University, New York.

The origins of chronic fatigue syndrome date back to 1985, when the Centers for Disease Control and Prevention received a request from two physicians – Paul Cheney, MD, and Daniel Peterson, MD – to investigate a mysterious disease outbreak in Nevada. In November 1984, residents in and around the idyllic vacation spot of Incline Village, a small town tucked into the north shore of Lake Tahoe, had begun reporting flu-like symptoms that persisted for weeks, even months. The doctors had searched high and low for a cause, but they couldn’t figure out what was making their patients sick.

They reported a range of symptoms – including muscle aches and pains, low-grade fevers, sore throats, and headaches – but everyone said that crippling fatigue was the most debilitating issue. This wasn’t the kind of fatigue that could be cured by a nap or even a long holiday. No matter how much their patients slept – and some were almost completely bedbound – their fatigue didn’t abate. What’s more, the fatigue got worse whenever they tried to push themselves to do more. Puzzled, the CDC sent two epidemic intelligence service (EIS) officers to try to get to the bottom of what might be happening.


 

Muscle aches and pains with crippling fatigue

After their visit to Incline Village, however, the CDC was just as perplexed as Dr. Cheney and Dr. Peterson. Many of the people with the condition reported flu-like symptoms right around the time they first got sick, and the physicians’ leading hypothesis was that the outbreak and its lasting symptoms were caused by chronic Epstein-Barr virus infection. But neither the CDC nor anyone else could identify the infection or any other microbial cause. The two EIS officers duly wrote up a report for the CDC’s flagship publication, Morbidity and Mortality Weekly ReportI, titled “Chronic Fatigue Possibly Related to Epstein-Barr Virus – Nevada”.

That investigators focused on the fatigue aspect made sense, says Leonard A. Jason, PhD, professor of psychology at DePaul University and director of the Center for Community Research, both in Chicago, because it was one of the few symptoms shared by all the individuals studied and it was also the most debilitating. But that focus – and the name “chronic fatigue syndrome” – led to broad public dismissal of the condition’s severity, as did an editorial note in MMWR urging physicians to look for “more definable, and possibly treatable, conditions.” Subsequent research failed to confirm a specific link to the Epstein-Barr virus, which only added to the condition’s phony reputation. Rather than being considered a potentially disabling illness, it was disregarded as a “yuppie flu” or a fancy name for malingering.

“It’s not a surprise that patients are being dismissed because there’s already this sort of grandfathered-in sense that fatigue is not real,” said Jennifer Frankovich, MD, a pediatric rheumatologist at Stanford (Calif.) University’s Lucile Packard Children’s Hospital in Palo Alto. “I’m sure that’s frustrating for them to be tired and then to have the clinician not believe them or dismiss them or think they’re making it up. It would be more helpful to the families to say: ‘You know what, we don’t know, we do not have the answer, and we believe you.’ ”
 

A syndrome’s shame

As time passed, patient advocacy groups began pushing back against the negative way the condition was being perceived. This criticism came as organizations like the CDC worked to develop a set of diagnostic criteria that researchers and clinicians dealing with chronic fatigue syndrome could use. With such a heterogeneous group of patients and symptoms, the task was no small challenge. The discussions, which took place over nearly 2 decades, played a key role in helping scientists home in on the single factor that was central to chronic fatigue: postexertional malaise.

“This is quite unique for chronic fatigue syndrome. With other diseases, yes, you may have fatigue as one of the components of the disease, but postexertional fatigue is very specific,” said Alain Moreau, PhD, a molecular biologist at the University of Montreal.

Of course, plenty of people have pushed themselves too hard physically and paid the price the next day. But those with chronic fatigue syndrome weren’t running marathons. To them, exertion could be anything from getting the mail to reading a book. Nor could the resulting exhaustion be resolved by an afternoon on the couch or a long vacation.

“If they do these activities, they can crash for weeks, even months,” Dr. Moreau said. It was deep, persistent, and – for 40% of those with chronic fatigue syndrome – disabling. In 2015, a study group from the Institute of Medicine proposed renaming chronic fatigue to “systemic exercise intolerance disease” because of the centrality of this symptom. Although that effort mostly stalled, their report did bring the condition out of its historic place as a scientific backwater. What resulted was an uptick in research on chronic fatigue syndrome, which helped define some of the physiological issues that either contribute to or result from the condition.

Researchers had long known about the link between infection and fatigue, said Dr. Frankovich. Work included mysterious outbreaks like the one in Lake Tahoe and well-documented issues like the wave of encephalitis lethargica (a condition that leaves patients in an almost vegetative state) that followed the 1918 H1N1 influenza pandemic.

“As a clinician, when you see someone who comes in with a chronic infection, they’re tired. I think that’s why, in the chronic-fatigue world, people are desperately looking for the infection so we can treat it, and maybe these poor suffering people will feel better,” Dr. Frankovich added. Then the pandemic struck, giving him yet another opportunity to study postviral syndromes.
 

Immunologic symptoms

Given the close link between a nonspecific viral illness and the onset of symptoms in chronic fatigue syndrome, scientists like Dr. Hornig opted to focus on immunologic symptoms. In a 2015 analysis published in Science, Dr. Hornig and colleagues showed that immune problems can be found in the earliest stages of chronic fatigue syndrome, and that they change as the illness progresses. Patients who had been sick for less than 3 years showed significant increases in levels of both pro- and anti-inflammatory cytokines, and the factor most strongly correlated to this inability to regulate cytokine levels was the duration of symptoms, not their severity. A series of other studies also revealed problems with regulation of the immune system, although no one could show what might have set these problems in motion.

Other researchers found signs of mitochondrial dysfunction in those with chronic fatigue syndrome. Because mitochondria make energy for cells, it wasn’t an intellectual stretch to believe that glitches in this process could contribute to fatigue. As early as 1991, scientists had discovered signs of mitochondrial degeneration in muscle biopsies from people with chronic fatigue syndrome. Subsequent studies showed that those affected by chronic fatigue were missing segments of mitochondrial DNA and had significantly reduced levels of mitochondrial activity. Although exercise normally improves mitochondrial functioning, the opposite appears to happen in chronic fatigue.

To Dr. Nath, these dual hypotheses aren’t necessarily mutually exclusive. Some studies have hinted that infection with the common human herpesvirus–6 (HHV-6) can lead to an autoimmune condition in which the body makes antibodies against the mitochondria. Mitochondria also play a key role in the ability of the innate immune system to produce interferon and other proinflammatory cytokines. It might also be that the link between immune and mitochondrial problems is more convoluted than originally thought, or that the two systems are affected independent of one another, Dr. Nath said.

Finding answers, especially those that could lead to potential treatments, wouldn’t be easy, however. In 2016, the NIH launched an in-depth study of a small number of individuals with chronic fatigue, hoping to find clues about what the condition was and how it might be treated.

For scientists like Dr. Nath, the NIH study provided a way to get at the underlying biology of chronic fatigue syndrome. Then the pandemic struck, giving him yet another opportunity to study postviral syndromes.
 

Chronic post-SARS syndrome

In March 2020, retired physician Harvey Moldofsky, MD, began receiving inquiries about a 2011 study he and his colleague, John Patcai, MD, had published in BMC Neurology about something they dubbed “chronic post-SARS syndrome.” The small case-control study, which involved mainly health care workers in Toronto, received little attention when it was first published, but with COVID-19, it was suddenly relevant.

Early clusters of similar cases in Miami made local physicians desperate for Dr. Moldofsky’s expertise. Luckily, he was nearby; he had fled the frigid Canadian winter for the warmth of Sarasota, Fla.

“I had people from various countries around the world writing to me and asking what they should do. And of course I don’t have any answers,” he said. But the study contained one of the world’s only references to the syndrome.

In 2003, a woman arrived in Toronto from Hong Kong. She didn’t know it at the time, but her preairport stay at the Hotel Metropole had infected her with the first SARS (severe acute respiratory syndrome) coronavirus. Her subsequent hospitalization in Toronto sparked a city-wide outbreak of SARS in which 273 people became ill and 44 died. Many of those affected were health care workers, including nurses and respiratory therapists. Although most eventually returned to work, a subset couldn’t. They complained of energy-sapping fatigue, poor sleep, brain fog, and assorted body aches and pains that persisted for more than 18 months. The aches and pains brought them to the attention of Dr. Moldofsky, then director of the Centre for the Study of Pain at the University of Toronto.

His primary interest at the time was fibromyalgia, which caused symptoms similar to those reported by the original SARS long-haulers. Intrigued, Dr. Moldofsky agreed to take a look. Their chest x-rays were clear and the nurses showed no signs of lingering viral infection. Dr. Moldofsky could see that the nurses were ill and suffering, but no lab tests or anything else could identify what was causing their symptoms.

In 2011, Dr. Moldofsky and Dr. Patcai found a strong overlap between chronic SARS, fibromyalgia, and chronic fatigue syndrome when they compared 22 patients with long-term SARS issues with 21 who had fibromyalgia. “Their problems are exactly the same. They have strange symptoms and nobody can figure out what they’re about. And these symptoms are aches and pains, and they have trouble thinking and concentrating,” Dr. Moldofsky said. Reports of COVID-19 long-haulers didn’t surprise Dr. Moldofsky, and he immediately recognized that Nath’s intention to follow these patients could provide insights into both fibromyalgia and chronic fatigue syndrome.

That’s exactly what Dr. Nath is proposing with the two NIH studies. One will focus solely on the neurologic impacts of COVID-19, including stroke, loss of taste and smell, and brain fog. The other will bring patients who have had COVID-19 symptoms for at least 6 months to the NIH Clinical Center for an inpatient stay during which they will undergo detailed physiologic tests.

Scientists around the world are launching their own post–COVID-19 studies. Dr. Moreau’s group in Montreal has laid the groundwork for such an endeavor, and the CoroNerve group in the United Kingdom is monitoring neurologic complications from the coronavirus. Many of them have the same goals as the NIH studies: Leverage the large number of COVID-19 long-haulers to better understand the earliest stages of postviral syndrome.

“At this juncture, after all the reports that we’ve seen so far, I think it’s very unlikely that there will be no relationship whatsoever between COVID-19 and chronic fatigue syndrome,” Dr. Hornig said. “I think there certainly will be some, but again, what’s the scope, what’s the size? And then, of course, even more importantly, if it is happening, what is the mechanism and how is it happening?”

For people like Ms. Gage-Witvliet, the answers can’t come soon enough. For the first time in more than a decade, the full-time professor of epidemiology didn’t prepare to teach this year because she simply can’t. It’s too taxing for her brain to deal with impromptu student questions. Ms. Gage-Witvliet hopes that, by sharing her own experiences with post COVID-19, she can help others.

“In my work, I use data to give a voice to people who don’t have a voice,” she said. “Now, I am one of those people.”

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

When Margot Gage-Witvliet began feeling run down after her family returned from a trip to the Netherlands in late February 2020, she initially chalked up her symptoms to jet lag. Three days later, however, her situation went from concerning to alarming as she struggled to breathe. “It felt like there was an elephant sitting on my chest,” she said.

Her husband and daughters also became ill with COVID-19, but Ms. Gage-Witvliet was the only one in her family who didn’t get better. After an early improvement, a rare coronavirus-induced tonic-clonic seizure in early April sent her spiraling back down. Ms. Gage-Witvliet spent the next several weeks in bed with the curtains drawn, unable to tolerate light or sound.

Today, Ms. Gage-Witvliet’s life looks nothing like it did 6 months ago when she first got sick. As one of COVID-19’s so called long-haulers, she continues to struggle with crushing fatigue, brain fog, and headaches – symptoms that worsen when she pushes herself to do more. Across the country, as many as 1 in 10 COVID-19 patients are reporting illnesses that continue for weeks and months after their initial diagnosis. Nearly all report neurologic issues like Ms. Gage-Witvliet, as well as shortness of breath and psychiatric concerns.

For Avindra Nath, MD, a neurologist at the National Institutes of Health, the experience of these long-haul COVID-19 patients feels familiar and reminds him of myalgic encephalomyelitis, also known as chronic fatigue syndrome.

Dr. Nath has long been interested in the lingering neurologic issues connected to chronic fatigue. An estimated three-quarters of all patients with chronic fatigue syndrome report that their symptoms started after a viral infection, and they suffer unrelenting exhaustion, difficulties regulating pulse and blood pressure, aches and pains, and brain fog. When Dr. Nath first read about the novel coronavirus, he began to worry that the virus would trigger symptoms in a subset of those infected. Hearing about the experiences of long-haulers like Ms. Gage-Witvliet raised his suspicions even more.

Unlike COVID-19 long-haulers, however, many patients with chronic fatigue syndrome go at least a year with these symptoms before receiving a diagnosis, according to a British survey. That means researchers have had few opportunities to study the early stages of the syndrome. “When we see patients with myalgic encephalomyelitis, whatever infection they might have had occurred in the remote past, so there’s no way for us to know how they got infected with it, what the infection was, or what the effects of it were in that early phase. We’re seeing them 2 years afterward,” Dr. Nath said.

Dr. Nath quickly realized that studying patients like Ms. Gage-Witvliet would give physicians and scientists a unique opportunity to understand not only long-term outcomes of COVID-19 infections, but also other postviral syndromes, including chronic fatigue syndrome at their earliest stages. It’s why Dr. Nath has spent the past several months scrambling to launch two NIH studies to examine the phenomenon.

Although Dr. Nath said that the parallels between COVID-19 long-haulers and those with chronic fatigue syndrome are obvious, he cautions against assuming that they are the same phenomenon. Some long-haulers might simply be taking a much slower path to recovery, or they might have a condition that looks similar on the surface but differs from chronic fatigue syndrome on a molecular level. But even if Dr. Nath fails to see links to chronic fatigue syndrome, with more than 92.5 million documented cases of COVID-19 around the world, the work will be relevant to the substantial number of infected individuals who don’t recover quickly.

“With so many people having exposure to the same virus over a similar time period, we really have the opportunity to look at these manifestations and at the very least to understand postviral syndromes,” said Mady Hornig, MD, a psychiatrist at Columbia University, New York.

The origins of chronic fatigue syndrome date back to 1985, when the Centers for Disease Control and Prevention received a request from two physicians – Paul Cheney, MD, and Daniel Peterson, MD – to investigate a mysterious disease outbreak in Nevada. In November 1984, residents in and around the idyllic vacation spot of Incline Village, a small town tucked into the north shore of Lake Tahoe, had begun reporting flu-like symptoms that persisted for weeks, even months. The doctors had searched high and low for a cause, but they couldn’t figure out what was making their patients sick.

They reported a range of symptoms – including muscle aches and pains, low-grade fevers, sore throats, and headaches – but everyone said that crippling fatigue was the most debilitating issue. This wasn’t the kind of fatigue that could be cured by a nap or even a long holiday. No matter how much their patients slept – and some were almost completely bedbound – their fatigue didn’t abate. What’s more, the fatigue got worse whenever they tried to push themselves to do more. Puzzled, the CDC sent two epidemic intelligence service (EIS) officers to try to get to the bottom of what might be happening.


 

Muscle aches and pains with crippling fatigue

After their visit to Incline Village, however, the CDC was just as perplexed as Dr. Cheney and Dr. Peterson. Many of the people with the condition reported flu-like symptoms right around the time they first got sick, and the physicians’ leading hypothesis was that the outbreak and its lasting symptoms were caused by chronic Epstein-Barr virus infection. But neither the CDC nor anyone else could identify the infection or any other microbial cause. The two EIS officers duly wrote up a report for the CDC’s flagship publication, Morbidity and Mortality Weekly ReportI, titled “Chronic Fatigue Possibly Related to Epstein-Barr Virus – Nevada”.

That investigators focused on the fatigue aspect made sense, says Leonard A. Jason, PhD, professor of psychology at DePaul University and director of the Center for Community Research, both in Chicago, because it was one of the few symptoms shared by all the individuals studied and it was also the most debilitating. But that focus – and the name “chronic fatigue syndrome” – led to broad public dismissal of the condition’s severity, as did an editorial note in MMWR urging physicians to look for “more definable, and possibly treatable, conditions.” Subsequent research failed to confirm a specific link to the Epstein-Barr virus, which only added to the condition’s phony reputation. Rather than being considered a potentially disabling illness, it was disregarded as a “yuppie flu” or a fancy name for malingering.

