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TOPLINE:

Tumor necrosis factor (TNF) inhibitors led to no significant difference in survival or respiratory-related hospitalizations, compared with non-TNF inhibitors, in patients with rheumatoid arthritis–associated interstitial lung disease (RA-ILD).

METHODOLOGY:

• Guidelines from the American College of Rheumatology and the American College of Chest Physicians conditionally advise against the use of TNF inhibitors for treating ILD in patients with RA-ILD, with persisting uncertainty about the safety of TNF inhibitors.
• Researchers conducted a retrospective cohort study using data from the US Department of Veterans Affairs, with a focus on comparing outcomes in patients with RA-ILD who initiated TNF or non-TNF inhibitors between 2006 and 2018.
• A total of 1047 US veterans with RA-ILD were included, with 237 who initiated TNF inhibitors propensity matched in a 1:1 ratio with 237 who initiated non-TNF inhibitors (mean age, 68 years; 92% men).
• The primary composite outcome was time to death or respiratory-related hospitalization over a follow-up period of up to 3 years.
• The secondary outcomes included all-cause mortality, respiratory-related mortality, and respiratory-related hospitalization, with additional assessments over a 1-year period.

TAKEAWAY:

• No significant difference was observed in the composite outcome of death or respiratory-related hospitalization between the TNF and non-TNF inhibitor groups (adjusted hazard ratio, 1.21; 95% CI, 0.92-1.58).
• No significant differences in the risk for respiratory-related hospitalization and all-cause or respiratory-related mortality were found between the TNF and non-TNF inhibitor groups. Similar findings were observed for all the outcomes during 1 year of follow-up.
• The mean duration of medication use prior to discontinuation, the time to discontinuation, and the mean predicted forced vital capacity percentage were similar for both groups.
• In a subgroup analysis of patients aged ≥ 65 years, those treated with non-TNF inhibitors had a higher risk for the composite outcome and all-cause and respiratory-related mortality than those treated with TNF inhibitors. No significant differences in outcomes were observed between the two treatment groups among patients aged < 65 years.

IN PRACTICE:

“Our results do not suggest that systematic avoidance of TNF inhibitors is required in all patients with rheumatoid arthritis–associated ILD. However, given disease heterogeneity and imprecision of our estimates, some subpopulations of patients with rheumatoid arthritis–associated ILD might benefit from specific biological or targeted synthetic DMARD [disease-modifying antirheumatic drug] treatment strategies,” the authors wrote.

SOURCE:

The study was led by Bryant R. England, MD, PhD, University of Nebraska Medical Center, Omaha It was published online on January 7, 2025, in The Lancet Rheumatology.

LIMITATIONS:

Administrative algorithms were used for identifying RA-ILD, potentially leading to misclassification and limiting phenotyping accuracy. Even with the use of propensity score methods, there might still be residual selection bias or unmeasured confounding. The study lacked comprehensive measures of posttreatment forced vital capacity and other indicators of ILD severity. The study population, predominantly men and those with a smoking history, may limit the generalizability of the findings to other groups.

DISCLOSURES:

The study was primarily funded by the US Department of Veterans Affairs. Some authors reported having financial relationships with pharmaceutical companies unrelated to the submitted work.

This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Tumor necrosis factor (TNF) inhibitors led to no significant difference in survival or respiratory-related hospitalizations, compared with non-TNF inhibitors, in patients with rheumatoid arthritis–associated interstitial lung disease (RA-ILD).

METHODOLOGY:

• Guidelines from the American College of Rheumatology and the American College of Chest Physicians conditionally advise against the use of TNF inhibitors for treating ILD in patients with RA-ILD, with persisting uncertainty about the safety of TNF inhibitors.
• Researchers conducted a retrospective cohort study using data from the US Department of Veterans Affairs, with a focus on comparing outcomes in patients with RA-ILD who initiated TNF or non-TNF inhibitors between 2006 and 2018.
• A total of 1047 US veterans with RA-ILD were included, with 237 who initiated TNF inhibitors propensity matched in a 1:1 ratio with 237 who initiated non-TNF inhibitors (mean age, 68 years; 92% men).
• The primary composite outcome was time to death or respiratory-related hospitalization over a follow-up period of up to 3 years.
• The secondary outcomes included all-cause mortality, respiratory-related mortality, and respiratory-related hospitalization, with additional assessments over a 1-year period.

TAKEAWAY:

• No significant difference was observed in the composite outcome of death or respiratory-related hospitalization between the TNF and non-TNF inhibitor groups (adjusted hazard ratio, 1.21; 95% CI, 0.92-1.58).
• No significant differences in the risk for respiratory-related hospitalization and all-cause or respiratory-related mortality were found between the TNF and non-TNF inhibitor groups. Similar findings were observed for all the outcomes during 1 year of follow-up.
• The mean duration of medication use prior to discontinuation, the time to discontinuation, and the mean predicted forced vital capacity percentage were similar for both groups.
• In a subgroup analysis of patients aged ≥ 65 years, those treated with non-TNF inhibitors had a higher risk for the composite outcome and all-cause and respiratory-related mortality than those treated with TNF inhibitors. No significant differences in outcomes were observed between the two treatment groups among patients aged < 65 years.

IN PRACTICE:

“Our results do not suggest that systematic avoidance of TNF inhibitors is required in all patients with rheumatoid arthritis–associated ILD. However, given disease heterogeneity and imprecision of our estimates, some subpopulations of patients with rheumatoid arthritis–associated ILD might benefit from specific biological or targeted synthetic DMARD [disease-modifying antirheumatic drug] treatment strategies,” the authors wrote.

SOURCE:

The study was led by Bryant R. England, MD, PhD, University of Nebraska Medical Center, Omaha It was published online on January 7, 2025, in The Lancet Rheumatology.

LIMITATIONS:

Administrative algorithms were used for identifying RA-ILD, potentially leading to misclassification and limiting phenotyping accuracy. Even with the use of propensity score methods, there might still be residual selection bias or unmeasured confounding. The study lacked comprehensive measures of posttreatment forced vital capacity and other indicators of ILD severity. The study population, predominantly men and those with a smoking history, may limit the generalizability of the findings to other groups.

DISCLOSURES:

The study was primarily funded by the US Department of Veterans Affairs. Some authors reported having financial relationships with pharmaceutical companies unrelated to the submitted work.

This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Tumor necrosis factor (TNF) inhibitors led to no significant difference in survival or respiratory-related hospitalizations, compared with non-TNF inhibitors, in patients with rheumatoid arthritis–associated interstitial lung disease (RA-ILD).

METHODOLOGY:

• Guidelines from the American College of Rheumatology and the American College of Chest Physicians conditionally advise against the use of TNF inhibitors for treating ILD in patients with RA-ILD, with persisting uncertainty about the safety of TNF inhibitors.
• Researchers conducted a retrospective cohort study using data from the US Department of Veterans Affairs, with a focus on comparing outcomes in patients with RA-ILD who initiated TNF or non-TNF inhibitors between 2006 and 2018.
• A total of 1047 US veterans with RA-ILD were included, with 237 who initiated TNF inhibitors propensity matched in a 1:1 ratio with 237 who initiated non-TNF inhibitors (mean age, 68 years; 92% men).
• The primary composite outcome was time to death or respiratory-related hospitalization over a follow-up period of up to 3 years.
• The secondary outcomes included all-cause mortality, respiratory-related mortality, and respiratory-related hospitalization, with additional assessments over a 1-year period.

TAKEAWAY:

• No significant difference was observed in the composite outcome of death or respiratory-related hospitalization between the TNF and non-TNF inhibitor groups (adjusted hazard ratio, 1.21; 95% CI, 0.92-1.58).
• No significant differences in the risk for respiratory-related hospitalization and all-cause or respiratory-related mortality were found between the TNF and non-TNF inhibitor groups. Similar findings were observed for all the outcomes during 1 year of follow-up.
• The mean duration of medication use prior to discontinuation, the time to discontinuation, and the mean predicted forced vital capacity percentage were similar for both groups.
• In a subgroup analysis of patients aged ≥ 65 years, those treated with non-TNF inhibitors had a higher risk for the composite outcome and all-cause and respiratory-related mortality than those treated with TNF inhibitors. No significant differences in outcomes were observed between the two treatment groups among patients aged < 65 years.

IN PRACTICE:

“Our results do not suggest that systematic avoidance of TNF inhibitors is required in all patients with rheumatoid arthritis–associated ILD. However, given disease heterogeneity and imprecision of our estimates, some subpopulations of patients with rheumatoid arthritis–associated ILD might benefit from specific biological or targeted synthetic DMARD [disease-modifying antirheumatic drug] treatment strategies,” the authors wrote.

SOURCE:

The study was led by Bryant R. England, MD, PhD, University of Nebraska Medical Center, Omaha It was published online on January 7, 2025, in The Lancet Rheumatology.

LIMITATIONS:

Administrative algorithms were used for identifying RA-ILD, potentially leading to misclassification and limiting phenotyping accuracy. Even with the use of propensity score methods, there might still be residual selection bias or unmeasured confounding. The study lacked comprehensive measures of posttreatment forced vital capacity and other indicators of ILD severity. The study population, predominantly men and those with a smoking history, may limit the generalizability of the findings to other groups.

DISCLOSURES:

The study was primarily funded by the US Department of Veterans Affairs. Some authors reported having financial relationships with pharmaceutical companies unrelated to the submitted work.

This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

Children who were severely ill with multisystem inflammatory syndrome in children (MIS-C) related to COVID-19 infection appear to show excellent cardiovascular and noncardiovascular outcomes by 6 months, according to data published in JAMA Pediatrics.

MIS-C is a life-threatening complication of COVID-19 infection and data on outcomes are limited, wrote the authors, led by Dongngan T. Truong, MD, MSSI, with Children’s Healthcare of Atlanta Cardiology, Emory University School of Medicine in Atlanta, Georgia. These 6-month results are from the Long-Term Outcomes After the Multisystem Inflammatory Syndrome in Children (MUSIC) study, sponsored by the National Heart, Lung, and Blood Institute.

Researchers found in this cohort study of 1204 participants that by 6 months after hospital discharge, 99% had normalization of left ventricular systolic function, and 92.3% had normalized coronary artery dimensions. More than 95% reported being more than 90% back to baseline health.

Patient-Reported Outcomes Measurement Information Systems (PROMIS) Global Health scores were at least equivalent to prepandemic population normative values. PROMIS Global Health parent/guardian proxy median T scores for fatigue, global health, and pain interference improved significantly from 2 weeks to 6 months: fatigue, 56.1 vs 48.9; global health, 48.8 vs 51.3; pain interference, 53.0 vs 43.3 (P < .001).

The most common symptoms reported at 2 weeks were fatigue (15.9%) and low stamina/energy (9.2%); both decreased to 3.4% and 3.3%, respectively, by 6 months. The most common cardiovascular symptom at 2 weeks was palpitations (1.5%), which decreased to 0.6%.

 

Chest Pain Increased Over Time

Reports of chest pain, however, reportedly increased over time, with 1.3% reporting chest pain at rest at 2 weeks and 2.2% at 6 months. Although gastrointestinal symptoms were common during the acute MIS-C, only 5.3% of respondents reported those symptoms at 2 weeks.

Children in the cohort had a median age of 9 years, and 60% were men. They self-identified with the following races and ethnicities: American Indian or Alaska Native (0.1%), Asian (3.3%), Black (27.0%), Hawaiian Native or Other Pacific Islander (0.2%), Hispanic or Latino (26.9%), multiracial (2.7%), White (31.2%), other (1.0%), and unknown or refused to specify (7.6%). Authors wrote that the cohort was followed-up to 2 years after illness onset and long-term results are not yet known.

 

Time to Exhale

David J. Goldberg, MD, with the Cardiac Center, Children’s Hospital of Philadelphia, Pennsylvania, and colleagues, wrote in an accompanying editorial that “the decreased frequency of the disease along (with) the reassuring reports on midterm outcomes can allow the pediatric community a moment of collective exhale.”

The editorialists note that of those who initially presented with myocardial dysfunction, all but one patient evaluated had a normal ejection fraction at follow-up. Energy, sleep, appetite, cognition, and mood also normalized by midterm.

“The results of the MUSIC study add to the emerging midterm outcomes data suggesting a near-complete cardiovascular recovery in the overwhelming majority of patients who develop MIS-C,” Goldberg and colleagues wrote. “Despite initial concerns, driven by the severity of acute presentation at diagnosis and longer-term questions that remain (for example, does coronary microvascular dysfunction persist even after normalization of coronary artery z score?), these data suggest an encouraging outlook for the long-term health of affected children.”

The Centers for Disease Control and Prevention and other agencies have reported a declining overall incidence of MIS-C and highlighted the protective value of vaccination. 

The editorialists add, however, that while the drop in MIS-C cases is encouraging, cases are still reported, especially amid high viral activity periods, “and nearly half of affected children continue to require intensive care in the acute phase of illness.”

Truong reported grants from the National Institutes of Health and serving as coprincipal investigator for Pfizer for research on COVID-19 vaccine-associated myocarditis funded by Pfizer and occurring through the framework of the National Heart, Lung, and Blood Institute’s Pediatric Heart Network outside the submitted work. One coauthor reported grants from Pfizer and Boston Scientific outside the submitted work. One coauthor reported receiving grants from Additional Ventures Foundation outside the submitted work. One coauthor reported receiving consultant fees from Amryt Pharma, Chiesi, Esperion, and Ultragenyx outside the submitted work. A coauthor reported receiving consultant fees from Larimar Therapeutics for mitochondrial therapies outside the submitted work. One coauthor reported being an employee of Takeda Pharmaceuticals since July 2023. One editorialist reported grants from Childhood Arthritis and Rheumatology Research Alliance and the Arthritis Foundation, Academy Health, and the Gordon and Betty Moore Foundation during the conduct of the study.

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

Children who were severely ill with multisystem inflammatory syndrome in children (MIS-C) related to COVID-19 infection appear to show excellent cardiovascular and noncardiovascular outcomes by 6 months, according to data published in JAMA Pediatrics.

MIS-C is a life-threatening complication of COVID-19 infection and data on outcomes are limited, wrote the authors, led by Dongngan T. Truong, MD, MSSI, with Children’s Healthcare of Atlanta Cardiology, Emory University School of Medicine in Atlanta, Georgia. These 6-month results are from the Long-Term Outcomes After the Multisystem Inflammatory Syndrome in Children (MUSIC) study, sponsored by the National Heart, Lung, and Blood Institute.

Researchers found in this cohort study of 1204 participants that by 6 months after hospital discharge, 99% had normalization of left ventricular systolic function, and 92.3% had normalized coronary artery dimensions. More than 95% reported being more than 90% back to baseline health.

Patient-Reported Outcomes Measurement Information Systems (PROMIS) Global Health scores were at least equivalent to prepandemic population normative values. PROMIS Global Health parent/guardian proxy median T scores for fatigue, global health, and pain interference improved significantly from 2 weeks to 6 months: fatigue, 56.1 vs 48.9; global health, 48.8 vs 51.3; pain interference, 53.0 vs 43.3 (P < .001).

The most common symptoms reported at 2 weeks were fatigue (15.9%) and low stamina/energy (9.2%); both decreased to 3.4% and 3.3%, respectively, by 6 months. The most common cardiovascular symptom at 2 weeks was palpitations (1.5%), which decreased to 0.6%.

 

Chest Pain Increased Over Time

Reports of chest pain, however, reportedly increased over time, with 1.3% reporting chest pain at rest at 2 weeks and 2.2% at 6 months. Although gastrointestinal symptoms were common during the acute MIS-C, only 5.3% of respondents reported those symptoms at 2 weeks.

Children in the cohort had a median age of 9 years, and 60% were men. They self-identified with the following races and ethnicities: American Indian or Alaska Native (0.1%), Asian (3.3%), Black (27.0%), Hawaiian Native or Other Pacific Islander (0.2%), Hispanic or Latino (26.9%), multiracial (2.7%), White (31.2%), other (1.0%), and unknown or refused to specify (7.6%). Authors wrote that the cohort was followed-up to 2 years after illness onset and long-term results are not yet known.

