Clinician Reviews

Scent-detecting dogs have long been used to sniff out medical conditions ranging from low blood sugar and cancer to malaria, impending seizures, and migraines – not to mention explosives and narcotics.

Recently, the sensitivity of the canine nose has been tested as a strategy for screening for SARS-CoV-2 infection in schoolchildren showing no outward symptoms of the virus. A pilot study led by Carol A. Glaser, DVM, MD, of the California Department of Public Health in Richmond, found that trained dogs had an accuracy of more than 95% for detecting the odor of volatile organic compounds, or VOCs, produced by COVID-infected individuals.

California Department of Public Health

The authors believe that odor-based diagnosis with dogs could eventually provide a rapid, inexpensive, and noninvasive way to screen large groups for COVID-19 without the need for antigen testing.

“This is a new program with research ongoing, so it would be premature to consider it from a consumer’s perspective,” Dr. Glaser said in an interview. “However, the data look promising and we are hopeful we can continue to pilot various programs in various settings to see where, and if, dogs can be used for biomedical detection.”
 

In the lab and in the field

In a study published online in JAMA Pediatrics, Dr. Glaser’s group found that after 2 months’ training on COVID-19 scent samples in the laboratory, the dogs detected the presence of the virus more than 95% of the time. Antigen tests were used as a comparative reference.

In medical terms, the dogs achieved a greater than 95% accuracy on two important measures of effectiveness: sensitivity – a test’s ability to correctly detect the positive presence of disease – and specificity – the ability of a test to accurately rule out the presence of disease and identify as negative an uninfected person.

Next, the researchers piloted field tests in 50 visits at 27 schools from April 1 to May 25, 2022, to compare dogs’ detection ability with that of standard laboratory antigen testing. Participants in the completely voluntary screening numbered 1,558 and ranged in age from 9 to 17 years. Of these, 56% were girls and 89% were students. Almost 70% were screened at least twice.

Overall, the field test compared 3,897 paired antigen-vs.-dog screenings. The dogs accurately signaled the presence of 85 infections and ruled out 3,411 infections, for an overall accuracy of 90%. In 383 cases, however, they inaccurately signaled the presence of infection (false positives) and missed 18 actual infections (false negatives). That translated to a sensitivity in the field of 83%, considerably lower than that of their lab performance.

Direct screening of individuals with dogs outside of the lab involved circumstantial factors that likely contributed to decreased sensitivity and specificity, the authors acknowledged. These included such distractions as noise and the presence of excitable young children as well environmental conditions such as wind and other odors. What about dog phobia and dog hair allergy? “Dog screening takes only a few seconds per student and the dogs do not generally touch the participant as they run a line and sniff at ankles,” Dr. Glaser explained.

As for allergies, the rapid, ankle-level screening occurred in outdoor settings. “The chance of allergies is very low. This would be similar to someone who is out walking on the sidewalk and walks by a dog,” Dr. Glaser said.

Last year, a British trial of almost 4,000 adults tested six dogs trained to detect differences in VOCs between COVID-infected and uninfected individuals. Given samples from both groups, the dogs were able to distinguish between infected and uninfected samples with a sensitivity for detecting the virus ranging from 82% to 94% and a specificity for ruling it out of 76% to 92%. And they were able to smell the VOCs even when the viral load was low. The study also tested organic sensors, which proved even more accurate than the canines.

According to lead author James G. Logan, PhD, a disease control expert at the London School of Hygiene & Tropical Medicine in London, “Odour-based diagnostics using dogs and/or sensors may prove a rapid and effective tool for screening large numbers of people. Mathematical modelling suggests that dog screening plus a confirmatory PCR test could detect up to 89% of SARS-CoV-2 infections, averting up to 2.2 times as much transmission compared to isolation of symptomatic individuals only.”

Funding was provided by the Centers for Disease Control and Prevention Foundation (CDCF) to Early Alert Canines for the purchase and care of the dogs and the support of the handlers and trainers. The CDCF had no other role in the study. Coauthor Carol A. Edwards of Early Alert Canines reported receiving grants from the CDCF.

Scent-detecting dogs have long been used to sniff out medical conditions ranging from low blood sugar and cancer to malaria, impending seizures, and migraines – not to mention explosives and narcotics.

Recently, the sensitivity of the canine nose has been tested as a strategy for screening for SARS-CoV-2 infection in schoolchildren showing no outward symptoms of the virus. A pilot study led by Carol A. Glaser, DVM, MD, of the California Department of Public Health in Richmond, found that trained dogs had an accuracy of more than 95% for detecting the odor of volatile organic compounds, or VOCs, produced by COVID-infected individuals.

California Department of Public Health

The authors believe that odor-based diagnosis with dogs could eventually provide a rapid, inexpensive, and noninvasive way to screen large groups for COVID-19 without the need for antigen testing.

“This is a new program with research ongoing, so it would be premature to consider it from a consumer’s perspective,” Dr. Glaser said in an interview. “However, the data look promising and we are hopeful we can continue to pilot various programs in various settings to see where, and if, dogs can be used for biomedical detection.”
 

In the lab and in the field

In a study published online in JAMA Pediatrics, Dr. Glaser’s group found that after 2 months’ training on COVID-19 scent samples in the laboratory, the dogs detected the presence of the virus more than 95% of the time. Antigen tests were used as a comparative reference.

In medical terms, the dogs achieved a greater than 95% accuracy on two important measures of effectiveness: sensitivity – a test’s ability to correctly detect the positive presence of disease – and specificity – the ability of a test to accurately rule out the presence of disease and identify as negative an uninfected person.

Next, the researchers piloted field tests in 50 visits at 27 schools from April 1 to May 25, 2022, to compare dogs’ detection ability with that of standard laboratory antigen testing. Participants in the completely voluntary screening numbered 1,558 and ranged in age from 9 to 17 years. Of these, 56% were girls and 89% were students. Almost 70% were screened at least twice.

Overall, the field test compared 3,897 paired antigen-vs.-dog screenings. The dogs accurately signaled the presence of 85 infections and ruled out 3,411 infections, for an overall accuracy of 90%. In 383 cases, however, they inaccurately signaled the presence of infection (false positives) and missed 18 actual infections (false negatives). That translated to a sensitivity in the field of 83%, considerably lower than that of their lab performance.

Direct screening of individuals with dogs outside of the lab involved circumstantial factors that likely contributed to decreased sensitivity and specificity, the authors acknowledged. These included such distractions as noise and the presence of excitable young children as well environmental conditions such as wind and other odors. What about dog phobia and dog hair allergy? “Dog screening takes only a few seconds per student and the dogs do not generally touch the participant as they run a line and sniff at ankles,” Dr. Glaser explained.

As for allergies, the rapid, ankle-level screening occurred in outdoor settings. “The chance of allergies is very low. This would be similar to someone who is out walking on the sidewalk and walks by a dog,” Dr. Glaser said.

Last year, a British trial of almost 4,000 adults tested six dogs trained to detect differences in VOCs between COVID-infected and uninfected individuals. Given samples from both groups, the dogs were able to distinguish between infected and uninfected samples with a sensitivity for detecting the virus ranging from 82% to 94% and a specificity for ruling it out of 76% to 92%. And they were able to smell the VOCs even when the viral load was low. The study also tested organic sensors, which proved even more accurate than the canines.

According to lead author James G. Logan, PhD, a disease control expert at the London School of Hygiene & Tropical Medicine in London, “Odour-based diagnostics using dogs and/or sensors may prove a rapid and effective tool for screening large numbers of people. Mathematical modelling suggests that dog screening plus a confirmatory PCR test could detect up to 89% of SARS-CoV-2 infections, averting up to 2.2 times as much transmission compared to isolation of symptomatic individuals only.”

Funding was provided by the Centers for Disease Control and Prevention Foundation (CDCF) to Early Alert Canines for the purchase and care of the dogs and the support of the handlers and trainers. The CDCF had no other role in the study. Coauthor Carol A. Edwards of Early Alert Canines reported receiving grants from the CDCF.

Scent-detecting dogs have long been used to sniff out medical conditions ranging from low blood sugar and cancer to malaria, impending seizures, and migraines – not to mention explosives and narcotics.

Recently, the sensitivity of the canine nose has been tested as a strategy for screening for SARS-CoV-2 infection in schoolchildren showing no outward symptoms of the virus. A pilot study led by Carol A. Glaser, DVM, MD, of the California Department of Public Health in Richmond, found that trained dogs had an accuracy of more than 95% for detecting the odor of volatile organic compounds, or VOCs, produced by COVID-infected individuals.

California Department of Public Health

The authors believe that odor-based diagnosis with dogs could eventually provide a rapid, inexpensive, and noninvasive way to screen large groups for COVID-19 without the need for antigen testing.

“This is a new program with research ongoing, so it would be premature to consider it from a consumer’s perspective,” Dr. Glaser said in an interview. “However, the data look promising and we are hopeful we can continue to pilot various programs in various settings to see where, and if, dogs can be used for biomedical detection.”
 

In the lab and in the field

In a study published online in JAMA Pediatrics, Dr. Glaser’s group found that after 2 months’ training on COVID-19 scent samples in the laboratory, the dogs detected the presence of the virus more than 95% of the time. Antigen tests were used as a comparative reference.

In medical terms, the dogs achieved a greater than 95% accuracy on two important measures of effectiveness: sensitivity – a test’s ability to correctly detect the positive presence of disease – and specificity – the ability of a test to accurately rule out the presence of disease and identify as negative an uninfected person.

Next, the researchers piloted field tests in 50 visits at 27 schools from April 1 to May 25, 2022, to compare dogs’ detection ability with that of standard laboratory antigen testing. Participants in the completely voluntary screening numbered 1,558 and ranged in age from 9 to 17 years. Of these, 56% were girls and 89% were students. Almost 70% were screened at least twice.

Overall, the field test compared 3,897 paired antigen-vs.-dog screenings. The dogs accurately signaled the presence of 85 infections and ruled out 3,411 infections, for an overall accuracy of 90%. In 383 cases, however, they inaccurately signaled the presence of infection (false positives) and missed 18 actual infections (false negatives). That translated to a sensitivity in the field of 83%, considerably lower than that of their lab performance.

Direct screening of individuals with dogs outside of the lab involved circumstantial factors that likely contributed to decreased sensitivity and specificity, the authors acknowledged. These included such distractions as noise and the presence of excitable young children as well environmental conditions such as wind and other odors. What about dog phobia and dog hair allergy? “Dog screening takes only a few seconds per student and the dogs do not generally touch the participant as they run a line and sniff at ankles,” Dr. Glaser explained.

As for allergies, the rapid, ankle-level screening occurred in outdoor settings. “The chance of allergies is very low. This would be similar to someone who is out walking on the sidewalk and walks by a dog,” Dr. Glaser said.

Last year, a British trial of almost 4,000 adults tested six dogs trained to detect differences in VOCs between COVID-infected and uninfected individuals. Given samples from both groups, the dogs were able to distinguish between infected and uninfected samples with a sensitivity for detecting the virus ranging from 82% to 94% and a specificity for ruling it out of 76% to 92%. And they were able to smell the VOCs even when the viral load was low. The study also tested organic sensors, which proved even more accurate than the canines.

According to lead author James G. Logan, PhD, a disease control expert at the London School of Hygiene & Tropical Medicine in London, “Odour-based diagnostics using dogs and/or sensors may prove a rapid and effective tool for screening large numbers of people. Mathematical modelling suggests that dog screening plus a confirmatory PCR test could detect up to 89% of SARS-CoV-2 infections, averting up to 2.2 times as much transmission compared to isolation of symptomatic individuals only.”

Funding was provided by the Centers for Disease Control and Prevention Foundation (CDCF) to Early Alert Canines for the purchase and care of the dogs and the support of the handlers and trainers. The CDCF had no other role in the study. Coauthor Carol A. Edwards of Early Alert Canines reported receiving grants from the CDCF.

Cardiovascular disease (CVD) is the main cause of premature death and disability in the general population, and according to the World Health Organization, the incidence of CVD is increasing throughout the world. Conventional risk factors that contribute to the occurrence and worsening of CVD have been identified and widely studied. They include high cholesterol levels, high blood pressure, diabetes, obesity, smoking, and lack of physical activity. Despite the introduction of measures to prevent and treat these risk factors with lipid-lowering drugs, antihypertensives, antiplatelet drugs, and anticoagulants, the mortality rate related to CVD remains high.
 

Despite the effectiveness of many currently available treatment options, there are still significant gaps in risk assessment and treatment of CVD.

In the past few years, new coronary risk factors have emerged. They are detailed in an editorial published in The American Journal of Medicine that describes their role and their impact on our cardiovascular health.
 

Systemic inflammation

The new coronary risk factors include the following diseases characterized by systemic inflammation:

• Gout – Among patients who have experienced a recent flare of gout, the probability of experiencing an acute cardiovascular event such as a myocardial infarction or stroke is increased.
• Rheumatoid arthritis and systemic lupus erythematous – Patients with one or both of these conditions are at higher odds of experiencing concomitant premature and extremely premature coronary artery disease.
• Inflammatory bowel disease (Crohn’s disease or ulcerative colitis) – Patients with this disease have increased odds of developing coronary artery disease.
• Psoriasis – Patients with psoriasis are up to 50% more likely to develop CVD.

Maternal and childhood factors

The following maternal and childhood factors are associated with an increased risk of developing coronary artery disease: gestational diabetes; preeclampsia; delivering a child of low birth weight; preterm delivery; and premature or surgical menopause. The factor or factors that increase the risk of coronary artery disease associated with each of these conditions are not known but may be the result of increased cytokine and oxidative stress.

An unusual and yet unexplained association has been observed between migraine headaches with aura in women and incident CVD.

Also of interest is the association of early life trauma and the risk of adverse cardiovascular outcomes in young and middle-aged individuals who have a history of myocardial infarction.

Transgender patients who present for gender-affirming care are also at increased cardiovascular risk. Among these patients, the increase in coronary artery disease risk may be related to high rates of anxiety and depression.
 

Environmental factors

Low socioeconomic status has emerged as a risk factor. Increased psychosocial stressors, limited educational and economic opportunities, and lack of peer influence favoring healthier lifestyle choices may be causative elements leading to enhanced coronary artery disease among individuals with low socioeconomic living conditions.

Air pollution was estimated to have caused 9 million deaths worldwide in 2019, with 62% due to CVD and 31.7% to coronary artery disease. Severely polluted environmental aerosols contain several toxic metals, such as lead, mercury, arsenic, and cadmium. Transient exposure to various air pollutants may trigger the onset of an acute coronary syndrome.
 

Lifestyle factors

Long working hours by patients who have experienced a first myocardial infarction increase the risk for a recurrent event, possibly because of prolonged exposure to work stressors.

Skipping breakfast has been linked to increased cardiovascular and all-cause mortality.

Long-term consumption of drinks containing sugar and artificial sweeteners has also been associated with increased cardiovascular mortality.

Recognizing the presence of one or more of these new risk factors could help prompt and improve behaviors for reducing more conventional CV risk factors to a minimum.

This article was translated from Univadis Italy, which is part of the Medscape Professional Network.

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

Cardiovascular disease (CVD) is the main cause of premature death and disability in the general population, and according to the World Health Organization, the incidence of CVD is increasing throughout the world. Conventional risk factors that contribute to the occurrence and worsening of CVD have been identified and widely studied. They include high cholesterol levels, high blood pressure, diabetes, obesity, smoking, and lack of physical activity. Despite the introduction of measures to prevent and treat these risk factors with lipid-lowering drugs, antihypertensives, antiplatelet drugs, and anticoagulants, the mortality rate related to CVD remains high.
 

Despite the effectiveness of many currently available treatment options, there are still significant gaps in risk assessment and treatment of CVD.

In the past few years, new coronary risk factors have emerged. They are detailed in an editorial published in The American Journal of Medicine that describes their role and their impact on our cardiovascular health.
 

