With the discovery of autoantibodies and other risk factors for rheumatoid arthritis (RA), researchers developed clinical trials to see whether the disease can be prevented entirely. In the past 10 years, a number of these trials have concluded, with variable results.

While some trials demonstrated no effect at all, others showed that medical intervention can delay the onset of disease in certain populations and even reduce the rates of progression to RA. These completed trials also offer researchers the chance to identify opportunities to improve RA prevention trials moving forward.

“We’re looking at all that data and trying to figure out what the next step is going to be,” said Kevin Deane, MD, PhD, a professor of medicine and a rheumatologist at the University of Colorado School of Medicine, Aurora.

Key lessons include the need for improved risk stratification tools and better understanding of RA pathogenesis, he said.
 

The Research So Far

All RA prevention trials except for one have been completed and/or published within the past decade, bringing valuable insights to the field. (See chart below.)

MDedge News

Atorvastatin (STAPRA) and hydroxychloroquine (StopRA) proved ineffective in preventing the onset of RA, and both trials were stopped early. Rituximab and methotrexate (MTX) both delayed the onset of RA, but the effect disappeared by the end of the follow-up periods.

However, the 2-year results from the TREAT EARLIER trial showed that compared with patients given placebo, those given MTX showed improved MRI-detected joint inflammation, physical functioning, and reported symptoms.

The 4-year analysis of the trial further risk stratified participants and found that MTX showed a preventive effect in anti–citrullinated protein antibody (ACPA)–negative participants at an increased risk for RA.

Abatacept also showed promise in preventing RA in two separate trials. In the ARIAA trial, compared with placebo, 6 months of treatment with abatacept reduced MRI inflammation and symptoms and lowered the rates of progression to RA. This treatment effect lessened during the 1-year follow-up period, but the difference between the two groups was still significant at 18 months.

In the APIPPRA trial, 12 months of treatment with abatacept improved subclinical inflammation and quality-of-life measures in participants and reduced the rates of progression to RA through another 12 months of observation. However, during this post-treatment follow-up period, the treatment effect began to diminish.

While there have been some promising findings — not only in disease prevention but also in disease modification — these studies all looked at different patient groups, noted Kulveer Mankia, MA, DM, an associate professor and consulting rheumatologist at the Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds in England.

“You have disparate, different inclusion criteria in different studies, all of which take years to complete,” he said. For example, while the TREAT EARLIER trial recruited patients with joint pain and subclinical joint inflammation via MRI, regardless of autoantibody status, the APIPPRA trial enrolled patients that were both ACPA+ and rheumatoid factor (RF)+ with joint pain.

“You’re left extrapolating as to whether [these interventions] will work in different at-risk populations,” he said.

Even with specific inclusion criteria in each study, there can still be heterogeneity in risk within a study group, Deane said. In the TREAT EARLIER study, 18%-20% of participants ultimately developed RA over the study period, which is lower than expected.

“While it seemed like a pretty high-risk group, it wasn’t as high risk as we thought,” he said, “and that’s why we’ve gone back to the drawing board.”
 

Risk Stratification Efforts

There are now two ongoing joint efforts by the American College of Rheumatology (ACR) and the European Alliance of Associations for Rheumatology (EULAR) to define these populations and “bring some consensus to the field,” Mankia said.

Voisin / Science Source

The first aims to create a unanimous risk stratification tool for future RA prevention studies. The proposed system, devised for individuals with new joint symptoms who are at a risk for RA, was presented at the EULAR 2024 annual meeting and will be further discussed at the upcoming ACR 2024 annual meeting in Washington, DC.

The system uses a point system based on six criteria — three lab tests and three criteria commonly assessed in clinical practice:

• Morning stiffness
• Patient-reported joint swelling
• Difficulty making a fist
• Increased C-reactive protein
• RF positivity
• ACPA positivity

These criteria were picked so that the risk stratification tool can be used without imaging; however, the inclusion of MRI can further refine the score.

The ACR-EULAR task force that created the tool has emphasized that this criterion is specifically designed for research purposes and should not be used in clinical practice. Using this stratification tool should allow future clinical studies to group patients by similar risk, Deane said.

“Not that all studies have to look at exactly the same people, but each study should have similar risk stratification,” he said.

The second ACR-EULAR joint effort is taking a population-based approach to risk stratification, Deane said, to better predict RA risk in individuals without common symptoms like joint pain.

The aim is to create something analogous to the Framingham Risk Score in predicting cardiovascular disease, in which simple variables like total cholesterol, high-density lipoprotein cholesterol, systolic blood pressure, and smoking status can be used to calculate an individual’s 10-year risk for CVD, Deane explained.

The second approach could also identify patients earlier in the progression to RA, which may be easier to treat than later stages of disease.
 

Understanding RA Origins

However, treating an earlier stage of disease might require a different approach. Up to this point, medical interventions for RA prevention used drugs approved to treat RA, but inventions during the pre-RA stage — before any joint symptoms appear — might require targeting different immunologic pathways.

“The general concept is if there is a pre-RA stage when joints are not involved, that means all the immunologic abnormalities are probably happening somewhere else in the body,” he said. “The big question is: Where is that, and how exactly is that happening?”

One theory is that RA begins to develop in mucosal sites, such as the intestines or lungs, before it involves synovial joints.

“In the absence of resolution, these localized immune processes transition into a systemic process that targets the joints, either by direct effects of microbiota, molecular mimicry, and/or immune amplification,” wrote Deane and coauthors in a recent review article in Annals of the Rheumatic Diseases. “This, in turn, leads to inappropriate engagement of a range of effector mechanisms in both synovium and periarticular sites.”

Following this logic, the progression of the at-risk stage of RA could be considered a continuum along which there are multiple possible points for intervention. It’s also probable that the disease can develop through multiple pathways, Deane said.

“If you look at all the people who get rheumatoid arthritis, there’s probably no way those could have the same exact pathways,” he said. “There’s probably going to be different endotypes and understanding that is going to help us prevent disease in a better way.”
 

Looking Forward

Beyond improving risk stratification and understanding RA pathogenesis, researchers are also considering novel therapeutic approaches for future trials. Glucagon-like peptide 1 (GLP-1) receptor agonists could be worth exploring in RA prevention and treatment, said Jeffrey A. Sparks, MD, MMSc, a rheumatologist at Brigham and Women’s Hospital, Boston, Massachusetts.

These drugs — initially developed for diabetes — have already shown anti-inflammatory effects, and one study suggested that GLP-1s lowered the risk for major adverse cardiovascular events and all-cause mortality in individuals with immune-mediated inflammatory diseases. Obesity is a known risk factor for RA, so weight loss aided by GLP-1 drugs could also help reduce risk in certain patients. Clinical trials are needed to explore GLP-1s for both RA prevention and treatment, he said.

While prevention trials up to this point have used one-time, time-limited interventions, longer durations of medication or multiple rounds of therapy may be more efficacious. Even for trials that demonstrated the intervention arms had less progression to RA, this effect diminished once participants stopped the medication. In the ARIAA and APIPPRA trials using abatacept, “it wasn’t like we hit a reset button and [patients] just permanently now did not get rheumatoid arthritis,” Deane said, suggesting that alternative approaches should be explored.