 

Time to Exhale

David J. Goldberg, MD, with the Cardiac Center, Children’s Hospital of Philadelphia, Pennsylvania, and colleagues, wrote in an accompanying editorial that “the decreased frequency of the disease along (with) the reassuring reports on midterm outcomes can allow the pediatric community a moment of collective exhale.”

The editorialists note that of those who initially presented with myocardial dysfunction, all but one patient evaluated had a normal ejection fraction at follow-up. Energy, sleep, appetite, cognition, and mood also normalized by midterm.

“The results of the MUSIC study add to the emerging midterm outcomes data suggesting a near-complete cardiovascular recovery in the overwhelming majority of patients who develop MIS-C,” Goldberg and colleagues wrote. “Despite initial concerns, driven by the severity of acute presentation at diagnosis and longer-term questions that remain (for example, does coronary microvascular dysfunction persist even after normalization of coronary artery z score?), these data suggest an encouraging outlook for the long-term health of affected children.”

The Centers for Disease Control and Prevention and other agencies have reported a declining overall incidence of MIS-C and highlighted the protective value of vaccination. 

The editorialists add, however, that while the drop in MIS-C cases is encouraging, cases are still reported, especially amid high viral activity periods, “and nearly half of affected children continue to require intensive care in the acute phase of illness.”

Truong reported grants from the National Institutes of Health and serving as coprincipal investigator for Pfizer for research on COVID-19 vaccine-associated myocarditis funded by Pfizer and occurring through the framework of the National Heart, Lung, and Blood Institute’s Pediatric Heart Network outside the submitted work. One coauthor reported grants from Pfizer and Boston Scientific outside the submitted work. One coauthor reported receiving grants from Additional Ventures Foundation outside the submitted work. One coauthor reported receiving consultant fees from Amryt Pharma, Chiesi, Esperion, and Ultragenyx outside the submitted work. A coauthor reported receiving consultant fees from Larimar Therapeutics for mitochondrial therapies outside the submitted work. One coauthor reported being an employee of Takeda Pharmaceuticals since July 2023. One editorialist reported grants from Childhood Arthritis and Rheumatology Research Alliance and the Arthritis Foundation, Academy Health, and the Gordon and Betty Moore Foundation during the conduct of the study.

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

Children who were severely ill with multisystem inflammatory syndrome in children (MIS-C) related to COVID-19 infection appear to show excellent cardiovascular and noncardiovascular outcomes by 6 months, according to data published in JAMA Pediatrics.

MIS-C is a life-threatening complication of COVID-19 infection and data on outcomes are limited, wrote the authors, led by Dongngan T. Truong, MD, MSSI, with Children’s Healthcare of Atlanta Cardiology, Emory University School of Medicine in Atlanta, Georgia. These 6-month results are from the Long-Term Outcomes After the Multisystem Inflammatory Syndrome in Children (MUSIC) study, sponsored by the National Heart, Lung, and Blood Institute.

Researchers found in this cohort study of 1204 participants that by 6 months after hospital discharge, 99% had normalization of left ventricular systolic function, and 92.3% had normalized coronary artery dimensions. More than 95% reported being more than 90% back to baseline health.

Patient-Reported Outcomes Measurement Information Systems (PROMIS) Global Health scores were at least equivalent to prepandemic population normative values. PROMIS Global Health parent/guardian proxy median T scores for fatigue, global health, and pain interference improved significantly from 2 weeks to 6 months: fatigue, 56.1 vs 48.9; global health, 48.8 vs 51.3; pain interference, 53.0 vs 43.3 (P < .001).

The most common symptoms reported at 2 weeks were fatigue (15.9%) and low stamina/energy (9.2%); both decreased to 3.4% and 3.3%, respectively, by 6 months. The most common cardiovascular symptom at 2 weeks was palpitations (1.5%), which decreased to 0.6%.

 

Chest Pain Increased Over Time

Reports of chest pain, however, reportedly increased over time, with 1.3% reporting chest pain at rest at 2 weeks and 2.2% at 6 months. Although gastrointestinal symptoms were common during the acute MIS-C, only 5.3% of respondents reported those symptoms at 2 weeks.

Children in the cohort had a median age of 9 years, and 60% were men. They self-identified with the following races and ethnicities: American Indian or Alaska Native (0.1%), Asian (3.3%), Black (27.0%), Hawaiian Native or Other Pacific Islander (0.2%), Hispanic or Latino (26.9%), multiracial (2.7%), White (31.2%), other (1.0%), and unknown or refused to specify (7.6%). Authors wrote that the cohort was followed-up to 2 years after illness onset and long-term results are not yet known.

 

Time to Exhale

David J. Goldberg, MD, with the Cardiac Center, Children’s Hospital of Philadelphia, Pennsylvania, and colleagues, wrote in an accompanying editorial that “the decreased frequency of the disease along (with) the reassuring reports on midterm outcomes can allow the pediatric community a moment of collective exhale.”

The editorialists note that of those who initially presented with myocardial dysfunction, all but one patient evaluated had a normal ejection fraction at follow-up. Energy, sleep, appetite, cognition, and mood also normalized by midterm.

“The results of the MUSIC study add to the emerging midterm outcomes data suggesting a near-complete cardiovascular recovery in the overwhelming majority of patients who develop MIS-C,” Goldberg and colleagues wrote. “Despite initial concerns, driven by the severity of acute presentation at diagnosis and longer-term questions that remain (for example, does coronary microvascular dysfunction persist even after normalization of coronary artery z score?), these data suggest an encouraging outlook for the long-term health of affected children.”

The Centers for Disease Control and Prevention and other agencies have reported a declining overall incidence of MIS-C and highlighted the protective value of vaccination. 

The editorialists add, however, that while the drop in MIS-C cases is encouraging, cases are still reported, especially amid high viral activity periods, “and nearly half of affected children continue to require intensive care in the acute phase of illness.”

Truong reported grants from the National Institutes of Health and serving as coprincipal investigator for Pfizer for research on COVID-19 vaccine-associated myocarditis funded by Pfizer and occurring through the framework of the National Heart, Lung, and Blood Institute’s Pediatric Heart Network outside the submitted work. One coauthor reported grants from Pfizer and Boston Scientific outside the submitted work. One coauthor reported receiving grants from Additional Ventures Foundation outside the submitted work. One coauthor reported receiving consultant fees from Amryt Pharma, Chiesi, Esperion, and Ultragenyx outside the submitted work. A coauthor reported receiving consultant fees from Larimar Therapeutics for mitochondrial therapies outside the submitted work. One coauthor reported being an employee of Takeda Pharmaceuticals since July 2023. One editorialist reported grants from Childhood Arthritis and Rheumatology Research Alliance and the Arthritis Foundation, Academy Health, and the Gordon and Betty Moore Foundation during the conduct of the study.

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

TOPLINE:

The use of valaciclovir as prophylaxis prevents herpes zoster (HZ) in patients with systemic lupus erythematosus (SLE) receiving anifrolumab treatment, with no cases of zoster reported during the follow-up period in patients receiving valaciclovir.

METHODOLOGY:

• Anifrolumab, a human monoclonal antibody binding to type I interferon receptor subunit 1, increases the risk for HZ in patients with SLE; however, specific recommendations to prevent HZ are currently nonexistent for patients with SLE receiving anifrolumab.
• Researchers conducted a multicenter observational study in France from November 2021 to July 2024 to evaluate the prophylactic benefits of valaciclovir in 132 patients with SLE (mean age, 42 years; 92% women) treated with anifrolumab for ≥ 3 months.
• Among these patients, 87 received either 500 mg/d valaciclovir (n = 69) or 1000 mg/d valaciclovir (n = 18) as prophylaxis, whereas 45 did not receive valaciclovir.
• The patients were followed up for a median duration of 234 days under anifrolumab treatment, with monitoring for the development of herpes zoster.

TAKEAWAY:

• The risk for HZ was significantly lower in patients who received valaciclovir than in those who did not (hazard ratio, 0.08; P = .01).
• None of the patients treated with valaciclovir developed HZ during the survey period.
• The frequency of HZ in patients who did not receive valaciclovir increased progressively from 2.2% at 3 months to 6.2% at 6 months, reaching 23% at 12 months.
• None of the reported cases of HZ required hospitalization or led to anifrolumab discontinuation, although one patient developed neuralgia.

IN PRACTICE:

“Prophylactic treatment with valaciclovir is effective for preventing HZ [herpes zoster] infection in SLE patients treated with anifrolumab,” the authors wrote. “This finding is particularly relevant for SLE patients who cannot receive the recombinant HZ vaccine or for whom it is unavailable,” they added.

SOURCE:

The study was led by Ludovic Trefond, MD, PhD, Centre Hospitalier Universitaire de Clermont-Ferrand in France. It was published online on January 4, 2025, in RMD Open.

LIMITATIONS:

The observational design of the study and the low number of herpes zoster events during the follow-up period may have affected the robustness of the findings.

DISCLOSURES:

The authors did not receive any specific grants. Some authors reported having financial relationships with various pharmaceutical companies.

This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

The use of valaciclovir as prophylaxis prevents herpes zoster (HZ) in patients with systemic lupus erythematosus (SLE) receiving anifrolumab treatment, with no cases of zoster reported during the follow-up period in patients receiving valaciclovir.

METHODOLOGY:

• Anifrolumab, a human monoclonal antibody binding to type I interferon receptor subunit 1, increases the risk for HZ in patients with SLE; however, specific recommendations to prevent HZ are currently nonexistent for patients with SLE receiving anifrolumab.
• Researchers conducted a multicenter observational study in France from November 2021 to July 2024 to evaluate the prophylactic benefits of valaciclovir in 132 patients with SLE (mean age, 42 years; 92% women) treated with anifrolumab for ≥ 3 months.
• Among these patients, 87 received either 500 mg/d valaciclovir (n = 69) or 1000 mg/d valaciclovir (n = 18) as prophylaxis, whereas 45 did not receive valaciclovir.
• The patients were followed up for a median duration of 234 days under anifrolumab treatment, with monitoring for the development of herpes zoster.

TAKEAWAY:

• The risk for HZ was significantly lower in patients who received valaciclovir than in those who did not (hazard ratio, 0.08; P = .01).
• None of the patients treated with valaciclovir developed HZ during the survey period.
• The frequency of HZ in patients who did not receive valaciclovir increased progressively from 2.2% at 3 months to 6.2% at 6 months, reaching 23% at 12 months.
• None of the reported cases of HZ required hospitalization or led to anifrolumab discontinuation, although one patient developed neuralgia.

IN PRACTICE:

“Prophylactic treatment with valaciclovir is effective for preventing HZ [herpes zoster] infection in SLE patients treated with anifrolumab,” the authors wrote. “This finding is particularly relevant for SLE patients who cannot receive the recombinant HZ vaccine or for whom it is unavailable,” they added.

SOURCE:

The study was led by Ludovic Trefond, MD, PhD, Centre Hospitalier Universitaire de Clermont-Ferrand in France. It was published online on January 4, 2025, in RMD Open.

LIMITATIONS:

The observational design of the study and the low number of herpes zoster events during the follow-up period may have affected the robustness of the findings.

DISCLOSURES:

The authors did not receive any specific grants. Some authors reported having financial relationships with various pharmaceutical companies.

This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

The use of valaciclovir as prophylaxis prevents herpes zoster (HZ) in patients with systemic lupus erythematosus (SLE) receiving anifrolumab treatment, with no cases of zoster reported during the follow-up period in patients receiving valaciclovir.

METHODOLOGY:

• Anifrolumab, a human monoclonal antibody binding to type I interferon receptor subunit 1, increases the risk for HZ in patients with SLE; however, specific recommendations to prevent HZ are currently nonexistent for patients with SLE receiving anifrolumab.
• Researchers conducted a multicenter observational study in France from November 2021 to July 2024 to evaluate the prophylactic benefits of valaciclovir in 132 patients with SLE (mean age, 42 years; 92% women) treated with anifrolumab for ≥ 3 months.
• Among these patients, 87 received either 500 mg/d valaciclovir (n = 69) or 1000 mg/d valaciclovir (n = 18) as prophylaxis, whereas 45 did not receive valaciclovir.
• The patients were followed up for a median duration of 234 days under anifrolumab treatment, with monitoring for the development of herpes zoster.

TAKEAWAY:

• The risk for HZ was significantly lower in patients who received valaciclovir than in those who did not (hazard ratio, 0.08; P = .01).
• None of the patients treated with valaciclovir developed HZ during the survey period.
• The frequency of HZ in patients who did not receive valaciclovir increased progressively from 2.2% at 3 months to 6.2% at 6 months, reaching 23% at 12 months.
• None of the reported cases of HZ required hospitalization or led to anifrolumab discontinuation, although one patient developed neuralgia.

IN PRACTICE:

“Prophylactic treatment with valaciclovir is effective for preventing HZ [herpes zoster] infection in SLE patients treated with anifrolumab,” the authors wrote. “This finding is particularly relevant for SLE patients who cannot receive the recombinant HZ vaccine or for whom it is unavailable,” they added.

SOURCE:

The study was led by Ludovic Trefond, MD, PhD, Centre Hospitalier Universitaire de Clermont-Ferrand in France. It was published online on January 4, 2025, in RMD Open.

LIMITATIONS:

The observational design of the study and the low number of herpes zoster events during the follow-up period may have affected the robustness of the findings.

DISCLOSURES:

The authors did not receive any specific grants. Some authors reported having financial relationships with various pharmaceutical companies.

This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

Children with asthma scored significantly lower than those without asthma on measures of episodic memory, based on longitudinal data from nearly 500 individuals.

Animal models have shown associations between asthma and memory problems, but data for children are lacking, wrote Nicholas J. Christopher-Hayes, MA, of the University of California, Davis, and colleagues.

“Asthma is very frequent among children, and there is mounting evidence from rodent models that asthma may result in neural injury in the hippocampus, which in turn may cause memory loss,” Christopher-Hayes said in an interview. “Although there is also a good amount of research with older adults, very little research has been done with children, the period that is most frequently linked to asthma onset,” he said. Therefore, the researchers leveraged a large national study on child development to examine development of memory as a function of asthma exposure.

In this study published in JAMA Network Open, the researchers conducted both a longitudinal and cross-sectional analysis of data from the Adolescent Brain Cognitive Development Study, which began in 2015. Children were enrolled at ages 9-10 years with a follow-up assessment 1-2 years later.

The participants were categorized as early childhood-onset asthma (asthma at baseline and follow-up), later childhood-onset asthma (asthma at follow-up only), or no asthma history. The primary outcome of the longitudinal analysis was episodic memory. Approximately half of the participants were boys, and slightly more than half were White.

Among 474 children reviewed in the longitudinal analysis, 135 had early-onset asthma, 102 had later-onset asthma, and 237 had no asthma and served as control individuals. Overall, those with early-onset asthma showed significantly lower rates of longitudinal memory improvements at follow-up compared with the comparison group (P < .01).

Developmental memory improvement in children with later-onset asthma was not significantly different from the control individuals. 

Secondary outcomes included processing speed and inhibition, and attention. In a cross-sectional analysis with a larger sample of 2062 children from the same database (1031 with any asthma), those with asthma scored significantly lower on measures not only of episodic memory but also processing speed and inhibition/attention than children with no asthma, with P values of .04, .01, and .02, respectively.

The results were limited by several factors, including the reliance on parent reports for indicators of asthma and the lack of data on the potential effect of prescription corticosteroid use on neurocognitive development, the researchers noted.

The mechanism behind the association remains unclear; the inflammation associated with asthma may disrupt neural processing and manifest as cognitive dysfunction, as has been seen in rodent models of asthma, the researchers wrote. “It is possible that associations between asthma and developmental trajectories emerge earlier for memory, perhaps due to its sensitivity to subtle hippocampal injury,” they noted.