“It’s not a surprise that patients are being dismissed because there’s already this sort of grandfathered-in sense that fatigue is not real,” said Jennifer Frankovich, MD, a pediatric rheumatologist at Stanford (Calif.) University’s Lucile Packard Children’s Hospital in Palo Alto. “I’m sure that’s frustrating for them to be tired and then to have the clinician not believe them or dismiss them or think they’re making it up. It would be more helpful to the families to say: ‘You know what, we don’t know, we do not have the answer, and we believe you.’ ”
 

A syndrome’s shame

As time passed, patient advocacy groups began pushing back against the negative way the condition was being perceived. This criticism came as organizations like the CDC worked to develop a set of diagnostic criteria that researchers and clinicians dealing with chronic fatigue syndrome could use. With such a heterogeneous group of patients and symptoms, the task was no small challenge. The discussions, which took place over nearly 2 decades, played a key role in helping scientists home in on the single factor that was central to chronic fatigue: postexertional malaise.

“This is quite unique for chronic fatigue syndrome. With other diseases, yes, you may have fatigue as one of the components of the disease, but postexertional fatigue is very specific,” said Alain Moreau, PhD, a molecular biologist at the University of Montreal.

Of course, plenty of people have pushed themselves too hard physically and paid the price the next day. But those with chronic fatigue syndrome weren’t running marathons. To them, exertion could be anything from getting the mail to reading a book. Nor could the resulting exhaustion be resolved by an afternoon on the couch or a long vacation.

“If they do these activities, they can crash for weeks, even months,” Dr. Moreau said. It was deep, persistent, and – for 40% of those with chronic fatigue syndrome – disabling. In 2015, a study group from the Institute of Medicine proposed renaming chronic fatigue to “systemic exercise intolerance disease” because of the centrality of this symptom. Although that effort mostly stalled, their report did bring the condition out of its historic place as a scientific backwater. What resulted was an uptick in research on chronic fatigue syndrome, which helped define some of the physiological issues that either contribute to or result from the condition.

Researchers had long known about the link between infection and fatigue, said Dr. Frankovich. Work included mysterious outbreaks like the one in Lake Tahoe and well-documented issues like the wave of encephalitis lethargica (a condition that leaves patients in an almost vegetative state) that followed the 1918 H1N1 influenza pandemic.

“As a clinician, when you see someone who comes in with a chronic infection, they’re tired. I think that’s why, in the chronic-fatigue world, people are desperately looking for the infection so we can treat it, and maybe these poor suffering people will feel better,” Dr. Frankovich added. Then the pandemic struck, giving him yet another opportunity to study postviral syndromes.
 

Immunologic symptoms

Given the close link between a nonspecific viral illness and the onset of symptoms in chronic fatigue syndrome, scientists like Dr. Hornig opted to focus on immunologic symptoms. In a 2015 analysis published in Science, Dr. Hornig and colleagues showed that immune problems can be found in the earliest stages of chronic fatigue syndrome, and that they change as the illness progresses. Patients who had been sick for less than 3 years showed significant increases in levels of both pro- and anti-inflammatory cytokines, and the factor most strongly correlated to this inability to regulate cytokine levels was the duration of symptoms, not their severity. A series of other studies also revealed problems with regulation of the immune system, although no one could show what might have set these problems in motion.

Other researchers found signs of mitochondrial dysfunction in those with chronic fatigue syndrome. Because mitochondria make energy for cells, it wasn’t an intellectual stretch to believe that glitches in this process could contribute to fatigue. As early as 1991, scientists had discovered signs of mitochondrial degeneration in muscle biopsies from people with chronic fatigue syndrome. Subsequent studies showed that those affected by chronic fatigue were missing segments of mitochondrial DNA and had significantly reduced levels of mitochondrial activity. Although exercise normally improves mitochondrial functioning, the opposite appears to happen in chronic fatigue.

To Dr. Nath, these dual hypotheses aren’t necessarily mutually exclusive. Some studies have hinted that infection with the common human herpesvirus–6 (HHV-6) can lead to an autoimmune condition in which the body makes antibodies against the mitochondria. Mitochondria also play a key role in the ability of the innate immune system to produce interferon and other proinflammatory cytokines. It might also be that the link between immune and mitochondrial problems is more convoluted than originally thought, or that the two systems are affected independent of one another, Dr. Nath said.

Finding answers, especially those that could lead to potential treatments, wouldn’t be easy, however. In 2016, the NIH launched an in-depth study of a small number of individuals with chronic fatigue, hoping to find clues about what the condition was and how it might be treated.

For scientists like Dr. Nath, the NIH study provided a way to get at the underlying biology of chronic fatigue syndrome. Then the pandemic struck, giving him yet another opportunity to study postviral syndromes.
 

Chronic post-SARS syndrome

In March 2020, retired physician Harvey Moldofsky, MD, began receiving inquiries about a 2011 study he and his colleague, John Patcai, MD, had published in BMC Neurology about something they dubbed “chronic post-SARS syndrome.” The small case-control study, which involved mainly health care workers in Toronto, received little attention when it was first published, but with COVID-19, it was suddenly relevant.

Early clusters of similar cases in Miami made local physicians desperate for Dr. Moldofsky’s expertise. Luckily, he was nearby; he had fled the frigid Canadian winter for the warmth of Sarasota, Fla.

“I had people from various countries around the world writing to me and asking what they should do. And of course I don’t have any answers,” he said. But the study contained one of the world’s only references to the syndrome.

In 2003, a woman arrived in Toronto from Hong Kong. She didn’t know it at the time, but her preairport stay at the Hotel Metropole had infected her with the first SARS (severe acute respiratory syndrome) coronavirus. Her subsequent hospitalization in Toronto sparked a city-wide outbreak of SARS in which 273 people became ill and 44 died. Many of those affected were health care workers, including nurses and respiratory therapists. Although most eventually returned to work, a subset couldn’t. They complained of energy-sapping fatigue, poor sleep, brain fog, and assorted body aches and pains that persisted for more than 18 months. The aches and pains brought them to the attention of Dr. Moldofsky, then director of the Centre for the Study of Pain at the University of Toronto.

His primary interest at the time was fibromyalgia, which caused symptoms similar to those reported by the original SARS long-haulers. Intrigued, Dr. Moldofsky agreed to take a look. Their chest x-rays were clear and the nurses showed no signs of lingering viral infection. Dr. Moldofsky could see that the nurses were ill and suffering, but no lab tests or anything else could identify what was causing their symptoms.

In 2011, Dr. Moldofsky and Dr. Patcai found a strong overlap between chronic SARS, fibromyalgia, and chronic fatigue syndrome when they compared 22 patients with long-term SARS issues with 21 who had fibromyalgia. “Their problems are exactly the same. They have strange symptoms and nobody can figure out what they’re about. And these symptoms are aches and pains, and they have trouble thinking and concentrating,” Dr. Moldofsky said. Reports of COVID-19 long-haulers didn’t surprise Dr. Moldofsky, and he immediately recognized that Nath’s intention to follow these patients could provide insights into both fibromyalgia and chronic fatigue syndrome.

That’s exactly what Dr. Nath is proposing with the two NIH studies. One will focus solely on the neurologic impacts of COVID-19, including stroke, loss of taste and smell, and brain fog. The other will bring patients who have had COVID-19 symptoms for at least 6 months to the NIH Clinical Center for an inpatient stay during which they will undergo detailed physiologic tests.

Scientists around the world are launching their own post–COVID-19 studies. Dr. Moreau’s group in Montreal has laid the groundwork for such an endeavor, and the CoroNerve group in the United Kingdom is monitoring neurologic complications from the coronavirus. Many of them have the same goals as the NIH studies: Leverage the large number of COVID-19 long-haulers to better understand the earliest stages of postviral syndrome.

“At this juncture, after all the reports that we’ve seen so far, I think it’s very unlikely that there will be no relationship whatsoever between COVID-19 and chronic fatigue syndrome,” Dr. Hornig said. “I think there certainly will be some, but again, what’s the scope, what’s the size? And then, of course, even more importantly, if it is happening, what is the mechanism and how is it happening?”

For people like Ms. Gage-Witvliet, the answers can’t come soon enough. For the first time in more than a decade, the full-time professor of epidemiology didn’t prepare to teach this year because she simply can’t. It’s too taxing for her brain to deal with impromptu student questions. Ms. Gage-Witvliet hopes that, by sharing her own experiences with post COVID-19, she can help others.

“In my work, I use data to give a voice to people who don’t have a voice,” she said. “Now, I am one of those people.”

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

The American Diabetes Association, along with 18 other organizations, has sent a letter to the U.S. Centers for Disease Control and Prevention urging them to rank people with type 1 diabetes as equally high risk for COVID-19 severity, and therefore vaccination, as those with type 2 diabetes.

On Jan. 12, the CDC recommended states vaccinate all Americans over age 65 and those with underlying health conditions that make them more vulnerable to COVID-19.

Currently, type 2 diabetes is listed among 12 conditions that place adults “at increased risk of severe illness from the virus that causes COVID-19,” with the latter defined as “hospitalization, admission to the intensive care unit, intubation or mechanical ventilation, or death.”

On the other hand, the autoimmune condition type 1 diabetes is among 11 conditions the CDC says “might be at increased risk” for COVID-19, but limited data were available at the time of the last update on Dec. 23, 2020.

“States are utilizing the CDC risk classification when designing their vaccine distribution plans. This raises an obvious concern as it could result in the approximately 1.6 million with type 1 diabetes receiving the vaccination later than others with the same risk,” states the ADA letter, sent to the CDC on Jan. 13.

Representatives from the Endocrine Society, American Association of Clinical Endocrinology, Pediatric Endocrine Society, Association of Diabetes Care & Education Specialists, and JDRF, among others, cosigned the letter.
 

Newer data show those with type 1 diabetes at equally high risk

While acknowledging that “early data did not provide as much clarity about the extent to which those with type 1 diabetes are at high risk,” the ADA says newer evidence has emerged, as previously reported by this news organization, that “convincingly demonstrates that COVID-19 severity is more than tripled in individuals with type 1 diabetes.”

The letter also cites another study showing that people with type 1 diabetes “have a 3.3-fold greater risk of severe illness, are 3.9 times more likely to be hospitalized with COVID-19, and have a 3-fold increase in mortality compared to those without type 1 diabetes.”

Those risks, they note, are comparable to the increased risk established for those with type 2 diabetes, as shown in a third study from Scotland, published last month.

Asked for comment, CDC representative Kirsten Nordlund said in an interview, “This list is a living document that will be periodically updated by CDC, and it could rapidly change as the science evolves.”

In addition, Ms. Nordlund said, “Decisions about transitioning to subsequent phases should depend on supply; demand; equitable vaccine distribution; and local, state, or territorial context.”

“Phased vaccine recommendations are meant to be fluid and not restrictive for jurisdictions. It is not necessary to vaccinate all individuals in one phase before initiating the next phase; phases may overlap,” she noted. More information is available here.
 

Tennessee gives type 1 and type 2 diabetes equal priority for vaccination

Meanwhile, at least one state, Tennessee, has updated its guidance to include both types of diabetes as being priority for COVID-19 vaccination.

Vanderbilt University pediatric endocrinologist Justin M. Gregory, MD, said in an interview: “I was thrilled when our state modified its guidance on December 30th to include both type 1 and type 2 diabetes in the ‘high-risk category.’ Other states have not modified that guidance though.”

It’s unclear how this might play out on the ground, noted Dr. Gregory, who led one of the three studies demonstrating increased COVID-19 risk for people with type 1 diabetes.

“To tell you the truth, I don’t really know how individual organizations dispensing the vaccination [will handle] people who come to their facility saying they have ‘diabetes.’ Individual states set the vaccine-dispensing guidance and individual county health departments and health care systems mirror that guidance,” he said.

Thus, he added, “Although it’s possible an individual nurse may take the ‘I’ll ask you no questions, and you’ll tell me no lies’ approach if someone with type 1 diabetes says they have ‘diabetes’, websites and health department–recorded telephone messages are going to tell people with type 1 diabetes they have to wait further back in line if that is what their state’s guidance directs.”

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

The American Diabetes Association, along with 18 other organizations, has sent a letter to the U.S. Centers for Disease Control and Prevention urging them to rank people with type 1 diabetes as equally high risk for COVID-19 severity, and therefore vaccination, as those with type 2 diabetes.

On Jan. 12, the CDC recommended states vaccinate all Americans over age 65 and those with underlying health conditions that make them more vulnerable to COVID-19.

Currently, type 2 diabetes is listed among 12 conditions that place adults “at increased risk of severe illness from the virus that causes COVID-19,” with the latter defined as “hospitalization, admission to the intensive care unit, intubation or mechanical ventilation, or death.”

On the other hand, the autoimmune condition type 1 diabetes is among 11 conditions the CDC says “might be at increased risk” for COVID-19, but limited data were available at the time of the last update on Dec. 23, 2020.

“States are utilizing the CDC risk classification when designing their vaccine distribution plans. This raises an obvious concern as it could result in the approximately 1.6 million with type 1 diabetes receiving the vaccination later than others with the same risk,” states the ADA letter, sent to the CDC on Jan. 13.

Representatives from the Endocrine Society, American Association of Clinical Endocrinology, Pediatric Endocrine Society, Association of Diabetes Care & Education Specialists, and JDRF, among others, cosigned the letter.
 

Newer data show those with type 1 diabetes at equally high risk

While acknowledging that “early data did not provide as much clarity about the extent to which those with type 1 diabetes are at high risk,” the ADA says newer evidence has emerged, as previously reported by this news organization, that “convincingly demonstrates that COVID-19 severity is more than tripled in individuals with type 1 diabetes.”

The letter also cites another study showing that people with type 1 diabetes “have a 3.3-fold greater risk of severe illness, are 3.9 times more likely to be hospitalized with COVID-19, and have a 3-fold increase in mortality compared to those without type 1 diabetes.”

Those risks, they note, are comparable to the increased risk established for those with type 2 diabetes, as shown in a third study from Scotland, published last month.

Asked for comment, CDC representative Kirsten Nordlund said in an interview, “This list is a living document that will be periodically updated by CDC, and it could rapidly change as the science evolves.”

In addition, Ms. Nordlund said, “Decisions about transitioning to subsequent phases should depend on supply; demand; equitable vaccine distribution; and local, state, or territorial context.”

“Phased vaccine recommendations are meant to be fluid and not restrictive for jurisdictions. It is not necessary to vaccinate all individuals in one phase before initiating the next phase; phases may overlap,” she noted. More information is available here.
 

Tennessee gives type 1 and type 2 diabetes equal priority for vaccination

Meanwhile, at least one state, Tennessee, has updated its guidance to include both types of diabetes as being priority for COVID-19 vaccination.

Vanderbilt University pediatric endocrinologist Justin M. Gregory, MD, said in an interview: “I was thrilled when our state modified its guidance on December 30th to include both type 1 and type 2 diabetes in the ‘high-risk category.’ Other states have not modified that guidance though.”

It’s unclear how this might play out on the ground, noted Dr. Gregory, who led one of the three studies demonstrating increased COVID-19 risk for people with type 1 diabetes.

“To tell you the truth, I don’t really know how individual organizations dispensing the vaccination [will handle] people who come to their facility saying they have ‘diabetes.’ Individual states set the vaccine-dispensing guidance and individual county health departments and health care systems mirror that guidance,” he said.

Thus, he added, “Although it’s possible an individual nurse may take the ‘I’ll ask you no questions, and you’ll tell me no lies’ approach if someone with type 1 diabetes says they have ‘diabetes’, websites and health department–recorded telephone messages are going to tell people with type 1 diabetes they have to wait further back in line if that is what their state’s guidance directs.”

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

The American Diabetes Association, along with 18 other organizations, has sent a letter to the U.S. Centers for Disease Control and Prevention urging them to rank people with type 1 diabetes as equally high risk for COVID-19 severity, and therefore vaccination, as those with type 2 diabetes.

On Jan. 12, the CDC recommended states vaccinate all Americans over age 65 and those with underlying health conditions that make them more vulnerable to COVID-19.

Currently, type 2 diabetes is listed among 12 conditions that place adults “at increased risk of severe illness from the virus that causes COVID-19,” with the latter defined as “hospitalization, admission to the intensive care unit, intubation or mechanical ventilation, or death.”

On the other hand, the autoimmune condition type 1 diabetes is among 11 conditions the CDC says “might be at increased risk” for COVID-19, but limited data were available at the time of the last update on Dec. 23, 2020.

“States are utilizing the CDC risk classification when designing their vaccine distribution plans. This raises an obvious concern as it could result in the approximately 1.6 million with type 1 diabetes receiving the vaccination later than others with the same risk,” states the ADA letter, sent to the CDC on Jan. 13.