“Future studies need to look at potentially longer doses of drug or lower doses of drug, or some combination that might be effective,” he said.

Deane received honoraria from Bristol-Myers Squibb, Thermo Fisher, and Werfen and grant funding from Janssen Research and Development and Gilead Sciences. Mankia received grant support from Gilead, Lilly, AstraZeneca, and Serac Life Sciences and honoraria or consultant fees from AbbVie, UCB, Lilly, Galapagos, DeepCure, Serac Life Sciences, AstraZeneca, and Zura Bio. Sparks received research support from Boehringer Ingelheim, Bristol-Myers Squibb, Janssen, and Sonoma Biotherapeutics. He consulted for AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Gilead, Inova Diagnostics, Janssen, Merck, Mustang, Optum, Pfizer, ReCor Medical, Sana, Sobi, and UCB.

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

With the discovery of autoantibodies and other risk factors for rheumatoid arthritis (RA), researchers developed clinical trials to see whether the disease can be prevented entirely. In the past 10 years, a number of these trials have concluded, with variable results.

While some trials demonstrated no effect at all, others showed that medical intervention can delay the onset of disease in certain populations and even reduce the rates of progression to RA. These completed trials also offer researchers the chance to identify opportunities to improve RA prevention trials moving forward.

“We’re looking at all that data and trying to figure out what the next step is going to be,” said Kevin Deane, MD, PhD, a professor of medicine and a rheumatologist at the University of Colorado School of Medicine, Aurora.

Key lessons include the need for improved risk stratification tools and better understanding of RA pathogenesis, he said.
 

The Research So Far

All RA prevention trials except for one have been completed and/or published within the past decade, bringing valuable insights to the field. (See chart below.)

MDedge News

Atorvastatin (STAPRA) and hydroxychloroquine (StopRA) proved ineffective in preventing the onset of RA, and both trials were stopped early. Rituximab and methotrexate (MTX) both delayed the onset of RA, but the effect disappeared by the end of the follow-up periods.

However, the 2-year results from the TREAT EARLIER trial showed that compared with patients given placebo, those given MTX showed improved MRI-detected joint inflammation, physical functioning, and reported symptoms.

The 4-year analysis of the trial further risk stratified participants and found that MTX showed a preventive effect in anti–citrullinated protein antibody (ACPA)–negative participants at an increased risk for RA.

Abatacept also showed promise in preventing RA in two separate trials. In the ARIAA trial, compared with placebo, 6 months of treatment with abatacept reduced MRI inflammation and symptoms and lowered the rates of progression to RA. This treatment effect lessened during the 1-year follow-up period, but the difference between the two groups was still significant at 18 months.

In the APIPPRA trial, 12 months of treatment with abatacept improved subclinical inflammation and quality-of-life measures in participants and reduced the rates of progression to RA through another 12 months of observation. However, during this post-treatment follow-up period, the treatment effect began to diminish.

While there have been some promising findings — not only in disease prevention but also in disease modification — these studies all looked at different patient groups, noted Kulveer Mankia, MA, DM, an associate professor and consulting rheumatologist at the Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds in England.

“You have disparate, different inclusion criteria in different studies, all of which take years to complete,” he said. For example, while the TREAT EARLIER trial recruited patients with joint pain and subclinical joint inflammation via MRI, regardless of autoantibody status, the APIPPRA trial enrolled patients that were both ACPA+ and rheumatoid factor (RF)+ with joint pain.

“You’re left extrapolating as to whether [these interventions] will work in different at-risk populations,” he said.

Even with specific inclusion criteria in each study, there can still be heterogeneity in risk within a study group, Deane said. In the TREAT EARLIER study, 18%-20% of participants ultimately developed RA over the study period, which is lower than expected.

“While it seemed like a pretty high-risk group, it wasn’t as high risk as we thought,” he said, “and that’s why we’ve gone back to the drawing board.”
 

Risk Stratification Efforts

There are now two ongoing joint efforts by the American College of Rheumatology (ACR) and the European Alliance of Associations for Rheumatology (EULAR) to define these populations and “bring some consensus to the field,” Mankia said.

Voisin / Science Source

The first aims to create a unanimous risk stratification tool for future RA prevention studies. The proposed system, devised for individuals with new joint symptoms who are at a risk for RA, was presented at the EULAR 2024 annual meeting and will be further discussed at the upcoming ACR 2024 annual meeting in Washington, DC.

The system uses a point system based on six criteria — three lab tests and three criteria commonly assessed in clinical practice:

• Morning stiffness
• Patient-reported joint swelling
• Difficulty making a fist
• Increased C-reactive protein
• RF positivity
• ACPA positivity

These criteria were picked so that the risk stratification tool can be used without imaging; however, the inclusion of MRI can further refine the score.

The ACR-EULAR task force that created the tool has emphasized that this criterion is specifically designed for research purposes and should not be used in clinical practice. Using this stratification tool should allow future clinical studies to group patients by similar risk, Deane said.

“Not that all studies have to look at exactly the same people, but each study should have similar risk stratification,” he said.

The second ACR-EULAR joint effort is taking a population-based approach to risk stratification, Deane said, to better predict RA risk in individuals without common symptoms like joint pain.

The aim is to create something analogous to the Framingham Risk Score in predicting cardiovascular disease, in which simple variables like total cholesterol, high-density lipoprotein cholesterol, systolic blood pressure, and smoking status can be used to calculate an individual’s 10-year risk for CVD, Deane explained.

The second approach could also identify patients earlier in the progression to RA, which may be easier to treat than later stages of disease.
 

Understanding RA Origins

However, treating an earlier stage of disease might require a different approach. Up to this point, medical interventions for RA prevention used drugs approved to treat RA, but inventions during the pre-RA stage — before any joint symptoms appear — might require targeting different immunologic pathways.

“The general concept is if there is a pre-RA stage when joints are not involved, that means all the immunologic abnormalities are probably happening somewhere else in the body,” he said. “The big question is: Where is that, and how exactly is that happening?”

One theory is that RA begins to develop in mucosal sites, such as the intestines or lungs, before it involves synovial joints.

“In the absence of resolution, these localized immune processes transition into a systemic process that targets the joints, either by direct effects of microbiota, molecular mimicry, and/or immune amplification,” wrote Deane and coauthors in a recent review article in Annals of the Rheumatic Diseases. “This, in turn, leads to inappropriate engagement of a range of effector mechanisms in both synovium and periarticular sites.”

Following this logic, the progression of the at-risk stage of RA could be considered a continuum along which there are multiple possible points for intervention. It’s also probable that the disease can develop through multiple pathways, Deane said.

“If you look at all the people who get rheumatoid arthritis, there’s probably no way those could have the same exact pathways,” he said. “There’s probably going to be different endotypes and understanding that is going to help us prevent disease in a better way.”
 

Looking Forward

Beyond improving risk stratification and understanding RA pathogenesis, researchers are also considering novel therapeutic approaches for future trials. Glucagon-like peptide 1 (GLP-1) receptor agonists could be worth exploring in RA prevention and treatment, said Jeffrey A. Sparks, MD, MMSc, a rheumatologist at Brigham and Women’s Hospital, Boston, Massachusetts.

