Journal of Clinical Outcomes Management

People with long COVID have specific biomarkers in their blood, according to results of a study published in Nature. 

The findings may be a step toward creating blood tests to positively identify people with long COVID so specialized treatments can be employed, researchers said.

 “This is a decisive step forward in the development of valid and reliable blood testing protocols for long COVID,” said David Putrino, PhD., lead author and professor of rehabilitation and human performance and director of the Abilities Research Center at Icahn Mount Sinai Health System, New York.

Researchers from the Icahn School of Medicine at Mount Sinai and Yale School of Medicine looked at blood samples from about 270 people between January 2021 and June 2022. The people had never been infected with COVID, had fully recovered from an infection, or still showed symptoms at least four months after infection.

Using machine learning, the research teams were able to differentiate between people with and without long COVID with 96% accuracy based on distinctive features in the blood samples, according to a news release from Mount Sinai.

People with long COVID had abnormal T-cell activity and low levels of the hormone cortisol. Cortisol helps people feel alert and awake, which would explain why people with long COVID often report fatigue, NBC News said in a report on the study.

“It was one of the findings that most definitively separated the folks with long Covid from the people without long Covid,” Dr. Putrino told NBC News.

The study also found that long COVID appears to reactivate latent viruses including Epstein-Barr and mononucleosis, the study said.

The blood tests could allow doctors to come up with specialized treatments in people who report a wide variety of long COVID symptoms, Dr. Putrino said. 

“There is no ‘silver bullet’ for treating long COVID, because it is an illness that infiltrates complex systems such as the immune and hormonal regulation,” he said.

The Centers for Disease Control and Prevention says about one in five Americans who had COVID still have long COVID. Symptoms include fatigue, brain fog, dizziness, digestive problems, and loss of smell and taste.

A version of this article appeared on WebMD.com.

People with long COVID have specific biomarkers in their blood, according to results of a study published in Nature. 

The findings may be a step toward creating blood tests to positively identify people with long COVID so specialized treatments can be employed, researchers said.

 “This is a decisive step forward in the development of valid and reliable blood testing protocols for long COVID,” said David Putrino, PhD., lead author and professor of rehabilitation and human performance and director of the Abilities Research Center at Icahn Mount Sinai Health System, New York.

Researchers from the Icahn School of Medicine at Mount Sinai and Yale School of Medicine looked at blood samples from about 270 people between January 2021 and June 2022. The people had never been infected with COVID, had fully recovered from an infection, or still showed symptoms at least four months after infection.

Using machine learning, the research teams were able to differentiate between people with and without long COVID with 96% accuracy based on distinctive features in the blood samples, according to a news release from Mount Sinai.

People with long COVID had abnormal T-cell activity and low levels of the hormone cortisol. Cortisol helps people feel alert and awake, which would explain why people with long COVID often report fatigue, NBC News said in a report on the study.

“It was one of the findings that most definitively separated the folks with long Covid from the people without long Covid,” Dr. Putrino told NBC News.

The study also found that long COVID appears to reactivate latent viruses including Epstein-Barr and mononucleosis, the study said.

The blood tests could allow doctors to come up with specialized treatments in people who report a wide variety of long COVID symptoms, Dr. Putrino said. 

“There is no ‘silver bullet’ for treating long COVID, because it is an illness that infiltrates complex systems such as the immune and hormonal regulation,” he said.

The Centers for Disease Control and Prevention says about one in five Americans who had COVID still have long COVID. Symptoms include fatigue, brain fog, dizziness, digestive problems, and loss of smell and taste.

A version of this article appeared on WebMD.com.

People with long COVID have specific biomarkers in their blood, according to results of a study published in Nature. 

The findings may be a step toward creating blood tests to positively identify people with long COVID so specialized treatments can be employed, researchers said.

 “This is a decisive step forward in the development of valid and reliable blood testing protocols for long COVID,” said David Putrino, PhD., lead author and professor of rehabilitation and human performance and director of the Abilities Research Center at Icahn Mount Sinai Health System, New York.

Researchers from the Icahn School of Medicine at Mount Sinai and Yale School of Medicine looked at blood samples from about 270 people between January 2021 and June 2022. The people had never been infected with COVID, had fully recovered from an infection, or still showed symptoms at least four months after infection.

Using machine learning, the research teams were able to differentiate between people with and without long COVID with 96% accuracy based on distinctive features in the blood samples, according to a news release from Mount Sinai.

People with long COVID had abnormal T-cell activity and low levels of the hormone cortisol. Cortisol helps people feel alert and awake, which would explain why people with long COVID often report fatigue, NBC News said in a report on the study.

“It was one of the findings that most definitively separated the folks with long Covid from the people without long Covid,” Dr. Putrino told NBC News.

The study also found that long COVID appears to reactivate latent viruses including Epstein-Barr and mononucleosis, the study said.

The blood tests could allow doctors to come up with specialized treatments in people who report a wide variety of long COVID symptoms, Dr. Putrino said. 

“There is no ‘silver bullet’ for treating long COVID, because it is an illness that infiltrates complex systems such as the immune and hormonal regulation,” he said.

The Centers for Disease Control and Prevention says about one in five Americans who had COVID still have long COVID. Symptoms include fatigue, brain fog, dizziness, digestive problems, and loss of smell and taste.

A version of this article appeared on WebMD.com.

The antiviral COVID medication made by Merck can cause mutations in the coronavirus that occasionally spread to other people, according to a study published in the online journal Nature.

There’s no evidence that molnupiravir, sold under the brand name Lagevrio, has caused the creation of more transmissible or severe variants of COVID, the study says, but researchers called for more scrutiny of the drug.

Researchers looked at 15 million COVID genomes and discovered that hallmark mutations linked to molnupiravir increased in 2022, especially in places where the drug was widely used, such as the United States and the United Kingdom. Levels of the mutations were also found in populations where the drug was heavily prescribed, such as seniors.

Molnupiravir is an antiviral given to people after they show signs of having COVID-19. It interferes with the COVID-19 virus’s ability to make copies of itself, thus stopping the spread of the virus throughout the body and keeping the virus level low.

The study found the virus can sometimes survive molnupiravir, resulting in mutations that have spread to other people.

Theo Sanderson, PhD, the lead author on the study and a postdoctoral researcher at the Francis Crick Institute in London, told The Guardian that the implications of the mutations were unclear.

“The signature is very clear, but there aren’t any widely circulating variants that have the signature. At the moment there’s nothing that’s transmitted very widely that’s due to molnupiravir,” he said.

The study doesn’t say people should not use molnupiravir but calls for public health officials to scrutinize it.

“The observation that molnupiravir treatment has left a visible trace in global sequencing databases, including onwards transmission of molnupiravir-derived sequences, will be an important consideration for assessing the effects and evolutionary safety of this drug,” the researchers concluded.

When reached for comment, Merck questioned the evidence.

“The authors assume these mutations were associated with viral spread from molnupiravir-treated patients without documented evidence of that transmission. Instead, the authors rely on circumstantial associations between the region from which the sequence was identified and time frame of sequence collection in countries where molnupiravir is available to draw their conclusions,” the company said.

The Food and Drug Administration authorized the use of molnupiravir for the treatment of mild to moderate COVID-19 in adults in December 2021. The FDA has also authorized the use of nirmatrelvir/ritonavir (Paxlovid), an antiviral made by Pfizer.

A version of this article appeared on WebMD.com.

The antiviral COVID medication made by Merck can cause mutations in the coronavirus that occasionally spread to other people, according to a study published in the online journal Nature.

There’s no evidence that molnupiravir, sold under the brand name Lagevrio, has caused the creation of more transmissible or severe variants of COVID, the study says, but researchers called for more scrutiny of the drug.

Researchers looked at 15 million COVID genomes and discovered that hallmark mutations linked to molnupiravir increased in 2022, especially in places where the drug was widely used, such as the United States and the United Kingdom. Levels of the mutations were also found in populations where the drug was heavily prescribed, such as seniors.

Molnupiravir is an antiviral given to people after they show signs of having COVID-19. It interferes with the COVID-19 virus’s ability to make copies of itself, thus stopping the spread of the virus throughout the body and keeping the virus level low.

The study found the virus can sometimes survive molnupiravir, resulting in mutations that have spread to other people.

Theo Sanderson, PhD, the lead author on the study and a postdoctoral researcher at the Francis Crick Institute in London, told The Guardian that the implications of the mutations were unclear.

“The signature is very clear, but there aren’t any widely circulating variants that have the signature. At the moment there’s nothing that’s transmitted very widely that’s due to molnupiravir,” he said.

The study doesn’t say people should not use molnupiravir but calls for public health officials to scrutinize it.

“The observation that molnupiravir treatment has left a visible trace in global sequencing databases, including onwards transmission of molnupiravir-derived sequences, will be an important consideration for assessing the effects and evolutionary safety of this drug,” the researchers concluded.

When reached for comment, Merck questioned the evidence.

“The authors assume these mutations were associated with viral spread from molnupiravir-treated patients without documented evidence of that transmission. Instead, the authors rely on circumstantial associations between the region from which the sequence was identified and time frame of sequence collection in countries where molnupiravir is available to draw their conclusions,” the company said.

The Food and Drug Administration authorized the use of molnupiravir for the treatment of mild to moderate COVID-19 in adults in December 2021. The FDA has also authorized the use of nirmatrelvir/ritonavir (Paxlovid), an antiviral made by Pfizer.

A version of this article appeared on WebMD.com.

The antiviral COVID medication made by Merck can cause mutations in the coronavirus that occasionally spread to other people, according to a study published in the online journal Nature.

There’s no evidence that molnupiravir, sold under the brand name Lagevrio, has caused the creation of more transmissible or severe variants of COVID, the study says, but researchers called for more scrutiny of the drug.

Researchers looked at 15 million COVID genomes and discovered that hallmark mutations linked to molnupiravir increased in 2022, especially in places where the drug was widely used, such as the United States and the United Kingdom. Levels of the mutations were also found in populations where the drug was heavily prescribed, such as seniors.

Molnupiravir is an antiviral given to people after they show signs of having COVID-19. It interferes with the COVID-19 virus’s ability to make copies of itself, thus stopping the spread of the virus throughout the body and keeping the virus level low.

The study found the virus can sometimes survive molnupiravir, resulting in mutations that have spread to other people.

Theo Sanderson, PhD, the lead author on the study and a postdoctoral researcher at the Francis Crick Institute in London, told The Guardian that the implications of the mutations were unclear.

“The signature is very clear, but there aren’t any widely circulating variants that have the signature. At the moment there’s nothing that’s transmitted very widely that’s due to molnupiravir,” he said.

The study doesn’t say people should not use molnupiravir but calls for public health officials to scrutinize it.

“The observation that molnupiravir treatment has left a visible trace in global sequencing databases, including onwards transmission of molnupiravir-derived sequences, will be an important consideration for assessing the effects and evolutionary safety of this drug,” the researchers concluded.

When reached for comment, Merck questioned the evidence.

“The authors assume these mutations were associated with viral spread from molnupiravir-treated patients without documented evidence of that transmission. Instead, the authors rely on circumstantial associations between the region from which the sequence was identified and time frame of sequence collection in countries where molnupiravir is available to draw their conclusions,” the company said.

The Food and Drug Administration authorized the use of molnupiravir for the treatment of mild to moderate COVID-19 in adults in December 2021. The FDA has also authorized the use of nirmatrelvir/ritonavir (Paxlovid), an antiviral made by Pfizer.