Representatives from the Endocrine Society, American Association of Clinical Endocrinology, Pediatric Endocrine Society, Association of Diabetes Care & Education Specialists, and JDRF, among others, cosigned the letter.
 

Newer data show those with type 1 diabetes at equally high risk

While acknowledging that “early data did not provide as much clarity about the extent to which those with type 1 diabetes are at high risk,” the ADA says newer evidence has emerged, as previously reported by this news organization, that “convincingly demonstrates that COVID-19 severity is more than tripled in individuals with type 1 diabetes.”

The letter also cites another study showing that people with type 1 diabetes “have a 3.3-fold greater risk of severe illness, are 3.9 times more likely to be hospitalized with COVID-19, and have a 3-fold increase in mortality compared to those without type 1 diabetes.”

Those risks, they note, are comparable to the increased risk established for those with type 2 diabetes, as shown in a third study from Scotland, published last month.

Asked for comment, CDC representative Kirsten Nordlund said in an interview, “This list is a living document that will be periodically updated by CDC, and it could rapidly change as the science evolves.”

In addition, Ms. Nordlund said, “Decisions about transitioning to subsequent phases should depend on supply; demand; equitable vaccine distribution; and local, state, or territorial context.”

“Phased vaccine recommendations are meant to be fluid and not restrictive for jurisdictions. It is not necessary to vaccinate all individuals in one phase before initiating the next phase; phases may overlap,” she noted. More information is available here.
 

Tennessee gives type 1 and type 2 diabetes equal priority for vaccination

Meanwhile, at least one state, Tennessee, has updated its guidance to include both types of diabetes as being priority for COVID-19 vaccination.

Vanderbilt University pediatric endocrinologist Justin M. Gregory, MD, said in an interview: “I was thrilled when our state modified its guidance on December 30th to include both type 1 and type 2 diabetes in the ‘high-risk category.’ Other states have not modified that guidance though.”

It’s unclear how this might play out on the ground, noted Dr. Gregory, who led one of the three studies demonstrating increased COVID-19 risk for people with type 1 diabetes.

“To tell you the truth, I don’t really know how individual organizations dispensing the vaccination [will handle] people who come to their facility saying they have ‘diabetes.’ Individual states set the vaccine-dispensing guidance and individual county health departments and health care systems mirror that guidance,” he said.

Thus, he added, “Although it’s possible an individual nurse may take the ‘I’ll ask you no questions, and you’ll tell me no lies’ approach if someone with type 1 diabetes says they have ‘diabetes’, websites and health department–recorded telephone messages are going to tell people with type 1 diabetes they have to wait further back in line if that is what their state’s guidance directs.”

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

Cardiologist Ethan J. Weiss, MD, followed an intermittent-fasting diet for 7 years. He lost about 3.6 kg (8 lb) and began recommending the approach to friends and patients who wanted to lose weight.

“I liked the way the diet was so simple,” said Dr. Weiss, an associate professor at the Cardiovascular Research Institute, University of California, San Francisco. But he also felt “it was too good to be true because you can eat what you want as long as it’s within a narrow window.”

So when, last year, he conducted a randomized, controlled trial, TREAT, testing such an approach – eating during just 8 hours a day, fasting for the remaining 16 hours – versus an eating plan of three meals a day without restrictions, he was somewhat dismayed to find the group of people who fasted didn’t lose any more weight than the other group.

The approach used in this study is known as time-restricted eating. It involves designating periods of time within the day when people can consume whatever they want; they then “fast” at times outside those eating windows. Other methods include alternate-day fasting, or the well-known 5:2 diet. In the latter, people eat a “normal” amount of around 2,000 calories per day on 5 days of the week, but for the other 2 days, they restrict caloric intake to 500 calories per day.

Intermittent fasting is an umbrella term encompassing all of these different approaches.

Dr. Weiss’s work builds on more than a decade of research into this type of eating plan by scientists, including Krista Varady, PhD, professor of nutrition at the University of Illinois at Chicago, who presented an overview of her own studies last fall at the virtual annual meeting of the European Association for the Study of Diabetes.

Although much of the work has suggested that the shorter duration of eating period in this type of diet leads to lower calorie intake and weight loss while avoiding the need for the tedious calorie-counting of conventional diets, Dr. Weiss’s data – published last year – throws a spanner in the works and now complicates the evidence base.
 

A promise of simplicity: ‘All you have to do is watch the clock’

Dr. Varady said she, too, is intrigued by the simplicity of intermittent-fasting diets.

In 2018, Dr. Varady and colleagues tested the weight-loss efficacy of 12 weeks of time-restricted feeding in a pilot study of 23 people with obesity.

Participants were permitted an 8-hour eating window (10 a.m. to 6 p.m.) followed by water-only fasting of 16 hours (6 p.m. to 10 a.m.) the next day (sometimes referred to as the 16:8 diet). Researchers measured weight loss and fat mass, as well as metabolic parameters, and compared the active group with 23 matched-control participants who ate freely.

There were no restrictions on type or quantity of food consumed by the control group during the 8-hour period, but individuals in the time-restricted feeding group consumed around 350 calories less than the comparator group.

Dr. Varady thinks this is most likely because of the fact that people normally eat during a 14-hour window and time-restricted feeding cuts that down by 6 hours.

“One of the most beautiful things about time-restricted feeding is that it doesn’t require calorie monitoring,” she explained. “People get burnt out with having to constantly monitor calories. All you have to do is watch the clock.”

Adherence was quite high, she reported, although most people skipped 1 day, often a Saturday, likely because of social engagements.

Weight loss in the time-restricted feeding group was mild to moderate. After 3 months, mean body weight decreased by 2.6%, or approximately 3 kg (7-8 lb), relative to those who ate freely, but this was a significant difference (P  < .05).

But the researchers observed little change in metabolic disease risk factors between the groups.

In the time-restricted feeding group, systolic blood pressure dropped from 128 mm Hg to 121 mm Hg over the 12-week period, which was significant relative to the control group (P  <  .05) but there were no significant changes in fasting glucose, fasting lipids, fasting insulin, or insulin resistance relative to the comparator group.

In contrast to Dr. Varady’s findings, Dr. Weiss’s randomized TREAT trial, which used a similar 16:8 period of time-restricted versus unrestricted eating in 116 individuals with overweight or obesity, did not find greater weight loss in the group restricted to eating within the 8-hour window.

As previously reported by this news organization, those who fasted for 16 hours of each day (n = 59) did lose some weight, compared with the control group (n = 57) over 12 weeks, but the difference in weight loss between the groups was not significant (−0.26 kg; P = .63).

And there were no significant differences in any of the secondary outcomes of fat mass, fasting insulin, fasting glucose, hemoglobin A1c levels, estimated energy intake, total energy expenditure, and resting energy expenditure between the time-restricted eating and regular feeding groups.

“I don’t claim time-restricted eating is dead,” Dr. Weiss said, “but the hope that you can eat for a limited time each day and solve metabolic disease is not there.”

Does the length of the eating window matter?

Following her pilot study of an 8-hour eating window, Dr. Varady conducted further research with 4- or 6-hour eating windows to see if even shorter periods would precipitate greater weight loss, ideally a clinically significant loss of 5% of body weight.

She ran a 2-month randomized, controlled study in people with obesity, published in 2020, which was the first to examine both a 4-hour (3 p.m. to 7 p.m.; n = 19) or 6-hour (1 p.m to 7 p.m.; n = 20) eating window versus a diet without any food restrictions as a control (n = 19) (Cell Metab. 2020;32:366-78.e3).

Dr. Varady explained that they decided to shift the eating window to later in the day for this trial (in contrast to the earlier 8-hour study) to allow people to eat dinner at a sociable time, and thereby hopefully reduce dropouts from the study. 

“Unlike with alternate-day fasting, most people find time-restricted feeding easy to incorporate into their lifestyles,” she remarked.

Both the 4- and 6-hour eating window groups experienced a mean 3.2% body weight loss, compared with controls, and this correlated with a 550-calorie reduction in their daily consumption, compared with their baseline calorie intake.

In terms of other outcomes – and in contrast to the 8-hour window study which showed very little changed other than a minor decrease in blood pressure – researchers saw some changes in metabolic risk factors with the 4- and 6-hour eating windows, Dr. Varady reported.

Compared with the control group, fasting insulin decreased in both time-restricted feeding groups by a mean of 15% (P < .05). Insulin resistance also decreased by 25% in the 4-hour group and by 15% in the 6-hour group, compared with the control group. Fasting glucose did not change in either group, however.

The researchers did not observe any effect on blood pressure or plasma lipids in the 4- or 6-hour eating window groups, compared with controls. However, measures of oxidative stress and inflammation decreased in both groups versus controls by approximately 35% (P < .05).

“These findings suggest that this form of severe time-restricted feeding is achievable and can help adults with obesity lose weight, without having to count calories,” Dr. Varady and colleagues conclude.
 

Is intermittent fasting better for weight loss than calorie restriction?

Ultimately, if weight loss is the primary goal, many want to know how time-restricted feeding compares with conventional daily calorie restriction.

Back in 2017, Dr. Varady published a year-long randomized, controlled study that compared alternate-day fasting with a calorie-restriction diet and a conventional/usual diet among 100 participants with obesity who were otherwise healthy.  

Participants on the alternate-day fasting plan (n = 34) consumed 500 calories on fasting days for the first 6 months for weight loss (approximately 25% of energy needs) followed by 125% of energy needs on alternating “feast days”. For an additional 6 months, they ate 1,000 calories on fasting days – aimed at weight maintenance.

Those following the calorie-restriction diet (n = 35) reduced energy intake by 25% (approximately 500 kcal) for the first 6 months for weight loss, followed by enough calories sufficient for weight maintenance (so no further loss nor gain).

However, the study showed alternate-day fasting did not produce better weight loss than conventional calorie counting.

“Over the first 6 months [during the weight-loss period] both groups lost an average of 6% body weight. After 12 months it crept back to 5% weight loss,” reported Dr. Varady.

“Realistically, if the study continued for 2 or 3 years, they probably would have regained much of their weight,” she admitted.

Dr. Varady suspects it might be better for the alternate-day fasting participants to continue eating only 500 calories on their fast day during the weight-loss maintenance period rather than increasing calorie intake during this phase.

Heart rate and blood pressure did not change in either group, while triglycerides decreased in the alternate-day fasting group, and LDL cholesterol decreased in the calorie-restriction group.

Glucose level decreased in the calorie-restriction group but not the alternate-day fasting group, and insulin and HOMA-IR were unaffected in both groups, reported Dr. Varady, noting that these findings were in healthy people with obesity.

In people with obesity and insulin resistance – evaluated as a subgroup in a separate study by Dr. Varady of alternate-day fasting versus daily calorie restriction published in 2019 – she noted that when insulin levels and HOMA-IR were measured, there was a greater reduction in both variables in the fasting group, compared with the calorie-restriction group.

“For people at risk of diabetes, maybe fasting produces more potent effects on glycemic control?” she ventured.
 

Who fares best with which fasting diets?

Summing up, Dr. Varady provided some practical pointers regarding who she feels is best suited to intermittent fasting and who should avoid it.

Those who binge eat, shift-workers, and frequent snackers do not do well with fasting, she said.

The first 10 days of intermittent fasting are rough, she pointed out, with the most common complaint being headaches.

“Eventually, people do feel an energy boost on fast days, and they say they concentrate better and have lots of energy. People won’t feel lethargic. Also, eating protein on fast days has been shown to keep hunger at bay.”

She cautiously concluded that weight loss with “alternate-day fasting” is quicker than some other methods, at 4.5-7 kg (10-15 lb) in 3 months, but is harder to follow and requires some calorie counting.

“In comparison, with time-restricted feeding, for which there have been very few ... studies to date, weight loss is slower at 2-4.5 kg (5-10 lb) in 3 months, but it is easier to follow and tolerable because you don’t need to count calories.”

Dr. Weiss has reported no relevant financial relationships. Dr. Varady has reported receiving author fees from Hachette for her book, “Every Other Day Diet.” (New York: Hachette, 2013)

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

Cardiologist Ethan J. Weiss, MD, followed an intermittent-fasting diet for 7 years. He lost about 3.6 kg (8 lb) and began recommending the approach to friends and patients who wanted to lose weight.

“I liked the way the diet was so simple,” said Dr. Weiss, an associate professor at the Cardiovascular Research Institute, University of California, San Francisco. But he also felt “it was too good to be true because you can eat what you want as long as it’s within a narrow window.”

So when, last year, he conducted a randomized, controlled trial, TREAT, testing such an approach – eating during just 8 hours a day, fasting for the remaining 16 hours – versus an eating plan of three meals a day without restrictions, he was somewhat dismayed to find the group of people who fasted didn’t lose any more weight than the other group.

The approach used in this study is known as time-restricted eating. It involves designating periods of time within the day when people can consume whatever they want; they then “fast” at times outside those eating windows. Other methods include alternate-day fasting, or the well-known 5:2 diet. In the latter, people eat a “normal” amount of around 2,000 calories per day on 5 days of the week, but for the other 2 days, they restrict caloric intake to 500 calories per day.

Intermittent fasting is an umbrella term encompassing all of these different approaches.

Dr. Weiss’s work builds on more than a decade of research into this type of eating plan by scientists, including Krista Varady, PhD, professor of nutrition at the University of Illinois at Chicago, who presented an overview of her own studies last fall at the virtual annual meeting of the European Association for the Study of Diabetes.

Although much of the work has suggested that the shorter duration of eating period in this type of diet leads to lower calorie intake and weight loss while avoiding the need for the tedious calorie-counting of conventional diets, Dr. Weiss’s data – published last year – throws a spanner in the works and now complicates the evidence base.
 

A promise of simplicity: ‘All you have to do is watch the clock’

Dr. Varady said she, too, is intrigued by the simplicity of intermittent-fasting diets.

In 2018, Dr. Varady and colleagues tested the weight-loss efficacy of 12 weeks of time-restricted feeding in a pilot study of 23 people with obesity.

Participants were permitted an 8-hour eating window (10 a.m. to 6 p.m.) followed by water-only fasting of 16 hours (6 p.m. to 10 a.m.) the next day (sometimes referred to as the 16:8 diet). Researchers measured weight loss and fat mass, as well as metabolic parameters, and compared the active group with 23 matched-control participants who ate freely.

There were no restrictions on type or quantity of food consumed by the control group during the 8-hour period, but individuals in the time-restricted feeding group consumed around 350 calories less than the comparator group.

Dr. Varady thinks this is most likely because of the fact that people normally eat during a 14-hour window and time-restricted feeding cuts that down by 6 hours.

“One of the most beautiful things about time-restricted feeding is that it doesn’t require calorie monitoring,” she explained. “People get burnt out with having to constantly monitor calories. All you have to do is watch the clock.”

Adherence was quite high, she reported, although most people skipped 1 day, often a Saturday, likely because of social engagements.

Weight loss in the time-restricted feeding group was mild to moderate. After 3 months, mean body weight decreased by 2.6%, or approximately 3 kg (7-8 lb), relative to those who ate freely, but this was a significant difference (P  < .05).

But the researchers observed little change in metabolic disease risk factors between the groups.

In the time-restricted feeding group, systolic blood pressure dropped from 128 mm Hg to 121 mm Hg over the 12-week period, which was significant relative to the control group (P  <  .05) but there were no significant changes in fasting glucose, fasting lipids, fasting insulin, or insulin resistance relative to the comparator group.

In contrast to Dr. Varady’s findings, Dr. Weiss’s randomized TREAT trial, which used a similar 16:8 period of time-restricted versus unrestricted eating in 116 individuals with overweight or obesity, did not find greater weight loss in the group restricted to eating within the 8-hour window.

As previously reported by this news organization, those who fasted for 16 hours of each day (n = 59) did lose some weight, compared with the control group (n = 57) over 12 weeks, but the difference in weight loss between the groups was not significant (−0.26 kg; P = .63).

And there were no significant differences in any of the secondary outcomes of fat mass, fasting insulin, fasting glucose, hemoglobin A1c levels, estimated energy intake, total energy expenditure, and resting energy expenditure between the time-restricted eating and regular feeding groups.

“I don’t claim time-restricted eating is dead,” Dr. Weiss said, “but the hope that you can eat for a limited time each day and solve metabolic disease is not there.”

Does the length of the eating window matter?

Following her pilot study of an 8-hour eating window, Dr. Varady conducted further research with 4- or 6-hour eating windows to see if even shorter periods would precipitate greater weight loss, ideally a clinically significant loss of 5% of body weight.