Systemic inflammation

The new coronary risk factors include the following diseases characterized by systemic inflammation:

• Gout – Among patients who have experienced a recent flare of gout, the probability of experiencing an acute cardiovascular event such as a myocardial infarction or stroke is increased.
• Rheumatoid arthritis and systemic lupus erythematous – Patients with one or both of these conditions are at higher odds of experiencing concomitant premature and extremely premature coronary artery disease.
• Inflammatory bowel disease (Crohn’s disease or ulcerative colitis) – Patients with this disease have increased odds of developing coronary artery disease.
• Psoriasis – Patients with psoriasis are up to 50% more likely to develop CVD.

Maternal and childhood factors

The following maternal and childhood factors are associated with an increased risk of developing coronary artery disease: gestational diabetes; preeclampsia; delivering a child of low birth weight; preterm delivery; and premature or surgical menopause. The factor or factors that increase the risk of coronary artery disease associated with each of these conditions are not known but may be the result of increased cytokine and oxidative stress.

An unusual and yet unexplained association has been observed between migraine headaches with aura in women and incident CVD.

Also of interest is the association of early life trauma and the risk of adverse cardiovascular outcomes in young and middle-aged individuals who have a history of myocardial infarction.

Transgender patients who present for gender-affirming care are also at increased cardiovascular risk. Among these patients, the increase in coronary artery disease risk may be related to high rates of anxiety and depression.
 

Environmental factors

Low socioeconomic status has emerged as a risk factor. Increased psychosocial stressors, limited educational and economic opportunities, and lack of peer influence favoring healthier lifestyle choices may be causative elements leading to enhanced coronary artery disease among individuals with low socioeconomic living conditions.

Air pollution was estimated to have caused 9 million deaths worldwide in 2019, with 62% due to CVD and 31.7% to coronary artery disease. Severely polluted environmental aerosols contain several toxic metals, such as lead, mercury, arsenic, and cadmium. Transient exposure to various air pollutants may trigger the onset of an acute coronary syndrome.
 

Lifestyle factors

Long working hours by patients who have experienced a first myocardial infarction increase the risk for a recurrent event, possibly because of prolonged exposure to work stressors.

Skipping breakfast has been linked to increased cardiovascular and all-cause mortality.

Long-term consumption of drinks containing sugar and artificial sweeteners has also been associated with increased cardiovascular mortality.

Recognizing the presence of one or more of these new risk factors could help prompt and improve behaviors for reducing more conventional CV risk factors to a minimum.

This article was translated from Univadis Italy, which is part of the Medscape Professional Network.

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

Cardiovascular disease (CVD) is the main cause of premature death and disability in the general population, and according to the World Health Organization, the incidence of CVD is increasing throughout the world. Conventional risk factors that contribute to the occurrence and worsening of CVD have been identified and widely studied. They include high cholesterol levels, high blood pressure, diabetes, obesity, smoking, and lack of physical activity. Despite the introduction of measures to prevent and treat these risk factors with lipid-lowering drugs, antihypertensives, antiplatelet drugs, and anticoagulants, the mortality rate related to CVD remains high.
 

Despite the effectiveness of many currently available treatment options, there are still significant gaps in risk assessment and treatment of CVD.

In the past few years, new coronary risk factors have emerged. They are detailed in an editorial published in The American Journal of Medicine that describes their role and their impact on our cardiovascular health.
 

Systemic inflammation

The new coronary risk factors include the following diseases characterized by systemic inflammation:

• Gout – Among patients who have experienced a recent flare of gout, the probability of experiencing an acute cardiovascular event such as a myocardial infarction or stroke is increased.
• Rheumatoid arthritis and systemic lupus erythematous – Patients with one or both of these conditions are at higher odds of experiencing concomitant premature and extremely premature coronary artery disease.
• Inflammatory bowel disease (Crohn’s disease or ulcerative colitis) – Patients with this disease have increased odds of developing coronary artery disease.
• Psoriasis – Patients with psoriasis are up to 50% more likely to develop CVD.

Maternal and childhood factors

The following maternal and childhood factors are associated with an increased risk of developing coronary artery disease: gestational diabetes; preeclampsia; delivering a child of low birth weight; preterm delivery; and premature or surgical menopause. The factor or factors that increase the risk of coronary artery disease associated with each of these conditions are not known but may be the result of increased cytokine and oxidative stress.

An unusual and yet unexplained association has been observed between migraine headaches with aura in women and incident CVD.

Also of interest is the association of early life trauma and the risk of adverse cardiovascular outcomes in young and middle-aged individuals who have a history of myocardial infarction.

Transgender patients who present for gender-affirming care are also at increased cardiovascular risk. Among these patients, the increase in coronary artery disease risk may be related to high rates of anxiety and depression.
 

Environmental factors

Low socioeconomic status has emerged as a risk factor. Increased psychosocial stressors, limited educational and economic opportunities, and lack of peer influence favoring healthier lifestyle choices may be causative elements leading to enhanced coronary artery disease among individuals with low socioeconomic living conditions.

Air pollution was estimated to have caused 9 million deaths worldwide in 2019, with 62% due to CVD and 31.7% to coronary artery disease. Severely polluted environmental aerosols contain several toxic metals, such as lead, mercury, arsenic, and cadmium. Transient exposure to various air pollutants may trigger the onset of an acute coronary syndrome.
 

Lifestyle factors

Long working hours by patients who have experienced a first myocardial infarction increase the risk for a recurrent event, possibly because of prolonged exposure to work stressors.

Skipping breakfast has been linked to increased cardiovascular and all-cause mortality.

Long-term consumption of drinks containing sugar and artificial sweeteners has also been associated with increased cardiovascular mortality.

Recognizing the presence of one or more of these new risk factors could help prompt and improve behaviors for reducing more conventional CV risk factors to a minimum.

This article was translated from Univadis Italy, which is part of the Medscape Professional Network.

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

Seasonal variation in one of the hormones used to monitor thyroid function could in turn lead to false diagnoses of subclinical hypothyroidism and unnecessary prescriptions of levothyroxine, according to Yale clinical chemist Joe M. El-Khoury, PhD.

A Japanese study of more than 7,000 healthy individuals showed that thyrotropin-stimulating hormone (TSH) varies widely throughout the seasons, he said, peaking in the northern hemisphere’s winter months (January to February) with its low in the summer months (June to August). That paper was published last year in the Journal of the Endocrine Society.

Sebastian Kaulitzki/Fotolia

But free thyroxine (FT4) levels in the Japanese population remained relatively stable, he wrote in a letter recently published in Clinical Chemistry.

“If you end up with a mildly elevated TSH result and a normal FT4, try getting retested 2-3 months later to make sure this is not a seasonal artifact or transient increase before prescribing/taking levothyroxine unnecessarily,” advised Dr. El-Khoury, director of Yale University’s Clinical Chemistry Laboratory, New Haven, Conn.

“Because the [population-based, laboratory] reference ranges don’t account for seasonal variation, we’re flagging a significant number of people as high TSH when they’re normal, and physicians are prescribing levothyroxine inappropriately to healthy people who don’t need it,” he told this news organization, adding that overtreatment can be harmful, particularly for elderly people.

This seasonal variation in TSH could account for between a third to a half of the 90% of all levothyroxine prescriptions that were found to be unnecessary, according to a U.S. study in 2021, Dr. El-Khoury added.

In a comment, Trisha Cubb, MD, said that Dr. El-Khoury’s letter “raises a good point, that we really need to look at our reference ranges, especially when more and more studies are showing that so many thyroid hormone prescriptions may not be necessary.”

Dr. Cubb, thyroid section director and assistant professor of clinical medicine at Weill Cornell Medical College/Houston Methodist Academic Institute, Texas, also agrees with Dr. El-Khoury’s suggestion to repeat lab results in some instances.

“I think repeating results, especially in our patients with subclinical disease, is important,” she noted.

And she pointed out that seasonal variation isn’t the only relevant variable. “We also know that multiple clinical factors like pregnancy status, coexisting comorbidities, or age can all influence what we as clinicians consider an acceptable TSH range in an individual patient.” And other medications, such as steroids, or supplements like biotin, “can all affect thyroid lab values,” she noted.

“Ensuring that minor abnormalities aren’t transient is important prior to initiating medical therapy. With any medical therapy there are possible side effects, along with time, cost, [and] monitoring, all of which can be associated with thyroid hormone replacement.”
 

TSH reference ranges should be adapted for subpopulations

Dr. El-Khoury explained that to get an idea of how big the seasonal differences in TSH observed in the Japanese study were, “the upper end of the population they tracked goes from 5.2 [mIU/L] in January to 3.4 [mIU/L] in August. So you have almost a 2-unit change in concentration that can happen in the reference population. But laboratory reference ranges, or ‘normal ranges,’ are usually fixed and don’t change by season.”

The higher the TSH, the more likely a person is to have hypothyroidism. Major recent studies have found no benefit of levothyroxine treatment with TSH levels below 7.0-10.0 mIU/L, he said.

“So, I suggest that the limit should be 7.0 [mIU/L] to be safe, but it could be as high as 10 [mIU/L]. In any case, let’s shift the mindset to clinical outcome–based treatment cutoffs,” he said, noting that this approach is currently used for decisions on cholesterol-lowering therapy or vitamin D supplementation, for example.

Regarding this suggestion of using a TSH cutoff of 7 mIU/L to diagnose subclinical hypothyroidism, Dr. Cubb said: “It really depends on the specific population. In an elderly patient, a higher TSH may be of less clinical concern when compared to a female who is actively trying to get pregnant.

“Overall, I think we do need to better understand what appropriate TSH ranges are in specific subpopulations, and then with time, make this more understandable and available for general medicine as well as subspecialty providers to be able to utilize,” she noted.

Regarding the particular Japanese findings cited by Dr. El-Khoury, Dr. Cubb observed that this was a very specific study population, “so we would need more data showing that this is more generalizable.”

And she noted that there’s also diurnal variation in TSH. “In the [Japanese] paper, patients had their thyroid labs drawn between 8:00 a.m. and 9:00 a.m. in a fasting state. Oftentimes in the U.S., thyroid labs are not drawn at specific times or [during] fasting. I think this is one of many factors that should be considered.”
 

Acknowledging seasonal variation would be a start

But overall, Dr. Cubb said that both the Japanese study and Dr. El-Khoury’s letter highlight “how season, in and of itself, which is not something we usually think about, can affect thyroid lab results. I believe as more data come out, more generalizable data, that’s how evidence-based guidelines are generated over time.”

According to Dr. El-Khoury, fixing the laboratory reference range issues would likely require a joint effort of professional medical societies, reference laboratories, and assay manufacturers. But with seasonal variation, that might be a difficult task.

“The problem is, in laboratory medicine, we don’t have rules for an analyte that changes by season to do anything different. My goal is to get people to at least acknowledge this is a problem and do something,” he concluded.

Dr. El-Khoury and Dr. Cubb have reported no relevant financial relationships.
 

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

Seasonal variation in one of the hormones used to monitor thyroid function could in turn lead to false diagnoses of subclinical hypothyroidism and unnecessary prescriptions of levothyroxine, according to Yale clinical chemist Joe M. El-Khoury, PhD.

A Japanese study of more than 7,000 healthy individuals showed that thyrotropin-stimulating hormone (TSH) varies widely throughout the seasons, he said, peaking in the northern hemisphere’s winter months (January to February) with its low in the summer months (June to August). That paper was published last year in the Journal of the Endocrine Society.

Sebastian Kaulitzki/Fotolia

But free thyroxine (FT4) levels in the Japanese population remained relatively stable, he wrote in a letter recently published in Clinical Chemistry.

“If you end up with a mildly elevated TSH result and a normal FT4, try getting retested 2-3 months later to make sure this is not a seasonal artifact or transient increase before prescribing/taking levothyroxine unnecessarily,” advised Dr. El-Khoury, director of Yale University’s Clinical Chemistry Laboratory, New Haven, Conn.

“Because the [population-based, laboratory] reference ranges don’t account for seasonal variation, we’re flagging a significant number of people as high TSH when they’re normal, and physicians are prescribing levothyroxine inappropriately to healthy people who don’t need it,” he told this news organization, adding that overtreatment can be harmful, particularly for elderly people.

This seasonal variation in TSH could account for between a third to a half of the 90% of all levothyroxine prescriptions that were found to be unnecessary, according to a U.S. study in 2021, Dr. El-Khoury added.

In a comment, Trisha Cubb, MD, said that Dr. El-Khoury’s letter “raises a good point, that we really need to look at our reference ranges, especially when more and more studies are showing that so many thyroid hormone prescriptions may not be necessary.”

Dr. Cubb, thyroid section director and assistant professor of clinical medicine at Weill Cornell Medical College/Houston Methodist Academic Institute, Texas, also agrees with Dr. El-Khoury’s suggestion to repeat lab results in some instances.

“I think repeating results, especially in our patients with subclinical disease, is important,” she noted.

And she pointed out that seasonal variation isn’t the only relevant variable. “We also know that multiple clinical factors like pregnancy status, coexisting comorbidities, or age can all influence what we as clinicians consider an acceptable TSH range in an individual patient.” And other medications, such as steroids, or supplements like biotin, “can all affect thyroid lab values,” she noted.

“Ensuring that minor abnormalities aren’t transient is important prior to initiating medical therapy. With any medical therapy there are possible side effects, along with time, cost, [and] monitoring, all of which can be associated with thyroid hormone replacement.”
 

TSH reference ranges should be adapted for subpopulations

Dr. El-Khoury explained that to get an idea of how big the seasonal differences in TSH observed in the Japanese study were, “the upper end of the population they tracked goes from 5.2 [mIU/L] in January to 3.4 [mIU/L] in August. So you have almost a 2-unit change in concentration that can happen in the reference population. But laboratory reference ranges, or ‘normal ranges,’ are usually fixed and don’t change by season.”

The higher the TSH, the more likely a person is to have hypothyroidism. Major recent studies have found no benefit of levothyroxine treatment with TSH levels below 7.0-10.0 mIU/L, he said.

“So, I suggest that the limit should be 7.0 [mIU/L] to be safe, but it could be as high as 10 [mIU/L]. In any case, let’s shift the mindset to clinical outcome–based treatment cutoffs,” he said, noting that this approach is currently used for decisions on cholesterol-lowering therapy or vitamin D supplementation, for example.

Regarding this suggestion of using a TSH cutoff of 7 mIU/L to diagnose subclinical hypothyroidism, Dr. Cubb said: “It really depends on the specific population. In an elderly patient, a higher TSH may be of less clinical concern when compared to a female who is actively trying to get pregnant.

“Overall, I think we do need to better understand what appropriate TSH ranges are in specific subpopulations, and then with time, make this more understandable and available for general medicine as well as subspecialty providers to be able to utilize,” she noted.

Regarding the particular Japanese findings cited by Dr. El-Khoury, Dr. Cubb observed that this was a very specific study population, “so we would need more data showing that this is more generalizable.”

And she noted that there’s also diurnal variation in TSH. “In the [Japanese] paper, patients had their thyroid labs drawn between 8:00 a.m. and 9:00 a.m. in a fasting state. Oftentimes in the U.S., thyroid labs are not drawn at specific times or [during] fasting. I think this is one of many factors that should be considered.”
 

Acknowledging seasonal variation would be a start

But overall, Dr. Cubb said that both the Japanese study and Dr. El-Khoury’s letter highlight “how season, in and of itself, which is not something we usually think about, can affect thyroid lab results. I believe as more data come out, more generalizable data, that’s how evidence-based guidelines are generated over time.”

According to Dr. El-Khoury, fixing the laboratory reference range issues would likely require a joint effort of professional medical societies, reference laboratories, and assay manufacturers. But with seasonal variation, that might be a difficult task.

“The problem is, in laboratory medicine, we don’t have rules for an analyte that changes by season to do anything different. My goal is to get people to at least acknowledge this is a problem and do something,” he concluded.

Dr. El-Khoury and Dr. Cubb have reported no relevant financial relationships.
 

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

Seasonal variation in one of the hormones used to monitor thyroid function could in turn lead to false diagnoses of subclinical hypothyroidism and unnecessary prescriptions of levothyroxine, according to Yale clinical chemist Joe M. El-Khoury, PhD.