These drugs — initially developed for diabetes — have already shown anti-inflammatory effects, and one study suggested that GLP-1s lowered the risk for major adverse cardiovascular events and all-cause mortality in individuals with immune-mediated inflammatory diseases. Obesity is a known risk factor for RA, so weight loss aided by GLP-1 drugs could also help reduce risk in certain patients. Clinical trials are needed to explore GLP-1s for both RA prevention and treatment, he said.

While prevention trials up to this point have used one-time, time-limited interventions, longer durations of medication or multiple rounds of therapy may be more efficacious. Even for trials that demonstrated the intervention arms had less progression to RA, this effect diminished once participants stopped the medication. In the ARIAA and APIPPRA trials using abatacept, “it wasn’t like we hit a reset button and [patients] just permanently now did not get rheumatoid arthritis,” Deane said, suggesting that alternative approaches should be explored.

“Future studies need to look at potentially longer doses of drug or lower doses of drug, or some combination that might be effective,” he said.

Deane received honoraria from Bristol-Myers Squibb, Thermo Fisher, and Werfen and grant funding from Janssen Research and Development and Gilead Sciences. Mankia received grant support from Gilead, Lilly, AstraZeneca, and Serac Life Sciences and honoraria or consultant fees from AbbVie, UCB, Lilly, Galapagos, DeepCure, Serac Life Sciences, AstraZeneca, and Zura Bio. Sparks received research support from Boehringer Ingelheim, Bristol-Myers Squibb, Janssen, and Sonoma Biotherapeutics. He consulted for AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Gilead, Inova Diagnostics, Janssen, Merck, Mustang, Optum, Pfizer, ReCor Medical, Sana, Sobi, and UCB.

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

With the discovery of autoantibodies and other risk factors for rheumatoid arthritis (RA), researchers developed clinical trials to see whether the disease can be prevented entirely. In the past 10 years, a number of these trials have concluded, with variable results.

While some trials demonstrated no effect at all, others showed that medical intervention can delay the onset of disease in certain populations and even reduce the rates of progression to RA. These completed trials also offer researchers the chance to identify opportunities to improve RA prevention trials moving forward.

“We’re looking at all that data and trying to figure out what the next step is going to be,” said Kevin Deane, MD, PhD, a professor of medicine and a rheumatologist at the University of Colorado School of Medicine, Aurora.

Key lessons include the need for improved risk stratification tools and better understanding of RA pathogenesis, he said.
 

The Research So Far

All RA prevention trials except for one have been completed and/or published within the past decade, bringing valuable insights to the field. (See chart below.)

MDedge News

Atorvastatin (STAPRA) and hydroxychloroquine (StopRA) proved ineffective in preventing the onset of RA, and both trials were stopped early. Rituximab and methotrexate (MTX) both delayed the onset of RA, but the effect disappeared by the end of the follow-up periods.

However, the 2-year results from the TREAT EARLIER trial showed that compared with patients given placebo, those given MTX showed improved MRI-detected joint inflammation, physical functioning, and reported symptoms.

The 4-year analysis of the trial further risk stratified participants and found that MTX showed a preventive effect in anti–citrullinated protein antibody (ACPA)–negative participants at an increased risk for RA.

Abatacept also showed promise in preventing RA in two separate trials. In the ARIAA trial, compared with placebo, 6 months of treatment with abatacept reduced MRI inflammation and symptoms and lowered the rates of progression to RA. This treatment effect lessened during the 1-year follow-up period, but the difference between the two groups was still significant at 18 months.

In the APIPPRA trial, 12 months of treatment with abatacept improved subclinical inflammation and quality-of-life measures in participants and reduced the rates of progression to RA through another 12 months of observation. However, during this post-treatment follow-up period, the treatment effect began to diminish.

While there have been some promising findings — not only in disease prevention but also in disease modification — these studies all looked at different patient groups, noted Kulveer Mankia, MA, DM, an associate professor and consulting rheumatologist at the Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds in England.

“You have disparate, different inclusion criteria in different studies, all of which take years to complete,” he said. For example, while the TREAT EARLIER trial recruited patients with joint pain and subclinical joint inflammation via MRI, regardless of autoantibody status, the APIPPRA trial enrolled patients that were both ACPA+ and rheumatoid factor (RF)+ with joint pain.

“You’re left extrapolating as to whether [these interventions] will work in different at-risk populations,” he said.

Even with specific inclusion criteria in each study, there can still be heterogeneity in risk within a study group, Deane said. In the TREAT EARLIER study, 18%-20% of participants ultimately developed RA over the study period, which is lower than expected.

“While it seemed like a pretty high-risk group, it wasn’t as high risk as we thought,” he said, “and that’s why we’ve gone back to the drawing board.”
 

Risk Stratification Efforts

There are now two ongoing joint efforts by the American College of Rheumatology (ACR) and the European Alliance of Associations for Rheumatology (EULAR) to define these populations and “bring some consensus to the field,” Mankia said.

Voisin / Science Source

The first aims to create a unanimous risk stratification tool for future RA prevention studies. The proposed system, devised for individuals with new joint symptoms who are at a risk for RA, was presented at the EULAR 2024 annual meeting and will be further discussed at the upcoming ACR 2024 annual meeting in Washington, DC.

The system uses a point system based on six criteria — three lab tests and three criteria commonly assessed in clinical practice:

• Morning stiffness
• Patient-reported joint swelling
• Difficulty making a fist
• Increased C-reactive protein
• RF positivity
• ACPA positivity

These criteria were picked so that the risk stratification tool can be used without imaging; however, the inclusion of MRI can further refine the score.

The ACR-EULAR task force that created the tool has emphasized that this criterion is specifically designed for research purposes and should not be used in clinical practice. Using this stratification tool should allow future clinical studies to group patients by similar risk, Deane said.

“Not that all studies have to look at exactly the same people, but each study should have similar risk stratification,” he said.

The second ACR-EULAR joint effort is taking a population-based approach to risk stratification, Deane said, to better predict RA risk in individuals without common symptoms like joint pain.

The aim is to create something analogous to the Framingham Risk Score in predicting cardiovascular disease, in which simple variables like total cholesterol, high-density lipoprotein cholesterol, systolic blood pressure, and smoking status can be used to calculate an individual’s 10-year risk for CVD, Deane explained.

The second approach could also identify patients earlier in the progression to RA, which may be easier to treat than later stages of disease.
 

Understanding RA Origins

However, treating an earlier stage of disease might require a different approach. Up to this point, medical interventions for RA prevention used drugs approved to treat RA, but inventions during the pre-RA stage — before any joint symptoms appear — might require targeting different immunologic pathways.

“The general concept is if there is a pre-RA stage when joints are not involved, that means all the immunologic abnormalities are probably happening somewhere else in the body,” he said. “The big question is: Where is that, and how exactly is that happening?”

One theory is that RA begins to develop in mucosal sites, such as the intestines or lungs, before it involves synovial joints.