She ran a 2-month randomized, controlled study in people with obesity, published in 2020, which was the first to examine both a 4-hour (3 p.m. to 7 p.m.; n = 19) or 6-hour (1 p.m to 7 p.m.; n = 20) eating window versus a diet without any food restrictions as a control (n = 19) (Cell Metab. 2020;32:366-78.e3).

Dr. Varady explained that they decided to shift the eating window to later in the day for this trial (in contrast to the earlier 8-hour study) to allow people to eat dinner at a sociable time, and thereby hopefully reduce dropouts from the study. 

“Unlike with alternate-day fasting, most people find time-restricted feeding easy to incorporate into their lifestyles,” she remarked.

Both the 4- and 6-hour eating window groups experienced a mean 3.2% body weight loss, compared with controls, and this correlated with a 550-calorie reduction in their daily consumption, compared with their baseline calorie intake.

In terms of other outcomes – and in contrast to the 8-hour window study which showed very little changed other than a minor decrease in blood pressure – researchers saw some changes in metabolic risk factors with the 4- and 6-hour eating windows, Dr. Varady reported.

Compared with the control group, fasting insulin decreased in both time-restricted feeding groups by a mean of 15% (P < .05). Insulin resistance also decreased by 25% in the 4-hour group and by 15% in the 6-hour group, compared with the control group. Fasting glucose did not change in either group, however.

The researchers did not observe any effect on blood pressure or plasma lipids in the 4- or 6-hour eating window groups, compared with controls. However, measures of oxidative stress and inflammation decreased in both groups versus controls by approximately 35% (P < .05).

“These findings suggest that this form of severe time-restricted feeding is achievable and can help adults with obesity lose weight, without having to count calories,” Dr. Varady and colleagues conclude.
 

Is intermittent fasting better for weight loss than calorie restriction?

Ultimately, if weight loss is the primary goal, many want to know how time-restricted feeding compares with conventional daily calorie restriction.

Back in 2017, Dr. Varady published a year-long randomized, controlled study that compared alternate-day fasting with a calorie-restriction diet and a conventional/usual diet among 100 participants with obesity who were otherwise healthy.  

Participants on the alternate-day fasting plan (n = 34) consumed 500 calories on fasting days for the first 6 months for weight loss (approximately 25% of energy needs) followed by 125% of energy needs on alternating “feast days”. For an additional 6 months, they ate 1,000 calories on fasting days – aimed at weight maintenance.

Those following the calorie-restriction diet (n = 35) reduced energy intake by 25% (approximately 500 kcal) for the first 6 months for weight loss, followed by enough calories sufficient for weight maintenance (so no further loss nor gain).

However, the study showed alternate-day fasting did not produce better weight loss than conventional calorie counting.

“Over the first 6 months [during the weight-loss period] both groups lost an average of 6% body weight. After 12 months it crept back to 5% weight loss,” reported Dr. Varady.

“Realistically, if the study continued for 2 or 3 years, they probably would have regained much of their weight,” she admitted.

Dr. Varady suspects it might be better for the alternate-day fasting participants to continue eating only 500 calories on their fast day during the weight-loss maintenance period rather than increasing calorie intake during this phase.

Heart rate and blood pressure did not change in either group, while triglycerides decreased in the alternate-day fasting group, and LDL cholesterol decreased in the calorie-restriction group.

Glucose level decreased in the calorie-restriction group but not the alternate-day fasting group, and insulin and HOMA-IR were unaffected in both groups, reported Dr. Varady, noting that these findings were in healthy people with obesity.

In people with obesity and insulin resistance – evaluated as a subgroup in a separate study by Dr. Varady of alternate-day fasting versus daily calorie restriction published in 2019 – she noted that when insulin levels and HOMA-IR were measured, there was a greater reduction in both variables in the fasting group, compared with the calorie-restriction group.

“For people at risk of diabetes, maybe fasting produces more potent effects on glycemic control?” she ventured.
 

Who fares best with which fasting diets?

Summing up, Dr. Varady provided some practical pointers regarding who she feels is best suited to intermittent fasting and who should avoid it.

Those who binge eat, shift-workers, and frequent snackers do not do well with fasting, she said.

The first 10 days of intermittent fasting are rough, she pointed out, with the most common complaint being headaches.

“Eventually, people do feel an energy boost on fast days, and they say they concentrate better and have lots of energy. People won’t feel lethargic. Also, eating protein on fast days has been shown to keep hunger at bay.”

She cautiously concluded that weight loss with “alternate-day fasting” is quicker than some other methods, at 4.5-7 kg (10-15 lb) in 3 months, but is harder to follow and requires some calorie counting.

“In comparison, with time-restricted feeding, for which there have been very few ... studies to date, weight loss is slower at 2-4.5 kg (5-10 lb) in 3 months, but it is easier to follow and tolerable because you don’t need to count calories.”

Dr. Weiss has reported no relevant financial relationships. Dr. Varady has reported receiving author fees from Hachette for her book, “Every Other Day Diet.” (New York: Hachette, 2013)

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

Cardiologist Ethan J. Weiss, MD, followed an intermittent-fasting diet for 7 years. He lost about 3.6 kg (8 lb) and began recommending the approach to friends and patients who wanted to lose weight.

“I liked the way the diet was so simple,” said Dr. Weiss, an associate professor at the Cardiovascular Research Institute, University of California, San Francisco. But he also felt “it was too good to be true because you can eat what you want as long as it’s within a narrow window.”

So when, last year, he conducted a randomized, controlled trial, TREAT, testing such an approach – eating during just 8 hours a day, fasting for the remaining 16 hours – versus an eating plan of three meals a day without restrictions, he was somewhat dismayed to find the group of people who fasted didn’t lose any more weight than the other group.

The approach used in this study is known as time-restricted eating. It involves designating periods of time within the day when people can consume whatever they want; they then “fast” at times outside those eating windows. Other methods include alternate-day fasting, or the well-known 5:2 diet. In the latter, people eat a “normal” amount of around 2,000 calories per day on 5 days of the week, but for the other 2 days, they restrict caloric intake to 500 calories per day.

Intermittent fasting is an umbrella term encompassing all of these different approaches.

Dr. Weiss’s work builds on more than a decade of research into this type of eating plan by scientists, including Krista Varady, PhD, professor of nutrition at the University of Illinois at Chicago, who presented an overview of her own studies last fall at the virtual annual meeting of the European Association for the Study of Diabetes.

Although much of the work has suggested that the shorter duration of eating period in this type of diet leads to lower calorie intake and weight loss while avoiding the need for the tedious calorie-counting of conventional diets, Dr. Weiss’s data – published last year – throws a spanner in the works and now complicates the evidence base.
 

A promise of simplicity: ‘All you have to do is watch the clock’

Dr. Varady said she, too, is intrigued by the simplicity of intermittent-fasting diets.

In 2018, Dr. Varady and colleagues tested the weight-loss efficacy of 12 weeks of time-restricted feeding in a pilot study of 23 people with obesity.

Participants were permitted an 8-hour eating window (10 a.m. to 6 p.m.) followed by water-only fasting of 16 hours (6 p.m. to 10 a.m.) the next day (sometimes referred to as the 16:8 diet). Researchers measured weight loss and fat mass, as well as metabolic parameters, and compared the active group with 23 matched-control participants who ate freely.

There were no restrictions on type or quantity of food consumed by the control group during the 8-hour period, but individuals in the time-restricted feeding group consumed around 350 calories less than the comparator group.

Dr. Varady thinks this is most likely because of the fact that people normally eat during a 14-hour window and time-restricted feeding cuts that down by 6 hours.

“One of the most beautiful things about time-restricted feeding is that it doesn’t require calorie monitoring,” she explained. “People get burnt out with having to constantly monitor calories. All you have to do is watch the clock.”

Adherence was quite high, she reported, although most people skipped 1 day, often a Saturday, likely because of social engagements.

Weight loss in the time-restricted feeding group was mild to moderate. After 3 months, mean body weight decreased by 2.6%, or approximately 3 kg (7-8 lb), relative to those who ate freely, but this was a significant difference (P  < .05).

But the researchers observed little change in metabolic disease risk factors between the groups.

In the time-restricted feeding group, systolic blood pressure dropped from 128 mm Hg to 121 mm Hg over the 12-week period, which was significant relative to the control group (P  <  .05) but there were no significant changes in fasting glucose, fasting lipids, fasting insulin, or insulin resistance relative to the comparator group.

In contrast to Dr. Varady’s findings, Dr. Weiss’s randomized TREAT trial, which used a similar 16:8 period of time-restricted versus unrestricted eating in 116 individuals with overweight or obesity, did not find greater weight loss in the group restricted to eating within the 8-hour window.

As previously reported by this news organization, those who fasted for 16 hours of each day (n = 59) did lose some weight, compared with the control group (n = 57) over 12 weeks, but the difference in weight loss between the groups was not significant (−0.26 kg; P = .63).

And there were no significant differences in any of the secondary outcomes of fat mass, fasting insulin, fasting glucose, hemoglobin A1c levels, estimated energy intake, total energy expenditure, and resting energy expenditure between the time-restricted eating and regular feeding groups.

“I don’t claim time-restricted eating is dead,” Dr. Weiss said, “but the hope that you can eat for a limited time each day and solve metabolic disease is not there.”

Does the length of the eating window matter?

Following her pilot study of an 8-hour eating window, Dr. Varady conducted further research with 4- or 6-hour eating windows to see if even shorter periods would precipitate greater weight loss, ideally a clinically significant loss of 5% of body weight.

She ran a 2-month randomized, controlled study in people with obesity, published in 2020, which was the first to examine both a 4-hour (3 p.m. to 7 p.m.; n = 19) or 6-hour (1 p.m to 7 p.m.; n = 20) eating window versus a diet without any food restrictions as a control (n = 19) (Cell Metab. 2020;32:366-78.e3).

Dr. Varady explained that they decided to shift the eating window to later in the day for this trial (in contrast to the earlier 8-hour study) to allow people to eat dinner at a sociable time, and thereby hopefully reduce dropouts from the study. 

“Unlike with alternate-day fasting, most people find time-restricted feeding easy to incorporate into their lifestyles,” she remarked.

Both the 4- and 6-hour eating window groups experienced a mean 3.2% body weight loss, compared with controls, and this correlated with a 550-calorie reduction in their daily consumption, compared with their baseline calorie intake.

In terms of other outcomes – and in contrast to the 8-hour window study which showed very little changed other than a minor decrease in blood pressure – researchers saw some changes in metabolic risk factors with the 4- and 6-hour eating windows, Dr. Varady reported.

Compared with the control group, fasting insulin decreased in both time-restricted feeding groups by a mean of 15% (P < .05). Insulin resistance also decreased by 25% in the 4-hour group and by 15% in the 6-hour group, compared with the control group. Fasting glucose did not change in either group, however.

The researchers did not observe any effect on blood pressure or plasma lipids in the 4- or 6-hour eating window groups, compared with controls. However, measures of oxidative stress and inflammation decreased in both groups versus controls by approximately 35% (P < .05).

“These findings suggest that this form of severe time-restricted feeding is achievable and can help adults with obesity lose weight, without having to count calories,” Dr. Varady and colleagues conclude.
 

Is intermittent fasting better for weight loss than calorie restriction?

Ultimately, if weight loss is the primary goal, many want to know how time-restricted feeding compares with conventional daily calorie restriction.

Back in 2017, Dr. Varady published a year-long randomized, controlled study that compared alternate-day fasting with a calorie-restriction diet and a conventional/usual diet among 100 participants with obesity who were otherwise healthy.  

Participants on the alternate-day fasting plan (n = 34) consumed 500 calories on fasting days for the first 6 months for weight loss (approximately 25% of energy needs) followed by 125% of energy needs on alternating “feast days”. For an additional 6 months, they ate 1,000 calories on fasting days – aimed at weight maintenance.

Those following the calorie-restriction diet (n = 35) reduced energy intake by 25% (approximately 500 kcal) for the first 6 months for weight loss, followed by enough calories sufficient for weight maintenance (so no further loss nor gain).

However, the study showed alternate-day fasting did not produce better weight loss than conventional calorie counting.

“Over the first 6 months [during the weight-loss period] both groups lost an average of 6% body weight. After 12 months it crept back to 5% weight loss,” reported Dr. Varady.

“Realistically, if the study continued for 2 or 3 years, they probably would have regained much of their weight,” she admitted.

Dr. Varady suspects it might be better for the alternate-day fasting participants to continue eating only 500 calories on their fast day during the weight-loss maintenance period rather than increasing calorie intake during this phase.

Heart rate and blood pressure did not change in either group, while triglycerides decreased in the alternate-day fasting group, and LDL cholesterol decreased in the calorie-restriction group.

Glucose level decreased in the calorie-restriction group but not the alternate-day fasting group, and insulin and HOMA-IR were unaffected in both groups, reported Dr. Varady, noting that these findings were in healthy people with obesity.

In people with obesity and insulin resistance – evaluated as a subgroup in a separate study by Dr. Varady of alternate-day fasting versus daily calorie restriction published in 2019 – she noted that when insulin levels and HOMA-IR were measured, there was a greater reduction in both variables in the fasting group, compared with the calorie-restriction group.

“For people at risk of diabetes, maybe fasting produces more potent effects on glycemic control?” she ventured.
 

Who fares best with which fasting diets?

Summing up, Dr. Varady provided some practical pointers regarding who she feels is best suited to intermittent fasting and who should avoid it.

Those who binge eat, shift-workers, and frequent snackers do not do well with fasting, she said.

The first 10 days of intermittent fasting are rough, she pointed out, with the most common complaint being headaches.

“Eventually, people do feel an energy boost on fast days, and they say they concentrate better and have lots of energy. People won’t feel lethargic. Also, eating protein on fast days has been shown to keep hunger at bay.”

She cautiously concluded that weight loss with “alternate-day fasting” is quicker than some other methods, at 4.5-7 kg (10-15 lb) in 3 months, but is harder to follow and requires some calorie counting.

“In comparison, with time-restricted feeding, for which there have been very few ... studies to date, weight loss is slower at 2-4.5 kg (5-10 lb) in 3 months, but it is easier to follow and tolerable because you don’t need to count calories.”

Dr. Weiss has reported no relevant financial relationships. Dr. Varady has reported receiving author fees from Hachette for her book, “Every Other Day Diet.” (New York: Hachette, 2013)

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

In an effort to counteract alarming trends in rising hepatitis infections, the U.S. Department of Health and Human Services has developed and released its Viral Hepatitis National Strategic Plan 2021-2025, which aims to eliminate viral hepatitis infection in the United States by 2030.

VashiDonsk/Wikimedia Commons/Creative Commons BY-SA 3.0

An estimated 3.3 million people in the United States were chronically infected with hepatitis B (HBV) and hepatitis C (HCV) as of 2016. In addition, the country “is currently facing unprecedented hepatitis A (HAV) outbreaks, while progress in preventing hepatitis B has stalled, and hepatitis C rates nearly tripled from 2011 to 2018,” according to the HHS.

The new plan, “A Roadmap to Elimination for the United States,” builds upon previous initiatives the HHS has made to tackle the diseases and was coordinated by the Office of the Assistant Secretary for Health through the Office of Infectious Disease and HIV/AIDS Policy.

The plan focuses on HAV, HBV, and HCV, which have the largest impact on the health of the nation, according to the HHS. The plan addresses populations with the highest burden of viral hepatitis based on nationwide data so that resources can be focused there to achieve the greatest impact. Persons who inject drugs are a priority population for all three hepatitis viruses. HAV efforts will also include a focus on the homeless population. HBV efforts will also focus on Asian and Pacific Islander and the Black, non-Hispanic populations, while HCV efforts will include a focus on Black, non-Hispanic people, people born during 1945-1965, people with HIV, and the American Indian/Alaska Native population.
 

Goal-setting

There are five main goals outlined in the plan, according to the HHS:

• Prevent new hepatitis infections.
• Improve hepatitis-related health outcomes of people with viral hepatitis.
• Reduce hepatitis-related disparities and health inequities.
• Improve hepatitis surveillance and data use.
• Achieve integrated, coordinated efforts that address the viral hepatitis epidemics among all partners and stakeholders.

“The United States will be a place where new viral hepatitis infections are prevented, every person knows their status, and every person with viral hepatitis has high-quality health care and treatment and lives free from stigma and discrimination. This vision includes all people, regardless of age, sex, gender identity, sexual orientation, race, ethnicity, religion, disability, geographic location, or socioeconomic circumstance,” according to the HHS vision statement.

mlesney@mdedge.com

In an effort to counteract alarming trends in rising hepatitis infections, the U.S. Department of Health and Human Services has developed and released its Viral Hepatitis National Strategic Plan 2021-2025, which aims to eliminate viral hepatitis infection in the United States by 2030.