A version of this article appeared on WebMD.com.

A real-world study published in  JAMA Open Network found that Pfizer’s COVID-19 antiviral Paxlovid is now less effective at preventing hospitalization or death in high-risk patients, compared with earlier studies. But when looking at death alone, the antiviral was still highly effective. 

Paxlovid was about 37% effective at preventing death or hospitalization in high-risk patients, compared with no treatment. The study also looked at the antiviral Lagevrio, made by Merck, and found it was about 41% effective. In preventing death alone, Paxlovid was about 84% effective, compared with no treatment, and Lagevrio was about 77% effective.

The investigators, of the University of North Carolina at Chapel Hill and the Cleveland Clinic, examined electronic health records of 68,867 patients at hospitals in Cleveland and Florida who were diagnosed with COVID from April 1, 2022, to Feb. 20, 2023.

For Paxlovid, the effectiveness against death and hospitalization was lower than the effectiveness rate of about 86% found in clinical trials in 2021, according to Bloomberg. 

The difference in effectiveness in the real-world and clinical studies may have occurred because the early studies were conducted with unvaccinated people. Also, the virus has evolved since those first studies, Bloomberg reported. 

The researchers said Paxlovid and Lagevrio are recommended for use because they reduce hospitalization and death among high-risk patients who get COVID, even taking recent Omicron subvariants into account.

“These findings suggest that the use of either nirmatrelvir (Paxlovid) or molnupiravir (Lagevrio) is associated with reductions in mortality and hospitalization in patients infected with Omicron, regardless of age, race and ethnicity, virus strain, vaccination status, previous infection status, or coexisting conditions,” the researchers wrote. “Both drugs can, therefore, be used to treat nonhospitalized patients who are at high risk of progressing to severe COVID-19.”

Both drugs should be taken within 5 days of the onset of COVID symptoms.

The study was supported by the National Institutes of Health. Three coauthors reported conflicts of interest with various companies and organizations.

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

A real-world study published in  JAMA Open Network found that Pfizer’s COVID-19 antiviral Paxlovid is now less effective at preventing hospitalization or death in high-risk patients, compared with earlier studies. But when looking at death alone, the antiviral was still highly effective. 

Paxlovid was about 37% effective at preventing death or hospitalization in high-risk patients, compared with no treatment. The study also looked at the antiviral Lagevrio, made by Merck, and found it was about 41% effective. In preventing death alone, Paxlovid was about 84% effective, compared with no treatment, and Lagevrio was about 77% effective.

The investigators, of the University of North Carolina at Chapel Hill and the Cleveland Clinic, examined electronic health records of 68,867 patients at hospitals in Cleveland and Florida who were diagnosed with COVID from April 1, 2022, to Feb. 20, 2023.

For Paxlovid, the effectiveness against death and hospitalization was lower than the effectiveness rate of about 86% found in clinical trials in 2021, according to Bloomberg. 

The difference in effectiveness in the real-world and clinical studies may have occurred because the early studies were conducted with unvaccinated people. Also, the virus has evolved since those first studies, Bloomberg reported. 

The researchers said Paxlovid and Lagevrio are recommended for use because they reduce hospitalization and death among high-risk patients who get COVID, even taking recent Omicron subvariants into account.

“These findings suggest that the use of either nirmatrelvir (Paxlovid) or molnupiravir (Lagevrio) is associated with reductions in mortality and hospitalization in patients infected with Omicron, regardless of age, race and ethnicity, virus strain, vaccination status, previous infection status, or coexisting conditions,” the researchers wrote. “Both drugs can, therefore, be used to treat nonhospitalized patients who are at high risk of progressing to severe COVID-19.”

Both drugs should be taken within 5 days of the onset of COVID symptoms.

The study was supported by the National Institutes of Health. Three coauthors reported conflicts of interest with various companies and organizations.

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

A real-world study published in  JAMA Open Network found that Pfizer’s COVID-19 antiviral Paxlovid is now less effective at preventing hospitalization or death in high-risk patients, compared with earlier studies. But when looking at death alone, the antiviral was still highly effective. 

Paxlovid was about 37% effective at preventing death or hospitalization in high-risk patients, compared with no treatment. The study also looked at the antiviral Lagevrio, made by Merck, and found it was about 41% effective. In preventing death alone, Paxlovid was about 84% effective, compared with no treatment, and Lagevrio was about 77% effective.

The investigators, of the University of North Carolina at Chapel Hill and the Cleveland Clinic, examined electronic health records of 68,867 patients at hospitals in Cleveland and Florida who were diagnosed with COVID from April 1, 2022, to Feb. 20, 2023.

For Paxlovid, the effectiveness against death and hospitalization was lower than the effectiveness rate of about 86% found in clinical trials in 2021, according to Bloomberg. 

The difference in effectiveness in the real-world and clinical studies may have occurred because the early studies were conducted with unvaccinated people. Also, the virus has evolved since those first studies, Bloomberg reported. 

The researchers said Paxlovid and Lagevrio are recommended for use because they reduce hospitalization and death among high-risk patients who get COVID, even taking recent Omicron subvariants into account.

“These findings suggest that the use of either nirmatrelvir (Paxlovid) or molnupiravir (Lagevrio) is associated with reductions in mortality and hospitalization in patients infected with Omicron, regardless of age, race and ethnicity, virus strain, vaccination status, previous infection status, or coexisting conditions,” the researchers wrote. “Both drugs can, therefore, be used to treat nonhospitalized patients who are at high risk of progressing to severe COVID-19.”

Both drugs should be taken within 5 days of the onset of COVID symptoms.

The study was supported by the National Institutes of Health. Three coauthors reported conflicts of interest with various companies and organizations.

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

TOPLINE:

The COVID-19 booster vaccine typically causes transient, clinically insignificant elevations in glucose levels in people with type 1 diabetes, but some individuals may develop more pronounced hyperglycemia.

METHODOLOGY:

• In a single-center prospective cohort study of 21 adults with type 1 diabetes, patients were given a blinded Dexcom G6 Pro continuous glucose monitor (CGM) at the first research clinic visit.
• After 3-4 days, participants received a COVID-19 booster vaccine.
• They returned to the clinic 10 days after the initial visit (5-6 days after booster vaccination) to have the CGM removed and glycemia assessed.

TAKEAWAY:

• Compared with baseline, the mean daily glucose level was significantly increased at day 2 (162.9 mg/dL vs. 172.8 mg/dL; P = .04) and day 3 (173.1 mg/dL; P = .02) post vaccination.
• Glucose excursions at day 0 (173.2 mg/dL; P = .058) and day 1 (173.1 mg/dL; P = .078) didn’t quite reach statistical significance.
• One participant experienced increases in glucose of 36%, 69%, 35%, 26%, 22%, and 19% on days 0-5, respectively, compared with baseline.
• Glucose excursions of at least 25% above baseline occurred in four participants on day 0 and day 1 and in three participants on days 2 and 5.
• Insulin resistance, as measured by Total Daily Insulin Resistance (a metric that integrates daily mean glucose concentration with total daily insulin dose), was also significantly increased from baseline to day 2 post vaccination (7,171 mg/dL vs. 8,070 mg/dL units; P = .03).
• No other measures of glycemia differed significantly, compared with baseline.
• Outcomes didn’t differ significantly by sex, age, or vaccine manufacturer.

IN PRACTICE:

• “To our knowledge this is the first study investigating the effect of the COVID-19 booster vaccine on glycemia specifically in people with type 1 diabetes,” say the authors.
• “Clinicians, pharmacists, and other health care providers may need to counsel people with T1D to be more vigilant with glucose testing and insulin dosing for the first 5 days after vaccination. Most importantly, insulin, required to control glycemia, may need to be transiently increased.”
• “Further studies are warranted to investigate whether other vaccines have similar glycemic effects, and which individuals are at highest risk for profound glucose perturbations post vaccination.”

SOURCE:

The study was conducted by Mihail Zilbermint, MD, of the division of hospital medicine, Johns Hopkins Medicine, Bethesda, Md., and colleagues. It was published in Diabetes Research and Clinical Practice.

LIMITATIONS:

• The sample size was small.
• There were no measurements of inflammatory markers, dietary intake, physical activity, or survey patient symptomatology to adjust for variables that may have influenced glycemic control.
• In the study cohort, glycemia was moderately well controlled at baseline.

DISCLOSURES:

The study was supported by an investigator-initiated study grant from DexCom Inc. Dr. Zilbermint has consulted for EMD Serono.

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

TOPLINE:

The COVID-19 booster vaccine typically causes transient, clinically insignificant elevations in glucose levels in people with type 1 diabetes, but some individuals may develop more pronounced hyperglycemia.

METHODOLOGY:

• In a single-center prospective cohort study of 21 adults with type 1 diabetes, patients were given a blinded Dexcom G6 Pro continuous glucose monitor (CGM) at the first research clinic visit.
• After 3-4 days, participants received a COVID-19 booster vaccine.
• They returned to the clinic 10 days after the initial visit (5-6 days after booster vaccination) to have the CGM removed and glycemia assessed.

TAKEAWAY:

• Compared with baseline, the mean daily glucose level was significantly increased at day 2 (162.9 mg/dL vs. 172.8 mg/dL; P = .04) and day 3 (173.1 mg/dL; P = .02) post vaccination.
• Glucose excursions at day 0 (173.2 mg/dL; P = .058) and day 1 (173.1 mg/dL; P = .078) didn’t quite reach statistical significance.
• One participant experienced increases in glucose of 36%, 69%, 35%, 26%, 22%, and 19% on days 0-5, respectively, compared with baseline.
• Glucose excursions of at least 25% above baseline occurred in four participants on day 0 and day 1 and in three participants on days 2 and 5.
• Insulin resistance, as measured by Total Daily Insulin Resistance (a metric that integrates daily mean glucose concentration with total daily insulin dose), was also significantly increased from baseline to day 2 post vaccination (7,171 mg/dL vs. 8,070 mg/dL units; P = .03).
• No other measures of glycemia differed significantly, compared with baseline.
• Outcomes didn’t differ significantly by sex, age, or vaccine manufacturer.

IN PRACTICE:

• “To our knowledge this is the first study investigating the effect of the COVID-19 booster vaccine on glycemia specifically in people with type 1 diabetes,” say the authors.
• “Clinicians, pharmacists, and other health care providers may need to counsel people with T1D to be more vigilant with glucose testing and insulin dosing for the first 5 days after vaccination. Most importantly, insulin, required to control glycemia, may need to be transiently increased.”
• “Further studies are warranted to investigate whether other vaccines have similar glycemic effects, and which individuals are at highest risk for profound glucose perturbations post vaccination.”

SOURCE:

The study was conducted by Mihail Zilbermint, MD, of the division of hospital medicine, Johns Hopkins Medicine, Bethesda, Md., and colleagues. It was published in Diabetes Research and Clinical Practice.

LIMITATIONS:

• The sample size was small.
• There were no measurements of inflammatory markers, dietary intake, physical activity, or survey patient symptomatology to adjust for variables that may have influenced glycemic control.
• In the study cohort, glycemia was moderately well controlled at baseline.

DISCLOSURES:

The study was supported by an investigator-initiated study grant from DexCom Inc. Dr. Zilbermint has consulted for EMD Serono.

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

TOPLINE:

The COVID-19 booster vaccine typically causes transient, clinically insignificant elevations in glucose levels in people with type 1 diabetes, but some individuals may develop more pronounced hyperglycemia.