Longer follow-up studies are needed to fully understand how childhood asthma predicts memory declines or difficulties in childhood and beyond, said Christopher-Hayes. “We also need additional studies to understand why children who were diagnosed earlier and had asthma for longer seem to be particularly affected,” he said.

The results of this study were consistent with previous findings and therefore not surprising, senior author Simona Ghetti, PhD, a professor of psychology at the University of California, Davis, said in an interview. However, the finding that the extent of exposure to asthma was associated with slower memory improvement in childhood was striking, she said. That children with an earlier asthma onset who had disease indicators for a longer period showed a slower development of memory over time, suggests that asthma exposure may affect the developmental trajectory of memory, Ghetti noted. 

“Recommendations to clinicians are premature because we need a better understanding of the boundary conditions, such as the minimal level of asthma exposure that might generate memory difficulties,” said Ghetti.

“Nevertheless, our results underscore the importance of looking at asthma as a potential source of cognitive difficulty in children,” she said.

 

Asthma’s Extensive Effect

Evidence is mounting that a diagnosis of asthma may have implications outside the pulmonary system, Diego J. Maselli, MD, professor and chief of the Division of Pulmonary Diseases & Critical Care at UT Health, San Antonio, said in an interview. 

“Asthmatics may be at risk of nasal polyps, allergic rhinitis, and other allergic conditions, but there is emerging of evidence inflammation associated with asthma may affect other organ systems,” said Maselli, who was not involved in the study.

“For example, chronic inflammation in asthmatics may increase the risk of cardiovascular disease,” he said.

Although less is known about the effects of asthma on the nervous system, animal models suggest that inflammation associated with asthma may result in neuronal injury and potential effects on memory, said Maselli.

The findings of this study provide evidence of potential detrimental effects on the memory of children with asthma but should be interpreted with caution, Maselli said. “Children with chronic medical conditions may have an inherent disadvantage compared with their peers due to the burden of their disease, medication utilization and side effects, absenteeism from school, physical limitations, and other disease-specific circumstances,” he noted.

“Uncontrolled asthma, in particular, has strong links to low socioeconomic factors that are closely tied to access to adequate medical care, nutrition, educational institutions, and other relevant contributors to normal cognitive development,” Maselli said. Although the authors account for some of these socioeconomic factors by evaluating income and race, other variables may have influenced the results, he added.

Overall, this study’s findings suggested that the diagnosis of asthma in children may be associated with memory deficits and may influence neurodevelopment; however, more research is needed to determine whether the findings are replicated in other cohorts, said Maselli. “In particular, evaluating the effects of the severity of asthma and different asthma endotypes would be crucial to identify children with a higher risk of memory or cognitive deficits and confirm these associations,” he said.

This study was funded by the Memory and Plasticity Program at the University of California, Davis, and by a Learning, Memory, and Plasticity Training Program Fellowship grant from the National Institutes of Health. The researchers and Maselli had no financial conflicts to disclose. 

 

A version of this article appeared on Medscape.com.

Children with asthma scored significantly lower than those without asthma on measures of episodic memory, based on longitudinal data from nearly 500 individuals.

Animal models have shown associations between asthma and memory problems, but data for children are lacking, wrote Nicholas J. Christopher-Hayes, MA, of the University of California, Davis, and colleagues.

“Asthma is very frequent among children, and there is mounting evidence from rodent models that asthma may result in neural injury in the hippocampus, which in turn may cause memory loss,” Christopher-Hayes said in an interview. “Although there is also a good amount of research with older adults, very little research has been done with children, the period that is most frequently linked to asthma onset,” he said. Therefore, the researchers leveraged a large national study on child development to examine development of memory as a function of asthma exposure.

In this study published in JAMA Network Open, the researchers conducted both a longitudinal and cross-sectional analysis of data from the Adolescent Brain Cognitive Development Study, which began in 2015. Children were enrolled at ages 9-10 years with a follow-up assessment 1-2 years later.

The participants were categorized as early childhood-onset asthma (asthma at baseline and follow-up), later childhood-onset asthma (asthma at follow-up only), or no asthma history. The primary outcome of the longitudinal analysis was episodic memory. Approximately half of the participants were boys, and slightly more than half were White.

Among 474 children reviewed in the longitudinal analysis, 135 had early-onset asthma, 102 had later-onset asthma, and 237 had no asthma and served as control individuals. Overall, those with early-onset asthma showed significantly lower rates of longitudinal memory improvements at follow-up compared with the comparison group (P < .01).

Developmental memory improvement in children with later-onset asthma was not significantly different from the control individuals. 

Secondary outcomes included processing speed and inhibition, and attention. In a cross-sectional analysis with a larger sample of 2062 children from the same database (1031 with any asthma), those with asthma scored significantly lower on measures not only of episodic memory but also processing speed and inhibition/attention than children with no asthma, with P values of .04, .01, and .02, respectively.

The results were limited by several factors, including the reliance on parent reports for indicators of asthma and the lack of data on the potential effect of prescription corticosteroid use on neurocognitive development, the researchers noted.

The mechanism behind the association remains unclear; the inflammation associated with asthma may disrupt neural processing and manifest as cognitive dysfunction, as has been seen in rodent models of asthma, the researchers wrote. “It is possible that associations between asthma and developmental trajectories emerge earlier for memory, perhaps due to its sensitivity to subtle hippocampal injury,” they noted.

Longer follow-up studies are needed to fully understand how childhood asthma predicts memory declines or difficulties in childhood and beyond, said Christopher-Hayes. “We also need additional studies to understand why children who were diagnosed earlier and had asthma for longer seem to be particularly affected,” he said.

The results of this study were consistent with previous findings and therefore not surprising, senior author Simona Ghetti, PhD, a professor of psychology at the University of California, Davis, said in an interview. However, the finding that the extent of exposure to asthma was associated with slower memory improvement in childhood was striking, she said. That children with an earlier asthma onset who had disease indicators for a longer period showed a slower development of memory over time, suggests that asthma exposure may affect the developmental trajectory of memory, Ghetti noted. 

“Recommendations to clinicians are premature because we need a better understanding of the boundary conditions, such as the minimal level of asthma exposure that might generate memory difficulties,” said Ghetti.

“Nevertheless, our results underscore the importance of looking at asthma as a potential source of cognitive difficulty in children,” she said.

 

Asthma’s Extensive Effect

Evidence is mounting that a diagnosis of asthma may have implications outside the pulmonary system, Diego J. Maselli, MD, professor and chief of the Division of Pulmonary Diseases & Critical Care at UT Health, San Antonio, said in an interview. 

“Asthmatics may be at risk of nasal polyps, allergic rhinitis, and other allergic conditions, but there is emerging of evidence inflammation associated with asthma may affect other organ systems,” said Maselli, who was not involved in the study.

“For example, chronic inflammation in asthmatics may increase the risk of cardiovascular disease,” he said.

Although less is known about the effects of asthma on the nervous system, animal models suggest that inflammation associated with asthma may result in neuronal injury and potential effects on memory, said Maselli.

The findings of this study provide evidence of potential detrimental effects on the memory of children with asthma but should be interpreted with caution, Maselli said. “Children with chronic medical conditions may have an inherent disadvantage compared with their peers due to the burden of their disease, medication utilization and side effects, absenteeism from school, physical limitations, and other disease-specific circumstances,” he noted.

“Uncontrolled asthma, in particular, has strong links to low socioeconomic factors that are closely tied to access to adequate medical care, nutrition, educational institutions, and other relevant contributors to normal cognitive development,” Maselli said. Although the authors account for some of these socioeconomic factors by evaluating income and race, other variables may have influenced the results, he added.

Overall, this study’s findings suggested that the diagnosis of asthma in children may be associated with memory deficits and may influence neurodevelopment; however, more research is needed to determine whether the findings are replicated in other cohorts, said Maselli. “In particular, evaluating the effects of the severity of asthma and different asthma endotypes would be crucial to identify children with a higher risk of memory or cognitive deficits and confirm these associations,” he said.

This study was funded by the Memory and Plasticity Program at the University of California, Davis, and by a Learning, Memory, and Plasticity Training Program Fellowship grant from the National Institutes of Health. The researchers and Maselli had no financial conflicts to disclose. 

 

A version of this article appeared on Medscape.com.

Children with asthma scored significantly lower than those without asthma on measures of episodic memory, based on longitudinal data from nearly 500 individuals.

Animal models have shown associations between asthma and memory problems, but data for children are lacking, wrote Nicholas J. Christopher-Hayes, MA, of the University of California, Davis, and colleagues.

“Asthma is very frequent among children, and there is mounting evidence from rodent models that asthma may result in neural injury in the hippocampus, which in turn may cause memory loss,” Christopher-Hayes said in an interview. “Although there is also a good amount of research with older adults, very little research has been done with children, the period that is most frequently linked to asthma onset,” he said. Therefore, the researchers leveraged a large national study on child development to examine development of memory as a function of asthma exposure.

In this study published in JAMA Network Open, the researchers conducted both a longitudinal and cross-sectional analysis of data from the Adolescent Brain Cognitive Development Study, which began in 2015. Children were enrolled at ages 9-10 years with a follow-up assessment 1-2 years later.

The participants were categorized as early childhood-onset asthma (asthma at baseline and follow-up), later childhood-onset asthma (asthma at follow-up only), or no asthma history. The primary outcome of the longitudinal analysis was episodic memory. Approximately half of the participants were boys, and slightly more than half were White.

Among 474 children reviewed in the longitudinal analysis, 135 had early-onset asthma, 102 had later-onset asthma, and 237 had no asthma and served as control individuals. Overall, those with early-onset asthma showed significantly lower rates of longitudinal memory improvements at follow-up compared with the comparison group (P < .01).

Developmental memory improvement in children with later-onset asthma was not significantly different from the control individuals. 

Secondary outcomes included processing speed and inhibition, and attention. In a cross-sectional analysis with a larger sample of 2062 children from the same database (1031 with any asthma), those with asthma scored significantly lower on measures not only of episodic memory but also processing speed and inhibition/attention than children with no asthma, with P values of .04, .01, and .02, respectively.

The results were limited by several factors, including the reliance on parent reports for indicators of asthma and the lack of data on the potential effect of prescription corticosteroid use on neurocognitive development, the researchers noted.

The mechanism behind the association remains unclear; the inflammation associated with asthma may disrupt neural processing and manifest as cognitive dysfunction, as has been seen in rodent models of asthma, the researchers wrote. “It is possible that associations between asthma and developmental trajectories emerge earlier for memory, perhaps due to its sensitivity to subtle hippocampal injury,” they noted.

Longer follow-up studies are needed to fully understand how childhood asthma predicts memory declines or difficulties in childhood and beyond, said Christopher-Hayes. “We also need additional studies to understand why children who were diagnosed earlier and had asthma for longer seem to be particularly affected,” he said.

The results of this study were consistent with previous findings and therefore not surprising, senior author Simona Ghetti, PhD, a professor of psychology at the University of California, Davis, said in an interview. However, the finding that the extent of exposure to asthma was associated with slower memory improvement in childhood was striking, she said. That children with an earlier asthma onset who had disease indicators for a longer period showed a slower development of memory over time, suggests that asthma exposure may affect the developmental trajectory of memory, Ghetti noted. 

“Recommendations to clinicians are premature because we need a better understanding of the boundary conditions, such as the minimal level of asthma exposure that might generate memory difficulties,” said Ghetti.

“Nevertheless, our results underscore the importance of looking at asthma as a potential source of cognitive difficulty in children,” she said.

 

Asthma’s Extensive Effect

Evidence is mounting that a diagnosis of asthma may have implications outside the pulmonary system, Diego J. Maselli, MD, professor and chief of the Division of Pulmonary Diseases & Critical Care at UT Health, San Antonio, said in an interview. 

“Asthmatics may be at risk of nasal polyps, allergic rhinitis, and other allergic conditions, but there is emerging of evidence inflammation associated with asthma may affect other organ systems,” said Maselli, who was not involved in the study.

“For example, chronic inflammation in asthmatics may increase the risk of cardiovascular disease,” he said.

Although less is known about the effects of asthma on the nervous system, animal models suggest that inflammation associated with asthma may result in neuronal injury and potential effects on memory, said Maselli.

The findings of this study provide evidence of potential detrimental effects on the memory of children with asthma but should be interpreted with caution, Maselli said. “Children with chronic medical conditions may have an inherent disadvantage compared with their peers due to the burden of their disease, medication utilization and side effects, absenteeism from school, physical limitations, and other disease-specific circumstances,” he noted.

“Uncontrolled asthma, in particular, has strong links to low socioeconomic factors that are closely tied to access to adequate medical care, nutrition, educational institutions, and other relevant contributors to normal cognitive development,” Maselli said. Although the authors account for some of these socioeconomic factors by evaluating income and race, other variables may have influenced the results, he added.

Overall, this study’s findings suggested that the diagnosis of asthma in children may be associated with memory deficits and may influence neurodevelopment; however, more research is needed to determine whether the findings are replicated in other cohorts, said Maselli. “In particular, evaluating the effects of the severity of asthma and different asthma endotypes would be crucial to identify children with a higher risk of memory or cognitive deficits and confirm these associations,” he said.

This study was funded by the Memory and Plasticity Program at the University of California, Davis, and by a Learning, Memory, and Plasticity Training Program Fellowship grant from the National Institutes of Health. The researchers and Maselli had no financial conflicts to disclose. 

 

A version of this article appeared on Medscape.com.

The latest glucagon-like peptide 1 (GLP-1) receptor agonists have been heralded for their potential to not only boost weight loss and glucose control but also improve cardiovascular, gastric, hepatic, and renal values.

Throughout 2024, research has also indicated GLP-1 drugs may reduce risks for obesity-related cancer.

In a US study of more than 1.6 million patients with type 2 diabetes, cancer researchers found that patients who took a GLP-1 drug had significant risk reductions for 10 of 13 obesity-associated cancers, as compared with patients who only took insulin.

The research team found a reduction in esophageal, colorectal, endometrial, gallbladder, kidney, liver, ovarian, and pancreatic cancers, as well as meningioma and multiple myeloma. They also saw a declining risk for stomach cancer, though it wasn’t considered statistically significant, but not a reduced risk for postmenopausal breast cancer or thyroid cancer.

The associations make sense, particularly because GLP-1 drugs have unexpected effects on modulating immune functions linked to obesity-associated cancers.

“The protective effects of GLP-1s against obesity-associated cancers likely stem from multiple mechanisms,” said lead author Lindsey Wang, a medical student and research scholar at Case Western Reserve University in Cleveland.

“These drugs promote substantial weight loss, reducing obesity-related cancer risks,” she said. “They also enhance insulin sensitivity and lower insulin levels, decreasing cancer cell growth signals.”

 

Additional GLP-1 Studies

The Case Western team also published a study in December 2023 that found people with type 2 diabetes who took GLP-1s had a 44% lower risk for colorectal cancer than those who took insulin and a 25% lower risk than those who took metformin. The research suggested even greater risk reductions among those with overweight or obesity, with GLP-1 users having a 50% lower risk than those who took insulin and a 42% lower risk than those who took metformin.

In another recent Case Western study, both bariatric surgery and GLP-1 drugs reduced the risk for obesity-related cancers. While those who had bariatric surgery had a 22% risk reduction over 10 years, as compared with those who received no treatment, those taking GLP-1 had a 39% risk reduction.

Other studies worldwide have looked at GLP-1 drugs and tumor effects among various cancer cell lines. In a study using pancreatic cancer cell lines, GLP-1 liraglutide suppressed cancer cell growth and led to cell death. Similarly, a study using breast cancer cells found liraglutide reduced cancer cell viability and the ability for cells to migrate.

As researchers identify additional links between GLP-1s and improvements across organ systems, the knock-on effects could lead to lower cancer risks as well. For example, studies presented at The Liver Meeting in San Diego in November pointed to GLP-1s reducing fatty liver disease, which can slow the progression to liver cancer.