A Japanese study of more than 7,000 healthy individuals showed that thyrotropin-stimulating hormone (TSH) varies widely throughout the seasons, he said, peaking in the northern hemisphere’s winter months (January to February) with its low in the summer months (June to August). That paper was published last year in the Journal of the Endocrine Society.

Sebastian Kaulitzki/Fotolia

But free thyroxine (FT4) levels in the Japanese population remained relatively stable, he wrote in a letter recently published in Clinical Chemistry.

“If you end up with a mildly elevated TSH result and a normal FT4, try getting retested 2-3 months later to make sure this is not a seasonal artifact or transient increase before prescribing/taking levothyroxine unnecessarily,” advised Dr. El-Khoury, director of Yale University’s Clinical Chemistry Laboratory, New Haven, Conn.

“Because the [population-based, laboratory] reference ranges don’t account for seasonal variation, we’re flagging a significant number of people as high TSH when they’re normal, and physicians are prescribing levothyroxine inappropriately to healthy people who don’t need it,” he told this news organization, adding that overtreatment can be harmful, particularly for elderly people.

This seasonal variation in TSH could account for between a third to a half of the 90% of all levothyroxine prescriptions that were found to be unnecessary, according to a U.S. study in 2021, Dr. El-Khoury added.

In a comment, Trisha Cubb, MD, said that Dr. El-Khoury’s letter “raises a good point, that we really need to look at our reference ranges, especially when more and more studies are showing that so many thyroid hormone prescriptions may not be necessary.”

Dr. Cubb, thyroid section director and assistant professor of clinical medicine at Weill Cornell Medical College/Houston Methodist Academic Institute, Texas, also agrees with Dr. El-Khoury’s suggestion to repeat lab results in some instances.

“I think repeating results, especially in our patients with subclinical disease, is important,” she noted.

And she pointed out that seasonal variation isn’t the only relevant variable. “We also know that multiple clinical factors like pregnancy status, coexisting comorbidities, or age can all influence what we as clinicians consider an acceptable TSH range in an individual patient.” And other medications, such as steroids, or supplements like biotin, “can all affect thyroid lab values,” she noted.

“Ensuring that minor abnormalities aren’t transient is important prior to initiating medical therapy. With any medical therapy there are possible side effects, along with time, cost, [and] monitoring, all of which can be associated with thyroid hormone replacement.”
 

TSH reference ranges should be adapted for subpopulations

Dr. El-Khoury explained that to get an idea of how big the seasonal differences in TSH observed in the Japanese study were, “the upper end of the population they tracked goes from 5.2 [mIU/L] in January to 3.4 [mIU/L] in August. So you have almost a 2-unit change in concentration that can happen in the reference population. But laboratory reference ranges, or ‘normal ranges,’ are usually fixed and don’t change by season.”

The higher the TSH, the more likely a person is to have hypothyroidism. Major recent studies have found no benefit of levothyroxine treatment with TSH levels below 7.0-10.0 mIU/L, he said.

“So, I suggest that the limit should be 7.0 [mIU/L] to be safe, but it could be as high as 10 [mIU/L]. In any case, let’s shift the mindset to clinical outcome–based treatment cutoffs,” he said, noting that this approach is currently used for decisions on cholesterol-lowering therapy or vitamin D supplementation, for example.

Regarding this suggestion of using a TSH cutoff of 7 mIU/L to diagnose subclinical hypothyroidism, Dr. Cubb said: “It really depends on the specific population. In an elderly patient, a higher TSH may be of less clinical concern when compared to a female who is actively trying to get pregnant.

“Overall, I think we do need to better understand what appropriate TSH ranges are in specific subpopulations, and then with time, make this more understandable and available for general medicine as well as subspecialty providers to be able to utilize,” she noted.

Regarding the particular Japanese findings cited by Dr. El-Khoury, Dr. Cubb observed that this was a very specific study population, “so we would need more data showing that this is more generalizable.”

And she noted that there’s also diurnal variation in TSH. “In the [Japanese] paper, patients had their thyroid labs drawn between 8:00 a.m. and 9:00 a.m. in a fasting state. Oftentimes in the U.S., thyroid labs are not drawn at specific times or [during] fasting. I think this is one of many factors that should be considered.”
 

Acknowledging seasonal variation would be a start

But overall, Dr. Cubb said that both the Japanese study and Dr. El-Khoury’s letter highlight “how season, in and of itself, which is not something we usually think about, can affect thyroid lab results. I believe as more data come out, more generalizable data, that’s how evidence-based guidelines are generated over time.”

According to Dr. El-Khoury, fixing the laboratory reference range issues would likely require a joint effort of professional medical societies, reference laboratories, and assay manufacturers. But with seasonal variation, that might be a difficult task.

“The problem is, in laboratory medicine, we don’t have rules for an analyte that changes by season to do anything different. My goal is to get people to at least acknowledge this is a problem and do something,” he concluded.

Dr. El-Khoury and Dr. Cubb have reported no relevant financial relationships.
 

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

The Food and Drug Administration has approved Medtronic Minimed’s 780G automated insulin delivery system with the Guardian 4 sensor.

The latest so-called artificial pancreas system is approved for people aged 7 years and older who have type 1 diabetes. Medtronic will begin taking preorders for the 780G on May 15, 2023. Users of the current MiniMed 770G will be eligible for no-cost remote software upgrades.

Olivier Le Moal/Getty Images

The 780G is currently available in 105 countries. It has been available in Europe since 2020 and in the United Kingdom since 2021. It is the first automated insulin delivery system to automatically administer bolus correction insulin doses every 5 minutes to correct meal-related hyperglycemia.

This so-called meal detection technology doesn’t replace manual premeal boluses but does provide extra insulin if the premeal bolus is skipped or is insufficient.

As with other automated systems, the 780G automatically adjusts basal insulin doses up or down based on glucose levels and trends and shuts off insulin delivery to prevent hypoglycemia. The insulin pump’s infusion set can be worn for 7 days, rather than 3 days as with the older system, and the glucose target level can be set as low as 100 mg/dL.

And in contrast to the older MiniMed 670G system, which tended to frequently boot users out of automated mode, with the 780G, users spent an average of 95% of the time in the automated “SmartGuard” mode.

In the pivotal U.S. trial, overall, patients who used the 780G spent 75% of the time in ideal glucose range (70-180 mg/dL) and 1.8% of the time below that range. Overnight, the figures were 82% and 1.5%, respectively. With the glucose target set at 100 mg/dL and active insulin time set to 2 hours, patients spent 78.8% of time in range without increased hyperglycemia.

In the ADAPT study, with the 780G, there was a 26% increase in time in ideal glucose range and a 1.4% reduction in A1c compared with results for patients who received multiple daily insulin injections with intermittently scanned continuous glucose monitoring, without an increase in hypoglycemia. Overnight, time in range increased 30.2%. The results were sustained at 1 year.

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

The Food and Drug Administration has approved Medtronic Minimed’s 780G automated insulin delivery system with the Guardian 4 sensor.

The latest so-called artificial pancreas system is approved for people aged 7 years and older who have type 1 diabetes. Medtronic will begin taking preorders for the 780G on May 15, 2023. Users of the current MiniMed 770G will be eligible for no-cost remote software upgrades.

Olivier Le Moal/Getty Images

The 780G is currently available in 105 countries. It has been available in Europe since 2020 and in the United Kingdom since 2021. It is the first automated insulin delivery system to automatically administer bolus correction insulin doses every 5 minutes to correct meal-related hyperglycemia.

This so-called meal detection technology doesn’t replace manual premeal boluses but does provide extra insulin if the premeal bolus is skipped or is insufficient.

As with other automated systems, the 780G automatically adjusts basal insulin doses up or down based on glucose levels and trends and shuts off insulin delivery to prevent hypoglycemia. The insulin pump’s infusion set can be worn for 7 days, rather than 3 days as with the older system, and the glucose target level can be set as low as 100 mg/dL.

And in contrast to the older MiniMed 670G system, which tended to frequently boot users out of automated mode, with the 780G, users spent an average of 95% of the time in the automated “SmartGuard” mode.

In the pivotal U.S. trial, overall, patients who used the 780G spent 75% of the time in ideal glucose range (70-180 mg/dL) and 1.8% of the time below that range. Overnight, the figures were 82% and 1.5%, respectively. With the glucose target set at 100 mg/dL and active insulin time set to 2 hours, patients spent 78.8% of time in range without increased hyperglycemia.

In the ADAPT study, with the 780G, there was a 26% increase in time in ideal glucose range and a 1.4% reduction in A1c compared with results for patients who received multiple daily insulin injections with intermittently scanned continuous glucose monitoring, without an increase in hypoglycemia. Overnight, time in range increased 30.2%. The results were sustained at 1 year.

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

The Food and Drug Administration has approved Medtronic Minimed’s 780G automated insulin delivery system with the Guardian 4 sensor.

The latest so-called artificial pancreas system is approved for people aged 7 years and older who have type 1 diabetes. Medtronic will begin taking preorders for the 780G on May 15, 2023. Users of the current MiniMed 770G will be eligible for no-cost remote software upgrades.

Olivier Le Moal/Getty Images

The 780G is currently available in 105 countries. It has been available in Europe since 2020 and in the United Kingdom since 2021. It is the first automated insulin delivery system to automatically administer bolus correction insulin doses every 5 minutes to correct meal-related hyperglycemia.

This so-called meal detection technology doesn’t replace manual premeal boluses but does provide extra insulin if the premeal bolus is skipped or is insufficient.

As with other automated systems, the 780G automatically adjusts basal insulin doses up or down based on glucose levels and trends and shuts off insulin delivery to prevent hypoglycemia. The insulin pump’s infusion set can be worn for 7 days, rather than 3 days as with the older system, and the glucose target level can be set as low as 100 mg/dL.

And in contrast to the older MiniMed 670G system, which tended to frequently boot users out of automated mode, with the 780G, users spent an average of 95% of the time in the automated “SmartGuard” mode.

In the pivotal U.S. trial, overall, patients who used the 780G spent 75% of the time in ideal glucose range (70-180 mg/dL) and 1.8% of the time below that range. Overnight, the figures were 82% and 1.5%, respectively. With the glucose target set at 100 mg/dL and active insulin time set to 2 hours, patients spent 78.8% of time in range without increased hyperglycemia.

In the ADAPT study, with the 780G, there was a 26% increase in time in ideal glucose range and a 1.4% reduction in A1c compared with results for patients who received multiple daily insulin injections with intermittently scanned continuous glucose monitoring, without an increase in hypoglycemia. Overnight, time in range increased 30.2%. The results were sustained at 1 year.

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

BOSTON – The neurologic symptoms of long COVID appear to be explained by a phenomenon known as antigenic imprinting, which involves a misdirected immune response to the SARS-CoV2 virus, according to a collaborative study presented at the 2023 annual meeting of the American Academy of Neurology.

Already documented in several other viral infections, such as influenza and human immunodeficiency virus, antigenic imprinting results in production of antibodies to previously encountered viral infections rather than to the immediate threat, according to Marianna Spatola, MD, PhD, a research fellow at the Ragon Institute, Harvard University, Cambridge, Mass.
 

Original antigenic sin

In the case of persistent neurologic symptoms after COVID, a condition known as neuroPASC (neurological postacute sequelae of SARS-CoV2 infection), antibodies produced for previously encountered coronaviruses rather than for SARS-CoV2 might explain most or all cases, according to the data Dr. Spatola presented.

The evidence for this explanation was drawn from a study of 112 patients evaluated months after an acute episode of COVID-19. Of these, 18 patients had persistent neurologic dysfunction. When compared with the 94 whose infection resolved without sequelae, the patients with prolonged neurologic impairments had relatively low systemic antibody response to SARS-CoV2. However, they showed relatively high antibody responses against other coronaviruses.

This is a pattern consistent with antigenic imprinting, a concept first described more than 60 years ago as original antigenic sin. When the immune system becomes imprinted with an antigen from the first encountered virus from a family of pathogens, it governs all subsequent antibody responses, according to several published studies that have described and evaluated this concept.
 

Additional evidence

In Dr. Spatola’s study, other differences, particularly in regard to the cerebrospinal fluid (CSF), further supported the role of antigenic imprinting as a cause of neuroPASC. For one, those with elevated immune responses to other common coronaviruses rather than SARS-CoV2 in the CSF relative to the periphery were more likely to have a bad outcome in regard to neurologic symptoms.

Moreover, the CSF in neuroPASC patients “was characterized by increased IgG1 and absence of IgM, suggesting compartmentalized humoral responses within the CSF through selective transfer of antibodies from the serum to the CSF across the blood-brain barrier rather than through intrathecal synthesis,” Dr. Spatola reported.

In the case of COVID-19, the propensity for antigenic imprinting is not difficult to understand.

“The common cold coronaviruses are pretty similar to SARS-CoV2, but they are not exactly the same,” Dr. Spatola said. Her work and studies by others suggest that when antigenic imprinting occurs, “it prevents full maturation of the antibody response.”

NeuroPASC is one of many manifestations of long COVID, but Dr. Spatola pointed out that the immune response in the CSF is unique and the causes of prolonged neurologic impairment after COVID-19 are likely to involve different mechanisms than other long-COVID symptoms.

“Antibodies in the brain are functionally different,” said Dr. Spatola, noting for example that antibody-directed defenses against viral threats show a greater relative reliance on phagocytosis. This might become important in the development of therapeutics for neurologic symptoms of long COVID.
 

A different phenomenon

The manifestations of neuroPASC are heterogeneous and can include confusion, cognitive dysfunction, headache, encephalitis, and other impairments. Neurologic symptoms occur during acute SARS-CoV2 infections, but neuroPASC appears to be a different phenomenon. These symptoms, which develop after the initial respiratory disease has resolved, were attributed by Dr. Spatola to persistent inflammation that is not necessarily directly related to ongoing infection.

“The reason why some patients develop neuroPASC is unknown, but I think the evidence has pointed to a role for the immune system rather than the virus itself,” Dr. Spatola said.

Currently, neuroPASC is a clinical diagnosis but Dr. Spatola and her coinvestigators are conducting research to identify biomarkers. A viable diagnostic test is not expected imminently. They have identified 150 different features with potential relevance to neuroPASC.

In their comparison of those who did relative to those who did not develop neuroPASC, the initial studies were undertaken 2-4 months after the acute COVID-19 symptoms had resolved. The patients with neuroPASC and those without neurologic sequelae have now been followed for 6-8 months, which Dr. Spatola said was too short to draw firm conclusions about outcomes.
 

An evolving concept

Despite the small sample size of this study, these are “very interesting data” for considering the pathogenesis of neuroPASC, which is “a concept that is still evolving,” according to Natalia S. Rost, MD, chief of the stroke division, department of neurology, Massachusetts General Hospital, Boston.

Applied to SARS-CoV2, the concept of original antigenic sin “is new” but Dr. Rost said that it might help differentiate neuroPASC from acute neurologic symptoms of COVID-19, which include stroke. She indicated that the work performed by Dr. Spatola and others might eventually explain the pathology while leading to treatment strategies. She cautioned that the concepts explored in this study “need to be further developed” through larger sample sizes and the exploration of other variables that support the hypothesis.

Dr. Spatola and Dr. Rost report no potential conflicts of interest.

BOSTON – The neurologic symptoms of long COVID appear to be explained by a phenomenon known as antigenic imprinting, which involves a misdirected immune response to the SARS-CoV2 virus, according to a collaborative study presented at the 2023 annual meeting of the American Academy of Neurology.

Already documented in several other viral infections, such as influenza and human immunodeficiency virus, antigenic imprinting results in production of antibodies to previously encountered viral infections rather than to the immediate threat, according to Marianna Spatola, MD, PhD, a research fellow at the Ragon Institute, Harvard University, Cambridge, Mass.
 

Original antigenic sin

In the case of persistent neurologic symptoms after COVID, a condition known as neuroPASC (neurological postacute sequelae of SARS-CoV2 infection), antibodies produced for previously encountered coronaviruses rather than for SARS-CoV2 might explain most or all cases, according to the data Dr. Spatola presented.