VashiDonsk/Wikimedia Commons/Creative Commons BY-SA 3.0

An estimated 3.3 million people in the United States were chronically infected with hepatitis B (HBV) and hepatitis C (HCV) as of 2016. In addition, the country “is currently facing unprecedented hepatitis A (HAV) outbreaks, while progress in preventing hepatitis B has stalled, and hepatitis C rates nearly tripled from 2011 to 2018,” according to the HHS.

The new plan, “A Roadmap to Elimination for the United States,” builds upon previous initiatives the HHS has made to tackle the diseases and was coordinated by the Office of the Assistant Secretary for Health through the Office of Infectious Disease and HIV/AIDS Policy.

The plan focuses on HAV, HBV, and HCV, which have the largest impact on the health of the nation, according to the HHS. The plan addresses populations with the highest burden of viral hepatitis based on nationwide data so that resources can be focused there to achieve the greatest impact. Persons who inject drugs are a priority population for all three hepatitis viruses. HAV efforts will also include a focus on the homeless population. HBV efforts will also focus on Asian and Pacific Islander and the Black, non-Hispanic populations, while HCV efforts will include a focus on Black, non-Hispanic people, people born during 1945-1965, people with HIV, and the American Indian/Alaska Native population.
 

Goal-setting

There are five main goals outlined in the plan, according to the HHS:

• Prevent new hepatitis infections.
• Improve hepatitis-related health outcomes of people with viral hepatitis.
• Reduce hepatitis-related disparities and health inequities.
• Improve hepatitis surveillance and data use.
• Achieve integrated, coordinated efforts that address the viral hepatitis epidemics among all partners and stakeholders.

“The United States will be a place where new viral hepatitis infections are prevented, every person knows their status, and every person with viral hepatitis has high-quality health care and treatment and lives free from stigma and discrimination. This vision includes all people, regardless of age, sex, gender identity, sexual orientation, race, ethnicity, religion, disability, geographic location, or socioeconomic circumstance,” according to the HHS vision statement.

mlesney@mdedge.com

In an effort to counteract alarming trends in rising hepatitis infections, the U.S. Department of Health and Human Services has developed and released its Viral Hepatitis National Strategic Plan 2021-2025, which aims to eliminate viral hepatitis infection in the United States by 2030.

VashiDonsk/Wikimedia Commons/Creative Commons BY-SA 3.0

An estimated 3.3 million people in the United States were chronically infected with hepatitis B (HBV) and hepatitis C (HCV) as of 2016. In addition, the country “is currently facing unprecedented hepatitis A (HAV) outbreaks, while progress in preventing hepatitis B has stalled, and hepatitis C rates nearly tripled from 2011 to 2018,” according to the HHS.

The new plan, “A Roadmap to Elimination for the United States,” builds upon previous initiatives the HHS has made to tackle the diseases and was coordinated by the Office of the Assistant Secretary for Health through the Office of Infectious Disease and HIV/AIDS Policy.

The plan focuses on HAV, HBV, and HCV, which have the largest impact on the health of the nation, according to the HHS. The plan addresses populations with the highest burden of viral hepatitis based on nationwide data so that resources can be focused there to achieve the greatest impact. Persons who inject drugs are a priority population for all three hepatitis viruses. HAV efforts will also include a focus on the homeless population. HBV efforts will also focus on Asian and Pacific Islander and the Black, non-Hispanic populations, while HCV efforts will include a focus on Black, non-Hispanic people, people born during 1945-1965, people with HIV, and the American Indian/Alaska Native population.
 

Goal-setting

There are five main goals outlined in the plan, according to the HHS:

• Prevent new hepatitis infections.
• Improve hepatitis-related health outcomes of people with viral hepatitis.
• Reduce hepatitis-related disparities and health inequities.
• Improve hepatitis surveillance and data use.
• Achieve integrated, coordinated efforts that address the viral hepatitis epidemics among all partners and stakeholders.

“The United States will be a place where new viral hepatitis infections are prevented, every person knows their status, and every person with viral hepatitis has high-quality health care and treatment and lives free from stigma and discrimination. This vision includes all people, regardless of age, sex, gender identity, sexual orientation, race, ethnicity, religion, disability, geographic location, or socioeconomic circumstance,” according to the HHS vision statement.

mlesney@mdedge.com

Infection with the SARS-CoV-2 virus may provide some immunity for at least 5 months, interim results from a study has found.

The first report from the Sarscov2 Immunity & Reinfection Evaluation (SIREN) study suggested that antibodies from people who had recovered from COVID-19 gave at least 83% protection against reinfection compared with people who had not had the disease before.

However, Public Health England (PHE) researchers said some people with antibodies may still be able to carry and transmit the SARS-CoV-2 virus.

‘Strongly encouraged’

Susan Hopkins, PhD, senior medical advisor at PHE, who is leading the study, said the overall findings were good news. She told a briefing hosted by the Science Media Centre: “I am strongly encouraged that people have immunity that is lasting much more than the few months that was speculated before the summer.”

She added: “It allows people to feel that their prior infection will protect them from future infections but at the same time it is not complete protection, and therefore they still need to be careful when they are out and about.”

PHE scientists said they would continue to assess whether protection might last longer than 5 months.

Eleanor Riley, PhD, professor of immunology and infectious disease at the University of Edinburgh, said the report suggested that “natural infection provides short-term protection against COVID-19 that is very similar to that conferred by vaccination.”

Simon Clarke, PhD, associate professor in cellular microbiology at the University of Reading, said: “The concerning finding is that some people who have COVID antibodies appear to still be able to carry the coronavirus and could spread it to others. This means that the vast majority of the population will either need to have natural immunity or have been immunised for us to fully lift restrictions on our lives.”

The analysis took place before the new variant of SARS-CoV-2 became widespread in the UK. The PHE scientists said that further work was underway to establish whether and to what extent antibodies also provide protection from the VOC202012/01 variant.

Healthcare Workers

The SIREN preprint analysed data from 20,787 health care workers from 102 NHS trusts who had undergone antibody and PCR testing from June 18 to November 9, 2020.

Of those, 6614 tested positive for COVID-19 antibodies.

Of the 44 potential reinfections identified, two were designated ‘probable’ and 42 ‘possible’, based on available evidence.

Both of the two individuals classified as probable reinfections reported having experienced COVID-19 symptoms during the first wave of the pandemic but were not tested at the time. Both reported that their symptoms were less severe the second time.

None of the 44 potential reinfection cases were PCR tested during the first wave, but all tested positive for COVID-19 antibodies at the time they were recruited to the study.

Tom Wingfield, PhD, senior clinical lecturer at the Liverpool School of Tropical Medicine, said that given the high risk of SARS-CoV-2 infection for frontline NHS staff, it was “vital that we do all that we can to understand, predict, and prevent risk of SARS-CoV-2 amongst healthcare workers”.

The study will continue to follow participants for 12 months to explore how long any immunity may last, the effectiveness of vaccines, and to what extent people with immunity are able to carry and transmit the virus.

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

Infection with the SARS-CoV-2 virus may provide some immunity for at least 5 months, interim results from a study has found.

The first report from the Sarscov2 Immunity & Reinfection Evaluation (SIREN) study suggested that antibodies from people who had recovered from COVID-19 gave at least 83% protection against reinfection compared with people who had not had the disease before.

However, Public Health England (PHE) researchers said some people with antibodies may still be able to carry and transmit the SARS-CoV-2 virus.

‘Strongly encouraged’

Susan Hopkins, PhD, senior medical advisor at PHE, who is leading the study, said the overall findings were good news. She told a briefing hosted by the Science Media Centre: “I am strongly encouraged that people have immunity that is lasting much more than the few months that was speculated before the summer.”

She added: “It allows people to feel that their prior infection will protect them from future infections but at the same time it is not complete protection, and therefore they still need to be careful when they are out and about.”

PHE scientists said they would continue to assess whether protection might last longer than 5 months.

Eleanor Riley, PhD, professor of immunology and infectious disease at the University of Edinburgh, said the report suggested that “natural infection provides short-term protection against COVID-19 that is very similar to that conferred by vaccination.”

Simon Clarke, PhD, associate professor in cellular microbiology at the University of Reading, said: “The concerning finding is that some people who have COVID antibodies appear to still be able to carry the coronavirus and could spread it to others. This means that the vast majority of the population will either need to have natural immunity or have been immunised for us to fully lift restrictions on our lives.”

The analysis took place before the new variant of SARS-CoV-2 became widespread in the UK. The PHE scientists said that further work was underway to establish whether and to what extent antibodies also provide protection from the VOC202012/01 variant.

Healthcare Workers

The SIREN preprint analysed data from 20,787 health care workers from 102 NHS trusts who had undergone antibody and PCR testing from June 18 to November 9, 2020.

Of those, 6614 tested positive for COVID-19 antibodies.

Of the 44 potential reinfections identified, two were designated ‘probable’ and 42 ‘possible’, based on available evidence.

Both of the two individuals classified as probable reinfections reported having experienced COVID-19 symptoms during the first wave of the pandemic but were not tested at the time. Both reported that their symptoms were less severe the second time.

None of the 44 potential reinfection cases were PCR tested during the first wave, but all tested positive for COVID-19 antibodies at the time they were recruited to the study.

Tom Wingfield, PhD, senior clinical lecturer at the Liverpool School of Tropical Medicine, said that given the high risk of SARS-CoV-2 infection for frontline NHS staff, it was “vital that we do all that we can to understand, predict, and prevent risk of SARS-CoV-2 amongst healthcare workers”.

The study will continue to follow participants for 12 months to explore how long any immunity may last, the effectiveness of vaccines, and to what extent people with immunity are able to carry and transmit the virus.

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

Infection with the SARS-CoV-2 virus may provide some immunity for at least 5 months, interim results from a study has found.

The first report from the Sarscov2 Immunity & Reinfection Evaluation (SIREN) study suggested that antibodies from people who had recovered from COVID-19 gave at least 83% protection against reinfection compared with people who had not had the disease before.

However, Public Health England (PHE) researchers said some people with antibodies may still be able to carry and transmit the SARS-CoV-2 virus.

‘Strongly encouraged’

Susan Hopkins, PhD, senior medical advisor at PHE, who is leading the study, said the overall findings were good news. She told a briefing hosted by the Science Media Centre: “I am strongly encouraged that people have immunity that is lasting much more than the few months that was speculated before the summer.”

She added: “It allows people to feel that their prior infection will protect them from future infections but at the same time it is not complete protection, and therefore they still need to be careful when they are out and about.”

PHE scientists said they would continue to assess whether protection might last longer than 5 months.

Eleanor Riley, PhD, professor of immunology and infectious disease at the University of Edinburgh, said the report suggested that “natural infection provides short-term protection against COVID-19 that is very similar to that conferred by vaccination.”

Simon Clarke, PhD, associate professor in cellular microbiology at the University of Reading, said: “The concerning finding is that some people who have COVID antibodies appear to still be able to carry the coronavirus and could spread it to others. This means that the vast majority of the population will either need to have natural immunity or have been immunised for us to fully lift restrictions on our lives.”

The analysis took place before the new variant of SARS-CoV-2 became widespread in the UK. The PHE scientists said that further work was underway to establish whether and to what extent antibodies also provide protection from the VOC202012/01 variant.

Healthcare Workers

The SIREN preprint analysed data from 20,787 health care workers from 102 NHS trusts who had undergone antibody and PCR testing from June 18 to November 9, 2020.

Of those, 6614 tested positive for COVID-19 antibodies.

Of the 44 potential reinfections identified, two were designated ‘probable’ and 42 ‘possible’, based on available evidence.

Both of the two individuals classified as probable reinfections reported having experienced COVID-19 symptoms during the first wave of the pandemic but were not tested at the time. Both reported that their symptoms were less severe the second time.

None of the 44 potential reinfection cases were PCR tested during the first wave, but all tested positive for COVID-19 antibodies at the time they were recruited to the study.

Tom Wingfield, PhD, senior clinical lecturer at the Liverpool School of Tropical Medicine, said that given the high risk of SARS-CoV-2 infection for frontline NHS staff, it was “vital that we do all that we can to understand, predict, and prevent risk of SARS-CoV-2 amongst healthcare workers”.

The study will continue to follow participants for 12 months to explore how long any immunity may last, the effectiveness of vaccines, and to what extent people with immunity are able to carry and transmit the virus.

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

Last fall, health experts said it was possible the United States could experience an easy 2020-21 flu season because health measures to fight COVID-19 would also thwart the spread of influenza.

It looks like that happened – and then some. Numbers are strikingly low for cases of the flu and other common respiratory and gastrointestinal viruses, health experts told the Washington Post.

“It’s crazy,” Lynnette Brammer, MPH, who leads the domestic influenza surveillance team at the Centers for Disease Control and Prevention, told the Washington Post. “This is my 30th flu season. I never would have expected to see flu activity this low.”

Influenza A, influenza B, parainfluenza, norovirus, respiratory syncytial virus, human metapneumovirus, and the bacteria that cause whooping cough and pneumonia are circulating at near-record-low levels.

As an example, the Washington Post said in the third week of December 2019, the CDC’s network of clinical labs reported 16.2% of almost 30,000 samples tested positive for influenza A. During the same period in 2020, only 0.3% tested positive.

But there’s a possible downside to this suppression of viruses, because flu and other viruses may rebound once the coronavirus is brought under control.

“The best analogy is to a forest fire,” Bryan Grenfell, PhD, an epidemiologist and population biologist at Princeton (N.J.) University, told the Washington Post. “For the fire to spread, it needs to have unburned wood. For epidemics to spread, they require people who haven’t previously been infected. So if people don’t get infected this year by these viruses, they likely will at some point later on.”

American health experts like Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Disease, said last fall that they noticed Australia and other nations in the southern hemisphere had easy flu seasons, apparently because of COVID protection measures. The flu season there runs March through August.

COVID-19 now has a very low presence in Australia, but in recent months the flu has been making a comeback. Flu cases among children aged 5 and younger rose sixfold by December, when such cases are usually at their lowest, the Washington Post said.

“That’s an important cautionary tale for us,” said Kevin Messacar, MD, an infectious disease doctor at Children’s Hospital Colorado, Aurora. “Just because we get through the winter and don’t see much RSV or influenza doesn’t mean we’ll be out of the woods.”

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

Last fall, health experts said it was possible the United States could experience an easy 2020-21 flu season because health measures to fight COVID-19 would also thwart the spread of influenza.

It looks like that happened – and then some. Numbers are strikingly low for cases of the flu and other common respiratory and gastrointestinal viruses, health experts told the Washington Post.

“It’s crazy,” Lynnette Brammer, MPH, who leads the domestic influenza surveillance team at the Centers for Disease Control and Prevention, told the Washington Post. “This is my 30th flu season. I never would have expected to see flu activity this low.”

Influenza A, influenza B, parainfluenza, norovirus, respiratory syncytial virus, human metapneumovirus, and the bacteria that cause whooping cough and pneumonia are circulating at near-record-low levels.

As an example, the Washington Post said in the third week of December 2019, the CDC’s network of clinical labs reported 16.2% of almost 30,000 samples tested positive for influenza A. During the same period in 2020, only 0.3% tested positive.

But there’s a possible downside to this suppression of viruses, because flu and other viruses may rebound once the coronavirus is brought under control.

“The best analogy is to a forest fire,” Bryan Grenfell, PhD, an epidemiologist and population biologist at Princeton (N.J.) University, told the Washington Post. “For the fire to spread, it needs to have unburned wood. For epidemics to spread, they require people who haven’t previously been infected. So if people don’t get infected this year by these viruses, they likely will at some point later on.”

American health experts like Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Disease, said last fall that they noticed Australia and other nations in the southern hemisphere had easy flu seasons, apparently because of COVID protection measures. The flu season there runs March through August.

COVID-19 now has a very low presence in Australia, but in recent months the flu has been making a comeback. Flu cases among children aged 5 and younger rose sixfold by December, when such cases are usually at their lowest, the Washington Post said.

“That’s an important cautionary tale for us,” said Kevin Messacar, MD, an infectious disease doctor at Children’s Hospital Colorado, Aurora. “Just because we get through the winter and don’t see much RSV or influenza doesn’t mean we’ll be out of the woods.”