“Separate from obesity, having higher levels of body fat is associated with an increased risk of several forms of cancer,” said Neil Iyengar, MD, an oncologist at Memorial Sloan Kettering Cancer Center in New York City. Iyengar researches the relationship between obesity and cancer.

“I foresee that this class of drugs will revolutionize obesity and the cancer burden that comes with it, if people can get access,” he said. “This really is an exciting development.”

 

Ongoing GLP-1 Research

On the other hand, cancer researchers have also expressed concerns about potential associations between GLP-1s and increased cancer risks. In the obesity-associated cancer study by Case Western researchers, patients with type 2 diabetes taking a GLP-1 drug appeared to have a slightly higher risk for kidney cancer than those taking metformin.

In addition, GLP-1 studies in animals have indicated that the drugs may increase the risks for medullary thyroid cancer and pancreatic cancer. However, the data on increased risks in humans remain inconclusive, and more recent studies refute these findings.

For instance, cancer researchers in India conducted a systematic review and meta-analysis of semaglutide and cancer risks, finding that 37 randomized controlled trials and 19 real-world studies didn’t find increased risks for any cancer, including pancreatic and thyroid cancers.

In another systematic review by Brazilian researchers, 50 trials found GLP-1s didn’t increase the risk for breast cancer or benign breast neoplasms.

In 2025, new retrospective studies will show more nuanced data, especially as more patients — both with and without type 2 diabetes — take semaglutide, tirzepatide, and new GLP-1 drugs in the research pipeline.

“The holy grail has always been getting a medication to treat obesity,” said Anne McTiernan, MD, PhD, an epidemiologist and obesity researcher at the Fred Hutchinson Cancer Center in Seattle.

“There have been trials focused on these medications’ effects on diabetes and cardiovascular disease treatment, but no trials have tested their effects on cancer risk,” she said. “Usually, many years of follow-up of large numbers of patients are needed to see cancer effects of a carcinogen or cancer-preventing intervention.”

Those clinical trials are likely coming soon, she said. Researchers will need to conduct prospective clinical trials to examine the direct relationship between GLP-1 drugs and cancer risks, as well as the underlying mechanisms linked to cancer cell growth, activation of immune cells, and anti-inflammatory properties.

Because GLP-1 medications aren’t intended to be taken forever, researchers will also need to consider the associations with long-term cancer risks. Even so, weight loss and other obesity-related improvements could contribute to overall lower cancer risks in the end.

“If taking these drugs for a limited amount of time can help people lose weight and get on an exercise plan, then that’s helping lower cancer risk long-term,” said Sonali Thosani, MD, associate professor of endocrine neoplasia and hormonal disorders at the University of Texas MD Anderson Cancer Center in Houston.

“But it all comes back to someone making lifestyle changes and sticking to them, even after they stop taking the drugs,” she said. “If they can do that, then you’ll probably see a net positive for long-term cancer risks and other long-term health risks.”

 

A version of this article appeared on Medscape.com.

The latest glucagon-like peptide 1 (GLP-1) receptor agonists have been heralded for their potential to not only boost weight loss and glucose control but also improve cardiovascular, gastric, hepatic, and renal values.

Throughout 2024, research has also indicated GLP-1 drugs may reduce risks for obesity-related cancer.

In a US study of more than 1.6 million patients with type 2 diabetes, cancer researchers found that patients who took a GLP-1 drug had significant risk reductions for 10 of 13 obesity-associated cancers, as compared with patients who only took insulin.

The research team found a reduction in esophageal, colorectal, endometrial, gallbladder, kidney, liver, ovarian, and pancreatic cancers, as well as meningioma and multiple myeloma. They also saw a declining risk for stomach cancer, though it wasn’t considered statistically significant, but not a reduced risk for postmenopausal breast cancer or thyroid cancer.

The associations make sense, particularly because GLP-1 drugs have unexpected effects on modulating immune functions linked to obesity-associated cancers.

“The protective effects of GLP-1s against obesity-associated cancers likely stem from multiple mechanisms,” said lead author Lindsey Wang, a medical student and research scholar at Case Western Reserve University in Cleveland.

“These drugs promote substantial weight loss, reducing obesity-related cancer risks,” she said. “They also enhance insulin sensitivity and lower insulin levels, decreasing cancer cell growth signals.”

 

Additional GLP-1 Studies

The Case Western team also published a study in December 2023 that found people with type 2 diabetes who took GLP-1s had a 44% lower risk for colorectal cancer than those who took insulin and a 25% lower risk than those who took metformin. The research suggested even greater risk reductions among those with overweight or obesity, with GLP-1 users having a 50% lower risk than those who took insulin and a 42% lower risk than those who took metformin.

In another recent Case Western study, both bariatric surgery and GLP-1 drugs reduced the risk for obesity-related cancers. While those who had bariatric surgery had a 22% risk reduction over 10 years, as compared with those who received no treatment, those taking GLP-1 had a 39% risk reduction.

Other studies worldwide have looked at GLP-1 drugs and tumor effects among various cancer cell lines. In a study using pancreatic cancer cell lines, GLP-1 liraglutide suppressed cancer cell growth and led to cell death. Similarly, a study using breast cancer cells found liraglutide reduced cancer cell viability and the ability for cells to migrate.

As researchers identify additional links between GLP-1s and improvements across organ systems, the knock-on effects could lead to lower cancer risks as well. For example, studies presented at The Liver Meeting in San Diego in November pointed to GLP-1s reducing fatty liver disease, which can slow the progression to liver cancer.

“Separate from obesity, having higher levels of body fat is associated with an increased risk of several forms of cancer,” said Neil Iyengar, MD, an oncologist at Memorial Sloan Kettering Cancer Center in New York City. Iyengar researches the relationship between obesity and cancer.

“I foresee that this class of drugs will revolutionize obesity and the cancer burden that comes with it, if people can get access,” he said. “This really is an exciting development.”

 

Ongoing GLP-1 Research

On the other hand, cancer researchers have also expressed concerns about potential associations between GLP-1s and increased cancer risks. In the obesity-associated cancer study by Case Western researchers, patients with type 2 diabetes taking a GLP-1 drug appeared to have a slightly higher risk for kidney cancer than those taking metformin.

In addition, GLP-1 studies in animals have indicated that the drugs may increase the risks for medullary thyroid cancer and pancreatic cancer. However, the data on increased risks in humans remain inconclusive, and more recent studies refute these findings.

For instance, cancer researchers in India conducted a systematic review and meta-analysis of semaglutide and cancer risks, finding that 37 randomized controlled trials and 19 real-world studies didn’t find increased risks for any cancer, including pancreatic and thyroid cancers.

In another systematic review by Brazilian researchers, 50 trials found GLP-1s didn’t increase the risk for breast cancer or benign breast neoplasms.

In 2025, new retrospective studies will show more nuanced data, especially as more patients — both with and without type 2 diabetes — take semaglutide, tirzepatide, and new GLP-1 drugs in the research pipeline.

“The holy grail has always been getting a medication to treat obesity,” said Anne McTiernan, MD, PhD, an epidemiologist and obesity researcher at the Fred Hutchinson Cancer Center in Seattle.

“There have been trials focused on these medications’ effects on diabetes and cardiovascular disease treatment, but no trials have tested their effects on cancer risk,” she said. “Usually, many years of follow-up of large numbers of patients are needed to see cancer effects of a carcinogen or cancer-preventing intervention.”

Those clinical trials are likely coming soon, she said. Researchers will need to conduct prospective clinical trials to examine the direct relationship between GLP-1 drugs and cancer risks, as well as the underlying mechanisms linked to cancer cell growth, activation of immune cells, and anti-inflammatory properties.

Because GLP-1 medications aren’t intended to be taken forever, researchers will also need to consider the associations with long-term cancer risks. Even so, weight loss and other obesity-related improvements could contribute to overall lower cancer risks in the end.

“If taking these drugs for a limited amount of time can help people lose weight and get on an exercise plan, then that’s helping lower cancer risk long-term,” said Sonali Thosani, MD, associate professor of endocrine neoplasia and hormonal disorders at the University of Texas MD Anderson Cancer Center in Houston.

“But it all comes back to someone making lifestyle changes and sticking to them, even after they stop taking the drugs,” she said. “If they can do that, then you’ll probably see a net positive for long-term cancer risks and other long-term health risks.”

 

A version of this article appeared on Medscape.com.

The latest glucagon-like peptide 1 (GLP-1) receptor agonists have been heralded for their potential to not only boost weight loss and glucose control but also improve cardiovascular, gastric, hepatic, and renal values.

Throughout 2024, research has also indicated GLP-1 drugs may reduce risks for obesity-related cancer.

In a US study of more than 1.6 million patients with type 2 diabetes, cancer researchers found that patients who took a GLP-1 drug had significant risk reductions for 10 of 13 obesity-associated cancers, as compared with patients who only took insulin.

The research team found a reduction in esophageal, colorectal, endometrial, gallbladder, kidney, liver, ovarian, and pancreatic cancers, as well as meningioma and multiple myeloma. They also saw a declining risk for stomach cancer, though it wasn’t considered statistically significant, but not a reduced risk for postmenopausal breast cancer or thyroid cancer.

The associations make sense, particularly because GLP-1 drugs have unexpected effects on modulating immune functions linked to obesity-associated cancers.

“The protective effects of GLP-1s against obesity-associated cancers likely stem from multiple mechanisms,” said lead author Lindsey Wang, a medical student and research scholar at Case Western Reserve University in Cleveland.

“These drugs promote substantial weight loss, reducing obesity-related cancer risks,” she said. “They also enhance insulin sensitivity and lower insulin levels, decreasing cancer cell growth signals.”

 

Additional GLP-1 Studies

The Case Western team also published a study in December 2023 that found people with type 2 diabetes who took GLP-1s had a 44% lower risk for colorectal cancer than those who took insulin and a 25% lower risk than those who took metformin. The research suggested even greater risk reductions among those with overweight or obesity, with GLP-1 users having a 50% lower risk than those who took insulin and a 42% lower risk than those who took metformin.

In another recent Case Western study, both bariatric surgery and GLP-1 drugs reduced the risk for obesity-related cancers. While those who had bariatric surgery had a 22% risk reduction over 10 years, as compared with those who received no treatment, those taking GLP-1 had a 39% risk reduction.

Other studies worldwide have looked at GLP-1 drugs and tumor effects among various cancer cell lines. In a study using pancreatic cancer cell lines, GLP-1 liraglutide suppressed cancer cell growth and led to cell death. Similarly, a study using breast cancer cells found liraglutide reduced cancer cell viability and the ability for cells to migrate.

As researchers identify additional links between GLP-1s and improvements across organ systems, the knock-on effects could lead to lower cancer risks as well. For example, studies presented at The Liver Meeting in San Diego in November pointed to GLP-1s reducing fatty liver disease, which can slow the progression to liver cancer.

“Separate from obesity, having higher levels of body fat is associated with an increased risk of several forms of cancer,” said Neil Iyengar, MD, an oncologist at Memorial Sloan Kettering Cancer Center in New York City. Iyengar researches the relationship between obesity and cancer.

“I foresee that this class of drugs will revolutionize obesity and the cancer burden that comes with it, if people can get access,” he said. “This really is an exciting development.”

 

Ongoing GLP-1 Research

On the other hand, cancer researchers have also expressed concerns about potential associations between GLP-1s and increased cancer risks. In the obesity-associated cancer study by Case Western researchers, patients with type 2 diabetes taking a GLP-1 drug appeared to have a slightly higher risk for kidney cancer than those taking metformin.

In addition, GLP-1 studies in animals have indicated that the drugs may increase the risks for medullary thyroid cancer and pancreatic cancer. However, the data on increased risks in humans remain inconclusive, and more recent studies refute these findings.

For instance, cancer researchers in India conducted a systematic review and meta-analysis of semaglutide and cancer risks, finding that 37 randomized controlled trials and 19 real-world studies didn’t find increased risks for any cancer, including pancreatic and thyroid cancers.

In another systematic review by Brazilian researchers, 50 trials found GLP-1s didn’t increase the risk for breast cancer or benign breast neoplasms.

In 2025, new retrospective studies will show more nuanced data, especially as more patients — both with and without type 2 diabetes — take semaglutide, tirzepatide, and new GLP-1 drugs in the research pipeline.

“The holy grail has always been getting a medication to treat obesity,” said Anne McTiernan, MD, PhD, an epidemiologist and obesity researcher at the Fred Hutchinson Cancer Center in Seattle.

“There have been trials focused on these medications’ effects on diabetes and cardiovascular disease treatment, but no trials have tested their effects on cancer risk,” she said. “Usually, many years of follow-up of large numbers of patients are needed to see cancer effects of a carcinogen or cancer-preventing intervention.”

Those clinical trials are likely coming soon, she said. Researchers will need to conduct prospective clinical trials to examine the direct relationship between GLP-1 drugs and cancer risks, as well as the underlying mechanisms linked to cancer cell growth, activation of immune cells, and anti-inflammatory properties.

Because GLP-1 medications aren’t intended to be taken forever, researchers will also need to consider the associations with long-term cancer risks. Even so, weight loss and other obesity-related improvements could contribute to overall lower cancer risks in the end.

“If taking these drugs for a limited amount of time can help people lose weight and get on an exercise plan, then that’s helping lower cancer risk long-term,” said Sonali Thosani, MD, associate professor of endocrine neoplasia and hormonal disorders at the University of Texas MD Anderson Cancer Center in Houston.

“But it all comes back to someone making lifestyle changes and sticking to them, even after they stop taking the drugs,” she said. “If they can do that, then you’ll probably see a net positive for long-term cancer risks and other long-term health risks.”

 

A version of this article appeared on Medscape.com.

TOPLINE:

Both low and high levels of high-density lipoprotein (HDL) are associated with an increased risk for age-related macular degeneration (AMD). This study also identified a potential novel single-nucleotide polymorphism linked to an elevated risk for the retina condition.

METHODOLOGY:

• Researchers conducted a cross-sectional retrospective analysis using data from the All of Us research program to assess the association between lipoprotein and the risk for AMD.
• They analyzed data from 2328 patients with AMD (mean age, 75.5 years; 46.7% women; 84.2% White individuals) and 5028 matched controls (mean age, 75.6 years; 52.5% women; 82.9% White individuals).
• Data were extracted for smoking status, history of hyperlipidemia, use of statins (categorized as hepatically and non-hepatically metabolized), and laboratory values for total triglyceride, low-density lipoprotein (LDL), and HDL levels.
• Data for single-nucleotide polymorphisms associated with the dysregulation of LDL and HDL metabolism were extracted using the PLINK toolkit.

TAKEAWAY:

• Both high and low HDL levels were associated with an increased risk for AMD (adjusted odds ratio [aOR], 1.28 for both; both P < .001), whereas low and high levels of triglyceride and LDL did not demonstrate a statistically significant association with the risk for AMD.
• A history of smoking and statin use showed significant associations with an increased risk for AMD (aOR, 1.30 and 1.36, respectively; both P < .001).
• Single-nucleotide polymorphisms in the genes associated with HDL metabolism, ABCA1 and LIPC, were negatively associated with the risk for AMD (aOR, 0.88; P = .04 and aOR, 0.86; P = .001, respectively).
• Lipoprotein(a) or Lp(a) was identified as a novel single nucleotide polymorphism linked to an increased risk for AMD (aOR, 1.37; P = .007).

IN PRACTICE:

“Despite conflicting evidence regarding the relationship with elevated HDL and AMD risk, this is to our knowledge the first time a U-shaped relationship with low and high HDL and AMD has been described. In fact, the presence of a U-shaped relationship may explain inconsistency in prior analyses comparing mean HDL levels in AMD and control populations,” the study authors wrote. 

SOURCE:

The study was led by Jimmy S. Chen, MD, of the Viterbi Family Department of Ophthalmology and Shiley Eye Institute at the University of California, San Diego. It was published online on January 3, 2025, in Ophthalmology.