The evidence for this explanation was drawn from a study of 112 patients evaluated months after an acute episode of COVID-19. Of these, 18 patients had persistent neurologic dysfunction. When compared with the 94 whose infection resolved without sequelae, the patients with prolonged neurologic impairments had relatively low systemic antibody response to SARS-CoV2. However, they showed relatively high antibody responses against other coronaviruses.

This is a pattern consistent with antigenic imprinting, a concept first described more than 60 years ago as original antigenic sin. When the immune system becomes imprinted with an antigen from the first encountered virus from a family of pathogens, it governs all subsequent antibody responses, according to several published studies that have described and evaluated this concept.
 

Additional evidence

In Dr. Spatola’s study, other differences, particularly in regard to the cerebrospinal fluid (CSF), further supported the role of antigenic imprinting as a cause of neuroPASC. For one, those with elevated immune responses to other common coronaviruses rather than SARS-CoV2 in the CSF relative to the periphery were more likely to have a bad outcome in regard to neurologic symptoms.

Moreover, the CSF in neuroPASC patients “was characterized by increased IgG1 and absence of IgM, suggesting compartmentalized humoral responses within the CSF through selective transfer of antibodies from the serum to the CSF across the blood-brain barrier rather than through intrathecal synthesis,” Dr. Spatola reported.

In the case of COVID-19, the propensity for antigenic imprinting is not difficult to understand.

“The common cold coronaviruses are pretty similar to SARS-CoV2, but they are not exactly the same,” Dr. Spatola said. Her work and studies by others suggest that when antigenic imprinting occurs, “it prevents full maturation of the antibody response.”

NeuroPASC is one of many manifestations of long COVID, but Dr. Spatola pointed out that the immune response in the CSF is unique and the causes of prolonged neurologic impairment after COVID-19 are likely to involve different mechanisms than other long-COVID symptoms.

“Antibodies in the brain are functionally different,” said Dr. Spatola, noting for example that antibody-directed defenses against viral threats show a greater relative reliance on phagocytosis. This might become important in the development of therapeutics for neurologic symptoms of long COVID.
 

A different phenomenon

The manifestations of neuroPASC are heterogeneous and can include confusion, cognitive dysfunction, headache, encephalitis, and other impairments. Neurologic symptoms occur during acute SARS-CoV2 infections, but neuroPASC appears to be a different phenomenon. These symptoms, which develop after the initial respiratory disease has resolved, were attributed by Dr. Spatola to persistent inflammation that is not necessarily directly related to ongoing infection.

“The reason why some patients develop neuroPASC is unknown, but I think the evidence has pointed to a role for the immune system rather than the virus itself,” Dr. Spatola said.

Currently, neuroPASC is a clinical diagnosis but Dr. Spatola and her coinvestigators are conducting research to identify biomarkers. A viable diagnostic test is not expected imminently. They have identified 150 different features with potential relevance to neuroPASC.

In their comparison of those who did relative to those who did not develop neuroPASC, the initial studies were undertaken 2-4 months after the acute COVID-19 symptoms had resolved. The patients with neuroPASC and those without neurologic sequelae have now been followed for 6-8 months, which Dr. Spatola said was too short to draw firm conclusions about outcomes.
 

An evolving concept

Despite the small sample size of this study, these are “very interesting data” for considering the pathogenesis of neuroPASC, which is “a concept that is still evolving,” according to Natalia S. Rost, MD, chief of the stroke division, department of neurology, Massachusetts General Hospital, Boston.

Applied to SARS-CoV2, the concept of original antigenic sin “is new” but Dr. Rost said that it might help differentiate neuroPASC from acute neurologic symptoms of COVID-19, which include stroke. She indicated that the work performed by Dr. Spatola and others might eventually explain the pathology while leading to treatment strategies. She cautioned that the concepts explored in this study “need to be further developed” through larger sample sizes and the exploration of other variables that support the hypothesis.

Dr. Spatola and Dr. Rost report no potential conflicts of interest.

BOSTON – The neurologic symptoms of long COVID appear to be explained by a phenomenon known as antigenic imprinting, which involves a misdirected immune response to the SARS-CoV2 virus, according to a collaborative study presented at the 2023 annual meeting of the American Academy of Neurology.

Already documented in several other viral infections, such as influenza and human immunodeficiency virus, antigenic imprinting results in production of antibodies to previously encountered viral infections rather than to the immediate threat, according to Marianna Spatola, MD, PhD, a research fellow at the Ragon Institute, Harvard University, Cambridge, Mass.
 

Original antigenic sin

In the case of persistent neurologic symptoms after COVID, a condition known as neuroPASC (neurological postacute sequelae of SARS-CoV2 infection), antibodies produced for previously encountered coronaviruses rather than for SARS-CoV2 might explain most or all cases, according to the data Dr. Spatola presented.

The evidence for this explanation was drawn from a study of 112 patients evaluated months after an acute episode of COVID-19. Of these, 18 patients had persistent neurologic dysfunction. When compared with the 94 whose infection resolved without sequelae, the patients with prolonged neurologic impairments had relatively low systemic antibody response to SARS-CoV2. However, they showed relatively high antibody responses against other coronaviruses.

This is a pattern consistent with antigenic imprinting, a concept first described more than 60 years ago as original antigenic sin. When the immune system becomes imprinted with an antigen from the first encountered virus from a family of pathogens, it governs all subsequent antibody responses, according to several published studies that have described and evaluated this concept.
 

Additional evidence

In Dr. Spatola’s study, other differences, particularly in regard to the cerebrospinal fluid (CSF), further supported the role of antigenic imprinting as a cause of neuroPASC. For one, those with elevated immune responses to other common coronaviruses rather than SARS-CoV2 in the CSF relative to the periphery were more likely to have a bad outcome in regard to neurologic symptoms.

Moreover, the CSF in neuroPASC patients “was characterized by increased IgG1 and absence of IgM, suggesting compartmentalized humoral responses within the CSF through selective transfer of antibodies from the serum to the CSF across the blood-brain barrier rather than through intrathecal synthesis,” Dr. Spatola reported.

In the case of COVID-19, the propensity for antigenic imprinting is not difficult to understand.

“The common cold coronaviruses are pretty similar to SARS-CoV2, but they are not exactly the same,” Dr. Spatola said. Her work and studies by others suggest that when antigenic imprinting occurs, “it prevents full maturation of the antibody response.”

NeuroPASC is one of many manifestations of long COVID, but Dr. Spatola pointed out that the immune response in the CSF is unique and the causes of prolonged neurologic impairment after COVID-19 are likely to involve different mechanisms than other long-COVID symptoms.

“Antibodies in the brain are functionally different,” said Dr. Spatola, noting for example that antibody-directed defenses against viral threats show a greater relative reliance on phagocytosis. This might become important in the development of therapeutics for neurologic symptoms of long COVID.
 

A different phenomenon

The manifestations of neuroPASC are heterogeneous and can include confusion, cognitive dysfunction, headache, encephalitis, and other impairments. Neurologic symptoms occur during acute SARS-CoV2 infections, but neuroPASC appears to be a different phenomenon. These symptoms, which develop after the initial respiratory disease has resolved, were attributed by Dr. Spatola to persistent inflammation that is not necessarily directly related to ongoing infection.

“The reason why some patients develop neuroPASC is unknown, but I think the evidence has pointed to a role for the immune system rather than the virus itself,” Dr. Spatola said.

Currently, neuroPASC is a clinical diagnosis but Dr. Spatola and her coinvestigators are conducting research to identify biomarkers. A viable diagnostic test is not expected imminently. They have identified 150 different features with potential relevance to neuroPASC.

In their comparison of those who did relative to those who did not develop neuroPASC, the initial studies were undertaken 2-4 months after the acute COVID-19 symptoms had resolved. The patients with neuroPASC and those without neurologic sequelae have now been followed for 6-8 months, which Dr. Spatola said was too short to draw firm conclusions about outcomes.
 

An evolving concept

Despite the small sample size of this study, these are “very interesting data” for considering the pathogenesis of neuroPASC, which is “a concept that is still evolving,” according to Natalia S. Rost, MD, chief of the stroke division, department of neurology, Massachusetts General Hospital, Boston.

Applied to SARS-CoV2, the concept of original antigenic sin “is new” but Dr. Rost said that it might help differentiate neuroPASC from acute neurologic symptoms of COVID-19, which include stroke. She indicated that the work performed by Dr. Spatola and others might eventually explain the pathology while leading to treatment strategies. She cautioned that the concepts explored in this study “need to be further developed” through larger sample sizes and the exploration of other variables that support the hypothesis.

Dr. Spatola and Dr. Rost report no potential conflicts of interest.

The American College of Cardiology has released an Expert Consensus Decision Pathway (ECDP) on the management of heart failure with preserved ejection fraction (HFpEF).

The 44-page document highlights the “critical need” to accurately diagnose HFpEF to permit timely implementation of evidence- and guideline-based therapies to improve patient outcomes.

Although the incidence of overall HF in the United States appears to be stable or declining, the incidence of HFpEF continues to rise in tandem with increasing age and burdens of obesity, sedentary lifestyle, and cardiometabolic disorders.

HFpEF now accounts for more than one half of HF cases but remains “underrecognized” in everyday clinical practice, said the writing group, led by Michelle Kittleson, MD, PhD, professor of medicine, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles.

HFpEF is a complex condition, often with multiple overlapping comorbidities, including hypertension, diabetes, obesity, and sleep apnea; optimal management requires a multidisciplinary approach, the writing group said.

The ECDP on HFpEF lays out a structure for diagnosis, clinical decision-making, management of comorbidities, implementation of the latest guideline-directed medical therapy (pharmacologic and nonpharmacologic), and equitable delivery of care.

The document was published online in the Journal of the American College of Cardiology.

It aligns with and builds on recommendations from the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

“HFpEF is one of the most pressing diagnostic and therapeutic challenges in clinical medicine today given its increasing prevalence, under diagnosis, poor prognosis, limited therapeutic options, and substantial burden on the health care system worldwide,” wrote the authors of a companion scientific statement on HFpEF.

Despite these challenges, the success of recent sodium-glucose cotransporter 2 inhibitor trials has shown that HFpEF is treatable, Barry Borlaug, MD, department of cardiovascular medicine, Mayo Clinic, Rochester, Minn., and coauthors pointed out.

They noted that “ongoing large-scale studies of HFpEF pathobiology, an increasing number of translational studies spanning the gap between the bedside and the bench, and numerous clinical trials of novel therapeutics in HFpEF offer a glimpse of hope toward a future of reduced prevalence, morbidity, and mortality associated with HFpEF, which would be a major advance for population health.”

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

The American College of Cardiology has released an Expert Consensus Decision Pathway (ECDP) on the management of heart failure with preserved ejection fraction (HFpEF).

The 44-page document highlights the “critical need” to accurately diagnose HFpEF to permit timely implementation of evidence- and guideline-based therapies to improve patient outcomes.

Although the incidence of overall HF in the United States appears to be stable or declining, the incidence of HFpEF continues to rise in tandem with increasing age and burdens of obesity, sedentary lifestyle, and cardiometabolic disorders.

HFpEF now accounts for more than one half of HF cases but remains “underrecognized” in everyday clinical practice, said the writing group, led by Michelle Kittleson, MD, PhD, professor of medicine, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles.

HFpEF is a complex condition, often with multiple overlapping comorbidities, including hypertension, diabetes, obesity, and sleep apnea; optimal management requires a multidisciplinary approach, the writing group said.

The ECDP on HFpEF lays out a structure for diagnosis, clinical decision-making, management of comorbidities, implementation of the latest guideline-directed medical therapy (pharmacologic and nonpharmacologic), and equitable delivery of care.

The document was published online in the Journal of the American College of Cardiology.

It aligns with and builds on recommendations from the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

“HFpEF is one of the most pressing diagnostic and therapeutic challenges in clinical medicine today given its increasing prevalence, under diagnosis, poor prognosis, limited therapeutic options, and substantial burden on the health care system worldwide,” wrote the authors of a companion scientific statement on HFpEF.

Despite these challenges, the success of recent sodium-glucose cotransporter 2 inhibitor trials has shown that HFpEF is treatable, Barry Borlaug, MD, department of cardiovascular medicine, Mayo Clinic, Rochester, Minn., and coauthors pointed out.

They noted that “ongoing large-scale studies of HFpEF pathobiology, an increasing number of translational studies spanning the gap between the bedside and the bench, and numerous clinical trials of novel therapeutics in HFpEF offer a glimpse of hope toward a future of reduced prevalence, morbidity, and mortality associated with HFpEF, which would be a major advance for population health.”

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

The American College of Cardiology has released an Expert Consensus Decision Pathway (ECDP) on the management of heart failure with preserved ejection fraction (HFpEF).

The 44-page document highlights the “critical need” to accurately diagnose HFpEF to permit timely implementation of evidence- and guideline-based therapies to improve patient outcomes.

Although the incidence of overall HF in the United States appears to be stable or declining, the incidence of HFpEF continues to rise in tandem with increasing age and burdens of obesity, sedentary lifestyle, and cardiometabolic disorders.

HFpEF now accounts for more than one half of HF cases but remains “underrecognized” in everyday clinical practice, said the writing group, led by Michelle Kittleson, MD, PhD, professor of medicine, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles.

HFpEF is a complex condition, often with multiple overlapping comorbidities, including hypertension, diabetes, obesity, and sleep apnea; optimal management requires a multidisciplinary approach, the writing group said.

The ECDP on HFpEF lays out a structure for diagnosis, clinical decision-making, management of comorbidities, implementation of the latest guideline-directed medical therapy (pharmacologic and nonpharmacologic), and equitable delivery of care.

The document was published online in the Journal of the American College of Cardiology.

It aligns with and builds on recommendations from the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.

“HFpEF is one of the most pressing diagnostic and therapeutic challenges in clinical medicine today given its increasing prevalence, under diagnosis, poor prognosis, limited therapeutic options, and substantial burden on the health care system worldwide,” wrote the authors of a companion scientific statement on HFpEF.

Despite these challenges, the success of recent sodium-glucose cotransporter 2 inhibitor trials has shown that HFpEF is treatable, Barry Borlaug, MD, department of cardiovascular medicine, Mayo Clinic, Rochester, Minn., and coauthors pointed out.

They noted that “ongoing large-scale studies of HFpEF pathobiology, an increasing number of translational studies spanning the gap between the bedside and the bench, and numerous clinical trials of novel therapeutics in HFpEF offer a glimpse of hope toward a future of reduced prevalence, morbidity, and mortality associated with HFpEF, which would be a major advance for population health.”

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

This discussion was recorded on April 6, 2023. This transcript has been edited for clarity.

Robert D. Glatter, MD: Welcome. I’m Dr. Robert Glatter, medical adviser for Medscape Emergency Medicine. Joining us today is Dr. Lewis Nelson, professor and chair of emergency medicine at Rutgers New Jersey Medical School and a certified medical toxicologist.

Today, we will be discussing an important and disturbing Gen Z trend circulating on social media, known as blackout rage gallon, or BORG.

Welcome, Lewis.

Lewis S. Nelson, MD: Thanks for having me.

Dr. Glatter: Thanks so much for joining us. This trend that’s been circulating on social media is really disturbing. It has elements that focus on binge drinking: Talking about taking a jug; emptying half of it out; and putting one fifth of vodka and some electrolytes, caffeine, or other things too is just incredibly disturbing. Teens and parents are looking at this. I’ll let you jump into the discussion.

Dr. Nelson: You’re totally right, it is disturbing. Binge drinking is a huge problem in this country in general. It’s a particular problem with young people – teenagers and young adults. I don’t think people appreciate the dangers associated with binge drinking, such as the amount of alcohol they consume and some of the unintended consequences of doing that.

To frame things quickly, we think there are probably around six people a day in the United States who die of alcohol poisoning. Alcohol poisoning basically is binge drinking to such an extent that you die of the alcohol itself. You’re not dying of a car crash or doing something that injures you. You’re dying of the alcohol. You’re drinking so much that your breathing slows, it stops, you have heart rhythm disturbances, and so on. It totals about 2,200 people a year in the United States.