“In the absence of resolution, these localized immune processes transition into a systemic process that targets the joints, either by direct effects of microbiota, molecular mimicry, and/or immune amplification,” wrote Deane and coauthors in a recent review article in Annals of the Rheumatic Diseases. “This, in turn, leads to inappropriate engagement of a range of effector mechanisms in both synovium and periarticular sites.”

Following this logic, the progression of the at-risk stage of RA could be considered a continuum along which there are multiple possible points for intervention. It’s also probable that the disease can develop through multiple pathways, Deane said.

“If you look at all the people who get rheumatoid arthritis, there’s probably no way those could have the same exact pathways,” he said. “There’s probably going to be different endotypes and understanding that is going to help us prevent disease in a better way.”
 

Looking Forward

Beyond improving risk stratification and understanding RA pathogenesis, researchers are also considering novel therapeutic approaches for future trials. Glucagon-like peptide 1 (GLP-1) receptor agonists could be worth exploring in RA prevention and treatment, said Jeffrey A. Sparks, MD, MMSc, a rheumatologist at Brigham and Women’s Hospital, Boston, Massachusetts.

These drugs — initially developed for diabetes — have already shown anti-inflammatory effects, and one study suggested that GLP-1s lowered the risk for major adverse cardiovascular events and all-cause mortality in individuals with immune-mediated inflammatory diseases. Obesity is a known risk factor for RA, so weight loss aided by GLP-1 drugs could also help reduce risk in certain patients. Clinical trials are needed to explore GLP-1s for both RA prevention and treatment, he said.

While prevention trials up to this point have used one-time, time-limited interventions, longer durations of medication or multiple rounds of therapy may be more efficacious. Even for trials that demonstrated the intervention arms had less progression to RA, this effect diminished once participants stopped the medication. In the ARIAA and APIPPRA trials using abatacept, “it wasn’t like we hit a reset button and [patients] just permanently now did not get rheumatoid arthritis,” Deane said, suggesting that alternative approaches should be explored.

“Future studies need to look at potentially longer doses of drug or lower doses of drug, or some combination that might be effective,” he said.

Deane received honoraria from Bristol-Myers Squibb, Thermo Fisher, and Werfen and grant funding from Janssen Research and Development and Gilead Sciences. Mankia received grant support from Gilead, Lilly, AstraZeneca, and Serac Life Sciences and honoraria or consultant fees from AbbVie, UCB, Lilly, Galapagos, DeepCure, Serac Life Sciences, AstraZeneca, and Zura Bio. Sparks received research support from Boehringer Ingelheim, Bristol-Myers Squibb, Janssen, and Sonoma Biotherapeutics. He consulted for AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Gilead, Inova Diagnostics, Janssen, Merck, Mustang, Optum, Pfizer, ReCor Medical, Sana, Sobi, and UCB.

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

Our current healthcare system, which is a costly and unending cycle of merely managing chronic disease symptoms, is failing us. What we truly need is a patient-centered approach that restores health by addressing not just diagnoses but also the physical, emotional, and social needs of each individual. This is the essence of whole-person health, and transformation toward this model of care is already underway.

This shift underscores why clinicians like me support placing lifestyle medicine at the foundation of health and healthcare. Evidence-based lifestyle medicine — which applies interventions in nutrition, physical activity, restorative sleep, stress management, positive social connections, and avoidance of risky substances to prevent, treat, and when used intensively, even reverse lifestyle-related chronic disease — is a medical specialty equipped to successfully address patients’ whole-person health in an effective, high-value clinical care delivery model.

As this transformation continues, here are four key lifestyle medicine trends for 2025.
 

Lifestyle Medicine Becomes More Ingrained in Primary Care

The 2021 National Academies of Science, Engineering, and Medicine report, “Implementing High-Quality Primary Care” sounded the alarm about the state of primary care and outlined a comprehensive approach to transform it. Lifestyle medicine emerged as a solution as clinicians found innovative ways to integrate lifestyle behavior interventions into existing care models in a financially sustainable, scalable manner. Examples include Blue Zones Health, a new delivery model that aligns lifestyle medicine–certified clinicians with community and payers in California, and the University of Pittsburgh Medical Center lifestyle medicine program, where primary care patients are referred to virtual group coaching, a teaching kitchen, and classes on food as medicine, obesity, type 2 diabetes, and more.

Organizations dedicated to advancing primary care are paying close attention to the potential of lifestyle medicine. Currently, The Primary Care Collaborative has launched a new multi-year initiative on whole-person care and lifestyle medicine. This initiative aims to broaden the primary care community’s understanding of whole health and lifestyle medicine concepts and the evidence behind them, as well as lay the groundwork for future work to promote whole-person primary care and lifestyle medicine among an engaged and committed community of members. 
 

Digital Tools and AI Spark Lifestyle Medicine Innovations

American College of Lifestyle Medicine partner organizations are increasingly utilizing digital tools, such as health apps tailored to lifestyle behavior interventions, to expand access to care and support behavior change. One of the biggest challenges in lifestyle interventions is the limited time during patient encounters. But artificial intelligence (AI) tools can record (with patient permission) and summarize encounters, enabling clinicians to turn away from their keyboards and be more present to learn about the unique living, environmental, and societal factors that impact every individual’s lifestyle choices. AI tools can create individualized whole-food, plant-predominant meal plans or physical activity schedules for patients in just a few seconds. The potential for AI in lifestyle medicine is vast, and its applications were further explored at the American College of Lifestyle Medicine’s annual conference in October.

Behavior Change and Sustainability of the Food-as-Medicine Movement

Significant investments have been made in food as medicine to address diet-related chronic diseases. But merely providing medically tailored meals or produce prescriptions is not enough because once the prescriptions end, so will the health benefits. Clinicians certified in lifestyle medicine are prepared to coach patients into long-term behavior change, supporting them with education and information to shop for and prepare tasty, nutritious, and affordable food. The same applies to the use of glucagon-like peptide 1 drugs. Although the initial weight loss offers motivation, lifestyle changes are necessary to sustain long-term health benefits beyond medications.

Lifestyle Medicine Emerges as a Strategy to Achieve Health Equity 

Lifestyle behavior interventions have the unique ability to address health status and social drivers of health. For example, food as medicine affects an individual’s health while also addressing nutrition security. Certainly, no medication can both improve health status and feed someone. The addition of payment for the screening of social drivers of health to the 2024 Medicare Physician Fee Schedule is an important step toward connecting clinicians with community health–based organizations that can address factors that influence patients’ ability to adhere to lifestyle behavior care plans. Lifestyle medicine clinicians are poised to lead this effort because they are already having conversations with patients about their environment, living conditions, and access to nutritious food. 

The changes coming to our healthcare system are exciting and long overdue. Lifestyle medicine is positioned to be at the forefront of this transformation now and in the future.

Dr. Patel, president of the American College of Lifestyle Medicine in St. Louis, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Our current healthcare system, which is a costly and unending cycle of merely managing chronic disease symptoms, is failing us. What we truly need is a patient-centered approach that restores health by addressing not just diagnoses but also the physical, emotional, and social needs of each individual. This is the essence of whole-person health, and transformation toward this model of care is already underway.