LIMITATIONS:

The study was limited by the retrospective collection and analysis of data. The use of billing codes for diagnosis extraction may have introduced documentation inaccuracies. The subgroup analysis by severity of AMD was not performed.

DISCLOSURES:

One of the authors was funded by grants from the National Eye Institute (NEI), Research to Prevent Blindness Career Development Award, Robert Machemer MD and International Retinal Research Foundation, and the UC San Diego Academic Senate. Another author reported receiving a grant from the National Heart, Lung, and Blood Institute, while a third author received funding from the National Institutes of Health (NIH), NEI, and Research to Prevent Blindness. The All of Us Research Program was supported by grants from the NIH and other sources. The authors reported no conflicts of interest.
 

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Both low and high levels of high-density lipoprotein (HDL) are associated with an increased risk for age-related macular degeneration (AMD). This study also identified a potential novel single-nucleotide polymorphism linked to an elevated risk for the retina condition.

METHODOLOGY:

• Researchers conducted a cross-sectional retrospective analysis using data from the All of Us research program to assess the association between lipoprotein and the risk for AMD.
• They analyzed data from 2328 patients with AMD (mean age, 75.5 years; 46.7% women; 84.2% White individuals) and 5028 matched controls (mean age, 75.6 years; 52.5% women; 82.9% White individuals).
• Data were extracted for smoking status, history of hyperlipidemia, use of statins (categorized as hepatically and non-hepatically metabolized), and laboratory values for total triglyceride, low-density lipoprotein (LDL), and HDL levels.
• Data for single-nucleotide polymorphisms associated with the dysregulation of LDL and HDL metabolism were extracted using the PLINK toolkit.

TAKEAWAY:

• Both high and low HDL levels were associated with an increased risk for AMD (adjusted odds ratio [aOR], 1.28 for both; both P < .001), whereas low and high levels of triglyceride and LDL did not demonstrate a statistically significant association with the risk for AMD.
• A history of smoking and statin use showed significant associations with an increased risk for AMD (aOR, 1.30 and 1.36, respectively; both P < .001).
• Single-nucleotide polymorphisms in the genes associated with HDL metabolism, ABCA1 and LIPC, were negatively associated with the risk for AMD (aOR, 0.88; P = .04 and aOR, 0.86; P = .001, respectively).
• Lipoprotein(a) or Lp(a) was identified as a novel single nucleotide polymorphism linked to an increased risk for AMD (aOR, 1.37; P = .007).

IN PRACTICE:

“Despite conflicting evidence regarding the relationship with elevated HDL and AMD risk, this is to our knowledge the first time a U-shaped relationship with low and high HDL and AMD has been described. In fact, the presence of a U-shaped relationship may explain inconsistency in prior analyses comparing mean HDL levels in AMD and control populations,” the study authors wrote. 

SOURCE:

The study was led by Jimmy S. Chen, MD, of the Viterbi Family Department of Ophthalmology and Shiley Eye Institute at the University of California, San Diego. It was published online on January 3, 2025, in Ophthalmology.

LIMITATIONS:

The study was limited by the retrospective collection and analysis of data. The use of billing codes for diagnosis extraction may have introduced documentation inaccuracies. The subgroup analysis by severity of AMD was not performed.

DISCLOSURES:

One of the authors was funded by grants from the National Eye Institute (NEI), Research to Prevent Blindness Career Development Award, Robert Machemer MD and International Retinal Research Foundation, and the UC San Diego Academic Senate. Another author reported receiving a grant from the National Heart, Lung, and Blood Institute, while a third author received funding from the National Institutes of Health (NIH), NEI, and Research to Prevent Blindness. The All of Us Research Program was supported by grants from the NIH and other sources. The authors reported no conflicts of interest.
 

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

TOPLINE:

Both low and high levels of high-density lipoprotein (HDL) are associated with an increased risk for age-related macular degeneration (AMD). This study also identified a potential novel single-nucleotide polymorphism linked to an elevated risk for the retina condition.

METHODOLOGY:

• Researchers conducted a cross-sectional retrospective analysis using data from the All of Us research program to assess the association between lipoprotein and the risk for AMD.
• They analyzed data from 2328 patients with AMD (mean age, 75.5 years; 46.7% women; 84.2% White individuals) and 5028 matched controls (mean age, 75.6 years; 52.5% women; 82.9% White individuals).
• Data were extracted for smoking status, history of hyperlipidemia, use of statins (categorized as hepatically and non-hepatically metabolized), and laboratory values for total triglyceride, low-density lipoprotein (LDL), and HDL levels.
• Data for single-nucleotide polymorphisms associated with the dysregulation of LDL and HDL metabolism were extracted using the PLINK toolkit.

TAKEAWAY:

• Both high and low HDL levels were associated with an increased risk for AMD (adjusted odds ratio [aOR], 1.28 for both; both P < .001), whereas low and high levels of triglyceride and LDL did not demonstrate a statistically significant association with the risk for AMD.
• A history of smoking and statin use showed significant associations with an increased risk for AMD (aOR, 1.30 and 1.36, respectively; both P < .001).
• Single-nucleotide polymorphisms in the genes associated with HDL metabolism, ABCA1 and LIPC, were negatively associated with the risk for AMD (aOR, 0.88; P = .04 and aOR, 0.86; P = .001, respectively).
• Lipoprotein(a) or Lp(a) was identified as a novel single nucleotide polymorphism linked to an increased risk for AMD (aOR, 1.37; P = .007).

IN PRACTICE:

“Despite conflicting evidence regarding the relationship with elevated HDL and AMD risk, this is to our knowledge the first time a U-shaped relationship with low and high HDL and AMD has been described. In fact, the presence of a U-shaped relationship may explain inconsistency in prior analyses comparing mean HDL levels in AMD and control populations,” the study authors wrote. 

SOURCE:

The study was led by Jimmy S. Chen, MD, of the Viterbi Family Department of Ophthalmology and Shiley Eye Institute at the University of California, San Diego. It was published online on January 3, 2025, in Ophthalmology.

LIMITATIONS:

The study was limited by the retrospective collection and analysis of data. The use of billing codes for diagnosis extraction may have introduced documentation inaccuracies. The subgroup analysis by severity of AMD was not performed.

DISCLOSURES:

One of the authors was funded by grants from the National Eye Institute (NEI), Research to Prevent Blindness Career Development Award, Robert Machemer MD and International Retinal Research Foundation, and the UC San Diego Academic Senate. Another author reported receiving a grant from the National Heart, Lung, and Blood Institute, while a third author received funding from the National Institutes of Health (NIH), NEI, and Research to Prevent Blindness. The All of Us Research Program was supported by grants from the NIH and other sources. The authors reported no conflicts of interest.
 

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Norovirus cases continue to rise in the United States this winter, at levels higher than the same time period in previous years, according to the latest data from the Centers for Disease Control and Prevention (CDC).

Current data from the CDC’s NoroSTAT monitoring system show 495 reported outbreaks during the period from August 1, 2024, to December 11, 2024, compared with 363 outbreaks during the same period last year. In addition, the total number of norovirus outbreaks in the current season are higher than those reported in the seasonal years: 2012-2020 and 2021-2024.

Circulating strains of norovirus change over time, which can affect disease burden and potential disease severity, Sara Mirza, MD, an epidemiologist in the CDC’s Division of Viral Diseases, said in an interview.

The numbers for the 2024 norovirus season (considered approximately November to April) have reached or exceeded the case numbers seen before the COVID-19 pandemic, Mirza said.

The increase in cases may be caused in part by a new predominant strain of norovirus. “For the fall/winter of 2024-2025 season, genogroup 2, genotype 17, known as GII.17, has become the most detected genotype (strain) in the US among laboratory confirmed outbreaks reported to CDC,” said Mirza. “At this time, there is no indication that GII.17 causes more severe illness or affects one population more than another, but we are continuing to conduct surveillance to assess,” she added.

 

Clinical Takeaways

“Norovirus affects all ages, but young children and older adults are most at risk from more severe outcomes,” said Mirza.

“Clinicians treating older patients for acute gastroenteritis should be aware of these elevated risks and be sure to include norovirus as a potentially serious diagnosis, particularly in vulnerable patients with other diseases and those living in congregate settings, such as nursing homes,” she said.

When treating a patient with norovirus during an outbreak, use soap and water for hand hygiene after caring for patients with suspected or confirmed norovirus gastroenteritis, said Mirza. If norovirus infection is suspected, PPE use is recommended for individuals in the patient care area, she added. 

Although state, local, and territorial health departments are not required to report individual cases of norovirus to the CDC, healthcare providers are encouraged to report all outbreaks of acute gastroenteritis, including suspected outbreaks of norovirus, to the appropriate state, local, or territorial health department, said Mirza. “Health departments are encouraged to report all suspected and confirmed norovirus outbreaks through the National Outbreak Reporting System and CaliciNet,” she added.

“Infection control measures, such as thorough hand washing, cleaning and disinfecting surfaces with bleach, and patient isolation and contact precautions in congregate or healthcare settings are the best ways to prevent norovirus and keep it from spreading to others,” Mirza said.

Remind patients that alcohol-based hand sanitizer is ineffective against norovirus, because the virus’s protective protein shell prevents the alcohol from penetrating and inactivating the virus, Mirza emphasized. “Soap and water work to remove germs from hands,” she said.

 

Cruise Ship Considerations

Cruise ships continue to be sources of increased risk for norovirus, according the CDC. The CDC’s Vessel Sanitation Program (VSP) was created to help the cruise industry prevent public health issues such as norovirus outbreaks, and to provide guidance for actions to take in the event of outbreaks. 

For example, the most recently reported outbreak of norovirus on a cruise ship reported to the VSP was January 4, 2025, and occurred on a Holland America cruise from December 30, 2024, through January 8, 2025. Overall, 4.0% of passengers and 1.0% of crew members reported illness. Following VSP guidance, the ship reported increased cleaning and disinfection procedures and the collection of stool specimens for testing, and isolation of ill passengers and crew.

 

Clinical Perspective

In clinical practice, the number of norovirus cases is significantly exceeding previous years, and the trend seems to be consistent nationwide, David J. Cennimo, MD, associate professor of medicine and pediatrics at Rutgers New Jersey Medical School, Newark, New Jersey, said in an interview.

“Norovirus is incredibly contagious and spreads very quickly, which is how you get entire cruise ships infected at once,” he said. Norovirus is notoriously difficult to disinfect or kill, he added.

One possible contributor to the surge in cases is increased travel, especially during the holiday season, when people are coming together and sharing food, Cennimo noted. “We have seen many infections such as pneumonia return to levels approaching the period before the COVID-19 pandemic,” he said. 

For norovirus prevention, strict attention to sanitation and handwashing is a must at home or when traveling, said Cennimo. For clinicians, it is important to report outbreaks of GI illness so appropriate control measures can be taken, he said.

Visit the CDC’s website on norovirus prevention for more information. 

Mirza and Cennimo had no financial conflicts to disclose.

 

A version of this article appeared on Medscape.com.

Norovirus cases continue to rise in the United States this winter, at levels higher than the same time period in previous years, according to the latest data from the Centers for Disease Control and Prevention (CDC).

Current data from the CDC’s NoroSTAT monitoring system show 495 reported outbreaks during the period from August 1, 2024, to December 11, 2024, compared with 363 outbreaks during the same period last year. In addition, the total number of norovirus outbreaks in the current season are higher than those reported in the seasonal years: 2012-2020 and 2021-2024.

Circulating strains of norovirus change over time, which can affect disease burden and potential disease severity, Sara Mirza, MD, an epidemiologist in the CDC’s Division of Viral Diseases, said in an interview.

The numbers for the 2024 norovirus season (considered approximately November to April) have reached or exceeded the case numbers seen before the COVID-19 pandemic, Mirza said.

The increase in cases may be caused in part by a new predominant strain of norovirus. “For the fall/winter of 2024-2025 season, genogroup 2, genotype 17, known as GII.17, has become the most detected genotype (strain) in the US among laboratory confirmed outbreaks reported to CDC,” said Mirza. “At this time, there is no indication that GII.17 causes more severe illness or affects one population more than another, but we are continuing to conduct surveillance to assess,” she added.

 

Clinical Takeaways

“Norovirus affects all ages, but young children and older adults are most at risk from more severe outcomes,” said Mirza.

“Clinicians treating older patients for acute gastroenteritis should be aware of these elevated risks and be sure to include norovirus as a potentially serious diagnosis, particularly in vulnerable patients with other diseases and those living in congregate settings, such as nursing homes,” she said.

When treating a patient with norovirus during an outbreak, use soap and water for hand hygiene after caring for patients with suspected or confirmed norovirus gastroenteritis, said Mirza. If norovirus infection is suspected, PPE use is recommended for individuals in the patient care area, she added. 

Although state, local, and territorial health departments are not required to report individual cases of norovirus to the CDC, healthcare providers are encouraged to report all outbreaks of acute gastroenteritis, including suspected outbreaks of norovirus, to the appropriate state, local, or territorial health department, said Mirza. “Health departments are encouraged to report all suspected and confirmed norovirus outbreaks through the National Outbreak Reporting System and CaliciNet,” she added.

“Infection control measures, such as thorough hand washing, cleaning and disinfecting surfaces with bleach, and patient isolation and contact precautions in congregate or healthcare settings are the best ways to prevent norovirus and keep it from spreading to others,” Mirza said.

Remind patients that alcohol-based hand sanitizer is ineffective against norovirus, because the virus’s protective protein shell prevents the alcohol from penetrating and inactivating the virus, Mirza emphasized. “Soap and water work to remove germs from hands,” she said.

 

Cruise Ship Considerations

Cruise ships continue to be sources of increased risk for norovirus, according the CDC. The CDC’s Vessel Sanitation Program (VSP) was created to help the cruise industry prevent public health issues such as norovirus outbreaks, and to provide guidance for actions to take in the event of outbreaks. 

For example, the most recently reported outbreak of norovirus on a cruise ship reported to the VSP was January 4, 2025, and occurred on a Holland America cruise from December 30, 2024, through January 8, 2025. Overall, 4.0% of passengers and 1.0% of crew members reported illness. Following VSP guidance, the ship reported increased cleaning and disinfection procedures and the collection of stool specimens for testing, and isolation of ill passengers and crew.

 

Clinical Perspective

In clinical practice, the number of norovirus cases is significantly exceeding previous years, and the trend seems to be consistent nationwide, David J. Cennimo, MD, associate professor of medicine and pediatrics at Rutgers New Jersey Medical School, Newark, New Jersey, said in an interview.

“Norovirus is incredibly contagious and spreads very quickly, which is how you get entire cruise ships infected at once,” he said. Norovirus is notoriously difficult to disinfect or kill, he added.

One possible contributor to the surge in cases is increased travel, especially during the holiday season, when people are coming together and sharing food, Cennimo noted. “We have seen many infections such as pneumonia return to levels approaching the period before the COVID-19 pandemic,” he said. 

For norovirus prevention, strict attention to sanitation and handwashing is a must at home or when traveling, said Cennimo. For clinicians, it is important to report outbreaks of GI illness so appropriate control measures can be taken, he said.

Visit the CDC’s website on norovirus prevention for more information. 

Mirza and Cennimo had no financial conflicts to disclose.

 

A version of this article appeared on Medscape.com.

Norovirus cases continue to rise in the United States this winter, at levels higher than the same time period in previous years, according to the latest data from the Centers for Disease Control and Prevention (CDC).

Current data from the CDC’s NoroSTAT monitoring system show 495 reported outbreaks during the period from August 1, 2024, to December 11, 2024, compared with 363 outbreaks during the same period last year. In addition, the total number of norovirus outbreaks in the current season are higher than those reported in the seasonal years: 2012-2020 and 2021-2024.