METHODOLOGY:

• In a single-center prospective cohort study of 21 adults with type 1 diabetes, patients were given a blinded Dexcom G6 Pro continuous glucose monitor (CGM) at the first research clinic visit.
• After 3-4 days, participants received a COVID-19 booster vaccine.
• They returned to the clinic 10 days after the initial visit (5-6 days after booster vaccination) to have the CGM removed and glycemia assessed.

TAKEAWAY:

• Compared with baseline, the mean daily glucose level was significantly increased at day 2 (162.9 mg/dL vs. 172.8 mg/dL; P = .04) and day 3 (173.1 mg/dL; P = .02) post vaccination.
• Glucose excursions at day 0 (173.2 mg/dL; P = .058) and day 1 (173.1 mg/dL; P = .078) didn’t quite reach statistical significance.
• One participant experienced increases in glucose of 36%, 69%, 35%, 26%, 22%, and 19% on days 0-5, respectively, compared with baseline.
• Glucose excursions of at least 25% above baseline occurred in four participants on day 0 and day 1 and in three participants on days 2 and 5.
• Insulin resistance, as measured by Total Daily Insulin Resistance (a metric that integrates daily mean glucose concentration with total daily insulin dose), was also significantly increased from baseline to day 2 post vaccination (7,171 mg/dL vs. 8,070 mg/dL units; P = .03).
• No other measures of glycemia differed significantly, compared with baseline.
• Outcomes didn’t differ significantly by sex, age, or vaccine manufacturer.

IN PRACTICE:

• “To our knowledge this is the first study investigating the effect of the COVID-19 booster vaccine on glycemia specifically in people with type 1 diabetes,” say the authors.
• “Clinicians, pharmacists, and other health care providers may need to counsel people with T1D to be more vigilant with glucose testing and insulin dosing for the first 5 days after vaccination. Most importantly, insulin, required to control glycemia, may need to be transiently increased.”
• “Further studies are warranted to investigate whether other vaccines have similar glycemic effects, and which individuals are at highest risk for profound glucose perturbations post vaccination.”

SOURCE:

The study was conducted by Mihail Zilbermint, MD, of the division of hospital medicine, Johns Hopkins Medicine, Bethesda, Md., and colleagues. It was published in Diabetes Research and Clinical Practice.

LIMITATIONS:

• The sample size was small.
• There were no measurements of inflammatory markers, dietary intake, physical activity, or survey patient symptomatology to adjust for variables that may have influenced glycemic control.
• In the study cohort, glycemia was moderately well controlled at baseline.

DISCLOSURES:

The study was supported by an investigator-initiated study grant from DexCom Inc. Dr. Zilbermint has consulted for EMD Serono.

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

A new meta-analysis has shown that SGLT2 inhibitors do not lead to lower 28-day all-cause mortality, compared with usual care or placebo, in patients hospitalized with COVID-19.

However, no major safety issues were identified with the use of SGLT2 inhibitors in these acutely ill patients, the researchers report.

“While these findings do not support the use of SGLT2-inhibitors as standard of care for patients hospitalized with COVID-19, I think the most important take home message here is that the use of these medications appears to be safe even in really acutely ill hospitalized patients,” lead investigator of the meta-analysis, Mikhail Kosiborod, MD, Saint Luke’s Mid America Heart Institute, Kansas City, Mo., concluded.

He said this was important because the list of indications for SGLT2 inhibitors is rapidly growing.

“These medications are being used in more and more patients. And we know that when we discontinue medications in the hospital they frequently don’t get restarted, which can lead to real risks if SGLT2 inhibitors are stopped in patients with heart failure, chronic kidney disease, or diabetes. So, the bottom line is that there is no compelling reason to stop these medications in the hospital,” he added.

The new meta-analysis was presented at the recent annual congress of the European Society of Cardiology, held in Amsterdam.

Discussant of the presentation at the ESC Hotline session, Muthiah Vaduganathan, MD, MPH, Brigham and Women’s Hospital, Boston, agreed with Dr. Kosiborod’s interpretation.

“Until today we have had very limited information on the safety of SGLT2-inhibitors in acute illness, as the pivotal trials which established the use of these drugs in diabetes and chronic kidney disease largely excluded patients who were hospitalized,” Dr. Vaduganathan said.

“While the overall results of this meta-analysis are neutral and SGLT2 inhibitors will not be added as drugs to be used in the primary care of patients with COVID-19, it certainly sends a strong message of safety in acutely ill patients,” he added.

Dr. Vaduganathan explained that from the beginning of the COVID-19 pandemic, there was great interest in repurposing established therapies for alternative indications for their use in the management of COVID-19.

“Conditions that strongly predispose to adverse COVID outcomes strongly overlap with established indications for SGLT2-inhibitors. So many wondered whether these drugs may be an ideal treatment candidate for the management of COVID-19. However, there have been many safety concerns about the use of SGLT2-inhibitors in this acute setting, with worries that they may induce hemodynamic changes such an excessive lowering of blood pressure, or metabolic changes such as ketoacidosis in acutely ill patients,” he noted.

The initial DARE-19 study investigating SGLT2-inhibitors in COVID-19, with 1,250 participants, found a 20% reduction in the primary outcome of organ dysfunction or death, but this did not reach statistical significance, and no safety issues were seen. This “intriguing” result led to two further larger trials – the ACTIV-4a and RECOVERY trials, Dr. Vaduganathan reported.

“Those early signals of benefit seen in DARE-19 were largely not substantiated in the ACTIV-4A and RECOVERY trials, or in this new meta-analysis, and now we have this much larger body of evidence and more stable estimates about the efficacy of these drugs in acutely ill COVID-19 patients,” he said.

“But the story that we will all take forward is one of safety. This set of trials was arguably conducted in some of the sickest patients we’ve seen who have been exposed to SGLT2-inhibitors, and they strongly affirm that these agents can be safely continued in the setting of acute illness, with very low rates of ketoacidosis and kidney injury, and there was no prolongation of hospital stay,” he commented.

In his presentation, Dr. Kosiborod explained that treatments targeting COVID-19 pathobiology such as dysregulated immune responses, endothelial damage, microvascular thrombosis, and inflammation have been shown to improve the key outcomes in this patient group.

SGLT2 inhibitors, which modulate similar pathobiology, provide cardiovascular protection and prevent the progression of kidney disease in patients at risk for these events, including those with type 2 diabetes, heart failure, and kidney disease, and may also lead to organ protection in a setting of acute illness such as COVID-19, he noted. However, the role of SGLT2 inhibitors in patients hospitalized with COVID-19 remains uncertain.

To address the need for more definitive efficacy data, the World Health Organization Rapid Evidence Appraisal for COVID-19 Therapies (REACT) Working Group conducted a prospective meta-analysis using data from the three randomized controlled trials, DARE-19, RECOVERY, and ACTIV-4a, evaluating SGLT2 inhibitors in patients hospitalized with COVID-19.

Overall, these trials randomized 6,096 participants: 3,025 to SGLT2 inhibitors and 3,071 to usual care or placebo. The average age of participants ranged between 62 and 73 years across the trials, 39% were women, and 25% had type 2 diabetes.

By 28 days after randomization, all-cause mortality, the primary endpoint, had occurred in 11.6% of the SGLT2-inhibitor patients, compared with 12.4% of those randomized to usual care or placebo, giving an odds ratio of 0.93 (95% confidence interval, 0.79-1.08; P = .33) for SGLT2 inhibitors, with consistency across trials.

Data on in-hospital and 90-day all-cause mortality were only available for two out of three trials (DARE-19 and ACTIV-4a), but the results were similar to the primary endpoint showing nonsignificant trends toward a possible benefit in the SGLT2-inhibitor group.

The results were also similar for the secondary outcomes of progression to acute kidney injury or requirement for dialysis or death, and progression to invasive mechanical ventilation, extracorporeal membrane oxygenation, or death, both assessed at 28 days.

The primary safety outcome of ketoacidosis by 28 days was observed in seven and two patients allocated to SGLT2 inhibitors and usual care or placebo, respectively, and overall, the incidence of reported serious adverse events was balanced between treatment groups.

The RECOVERY trial was supported by grants to the University of Oxford from UK Research and Innovation, the National Institute for Health and Care Research, and Wellcome. The ACTIV-4a platform was sponsored by the National Heart, Lung, and Blood Institute. DARE-19 was an investigator-initiated collaborative trial supported by AstraZeneca. Dr. Kosiborod reported numerous conflicts of interest.

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

A new meta-analysis has shown that SGLT2 inhibitors do not lead to lower 28-day all-cause mortality, compared with usual care or placebo, in patients hospitalized with COVID-19.

However, no major safety issues were identified with the use of SGLT2 inhibitors in these acutely ill patients, the researchers report.

“While these findings do not support the use of SGLT2-inhibitors as standard of care for patients hospitalized with COVID-19, I think the most important take home message here is that the use of these medications appears to be safe even in really acutely ill hospitalized patients,” lead investigator of the meta-analysis, Mikhail Kosiborod, MD, Saint Luke’s Mid America Heart Institute, Kansas City, Mo., concluded.

He said this was important because the list of indications for SGLT2 inhibitors is rapidly growing.

“These medications are being used in more and more patients. And we know that when we discontinue medications in the hospital they frequently don’t get restarted, which can lead to real risks if SGLT2 inhibitors are stopped in patients with heart failure, chronic kidney disease, or diabetes. So, the bottom line is that there is no compelling reason to stop these medications in the hospital,” he added.

The new meta-analysis was presented at the recent annual congress of the European Society of Cardiology, held in Amsterdam.

Discussant of the presentation at the ESC Hotline session, Muthiah Vaduganathan, MD, MPH, Brigham and Women’s Hospital, Boston, agreed with Dr. Kosiborod’s interpretation.

“Until today we have had very limited information on the safety of SGLT2-inhibitors in acute illness, as the pivotal trials which established the use of these drugs in diabetes and chronic kidney disease largely excluded patients who were hospitalized,” Dr. Vaduganathan said.

“While the overall results of this meta-analysis are neutral and SGLT2 inhibitors will not be added as drugs to be used in the primary care of patients with COVID-19, it certainly sends a strong message of safety in acutely ill patients,” he added.

Dr. Vaduganathan explained that from the beginning of the COVID-19 pandemic, there was great interest in repurposing established therapies for alternative indications for their use in the management of COVID-19.

“Conditions that strongly predispose to adverse COVID outcomes strongly overlap with established indications for SGLT2-inhibitors. So many wondered whether these drugs may be an ideal treatment candidate for the management of COVID-19. However, there have been many safety concerns about the use of SGLT2-inhibitors in this acute setting, with worries that they may induce hemodynamic changes such an excessive lowering of blood pressure, or metabolic changes such as ketoacidosis in acutely ill patients,” he noted.

The initial DARE-19 study investigating SGLT2-inhibitors in COVID-19, with 1,250 participants, found a 20% reduction in the primary outcome of organ dysfunction or death, but this did not reach statistical significance, and no safety issues were seen. This “intriguing” result led to two further larger trials – the ACTIV-4a and RECOVERY trials, Dr. Vaduganathan reported.

“Those early signals of benefit seen in DARE-19 were largely not substantiated in the ACTIV-4A and RECOVERY trials, or in this new meta-analysis, and now we have this much larger body of evidence and more stable estimates about the efficacy of these drugs in acutely ill COVID-19 patients,” he said.

“But the story that we will all take forward is one of safety. This set of trials was arguably conducted in some of the sickest patients we’ve seen who have been exposed to SGLT2-inhibitors, and they strongly affirm that these agents can be safely continued in the setting of acute illness, with very low rates of ketoacidosis and kidney injury, and there was no prolongation of hospital stay,” he commented.