Dr. Glatter: That’s alarming. For this trend, their argument is that half of the gallon is water. Therefore, I’m fine. I can drink it over 8-12 hours and it’s not an issue. How would you respond to that?

Dr. Nelson: Well, alcohol is alcohol. It’s all about how much you take in over what time period. I guess, in concept, it could be safer if you do it right. That’s not the way it’s been, so to speak, marketed on the various social media platforms. It’s meant to be a way to protect yourself from having your drink spiked or eating or ingesting contaminants from other people’s mouths when you share glasses or dip cups into communal pots like jungle juice or something.

Clearly, if you’re going to drink a large amount of alcohol over a short or long period of time, you do run the risk of having significant consequences, including bad decision-making if you’re just a little drunk all the way down to that of the complications you described about alcohol poisoning.

Dr. Glatter: There has been a comment made that this could be a form of harm reduction. The point of harm reduction is that we run trials, we validate it, and we test it. This, certainly in my mind, is no form of true harm reduction. I think you would agree.

Dr. Nelson: Many things that are marketed as harm reduction aren’t. There could be some aspects of this that could be considered harm reduction. You may believe – and there’s no reason not to – that protecting your drink is a good idea. If you’re at a bar and you leave your glass open and somebody put something in it, you can be drugged. Drug-facilitated sexual assault, for example, is a big issue. That means you have to leave your glass unattended. If you tend to your glass, it’s probably fine. One of the ways of harm reduction they mention is that by having a cap and having this bottle with you at all times, that can’t happen.

Now, in fairness, by far the drug most commonly associated with sexual assault is alcohol. It’s not gamma-hydroxybutyrate or ketamine. It’s not the other things that people are concerned about. Those happen, but those are small problems in the big picture. It’s drinking too much.

A form of harm reduction that you can comment on perhaps is that you make this drink concoction yourself, so you know what is in there. You can take that bottle, pour out half the water, and fill up the other half with water and nobody’s going to know. More likely, the way they say you should do it is you take your gallon jug, you pour it out, and you fill it up with one fifth of vodka.

One fifth of vodka is the same amount of volume as a bottle of wine. At 750 mL, that’s a huge amount of alcohol. If you measure the number of shots in that bottle, it’s about 17 shots. Even if you drink that over 6 hours, that’s still several shots an hour. That’s a large amount of alcohol. You might do two or three shots once and then not drink for a few hours. To sit and drink two or three shots an hour for 6 hours, that’s just an exceptional amount of alcohol.

They flavorize it and add caffeine, which only adds to the risk. It doesn’t make it in any way safer. With the volume, 1 gal of water or equivalent over a short period of time in and of itself could be a problem. There’s a large amount of mismessaging here. Whether something’s harm reduction, it could flip around to be easily construed or understood as being harmful.

Not to mention, the idea that when you make something safer, one of the unintended consequences of harm reduction is what we call risk compensation. This is best probably described as what’s called the Peltzman effect. The way that we think about airbags and seatbelts is that they’re going to reduce car crash deaths; and they do, but people drive faster and more recklessly because they know they’re safe.

This is a well-described problem in epidemiology: You expect a certain amount of harm reduction through some implemented process, but you don’t meet that because people take increased risks.

Dr. Glatter: Right. The idea of not developing a hangover is common among many teens and 20-somethings, thinking that because there’s hydration there, because half of it is water, it’s just not going to happen. There’s your “harm reduction,” but your judgment’s impaired. It’s day drinking at its best, all day long. Then someone has the idea to get behind the wheel. These are the disastrous consequences that we all fear.

Dr. Nelson: There is a great example, perhaps of an unintended consequence of harm reduction. By putting caffeine in it, depending on how much caffeine you put in, some of these mixtures can have up to 1,000 mg of caffeine. Remember, a cup of coffee is about 1-200 mg, so you’re talking about several cups of coffee. The idea is that you will not be able to sense, as you normally do, how drunk you are. You’re not going to be a sleepy drunk, you’re going to be an awake drunk.

The idea that you’re going to have to drive so you’re going to drink a strong cup of black coffee before you go driving, you’re not going to drive any better. I can assure you that. You’re going to be more awake, perhaps, and not fall asleep at the wheel, but you’re still going to have psychomotor impairment. Your judgment is going to be impaired. There’s nothing good that comes with adding caffeine except that you’re going to be awake.

From a hangover perspective, there are many things that we’ve guessed at or suggested as either prevention or cures for hangovers. I don’t doubt that you’re going to have some volume depletion if you drink a large amount of alcohol. Alcohol’s a diuretic, so you’re going to lose more volume than you bring in.

Hydrating is probably always a good idea, but there is hydrating and then there’s overhydrating. We don’t need volumes like that. If you drink a cup or two of water, you’re probably fine. You don’t need to drink half a gallon of water. That can lead to problems like delusional hyponatremia, and so forth. There’s not any clear benefit to doing it.

If you want to prevent a hangover, one of the ways you might do it is by using vodka. There are nice data that show that clear alcohols typically, particularly vodka, don’t have many of the congeners that make the specific forms of alcohol what they are. Bourbon smells and tastes like bourbon because of these little molecules, these alkalis and ketones and amino acids and things that make it taste and smell the way it does. That’s true for all the other alcohols.

Vodka has the least amount of that. Even wine and beer have those in them, but vodka is basically alcohol mixed with water. It’s probably the least hangover-prone of all the alcohols; but still, if you drink a lot of vodka, you’re going to have a hangover. It’s just a dose-response curve to how much alcohol you drink, to how drunk you get, and to how much of a hangover you’re going to have.

Dr. Glatter: The hangover is really what it’s about because people want to be functional the next day. There are many companies out there that market hangover remedies, but people are using this as the hangover remedy in a way that’s socially accepted. That’s a good point you make.

The question is how do we get the message out to parents and teens? What’s the best way you feel to really sound the alarm here?

Dr. Nelson: These are challenging issues. We face this all the time with all the sorts of social media in particular. Most parents are not as savvy on social media as their kids are. You have to know what your children are doing. You should know what they’re listening to and watching. You do have to pay attention to the media directed at parents that will inform you a little bit about what your kids are doing. You have to talk with your kids and make sure they understand what it is that they’re doing.

We do this with our kids for some things. Hopefully, we talk about drinking, smoking, sex, and other things with our children (like driving if they get to that stage) and make sure they understand what the risks are and how to mitigate those risks. Being an attentive parent is part of it.

Sometimes you need outside messengers to do it. We’d like to believe that these social media companies are able to police themselves – at least they pay lip service to the fact they do. They have warnings that they’ll take things down that aren’t socially appropriate. Whether they do or not, I don’t know, because you keep seeing things about BORG on these media sites. If they are doing it, they’re not doing it efficiently or quickly enough.

Dr. Glatter: There has to be some censorship. These are young persons who are impressionable, who have developing brains, who are looking at this, thinking that if it’s out there on social media, such as TikTok or Instagram, then it’s okay to do so. That message has to be driven home.

Dr. Nelson: That’s a great point, and it’s tough. We know there’s been debate over the liability of social media or what they post, and whether or not they should be held liable like a more conventional media company or not. That’s politics and philosophy, and we’re probably not going to solve it here.

All these things wind up going viral and there’s probably got to be some filter on things that go viral. Maybe they need to have a bit more attentiveness to that when those things start happening. Now, clearly not every one of these is viral. When you think about some of the challenges we’ve seen in the past, such as the Tide Pod challenge and cinnamon challenge, some of these things could be quickly figured out to be dangerous.

I remember that the ice bucket challenge for amyotrophic lateral sclerosis was pretty benign. You pour a bucket of water over your head, and people aren’t really getting hurt. That’s fun and good, and let people go out and do that. That could pass through the filter. When you start to see people drinking excessive amounts of alcohol, it doesn’t take an emergency physician to know that’s not a good thing. Any parent should know that if my kid drinks half a bottle or a bottle of vodka over a short period of time, that just can’t be okay.

Dr. Glatter: It’s a public health issue. That’s what we need to elevate it to because ultimately that’s what it impacts: welfare and safety.

Speaking of buckets, there’s a new bucket challenge, wherein unsuspecting people have a bucket put on their head, can’t breathe, and then pass out. There’s been a number of these reported and actually filmed on social media. Here’s another example of dangerous types of behavior that essentially are a form of assault. Unsuspecting people suffer injuries from young children and teens trying to play pranks.

Again, had there not been this medium, we wouldn’t necessarily see the extent of the injuries. I guess going forward, the next step would be to send a message to colleges that there should be some form of warning if this trend is seen, at least from a public health standpoint.

Dr. Nelson: Education is a necessary thing to do, but it’s almost never the real solution to a problem. We can educate people as best we can that they need to do things right. At some point, we’re going to need to regulate it or manage it somehow.

Whether it’s through a carrot or a stick approach, or whether you want to give people kudos for doing the right thing or punish them for doing something wrong, that’s a tough decision to make and one that is going to be made by a parent or guardian, a school official, or law enforcement. Somehow, we have to figure out how to make this happen.

There’s not going to be a single size that fits all for this. At some level, we have to do something to educate and regulate. The balance between those two things is going to be political and philosophical in nature.

Dr. Glatter: Right, and the element of peer pressure and conformity in this is really part of the element. If we try to remove that aspect of it, then often these trends would go away. That aspect of conformity and peer pressure is instrumental in fueling these trends. Maybe we can make a full gallon of water be the trend without any alcohol in there.

Dr. Nelson: We say water is only water, but as a medical toxicologist, I can tell you that one of the foundations in medical toxicology is that everything is toxic. It’s just the dose that determines the toxicity. Oxygen is toxic, water is toxic. Everything’s toxic if you take enough of it.

We know that whether it’s psychogenic or intentional, polydipsia by drinking excessive amounts of water, especially without electrolytes, is one of the reasons they say you should add electrolytes. That’s all relative as well, because depending on the electrolyte and how much you put in and things like that, that could also become dangerous. Drinking excessive amounts of water like they’re suggesting, which sounds like a good thing to prevent hangover and so on, can in and of itself be a problem too.

Dr. Glatter: Right, and we know that there’s no magic bullet for a hangover. Obviously, abstinence is the only thing that truly works.

Dr. Nelson: Or moderation.

Dr. Glatter: Until research proves further.

Thank you so much. You’ve made some really important points. Thank you for talking about the BORG phenomenon, how it relates to society in general, and what we can do to try to change people’s perception of alcohol and the bigger picture of binge drinking. I really appreciate it.

Dr. Nelson: Thanks, Rob, for having me. It’s an important topic and hopefully we can get a handle on this. I appreciate your time.

Dr. Glatter is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Hofstra University, Hempstead, N.Y. Dr. Nelson is professor and chair of the department of emergency medicine and chief of the division of medical toxicology at Rutgers New Jersey Medical School, Newark. He is a member of the board of directors of the American Board of Emergency Medicine, the Accreditation Council for Continuing Medical Education, and Association of Academic Chairs in Emergency Medicine and is past-president of the American College of Medical Toxicology. Dr. Glatter and Dr. Nelson disclosed no relevant financial relationships.

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

This discussion was recorded on April 6, 2023. This transcript has been edited for clarity.

Robert D. Glatter, MD: Welcome. I’m Dr. Robert Glatter, medical adviser for Medscape Emergency Medicine. Joining us today is Dr. Lewis Nelson, professor and chair of emergency medicine at Rutgers New Jersey Medical School and a certified medical toxicologist.

Today, we will be discussing an important and disturbing Gen Z trend circulating on social media, known as blackout rage gallon, or BORG.

Welcome, Lewis.

Lewis S. Nelson, MD: Thanks for having me.

Dr. Glatter: Thanks so much for joining us. This trend that’s been circulating on social media is really disturbing. It has elements that focus on binge drinking: Talking about taking a jug; emptying half of it out; and putting one fifth of vodka and some electrolytes, caffeine, or other things too is just incredibly disturbing. Teens and parents are looking at this. I’ll let you jump into the discussion.

Dr. Nelson: You’re totally right, it is disturbing. Binge drinking is a huge problem in this country in general. It’s a particular problem with young people – teenagers and young adults. I don’t think people appreciate the dangers associated with binge drinking, such as the amount of alcohol they consume and some of the unintended consequences of doing that.

To frame things quickly, we think there are probably around six people a day in the United States who die of alcohol poisoning. Alcohol poisoning basically is binge drinking to such an extent that you die of the alcohol itself. You’re not dying of a car crash or doing something that injures you. You’re dying of the alcohol. You’re drinking so much that your breathing slows, it stops, you have heart rhythm disturbances, and so on. It totals about 2,200 people a year in the United States.

Dr. Glatter: That’s alarming. For this trend, their argument is that half of the gallon is water. Therefore, I’m fine. I can drink it over 8-12 hours and it’s not an issue. How would you respond to that?

Dr. Nelson: Well, alcohol is alcohol. It’s all about how much you take in over what time period. I guess, in concept, it could be safer if you do it right. That’s not the way it’s been, so to speak, marketed on the various social media platforms. It’s meant to be a way to protect yourself from having your drink spiked or eating or ingesting contaminants from other people’s mouths when you share glasses or dip cups into communal pots like jungle juice or something.

Clearly, if you’re going to drink a large amount of alcohol over a short or long period of time, you do run the risk of having significant consequences, including bad decision-making if you’re just a little drunk all the way down to that of the complications you described about alcohol poisoning.

Dr. Glatter: There has been a comment made that this could be a form of harm reduction. The point of harm reduction is that we run trials, we validate it, and we test it. This, certainly in my mind, is no form of true harm reduction. I think you would agree.

Dr. Nelson: Many things that are marketed as harm reduction aren’t. There could be some aspects of this that could be considered harm reduction. You may believe – and there’s no reason not to – that protecting your drink is a good idea. If you’re at a bar and you leave your glass open and somebody put something in it, you can be drugged. Drug-facilitated sexual assault, for example, is a big issue. That means you have to leave your glass unattended. If you tend to your glass, it’s probably fine. One of the ways of harm reduction they mention is that by having a cap and having this bottle with you at all times, that can’t happen.

Now, in fairness, by far the drug most commonly associated with sexual assault is alcohol. It’s not gamma-hydroxybutyrate or ketamine. It’s not the other things that people are concerned about. Those happen, but those are small problems in the big picture. It’s drinking too much.

A form of harm reduction that you can comment on perhaps is that you make this drink concoction yourself, so you know what is in there. You can take that bottle, pour out half the water, and fill up the other half with water and nobody’s going to know. More likely, the way they say you should do it is you take your gallon jug, you pour it out, and you fill it up with one fifth of vodka.

One fifth of vodka is the same amount of volume as a bottle of wine. At 750 mL, that’s a huge amount of alcohol. If you measure the number of shots in that bottle, it’s about 17 shots. Even if you drink that over 6 hours, that’s still several shots an hour. That’s a large amount of alcohol. You might do two or three shots once and then not drink for a few hours. To sit and drink two or three shots an hour for 6 hours, that’s just an exceptional amount of alcohol.

They flavorize it and add caffeine, which only adds to the risk. It doesn’t make it in any way safer. With the volume, 1 gal of water or equivalent over a short period of time in and of itself could be a problem. There’s a large amount of mismessaging here. Whether something’s harm reduction, it could flip around to be easily construed or understood as being harmful.

Not to mention, the idea that when you make something safer, one of the unintended consequences of harm reduction is what we call risk compensation. This is best probably described as what’s called the Peltzman effect. The way that we think about airbags and seatbelts is that they’re going to reduce car crash deaths; and they do, but people drive faster and more recklessly because they know they’re safe.

This is a well-described problem in epidemiology: You expect a certain amount of harm reduction through some implemented process, but you don’t meet that because people take increased risks.