This shift underscores why clinicians like me support placing lifestyle medicine at the foundation of health and healthcare. Evidence-based lifestyle medicine — which applies interventions in nutrition, physical activity, restorative sleep, stress management, positive social connections, and avoidance of risky substances to prevent, treat, and when used intensively, even reverse lifestyle-related chronic disease — is a medical specialty equipped to successfully address patients’ whole-person health in an effective, high-value clinical care delivery model.

As this transformation continues, here are four key lifestyle medicine trends for 2025.
 

Lifestyle Medicine Becomes More Ingrained in Primary Care

The 2021 National Academies of Science, Engineering, and Medicine report, “Implementing High-Quality Primary Care” sounded the alarm about the state of primary care and outlined a comprehensive approach to transform it. Lifestyle medicine emerged as a solution as clinicians found innovative ways to integrate lifestyle behavior interventions into existing care models in a financially sustainable, scalable manner. Examples include Blue Zones Health, a new delivery model that aligns lifestyle medicine–certified clinicians with community and payers in California, and the University of Pittsburgh Medical Center lifestyle medicine program, where primary care patients are referred to virtual group coaching, a teaching kitchen, and classes on food as medicine, obesity, type 2 diabetes, and more.

Organizations dedicated to advancing primary care are paying close attention to the potential of lifestyle medicine. Currently, The Primary Care Collaborative has launched a new multi-year initiative on whole-person care and lifestyle medicine. This initiative aims to broaden the primary care community’s understanding of whole health and lifestyle medicine concepts and the evidence behind them, as well as lay the groundwork for future work to promote whole-person primary care and lifestyle medicine among an engaged and committed community of members. 
 

Digital Tools and AI Spark Lifestyle Medicine Innovations

American College of Lifestyle Medicine partner organizations are increasingly utilizing digital tools, such as health apps tailored to lifestyle behavior interventions, to expand access to care and support behavior change. One of the biggest challenges in lifestyle interventions is the limited time during patient encounters. But artificial intelligence (AI) tools can record (with patient permission) and summarize encounters, enabling clinicians to turn away from their keyboards and be more present to learn about the unique living, environmental, and societal factors that impact every individual’s lifestyle choices. AI tools can create individualized whole-food, plant-predominant meal plans or physical activity schedules for patients in just a few seconds. The potential for AI in lifestyle medicine is vast, and its applications were further explored at the American College of Lifestyle Medicine’s annual conference in October.

Behavior Change and Sustainability of the Food-as-Medicine Movement

Significant investments have been made in food as medicine to address diet-related chronic diseases. But merely providing medically tailored meals or produce prescriptions is not enough because once the prescriptions end, so will the health benefits. Clinicians certified in lifestyle medicine are prepared to coach patients into long-term behavior change, supporting them with education and information to shop for and prepare tasty, nutritious, and affordable food. The same applies to the use of glucagon-like peptide 1 drugs. Although the initial weight loss offers motivation, lifestyle changes are necessary to sustain long-term health benefits beyond medications.

Lifestyle Medicine Emerges as a Strategy to Achieve Health Equity 

Lifestyle behavior interventions have the unique ability to address health status and social drivers of health. For example, food as medicine affects an individual’s health while also addressing nutrition security. Certainly, no medication can both improve health status and feed someone. The addition of payment for the screening of social drivers of health to the 2024 Medicare Physician Fee Schedule is an important step toward connecting clinicians with community health–based organizations that can address factors that influence patients’ ability to adhere to lifestyle behavior care plans. Lifestyle medicine clinicians are poised to lead this effort because they are already having conversations with patients about their environment, living conditions, and access to nutritious food. 

The changes coming to our healthcare system are exciting and long overdue. Lifestyle medicine is positioned to be at the forefront of this transformation now and in the future.

Dr. Patel, president of the American College of Lifestyle Medicine in St. Louis, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Our current healthcare system, which is a costly and unending cycle of merely managing chronic disease symptoms, is failing us. What we truly need is a patient-centered approach that restores health by addressing not just diagnoses but also the physical, emotional, and social needs of each individual. This is the essence of whole-person health, and transformation toward this model of care is already underway.

This shift underscores why clinicians like me support placing lifestyle medicine at the foundation of health and healthcare. Evidence-based lifestyle medicine — which applies interventions in nutrition, physical activity, restorative sleep, stress management, positive social connections, and avoidance of risky substances to prevent, treat, and when used intensively, even reverse lifestyle-related chronic disease — is a medical specialty equipped to successfully address patients’ whole-person health in an effective, high-value clinical care delivery model.

As this transformation continues, here are four key lifestyle medicine trends for 2025.
 

Lifestyle Medicine Becomes More Ingrained in Primary Care

The 2021 National Academies of Science, Engineering, and Medicine report, “Implementing High-Quality Primary Care” sounded the alarm about the state of primary care and outlined a comprehensive approach to transform it. Lifestyle medicine emerged as a solution as clinicians found innovative ways to integrate lifestyle behavior interventions into existing care models in a financially sustainable, scalable manner. Examples include Blue Zones Health, a new delivery model that aligns lifestyle medicine–certified clinicians with community and payers in California, and the University of Pittsburgh Medical Center lifestyle medicine program, where primary care patients are referred to virtual group coaching, a teaching kitchen, and classes on food as medicine, obesity, type 2 diabetes, and more.

Organizations dedicated to advancing primary care are paying close attention to the potential of lifestyle medicine. Currently, The Primary Care Collaborative has launched a new multi-year initiative on whole-person care and lifestyle medicine. This initiative aims to broaden the primary care community’s understanding of whole health and lifestyle medicine concepts and the evidence behind them, as well as lay the groundwork for future work to promote whole-person primary care and lifestyle medicine among an engaged and committed community of members. 
 

Digital Tools and AI Spark Lifestyle Medicine Innovations

American College of Lifestyle Medicine partner organizations are increasingly utilizing digital tools, such as health apps tailored to lifestyle behavior interventions, to expand access to care and support behavior change. One of the biggest challenges in lifestyle interventions is the limited time during patient encounters. But artificial intelligence (AI) tools can record (with patient permission) and summarize encounters, enabling clinicians to turn away from their keyboards and be more present to learn about the unique living, environmental, and societal factors that impact every individual’s lifestyle choices. AI tools can create individualized whole-food, plant-predominant meal plans or physical activity schedules for patients in just a few seconds. The potential for AI in lifestyle medicine is vast, and its applications were further explored at the American College of Lifestyle Medicine’s annual conference in October.

Behavior Change and Sustainability of the Food-as-Medicine Movement

Significant investments have been made in food as medicine to address diet-related chronic diseases. But merely providing medically tailored meals or produce prescriptions is not enough because once the prescriptions end, so will the health benefits. Clinicians certified in lifestyle medicine are prepared to coach patients into long-term behavior change, supporting them with education and information to shop for and prepare tasty, nutritious, and affordable food. The same applies to the use of glucagon-like peptide 1 drugs. Although the initial weight loss offers motivation, lifestyle changes are necessary to sustain long-term health benefits beyond medications.