In his presentation, Dr. Kosiborod explained that treatments targeting COVID-19 pathobiology such as dysregulated immune responses, endothelial damage, microvascular thrombosis, and inflammation have been shown to improve the key outcomes in this patient group.

SGLT2 inhibitors, which modulate similar pathobiology, provide cardiovascular protection and prevent the progression of kidney disease in patients at risk for these events, including those with type 2 diabetes, heart failure, and kidney disease, and may also lead to organ protection in a setting of acute illness such as COVID-19, he noted. However, the role of SGLT2 inhibitors in patients hospitalized with COVID-19 remains uncertain.

To address the need for more definitive efficacy data, the World Health Organization Rapid Evidence Appraisal for COVID-19 Therapies (REACT) Working Group conducted a prospective meta-analysis using data from the three randomized controlled trials, DARE-19, RECOVERY, and ACTIV-4a, evaluating SGLT2 inhibitors in patients hospitalized with COVID-19.

Overall, these trials randomized 6,096 participants: 3,025 to SGLT2 inhibitors and 3,071 to usual care or placebo. The average age of participants ranged between 62 and 73 years across the trials, 39% were women, and 25% had type 2 diabetes.

By 28 days after randomization, all-cause mortality, the primary endpoint, had occurred in 11.6% of the SGLT2-inhibitor patients, compared with 12.4% of those randomized to usual care or placebo, giving an odds ratio of 0.93 (95% confidence interval, 0.79-1.08; P = .33) for SGLT2 inhibitors, with consistency across trials.

Data on in-hospital and 90-day all-cause mortality were only available for two out of three trials (DARE-19 and ACTIV-4a), but the results were similar to the primary endpoint showing nonsignificant trends toward a possible benefit in the SGLT2-inhibitor group.

The results were also similar for the secondary outcomes of progression to acute kidney injury or requirement for dialysis or death, and progression to invasive mechanical ventilation, extracorporeal membrane oxygenation, or death, both assessed at 28 days.

The primary safety outcome of ketoacidosis by 28 days was observed in seven and two patients allocated to SGLT2 inhibitors and usual care or placebo, respectively, and overall, the incidence of reported serious adverse events was balanced between treatment groups.

The RECOVERY trial was supported by grants to the University of Oxford from UK Research and Innovation, the National Institute for Health and Care Research, and Wellcome. The ACTIV-4a platform was sponsored by the National Heart, Lung, and Blood Institute. DARE-19 was an investigator-initiated collaborative trial supported by AstraZeneca. Dr. Kosiborod reported numerous conflicts of interest.

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

A new meta-analysis has shown that SGLT2 inhibitors do not lead to lower 28-day all-cause mortality, compared with usual care or placebo, in patients hospitalized with COVID-19.

However, no major safety issues were identified with the use of SGLT2 inhibitors in these acutely ill patients, the researchers report.

“While these findings do not support the use of SGLT2-inhibitors as standard of care for patients hospitalized with COVID-19, I think the most important take home message here is that the use of these medications appears to be safe even in really acutely ill hospitalized patients,” lead investigator of the meta-analysis, Mikhail Kosiborod, MD, Saint Luke’s Mid America Heart Institute, Kansas City, Mo., concluded.

He said this was important because the list of indications for SGLT2 inhibitors is rapidly growing.

“These medications are being used in more and more patients. And we know that when we discontinue medications in the hospital they frequently don’t get restarted, which can lead to real risks if SGLT2 inhibitors are stopped in patients with heart failure, chronic kidney disease, or diabetes. So, the bottom line is that there is no compelling reason to stop these medications in the hospital,” he added.

The new meta-analysis was presented at the recent annual congress of the European Society of Cardiology, held in Amsterdam.

Discussant of the presentation at the ESC Hotline session, Muthiah Vaduganathan, MD, MPH, Brigham and Women’s Hospital, Boston, agreed with Dr. Kosiborod’s interpretation.

“Until today we have had very limited information on the safety of SGLT2-inhibitors in acute illness, as the pivotal trials which established the use of these drugs in diabetes and chronic kidney disease largely excluded patients who were hospitalized,” Dr. Vaduganathan said.

“While the overall results of this meta-analysis are neutral and SGLT2 inhibitors will not be added as drugs to be used in the primary care of patients with COVID-19, it certainly sends a strong message of safety in acutely ill patients,” he added.

Dr. Vaduganathan explained that from the beginning of the COVID-19 pandemic, there was great interest in repurposing established therapies for alternative indications for their use in the management of COVID-19.

“Conditions that strongly predispose to adverse COVID outcomes strongly overlap with established indications for SGLT2-inhibitors. So many wondered whether these drugs may be an ideal treatment candidate for the management of COVID-19. However, there have been many safety concerns about the use of SGLT2-inhibitors in this acute setting, with worries that they may induce hemodynamic changes such an excessive lowering of blood pressure, or metabolic changes such as ketoacidosis in acutely ill patients,” he noted.

The initial DARE-19 study investigating SGLT2-inhibitors in COVID-19, with 1,250 participants, found a 20% reduction in the primary outcome of organ dysfunction or death, but this did not reach statistical significance, and no safety issues were seen. This “intriguing” result led to two further larger trials – the ACTIV-4a and RECOVERY trials, Dr. Vaduganathan reported.

“Those early signals of benefit seen in DARE-19 were largely not substantiated in the ACTIV-4A and RECOVERY trials, or in this new meta-analysis, and now we have this much larger body of evidence and more stable estimates about the efficacy of these drugs in acutely ill COVID-19 patients,” he said.

“But the story that we will all take forward is one of safety. This set of trials was arguably conducted in some of the sickest patients we’ve seen who have been exposed to SGLT2-inhibitors, and they strongly affirm that these agents can be safely continued in the setting of acute illness, with very low rates of ketoacidosis and kidney injury, and there was no prolongation of hospital stay,” he commented.

In his presentation, Dr. Kosiborod explained that treatments targeting COVID-19 pathobiology such as dysregulated immune responses, endothelial damage, microvascular thrombosis, and inflammation have been shown to improve the key outcomes in this patient group.

SGLT2 inhibitors, which modulate similar pathobiology, provide cardiovascular protection and prevent the progression of kidney disease in patients at risk for these events, including those with type 2 diabetes, heart failure, and kidney disease, and may also lead to organ protection in a setting of acute illness such as COVID-19, he noted. However, the role of SGLT2 inhibitors in patients hospitalized with COVID-19 remains uncertain.

To address the need for more definitive efficacy data, the World Health Organization Rapid Evidence Appraisal for COVID-19 Therapies (REACT) Working Group conducted a prospective meta-analysis using data from the three randomized controlled trials, DARE-19, RECOVERY, and ACTIV-4a, evaluating SGLT2 inhibitors in patients hospitalized with COVID-19.

Overall, these trials randomized 6,096 participants: 3,025 to SGLT2 inhibitors and 3,071 to usual care or placebo. The average age of participants ranged between 62 and 73 years across the trials, 39% were women, and 25% had type 2 diabetes.

By 28 days after randomization, all-cause mortality, the primary endpoint, had occurred in 11.6% of the SGLT2-inhibitor patients, compared with 12.4% of those randomized to usual care or placebo, giving an odds ratio of 0.93 (95% confidence interval, 0.79-1.08; P = .33) for SGLT2 inhibitors, with consistency across trials.

Data on in-hospital and 90-day all-cause mortality were only available for two out of three trials (DARE-19 and ACTIV-4a), but the results were similar to the primary endpoint showing nonsignificant trends toward a possible benefit in the SGLT2-inhibitor group.

The results were also similar for the secondary outcomes of progression to acute kidney injury or requirement for dialysis or death, and progression to invasive mechanical ventilation, extracorporeal membrane oxygenation, or death, both assessed at 28 days.

The primary safety outcome of ketoacidosis by 28 days was observed in seven and two patients allocated to SGLT2 inhibitors and usual care or placebo, respectively, and overall, the incidence of reported serious adverse events was balanced between treatment groups.

The RECOVERY trial was supported by grants to the University of Oxford from UK Research and Innovation, the National Institute for Health and Care Research, and Wellcome. The ACTIV-4a platform was sponsored by the National Heart, Lung, and Blood Institute. DARE-19 was an investigator-initiated collaborative trial supported by AstraZeneca. Dr. Kosiborod reported numerous conflicts of interest.

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

TOPLINE:

Globally, lead exposure is linked to more than 5.5 million adult cardiovascular deaths in 2019, as well as loss of 765 million intelligence quotient (IQ) points in children younger than 5 years, which cost U.S. $6 trillion in lost productivity, new research suggests.

METHODOLOGY:

• Global lead exposure has declined substantially since leaded gasoline was phased out, but several sources of lead remain, resulting in adverse health and economic effects, particularly in low- and middle-income countries (LMICs).
• Estimates of cardiovascular disease (CVD) deaths from lead exposure have been limited to effects of increased blood pressure, but studies show that lead exposure has cardiovascular impacts through mechanisms other than hypertension.
• Drawing from various sources and studies, researchers estimated global blood lead levels and the impact of lead exposure on CVD mortality in 2019 among adults aged 25 years or older, IQ loss in children younger than 5 years, and the related economic costs.

TAKEAWAY:

• Researchers estimated that there were 5,545,000 (95% confidence interval, 2,305,000-8,271,000) cardiovascular deaths in adults from lead exposure in 2019, with as many as 90.2% of these deaths in LMICs; however, this estimate may be incomplete because it does not include the effect of lead exposure on CVD mortality mediated through hypertension.
• The estimated global IQ loss in children younger than 5 years due to lead exposure was 765 million (95% CI, 443 million-1,098 million) IQ points in 2019, 95.3% of which occurred in LMICs.
• These estimates place lead exposure on a par with ambient particulate matter and household air pollution combined, and ahead of unsafe household drinking water, sanitation, and handwashing, as an environmental risk factor.
• The estimated global cost of lead exposure from CVD mortality and IQ loss combined is U.S. $6.0 trillion (range, $2.6 trillion-9.0 trillion) in 2019, equivalent to 6.9% of the 2019 global gross domestic product.

IN PRACTICE:

Given the magnitude of the estimated health effects of lead exposure, particularly in LMICs, “it is imperative that nationally representative periodic blood lead level measurements be institutionalized,” write the authors, adding that these measurements could be incorporated into existing household surveys.

STUDY DETAILS:

The study was conducted by Bjorn Larsen, PhD, environmental economist and consultant to the World Bank, and Ernesto Sánchez-Triana. It was published online in The Lancet Planetary Health.

LIMITATIONS:

• Global blood lead level estimates may be inaccurate, given that measurements are absent for many countries.
• Certain income projections and income losses are uncertain.
• Because the study does not capture the detrimental effects of lead exposure other than IQ loss and CVD mortality, the estimates of global costs are conservative.

DISCLOSURES:

The study received support from the Korea Green Growth Trust Fund and the World Bank’s Pollution Management and Environmental Health Program. The authors have no relevant conflicts of interest.

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

TOPLINE:

Globally, lead exposure is linked to more than 5.5 million adult cardiovascular deaths in 2019, as well as loss of 765 million intelligence quotient (IQ) points in children younger than 5 years, which cost U.S. $6 trillion in lost productivity, new research suggests.