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

Last fall, health experts said it was possible the United States could experience an easy 2020-21 flu season because health measures to fight COVID-19 would also thwart the spread of influenza.

It looks like that happened – and then some. Numbers are strikingly low for cases of the flu and other common respiratory and gastrointestinal viruses, health experts told the Washington Post.

“It’s crazy,” Lynnette Brammer, MPH, who leads the domestic influenza surveillance team at the Centers for Disease Control and Prevention, told the Washington Post. “This is my 30th flu season. I never would have expected to see flu activity this low.”

Influenza A, influenza B, parainfluenza, norovirus, respiratory syncytial virus, human metapneumovirus, and the bacteria that cause whooping cough and pneumonia are circulating at near-record-low levels.

As an example, the Washington Post said in the third week of December 2019, the CDC’s network of clinical labs reported 16.2% of almost 30,000 samples tested positive for influenza A. During the same period in 2020, only 0.3% tested positive.

But there’s a possible downside to this suppression of viruses, because flu and other viruses may rebound once the coronavirus is brought under control.

“The best analogy is to a forest fire,” Bryan Grenfell, PhD, an epidemiologist and population biologist at Princeton (N.J.) University, told the Washington Post. “For the fire to spread, it needs to have unburned wood. For epidemics to spread, they require people who haven’t previously been infected. So if people don’t get infected this year by these viruses, they likely will at some point later on.”

American health experts like Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Disease, said last fall that they noticed Australia and other nations in the southern hemisphere had easy flu seasons, apparently because of COVID protection measures. The flu season there runs March through August.

COVID-19 now has a very low presence in Australia, but in recent months the flu has been making a comeback. Flu cases among children aged 5 and younger rose sixfold by December, when such cases are usually at their lowest, the Washington Post said.

“That’s an important cautionary tale for us,” said Kevin Messacar, MD, an infectious disease doctor at Children’s Hospital Colorado, Aurora. “Just because we get through the winter and don’t see much RSV or influenza doesn’t mean we’ll be out of the woods.”

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

The Endocrine Society has issued a new position statement calling on all stakeholders, including clinicians, to play a role in reducing the cost of insulin for patients with diabetes in the United States.

“Addressing Insulin Access and Affordability: An Endocrine Society Position Statement,” was published online Jan. 12 in the Journal of Clinical Endocrinology and Metabolism.

“The society believes all stakeholders across the supply chain have a role to play in addressing the high price of insulin,” said the 11 authors, who are all members of the society’s advocacy and public outreach core committee.  

This is the first such statement from a major professional organization in 2021, which is the 100th anniversary of the discovery of insulin.

And the call for action was issued just a week prior to the inauguration of incoming U.S. President Joe Biden, who has pledged to “build on the Affordable Care Act by giving Americans more choice, reducing health care costs, and making our health care system less complex to navigate.”

The cost of insulin has nearly tripled in the past 15 years in the United States, and a lack of transparency in the drug supply chain has made it challenging to identify and address the causes of soaring costs.

The high cost of insulin has made access particularly difficult for people with diabetes with a low income, who have high-deductible health plans, are Medicare beneficiaries using Part B to cover insulin delivered via pump, or are in the Medicare Part D “donut hole,” as well as young adults once they reach their 26th birthday and can no longer be covered under their parents’ insurance.

“Inventors Frederick Banting and Charles Best sold the insulin patent for a mere $1 in the 1920s because they wanted their discovery to save lives and for insulin to be affordable and accessible to everyone who needed it,” said Endocrine Society President-elect Carol Wysham, MD, of the Rockwood/MultiCare Health Systems, Spokane, Wash.

“People with diabetes without full insurance are often paying increasing out-of-pocket costs for insulin resulting in many rationing their medication or skipping lifesaving doses altogether,” she said.

The society’s statement called for allowing government negotiation of drug prices and greater transparency across the supply chain to elucidate the reasons for rising insulin costs.  

For physicians in particular, they advised training in use of lower-cost human NPH and regular insulin for appropriate patients with type 2 diabetes, and considering patients’ individual financial and coverage status when prescribing insulin.

Pharmacists are advised to learn about and share information with patients about lower-cost options offered by manufacturers.

Other policy recommendations for relevant stakeholders include:

• Limit future insulin list price increases to the rate of inflation.
• Limit out-of-pocket costs without increasing premiums or deductibles by limiting cost sharing to copays of no more than $35, providing first-dollar coverage, or capping costs at no more than $100 per month.
• Eliminate rebates or pass savings from rebates along to consumers without increasing premiums or deductibles.
• Expedite approval of insulin biosimilars to create market competition.
• Include real-time benefit information in electronic medical records.
• Develop a payment model for Medicare Part B beneficiaries, as well as Part D, to lower out-of-pocket copays.

For manufacturers, the society also recommended improving patient assistance programs to be less restrictive and more accountable. And employers, they said, should limit copays without increasing premiums or deductibles, and seek plan options that benefit people with diabetes and provide education about these options during open enrollment.   

Of the 11 writing panel members, 4 have pharmaceutical industry disclosures.

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

The Endocrine Society has issued a new position statement calling on all stakeholders, including clinicians, to play a role in reducing the cost of insulin for patients with diabetes in the United States.

“Addressing Insulin Access and Affordability: An Endocrine Society Position Statement,” was published online Jan. 12 in the Journal of Clinical Endocrinology and Metabolism.

“The society believes all stakeholders across the supply chain have a role to play in addressing the high price of insulin,” said the 11 authors, who are all members of the society’s advocacy and public outreach core committee.  

This is the first such statement from a major professional organization in 2021, which is the 100th anniversary of the discovery of insulin.

And the call for action was issued just a week prior to the inauguration of incoming U.S. President Joe Biden, who has pledged to “build on the Affordable Care Act by giving Americans more choice, reducing health care costs, and making our health care system less complex to navigate.”

The cost of insulin has nearly tripled in the past 15 years in the United States, and a lack of transparency in the drug supply chain has made it challenging to identify and address the causes of soaring costs.

The high cost of insulin has made access particularly difficult for people with diabetes with a low income, who have high-deductible health plans, are Medicare beneficiaries using Part B to cover insulin delivered via pump, or are in the Medicare Part D “donut hole,” as well as young adults once they reach their 26th birthday and can no longer be covered under their parents’ insurance.

“Inventors Frederick Banting and Charles Best sold the insulin patent for a mere $1 in the 1920s because they wanted their discovery to save lives and for insulin to be affordable and accessible to everyone who needed it,” said Endocrine Society President-elect Carol Wysham, MD, of the Rockwood/MultiCare Health Systems, Spokane, Wash.

“People with diabetes without full insurance are often paying increasing out-of-pocket costs for insulin resulting in many rationing their medication or skipping lifesaving doses altogether,” she said.

The society’s statement called for allowing government negotiation of drug prices and greater transparency across the supply chain to elucidate the reasons for rising insulin costs.  

For physicians in particular, they advised training in use of lower-cost human NPH and regular insulin for appropriate patients with type 2 diabetes, and considering patients’ individual financial and coverage status when prescribing insulin.

Pharmacists are advised to learn about and share information with patients about lower-cost options offered by manufacturers.

Other policy recommendations for relevant stakeholders include:

• Limit future insulin list price increases to the rate of inflation.
• Limit out-of-pocket costs without increasing premiums or deductibles by limiting cost sharing to copays of no more than $35, providing first-dollar coverage, or capping costs at no more than $100 per month.
• Eliminate rebates or pass savings from rebates along to consumers without increasing premiums or deductibles.
• Expedite approval of insulin biosimilars to create market competition.
• Include real-time benefit information in electronic medical records.
• Develop a payment model for Medicare Part B beneficiaries, as well as Part D, to lower out-of-pocket copays.

For manufacturers, the society also recommended improving patient assistance programs to be less restrictive and more accountable. And employers, they said, should limit copays without increasing premiums or deductibles, and seek plan options that benefit people with diabetes and provide education about these options during open enrollment.   

Of the 11 writing panel members, 4 have pharmaceutical industry disclosures.

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

The Endocrine Society has issued a new position statement calling on all stakeholders, including clinicians, to play a role in reducing the cost of insulin for patients with diabetes in the United States.

“Addressing Insulin Access and Affordability: An Endocrine Society Position Statement,” was published online Jan. 12 in the Journal of Clinical Endocrinology and Metabolism.

“The society believes all stakeholders across the supply chain have a role to play in addressing the high price of insulin,” said the 11 authors, who are all members of the society’s advocacy and public outreach core committee.  

This is the first such statement from a major professional organization in 2021, which is the 100th anniversary of the discovery of insulin.

And the call for action was issued just a week prior to the inauguration of incoming U.S. President Joe Biden, who has pledged to “build on the Affordable Care Act by giving Americans more choice, reducing health care costs, and making our health care system less complex to navigate.”

The cost of insulin has nearly tripled in the past 15 years in the United States, and a lack of transparency in the drug supply chain has made it challenging to identify and address the causes of soaring costs.

The high cost of insulin has made access particularly difficult for people with diabetes with a low income, who have high-deductible health plans, are Medicare beneficiaries using Part B to cover insulin delivered via pump, or are in the Medicare Part D “donut hole,” as well as young adults once they reach their 26th birthday and can no longer be covered under their parents’ insurance.

“Inventors Frederick Banting and Charles Best sold the insulin patent for a mere $1 in the 1920s because they wanted their discovery to save lives and for insulin to be affordable and accessible to everyone who needed it,” said Endocrine Society President-elect Carol Wysham, MD, of the Rockwood/MultiCare Health Systems, Spokane, Wash.

“People with diabetes without full insurance are often paying increasing out-of-pocket costs for insulin resulting in many rationing their medication or skipping lifesaving doses altogether,” she said.

The society’s statement called for allowing government negotiation of drug prices and greater transparency across the supply chain to elucidate the reasons for rising insulin costs.  

For physicians in particular, they advised training in use of lower-cost human NPH and regular insulin for appropriate patients with type 2 diabetes, and considering patients’ individual financial and coverage status when prescribing insulin.

Pharmacists are advised to learn about and share information with patients about lower-cost options offered by manufacturers.

Other policy recommendations for relevant stakeholders include:

• Limit future insulin list price increases to the rate of inflation.
• Limit out-of-pocket costs without increasing premiums or deductibles by limiting cost sharing to copays of no more than $35, providing first-dollar coverage, or capping costs at no more than $100 per month.
• Eliminate rebates or pass savings from rebates along to consumers without increasing premiums or deductibles.
• Expedite approval of insulin biosimilars to create market competition.
• Include real-time benefit information in electronic medical records.
• Develop a payment model for Medicare Part B beneficiaries, as well as Part D, to lower out-of-pocket copays.

For manufacturers, the society also recommended improving patient assistance programs to be less restrictive and more accountable. And employers, they said, should limit copays without increasing premiums or deductibles, and seek plan options that benefit people with diabetes and provide education about these options during open enrollment.   

Of the 11 writing panel members, 4 have pharmaceutical industry disclosures.

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

Stephanie Florez-Pollack, MD, a dermatology resident at the University of Pennsylvania, Philadelphia, began considering the field of dermatology when, as part of the Latino Medical Students Association, she was invited by Amit Pandya, MD, to a pizza party and dermatology discussion during her first year of medical school at the University of Texas Southwestern Medical Center, Dallas.

Courtesy Dr. Stephanie Flores-Pollack

There, she met three Latinx residents who were part of the University of Texas Southwestern dermatology program. “I was so excited to hear their stories, where they came from, and how they ended up in dermatology,” she said. Dermatology had not been on her radar screen. Now there was a spark.

Volunteering at the free Agape dermatology clinic in Dallas later that year sharpened her interest. “For the first time, I really saw myself working in the field. Hearing patients’ stories and what they went through with what many people might think are very simple skin diseases made me realize there was potential to make a big impact in a person’s life,” said Dr. Florez-Pollack, who immigrated from Colombia with her family when she was 15.

Dr. Florez-Pollack’s journey into dermatology as an underrepresented-in-medicine (UIM) physician-in-training offers a window into a movement underway that aims to create a diverse dermatology workforce – one that reflects the ethnic and racial make-up of the population. It’s a movement that involves early outreach to medical students, stepped-up mentorship and sponsorship, implicit bias training, and holistic review of residency applicants.

There is no published study of all the changes being made – of how many dermatology programs have new outreach programs, for instance, or new approaches to resident application reviews. However, participation in the American Academy of Dermatology Diversity Champions program increased significantly between 2019 and 2020, and a sizable body of articles and editorials on diversity have been published in the dermatology literature in recent years, including at least several on holistic review of resident applications. Five years ago, there were few publications, sources said.

“The conversation is happening now at multiple levels, including in our peer-reviewed literature, where people are looking objectively at ... how we can make changes for the better,” said Nada Elbuluk, MD, director of the dermatology diversity and inclusion program at the University of Southern California, Los Angeles.

Unpublished findings also indicate that the number of UIM dermatology residents is inching upward. “Residency selection may not be on everyone’s mind, but an understanding of how we select people into our specialty is something every derm should know about and care about,” said Kanade Shinkai, MD, PhD, professor of dermatology at the University of California, San Francisco, and editor in chief of JAMA Dermatology.
 

The wake-up calls

The impetus for current changes first came in 2015, when Bruce Wintroub, MD, professor and chair of dermatology at UCSF, and interim dean of the medical school at the time, delivered a passionate plenary lecture at the annual AAD meeting about the lack of equity, diversity and inclusion in the specialty and the role of unconscious bias. Moved in part by a “White Coats for Black Lives” die-in by medical students on his campus following the killing of unarmed Black men, Dr. Wintroub called on his colleagues to recruit more UIM physicians into the specialty and to make the field more inclusive.

In 2016, Dr. Wintroub joined Dr. Pandya and two other academic dermatologists in authoring a commentary, published in the Journal of the American Academy of Dermatology, about the need to step up efforts and make diversity a priority. Dermatology was among the least ethnically and racially diverse specialties, second only to orthopedics, they wrote, with black dermatologists making up only 3% of all dermatologists and Hispanics only 4.2% in the United States, compared with 12.8% and 16.3% in the U.S. population, respectively.

For the next year or so, they and others from six academic institutions formed an incubator of sorts, actively tracking and sharing actions they were taking to improve diversity and the practice environment. “We wanted to learn from each other, then disseminate information to other programs,” said Dr. Pandya, who chaired the AAD diversity task force and led the self-branded “diversity champions.” (Dr. Pandya maintains his appointment at UTSW but now practices at the Palo Alto Foundation Medical Group in Sunnyvale, Calif.)

In 2017, at a President’s Conference on Diversity in Dermatology called for by then-AAD president Henry Lim, MD, leaders of the Association of Professors of Dermatology, the Society for Investigative Dermatology, and other dermatology organizations agreed on key action items, which they described in JAAD in 2018: Helping to increase the pipeline of UIM students applying to medical school, increasing UIM medical students’ early exposure to dermatology, and increasing the number of UIM students recruited into dermatology residency programs.

Diversity in the physician workforce has been shown to improve outcomes for all patients, and is important for ameliorating health care disparities and improving satisfaction and care for all patients, the authors of the 2018 paper wrote. “Multiple studies,” they noted, “have shown that UIM physicians are more likely to practice in areas where health care disparities exist.”

For specific proposed actions, the leaders attending the diversity conference drew largely upon the “diversity champions’” experiences, and agreed to fund and officially develop a diversity champions program. They also decided to invest in “bioskills” workshops for undergraduates and medical students at historically black colleges and universities, and other institutions at historically black colleges and universities at medical schools through a partnership with Nth Dimension – an organization founded in 2004 to bring more women and underrepresented minorities into orthopedic surgery.

In the last 2 years, more than 450 UIM students have attended these bioskills workshops, getting a taste of basic dermatology procedures and interacting with dermatologists.

And in September 2020, 157 dermatologists representing 80 programs throughout the country attended the second AAD Diversity Champions conference, up from 84 attendees and 30 programs in 2019. On the agenda: Discussions of holistic application review, mentorship, recruitment of UIM faculty, and a 2-hour session on microaggressions. Similar programs are being led by other dermatology organizations.

(UIM was coined by the American Association of Medical Colleges to describe racial and ethnic populations that are underrepresented in medicine relative to their numbers in the general population.)

Achievement of racial/ethnic diversity “won’t happen unless the field actively encourages people to look at it – which is not what we were doing,” Dr. Wintroub said in an interview. “I think that’s been the major change. We’re opening the door and saying: ‘We want you and we welcome you.’ ”


 

Rethinking traditional mentorship

For Dr. Florez-Pollack, the door almost shut when she began to hear from fellow medical students that dermatology is “too competitive ... a field for only the top people in the class.” She felt doubt settling in.