Dr. Glatter: Right. The idea of not developing a hangover is common among many teens and 20-somethings, thinking that because there’s hydration there, because half of it is water, it’s just not going to happen. There’s your “harm reduction,” but your judgment’s impaired. It’s day drinking at its best, all day long. Then someone has the idea to get behind the wheel. These are the disastrous consequences that we all fear.

Dr. Nelson: There is a great example, perhaps of an unintended consequence of harm reduction. By putting caffeine in it, depending on how much caffeine you put in, some of these mixtures can have up to 1,000 mg of caffeine. Remember, a cup of coffee is about 1-200 mg, so you’re talking about several cups of coffee. The idea is that you will not be able to sense, as you normally do, how drunk you are. You’re not going to be a sleepy drunk, you’re going to be an awake drunk.

The idea that you’re going to have to drive so you’re going to drink a strong cup of black coffee before you go driving, you’re not going to drive any better. I can assure you that. You’re going to be more awake, perhaps, and not fall asleep at the wheel, but you’re still going to have psychomotor impairment. Your judgment is going to be impaired. There’s nothing good that comes with adding caffeine except that you’re going to be awake.

From a hangover perspective, there are many things that we’ve guessed at or suggested as either prevention or cures for hangovers. I don’t doubt that you’re going to have some volume depletion if you drink a large amount of alcohol. Alcohol’s a diuretic, so you’re going to lose more volume than you bring in.

Hydrating is probably always a good idea, but there is hydrating and then there’s overhydrating. We don’t need volumes like that. If you drink a cup or two of water, you’re probably fine. You don’t need to drink half a gallon of water. That can lead to problems like delusional hyponatremia, and so forth. There’s not any clear benefit to doing it.

If you want to prevent a hangover, one of the ways you might do it is by using vodka. There are nice data that show that clear alcohols typically, particularly vodka, don’t have many of the congeners that make the specific forms of alcohol what they are. Bourbon smells and tastes like bourbon because of these little molecules, these alkalis and ketones and amino acids and things that make it taste and smell the way it does. That’s true for all the other alcohols.

Vodka has the least amount of that. Even wine and beer have those in them, but vodka is basically alcohol mixed with water. It’s probably the least hangover-prone of all the alcohols; but still, if you drink a lot of vodka, you’re going to have a hangover. It’s just a dose-response curve to how much alcohol you drink, to how drunk you get, and to how much of a hangover you’re going to have.

Dr. Glatter: The hangover is really what it’s about because people want to be functional the next day. There are many companies out there that market hangover remedies, but people are using this as the hangover remedy in a way that’s socially accepted. That’s a good point you make.

The question is how do we get the message out to parents and teens? What’s the best way you feel to really sound the alarm here?

Dr. Nelson: These are challenging issues. We face this all the time with all the sorts of social media in particular. Most parents are not as savvy on social media as their kids are. You have to know what your children are doing. You should know what they’re listening to and watching. You do have to pay attention to the media directed at parents that will inform you a little bit about what your kids are doing. You have to talk with your kids and make sure they understand what it is that they’re doing.

We do this with our kids for some things. Hopefully, we talk about drinking, smoking, sex, and other things with our children (like driving if they get to that stage) and make sure they understand what the risks are and how to mitigate those risks. Being an attentive parent is part of it.

Sometimes you need outside messengers to do it. We’d like to believe that these social media companies are able to police themselves – at least they pay lip service to the fact they do. They have warnings that they’ll take things down that aren’t socially appropriate. Whether they do or not, I don’t know, because you keep seeing things about BORG on these media sites. If they are doing it, they’re not doing it efficiently or quickly enough.

Dr. Glatter: There has to be some censorship. These are young persons who are impressionable, who have developing brains, who are looking at this, thinking that if it’s out there on social media, such as TikTok or Instagram, then it’s okay to do so. That message has to be driven home.

Dr. Nelson: That’s a great point, and it’s tough. We know there’s been debate over the liability of social media or what they post, and whether or not they should be held liable like a more conventional media company or not. That’s politics and philosophy, and we’re probably not going to solve it here.

All these things wind up going viral and there’s probably got to be some filter on things that go viral. Maybe they need to have a bit more attentiveness to that when those things start happening. Now, clearly not every one of these is viral. When you think about some of the challenges we’ve seen in the past, such as the Tide Pod challenge and cinnamon challenge, some of these things could be quickly figured out to be dangerous.

I remember that the ice bucket challenge for amyotrophic lateral sclerosis was pretty benign. You pour a bucket of water over your head, and people aren’t really getting hurt. That’s fun and good, and let people go out and do that. That could pass through the filter. When you start to see people drinking excessive amounts of alcohol, it doesn’t take an emergency physician to know that’s not a good thing. Any parent should know that if my kid drinks half a bottle or a bottle of vodka over a short period of time, that just can’t be okay.

Dr. Glatter: It’s a public health issue. That’s what we need to elevate it to because ultimately that’s what it impacts: welfare and safety.

Speaking of buckets, there’s a new bucket challenge, wherein unsuspecting people have a bucket put on their head, can’t breathe, and then pass out. There’s been a number of these reported and actually filmed on social media. Here’s another example of dangerous types of behavior that essentially are a form of assault. Unsuspecting people suffer injuries from young children and teens trying to play pranks.

Again, had there not been this medium, we wouldn’t necessarily see the extent of the injuries. I guess going forward, the next step would be to send a message to colleges that there should be some form of warning if this trend is seen, at least from a public health standpoint.

Dr. Nelson: Education is a necessary thing to do, but it’s almost never the real solution to a problem. We can educate people as best we can that they need to do things right. At some point, we’re going to need to regulate it or manage it somehow.

Whether it’s through a carrot or a stick approach, or whether you want to give people kudos for doing the right thing or punish them for doing something wrong, that’s a tough decision to make and one that is going to be made by a parent or guardian, a school official, or law enforcement. Somehow, we have to figure out how to make this happen.

There’s not going to be a single size that fits all for this. At some level, we have to do something to educate and regulate. The balance between those two things is going to be political and philosophical in nature.

Dr. Glatter: Right, and the element of peer pressure and conformity in this is really part of the element. If we try to remove that aspect of it, then often these trends would go away. That aspect of conformity and peer pressure is instrumental in fueling these trends. Maybe we can make a full gallon of water be the trend without any alcohol in there.

Dr. Nelson: We say water is only water, but as a medical toxicologist, I can tell you that one of the foundations in medical toxicology is that everything is toxic. It’s just the dose that determines the toxicity. Oxygen is toxic, water is toxic. Everything’s toxic if you take enough of it.

We know that whether it’s psychogenic or intentional, polydipsia by drinking excessive amounts of water, especially without electrolytes, is one of the reasons they say you should add electrolytes. That’s all relative as well, because depending on the electrolyte and how much you put in and things like that, that could also become dangerous. Drinking excessive amounts of water like they’re suggesting, which sounds like a good thing to prevent hangover and so on, can in and of itself be a problem too.

Dr. Glatter: Right, and we know that there’s no magic bullet for a hangover. Obviously, abstinence is the only thing that truly works.

Dr. Nelson: Or moderation.

Dr. Glatter: Until research proves further.

Thank you so much. You’ve made some really important points. Thank you for talking about the BORG phenomenon, how it relates to society in general, and what we can do to try to change people’s perception of alcohol and the bigger picture of binge drinking. I really appreciate it.

Dr. Nelson: Thanks, Rob, for having me. It’s an important topic and hopefully we can get a handle on this. I appreciate your time.

Dr. Glatter is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Hofstra University, Hempstead, N.Y. Dr. Nelson is professor and chair of the department of emergency medicine and chief of the division of medical toxicology at Rutgers New Jersey Medical School, Newark. He is a member of the board of directors of the American Board of Emergency Medicine, the Accreditation Council for Continuing Medical Education, and Association of Academic Chairs in Emergency Medicine and is past-president of the American College of Medical Toxicology. Dr. Glatter and Dr. Nelson disclosed no relevant financial relationships.

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

This discussion was recorded on April 6, 2023. This transcript has been edited for clarity.

Robert D. Glatter, MD: Welcome. I’m Dr. Robert Glatter, medical adviser for Medscape Emergency Medicine. Joining us today is Dr. Lewis Nelson, professor and chair of emergency medicine at Rutgers New Jersey Medical School and a certified medical toxicologist.

Today, we will be discussing an important and disturbing Gen Z trend circulating on social media, known as blackout rage gallon, or BORG.

Welcome, Lewis.

Lewis S. Nelson, MD: Thanks for having me.

Dr. Glatter: Thanks so much for joining us. This trend that’s been circulating on social media is really disturbing. It has elements that focus on binge drinking: Talking about taking a jug; emptying half of it out; and putting one fifth of vodka and some electrolytes, caffeine, or other things too is just incredibly disturbing. Teens and parents are looking at this. I’ll let you jump into the discussion.

Dr. Nelson: You’re totally right, it is disturbing. Binge drinking is a huge problem in this country in general. It’s a particular problem with young people – teenagers and young adults. I don’t think people appreciate the dangers associated with binge drinking, such as the amount of alcohol they consume and some of the unintended consequences of doing that.

To frame things quickly, we think there are probably around six people a day in the United States who die of alcohol poisoning. Alcohol poisoning basically is binge drinking to such an extent that you die of the alcohol itself. You’re not dying of a car crash or doing something that injures you. You’re dying of the alcohol. You’re drinking so much that your breathing slows, it stops, you have heart rhythm disturbances, and so on. It totals about 2,200 people a year in the United States.

Dr. Glatter: That’s alarming. For this trend, their argument is that half of the gallon is water. Therefore, I’m fine. I can drink it over 8-12 hours and it’s not an issue. How would you respond to that?

Dr. Nelson: Well, alcohol is alcohol. It’s all about how much you take in over what time period. I guess, in concept, it could be safer if you do it right. That’s not the way it’s been, so to speak, marketed on the various social media platforms. It’s meant to be a way to protect yourself from having your drink spiked or eating or ingesting contaminants from other people’s mouths when you share glasses or dip cups into communal pots like jungle juice or something.

Clearly, if you’re going to drink a large amount of alcohol over a short or long period of time, you do run the risk of having significant consequences, including bad decision-making if you’re just a little drunk all the way down to that of the complications you described about alcohol poisoning.

Dr. Glatter: There has been a comment made that this could be a form of harm reduction. The point of harm reduction is that we run trials, we validate it, and we test it. This, certainly in my mind, is no form of true harm reduction. I think you would agree.

Dr. Nelson: Many things that are marketed as harm reduction aren’t. There could be some aspects of this that could be considered harm reduction. You may believe – and there’s no reason not to – that protecting your drink is a good idea. If you’re at a bar and you leave your glass open and somebody put something in it, you can be drugged. Drug-facilitated sexual assault, for example, is a big issue. That means you have to leave your glass unattended. If you tend to your glass, it’s probably fine. One of the ways of harm reduction they mention is that by having a cap and having this bottle with you at all times, that can’t happen.

Now, in fairness, by far the drug most commonly associated with sexual assault is alcohol. It’s not gamma-hydroxybutyrate or ketamine. It’s not the other things that people are concerned about. Those happen, but those are small problems in the big picture. It’s drinking too much.

A form of harm reduction that you can comment on perhaps is that you make this drink concoction yourself, so you know what is in there. You can take that bottle, pour out half the water, and fill up the other half with water and nobody’s going to know. More likely, the way they say you should do it is you take your gallon jug, you pour it out, and you fill it up with one fifth of vodka.

One fifth of vodka is the same amount of volume as a bottle of wine. At 750 mL, that’s a huge amount of alcohol. If you measure the number of shots in that bottle, it’s about 17 shots. Even if you drink that over 6 hours, that’s still several shots an hour. That’s a large amount of alcohol. You might do two or three shots once and then not drink for a few hours. To sit and drink two or three shots an hour for 6 hours, that’s just an exceptional amount of alcohol.

They flavorize it and add caffeine, which only adds to the risk. It doesn’t make it in any way safer. With the volume, 1 gal of water or equivalent over a short period of time in and of itself could be a problem. There’s a large amount of mismessaging here. Whether something’s harm reduction, it could flip around to be easily construed or understood as being harmful.

Not to mention, the idea that when you make something safer, one of the unintended consequences of harm reduction is what we call risk compensation. This is best probably described as what’s called the Peltzman effect. The way that we think about airbags and seatbelts is that they’re going to reduce car crash deaths; and they do, but people drive faster and more recklessly because they know they’re safe.

This is a well-described problem in epidemiology: You expect a certain amount of harm reduction through some implemented process, but you don’t meet that because people take increased risks.

Dr. Glatter: Right. The idea of not developing a hangover is common among many teens and 20-somethings, thinking that because there’s hydration there, because half of it is water, it’s just not going to happen. There’s your “harm reduction,” but your judgment’s impaired. It’s day drinking at its best, all day long. Then someone has the idea to get behind the wheel. These are the disastrous consequences that we all fear.

Dr. Nelson: There is a great example, perhaps of an unintended consequence of harm reduction. By putting caffeine in it, depending on how much caffeine you put in, some of these mixtures can have up to 1,000 mg of caffeine. Remember, a cup of coffee is about 1-200 mg, so you’re talking about several cups of coffee. The idea is that you will not be able to sense, as you normally do, how drunk you are. You’re not going to be a sleepy drunk, you’re going to be an awake drunk.

The idea that you’re going to have to drive so you’re going to drink a strong cup of black coffee before you go driving, you’re not going to drive any better. I can assure you that. You’re going to be more awake, perhaps, and not fall asleep at the wheel, but you’re still going to have psychomotor impairment. Your judgment is going to be impaired. There’s nothing good that comes with adding caffeine except that you’re going to be awake.

From a hangover perspective, there are many things that we’ve guessed at or suggested as either prevention or cures for hangovers. I don’t doubt that you’re going to have some volume depletion if you drink a large amount of alcohol. Alcohol’s a diuretic, so you’re going to lose more volume than you bring in.

Hydrating is probably always a good idea, but there is hydrating and then there’s overhydrating. We don’t need volumes like that. If you drink a cup or two of water, you’re probably fine. You don’t need to drink half a gallon of water. That can lead to problems like delusional hyponatremia, and so forth. There’s not any clear benefit to doing it.

If you want to prevent a hangover, one of the ways you might do it is by using vodka. There are nice data that show that clear alcohols typically, particularly vodka, don’t have many of the congeners that make the specific forms of alcohol what they are. Bourbon smells and tastes like bourbon because of these little molecules, these alkalis and ketones and amino acids and things that make it taste and smell the way it does. That’s true for all the other alcohols.

Vodka has the least amount of that. Even wine and beer have those in them, but vodka is basically alcohol mixed with water. It’s probably the least hangover-prone of all the alcohols; but still, if you drink a lot of vodka, you’re going to have a hangover. It’s just a dose-response curve to how much alcohol you drink, to how drunk you get, and to how much of a hangover you’re going to have.

Dr. Glatter: The hangover is really what it’s about because people want to be functional the next day. There are many companies out there that market hangover remedies, but people are using this as the hangover remedy in a way that’s socially accepted. That’s a good point you make.

The question is how do we get the message out to parents and teens? What’s the best way you feel to really sound the alarm here?

Dr. Nelson: These are challenging issues. We face this all the time with all the sorts of social media in particular. Most parents are not as savvy on social media as their kids are. You have to know what your children are doing. You should know what they’re listening to and watching. You do have to pay attention to the media directed at parents that will inform you a little bit about what your kids are doing. You have to talk with your kids and make sure they understand what it is that they’re doing.

We do this with our kids for some things. Hopefully, we talk about drinking, smoking, sex, and other things with our children (like driving if they get to that stage) and make sure they understand what the risks are and how to mitigate those risks. Being an attentive parent is part of it.

Sometimes you need outside messengers to do it. We’d like to believe that these social media companies are able to police themselves – at least they pay lip service to the fact they do. They have warnings that they’ll take things down that aren’t socially appropriate. Whether they do or not, I don’t know, because you keep seeing things about BORG on these media sites. If they are doing it, they’re not doing it efficiently or quickly enough.