METHODOLOGY:

• Global lead exposure has declined substantially since leaded gasoline was phased out, but several sources of lead remain, resulting in adverse health and economic effects, particularly in low- and middle-income countries (LMICs).
• Estimates of cardiovascular disease (CVD) deaths from lead exposure have been limited to effects of increased blood pressure, but studies show that lead exposure has cardiovascular impacts through mechanisms other than hypertension.
• Drawing from various sources and studies, researchers estimated global blood lead levels and the impact of lead exposure on CVD mortality in 2019 among adults aged 25 years or older, IQ loss in children younger than 5 years, and the related economic costs.

TAKEAWAY:

• Researchers estimated that there were 5,545,000 (95% confidence interval, 2,305,000-8,271,000) cardiovascular deaths in adults from lead exposure in 2019, with as many as 90.2% of these deaths in LMICs; however, this estimate may be incomplete because it does not include the effect of lead exposure on CVD mortality mediated through hypertension.
• The estimated global IQ loss in children younger than 5 years due to lead exposure was 765 million (95% CI, 443 million-1,098 million) IQ points in 2019, 95.3% of which occurred in LMICs.
• These estimates place lead exposure on a par with ambient particulate matter and household air pollution combined, and ahead of unsafe household drinking water, sanitation, and handwashing, as an environmental risk factor.
• The estimated global cost of lead exposure from CVD mortality and IQ loss combined is U.S. $6.0 trillion (range, $2.6 trillion-9.0 trillion) in 2019, equivalent to 6.9% of the 2019 global gross domestic product.

IN PRACTICE:

Given the magnitude of the estimated health effects of lead exposure, particularly in LMICs, “it is imperative that nationally representative periodic blood lead level measurements be institutionalized,” write the authors, adding that these measurements could be incorporated into existing household surveys.

STUDY DETAILS:

The study was conducted by Bjorn Larsen, PhD, environmental economist and consultant to the World Bank, and Ernesto Sánchez-Triana. It was published online in The Lancet Planetary Health.

LIMITATIONS:

• Global blood lead level estimates may be inaccurate, given that measurements are absent for many countries.
• Certain income projections and income losses are uncertain.
• Because the study does not capture the detrimental effects of lead exposure other than IQ loss and CVD mortality, the estimates of global costs are conservative.

DISCLOSURES:

The study received support from the Korea Green Growth Trust Fund and the World Bank’s Pollution Management and Environmental Health Program. The authors have no relevant conflicts of interest.

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

TOPLINE:

Globally, lead exposure is linked to more than 5.5 million adult cardiovascular deaths in 2019, as well as loss of 765 million intelligence quotient (IQ) points in children younger than 5 years, which cost U.S. $6 trillion in lost productivity, new research suggests.

METHODOLOGY:

• Global lead exposure has declined substantially since leaded gasoline was phased out, but several sources of lead remain, resulting in adverse health and economic effects, particularly in low- and middle-income countries (LMICs).
• Estimates of cardiovascular disease (CVD) deaths from lead exposure have been limited to effects of increased blood pressure, but studies show that lead exposure has cardiovascular impacts through mechanisms other than hypertension.
• Drawing from various sources and studies, researchers estimated global blood lead levels and the impact of lead exposure on CVD mortality in 2019 among adults aged 25 years or older, IQ loss in children younger than 5 years, and the related economic costs.

TAKEAWAY:

• Researchers estimated that there were 5,545,000 (95% confidence interval, 2,305,000-8,271,000) cardiovascular deaths in adults from lead exposure in 2019, with as many as 90.2% of these deaths in LMICs; however, this estimate may be incomplete because it does not include the effect of lead exposure on CVD mortality mediated through hypertension.
• The estimated global IQ loss in children younger than 5 years due to lead exposure was 765 million (95% CI, 443 million-1,098 million) IQ points in 2019, 95.3% of which occurred in LMICs.
• These estimates place lead exposure on a par with ambient particulate matter and household air pollution combined, and ahead of unsafe household drinking water, sanitation, and handwashing, as an environmental risk factor.
• The estimated global cost of lead exposure from CVD mortality and IQ loss combined is U.S. $6.0 trillion (range, $2.6 trillion-9.0 trillion) in 2019, equivalent to 6.9% of the 2019 global gross domestic product.

IN PRACTICE:

Given the magnitude of the estimated health effects of lead exposure, particularly in LMICs, “it is imperative that nationally representative periodic blood lead level measurements be institutionalized,” write the authors, adding that these measurements could be incorporated into existing household surveys.

STUDY DETAILS:

The study was conducted by Bjorn Larsen, PhD, environmental economist and consultant to the World Bank, and Ernesto Sánchez-Triana. It was published online in The Lancet Planetary Health.

LIMITATIONS:

• Global blood lead level estimates may be inaccurate, given that measurements are absent for many countries.
• Certain income projections and income losses are uncertain.
• Because the study does not capture the detrimental effects of lead exposure other than IQ loss and CVD mortality, the estimates of global costs are conservative.

DISCLOSURES:

The study received support from the Korea Green Growth Trust Fund and the World Bank’s Pollution Management and Environmental Health Program. The authors have no relevant conflicts of interest.

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

More than 10 hours a day of sedentary behavior significantly increases the risk of dementia in older adults, a new study suggests.

The study of nearly 50,000 adults in the UK Biobank shows that dementia risk increased 8% with 10 hours of sedentary time and 63% with 12 hours. That’s particularly concerning because Americans spend an average of 9.5 hours a day sitting.

Sleep wasn’t factored into the sedentary time and how someone accumulated the 10 hours – either in one continuous block or broken up throughout the day – was irrelevant.

“Our analysis cannot determine whether there is a causal link, so prescriptive conclusions are not really possible; however. I think it is very reasonable to conclude that sitting less and moving more may help reduce risk of dementia,” lead investigator David Raichlen, PhD, professor of biological sciences and anthropology, University of Southern California, Los Angeles, said in an interview.

The findings were published online in JAMA.
 

A surprising find?

The study is a retrospective analysis of prospectively collected data from the UK Biobank of 49,841 adults aged 60 years or older who wore an accelerometer on their wrists 24 hours a day for a week. Participants had no history of dementia when they wore the movement monitoring device.

Investigators used machine-based learning to determine sedentary time based on readings from the accelerometers. Sleep was not included as sedentary behavior.

Over a mean follow-up of 6.72 years, 414 participants were diagnosed with dementia.

Investigators found that dementia risk rises by 8% at 10 hours a day (adjusted hazard ratio, 1.08; P < .001) and 63% at 12 hours a day (aHR, 1.63; P < .001), compared with 9.27 hours a day. Those who logged 15 hours of sedentary behavior a day had more than triple the dementia risk (aHR, 3.21; P < .001).

Although previous studies had found that breaking up sedentary periods with short bursts of activity help offset some negative health effects of sitting, that wasn’t the case here. Dementia risk was elevated whether participants were sedentary for 10 uninterrupted hours or multiple sedentary periods that totaled 10 hours over the whole day.

“This was surprising,” Dr. Raichlen said. “We expected to find that patterns of sedentary behavior would play a role in risk of dementia, but once you take into account the daily volume of time spent sedentary, how you get there doesn’t seem to matter as much.”

The study did not examine how participants spent sedentary time, but an earlier study by Dr. Raichlen found that watching TV was associated with a greater risk of dementia in older adults, compared with working on a computer.
 

More research welcome

Dr. Raichlen noted that the number of dementia cases in the study is low and that the view of sedentary behavior is based on 1 week of accelerometer readings. A longitudinal study is needed to determine if the findings last over a longer time period.

In a comment, Claire Sexton, DPhil, senior director of scientific programs and outreach for the Alzheimer’s Association, says that earlier studies reported an association between sedentary time and dementia, so these results aren’t “particularly surprising.”

“However, reports that did not find an association have also been published, so additional research on possible associations is welcome,” she said.

It’s also important to note that this observational study doesn’t establish a causal relationship between inactivity and cognitive function, which Dr. Sexton said means the influence of other dementia risk factors that are also exacerbated by sedentary behavior can’t be ruled out.

“Although results remained significant after adjusting for several of these factors, further research is required to better understand the various elements that may influence the observed relationship,” noted Dr. Sexton, who was not part of the study. “Reverse causality – that changes in the brain related to dementia are causing the sedentary behavior – cannot be ruled out.”

The study was funded by the National Institutes of Health, the state of Arizona, the Arizona Department of Health Services, and the McKnight Brain Research Foundation. Dr. Raichlen and Dr. Sexton report no relevant financial relationships.

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

More than 10 hours a day of sedentary behavior significantly increases the risk of dementia in older adults, a new study suggests.

The study of nearly 50,000 adults in the UK Biobank shows that dementia risk increased 8% with 10 hours of sedentary time and 63% with 12 hours. That’s particularly concerning because Americans spend an average of 9.5 hours a day sitting.

Sleep wasn’t factored into the sedentary time and how someone accumulated the 10 hours – either in one continuous block or broken up throughout the day – was irrelevant.

“Our analysis cannot determine whether there is a causal link, so prescriptive conclusions are not really possible; however. I think it is very reasonable to conclude that sitting less and moving more may help reduce risk of dementia,” lead investigator David Raichlen, PhD, professor of biological sciences and anthropology, University of Southern California, Los Angeles, said in an interview.

The findings were published online in JAMA.
 

A surprising find?

The study is a retrospective analysis of prospectively collected data from the UK Biobank of 49,841 adults aged 60 years or older who wore an accelerometer on their wrists 24 hours a day for a week. Participants had no history of dementia when they wore the movement monitoring device.

Investigators used machine-based learning to determine sedentary time based on readings from the accelerometers. Sleep was not included as sedentary behavior.

Over a mean follow-up of 6.72 years, 414 participants were diagnosed with dementia.

Investigators found that dementia risk rises by 8% at 10 hours a day (adjusted hazard ratio, 1.08; P < .001) and 63% at 12 hours a day (aHR, 1.63; P < .001), compared with 9.27 hours a day. Those who logged 15 hours of sedentary behavior a day had more than triple the dementia risk (aHR, 3.21; P < .001).

Although previous studies had found that breaking up sedentary periods with short bursts of activity help offset some negative health effects of sitting, that wasn’t the case here. Dementia risk was elevated whether participants were sedentary for 10 uninterrupted hours or multiple sedentary periods that totaled 10 hours over the whole day.

“This was surprising,” Dr. Raichlen said. “We expected to find that patterns of sedentary behavior would play a role in risk of dementia, but once you take into account the daily volume of time spent sedentary, how you get there doesn’t seem to matter as much.”

The study did not examine how participants spent sedentary time, but an earlier study by Dr. Raichlen found that watching TV was associated with a greater risk of dementia in older adults, compared with working on a computer.
 

More research welcome

Dr. Raichlen noted that the number of dementia cases in the study is low and that the view of sedentary behavior is based on 1 week of accelerometer readings. A longitudinal study is needed to determine if the findings last over a longer time period.

In a comment, Claire Sexton, DPhil, senior director of scientific programs and outreach for the Alzheimer’s Association, says that earlier studies reported an association between sedentary time and dementia, so these results aren’t “particularly surprising.”

“However, reports that did not find an association have also been published, so additional research on possible associations is welcome,” she said.

It’s also important to note that this observational study doesn’t establish a causal relationship between inactivity and cognitive function, which Dr. Sexton said means the influence of other dementia risk factors that are also exacerbated by sedentary behavior can’t be ruled out.