“I had peers who were throwing a lot of money toward prep materials ... peers who had siblings in medicine and had started studying from day one [for the step 1 exam],” she said. “I thought, was it really worth the effort? Do I really want to be perfect to get into the field when other fields would be happy to have me as I am right now?”

Her immense enjoyment of an “Art of Observation” elective course helped renew her interest in the field; it reinforced her visual abilities as well as the potential for her to address implicit bias as a dermatologist. She sought Dr. Pandya’s guidance and sponsorship to help her grow connections, polish her resume, and present herself to other faculty.

Doors were opened, she said, for her to secure a 1-year research experience before her final year of medical school with UTSW faculty, and then a 1-month rotation/mentorship with William D. James, MD, professor of dermatology at the University of Pennsylvania, an institution with a history of diversity initiatives and a longstanding skin of color program.

Dr. Florez-Pollack sees her experience reflected in the findings of a recently published study – a thematic content analysis of telephone interviews with applicants to the UTSW dermatology residency program during the 2013-14 and 2014-15 application cycles. Of the 44 applicants who participated in the study, 13 were UIM applicants.

Six of the seven UIM applicants who matched were involved in a pipeline or enrichment program – and were exposed to the field early – compared with one or two of the six UIM applicants who did not match. Underrepresented applicants were more often discouraged from applying (54%) – told, for instance, that they could better serve their communities through other specialties – than were non-UIM applicants (13%). They also were affected more often by a lack of equitable resources, according to comments made by 70% of applicants (UIM and non-UIM).

Also notably, the investigators said, all of the UIM applicants who matched (and the majority of non-UIMs who matched) reported having a mentor during the process of applying, compared with 44% of those who didn’t match.

Rebecca Vasquez, MD, assistant professor of dermatology at UTSW, who led the study, was herself a mentee of Dr. Pandya. “He believed in me and gave me the courage to consider dermatology,” she said. (Dr. Vasquez was one of the Latinx women who inspired Dr. Florez-Pollack, in turn, when they met at Dr. Pandya’s pizza party. Dr. Florez-Pollack assisted with the research and was a coauthor of the study.)

Amy McMichael, MD, professor and chair of dermatology at Wake Forest University, Winston-Salem, N.C., said that dermatology as a field has traditionally been “very good at mentoring.” Many of the dermatology societies have long had mentorship programs, for instance, that guide medical students, and sometimes residents, through defined experiences or through periods of time.

But she advocates going deeper. “When it comes to sponsorship, we fall a little short,” she said. “Sponsorship is about promoting that person to the next level, making sure they achieve what they want to achieve ... putting them up for opportunities they may not have known existed. It’s continuous and focused.”

Dr. Olabola Awosika

Olabola Awosika, MD, a fourth-year dermatology resident at Henry Ford Health System, Detroit, said her interest in dermatology was solidified during her participation in the AAD’s month-long mentorship program after her second year of medical school at Howard University, Washington. However, it wasn’t until her fourth year, when she did an away rotation at Wake Forest, that she realized that “gaining access to the field” takes years of mentorship, research opportunities, and networking. It was too late.

After initially not matching, she did a rotation at Johns Hopkins in dermatology during an internship year, followed by a 2-year research fellowship at George Washington University, Washington. As does Dr. Florez-Pollack, who now mentors medical students. She also serves on the Women’s Dermatologic Society diversity committee, which is now developing initiatives to help UIM dermatologists “become upwardly mobile in dermatology [after residency], so they have a seat at the table in various settings.”
 

Holistic review for residency

Dr. Vasquez, who grew up in South Texas in an uninsured family that received most of its medical care across the border in Mexico, believes that the “biggest stride being made today” with respect to diversity in the dermatology workforce – and in the larger physician workforce – is increased understanding of the role of social and cultural capital.

Dr. Vasquez?

“We’d never really talked about this concept ... about how, if you don’t have the same upbringing, education, and resources, you’re already behind … and you may not do as well on standardized tests,” she said. “Now people are listening to it and understand it. That’s why more programs are looking at how to practice a more holistic approach to selecting applicants to interview.”

Some dermatology programs – at Wake Forest, UCSF, USC, Vanderbilt, and George Washington University for instance – have eliminated the use of U.S. Medical Licensing Examination step 1 scores and Alpha Omega Alpha Medical Honor Society status as filtering/screening metrics. Some also take a “second look” at UIM applicants.

Overall, those making changes are looking “at everything the applicant brings to the table – their story, their experiences,” said Dr. Elbuluk. “We want to understand the full picture of who they are and their journey to becoming a physician.”

Implicit bias training for members of residency review committees is becoming more common, as is such training across the board in dermatology departments. “We have to bring it to the forefront so that we can create more inclusive environments,” said Sharon E. Albers, MD, a dermatologist at Vanderbilt University Medical Center, Nashville, Tenn., who serves as the dermatology department’s diversity liaison to the medical school, and who, as a former faculty member of Meharry Medical College, remains engaged with the historically black institution.

One of her recent efforts, inspired by participation in the diversity champions program, has been developing pipeline programs to speak to middle and high school students about medicine and dermatology. For now, however, she credits a holistic review process for change. Last year, three of the five matched dermatology residents at Vanderbilt were UIM physicians – unprecedented for the institution, Dr. Albers said, and “evidence that holistic review works if you’re very intentional about it.”

Dr. Vasquez?

Dr. Vasquez has analyzed data from the Accreditation Council of Graduate Medical Education and says that UIM dermatology residents comprised 8.0% of the total in 2019, marking an improvement over the prior 7 years. “We’ve introduced so many changes at the same time,” making it difficult to discern what’s most impactful, she said. “But something is working.”

(The AAMC, which has invested in pipeline programs for more than a decade and has championed holistic medical school admissions, states in its 2019 diversity data report that efforts to improve diversity in medicine have made “only marginal differences” – and that Black males in particular continue to be significantly underrepresented in medical schools. Persistent, structural racism was a common theme in the association’s 2015 report on Black males in medicine.)

Efforts to diversify the workforce – particularly holistic review – haven’t been without detractors. “It brings reaction,” Dr. Wintroub said. “Some people think you’re lowering quality in the field ... but that’s just not true.”

Diversity in the dermatology workforce is important not only for the care of patients from diverse backgrounds, but “perhaps more importantly, it brings new ideas and views and experiences into the field,” he said. “It pushes us to think in new directions ... that can only make our field better and richer.”

“We need to make sure our workforce is representative of the patients we serve – but also that all derms can manage patients of all skin types and demographics,” Dr. Shinkai said. “And we need more diversity in the leadership of our departments and dermatology organizations ... inclusivity needs to extend all the way to the highest reaches of our specialty.”

Adam Friedman, MD, professor and interim chair of dermatology at George Washington University and director of the department’s diversity, equity, and inclusion committee, agreed. “We need to both make sure our workforce mirrors the patients we serve, and said workforce is prepared to manage patients of all skin types and demographics. We need to cover the spectrum, from revamping medical education and mentorship opportunities to advancing diversity in the leadership of our departments, institutions, and societies. Addressing only part of the puzzle will not and can not be enough.”

Correction, 3/3/21: An earlier version of this article misstated Dr. Stephanie Florez-Pollack's name.

Stephanie Florez-Pollack, MD, a dermatology resident at the University of Pennsylvania, Philadelphia, began considering the field of dermatology when, as part of the Latino Medical Students Association, she was invited by Amit Pandya, MD, to a pizza party and dermatology discussion during her first year of medical school at the University of Texas Southwestern Medical Center, Dallas.

Courtesy Dr. Stephanie Flores-Pollack

There, she met three Latinx residents who were part of the University of Texas Southwestern dermatology program. “I was so excited to hear their stories, where they came from, and how they ended up in dermatology,” she said. Dermatology had not been on her radar screen. Now there was a spark.

Volunteering at the free Agape dermatology clinic in Dallas later that year sharpened her interest. “For the first time, I really saw myself working in the field. Hearing patients’ stories and what they went through with what many people might think are very simple skin diseases made me realize there was potential to make a big impact in a person’s life,” said Dr. Florez-Pollack, who immigrated from Colombia with her family when she was 15.

Dr. Florez-Pollack’s journey into dermatology as an underrepresented-in-medicine (UIM) physician-in-training offers a window into a movement underway that aims to create a diverse dermatology workforce – one that reflects the ethnic and racial make-up of the population. It’s a movement that involves early outreach to medical students, stepped-up mentorship and sponsorship, implicit bias training, and holistic review of residency applicants.

There is no published study of all the changes being made – of how many dermatology programs have new outreach programs, for instance, or new approaches to resident application reviews. However, participation in the American Academy of Dermatology Diversity Champions program increased significantly between 2019 and 2020, and a sizable body of articles and editorials on diversity have been published in the dermatology literature in recent years, including at least several on holistic review of resident applications. Five years ago, there were few publications, sources said.

“The conversation is happening now at multiple levels, including in our peer-reviewed literature, where people are looking objectively at ... how we can make changes for the better,” said Nada Elbuluk, MD, director of the dermatology diversity and inclusion program at the University of Southern California, Los Angeles.

Unpublished findings also indicate that the number of UIM dermatology residents is inching upward. “Residency selection may not be on everyone’s mind, but an understanding of how we select people into our specialty is something every derm should know about and care about,” said Kanade Shinkai, MD, PhD, professor of dermatology at the University of California, San Francisco, and editor in chief of JAMA Dermatology.
 

The wake-up calls

The impetus for current changes first came in 2015, when Bruce Wintroub, MD, professor and chair of dermatology at UCSF, and interim dean of the medical school at the time, delivered a passionate plenary lecture at the annual AAD meeting about the lack of equity, diversity and inclusion in the specialty and the role of unconscious bias. Moved in part by a “White Coats for Black Lives” die-in by medical students on his campus following the killing of unarmed Black men, Dr. Wintroub called on his colleagues to recruit more UIM physicians into the specialty and to make the field more inclusive.

In 2016, Dr. Wintroub joined Dr. Pandya and two other academic dermatologists in authoring a commentary, published in the Journal of the American Academy of Dermatology, about the need to step up efforts and make diversity a priority. Dermatology was among the least ethnically and racially diverse specialties, second only to orthopedics, they wrote, with black dermatologists making up only 3% of all dermatologists and Hispanics only 4.2% in the United States, compared with 12.8% and 16.3% in the U.S. population, respectively.

For the next year or so, they and others from six academic institutions formed an incubator of sorts, actively tracking and sharing actions they were taking to improve diversity and the practice environment. “We wanted to learn from each other, then disseminate information to other programs,” said Dr. Pandya, who chaired the AAD diversity task force and led the self-branded “diversity champions.” (Dr. Pandya maintains his appointment at UTSW but now practices at the Palo Alto Foundation Medical Group in Sunnyvale, Calif.)

In 2017, at a President’s Conference on Diversity in Dermatology called for by then-AAD president Henry Lim, MD, leaders of the Association of Professors of Dermatology, the Society for Investigative Dermatology, and other dermatology organizations agreed on key action items, which they described in JAAD in 2018: Helping to increase the pipeline of UIM students applying to medical school, increasing UIM medical students’ early exposure to dermatology, and increasing the number of UIM students recruited into dermatology residency programs.

Diversity in the physician workforce has been shown to improve outcomes for all patients, and is important for ameliorating health care disparities and improving satisfaction and care for all patients, the authors of the 2018 paper wrote. “Multiple studies,” they noted, “have shown that UIM physicians are more likely to practice in areas where health care disparities exist.”

For specific proposed actions, the leaders attending the diversity conference drew largely upon the “diversity champions’” experiences, and agreed to fund and officially develop a diversity champions program. They also decided to invest in “bioskills” workshops for undergraduates and medical students at historically black colleges and universities, and other institutions at historically black colleges and universities at medical schools through a partnership with Nth Dimension – an organization founded in 2004 to bring more women and underrepresented minorities into orthopedic surgery.

In the last 2 years, more than 450 UIM students have attended these bioskills workshops, getting a taste of basic dermatology procedures and interacting with dermatologists.

And in September 2020, 157 dermatologists representing 80 programs throughout the country attended the second AAD Diversity Champions conference, up from 84 attendees and 30 programs in 2019. On the agenda: Discussions of holistic application review, mentorship, recruitment of UIM faculty, and a 2-hour session on microaggressions. Similar programs are being led by other dermatology organizations.

(UIM was coined by the American Association of Medical Colleges to describe racial and ethnic populations that are underrepresented in medicine relative to their numbers in the general population.)

Achievement of racial/ethnic diversity “won’t happen unless the field actively encourages people to look at it – which is not what we were doing,” Dr. Wintroub said in an interview. “I think that’s been the major change. We’re opening the door and saying: ‘We want you and we welcome you.’ ”


 

Rethinking traditional mentorship

For Dr. Florez-Pollack, the door almost shut when she began to hear from fellow medical students that dermatology is “too competitive ... a field for only the top people in the class.” She felt doubt settling in.

“I had peers who were throwing a lot of money toward prep materials ... peers who had siblings in medicine and had started studying from day one [for the step 1 exam],” she said. “I thought, was it really worth the effort? Do I really want to be perfect to get into the field when other fields would be happy to have me as I am right now?”

Her immense enjoyment of an “Art of Observation” elective course helped renew her interest in the field; it reinforced her visual abilities as well as the potential for her to address implicit bias as a dermatologist. She sought Dr. Pandya’s guidance and sponsorship to help her grow connections, polish her resume, and present herself to other faculty.

Doors were opened, she said, for her to secure a 1-year research experience before her final year of medical school with UTSW faculty, and then a 1-month rotation/mentorship with William D. James, MD, professor of dermatology at the University of Pennsylvania, an institution with a history of diversity initiatives and a longstanding skin of color program.

Dr. Florez-Pollack sees her experience reflected in the findings of a recently published study – a thematic content analysis of telephone interviews with applicants to the UTSW dermatology residency program during the 2013-14 and 2014-15 application cycles. Of the 44 applicants who participated in the study, 13 were UIM applicants.

Six of the seven UIM applicants who matched were involved in a pipeline or enrichment program – and were exposed to the field early – compared with one or two of the six UIM applicants who did not match. Underrepresented applicants were more often discouraged from applying (54%) – told, for instance, that they could better serve their communities through other specialties – than were non-UIM applicants (13%). They also were affected more often by a lack of equitable resources, according to comments made by 70% of applicants (UIM and non-UIM).

Also notably, the investigators said, all of the UIM applicants who matched (and the majority of non-UIMs who matched) reported having a mentor during the process of applying, compared with 44% of those who didn’t match.

Rebecca Vasquez, MD, assistant professor of dermatology at UTSW, who led the study, was herself a mentee of Dr. Pandya. “He believed in me and gave me the courage to consider dermatology,” she said. (Dr. Vasquez was one of the Latinx women who inspired Dr. Florez-Pollack, in turn, when they met at Dr. Pandya’s pizza party. Dr. Florez-Pollack assisted with the research and was a coauthor of the study.)

Amy McMichael, MD, professor and chair of dermatology at Wake Forest University, Winston-Salem, N.C., said that dermatology as a field has traditionally been “very good at mentoring.” Many of the dermatology societies have long had mentorship programs, for instance, that guide medical students, and sometimes residents, through defined experiences or through periods of time.

But she advocates going deeper. “When it comes to sponsorship, we fall a little short,” she said. “Sponsorship is about promoting that person to the next level, making sure they achieve what they want to achieve ... putting them up for opportunities they may not have known existed. It’s continuous and focused.”

Dr. Olabola Awosika

Olabola Awosika, MD, a fourth-year dermatology resident at Henry Ford Health System, Detroit, said her interest in dermatology was solidified during her participation in the AAD’s month-long mentorship program after her second year of medical school at Howard University, Washington. However, it wasn’t until her fourth year, when she did an away rotation at Wake Forest, that she realized that “gaining access to the field” takes years of mentorship, research opportunities, and networking. It was too late.

After initially not matching, she did a rotation at Johns Hopkins in dermatology during an internship year, followed by a 2-year research fellowship at George Washington University, Washington. As does Dr. Florez-Pollack, who now mentors medical students. She also serves on the Women’s Dermatologic Society diversity committee, which is now developing initiatives to help UIM dermatologists “become upwardly mobile in dermatology [after residency], so they have a seat at the table in various settings.”
 