Dr. Glatter: There has to be some censorship. These are young persons who are impressionable, who have developing brains, who are looking at this, thinking that if it’s out there on social media, such as TikTok or Instagram, then it’s okay to do so. That message has to be driven home.

Dr. Nelson: That’s a great point, and it’s tough. We know there’s been debate over the liability of social media or what they post, and whether or not they should be held liable like a more conventional media company or not. That’s politics and philosophy, and we’re probably not going to solve it here.

All these things wind up going viral and there’s probably got to be some filter on things that go viral. Maybe they need to have a bit more attentiveness to that when those things start happening. Now, clearly not every one of these is viral. When you think about some of the challenges we’ve seen in the past, such as the Tide Pod challenge and cinnamon challenge, some of these things could be quickly figured out to be dangerous.

I remember that the ice bucket challenge for amyotrophic lateral sclerosis was pretty benign. You pour a bucket of water over your head, and people aren’t really getting hurt. That’s fun and good, and let people go out and do that. That could pass through the filter. When you start to see people drinking excessive amounts of alcohol, it doesn’t take an emergency physician to know that’s not a good thing. Any parent should know that if my kid drinks half a bottle or a bottle of vodka over a short period of time, that just can’t be okay.

Dr. Glatter: It’s a public health issue. That’s what we need to elevate it to because ultimately that’s what it impacts: welfare and safety.

Speaking of buckets, there’s a new bucket challenge, wherein unsuspecting people have a bucket put on their head, can’t breathe, and then pass out. There’s been a number of these reported and actually filmed on social media. Here’s another example of dangerous types of behavior that essentially are a form of assault. Unsuspecting people suffer injuries from young children and teens trying to play pranks.

Again, had there not been this medium, we wouldn’t necessarily see the extent of the injuries. I guess going forward, the next step would be to send a message to colleges that there should be some form of warning if this trend is seen, at least from a public health standpoint.

Dr. Nelson: Education is a necessary thing to do, but it’s almost never the real solution to a problem. We can educate people as best we can that they need to do things right. At some point, we’re going to need to regulate it or manage it somehow.

Whether it’s through a carrot or a stick approach, or whether you want to give people kudos for doing the right thing or punish them for doing something wrong, that’s a tough decision to make and one that is going to be made by a parent or guardian, a school official, or law enforcement. Somehow, we have to figure out how to make this happen.

There’s not going to be a single size that fits all for this. At some level, we have to do something to educate and regulate. The balance between those two things is going to be political and philosophical in nature.

Dr. Glatter: Right, and the element of peer pressure and conformity in this is really part of the element. If we try to remove that aspect of it, then often these trends would go away. That aspect of conformity and peer pressure is instrumental in fueling these trends. Maybe we can make a full gallon of water be the trend without any alcohol in there.

Dr. Nelson: We say water is only water, but as a medical toxicologist, I can tell you that one of the foundations in medical toxicology is that everything is toxic. It’s just the dose that determines the toxicity. Oxygen is toxic, water is toxic. Everything’s toxic if you take enough of it.

We know that whether it’s psychogenic or intentional, polydipsia by drinking excessive amounts of water, especially without electrolytes, is one of the reasons they say you should add electrolytes. That’s all relative as well, because depending on the electrolyte and how much you put in and things like that, that could also become dangerous. Drinking excessive amounts of water like they’re suggesting, which sounds like a good thing to prevent hangover and so on, can in and of itself be a problem too.

Dr. Glatter: Right, and we know that there’s no magic bullet for a hangover. Obviously, abstinence is the only thing that truly works.

Dr. Nelson: Or moderation.

Dr. Glatter: Until research proves further.

Thank you so much. You’ve made some really important points. Thank you for talking about the BORG phenomenon, how it relates to society in general, and what we can do to try to change people’s perception of alcohol and the bigger picture of binge drinking. I really appreciate it.

Dr. Nelson: Thanks, Rob, for having me. It’s an important topic and hopefully we can get a handle on this. I appreciate your time.

Dr. Glatter is an attending physician at Lenox Hill Hospital in New York City and assistant professor of emergency medicine at Hofstra University, Hempstead, N.Y. Dr. Nelson is professor and chair of the department of emergency medicine and chief of the division of medical toxicology at Rutgers New Jersey Medical School, Newark. He is a member of the board of directors of the American Board of Emergency Medicine, the Accreditation Council for Continuing Medical Education, and Association of Academic Chairs in Emergency Medicine and is past-president of the American College of Medical Toxicology. Dr. Glatter and Dr. Nelson disclosed no relevant financial relationships.

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

The combination of a patient-specific mRNA-based cancer vaccine (mRNA-4157/V940, Moderna and Merck) and the immune checkpoint inhibitor pembrolizumab significantly improved recurrence-free survival for patients with high-risk melanoma compared with pembrolizumab alone, according to the latest data from the KEYNOTE-942 trial.

This recurrence-free survival benefit corresponded to a 44% reduced risk of recurrence or death in patients who received the personalized vaccine plus pembrolizumab compared with the immunotherapy alone.

The randomized phase 2b trial is the first to show a positive result for a cancer vaccine in a randomized trial. The results, if confirmed in further studies, hold promise for treating other solid tumors with sensitivity to the programmed death-1 (PD-1) protein, investigators said.

“KEYNOTE-942 is the first randomized study to demonstrate improvement in recurrence-free survival in melanoma, or in any cancer in my view, with an individualized neoantigen vaccine approach,” trial investigator Jeffrey S. Weber, MD, PhD, of NYU Langone Perlmutter Cancer Center in New York, said during an oral abstract session at the annual meeting of the American Association for Cancer Research.

“I have every confidence that this strategy will be expanded to other histologies that are PD-1 sensitive, such as non–small cell lung cancer, renal cell cancer, hepatocellular cancer, gastroesophageal cancer, et cetera,” Dr. Weber said.

Invited discussant Margaret Callahan, MD, PhD, of Memorial Sloan Kettering Cancer Center in New York, called the results “exciting,” especially in light of previous results in cancer vaccine trials. “Despite hundreds of formulations and dozens of studies, cancer vaccines have been disappointing so far, and have largely failed to have a meaningful impact in oncology,” she said.
 

A promising personalized vaccine

The mRNA vaccine is individually tailored and encodes up to 34 patient-specific tumor neoantigens. The vaccine also acts as an adjuvant to strengthen the immune response.

Dr. Weber said that the “mRNA 4157 is what one would call an individualized neoantigen therapy. It will target an individual patient’s unique tumor mutations, and the revelation over the last 5-10 years, is that, for better or worse, virtually all the neoantigens are unique to an individual patient. There are very, very few true universal neoantigens, or at least universal neoantigens that could have clinical utility.”

The vaccines are developed from tumor biopsy tissues that then undergo whole exome and RNA sequencing to identify single nucleotide variants that are present in the tumor but not in normal tissue.

The findings are then fed into a computer algorithm that identifies potential neoepitope peptides that would bind well to the patient’s human leukocyte antigen (HLA) type and could evoke strong T-cell responses.

“Once they’re chosen, you concatenate the sequences together into a single-strand mRNA vaccine, it’s packaged with nanoparticles to encapsulate it, and there you have your mRNA vaccine,” Dr. Weber explained.

In the KEYNOTE-942 trial, the investigators randomly assigned patients with completely resected high-risk cutaneous melanoma on a 2:1 basis to receive mRNA-4157 via intramuscular injection every 3 weeks for a total of nine doses, plus intravenous pembrolizumab every 3 weeks for 18 cycles (107 patients) or pembrolizumab alone (50 patients). Median follow-up was 101 weeks in the combination group and 105 weeks in the pembrolizumab group.

Overall, the 18-month recurrence-free survival rates were 78.6% in the combination arm and 62.2% in the pembrolizumab arm. The recurrence-free survival rates corresponded to a 44% reduced risk of recurrence or death in patients who received the personalized vaccine plus pembrolizumab compared with those who received only pembrolizumab (hazard ratio [HR] for recurrence, 0.561; P =.0266).

Grade 3 or greater adverse events occurred in 25% of patients in the combination group and 18% of patients in the pembrolizumab group. The most common grade 3 event associated with the vaccine was fatigue. No grade 4 adverse events or deaths were associated with the vaccine, and the addition of the vaccine to pembrolizumab did not appear to increase risk for immune-mediated adverse events.

In a subanalysis, Dr. Weber and colleagues explored the relationship between tumor mutational burden and recurrence-free survival. Higher tumor mutational burden may mean more neoepitopes to target, which is helpful when developing personalized neoantigen vaccines, explained coinvestigator Ryan Sullivan, MD, associate director of the melanoma program at Mass General Cancer Center, Boston, who presented the subanalysis results.

The investigators performed whole exome and whole transcriptome sequencing of baseline tumor biopsy samples to determine the mutational burden of tumors and defined a high mutational burden as 10 or more mutations per megabase.

Overall, in the combination group, patients with a higher tumor mutational burden at baseline showed improved outcomes (HR, 0.652; 95% confidence interval [CI], 0.284-1.494), as did patients with a lower tumor mutational burden (HR, 0.586; 95% CI, 0.243-1.415).

The authors found the same was true for patients with high vs. low tumor inflammation scores (high: HR, 0.576; 95% CI, 0.209-1.591 vs. low: HR, 0.528; 95% CI, 0.253-1.101) and higher PD-L1 expression (PD-L1 positive: HR, 0.485; 95% CI, 0.226-1.039 vs. PD-L1 negative: HR, 0.162; 95% CI, 0.038-0.685).

The hazard ratios crossed 1, which suggest that the combination was similarly effective in all patient subsets, said Dr. Sullivan.

Dr. Callahan also highlighted that the P value was based on a one-side log-rank test, “a relatively low bar to jump over” and that there were slight imbalances in both PD-1 expression status and tumor mutational burden – both of which favored the vaccine group and may be associated with better recurrence-free survival.

The 16% difference in recurrence-free survival seen with the combination vs. pembrolizumab alone, if confirmed in further studies, “is clinically meaningful for high-risk patients,” said Dr. Callahan. “The authors are to be congratulated for presenting the first randomized study of a neoantigen vaccine with a clinical efficacy primary endpoint, and this is a trial that incorporates many of the lessons we’ve learned along the years.”

Dr. Sullivan also commented on the promising results. “The field of cancer vaccines is a wasteland of failed clinical trials after some initial promising data, so to have something like this where it does appear that this vaccine strategy works is good not only for patients with melanoma but for those people who have dedicated their lives to trying to develop cancer vaccines,” he said in an interview.

KEYNOTE-942 was funded by Moderna with collaboration from Merck. Dr. Weber has financial relationships with Merck, Moderna, and other companies. Dr. Sullivan has served as a paid consultant for Merck and has received research funding from the company. Dr. Callahan disclosed a consulting/advisory role with Moderna, Merck, and others.
 

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

The combination of a patient-specific mRNA-based cancer vaccine (mRNA-4157/V940, Moderna and Merck) and the immune checkpoint inhibitor pembrolizumab significantly improved recurrence-free survival for patients with high-risk melanoma compared with pembrolizumab alone, according to the latest data from the KEYNOTE-942 trial.

This recurrence-free survival benefit corresponded to a 44% reduced risk of recurrence or death in patients who received the personalized vaccine plus pembrolizumab compared with the immunotherapy alone.

The randomized phase 2b trial is the first to show a positive result for a cancer vaccine in a randomized trial. The results, if confirmed in further studies, hold promise for treating other solid tumors with sensitivity to the programmed death-1 (PD-1) protein, investigators said.

“KEYNOTE-942 is the first randomized study to demonstrate improvement in recurrence-free survival in melanoma, or in any cancer in my view, with an individualized neoantigen vaccine approach,” trial investigator Jeffrey S. Weber, MD, PhD, of NYU Langone Perlmutter Cancer Center in New York, said during an oral abstract session at the annual meeting of the American Association for Cancer Research.

“I have every confidence that this strategy will be expanded to other histologies that are PD-1 sensitive, such as non–small cell lung cancer, renal cell cancer, hepatocellular cancer, gastroesophageal cancer, et cetera,” Dr. Weber said.

Invited discussant Margaret Callahan, MD, PhD, of Memorial Sloan Kettering Cancer Center in New York, called the results “exciting,” especially in light of previous results in cancer vaccine trials. “Despite hundreds of formulations and dozens of studies, cancer vaccines have been disappointing so far, and have largely failed to have a meaningful impact in oncology,” she said.
 

A promising personalized vaccine

The mRNA vaccine is individually tailored and encodes up to 34 patient-specific tumor neoantigens. The vaccine also acts as an adjuvant to strengthen the immune response.

Dr. Weber said that the “mRNA 4157 is what one would call an individualized neoantigen therapy. It will target an individual patient’s unique tumor mutations, and the revelation over the last 5-10 years, is that, for better or worse, virtually all the neoantigens are unique to an individual patient. There are very, very few true universal neoantigens, or at least universal neoantigens that could have clinical utility.”

The vaccines are developed from tumor biopsy tissues that then undergo whole exome and RNA sequencing to identify single nucleotide variants that are present in the tumor but not in normal tissue.

The findings are then fed into a computer algorithm that identifies potential neoepitope peptides that would bind well to the patient’s human leukocyte antigen (HLA) type and could evoke strong T-cell responses.

“Once they’re chosen, you concatenate the sequences together into a single-strand mRNA vaccine, it’s packaged with nanoparticles to encapsulate it, and there you have your mRNA vaccine,” Dr. Weber explained.

In the KEYNOTE-942 trial, the investigators randomly assigned patients with completely resected high-risk cutaneous melanoma on a 2:1 basis to receive mRNA-4157 via intramuscular injection every 3 weeks for a total of nine doses, plus intravenous pembrolizumab every 3 weeks for 18 cycles (107 patients) or pembrolizumab alone (50 patients). Median follow-up was 101 weeks in the combination group and 105 weeks in the pembrolizumab group.

Overall, the 18-month recurrence-free survival rates were 78.6% in the combination arm and 62.2% in the pembrolizumab arm. The recurrence-free survival rates corresponded to a 44% reduced risk of recurrence or death in patients who received the personalized vaccine plus pembrolizumab compared with those who received only pembrolizumab (hazard ratio [HR] for recurrence, 0.561; P =.0266).

Grade 3 or greater adverse events occurred in 25% of patients in the combination group and 18% of patients in the pembrolizumab group. The most common grade 3 event associated with the vaccine was fatigue. No grade 4 adverse events or deaths were associated with the vaccine, and the addition of the vaccine to pembrolizumab did not appear to increase risk for immune-mediated adverse events.

In a subanalysis, Dr. Weber and colleagues explored the relationship between tumor mutational burden and recurrence-free survival. Higher tumor mutational burden may mean more neoepitopes to target, which is helpful when developing personalized neoantigen vaccines, explained coinvestigator Ryan Sullivan, MD, associate director of the melanoma program at Mass General Cancer Center, Boston, who presented the subanalysis results.

The investigators performed whole exome and whole transcriptome sequencing of baseline tumor biopsy samples to determine the mutational burden of tumors and defined a high mutational burden as 10 or more mutations per megabase.

Overall, in the combination group, patients with a higher tumor mutational burden at baseline showed improved outcomes (HR, 0.652; 95% confidence interval [CI], 0.284-1.494), as did patients with a lower tumor mutational burden (HR, 0.586; 95% CI, 0.243-1.415).

The authors found the same was true for patients with high vs. low tumor inflammation scores (high: HR, 0.576; 95% CI, 0.209-1.591 vs. low: HR, 0.528; 95% CI, 0.253-1.101) and higher PD-L1 expression (PD-L1 positive: HR, 0.485; 95% CI, 0.226-1.039 vs. PD-L1 negative: HR, 0.162; 95% CI, 0.038-0.685).

The hazard ratios crossed 1, which suggest that the combination was similarly effective in all patient subsets, said Dr. Sullivan.

Dr. Callahan also highlighted that the P value was based on a one-side log-rank test, “a relatively low bar to jump over” and that there were slight imbalances in both PD-1 expression status and tumor mutational burden – both of which favored the vaccine group and may be associated with better recurrence-free survival.