“Although results remained significant after adjusting for several of these factors, further research is required to better understand the various elements that may influence the observed relationship,” noted Dr. Sexton, who was not part of the study. “Reverse causality – that changes in the brain related to dementia are causing the sedentary behavior – cannot be ruled out.”

The study was funded by the National Institutes of Health, the state of Arizona, the Arizona Department of Health Services, and the McKnight Brain Research Foundation. Dr. Raichlen and Dr. Sexton report no relevant financial relationships.

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

More than 10 hours a day of sedentary behavior significantly increases the risk of dementia in older adults, a new study suggests.

The study of nearly 50,000 adults in the UK Biobank shows that dementia risk increased 8% with 10 hours of sedentary time and 63% with 12 hours. That’s particularly concerning because Americans spend an average of 9.5 hours a day sitting.

Sleep wasn’t factored into the sedentary time and how someone accumulated the 10 hours – either in one continuous block or broken up throughout the day – was irrelevant.

“Our analysis cannot determine whether there is a causal link, so prescriptive conclusions are not really possible; however. I think it is very reasonable to conclude that sitting less and moving more may help reduce risk of dementia,” lead investigator David Raichlen, PhD, professor of biological sciences and anthropology, University of Southern California, Los Angeles, said in an interview.

The findings were published online in JAMA.
 

A surprising find?

The study is a retrospective analysis of prospectively collected data from the UK Biobank of 49,841 adults aged 60 years or older who wore an accelerometer on their wrists 24 hours a day for a week. Participants had no history of dementia when they wore the movement monitoring device.

Investigators used machine-based learning to determine sedentary time based on readings from the accelerometers. Sleep was not included as sedentary behavior.

Over a mean follow-up of 6.72 years, 414 participants were diagnosed with dementia.

Investigators found that dementia risk rises by 8% at 10 hours a day (adjusted hazard ratio, 1.08; P < .001) and 63% at 12 hours a day (aHR, 1.63; P < .001), compared with 9.27 hours a day. Those who logged 15 hours of sedentary behavior a day had more than triple the dementia risk (aHR, 3.21; P < .001).

Although previous studies had found that breaking up sedentary periods with short bursts of activity help offset some negative health effects of sitting, that wasn’t the case here. Dementia risk was elevated whether participants were sedentary for 10 uninterrupted hours or multiple sedentary periods that totaled 10 hours over the whole day.

“This was surprising,” Dr. Raichlen said. “We expected to find that patterns of sedentary behavior would play a role in risk of dementia, but once you take into account the daily volume of time spent sedentary, how you get there doesn’t seem to matter as much.”

The study did not examine how participants spent sedentary time, but an earlier study by Dr. Raichlen found that watching TV was associated with a greater risk of dementia in older adults, compared with working on a computer.
 

More research welcome

Dr. Raichlen noted that the number of dementia cases in the study is low and that the view of sedentary behavior is based on 1 week of accelerometer readings. A longitudinal study is needed to determine if the findings last over a longer time period.

In a comment, Claire Sexton, DPhil, senior director of scientific programs and outreach for the Alzheimer’s Association, says that earlier studies reported an association between sedentary time and dementia, so these results aren’t “particularly surprising.”

“However, reports that did not find an association have also been published, so additional research on possible associations is welcome,” she said.

It’s also important to note that this observational study doesn’t establish a causal relationship between inactivity and cognitive function, which Dr. Sexton said means the influence of other dementia risk factors that are also exacerbated by sedentary behavior can’t be ruled out.

“Although results remained significant after adjusting for several of these factors, further research is required to better understand the various elements that may influence the observed relationship,” noted Dr. Sexton, who was not part of the study. “Reverse causality – that changes in the brain related to dementia are causing the sedentary behavior – cannot be ruled out.”

The study was funded by the National Institutes of Health, the state of Arizona, the Arizona Department of Health Services, and the McKnight Brain Research Foundation. Dr. Raichlen and Dr. Sexton report no relevant financial relationships.

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

COVID vaccines will have a new formulation in 2023, according to a decision announced by the U.S. Food and Drug Administration, that will focus efforts on circulating variants. The move pushes last year’s bivalent vaccines out of circulation because they will no longer be authorized for use in the United States.

The updated mRNA vaccines for 2023-2024 are being revised to include a single component that corresponds to the Omicron variant XBB.1.5. Like the bivalents offered before, the new monovalents are being manufactured by Moderna and Pfizer.

The new vaccines are authorized for use in individuals age 6 months and older.  And the new options are being developed using a similar process as previous formulations, according to the FDA.
 

Targeting circulating variants

In recent studies, regulators point out the extent of neutralization observed by the updated vaccines against currently circulating viral variants causing COVID-19, including EG.5, BA.2.86, appears to be of a similar magnitude to the extent of neutralization observed with previous versions of the vaccines against corresponding prior variants.

“This suggests that the vaccines are a good match for protecting against the currently circulating COVID-19 variants,” according to the report.

Hundreds of millions of people in the United States have already received previously approved mRNA COVID vaccines, according to regulators who say the benefit-to-risk profile is well understood as they move forward with new formulations.

“Vaccination remains critical to public health and continued protection against serious consequences of COVID-19, including hospitalization and death,” Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research, said in a statement. “The public can be assured that these updated vaccines have met the agency’s rigorous scientific standards for safety, effectiveness, and manufacturing quality. We very much encourage those who are eligible to consider getting vaccinated.”
 

Timing the effort

On Sept. 12 the U.S. Centers for Disease Control and Prevention recommended that everyone 6 months and older get an updated COVID-19 vaccine. Updated vaccines from Pfizer-BioNTech and Moderna will be available later this week, according to the agency.

This article was updated 9/14/23.

A version of this article appeared on Medscape.com.

COVID vaccines will have a new formulation in 2023, according to a decision announced by the U.S. Food and Drug Administration, that will focus efforts on circulating variants. The move pushes last year’s bivalent vaccines out of circulation because they will no longer be authorized for use in the United States.

The updated mRNA vaccines for 2023-2024 are being revised to include a single component that corresponds to the Omicron variant XBB.1.5. Like the bivalents offered before, the new monovalents are being manufactured by Moderna and Pfizer.

The new vaccines are authorized for use in individuals age 6 months and older.  And the new options are being developed using a similar process as previous formulations, according to the FDA.
 

Targeting circulating variants

In recent studies, regulators point out the extent of neutralization observed by the updated vaccines against currently circulating viral variants causing COVID-19, including EG.5, BA.2.86, appears to be of a similar magnitude to the extent of neutralization observed with previous versions of the vaccines against corresponding prior variants.

“This suggests that the vaccines are a good match for protecting against the currently circulating COVID-19 variants,” according to the report.

Hundreds of millions of people in the United States have already received previously approved mRNA COVID vaccines, according to regulators who say the benefit-to-risk profile is well understood as they move forward with new formulations.

“Vaccination remains critical to public health and continued protection against serious consequences of COVID-19, including hospitalization and death,” Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research, said in a statement. “The public can be assured that these updated vaccines have met the agency’s rigorous scientific standards for safety, effectiveness, and manufacturing quality. We very much encourage those who are eligible to consider getting vaccinated.”
 

Timing the effort

On Sept. 12 the U.S. Centers for Disease Control and Prevention recommended that everyone 6 months and older get an updated COVID-19 vaccine. Updated vaccines from Pfizer-BioNTech and Moderna will be available later this week, according to the agency.

This article was updated 9/14/23.

A version of this article appeared on Medscape.com.

COVID vaccines will have a new formulation in 2023, according to a decision announced by the U.S. Food and Drug Administration, that will focus efforts on circulating variants. The move pushes last year’s bivalent vaccines out of circulation because they will no longer be authorized for use in the United States.

The updated mRNA vaccines for 2023-2024 are being revised to include a single component that corresponds to the Omicron variant XBB.1.5. Like the bivalents offered before, the new monovalents are being manufactured by Moderna and Pfizer.

The new vaccines are authorized for use in individuals age 6 months and older.  And the new options are being developed using a similar process as previous formulations, according to the FDA.
 

Targeting circulating variants

In recent studies, regulators point out the extent of neutralization observed by the updated vaccines against currently circulating viral variants causing COVID-19, including EG.5, BA.2.86, appears to be of a similar magnitude to the extent of neutralization observed with previous versions of the vaccines against corresponding prior variants.

“This suggests that the vaccines are a good match for protecting against the currently circulating COVID-19 variants,” according to the report.

Hundreds of millions of people in the United States have already received previously approved mRNA COVID vaccines, according to regulators who say the benefit-to-risk profile is well understood as they move forward with new formulations.

“Vaccination remains critical to public health and continued protection against serious consequences of COVID-19, including hospitalization and death,” Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research, said in a statement. “The public can be assured that these updated vaccines have met the agency’s rigorous scientific standards for safety, effectiveness, and manufacturing quality. We very much encourage those who are eligible to consider getting vaccinated.”
 

Timing the effort

On Sept. 12 the U.S. Centers for Disease Control and Prevention recommended that everyone 6 months and older get an updated COVID-19 vaccine. Updated vaccines from Pfizer-BioNTech and Moderna will be available later this week, according to the agency.

This article was updated 9/14/23.

A version of this article appeared on Medscape.com.

New research provides strong evidence of an association between abdominal fat and reduced brain volumes, particularly those involved with cognitive function.

In a large study of healthy middle-aged adults, greater visceral and subcutaneous abdominal fat on abdominal MRI predicted brain atrophy on imaging, especially in women.

“The study shows that excess fat is bad for the brain and worse in women, including in Alzheimer’s disease risk regions,” lead author Cyrus Raji, MD, PhD, with the Mallinckrodt Institute of Radiology, Washington University, St. Louis, Mo., said in an interview.

The study was published online in the journal Aging and Disease
 

Modifiable risk factor

Multiple studies have suggested a connection between body fat accumulation and increased dementia risk. But few have examined the relationship between types of fat (visceral and subcutaneous) and brain volume.

For the new study, 10,000 healthy adults aged 20-80 years (mean age, 52.9 years; 53% men) underwent a short whole-body MRI protocol. Regression analyses of abdominal fat types and normalized brain volumes were evaluated, controlling for age and sex.

The research team found that higher amounts of both visceral and subcutaneous abdominal fat predicted lower total gray and white matter volume, as well as lower volume in the hippocampus, frontal cortex, and temporal, parietal, and occipital lobes.

“The findings are quite dramatic,” Dr. Raji told this news organization. “Overall, we found that both subcutaneous and visceral fat has similar levels of negative relationships with brain volumes.”

Women had a higher burden of brain atrophy with increased visceral fat than men. However, it’s difficult to place the sex differences in context because of the lack of prior work specifically investigating visceral fat, brain volume loss, and sex differences, the researchers caution.

They also note that while statistically significant relationships were observed between visceral fat levels and gray matter volume changes, their effect sizes were generally small. 

“Thus, the statistical significance of this work is influenced by the large sample size and less so by large effect size in any given set of regions,” the investigators write.

Other limitations include the cross-sectional nature of the study, which precludes conclusions about causality. The analysis also did not account for other lifestyle factors such as physical activity, diet, and genetic variables.

The researchers call for further investigation “to better elucidate underlying mechanisms and discover possible interventions targeting abdominal fat reduction as a strategy to maintain brain health.”
 

‘Helpful addition to the literature’

In a comment, Claire Sexton, DPhil, Alzheimer’s Association senior director of scientific programs and outreach, noted that “previous studies have linked obesity with cognitive decline and increased risk of dementia. Rather than using BMI as a proxy for body fat, the current study examined visceral and subcutaneous fat directly using imaging techniques.”