Holistic review for residency

Dr. Vasquez, who grew up in South Texas in an uninsured family that received most of its medical care across the border in Mexico, believes that the “biggest stride being made today” with respect to diversity in the dermatology workforce – and in the larger physician workforce – is increased understanding of the role of social and cultural capital.

Dr. Vasquez?

“We’d never really talked about this concept ... about how, if you don’t have the same upbringing, education, and resources, you’re already behind … and you may not do as well on standardized tests,” she said. “Now people are listening to it and understand it. That’s why more programs are looking at how to practice a more holistic approach to selecting applicants to interview.”

Some dermatology programs – at Wake Forest, UCSF, USC, Vanderbilt, and George Washington University for instance – have eliminated the use of U.S. Medical Licensing Examination step 1 scores and Alpha Omega Alpha Medical Honor Society status as filtering/screening metrics. Some also take a “second look” at UIM applicants.

Overall, those making changes are looking “at everything the applicant brings to the table – their story, their experiences,” said Dr. Elbuluk. “We want to understand the full picture of who they are and their journey to becoming a physician.”

Implicit bias training for members of residency review committees is becoming more common, as is such training across the board in dermatology departments. “We have to bring it to the forefront so that we can create more inclusive environments,” said Sharon E. Albers, MD, a dermatologist at Vanderbilt University Medical Center, Nashville, Tenn., who serves as the dermatology department’s diversity liaison to the medical school, and who, as a former faculty member of Meharry Medical College, remains engaged with the historically black institution.

One of her recent efforts, inspired by participation in the diversity champions program, has been developing pipeline programs to speak to middle and high school students about medicine and dermatology. For now, however, she credits a holistic review process for change. Last year, three of the five matched dermatology residents at Vanderbilt were UIM physicians – unprecedented for the institution, Dr. Albers said, and “evidence that holistic review works if you’re very intentional about it.”

Dr. Vasquez?

Dr. Vasquez has analyzed data from the Accreditation Council of Graduate Medical Education and says that UIM dermatology residents comprised 8.0% of the total in 2019, marking an improvement over the prior 7 years. “We’ve introduced so many changes at the same time,” making it difficult to discern what’s most impactful, she said. “But something is working.”

(The AAMC, which has invested in pipeline programs for more than a decade and has championed holistic medical school admissions, states in its 2019 diversity data report that efforts to improve diversity in medicine have made “only marginal differences” – and that Black males in particular continue to be significantly underrepresented in medical schools. Persistent, structural racism was a common theme in the association’s 2015 report on Black males in medicine.)

Efforts to diversify the workforce – particularly holistic review – haven’t been without detractors. “It brings reaction,” Dr. Wintroub said. “Some people think you’re lowering quality in the field ... but that’s just not true.”

Diversity in the dermatology workforce is important not only for the care of patients from diverse backgrounds, but “perhaps more importantly, it brings new ideas and views and experiences into the field,” he said. “It pushes us to think in new directions ... that can only make our field better and richer.”

“We need to make sure our workforce is representative of the patients we serve – but also that all derms can manage patients of all skin types and demographics,” Dr. Shinkai said. “And we need more diversity in the leadership of our departments and dermatology organizations ... inclusivity needs to extend all the way to the highest reaches of our specialty.”

Adam Friedman, MD, professor and interim chair of dermatology at George Washington University and director of the department’s diversity, equity, and inclusion committee, agreed. “We need to both make sure our workforce mirrors the patients we serve, and said workforce is prepared to manage patients of all skin types and demographics. We need to cover the spectrum, from revamping medical education and mentorship opportunities to advancing diversity in the leadership of our departments, institutions, and societies. Addressing only part of the puzzle will not and can not be enough.”

Correction, 3/3/21: An earlier version of this article misstated Dr. Stephanie Florez-Pollack's name.

Stephanie Florez-Pollack, MD, a dermatology resident at the University of Pennsylvania, Philadelphia, began considering the field of dermatology when, as part of the Latino Medical Students Association, she was invited by Amit Pandya, MD, to a pizza party and dermatology discussion during her first year of medical school at the University of Texas Southwestern Medical Center, Dallas.

Courtesy Dr. Stephanie Flores-Pollack

There, she met three Latinx residents who were part of the University of Texas Southwestern dermatology program. “I was so excited to hear their stories, where they came from, and how they ended up in dermatology,” she said. Dermatology had not been on her radar screen. Now there was a spark.

Volunteering at the free Agape dermatology clinic in Dallas later that year sharpened her interest. “For the first time, I really saw myself working in the field. Hearing patients’ stories and what they went through with what many people might think are very simple skin diseases made me realize there was potential to make a big impact in a person’s life,” said Dr. Florez-Pollack, who immigrated from Colombia with her family when she was 15.

Dr. Florez-Pollack’s journey into dermatology as an underrepresented-in-medicine (UIM) physician-in-training offers a window into a movement underway that aims to create a diverse dermatology workforce – one that reflects the ethnic and racial make-up of the population. It’s a movement that involves early outreach to medical students, stepped-up mentorship and sponsorship, implicit bias training, and holistic review of residency applicants.

There is no published study of all the changes being made – of how many dermatology programs have new outreach programs, for instance, or new approaches to resident application reviews. However, participation in the American Academy of Dermatology Diversity Champions program increased significantly between 2019 and 2020, and a sizable body of articles and editorials on diversity have been published in the dermatology literature in recent years, including at least several on holistic review of resident applications. Five years ago, there were few publications, sources said.

“The conversation is happening now at multiple levels, including in our peer-reviewed literature, where people are looking objectively at ... how we can make changes for the better,” said Nada Elbuluk, MD, director of the dermatology diversity and inclusion program at the University of Southern California, Los Angeles.

Unpublished findings also indicate that the number of UIM dermatology residents is inching upward. “Residency selection may not be on everyone’s mind, but an understanding of how we select people into our specialty is something every derm should know about and care about,” said Kanade Shinkai, MD, PhD, professor of dermatology at the University of California, San Francisco, and editor in chief of JAMA Dermatology.
 

The wake-up calls

The impetus for current changes first came in 2015, when Bruce Wintroub, MD, professor and chair of dermatology at UCSF, and interim dean of the medical school at the time, delivered a passionate plenary lecture at the annual AAD meeting about the lack of equity, diversity and inclusion in the specialty and the role of unconscious bias. Moved in part by a “White Coats for Black Lives” die-in by medical students on his campus following the killing of unarmed Black men, Dr. Wintroub called on his colleagues to recruit more UIM physicians into the specialty and to make the field more inclusive.

In 2016, Dr. Wintroub joined Dr. Pandya and two other academic dermatologists in authoring a commentary, published in the Journal of the American Academy of Dermatology, about the need to step up efforts and make diversity a priority. Dermatology was among the least ethnically and racially diverse specialties, second only to orthopedics, they wrote, with black dermatologists making up only 3% of all dermatologists and Hispanics only 4.2% in the United States, compared with 12.8% and 16.3% in the U.S. population, respectively.

For the next year or so, they and others from six academic institutions formed an incubator of sorts, actively tracking and sharing actions they were taking to improve diversity and the practice environment. “We wanted to learn from each other, then disseminate information to other programs,” said Dr. Pandya, who chaired the AAD diversity task force and led the self-branded “diversity champions.” (Dr. Pandya maintains his appointment at UTSW but now practices at the Palo Alto Foundation Medical Group in Sunnyvale, Calif.)

In 2017, at a President’s Conference on Diversity in Dermatology called for by then-AAD president Henry Lim, MD, leaders of the Association of Professors of Dermatology, the Society for Investigative Dermatology, and other dermatology organizations agreed on key action items, which they described in JAAD in 2018: Helping to increase the pipeline of UIM students applying to medical school, increasing UIM medical students’ early exposure to dermatology, and increasing the number of UIM students recruited into dermatology residency programs.

Diversity in the physician workforce has been shown to improve outcomes for all patients, and is important for ameliorating health care disparities and improving satisfaction and care for all patients, the authors of the 2018 paper wrote. “Multiple studies,” they noted, “have shown that UIM physicians are more likely to practice in areas where health care disparities exist.”

For specific proposed actions, the leaders attending the diversity conference drew largely upon the “diversity champions’” experiences, and agreed to fund and officially develop a diversity champions program. They also decided to invest in “bioskills” workshops for undergraduates and medical students at historically black colleges and universities, and other institutions at historically black colleges and universities at medical schools through a partnership with Nth Dimension – an organization founded in 2004 to bring more women and underrepresented minorities into orthopedic surgery.

In the last 2 years, more than 450 UIM students have attended these bioskills workshops, getting a taste of basic dermatology procedures and interacting with dermatologists.

And in September 2020, 157 dermatologists representing 80 programs throughout the country attended the second AAD Diversity Champions conference, up from 84 attendees and 30 programs in 2019. On the agenda: Discussions of holistic application review, mentorship, recruitment of UIM faculty, and a 2-hour session on microaggressions. Similar programs are being led by other dermatology organizations.

(UIM was coined by the American Association of Medical Colleges to describe racial and ethnic populations that are underrepresented in medicine relative to their numbers in the general population.)

Achievement of racial/ethnic diversity “won’t happen unless the field actively encourages people to look at it – which is not what we were doing,” Dr. Wintroub said in an interview. “I think that’s been the major change. We’re opening the door and saying: ‘We want you and we welcome you.’ ”


 

Rethinking traditional mentorship

For Dr. Florez-Pollack, the door almost shut when she began to hear from fellow medical students that dermatology is “too competitive ... a field for only the top people in the class.” She felt doubt settling in.

“I had peers who were throwing a lot of money toward prep materials ... peers who had siblings in medicine and had started studying from day one [for the step 1 exam],” she said. “I thought, was it really worth the effort? Do I really want to be perfect to get into the field when other fields would be happy to have me as I am right now?”

Her immense enjoyment of an “Art of Observation” elective course helped renew her interest in the field; it reinforced her visual abilities as well as the potential for her to address implicit bias as a dermatologist. She sought Dr. Pandya’s guidance and sponsorship to help her grow connections, polish her resume, and present herself to other faculty.

Doors were opened, she said, for her to secure a 1-year research experience before her final year of medical school with UTSW faculty, and then a 1-month rotation/mentorship with William D. James, MD, professor of dermatology at the University of Pennsylvania, an institution with a history of diversity initiatives and a longstanding skin of color program.

Dr. Florez-Pollack sees her experience reflected in the findings of a recently published study – a thematic content analysis of telephone interviews with applicants to the UTSW dermatology residency program during the 2013-14 and 2014-15 application cycles. Of the 44 applicants who participated in the study, 13 were UIM applicants.

Six of the seven UIM applicants who matched were involved in a pipeline or enrichment program – and were exposed to the field early – compared with one or two of the six UIM applicants who did not match. Underrepresented applicants were more often discouraged from applying (54%) – told, for instance, that they could better serve their communities through other specialties – than were non-UIM applicants (13%). They also were affected more often by a lack of equitable resources, according to comments made by 70% of applicants (UIM and non-UIM).

Also notably, the investigators said, all of the UIM applicants who matched (and the majority of non-UIMs who matched) reported having a mentor during the process of applying, compared with 44% of those who didn’t match.

Rebecca Vasquez, MD, assistant professor of dermatology at UTSW, who led the study, was herself a mentee of Dr. Pandya. “He believed in me and gave me the courage to consider dermatology,” she said. (Dr. Vasquez was one of the Latinx women who inspired Dr. Florez-Pollack, in turn, when they met at Dr. Pandya’s pizza party. Dr. Florez-Pollack assisted with the research and was a coauthor of the study.)

Amy McMichael, MD, professor and chair of dermatology at Wake Forest University, Winston-Salem, N.C., said that dermatology as a field has traditionally been “very good at mentoring.” Many of the dermatology societies have long had mentorship programs, for instance, that guide medical students, and sometimes residents, through defined experiences or through periods of time.

But she advocates going deeper. “When it comes to sponsorship, we fall a little short,” she said. “Sponsorship is about promoting that person to the next level, making sure they achieve what they want to achieve ... putting them up for opportunities they may not have known existed. It’s continuous and focused.”

Dr. Olabola Awosika

Olabola Awosika, MD, a fourth-year dermatology resident at Henry Ford Health System, Detroit, said her interest in dermatology was solidified during her participation in the AAD’s month-long mentorship program after her second year of medical school at Howard University, Washington. However, it wasn’t until her fourth year, when she did an away rotation at Wake Forest, that she realized that “gaining access to the field” takes years of mentorship, research opportunities, and networking. It was too late.

After initially not matching, she did a rotation at Johns Hopkins in dermatology during an internship year, followed by a 2-year research fellowship at George Washington University, Washington. As does Dr. Florez-Pollack, who now mentors medical students. She also serves on the Women’s Dermatologic Society diversity committee, which is now developing initiatives to help UIM dermatologists “become upwardly mobile in dermatology [after residency], so they have a seat at the table in various settings.”
 

Holistic review for residency

Dr. Vasquez, who grew up in South Texas in an uninsured family that received most of its medical care across the border in Mexico, believes that the “biggest stride being made today” with respect to diversity in the dermatology workforce – and in the larger physician workforce – is increased understanding of the role of social and cultural capital.

Dr. Vasquez?

“We’d never really talked about this concept ... about how, if you don’t have the same upbringing, education, and resources, you’re already behind … and you may not do as well on standardized tests,” she said. “Now people are listening to it and understand it. That’s why more programs are looking at how to practice a more holistic approach to selecting applicants to interview.”

Some dermatology programs – at Wake Forest, UCSF, USC, Vanderbilt, and George Washington University for instance – have eliminated the use of U.S. Medical Licensing Examination step 1 scores and Alpha Omega Alpha Medical Honor Society status as filtering/screening metrics. Some also take a “second look” at UIM applicants.

Overall, those making changes are looking “at everything the applicant brings to the table – their story, their experiences,” said Dr. Elbuluk. “We want to understand the full picture of who they are and their journey to becoming a physician.”

Implicit bias training for members of residency review committees is becoming more common, as is such training across the board in dermatology departments. “We have to bring it to the forefront so that we can create more inclusive environments,” said Sharon E. Albers, MD, a dermatologist at Vanderbilt University Medical Center, Nashville, Tenn., who serves as the dermatology department’s diversity liaison to the medical school, and who, as a former faculty member of Meharry Medical College, remains engaged with the historically black institution.

One of her recent efforts, inspired by participation in the diversity champions program, has been developing pipeline programs to speak to middle and high school students about medicine and dermatology. For now, however, she credits a holistic review process for change. Last year, three of the five matched dermatology residents at Vanderbilt were UIM physicians – unprecedented for the institution, Dr. Albers said, and “evidence that holistic review works if you’re very intentional about it.”

Dr. Vasquez?

Dr. Vasquez has analyzed data from the Accreditation Council of Graduate Medical Education and says that UIM dermatology residents comprised 8.0% of the total in 2019, marking an improvement over the prior 7 years. “We’ve introduced so many changes at the same time,” making it difficult to discern what’s most impactful, she said. “But something is working.”

(The AAMC, which has invested in pipeline programs for more than a decade and has championed holistic medical school admissions, states in its 2019 diversity data report that efforts to improve diversity in medicine have made “only marginal differences” – and that Black males in particular continue to be significantly underrepresented in medical schools. Persistent, structural racism was a common theme in the association’s 2015 report on Black males in medicine.)

Efforts to diversify the workforce – particularly holistic review – haven’t been without detractors. “It brings reaction,” Dr. Wintroub said. “Some people think you’re lowering quality in the field ... but that’s just not true.”

Diversity in the dermatology workforce is important not only for the care of patients from diverse backgrounds, but “perhaps more importantly, it brings new ideas and views and experiences into the field,” he said. “It pushes us to think in new directions ... that can only make our field better and richer.”

“We need to make sure our workforce is representative of the patients we serve – but also that all derms can manage patients of all skin types and demographics,” Dr. Shinkai said. “And we need more diversity in the leadership of our departments and dermatology organizations ... inclusivity needs to extend all the way to the highest reaches of our specialty.”

Adam Friedman, MD, professor and interim chair of dermatology at George Washington University and director of the department’s diversity, equity, and inclusion committee, agreed. “We need to both make sure our workforce mirrors the patients we serve, and said workforce is prepared to manage patients of all skin types and demographics. We need to cover the spectrum, from revamping medical education and mentorship opportunities to advancing diversity in the leadership of our departments, institutions, and societies. Addressing only part of the puzzle will not and can not be enough.”

Correction, 3/3/21: An earlier version of this article misstated Dr. Stephanie Florez-Pollack's name.