Circulating strains of norovirus change over time, which can affect disease burden and potential disease severity, Sara Mirza, MD, an epidemiologist in the CDC’s Division of Viral Diseases, said in an interview.

The numbers for the 2024 norovirus season (considered approximately November to April) have reached or exceeded the case numbers seen before the COVID-19 pandemic, Mirza said.

The increase in cases may be caused in part by a new predominant strain of norovirus. “For the fall/winter of 2024-2025 season, genogroup 2, genotype 17, known as GII.17, has become the most detected genotype (strain) in the US among laboratory confirmed outbreaks reported to CDC,” said Mirza. “At this time, there is no indication that GII.17 causes more severe illness or affects one population more than another, but we are continuing to conduct surveillance to assess,” she added.

 

Clinical Takeaways

“Norovirus affects all ages, but young children and older adults are most at risk from more severe outcomes,” said Mirza.

“Clinicians treating older patients for acute gastroenteritis should be aware of these elevated risks and be sure to include norovirus as a potentially serious diagnosis, particularly in vulnerable patients with other diseases and those living in congregate settings, such as nursing homes,” she said.

When treating a patient with norovirus during an outbreak, use soap and water for hand hygiene after caring for patients with suspected or confirmed norovirus gastroenteritis, said Mirza. If norovirus infection is suspected, PPE use is recommended for individuals in the patient care area, she added. 

Although state, local, and territorial health departments are not required to report individual cases of norovirus to the CDC, healthcare providers are encouraged to report all outbreaks of acute gastroenteritis, including suspected outbreaks of norovirus, to the appropriate state, local, or territorial health department, said Mirza. “Health departments are encouraged to report all suspected and confirmed norovirus outbreaks through the National Outbreak Reporting System and CaliciNet,” she added.

“Infection control measures, such as thorough hand washing, cleaning and disinfecting surfaces with bleach, and patient isolation and contact precautions in congregate or healthcare settings are the best ways to prevent norovirus and keep it from spreading to others,” Mirza said.

Remind patients that alcohol-based hand sanitizer is ineffective against norovirus, because the virus’s protective protein shell prevents the alcohol from penetrating and inactivating the virus, Mirza emphasized. “Soap and water work to remove germs from hands,” she said.

 

Cruise Ship Considerations

Cruise ships continue to be sources of increased risk for norovirus, according the CDC. The CDC’s Vessel Sanitation Program (VSP) was created to help the cruise industry prevent public health issues such as norovirus outbreaks, and to provide guidance for actions to take in the event of outbreaks. 

For example, the most recently reported outbreak of norovirus on a cruise ship reported to the VSP was January 4, 2025, and occurred on a Holland America cruise from December 30, 2024, through January 8, 2025. Overall, 4.0% of passengers and 1.0% of crew members reported illness. Following VSP guidance, the ship reported increased cleaning and disinfection procedures and the collection of stool specimens for testing, and isolation of ill passengers and crew.

 

Clinical Perspective

In clinical practice, the number of norovirus cases is significantly exceeding previous years, and the trend seems to be consistent nationwide, David J. Cennimo, MD, associate professor of medicine and pediatrics at Rutgers New Jersey Medical School, Newark, New Jersey, said in an interview.

“Norovirus is incredibly contagious and spreads very quickly, which is how you get entire cruise ships infected at once,” he said. Norovirus is notoriously difficult to disinfect or kill, he added.

One possible contributor to the surge in cases is increased travel, especially during the holiday season, when people are coming together and sharing food, Cennimo noted. “We have seen many infections such as pneumonia return to levels approaching the period before the COVID-19 pandemic,” he said. 

For norovirus prevention, strict attention to sanitation and handwashing is a must at home or when traveling, said Cennimo. For clinicians, it is important to report outbreaks of GI illness so appropriate control measures can be taken, he said.

Visit the CDC’s website on norovirus prevention for more information. 

Mirza and Cennimo had no financial conflicts to disclose.

 

A version of this article appeared on Medscape.com.

It is no secret that we have a daycare problem in this country. Twenty percent of families spend more than $36,000 for child care annually. Three quarters of a single parent’s income is spent on infant care. The result is that more than $122 billion is syphoned out of our economy in lost productivity and income.

How we got into this situation is less clear. Women who once were stay-at-home moms have moved into the workplace. Families are more mobile and grandparents who had been a source of childcare may live hours away. And, when they are nearby grandparents may themselves been forced to remain employed for economic reasons.

 

Despite the increase demand the market has failed to respond with more daycare providers because with a median hourly wage of less than $15.00 it is difficult to attract applicants from a pool of potential employees that is already in great demand.

And, let’s be honest, long hours cooped up inside with infants and toddlers isn’t the right job for everyone. For the most successful, although maybe not financially, providing daycare is truly a labor of love. There are high school and community college courses taught on child development and day care management. Experienced providers can be a source of tips-of-the trade to those just starting out. But, when there are three infants crying, two diapers to be changed, and a toddler heading toward a tantrum, two experienced providers may not be enough to calm the turbulent waters. 

A recent article in my local newspaper provided stark evidence of how serious our daycare situation has become. Although the daycare owner denies the allegation, the Department of Health and Human Service told the parents that the investigation currently supports their complaints that the children had been given melatonin gummies without their permission. Final action is pending but it is likely the daycare will lose its license. Not surprisingly the parents have already removed their children.

Curious about whether this situation was an isolated event, it didn’t take Google too long to find evidence of other daycares in which children had been given sleep-related medications without their parents’ permission. In May 2024 a daycare provider and three of her employees in Manchester, New Hampshire, were arrested and charged with endangering the welfare of a child after allegedly spiking their charges food with melatonin. Lest you think drugging infants in daycare is just a New England thing, my research found a news story dating back to 2003 that reported on several cases in which daycare providers had been administering diphenhydramine without parents permission. In one instance there was a fatal outcome. While melatonin does not pose a health risk on a par with diphenhydramine, the issue is the fact that the parents were not consulted.

I suspect that these two incidents in Maine and New Hampshire are not isolated events and melatonin has replaced diphenhydramine as the daycare provider’s “little helper” nationwide. It’s not clear how we as pediatricians can help police this practice, other than suggesting to parents that they initiate dialogues about napping strategies with their daycare providers. Not with an accusatory tone but more of a sharing about what tricks each party uses to make napping happen. It may be that the daycare provider has some valuable and sound advice that the parents can adapt to their home situation. However, if the daycare provider’s explanation for why the child naps well doesn’t sound right or the child is unusually drowsy after daycare visits they should share their concerns with us a pediatric health care advisors. 

 

Dr Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

It is no secret that we have a daycare problem in this country. Twenty percent of families spend more than $36,000 for child care annually. Three quarters of a single parent’s income is spent on infant care. The result is that more than $122 billion is syphoned out of our economy in lost productivity and income.

How we got into this situation is less clear. Women who once were stay-at-home moms have moved into the workplace. Families are more mobile and grandparents who had been a source of childcare may live hours away. And, when they are nearby grandparents may themselves been forced to remain employed for economic reasons.

 

Despite the increase demand the market has failed to respond with more daycare providers because with a median hourly wage of less than $15.00 it is difficult to attract applicants from a pool of potential employees that is already in great demand.

And, let’s be honest, long hours cooped up inside with infants and toddlers isn’t the right job for everyone. For the most successful, although maybe not financially, providing daycare is truly a labor of love. There are high school and community college courses taught on child development and day care management. Experienced providers can be a source of tips-of-the trade to those just starting out. But, when there are three infants crying, two diapers to be changed, and a toddler heading toward a tantrum, two experienced providers may not be enough to calm the turbulent waters. 

A recent article in my local newspaper provided stark evidence of how serious our daycare situation has become. Although the daycare owner denies the allegation, the Department of Health and Human Service told the parents that the investigation currently supports their complaints that the children had been given melatonin gummies without their permission. Final action is pending but it is likely the daycare will lose its license. Not surprisingly the parents have already removed their children.

Curious about whether this situation was an isolated event, it didn’t take Google too long to find evidence of other daycares in which children had been given sleep-related medications without their parents’ permission. In May 2024 a daycare provider and three of her employees in Manchester, New Hampshire, were arrested and charged with endangering the welfare of a child after allegedly spiking their charges food with melatonin. Lest you think drugging infants in daycare is just a New England thing, my research found a news story dating back to 2003 that reported on several cases in which daycare providers had been administering diphenhydramine without parents permission. In one instance there was a fatal outcome. While melatonin does not pose a health risk on a par with diphenhydramine, the issue is the fact that the parents were not consulted.

I suspect that these two incidents in Maine and New Hampshire are not isolated events and melatonin has replaced diphenhydramine as the daycare provider’s “little helper” nationwide. It’s not clear how we as pediatricians can help police this practice, other than suggesting to parents that they initiate dialogues about napping strategies with their daycare providers. Not with an accusatory tone but more of a sharing about what tricks each party uses to make napping happen. It may be that the daycare provider has some valuable and sound advice that the parents can adapt to their home situation. However, if the daycare provider’s explanation for why the child naps well doesn’t sound right or the child is unusually drowsy after daycare visits they should share their concerns with us a pediatric health care advisors. 

 

Dr Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

It is no secret that we have a daycare problem in this country. Twenty percent of families spend more than $36,000 for child care annually. Three quarters of a single parent’s income is spent on infant care. The result is that more than $122 billion is syphoned out of our economy in lost productivity and income.

How we got into this situation is less clear. Women who once were stay-at-home moms have moved into the workplace. Families are more mobile and grandparents who had been a source of childcare may live hours away. And, when they are nearby grandparents may themselves been forced to remain employed for economic reasons.

 

Despite the increase demand the market has failed to respond with more daycare providers because with a median hourly wage of less than $15.00 it is difficult to attract applicants from a pool of potential employees that is already in great demand.

And, let’s be honest, long hours cooped up inside with infants and toddlers isn’t the right job for everyone. For the most successful, although maybe not financially, providing daycare is truly a labor of love. There are high school and community college courses taught on child development and day care management. Experienced providers can be a source of tips-of-the trade to those just starting out. But, when there are three infants crying, two diapers to be changed, and a toddler heading toward a tantrum, two experienced providers may not be enough to calm the turbulent waters. 

A recent article in my local newspaper provided stark evidence of how serious our daycare situation has become. Although the daycare owner denies the allegation, the Department of Health and Human Service told the parents that the investigation currently supports their complaints that the children had been given melatonin gummies without their permission. Final action is pending but it is likely the daycare will lose its license. Not surprisingly the parents have already removed their children.

Curious about whether this situation was an isolated event, it didn’t take Google too long to find evidence of other daycares in which children had been given sleep-related medications without their parents’ permission. In May 2024 a daycare provider and three of her employees in Manchester, New Hampshire, were arrested and charged with endangering the welfare of a child after allegedly spiking their charges food with melatonin. Lest you think drugging infants in daycare is just a New England thing, my research found a news story dating back to 2003 that reported on several cases in which daycare providers had been administering diphenhydramine without parents permission. In one instance there was a fatal outcome. While melatonin does not pose a health risk on a par with diphenhydramine, the issue is the fact that the parents were not consulted.

I suspect that these two incidents in Maine and New Hampshire are not isolated events and melatonin has replaced diphenhydramine as the daycare provider’s “little helper” nationwide. It’s not clear how we as pediatricians can help police this practice, other than suggesting to parents that they initiate dialogues about napping strategies with their daycare providers. Not with an accusatory tone but more of a sharing about what tricks each party uses to make napping happen. It may be that the daycare provider has some valuable and sound advice that the parents can adapt to their home situation. However, if the daycare provider’s explanation for why the child naps well doesn’t sound right or the child is unusually drowsy after daycare visits they should share their concerns with us a pediatric health care advisors. 

 

Dr Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

The evidence is clear: Alcohol can cause cancer.

Earlier this month, US surgeon general Vivek Murthy, MD, issued an advisory, calling for alcoholic beverages to carry a warning label about cancer risk. The advisory flagged alcohol as the third leading preventable cause of cancer in the United States, after tobacco and obesity, and highlighted people’s limited awareness about the relationship between alcohol and cancer risk.

But, when it comes to cancer risk, are all types of alcohol created equal?

For many years, red wine seemed to be an outlier, with studies indicating that, in moderation, it might even be good for you. Red wine has anti-inflammatory and antioxidant properties — most notably, it contains the antioxidant resveratrol. Starting in the 1990s, research began to hint that the compound might protect against heart disease, aging, and cancer, though much of this work was done in animals or test tubes.

The idea that red wine carries health benefits, however, has been called into question more recently. A recent meta-analysis, for instance, suggests that many previous studies touting the health benefits of more moderate drinking were likely biased, potentially leading to “misleading positive health associations.” And one recent study found that alcohol consumption, largely red wine and beer, at all levels was linked to an increased risk for cardiovascular disease.

Although wine’s health halo is dwindling, there might be an exception: Cancer risk.

Overall, research shows that even light to moderate drinking increases the risk for at least seven types of cancer, but when focusing on red wine, in particular, that risk calculus can look different.

“It’s very complicated and nuanced,” said Timothy Rebbeck, PhD, professor of cancer prevention, Harvard T.H. Chan School of Public Health, Boston. “And ‘complicated and nuanced’ doesn’t work very well in public health messages.”

The Knowns About Alcohol and Cancer Risk

Some things about the relationship between alcohol and cancer risk are crystal clear. “There’s no question that alcohol is a group 1 carcinogen,” Rebbeck said. “Alcohol can cause cancer.”

Groups including the International Agency for Research on Cancer (IARC) and American Cancer Society agree that alcohol use is an established cause of seven types of cancer: Those of the oral cavity, larynx, pharynx, esophagus (squamous cell carcinoma), liver (hepatocellular carcinoma), breast, and colon/rectum. Heavy drinking — at least 8 standard drinks a week for women and 15 for men — and binge drinking — 4 or more drinks in 2 hours for women and 5 or more for men — only amplify that risk. (A “standard” drink has 14 g of alcohol, which translates to a 5-oz glass of wine.)

“We’re most concerned about high-risk drinking — more than 2 drinks a day — and/or binge drinking,” said Noelle LoConte, MD, of the Division of Hematology, Medical Oncology and Palliative Care, University of Wisconsin School of Medicine and Public Health, Madison, who authored a 2018 statement on alcohol and cancer risk from the American Society of Clinical Oncology (ASCO).

Compared with not drinking, heavy drinking is linked with a roughly fivefold increase in the risk for oral cavity, pharyngeal, and esophageal cancers, and a 61% increase in the risk for breast cancer, according to LoConte and colleagues.

Things get murkier when it comes to moderate drinking — defined as up to 1 standard drink per day for women and 2 per day for men. There is evidence, LoConte said, that moderate drinking is associated with increased cancer risks, though the magnitude is generally much less than heavier drinking.

Cancer type also matters. One analysis found that the risk for breast cancer increased with even light to moderate alcohol consumption. Compared with no drinking, light to moderate drinking has also been linked to increased risks for oral cavity, pharynx, larynx, and esophageal cancers.

As for whether the type of alcoholic beverage matters, LoConte said, there’s no clear physiological reason that wine would be less risky than beer or liquor. Research indicates that ethanol is the problematic ingredient: Once ingested, it’s metabolized into acetaldehyde, a DNA-damaging substance that’s considered a probable human carcinogen. Ethanol can also alter circulating levels of estrogens and androgens, LoConte said, which is thought to drive its association with breast cancer risk.

“It likely doesn’t matter how you choose to get your ethanol,” she said. “It’s a question of volume.”

Hints That Wine Is an Outlier

Still, some studies suggest that how people ingest ethanol could make a difference.

A study published in August in JAMA Network Open is a case in point. The study found that, among older adults, light to heavy drinkers had an increased risk of dying from cancer, compared with occasional drinkers (though the increased risk among light to moderate drinkers occurred only among people who also had chronic health conditions, such as diabetes or high blood pressure, or were of lower socioeconomic status).