Lifestyle Medicine Emerges as a Strategy to Achieve Health Equity 

Lifestyle behavior interventions have the unique ability to address health status and social drivers of health. For example, food as medicine affects an individual’s health while also addressing nutrition security. Certainly, no medication can both improve health status and feed someone. The addition of payment for the screening of social drivers of health to the 2024 Medicare Physician Fee Schedule is an important step toward connecting clinicians with community health–based organizations that can address factors that influence patients’ ability to adhere to lifestyle behavior care plans. Lifestyle medicine clinicians are poised to lead this effort because they are already having conversations with patients about their environment, living conditions, and access to nutritious food. 

The changes coming to our healthcare system are exciting and long overdue. Lifestyle medicine is positioned to be at the forefront of this transformation now and in the future.

Dr. Patel, president of the American College of Lifestyle Medicine in St. Louis, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

TOPLINE:

Patients with cutaneous lupus erythematosus (CLE) experienced improved symptoms with iberdomide, a cereblon modulator, added to standard lupus medications, particularly in subacute and chronic cases.

METHODOLOGY:

• Researchers conducted a randomized phase 2 trial to evaluate the efficacy and safety of iberdomide in 288 patients with CLE (mean age, 45 years; 97% women). Iberdomide is a cereblon modulator, which results in degradation of two transcription factors of immune cell development and homeostasis — Ikaros and Aiolos — that have been implicated in the genetic predisposition of systemic lupus.
• CLE Disease Area and Severity Index Activity (CLASI-A) endpoints included mean percent change from baseline and ≥ 50% reduction from baseline (CLASI-50), which were evaluated in all patients with baseline CLASI-A scores ≥ 8 and by CLE subtypes (acute, subacute, and chronic).
• At baseline, 56% of patients had acute CLE, 29% had chronic CLE, and 16% had subacute CLE; 28% of patients had a baseline CLASI-A score ≥ 8.
• Patients were randomly assigned to receive oral iberdomide (0.45 mg, 0.30 mg, 0.15 mg, or placebo daily) for 24 weeks while continuing standard lupus medications. At week 24, patients on placebo were rerandomized to iberdomide 0.45 mg or 0.30 mg once a day, while those on iberdomide continued their assigned dose through week 52.

TAKEAWAY:

• Among patients with baseline CLASI-A ≥ 8, the mean change in CLASI-A score from baseline at week 24 was −66.7% for those on iberdomide 0.45 mg vs −54.2% for placebo (P = .295).
• At week 24, patients with subacute CLE showed a significantly greater mean percent change from baseline in CLASI-A with iberdomide 0.45 mg vs placebo (−90.5% vs −51.2%; P = .007), while no significant differences were observed with the 0.45-mg dose vs placebo in patients with chronic or acute CLE.
• Overall, CLASI-50 responses were not significantly different among those on 0.45 mg vs placebo (55.6% vs 44.6%). The proportions of patients achieving CLASI-50 at week 24 were significantly greater for iberdomide 0.45 mg vs placebo for those with subacute CLE (91.7% vs 52.9%; P = .035) and chronic CLE (62.1% vs 27.8%; P = .029), but not for those with baseline CLASI-A ≥ 8 (66.7% vs 50%).
• More than 80% of patients had treatment-emergent adverse events (TEAEs), which were mostly mild to moderate. Over 2 years, the most common were urinary tract infections, upper respiratory tract infections, neutropenia, and nasopharyngitis. TEAEs leading to iberdomide discontinuation in one or more patients were neutropenia (n = 7), rash (n = 7), increased hepatic enzymes (n = 4), and deep vein thrombosis (n = 3).

IN PRACTICE:

“Data from this phase 2 trial of iberdomide in patients with SLE suggest that a greater proportion of patients with subacute or chronic CLE who received the higher dose of 0.45 mg iberdomide achieved CLASI-50 vs placebo. For the overall population, CLASI-50 response was not significantly different between treatment groups at week 24, partly due to a high placebo response that may have been driven by patients with acute CLE,” the authors wrote.

SOURCE:

The study was led by Victoria P. Werth, MD, of the University of Pennsylvania and the Veteran’s Administration Medical Center, both in Philadelphia, and was published online in the Journal of the American Academy of Dermatology.

LIMITATIONS:

The study included small patient subgroups for different CLE subtypes, which may affect the generalizability of the findings. CLE subtype was determined by the investigator without additional photographic adjudication. Additionally, the use of background lupus medications could have influenced the placebo group’s response, limiting the ability to observe the treatment effect of iberdomide monotherapy.

DISCLOSURES:

The study was funded by Bristol-Myers Squibb. Six authors reported being employed by Bristol-Myers Squibb, and several others reported consultancy and research support from various sources including Bristol-Myers Squibb.

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:

Patients with cutaneous lupus erythematosus (CLE) experienced improved symptoms with iberdomide, a cereblon modulator, added to standard lupus medications, particularly in subacute and chronic cases.

METHODOLOGY:

• Researchers conducted a randomized phase 2 trial to evaluate the efficacy and safety of iberdomide in 288 patients with CLE (mean age, 45 years; 97% women). Iberdomide is a cereblon modulator, which results in degradation of two transcription factors of immune cell development and homeostasis — Ikaros and Aiolos — that have been implicated in the genetic predisposition of systemic lupus.
• CLE Disease Area and Severity Index Activity (CLASI-A) endpoints included mean percent change from baseline and ≥ 50% reduction from baseline (CLASI-50), which were evaluated in all patients with baseline CLASI-A scores ≥ 8 and by CLE subtypes (acute, subacute, and chronic).
• At baseline, 56% of patients had acute CLE, 29% had chronic CLE, and 16% had subacute CLE; 28% of patients had a baseline CLASI-A score ≥ 8.
• Patients were randomly assigned to receive oral iberdomide (0.45 mg, 0.30 mg, 0.15 mg, or placebo daily) for 24 weeks while continuing standard lupus medications. At week 24, patients on placebo were rerandomized to iberdomide 0.45 mg or 0.30 mg once a day, while those on iberdomide continued their assigned dose through week 52.

TAKEAWAY:

• Among patients with baseline CLASI-A ≥ 8, the mean change in CLASI-A score from baseline at week 24 was −66.7% for those on iberdomide 0.45 mg vs −54.2% for placebo (P = .295).
• At week 24, patients with subacute CLE showed a significantly greater mean percent change from baseline in CLASI-A with iberdomide 0.45 mg vs placebo (−90.5% vs −51.2%; P = .007), while no significant differences were observed with the 0.45-mg dose vs placebo in patients with chronic or acute CLE.
• Overall, CLASI-50 responses were not significantly different among those on 0.45 mg vs placebo (55.6% vs 44.6%). The proportions of patients achieving CLASI-50 at week 24 were significantly greater for iberdomide 0.45 mg vs placebo for those with subacute CLE (91.7% vs 52.9%; P = .035) and chronic CLE (62.1% vs 27.8%; P = .029), but not for those with baseline CLASI-A ≥ 8 (66.7% vs 50%).
• More than 80% of patients had treatment-emergent adverse events (TEAEs), which were mostly mild to moderate. Over 2 years, the most common were urinary tract infections, upper respiratory tract infections, neutropenia, and nasopharyngitis. TEAEs leading to iberdomide discontinuation in one or more patients were neutropenia (n = 7), rash (n = 7), increased hepatic enzymes (n = 4), and deep vein thrombosis (n = 3).