Dr. Sexton, who was not associated with this study, said the finding that increased body fat was associated with reduced brain volumes suggests “a possible mechanism to explain the previously reported associations between obesity and cognition.”

“Though some degree of atrophy and brain shrinkage is common with old age, awareness of this association is important because reduced brain volume may be associated with problems with thinking, memory, and performing everyday tasks, and because rates of obesity continue to rise in the United States, along with obesity-related conditions including heart disease, stroke, type 2 diabetes and certain types of cancer,” she added.

“While a helpful addition to the literature, the study does have important limitations. As an observational study, it cannot establish whether higher levels of body fat directly causes reduced brain volumes,” Dr. Sexton cautioned.

In addition, the study did not take into account important related factors like physical activity and diet, which may influence any relationship between body fat and brain volumes, she noted. “Overall, it is not just one factor that is important to consider when considering risk for cognitive decline and dementia, but multiple factors.

“Obesity and the location of body fat must be considered in combination with one’s total lived experience and habits, including physical activity, education, head injury, sleep, mental health, and the health of your heart/cardiovascular system and other key bodily systems,” Dr. Sexton said.

The Alzheimer’s Association is leading a 2-year clinical trial known as U.S. POINTER to see whether combining physical activity, healthy nutrition, social and intellectual challenges, and improved self-management of medical conditions can protect cognitive function in older adults who are at increased risk for cognitive decline.

This work was supported in part by Providence St. Joseph Health in Seattle; Saint John’s Health Center Foundation; Pacific Neuroscience Institute and Foundation; Will and Cary Singleton; and the McLoughlin family. Dr. Raji is a consultant for Brainreader, Apollo Health, Voxelwise, Neurevolution, Pacific Neuroscience Institute Foundation, and Icometrix. Dr. Sexton reports no relevant financial relationships.

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

New research provides strong evidence of an association between abdominal fat and reduced brain volumes, particularly those involved with cognitive function.

In a large study of healthy middle-aged adults, greater visceral and subcutaneous abdominal fat on abdominal MRI predicted brain atrophy on imaging, especially in women.

“The study shows that excess fat is bad for the brain and worse in women, including in Alzheimer’s disease risk regions,” lead author Cyrus Raji, MD, PhD, with the Mallinckrodt Institute of Radiology, Washington University, St. Louis, Mo., said in an interview.

The study was published online in the journal Aging and Disease
 

Modifiable risk factor

Multiple studies have suggested a connection between body fat accumulation and increased dementia risk. But few have examined the relationship between types of fat (visceral and subcutaneous) and brain volume.

For the new study, 10,000 healthy adults aged 20-80 years (mean age, 52.9 years; 53% men) underwent a short whole-body MRI protocol. Regression analyses of abdominal fat types and normalized brain volumes were evaluated, controlling for age and sex.

The research team found that higher amounts of both visceral and subcutaneous abdominal fat predicted lower total gray and white matter volume, as well as lower volume in the hippocampus, frontal cortex, and temporal, parietal, and occipital lobes.

“The findings are quite dramatic,” Dr. Raji told this news organization. “Overall, we found that both subcutaneous and visceral fat has similar levels of negative relationships with brain volumes.”

Women had a higher burden of brain atrophy with increased visceral fat than men. However, it’s difficult to place the sex differences in context because of the lack of prior work specifically investigating visceral fat, brain volume loss, and sex differences, the researchers caution.

They also note that while statistically significant relationships were observed between visceral fat levels and gray matter volume changes, their effect sizes were generally small. 

“Thus, the statistical significance of this work is influenced by the large sample size and less so by large effect size in any given set of regions,” the investigators write.

Other limitations include the cross-sectional nature of the study, which precludes conclusions about causality. The analysis also did not account for other lifestyle factors such as physical activity, diet, and genetic variables.

The researchers call for further investigation “to better elucidate underlying mechanisms and discover possible interventions targeting abdominal fat reduction as a strategy to maintain brain health.”
 

‘Helpful addition to the literature’

In a comment, Claire Sexton, DPhil, Alzheimer’s Association senior director of scientific programs and outreach, noted that “previous studies have linked obesity with cognitive decline and increased risk of dementia. Rather than using BMI as a proxy for body fat, the current study examined visceral and subcutaneous fat directly using imaging techniques.”

Dr. Sexton, who was not associated with this study, said the finding that increased body fat was associated with reduced brain volumes suggests “a possible mechanism to explain the previously reported associations between obesity and cognition.”

“Though some degree of atrophy and brain shrinkage is common with old age, awareness of this association is important because reduced brain volume may be associated with problems with thinking, memory, and performing everyday tasks, and because rates of obesity continue to rise in the United States, along with obesity-related conditions including heart disease, stroke, type 2 diabetes and certain types of cancer,” she added.

“While a helpful addition to the literature, the study does have important limitations. As an observational study, it cannot establish whether higher levels of body fat directly causes reduced brain volumes,” Dr. Sexton cautioned.

In addition, the study did not take into account important related factors like physical activity and diet, which may influence any relationship between body fat and brain volumes, she noted. “Overall, it is not just one factor that is important to consider when considering risk for cognitive decline and dementia, but multiple factors.

“Obesity and the location of body fat must be considered in combination with one’s total lived experience and habits, including physical activity, education, head injury, sleep, mental health, and the health of your heart/cardiovascular system and other key bodily systems,” Dr. Sexton said.

The Alzheimer’s Association is leading a 2-year clinical trial known as U.S. POINTER to see whether combining physical activity, healthy nutrition, social and intellectual challenges, and improved self-management of medical conditions can protect cognitive function in older adults who are at increased risk for cognitive decline.

This work was supported in part by Providence St. Joseph Health in Seattle; Saint John’s Health Center Foundation; Pacific Neuroscience Institute and Foundation; Will and Cary Singleton; and the McLoughlin family. Dr. Raji is a consultant for Brainreader, Apollo Health, Voxelwise, Neurevolution, Pacific Neuroscience Institute Foundation, and Icometrix. Dr. Sexton reports no relevant financial relationships.

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

New research provides strong evidence of an association between abdominal fat and reduced brain volumes, particularly those involved with cognitive function.

In a large study of healthy middle-aged adults, greater visceral and subcutaneous abdominal fat on abdominal MRI predicted brain atrophy on imaging, especially in women.

“The study shows that excess fat is bad for the brain and worse in women, including in Alzheimer’s disease risk regions,” lead author Cyrus Raji, MD, PhD, with the Mallinckrodt Institute of Radiology, Washington University, St. Louis, Mo., said in an interview.

The study was published online in the journal Aging and Disease
 

Modifiable risk factor

Multiple studies have suggested a connection between body fat accumulation and increased dementia risk. But few have examined the relationship between types of fat (visceral and subcutaneous) and brain volume.

For the new study, 10,000 healthy adults aged 20-80 years (mean age, 52.9 years; 53% men) underwent a short whole-body MRI protocol. Regression analyses of abdominal fat types and normalized brain volumes were evaluated, controlling for age and sex.

The research team found that higher amounts of both visceral and subcutaneous abdominal fat predicted lower total gray and white matter volume, as well as lower volume in the hippocampus, frontal cortex, and temporal, parietal, and occipital lobes.

“The findings are quite dramatic,” Dr. Raji told this news organization. “Overall, we found that both subcutaneous and visceral fat has similar levels of negative relationships with brain volumes.”

Women had a higher burden of brain atrophy with increased visceral fat than men. However, it’s difficult to place the sex differences in context because of the lack of prior work specifically investigating visceral fat, brain volume loss, and sex differences, the researchers caution.

They also note that while statistically significant relationships were observed between visceral fat levels and gray matter volume changes, their effect sizes were generally small. 

“Thus, the statistical significance of this work is influenced by the large sample size and less so by large effect size in any given set of regions,” the investigators write.

Other limitations include the cross-sectional nature of the study, which precludes conclusions about causality. The analysis also did not account for other lifestyle factors such as physical activity, diet, and genetic variables.

The researchers call for further investigation “to better elucidate underlying mechanisms and discover possible interventions targeting abdominal fat reduction as a strategy to maintain brain health.”
 

‘Helpful addition to the literature’

In a comment, Claire Sexton, DPhil, Alzheimer’s Association senior director of scientific programs and outreach, noted that “previous studies have linked obesity with cognitive decline and increased risk of dementia. Rather than using BMI as a proxy for body fat, the current study examined visceral and subcutaneous fat directly using imaging techniques.”

Dr. Sexton, who was not associated with this study, said the finding that increased body fat was associated with reduced brain volumes suggests “a possible mechanism to explain the previously reported associations between obesity and cognition.”

“Though some degree of atrophy and brain shrinkage is common with old age, awareness of this association is important because reduced brain volume may be associated with problems with thinking, memory, and performing everyday tasks, and because rates of obesity continue to rise in the United States, along with obesity-related conditions including heart disease, stroke, type 2 diabetes and certain types of cancer,” she added.

“While a helpful addition to the literature, the study does have important limitations. As an observational study, it cannot establish whether higher levels of body fat directly causes reduced brain volumes,” Dr. Sexton cautioned.

In addition, the study did not take into account important related factors like physical activity and diet, which may influence any relationship between body fat and brain volumes, she noted. “Overall, it is not just one factor that is important to consider when considering risk for cognitive decline and dementia, but multiple factors.

“Obesity and the location of body fat must be considered in combination with one’s total lived experience and habits, including physical activity, education, head injury, sleep, mental health, and the health of your heart/cardiovascular system and other key bodily systems,” Dr. Sexton said.

The Alzheimer’s Association is leading a 2-year clinical trial known as U.S. POINTER to see whether combining physical activity, healthy nutrition, social and intellectual challenges, and improved self-management of medical conditions can protect cognitive function in older adults who are at increased risk for cognitive decline.

This work was supported in part by Providence St. Joseph Health in Seattle; Saint John’s Health Center Foundation; Pacific Neuroscience Institute and Foundation; Will and Cary Singleton; and the McLoughlin family. Dr. Raji is a consultant for Brainreader, Apollo Health, Voxelwise, Neurevolution, Pacific Neuroscience Institute Foundation, and Icometrix. Dr. Sexton reports no relevant financial relationships.

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

Crippling symptoms, lost careers, and eroded incomes: This is the harsh reality for doctors suffering with long COVID, according to the first major survey of physicians with the condition.

The survey, conducted by the British Medical Association and the Long COVID Doctors for Action support group, sheds light on the lingering effects of long COVID on more than 600 chronically ill and disabled doctors with the condition. It also spotlights what they describe as a lack of medical and financial support from their government and employers at the National Health Service.

“We feel betrayed and abandoned,” said Kelly Fearnley, MBChB, chair and cofounder of Long COVID Doctors for Action. “At a time of national crisis, when health care workers were asked to step up, we did. When the nation needed us, we stepped up. We put our lives on the line. We put our families’ lives on the line. And now that we are injured after knowingly being unprotected and deliberately and repeatedly exposed to a level 3 biohazard, we now find ourselves in this position.”

Dr. Fearnley fell ill while working in a hospital’s COVID ward in November 2020. She is one of an estimated 2 million people in the United Kingdom – including thousands of NHS employees – with long COVID. She hasn’t been able to return to work in nearly 3 years.

Long COVID affects more than 65 million people worldwide. It is estimated that 1 in 10 people infected with the virus develop long-term symptoms. In the United Kingdom, health care and social care workers are seven times more likely to have had severe COVID-19 than other types of employees.