Wine drinkers fared differently. Most notably, drinkers who “preferred” wine — consuming over 80% of total ethanol from wine — or those who drank only with meals showed a small reduction in their risk for cancer mortality and all-cause mortality (hazard ratio [HR], 0.94 for both). The small protective association was somewhat stronger among people who reported both patterns (HR, 0.88), especially if they were of lower socioeconomic status (HR, 0.79).

The findings are in line with other research suggesting that wine drinkers may be outliers when it comes to cancer risk. A 2023 meta-analysis of 26 observational studies, for instance, found no association between wine consumption and any cancer type, with the caveat that there was «substantial» heterogeneity among the studies.

This heterogeneity caveat speaks to the inherent limitations of observational research, said Tim Stockwell, PhD, of the Canadian Institute for Substance Use Research, University of Victoria in British Columbia, Canada.

“Individual studies of alcohol and cancer risk do find differences by type of drink, or patterns of drinking,” Stockwell said. “But it’s so hard to unpack the confounding that goes along with the type of person who’s a wine drinker or a beer drinker or a spirit drinker. The beverage of choice seems to come with a lot of baggage.”

Compared with people who favor beer or liquor, he noted, wine aficionados are typically higher-income, exercise more often, smoke less, and have different diets, for example. The “best” studies, Rebbeck said, try to adjust for those differences, but it’s challenging.

The authors of the 2023 meta-analysis noted that “many components in wine could have anticarcinogenic effects” that theoretically could counter the ill effects of ethanol. Besides resveratrol, which is mainly found in red wine, the list includes anthocyanins, quercetin, and tannins. However, the authors also acknowledged that they couldn’t account for whether other lifestyle habits might explain why wine drinkers, overall, showed no increased cancer risks and sometimes lower risks.

Still, groups such as the IARC and ASCO hold that there is no known “safe” level, or type, of alcohol when it comes to cancer.

In the latest Canadian guidelines on alcohol use, the scientific panel calculated that people who have 6 drinks a week throughout adulthood (whatever the source of the alcohol) could shave 11 weeks from their life expectancy, on average, said Stockwell, who was on the guideline panel. Compare that with heavy drinking, where 4 drinks a day could rob the average person of 2 or 3 years. “If you’re drinking a lot, you could get huge benefits from cutting down,” Stockwell explained. “If you’re a moderate drinker, the benefits would obviously be less.”

Stockwell said that choices around drinking and breast cancer risk, specifically, can be “tough.” Unlike many of the other alcohol-associated cancers, he noted, breast cancer is common — so even small relative risk increases may be concerning. Based on a 2020 meta-analysis of 22 cohort studies, the risk for breast cancer rises by about 10%, on average, for every 10 g of alcohol a woman drinks per day. This study also found no evidence that wine is any different from other types of alcohol.

In real life, the calculus around wine consumption and cancer risk will probably vary widely from person to person, Rebbeck said. One woman with a family history of breast cancer might decide that having wine with dinner isn’t worth it. Another with the same family history might see that glass of wine as a stress reliever and opt to focus on other ways to reduce her breast cancer risk — by exercising and maintaining a healthy weight, for example.

“The bottom line is, in human studies, the data on light to moderate drinking and cancer are limited and messy, and you can’t draw firm conclusions from them,” Rebbeck said. “It probably raises risk in some people, but we don’t know who those people are. And the risk increases are relatively small.”

A Conversation Few Are Having

Even with many studies highlighting the connection between alcohol consumption and cancer risk, most people remain unaware about this risk.

A 2023 study by the National Cancer Institute found that only a minority of US adults knew that drinking alcohol is linked to increased cancer risk, and they were much less likely to say that was true of wine: Only 20% did, vs 31% who said that liquor can boost cancer risk. Meanwhile, 10% believed that wine helps prevent cancer. Other studies show that even among cancer survivors and patients undergoing active cancer treatment, many drink — often heavily.

“What we know right now is, physicians almost never talk about this,” LoConte said.

That could be due to time constraints, according to Rebbeck, or clinicians’ perceptions that the subject is too complicated and/or their own confusion about the data. There could also be some “cognitive dissonance” at play, LoConte noted, because many doctors drink alcohol.

It’s critical, she said, that conversations about drinking habits become “normalized,” and that should include informing patients that alcohol use is associated with certain cancers. Again, LoConte said, it’s high-risk drinking that’s most concerning and where reducing intake could have the biggest impact on cancer risk and other health outcomes.

“From a cancer prevention standpoint, it’s probably best not to drink,” she said. “But people don’t make choices based solely on cancer risk. We don’t want to come out with recommendations saying no one should drink. I don’t think the data support that, and people would buck against that advice.”

Rebbeck made a similar point. Even if there’s uncertainty about the risks for a daily glass of wine, he said, people can use that information to make decisions. “Everybody’s preferences and choices are going to be different,” Rebbeck said. “And that’s all we can really do.”

A version of this article appeared on Medscape.com.

The evidence is clear: Alcohol can cause cancer.

Earlier this month, US surgeon general Vivek Murthy, MD, issued an advisory, calling for alcoholic beverages to carry a warning label about cancer risk. The advisory flagged alcohol as the third leading preventable cause of cancer in the United States, after tobacco and obesity, and highlighted people’s limited awareness about the relationship between alcohol and cancer risk.

But, when it comes to cancer risk, are all types of alcohol created equal?

For many years, red wine seemed to be an outlier, with studies indicating that, in moderation, it might even be good for you. Red wine has anti-inflammatory and antioxidant properties — most notably, it contains the antioxidant resveratrol. Starting in the 1990s, research began to hint that the compound might protect against heart disease, aging, and cancer, though much of this work was done in animals or test tubes.

The idea that red wine carries health benefits, however, has been called into question more recently. A recent meta-analysis, for instance, suggests that many previous studies touting the health benefits of more moderate drinking were likely biased, potentially leading to “misleading positive health associations.” And one recent study found that alcohol consumption, largely red wine and beer, at all levels was linked to an increased risk for cardiovascular disease.

Although wine’s health halo is dwindling, there might be an exception: Cancer risk.

Overall, research shows that even light to moderate drinking increases the risk for at least seven types of cancer, but when focusing on red wine, in particular, that risk calculus can look different.

“It’s very complicated and nuanced,” said Timothy Rebbeck, PhD, professor of cancer prevention, Harvard T.H. Chan School of Public Health, Boston. “And ‘complicated and nuanced’ doesn’t work very well in public health messages.”

The Knowns About Alcohol and Cancer Risk

Some things about the relationship between alcohol and cancer risk are crystal clear. “There’s no question that alcohol is a group 1 carcinogen,” Rebbeck said. “Alcohol can cause cancer.”

Groups including the International Agency for Research on Cancer (IARC) and American Cancer Society agree that alcohol use is an established cause of seven types of cancer: Those of the oral cavity, larynx, pharynx, esophagus (squamous cell carcinoma), liver (hepatocellular carcinoma), breast, and colon/rectum. Heavy drinking — at least 8 standard drinks a week for women and 15 for men — and binge drinking — 4 or more drinks in 2 hours for women and 5 or more for men — only amplify that risk. (A “standard” drink has 14 g of alcohol, which translates to a 5-oz glass of wine.)

“We’re most concerned about high-risk drinking — more than 2 drinks a day — and/or binge drinking,” said Noelle LoConte, MD, of the Division of Hematology, Medical Oncology and Palliative Care, University of Wisconsin School of Medicine and Public Health, Madison, who authored a 2018 statement on alcohol and cancer risk from the American Society of Clinical Oncology (ASCO).

Compared with not drinking, heavy drinking is linked with a roughly fivefold increase in the risk for oral cavity, pharyngeal, and esophageal cancers, and a 61% increase in the risk for breast cancer, according to LoConte and colleagues.

Things get murkier when it comes to moderate drinking — defined as up to 1 standard drink per day for women and 2 per day for men. There is evidence, LoConte said, that moderate drinking is associated with increased cancer risks, though the magnitude is generally much less than heavier drinking.

Cancer type also matters. One analysis found that the risk for breast cancer increased with even light to moderate alcohol consumption. Compared with no drinking, light to moderate drinking has also been linked to increased risks for oral cavity, pharynx, larynx, and esophageal cancers.

As for whether the type of alcoholic beverage matters, LoConte said, there’s no clear physiological reason that wine would be less risky than beer or liquor. Research indicates that ethanol is the problematic ingredient: Once ingested, it’s metabolized into acetaldehyde, a DNA-damaging substance that’s considered a probable human carcinogen. Ethanol can also alter circulating levels of estrogens and androgens, LoConte said, which is thought to drive its association with breast cancer risk.

“It likely doesn’t matter how you choose to get your ethanol,” she said. “It’s a question of volume.”

Hints That Wine Is an Outlier

Still, some studies suggest that how people ingest ethanol could make a difference.

A study published in August in JAMA Network Open is a case in point. The study found that, among older adults, light to heavy drinkers had an increased risk of dying from cancer, compared with occasional drinkers (though the increased risk among light to moderate drinkers occurred only among people who also had chronic health conditions, such as diabetes or high blood pressure, or were of lower socioeconomic status).

Wine drinkers fared differently. Most notably, drinkers who “preferred” wine — consuming over 80% of total ethanol from wine — or those who drank only with meals showed a small reduction in their risk for cancer mortality and all-cause mortality (hazard ratio [HR], 0.94 for both). The small protective association was somewhat stronger among people who reported both patterns (HR, 0.88), especially if they were of lower socioeconomic status (HR, 0.79).

The findings are in line with other research suggesting that wine drinkers may be outliers when it comes to cancer risk. A 2023 meta-analysis of 26 observational studies, for instance, found no association between wine consumption and any cancer type, with the caveat that there was «substantial» heterogeneity among the studies.

This heterogeneity caveat speaks to the inherent limitations of observational research, said Tim Stockwell, PhD, of the Canadian Institute for Substance Use Research, University of Victoria in British Columbia, Canada.

“Individual studies of alcohol and cancer risk do find differences by type of drink, or patterns of drinking,” Stockwell said. “But it’s so hard to unpack the confounding that goes along with the type of person who’s a wine drinker or a beer drinker or a spirit drinker. The beverage of choice seems to come with a lot of baggage.”

Compared with people who favor beer or liquor, he noted, wine aficionados are typically higher-income, exercise more often, smoke less, and have different diets, for example. The “best” studies, Rebbeck said, try to adjust for those differences, but it’s challenging.

The authors of the 2023 meta-analysis noted that “many components in wine could have anticarcinogenic effects” that theoretically could counter the ill effects of ethanol. Besides resveratrol, which is mainly found in red wine, the list includes anthocyanins, quercetin, and tannins. However, the authors also acknowledged that they couldn’t account for whether other lifestyle habits might explain why wine drinkers, overall, showed no increased cancer risks and sometimes lower risks.

Still, groups such as the IARC and ASCO hold that there is no known “safe” level, or type, of alcohol when it comes to cancer.

In the latest Canadian guidelines on alcohol use, the scientific panel calculated that people who have 6 drinks a week throughout adulthood (whatever the source of the alcohol) could shave 11 weeks from their life expectancy, on average, said Stockwell, who was on the guideline panel. Compare that with heavy drinking, where 4 drinks a day could rob the average person of 2 or 3 years. “If you’re drinking a lot, you could get huge benefits from cutting down,” Stockwell explained. “If you’re a moderate drinker, the benefits would obviously be less.”

Stockwell said that choices around drinking and breast cancer risk, specifically, can be “tough.” Unlike many of the other alcohol-associated cancers, he noted, breast cancer is common — so even small relative risk increases may be concerning. Based on a 2020 meta-analysis of 22 cohort studies, the risk for breast cancer rises by about 10%, on average, for every 10 g of alcohol a woman drinks per day. This study also found no evidence that wine is any different from other types of alcohol.

In real life, the calculus around wine consumption and cancer risk will probably vary widely from person to person, Rebbeck said. One woman with a family history of breast cancer might decide that having wine with dinner isn’t worth it. Another with the same family history might see that glass of wine as a stress reliever and opt to focus on other ways to reduce her breast cancer risk — by exercising and maintaining a healthy weight, for example.

“The bottom line is, in human studies, the data on light to moderate drinking and cancer are limited and messy, and you can’t draw firm conclusions from them,” Rebbeck said. “It probably raises risk in some people, but we don’t know who those people are. And the risk increases are relatively small.”

A Conversation Few Are Having

Even with many studies highlighting the connection between alcohol consumption and cancer risk, most people remain unaware about this risk.

A 2023 study by the National Cancer Institute found that only a minority of US adults knew that drinking alcohol is linked to increased cancer risk, and they were much less likely to say that was true of wine: Only 20% did, vs 31% who said that liquor can boost cancer risk. Meanwhile, 10% believed that wine helps prevent cancer. Other studies show that even among cancer survivors and patients undergoing active cancer treatment, many drink — often heavily.

“What we know right now is, physicians almost never talk about this,” LoConte said.

That could be due to time constraints, according to Rebbeck, or clinicians’ perceptions that the subject is too complicated and/or their own confusion about the data. There could also be some “cognitive dissonance” at play, LoConte noted, because many doctors drink alcohol.

It’s critical, she said, that conversations about drinking habits become “normalized,” and that should include informing patients that alcohol use is associated with certain cancers. Again, LoConte said, it’s high-risk drinking that’s most concerning and where reducing intake could have the biggest impact on cancer risk and other health outcomes.

“From a cancer prevention standpoint, it’s probably best not to drink,” she said. “But people don’t make choices based solely on cancer risk. We don’t want to come out with recommendations saying no one should drink. I don’t think the data support that, and people would buck against that advice.”

Rebbeck made a similar point. Even if there’s uncertainty about the risks for a daily glass of wine, he said, people can use that information to make decisions. “Everybody’s preferences and choices are going to be different,” Rebbeck said. “And that’s all we can really do.”

A version of this article appeared on Medscape.com.

The evidence is clear: Alcohol can cause cancer.

Earlier this month, US surgeon general Vivek Murthy, MD, issued an advisory, calling for alcoholic beverages to carry a warning label about cancer risk. The advisory flagged alcohol as the third leading preventable cause of cancer in the United States, after tobacco and obesity, and highlighted people’s limited awareness about the relationship between alcohol and cancer risk.

But, when it comes to cancer risk, are all types of alcohol created equal?

For many years, red wine seemed to be an outlier, with studies indicating that, in moderation, it might even be good for you. Red wine has anti-inflammatory and antioxidant properties — most notably, it contains the antioxidant resveratrol. Starting in the 1990s, research began to hint that the compound might protect against heart disease, aging, and cancer, though much of this work was done in animals or test tubes.

The idea that red wine carries health benefits, however, has been called into question more recently. A recent meta-analysis, for instance, suggests that many previous studies touting the health benefits of more moderate drinking were likely biased, potentially leading to “misleading positive health associations.” And one recent study found that alcohol consumption, largely red wine and beer, at all levels was linked to an increased risk for cardiovascular disease.

Although wine’s health halo is dwindling, there might be an exception: Cancer risk.

Overall, research shows that even light to moderate drinking increases the risk for at least seven types of cancer, but when focusing on red wine, in particular, that risk calculus can look different.

“It’s very complicated and nuanced,” said Timothy Rebbeck, PhD, professor of cancer prevention, Harvard T.H. Chan School of Public Health, Boston. “And ‘complicated and nuanced’ doesn’t work very well in public health messages.”

The Knowns About Alcohol and Cancer Risk

Some things about the relationship between alcohol and cancer risk are crystal clear. “There’s no question that alcohol is a group 1 carcinogen,” Rebbeck said. “Alcohol can cause cancer.”

Groups including the International Agency for Research on Cancer (IARC) and American Cancer Society agree that alcohol use is an established cause of seven types of cancer: Those of the oral cavity, larynx, pharynx, esophagus (squamous cell carcinoma), liver (hepatocellular carcinoma), breast, and colon/rectum. Heavy drinking — at least 8 standard drinks a week for women and 15 for men — and binge drinking — 4 or more drinks in 2 hours for women and 5 or more for men — only amplify that risk. (A “standard” drink has 14 g of alcohol, which translates to a 5-oz glass of wine.)