IN PRACTICE:

“Data from this phase 2 trial of iberdomide in patients with SLE suggest that a greater proportion of patients with subacute or chronic CLE who received the higher dose of 0.45 mg iberdomide achieved CLASI-50 vs placebo. For the overall population, CLASI-50 response was not significantly different between treatment groups at week 24, partly due to a high placebo response that may have been driven by patients with acute CLE,” the authors wrote.

SOURCE:

The study was led by Victoria P. Werth, MD, of the University of Pennsylvania and the Veteran’s Administration Medical Center, both in Philadelphia, and was published online in the Journal of the American Academy of Dermatology.

LIMITATIONS:

The study included small patient subgroups for different CLE subtypes, which may affect the generalizability of the findings. CLE subtype was determined by the investigator without additional photographic adjudication. Additionally, the use of background lupus medications could have influenced the placebo group’s response, limiting the ability to observe the treatment effect of iberdomide monotherapy.

DISCLOSURES:

The study was funded by Bristol-Myers Squibb. Six authors reported being employed by Bristol-Myers Squibb, and several others reported consultancy and research support from various sources including Bristol-Myers Squibb.

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:

Patients with cutaneous lupus erythematosus (CLE) experienced improved symptoms with iberdomide, a cereblon modulator, added to standard lupus medications, particularly in subacute and chronic cases.

METHODOLOGY:

• Researchers conducted a randomized phase 2 trial to evaluate the efficacy and safety of iberdomide in 288 patients with CLE (mean age, 45 years; 97% women). Iberdomide is a cereblon modulator, which results in degradation of two transcription factors of immune cell development and homeostasis — Ikaros and Aiolos — that have been implicated in the genetic predisposition of systemic lupus.
• CLE Disease Area and Severity Index Activity (CLASI-A) endpoints included mean percent change from baseline and ≥ 50% reduction from baseline (CLASI-50), which were evaluated in all patients with baseline CLASI-A scores ≥ 8 and by CLE subtypes (acute, subacute, and chronic).
• At baseline, 56% of patients had acute CLE, 29% had chronic CLE, and 16% had subacute CLE; 28% of patients had a baseline CLASI-A score ≥ 8.
• Patients were randomly assigned to receive oral iberdomide (0.45 mg, 0.30 mg, 0.15 mg, or placebo daily) for 24 weeks while continuing standard lupus medications. At week 24, patients on placebo were rerandomized to iberdomide 0.45 mg or 0.30 mg once a day, while those on iberdomide continued their assigned dose through week 52.

TAKEAWAY:

• Among patients with baseline CLASI-A ≥ 8, the mean change in CLASI-A score from baseline at week 24 was −66.7% for those on iberdomide 0.45 mg vs −54.2% for placebo (P = .295).
• At week 24, patients with subacute CLE showed a significantly greater mean percent change from baseline in CLASI-A with iberdomide 0.45 mg vs placebo (−90.5% vs −51.2%; P = .007), while no significant differences were observed with the 0.45-mg dose vs placebo in patients with chronic or acute CLE.
• Overall, CLASI-50 responses were not significantly different among those on 0.45 mg vs placebo (55.6% vs 44.6%). The proportions of patients achieving CLASI-50 at week 24 were significantly greater for iberdomide 0.45 mg vs placebo for those with subacute CLE (91.7% vs 52.9%; P = .035) and chronic CLE (62.1% vs 27.8%; P = .029), but not for those with baseline CLASI-A ≥ 8 (66.7% vs 50%).
• More than 80% of patients had treatment-emergent adverse events (TEAEs), which were mostly mild to moderate. Over 2 years, the most common were urinary tract infections, upper respiratory tract infections, neutropenia, and nasopharyngitis. TEAEs leading to iberdomide discontinuation in one or more patients were neutropenia (n = 7), rash (n = 7), increased hepatic enzymes (n = 4), and deep vein thrombosis (n = 3).

IN PRACTICE:

“Data from this phase 2 trial of iberdomide in patients with SLE suggest that a greater proportion of patients with subacute or chronic CLE who received the higher dose of 0.45 mg iberdomide achieved CLASI-50 vs placebo. For the overall population, CLASI-50 response was not significantly different between treatment groups at week 24, partly due to a high placebo response that may have been driven by patients with acute CLE,” the authors wrote.

SOURCE:

The study was led by Victoria P. Werth, MD, of the University of Pennsylvania and the Veteran’s Administration Medical Center, both in Philadelphia, and was published online in the Journal of the American Academy of Dermatology.

LIMITATIONS:

The study included small patient subgroups for different CLE subtypes, which may affect the generalizability of the findings. CLE subtype was determined by the investigator without additional photographic adjudication. Additionally, the use of background lupus medications could have influenced the placebo group’s response, limiting the ability to observe the treatment effect of iberdomide monotherapy.

DISCLOSURES:

The study was funded by Bristol-Myers Squibb. Six authors reported being employed by Bristol-Myers Squibb, and several others reported consultancy and research support from various sources including Bristol-Myers Squibb.

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.

BOSTON — Social adversity is associated with worse survival among patients with pulmonary hypertension (PH), according to a new retrospective study of a New York City population. Among HIV+ patients with heart failure, PH was associated with about a threefold increase in all-cause mortality, but that risk increased to about sevenfold when social adversity, identified by a licensed social worker, was also present.

A sub-analysis of both HIV+ and HIV– patients showed worse mortality outcomes with social adversity in both groups.

“Almost the majority of patients that we treat have either some social adversity or no insurance or are undocumented, so as a group of residents, we decided to study the impact of these factors on their health and the care that can be provided. We started using the two cohorts and now we keep it going with every new resident,” said Luca Biavati, MD, who presented the study at the CHEST Annual Meeting.

“The presence of any form of socioeconomic disadvantage is negatively impacting care and for a large part of the population, there are some factors that could probably be addressed by either an institutional or hospital policy,” said Dr. Biavati, who is an internal medicine resident at Jacobi Medical Center, New York.

Other factors are more difficult to address, such as lack of education. “[Some patients] don’t understand the gravity of their issue and medical condition until it’s too late, and then they’re not fit enough for the treatment, or just because of the social situation, they cannot qualify for advanced therapies,” said Dr. Biavati.

The researchers established two cohorts: One consisting of patients with HIV and heart failure who may or may not have had PH and one comprising patients with PH with or without HIV and heart failure. In the HIV/heart failure group, PH without social adversity was associated with a nearly threefold increase in all-cause mortality (hazard ratio [HR], 2.83; P = .004), whereas PH with social adversity was linked to a more than sevenfold increase in all-cause mortality (HR, 7.14; P < .001). Social adversity without PA was associated with a more than fourfold increase (HR, 4.47; P < .001).