The 16% difference in recurrence-free survival seen with the combination vs. pembrolizumab alone, if confirmed in further studies, “is clinically meaningful for high-risk patients,” said Dr. Callahan. “The authors are to be congratulated for presenting the first randomized study of a neoantigen vaccine with a clinical efficacy primary endpoint, and this is a trial that incorporates many of the lessons we’ve learned along the years.”

Dr. Sullivan also commented on the promising results. “The field of cancer vaccines is a wasteland of failed clinical trials after some initial promising data, so to have something like this where it does appear that this vaccine strategy works is good not only for patients with melanoma but for those people who have dedicated their lives to trying to develop cancer vaccines,” he said in an interview.

KEYNOTE-942 was funded by Moderna with collaboration from Merck. Dr. Weber has financial relationships with Merck, Moderna, and other companies. Dr. Sullivan has served as a paid consultant for Merck and has received research funding from the company. Dr. Callahan disclosed a consulting/advisory role with Moderna, Merck, and others.
 

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

The combination of a patient-specific mRNA-based cancer vaccine (mRNA-4157/V940, Moderna and Merck) and the immune checkpoint inhibitor pembrolizumab significantly improved recurrence-free survival for patients with high-risk melanoma compared with pembrolizumab alone, according to the latest data from the KEYNOTE-942 trial.

This recurrence-free survival benefit corresponded to a 44% reduced risk of recurrence or death in patients who received the personalized vaccine plus pembrolizumab compared with the immunotherapy alone.

The randomized phase 2b trial is the first to show a positive result for a cancer vaccine in a randomized trial. The results, if confirmed in further studies, hold promise for treating other solid tumors with sensitivity to the programmed death-1 (PD-1) protein, investigators said.

“KEYNOTE-942 is the first randomized study to demonstrate improvement in recurrence-free survival in melanoma, or in any cancer in my view, with an individualized neoantigen vaccine approach,” trial investigator Jeffrey S. Weber, MD, PhD, of NYU Langone Perlmutter Cancer Center in New York, said during an oral abstract session at the annual meeting of the American Association for Cancer Research.

“I have every confidence that this strategy will be expanded to other histologies that are PD-1 sensitive, such as non–small cell lung cancer, renal cell cancer, hepatocellular cancer, gastroesophageal cancer, et cetera,” Dr. Weber said.

Invited discussant Margaret Callahan, MD, PhD, of Memorial Sloan Kettering Cancer Center in New York, called the results “exciting,” especially in light of previous results in cancer vaccine trials. “Despite hundreds of formulations and dozens of studies, cancer vaccines have been disappointing so far, and have largely failed to have a meaningful impact in oncology,” she said.
 

A promising personalized vaccine

The mRNA vaccine is individually tailored and encodes up to 34 patient-specific tumor neoantigens. The vaccine also acts as an adjuvant to strengthen the immune response.

Dr. Weber said that the “mRNA 4157 is what one would call an individualized neoantigen therapy. It will target an individual patient’s unique tumor mutations, and the revelation over the last 5-10 years, is that, for better or worse, virtually all the neoantigens are unique to an individual patient. There are very, very few true universal neoantigens, or at least universal neoantigens that could have clinical utility.”

The vaccines are developed from tumor biopsy tissues that then undergo whole exome and RNA sequencing to identify single nucleotide variants that are present in the tumor but not in normal tissue.

The findings are then fed into a computer algorithm that identifies potential neoepitope peptides that would bind well to the patient’s human leukocyte antigen (HLA) type and could evoke strong T-cell responses.

“Once they’re chosen, you concatenate the sequences together into a single-strand mRNA vaccine, it’s packaged with nanoparticles to encapsulate it, and there you have your mRNA vaccine,” Dr. Weber explained.

In the KEYNOTE-942 trial, the investigators randomly assigned patients with completely resected high-risk cutaneous melanoma on a 2:1 basis to receive mRNA-4157 via intramuscular injection every 3 weeks for a total of nine doses, plus intravenous pembrolizumab every 3 weeks for 18 cycles (107 patients) or pembrolizumab alone (50 patients). Median follow-up was 101 weeks in the combination group and 105 weeks in the pembrolizumab group.

Overall, the 18-month recurrence-free survival rates were 78.6% in the combination arm and 62.2% in the pembrolizumab arm. The recurrence-free survival rates corresponded to a 44% reduced risk of recurrence or death in patients who received the personalized vaccine plus pembrolizumab compared with those who received only pembrolizumab (hazard ratio [HR] for recurrence, 0.561; P =.0266).

Grade 3 or greater adverse events occurred in 25% of patients in the combination group and 18% of patients in the pembrolizumab group. The most common grade 3 event associated with the vaccine was fatigue. No grade 4 adverse events or deaths were associated with the vaccine, and the addition of the vaccine to pembrolizumab did not appear to increase risk for immune-mediated adverse events.

In a subanalysis, Dr. Weber and colleagues explored the relationship between tumor mutational burden and recurrence-free survival. Higher tumor mutational burden may mean more neoepitopes to target, which is helpful when developing personalized neoantigen vaccines, explained coinvestigator Ryan Sullivan, MD, associate director of the melanoma program at Mass General Cancer Center, Boston, who presented the subanalysis results.

The investigators performed whole exome and whole transcriptome sequencing of baseline tumor biopsy samples to determine the mutational burden of tumors and defined a high mutational burden as 10 or more mutations per megabase.

Overall, in the combination group, patients with a higher tumor mutational burden at baseline showed improved outcomes (HR, 0.652; 95% confidence interval [CI], 0.284-1.494), as did patients with a lower tumor mutational burden (HR, 0.586; 95% CI, 0.243-1.415).

The authors found the same was true for patients with high vs. low tumor inflammation scores (high: HR, 0.576; 95% CI, 0.209-1.591 vs. low: HR, 0.528; 95% CI, 0.253-1.101) and higher PD-L1 expression (PD-L1 positive: HR, 0.485; 95% CI, 0.226-1.039 vs. PD-L1 negative: HR, 0.162; 95% CI, 0.038-0.685).

The hazard ratios crossed 1, which suggest that the combination was similarly effective in all patient subsets, said Dr. Sullivan.

Dr. Callahan also highlighted that the P value was based on a one-side log-rank test, “a relatively low bar to jump over” and that there were slight imbalances in both PD-1 expression status and tumor mutational burden – both of which favored the vaccine group and may be associated with better recurrence-free survival.

The 16% difference in recurrence-free survival seen with the combination vs. pembrolizumab alone, if confirmed in further studies, “is clinically meaningful for high-risk patients,” said Dr. Callahan. “The authors are to be congratulated for presenting the first randomized study of a neoantigen vaccine with a clinical efficacy primary endpoint, and this is a trial that incorporates many of the lessons we’ve learned along the years.”

Dr. Sullivan also commented on the promising results. “The field of cancer vaccines is a wasteland of failed clinical trials after some initial promising data, so to have something like this where it does appear that this vaccine strategy works is good not only for patients with melanoma but for those people who have dedicated their lives to trying to develop cancer vaccines,” he said in an interview.

KEYNOTE-942 was funded by Moderna with collaboration from Merck. Dr. Weber has financial relationships with Merck, Moderna, and other companies. Dr. Sullivan has served as a paid consultant for Merck and has received research funding from the company. Dr. Callahan disclosed a consulting/advisory role with Moderna, Merck, and others.
 

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

In a phase 2 clinical trial of a potential treatment for fatigue associated with long COVID-19, people who received the medicine reported positive results over those receiving a placebo.

The study was conducted by researchers at the University of Oxford, England, and published in eClinical Medicine.

It was one of the first randomized double-blind placebo controlled trial for a possible treatment for long COVID, according to a press release from the university. 

“People living with long COVID in the trial who received AXA1125 had a significant improvement in fatigue compared to those who received a placebo,” the university reported.

Forty-one people participated. They had fatigue for 18 months beforehand. All completed the study, and none reported serious side effects.

AXA1125 was developed by U.S. pharmaceutical company Axcella Therapeutics.

“Potential causes [of long COVID fatigue] include reduced mitochondrial function and cellular bioenergetics,” the researchers reported.

“AXA1125 was tested in long COVID fatigue as previous data from Axcella showed effects on cellular energetics and inflammation. Emerging data on long COVID suggests that the virus targets the mitochondrial, which are essential to normal energy generation and control of inflammation,” the university noted in its press release. “AXA1125 may improve energy generation and reduce the amount of inflammation in the body.”

The study’s authors wrote that AXA1125 was tied to a “significant reduction in 28-day Chalder Fatigue Questionnaire score relative to placebo.” They said participants who reported less fatigue also had better mitochondrial health and walked farther in a 6-minute test.
 

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

In a phase 2 clinical trial of a potential treatment for fatigue associated with long COVID-19, people who received the medicine reported positive results over those receiving a placebo.

The study was conducted by researchers at the University of Oxford, England, and published in eClinical Medicine.

It was one of the first randomized double-blind placebo controlled trial for a possible treatment for long COVID, according to a press release from the university. 

“People living with long COVID in the trial who received AXA1125 had a significant improvement in fatigue compared to those who received a placebo,” the university reported.

Forty-one people participated. They had fatigue for 18 months beforehand. All completed the study, and none reported serious side effects.

AXA1125 was developed by U.S. pharmaceutical company Axcella Therapeutics.

“Potential causes [of long COVID fatigue] include reduced mitochondrial function and cellular bioenergetics,” the researchers reported.

“AXA1125 was tested in long COVID fatigue as previous data from Axcella showed effects on cellular energetics and inflammation. Emerging data on long COVID suggests that the virus targets the mitochondrial, which are essential to normal energy generation and control of inflammation,” the university noted in its press release. “AXA1125 may improve energy generation and reduce the amount of inflammation in the body.”

The study’s authors wrote that AXA1125 was tied to a “significant reduction in 28-day Chalder Fatigue Questionnaire score relative to placebo.” They said participants who reported less fatigue also had better mitochondrial health and walked farther in a 6-minute test.
 

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

In a phase 2 clinical trial of a potential treatment for fatigue associated with long COVID-19, people who received the medicine reported positive results over those receiving a placebo.

The study was conducted by researchers at the University of Oxford, England, and published in eClinical Medicine.

It was one of the first randomized double-blind placebo controlled trial for a possible treatment for long COVID, according to a press release from the university. 

“People living with long COVID in the trial who received AXA1125 had a significant improvement in fatigue compared to those who received a placebo,” the university reported.

Forty-one people participated. They had fatigue for 18 months beforehand. All completed the study, and none reported serious side effects.

AXA1125 was developed by U.S. pharmaceutical company Axcella Therapeutics.

“Potential causes [of long COVID fatigue] include reduced mitochondrial function and cellular bioenergetics,” the researchers reported.

“AXA1125 was tested in long COVID fatigue as previous data from Axcella showed effects on cellular energetics and inflammation. Emerging data on long COVID suggests that the virus targets the mitochondrial, which are essential to normal energy generation and control of inflammation,” the university noted in its press release. “AXA1125 may improve energy generation and reduce the amount of inflammation in the body.”

The study’s authors wrote that AXA1125 was tied to a “significant reduction in 28-day Chalder Fatigue Questionnaire score relative to placebo.” They said participants who reported less fatigue also had better mitochondrial health and walked farther in a 6-minute test.
 

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

COVID can more than triple the chance of being diagnosed with type 2 diabetes within a year of being infected, according to a new Canadian study.

Men who had even a mild case of COVID were significantly more likely than were noninfected men to be diagnosed with type 2 diabetes. Women didn’t have an increased risk unless they were severely ill.

Both men and women who had severe cases were at the highest risk. People who were hospitalized for COVID treatment had more than a doubled risk of being diagnosed with type 2 diabetes, and those who were admitted to intensive care units had more than a tripled risk.

“This is definitely a concern in terms of long-term outcomes,” researcher and University of British Columbia professor Naveed Z. Janjua, PhD, told The New York Times. “With a respiratory infection, you usually think, ‘Seven or eight days and I’m done with it, that’s it.’ [But] here we’re seeing lingering effects that are lifelong.”

The study was published in JAMA Network Open. Researchers analyzed health data from 2020 and 2021 for 629,935 people, 20% of whom were diagnosed with COVID during that time. Most people in the study had not been vaccinated because vaccines were not widely available then. The health information came from a registry maintained by public health officials in British Columbia. The follow-up period was 257 days.

The authors cautioned that their findings could not say that COVID causes type 2 diabetes; rather, in a commentary published along with the study, Pamela B. Davis, MD, PhD, said the link makes sense because COVID is known to impact the pancreas.

“Such a stress may move a patient from a prediabetic state into diabetes,” wrote Dr. Davis, former dean of Case Western Reserve University, Cleveland, where she is now a professor.

The researchers estimated that the increased pattern of diagnoses of diabetes following COVID infection could increase the rate of the disease occurring in the general population by 3%-5% overall.
 

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

COVID can more than triple the chance of being diagnosed with type 2 diabetes within a year of being infected, according to a new Canadian study.

Men who had even a mild case of COVID were significantly more likely than were noninfected men to be diagnosed with type 2 diabetes. Women didn’t have an increased risk unless they were severely ill.

Both men and women who had severe cases were at the highest risk. People who were hospitalized for COVID treatment had more than a doubled risk of being diagnosed with type 2 diabetes, and those who were admitted to intensive care units had more than a tripled risk.

“This is definitely a concern in terms of long-term outcomes,” researcher and University of British Columbia professor Naveed Z. Janjua, PhD, told The New York Times. “With a respiratory infection, you usually think, ‘Seven or eight days and I’m done with it, that’s it.’ [But] here we’re seeing lingering effects that are lifelong.”

The study was published in JAMA Network Open. Researchers analyzed health data from 2020 and 2021 for 629,935 people, 20% of whom were diagnosed with COVID during that time. Most people in the study had not been vaccinated because vaccines were not widely available then. The health information came from a registry maintained by public health officials in British Columbia. The follow-up period was 257 days.

The authors cautioned that their findings could not say that COVID causes type 2 diabetes; rather, in a commentary published along with the study, Pamela B. Davis, MD, PhD, said the link makes sense because COVID is known to impact the pancreas.

“Such a stress may move a patient from a prediabetic state into diabetes,” wrote Dr. Davis, former dean of Case Western Reserve University, Cleveland, where she is now a professor.

The researchers estimated that the increased pattern of diagnoses of diabetes following COVID infection could increase the rate of the disease occurring in the general population by 3%-5% overall.
 

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

COVID can more than triple the chance of being diagnosed with type 2 diabetes within a year of being infected, according to a new Canadian study.

Men who had even a mild case of COVID were significantly more likely than were noninfected men to be diagnosed with type 2 diabetes. Women didn’t have an increased risk unless they were severely ill.

Both men and women who had severe cases were at the highest risk. People who were hospitalized for COVID treatment had more than a doubled risk of being diagnosed with type 2 diabetes, and those who were admitted to intensive care units had more than a tripled risk.

“This is definitely a concern in terms of long-term outcomes,” researcher and University of British Columbia professor Naveed Z. Janjua, PhD, told The New York Times. “With a respiratory infection, you usually think, ‘Seven or eight days and I’m done with it, that’s it.’ [But] here we’re seeing lingering effects that are lifelong.”

The study was published in JAMA Network Open. Researchers analyzed health data from 2020 and 2021 for 629,935 people, 20% of whom were diagnosed with COVID during that time. Most people in the study had not been vaccinated because vaccines were not widely available then. The health information came from a registry maintained by public health officials in British Columbia. The follow-up period was 257 days.

The authors cautioned that their findings could not say that COVID causes type 2 diabetes; rather, in a commentary published along with the study, Pamela B. Davis, MD, PhD, said the link makes sense because COVID is known to impact the pancreas.

“Such a stress may move a patient from a prediabetic state into diabetes,” wrote Dr. Davis, former dean of Case Western Reserve University, Cleveland, where she is now a professor.

The researchers estimated that the increased pattern of diagnoses of diabetes following COVID infection could increase the rate of the disease occurring in the general population by 3%-5% overall.
 

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