“We’re most concerned about high-risk drinking — more than 2 drinks a day — and/or binge drinking,” said Noelle LoConte, MD, of the Division of Hematology, Medical Oncology and Palliative Care, University of Wisconsin School of Medicine and Public Health, Madison, who authored a 2018 statement on alcohol and cancer risk from the American Society of Clinical Oncology (ASCO).

Compared with not drinking, heavy drinking is linked with a roughly fivefold increase in the risk for oral cavity, pharyngeal, and esophageal cancers, and a 61% increase in the risk for breast cancer, according to LoConte and colleagues.

Things get murkier when it comes to moderate drinking — defined as up to 1 standard drink per day for women and 2 per day for men. There is evidence, LoConte said, that moderate drinking is associated with increased cancer risks, though the magnitude is generally much less than heavier drinking.

Cancer type also matters. One analysis found that the risk for breast cancer increased with even light to moderate alcohol consumption. Compared with no drinking, light to moderate drinking has also been linked to increased risks for oral cavity, pharynx, larynx, and esophageal cancers.

As for whether the type of alcoholic beverage matters, LoConte said, there’s no clear physiological reason that wine would be less risky than beer or liquor. Research indicates that ethanol is the problematic ingredient: Once ingested, it’s metabolized into acetaldehyde, a DNA-damaging substance that’s considered a probable human carcinogen. Ethanol can also alter circulating levels of estrogens and androgens, LoConte said, which is thought to drive its association with breast cancer risk.

“It likely doesn’t matter how you choose to get your ethanol,” she said. “It’s a question of volume.”

Hints That Wine Is an Outlier

Still, some studies suggest that how people ingest ethanol could make a difference.

A study published in August in JAMA Network Open is a case in point. The study found that, among older adults, light to heavy drinkers had an increased risk of dying from cancer, compared with occasional drinkers (though the increased risk among light to moderate drinkers occurred only among people who also had chronic health conditions, such as diabetes or high blood pressure, or were of lower socioeconomic status).

Wine drinkers fared differently. Most notably, drinkers who “preferred” wine — consuming over 80% of total ethanol from wine — or those who drank only with meals showed a small reduction in their risk for cancer mortality and all-cause mortality (hazard ratio [HR], 0.94 for both). The small protective association was somewhat stronger among people who reported both patterns (HR, 0.88), especially if they were of lower socioeconomic status (HR, 0.79).

The findings are in line with other research suggesting that wine drinkers may be outliers when it comes to cancer risk. A 2023 meta-analysis of 26 observational studies, for instance, found no association between wine consumption and any cancer type, with the caveat that there was «substantial» heterogeneity among the studies.

This heterogeneity caveat speaks to the inherent limitations of observational research, said Tim Stockwell, PhD, of the Canadian Institute for Substance Use Research, University of Victoria in British Columbia, Canada.

“Individual studies of alcohol and cancer risk do find differences by type of drink, or patterns of drinking,” Stockwell said. “But it’s so hard to unpack the confounding that goes along with the type of person who’s a wine drinker or a beer drinker or a spirit drinker. The beverage of choice seems to come with a lot of baggage.”

Compared with people who favor beer or liquor, he noted, wine aficionados are typically higher-income, exercise more often, smoke less, and have different diets, for example. The “best” studies, Rebbeck said, try to adjust for those differences, but it’s challenging.

The authors of the 2023 meta-analysis noted that “many components in wine could have anticarcinogenic effects” that theoretically could counter the ill effects of ethanol. Besides resveratrol, which is mainly found in red wine, the list includes anthocyanins, quercetin, and tannins. However, the authors also acknowledged that they couldn’t account for whether other lifestyle habits might explain why wine drinkers, overall, showed no increased cancer risks and sometimes lower risks.

Still, groups such as the IARC and ASCO hold that there is no known “safe” level, or type, of alcohol when it comes to cancer.

In the latest Canadian guidelines on alcohol use, the scientific panel calculated that people who have 6 drinks a week throughout adulthood (whatever the source of the alcohol) could shave 11 weeks from their life expectancy, on average, said Stockwell, who was on the guideline panel. Compare that with heavy drinking, where 4 drinks a day could rob the average person of 2 or 3 years. “If you’re drinking a lot, you could get huge benefits from cutting down,” Stockwell explained. “If you’re a moderate drinker, the benefits would obviously be less.”

Stockwell said that choices around drinking and breast cancer risk, specifically, can be “tough.” Unlike many of the other alcohol-associated cancers, he noted, breast cancer is common — so even small relative risk increases may be concerning. Based on a 2020 meta-analysis of 22 cohort studies, the risk for breast cancer rises by about 10%, on average, for every 10 g of alcohol a woman drinks per day. This study also found no evidence that wine is any different from other types of alcohol.

In real life, the calculus around wine consumption and cancer risk will probably vary widely from person to person, Rebbeck said. One woman with a family history of breast cancer might decide that having wine with dinner isn’t worth it. Another with the same family history might see that glass of wine as a stress reliever and opt to focus on other ways to reduce her breast cancer risk — by exercising and maintaining a healthy weight, for example.

“The bottom line is, in human studies, the data on light to moderate drinking and cancer are limited and messy, and you can’t draw firm conclusions from them,” Rebbeck said. “It probably raises risk in some people, but we don’t know who those people are. And the risk increases are relatively small.”

A Conversation Few Are Having

Even with many studies highlighting the connection between alcohol consumption and cancer risk, most people remain unaware about this risk.

A 2023 study by the National Cancer Institute found that only a minority of US adults knew that drinking alcohol is linked to increased cancer risk, and they were much less likely to say that was true of wine: Only 20% did, vs 31% who said that liquor can boost cancer risk. Meanwhile, 10% believed that wine helps prevent cancer. Other studies show that even among cancer survivors and patients undergoing active cancer treatment, many drink — often heavily.

“What we know right now is, physicians almost never talk about this,” LoConte said.

That could be due to time constraints, according to Rebbeck, or clinicians’ perceptions that the subject is too complicated and/or their own confusion about the data. There could also be some “cognitive dissonance” at play, LoConte noted, because many doctors drink alcohol.

It’s critical, she said, that conversations about drinking habits become “normalized,” and that should include informing patients that alcohol use is associated with certain cancers. Again, LoConte said, it’s high-risk drinking that’s most concerning and where reducing intake could have the biggest impact on cancer risk and other health outcomes.

“From a cancer prevention standpoint, it’s probably best not to drink,” she said. “But people don’t make choices based solely on cancer risk. We don’t want to come out with recommendations saying no one should drink. I don’t think the data support that, and people would buck against that advice.”

Rebbeck made a similar point. Even if there’s uncertainty about the risks for a daily glass of wine, he said, people can use that information to make decisions. “Everybody’s preferences and choices are going to be different,” Rebbeck said. “And that’s all we can really do.”

A version of this article appeared on Medscape.com.

TOPLINE:

Risk for dementia is nearly 80% higher in stroke survivors than in those without stroke, a new study reveals. The data suggest risk declines within 1 year after stroke but remains elevated for up to 20 years.

METHODOLOGY:

• Researchers conducted a population-wide analysis of over 15 million people in Canada between 2002 and 2022. The study focused on adults hospitalized for ischemic stroke, intracerebral hemorrhage, or acute myocardial infarction (AMI).
• Of 175,980 stroke survivors, 99% were matched 1:1 to residents without stroke on the basis of age, sex, rural residence, neighborhood deprivation, and vascular comorbidities. In addition, 90% of patients were matched to those with AMI.
• Incident dementia diagnoses were tracked starting 90 days after stroke until death, emigration, or the end of the study, using a validated algorithm based on hospitalization for dementia, prescriptions for cholinesterase inhibitors, or physician claims within 2 years.
• The mean follow-up duration was 5.6 years.

TAKEAWAY:

• Among stroke survivors, 19% were diagnosed with dementia vs 12.5% in the reference population. The dementia rate per 100 person-years was higher among stroke survivors than in the reference population over the entire follow-up period (3.34 vs 1.89).
• Over the entire study period, dementia was 76% more likely among stroke patients (hazard ratio [HR], 1.76; 95% CI, 1.73-1.79) and 82% more likely in the AMI cohort (HR, 1.82; 95% CI, 1.79-1.85) than in the reference population.
• Time-varying analysis revealed that dementia risk was highest within the first year after stroke, with a > 2.5-fold increase at 6 months (HR, 2.51; 95% CI, 2.42-2.59), which decreased to a 1.5-fold increase at 5 years (HR, 1.51; 95% CI, 1.48-1.56) but remained elevated compared with the reference population even 20 years after the index stroke.
• Recurrent stroke was associated with an approximately threefold increased risk for dementia (single recurrent stroke adjusted HR, 2.64; 95% CI, 2.54-2.74; multiple recurrent strokes adjusted HR, 3.05; 95% CI, 2.81-3.33).

IN PRACTICE:

“While much research has been focused on reducing the risk of a second stroke, our findings make it clear that more research also is needed on developing interventions to help prevent dementia after stroke,” lead author Raed A. Joundi, MD, DPhil, McMaster University, Hamilton, Ontario, Canada, said in a press release.

“There is a need to accelerate the implementation of promising interventions or multipronged approaches into large randomized controlled trials to lower the risk of dementia,” the investigators wrote.
 

SOURCE:

The study was published online on December 4 in Neurology.

LIMITATIONS:

The study’s limitations included reliance on administrative coding without imaging data, potential underestimation of mild dementia, and lack of granular information on stroke severity, disability, and prestroke cognitive decline. While adjustments were made for healthcare contact and secondary prevention medications, residual biases may have persisted.

DISCLOSURES:

This study received funding from the Canada Brain Research Fund, Heart & Stroke Foundation of Canada, and Canadian Stroke Consortium. Two authors hold awards and positions from national organizations and academic institutions in Canada. Additional details are provided in the original article.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Risk for dementia is nearly 80% higher in stroke survivors than in those without stroke, a new study reveals. The data suggest risk declines within 1 year after stroke but remains elevated for up to 20 years.

METHODOLOGY:

• Researchers conducted a population-wide analysis of over 15 million people in Canada between 2002 and 2022. The study focused on adults hospitalized for ischemic stroke, intracerebral hemorrhage, or acute myocardial infarction (AMI).
• Of 175,980 stroke survivors, 99% were matched 1:1 to residents without stroke on the basis of age, sex, rural residence, neighborhood deprivation, and vascular comorbidities. In addition, 90% of patients were matched to those with AMI.
• Incident dementia diagnoses were tracked starting 90 days after stroke until death, emigration, or the end of the study, using a validated algorithm based on hospitalization for dementia, prescriptions for cholinesterase inhibitors, or physician claims within 2 years.
• The mean follow-up duration was 5.6 years.

TAKEAWAY:

• Among stroke survivors, 19% were diagnosed with dementia vs 12.5% in the reference population. The dementia rate per 100 person-years was higher among stroke survivors than in the reference population over the entire follow-up period (3.34 vs 1.89).
• Over the entire study period, dementia was 76% more likely among stroke patients (hazard ratio [HR], 1.76; 95% CI, 1.73-1.79) and 82% more likely in the AMI cohort (HR, 1.82; 95% CI, 1.79-1.85) than in the reference population.
• Time-varying analysis revealed that dementia risk was highest within the first year after stroke, with a > 2.5-fold increase at 6 months (HR, 2.51; 95% CI, 2.42-2.59), which decreased to a 1.5-fold increase at 5 years (HR, 1.51; 95% CI, 1.48-1.56) but remained elevated compared with the reference population even 20 years after the index stroke.
• Recurrent stroke was associated with an approximately threefold increased risk for dementia (single recurrent stroke adjusted HR, 2.64; 95% CI, 2.54-2.74; multiple recurrent strokes adjusted HR, 3.05; 95% CI, 2.81-3.33).

IN PRACTICE:

“While much research has been focused on reducing the risk of a second stroke, our findings make it clear that more research also is needed on developing interventions to help prevent dementia after stroke,” lead author Raed A. Joundi, MD, DPhil, McMaster University, Hamilton, Ontario, Canada, said in a press release.

“There is a need to accelerate the implementation of promising interventions or multipronged approaches into large randomized controlled trials to lower the risk of dementia,” the investigators wrote.
 

SOURCE:

The study was published online on December 4 in Neurology.

LIMITATIONS:

The study’s limitations included reliance on administrative coding without imaging data, potential underestimation of mild dementia, and lack of granular information on stroke severity, disability, and prestroke cognitive decline. While adjustments were made for healthcare contact and secondary prevention medications, residual biases may have persisted.

DISCLOSURES:

This study received funding from the Canada Brain Research Fund, Heart & Stroke Foundation of Canada, and Canadian Stroke Consortium. Two authors hold awards and positions from national organizations and academic institutions in Canada. Additional details are provided in the original article.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Risk for dementia is nearly 80% higher in stroke survivors than in those without stroke, a new study reveals. The data suggest risk declines within 1 year after stroke but remains elevated for up to 20 years.

METHODOLOGY:

• Researchers conducted a population-wide analysis of over 15 million people in Canada between 2002 and 2022. The study focused on adults hospitalized for ischemic stroke, intracerebral hemorrhage, or acute myocardial infarction (AMI).
• Of 175,980 stroke survivors, 99% were matched 1:1 to residents without stroke on the basis of age, sex, rural residence, neighborhood deprivation, and vascular comorbidities. In addition, 90% of patients were matched to those with AMI.
• Incident dementia diagnoses were tracked starting 90 days after stroke until death, emigration, or the end of the study, using a validated algorithm based on hospitalization for dementia, prescriptions for cholinesterase inhibitors, or physician claims within 2 years.
• The mean follow-up duration was 5.6 years.

TAKEAWAY:

• Among stroke survivors, 19% were diagnosed with dementia vs 12.5% in the reference population. The dementia rate per 100 person-years was higher among stroke survivors than in the reference population over the entire follow-up period (3.34 vs 1.89).
• Over the entire study period, dementia was 76% more likely among stroke patients (hazard ratio [HR], 1.76; 95% CI, 1.73-1.79) and 82% more likely in the AMI cohort (HR, 1.82; 95% CI, 1.79-1.85) than in the reference population.
• Time-varying analysis revealed that dementia risk was highest within the first year after stroke, with a > 2.5-fold increase at 6 months (HR, 2.51; 95% CI, 2.42-2.59), which decreased to a 1.5-fold increase at 5 years (HR, 1.51; 95% CI, 1.48-1.56) but remained elevated compared with the reference population even 20 years after the index stroke.
• Recurrent stroke was associated with an approximately threefold increased risk for dementia (single recurrent stroke adjusted HR, 2.64; 95% CI, 2.54-2.74; multiple recurrent strokes adjusted HR, 3.05; 95% CI, 2.81-3.33).

IN PRACTICE:

“While much research has been focused on reducing the risk of a second stroke, our findings make it clear that more research also is needed on developing interventions to help prevent dementia after stroke,” lead author Raed A. Joundi, MD, DPhil, McMaster University, Hamilton, Ontario, Canada, said in a press release.

“There is a need to accelerate the implementation of promising interventions or multipronged approaches into large randomized controlled trials to lower the risk of dementia,” the investigators wrote.
 

SOURCE:

The study was published online on December 4 in Neurology.

LIMITATIONS:

The study’s limitations included reliance on administrative coding without imaging data, potential underestimation of mild dementia, and lack of granular information on stroke severity, disability, and prestroke cognitive decline. While adjustments were made for healthcare contact and secondary prevention medications, residual biases may have persisted.

DISCLOSURES:

This study received funding from the Canada Brain Research Fund, Heart & Stroke Foundation of Canada, and Canadian Stroke Consortium. Two authors hold awards and positions from national organizations and academic institutions in Canada. Additional details are provided in the original article.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.