Doctors responding to the BMA survey reported a wide range of long COVID symptoms, including fatigue, headaches, muscular pain, nerve damage, joint pain, and respiratory problems.

Among the survey’s key findings, 60% of doctors said long COVID has affected their ability to carry out day-to-day tasks on a regular basis. Almost one in five (18%) said they were no longer able to work, while fewer than one in three (31%) were working full time. This compares with more than half (57%) of respondents working full time before the onset of their COVID illness – a decline of 46%.

Nearly half (48%) of respondents said they have experienced some form of loss of earnings as a result of long COVID, and almost half of the doctors were never referred to an NHS long COVID clinic. The survey included the following first-person accounts from doctors living with the condition.

• One doctor said: “I nearly lost my life, my home, my partner and my career. I have received little support to help keep these. The impact on my mental health nearly cost [me] my life again.”
• A senior consulting physician commented: “Life is absolutely miserable. Every day is a struggle. I wake up exhausted, the insomnia and night terrors are horrendous as I live through my worst fears every night. Any activity such as eating meals, washing, etc., will mean I have to go to bed for a few hours. I am unable to look after myself or my child, exercise or maintain social relationships. I have no financial security. Long COVID has totally destroyed my life.”
• A salaried general practitioner said: “I can no longer work, finances are ruined. I didn’t have employment protection so am now unemployed and penniless.”

Calls for action from the BMA include the following:

• Financial support for doctors and health care staff with long COVID.
• The recognition of long COVID as an occupational disease among health care workers, along with a definition of the condition that covers all of the debilitating disease’s symptoms.
• Improved access to physical and mental health services to help comprehensive assessment, investigations, and treatment.
• Greater workplace protection for health care staff who risk their lives for others.
• Better support for long COVID sufferers to return to work safely if they can, including a flexible approach to the use of workplace adjustments.

“One would think, given the circumstances under which we fell ill and current workforce shortages, NHS employers would be eager to do everything to facilitate the return to work of people with long COVID,” said Dr. Fearnley. “However, NHS employers are legally required to implement only ‘reasonable adjustments,’ and so things such as extended phased return or adjustments to shift patterns are not always being facilitated. Instead, an increasing number of employers are choosing to terminate contracts.”

Raymond Agius, the BMA’s occupational medicine committee cochair, also put the blame on inadequate safety measures for doctors. Those inadequate measures persist to this day, inasmuch as U.K. hospitals have dropped masking requirements.

“During the COVID-19 pandemic, doctors were left exposed and unprotected at work,” he said in a BMA press release. “They often did not have access to the right PPE. ... Too many risk assessments of workplaces and especially of vulnerable doctors were not undertaken.”

A small minority of doctors who were surveyed said they had access to respiratory protective equipment about the time they contracted COVID-19. Only 11% had access to an FFP2 respirator (the equivalent of an N95 mask); 16% had an FFP3 respirator (the equivalent of an N99 mask).

To date, the British government hasn’t issued much of a response to the survey, saying only that it has invested more than ₤50 million to better understand long COVID.

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

Crippling symptoms, lost careers, and eroded incomes: This is the harsh reality for doctors suffering with long COVID, according to the first major survey of physicians with the condition.

The survey, conducted by the British Medical Association and the Long COVID Doctors for Action support group, sheds light on the lingering effects of long COVID on more than 600 chronically ill and disabled doctors with the condition. It also spotlights what they describe as a lack of medical and financial support from their government and employers at the National Health Service.

“We feel betrayed and abandoned,” said Kelly Fearnley, MBChB, chair and cofounder of Long COVID Doctors for Action. “At a time of national crisis, when health care workers were asked to step up, we did. When the nation needed us, we stepped up. We put our lives on the line. We put our families’ lives on the line. And now that we are injured after knowingly being unprotected and deliberately and repeatedly exposed to a level 3 biohazard, we now find ourselves in this position.”

Dr. Fearnley fell ill while working in a hospital’s COVID ward in November 2020. She is one of an estimated 2 million people in the United Kingdom – including thousands of NHS employees – with long COVID. She hasn’t been able to return to work in nearly 3 years.

Long COVID affects more than 65 million people worldwide. It is estimated that 1 in 10 people infected with the virus develop long-term symptoms. In the United Kingdom, health care and social care workers are seven times more likely to have had severe COVID-19 than other types of employees.

Doctors responding to the BMA survey reported a wide range of long COVID symptoms, including fatigue, headaches, muscular pain, nerve damage, joint pain, and respiratory problems.

Among the survey’s key findings, 60% of doctors said long COVID has affected their ability to carry out day-to-day tasks on a regular basis. Almost one in five (18%) said they were no longer able to work, while fewer than one in three (31%) were working full time. This compares with more than half (57%) of respondents working full time before the onset of their COVID illness – a decline of 46%.

Nearly half (48%) of respondents said they have experienced some form of loss of earnings as a result of long COVID, and almost half of the doctors were never referred to an NHS long COVID clinic. The survey included the following first-person accounts from doctors living with the condition.

• One doctor said: “I nearly lost my life, my home, my partner and my career. I have received little support to help keep these. The impact on my mental health nearly cost [me] my life again.”
• A senior consulting physician commented: “Life is absolutely miserable. Every day is a struggle. I wake up exhausted, the insomnia and night terrors are horrendous as I live through my worst fears every night. Any activity such as eating meals, washing, etc., will mean I have to go to bed for a few hours. I am unable to look after myself or my child, exercise or maintain social relationships. I have no financial security. Long COVID has totally destroyed my life.”
• A salaried general practitioner said: “I can no longer work, finances are ruined. I didn’t have employment protection so am now unemployed and penniless.”

Calls for action from the BMA include the following:

• Financial support for doctors and health care staff with long COVID.
• The recognition of long COVID as an occupational disease among health care workers, along with a definition of the condition that covers all of the debilitating disease’s symptoms.
• Improved access to physical and mental health services to help comprehensive assessment, investigations, and treatment.
• Greater workplace protection for health care staff who risk their lives for others.
• Better support for long COVID sufferers to return to work safely if they can, including a flexible approach to the use of workplace adjustments.

“One would think, given the circumstances under which we fell ill and current workforce shortages, NHS employers would be eager to do everything to facilitate the return to work of people with long COVID,” said Dr. Fearnley. “However, NHS employers are legally required to implement only ‘reasonable adjustments,’ and so things such as extended phased return or adjustments to shift patterns are not always being facilitated. Instead, an increasing number of employers are choosing to terminate contracts.”

Raymond Agius, the BMA’s occupational medicine committee cochair, also put the blame on inadequate safety measures for doctors. Those inadequate measures persist to this day, inasmuch as U.K. hospitals have dropped masking requirements.

“During the COVID-19 pandemic, doctors were left exposed and unprotected at work,” he said in a BMA press release. “They often did not have access to the right PPE. ... Too many risk assessments of workplaces and especially of vulnerable doctors were not undertaken.”

A small minority of doctors who were surveyed said they had access to respiratory protective equipment about the time they contracted COVID-19. Only 11% had access to an FFP2 respirator (the equivalent of an N95 mask); 16% had an FFP3 respirator (the equivalent of an N99 mask).

To date, the British government hasn’t issued much of a response to the survey, saying only that it has invested more than ₤50 million to better understand long COVID.

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

Crippling symptoms, lost careers, and eroded incomes: This is the harsh reality for doctors suffering with long COVID, according to the first major survey of physicians with the condition.

The survey, conducted by the British Medical Association and the Long COVID Doctors for Action support group, sheds light on the lingering effects of long COVID on more than 600 chronically ill and disabled doctors with the condition. It also spotlights what they describe as a lack of medical and financial support from their government and employers at the National Health Service.

“We feel betrayed and abandoned,” said Kelly Fearnley, MBChB, chair and cofounder of Long COVID Doctors for Action. “At a time of national crisis, when health care workers were asked to step up, we did. When the nation needed us, we stepped up. We put our lives on the line. We put our families’ lives on the line. And now that we are injured after knowingly being unprotected and deliberately and repeatedly exposed to a level 3 biohazard, we now find ourselves in this position.”

Dr. Fearnley fell ill while working in a hospital’s COVID ward in November 2020. She is one of an estimated 2 million people in the United Kingdom – including thousands of NHS employees – with long COVID. She hasn’t been able to return to work in nearly 3 years.

Long COVID affects more than 65 million people worldwide. It is estimated that 1 in 10 people infected with the virus develop long-term symptoms. In the United Kingdom, health care and social care workers are seven times more likely to have had severe COVID-19 than other types of employees.

Doctors responding to the BMA survey reported a wide range of long COVID symptoms, including fatigue, headaches, muscular pain, nerve damage, joint pain, and respiratory problems.

Among the survey’s key findings, 60% of doctors said long COVID has affected their ability to carry out day-to-day tasks on a regular basis. Almost one in five (18%) said they were no longer able to work, while fewer than one in three (31%) were working full time. This compares with more than half (57%) of respondents working full time before the onset of their COVID illness – a decline of 46%.

Nearly half (48%) of respondents said they have experienced some form of loss of earnings as a result of long COVID, and almost half of the doctors were never referred to an NHS long COVID clinic. The survey included the following first-person accounts from doctors living with the condition.

• One doctor said: “I nearly lost my life, my home, my partner and my career. I have received little support to help keep these. The impact on my mental health nearly cost [me] my life again.”
• A senior consulting physician commented: “Life is absolutely miserable. Every day is a struggle. I wake up exhausted, the insomnia and night terrors are horrendous as I live through my worst fears every night. Any activity such as eating meals, washing, etc., will mean I have to go to bed for a few hours. I am unable to look after myself or my child, exercise or maintain social relationships. I have no financial security. Long COVID has totally destroyed my life.”
• A salaried general practitioner said: “I can no longer work, finances are ruined. I didn’t have employment protection so am now unemployed and penniless.”

Calls for action from the BMA include the following:

• Financial support for doctors and health care staff with long COVID.
• The recognition of long COVID as an occupational disease among health care workers, along with a definition of the condition that covers all of the debilitating disease’s symptoms.
• Improved access to physical and mental health services to help comprehensive assessment, investigations, and treatment.
• Greater workplace protection for health care staff who risk their lives for others.
• Better support for long COVID sufferers to return to work safely if they can, including a flexible approach to the use of workplace adjustments.

“One would think, given the circumstances under which we fell ill and current workforce shortages, NHS employers would be eager to do everything to facilitate the return to work of people with long COVID,” said Dr. Fearnley. “However, NHS employers are legally required to implement only ‘reasonable adjustments,’ and so things such as extended phased return or adjustments to shift patterns are not always being facilitated. Instead, an increasing number of employers are choosing to terminate contracts.”

Raymond Agius, the BMA’s occupational medicine committee cochair, also put the blame on inadequate safety measures for doctors. Those inadequate measures persist to this day, inasmuch as U.K. hospitals have dropped masking requirements.

“During the COVID-19 pandemic, doctors were left exposed and unprotected at work,” he said in a BMA press release. “They often did not have access to the right PPE. ... Too many risk assessments of workplaces and especially of vulnerable doctors were not undertaken.”

A small minority of doctors who were surveyed said they had access to respiratory protective equipment about the time they contracted COVID-19. Only 11% had access to an FFP2 respirator (the equivalent of an N95 mask); 16% had an FFP3 respirator (the equivalent of an N99 mask).

To date, the British government hasn’t issued much of a response to the survey, saying only that it has invested more than ₤50 million to better understand long COVID.

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