Within the PH cohort, social adversity was associated with lower survival (P < .001). When the researchers broke down the results by types of social adversity, they found statistically significant relationships between greater mortality risk and economic instability within the HIV+ population (HR, 2.59; P = .040), transportation issues within the HIV– population (HR, 12.8; P < .001), and lack of social or family support within both the HIV– (HR, 5.49; P < .001) and the HIV+ population (HR, 2.03; P = .028). 

The research has prompted interventions, which are now being studied at the institution, according to Dr. Biavati. “We have a policy of giving medications in bags when we discharge a patient with a social adversity. We literally go to the pharmacy, bring up the bag of medication, and we [put it] in their hands before they leave the hospital. They get a 1- or 3-month supply, depending on the medication, and then we usually discharge them with a clinical appointment already scheduled with either a pulmonary or primary care provider, and we usually call them before every appointment to confirm that they’re coming. That increases the chances of some success, but there’s still a very long way to go,” said Dr. Biavati.

Dr. Biavati was blinded to the results of the intervention, so he could not report on whether it was working. “But I can tell you that I’ve had busier clinics, so hopefully that means that they’re showing up more,” he said.

The problem is complex, according to Sandeep Jain, MD, who moderated the session. “Social adversity means lack of education. Lack of education means lack of compliance. Lack of compliance means what can you do if people are not taking medications? So it’s all matched together. It’s all lack of education and lack of money, lack of family support. And these drugs they have to take every single day. It’s not that easy. It’s very easy for us to say I had antiretroviral treatment for 6 months. It is almost impossible to continue regular treatment for that long [for a patient with social adversity]. You can’t blame them if they aren’t taking treatments. It’s very difficult for them,” said Dr. Jain.

That underscores the need for interventions that can address the needs of patients with social adversity. “We have to [practice] medicine considering the social situation of the patient and not just the medicine that we study in books. That’s kind of what we are faced with every day. We have therapies, and then life happens. It’s much harder to care for those patients,” said Dr. Biavati.

Dr. Biavati and Dr. Jain reported no relevant financial relationships.
 

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

BOSTON — Social adversity is associated with worse survival among patients with pulmonary hypertension (PH), according to a new retrospective study of a New York City population. Among HIV+ patients with heart failure, PH was associated with about a threefold increase in all-cause mortality, but that risk increased to about sevenfold when social adversity, identified by a licensed social worker, was also present.

A sub-analysis of both HIV+ and HIV– patients showed worse mortality outcomes with social adversity in both groups.

“Almost the majority of patients that we treat have either some social adversity or no insurance or are undocumented, so as a group of residents, we decided to study the impact of these factors on their health and the care that can be provided. We started using the two cohorts and now we keep it going with every new resident,” said Luca Biavati, MD, who presented the study at the CHEST Annual Meeting.

“The presence of any form of socioeconomic disadvantage is negatively impacting care and for a large part of the population, there are some factors that could probably be addressed by either an institutional or hospital policy,” said Dr. Biavati, who is an internal medicine resident at Jacobi Medical Center, New York.

Other factors are more difficult to address, such as lack of education. “[Some patients] don’t understand the gravity of their issue and medical condition until it’s too late, and then they’re not fit enough for the treatment, or just because of the social situation, they cannot qualify for advanced therapies,” said Dr. Biavati.

The researchers established two cohorts: One consisting of patients with HIV and heart failure who may or may not have had PH and one comprising patients with PH with or without HIV and heart failure. In the HIV/heart failure group, PH without social adversity was associated with a nearly threefold increase in all-cause mortality (hazard ratio [HR], 2.83; P = .004), whereas PH with social adversity was linked to a more than sevenfold increase in all-cause mortality (HR, 7.14; P < .001). Social adversity without PA was associated with a more than fourfold increase (HR, 4.47; P < .001).

Within the PH cohort, social adversity was associated with lower survival (P < .001). When the researchers broke down the results by types of social adversity, they found statistically significant relationships between greater mortality risk and economic instability within the HIV+ population (HR, 2.59; P = .040), transportation issues within the HIV– population (HR, 12.8; P < .001), and lack of social or family support within both the HIV– (HR, 5.49; P < .001) and the HIV+ population (HR, 2.03; P = .028). 

The research has prompted interventions, which are now being studied at the institution, according to Dr. Biavati. “We have a policy of giving medications in bags when we discharge a patient with a social adversity. We literally go to the pharmacy, bring up the bag of medication, and we [put it] in their hands before they leave the hospital. They get a 1- or 3-month supply, depending on the medication, and then we usually discharge them with a clinical appointment already scheduled with either a pulmonary or primary care provider, and we usually call them before every appointment to confirm that they’re coming. That increases the chances of some success, but there’s still a very long way to go,” said Dr. Biavati.

Dr. Biavati was blinded to the results of the intervention, so he could not report on whether it was working. “But I can tell you that I’ve had busier clinics, so hopefully that means that they’re showing up more,” he said.

The problem is complex, according to Sandeep Jain, MD, who moderated the session. “Social adversity means lack of education. Lack of education means lack of compliance. Lack of compliance means what can you do if people are not taking medications? So it’s all matched together. It’s all lack of education and lack of money, lack of family support. And these drugs they have to take every single day. It’s not that easy. It’s very easy for us to say I had antiretroviral treatment for 6 months. It is almost impossible to continue regular treatment for that long [for a patient with social adversity]. You can’t blame them if they aren’t taking treatments. It’s very difficult for them,” said Dr. Jain.

That underscores the need for interventions that can address the needs of patients with social adversity. “We have to [practice] medicine considering the social situation of the patient and not just the medicine that we study in books. That’s kind of what we are faced with every day. We have therapies, and then life happens. It’s much harder to care for those patients,” said Dr. Biavati.

Dr. Biavati and Dr. Jain reported no relevant financial relationships.
 

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

BOSTON — Social adversity is associated with worse survival among patients with pulmonary hypertension (PH), according to a new retrospective study of a New York City population. Among HIV+ patients with heart failure, PH was associated with about a threefold increase in all-cause mortality, but that risk increased to about sevenfold when social adversity, identified by a licensed social worker, was also present.

A sub-analysis of both HIV+ and HIV– patients showed worse mortality outcomes with social adversity in both groups.

“Almost the majority of patients that we treat have either some social adversity or no insurance or are undocumented, so as a group of residents, we decided to study the impact of these factors on their health and the care that can be provided. We started using the two cohorts and now we keep it going with every new resident,” said Luca Biavati, MD, who presented the study at the CHEST Annual Meeting.

“The presence of any form of socioeconomic disadvantage is negatively impacting care and for a large part of the population, there are some factors that could probably be addressed by either an institutional or hospital policy,” said Dr. Biavati, who is an internal medicine resident at Jacobi Medical Center, New York.

Other factors are more difficult to address, such as lack of education. “[Some patients] don’t understand the gravity of their issue and medical condition until it’s too late, and then they’re not fit enough for the treatment, or just because of the social situation, they cannot qualify for advanced therapies,” said Dr. Biavati.

The researchers established two cohorts: One consisting of patients with HIV and heart failure who may or may not have had PH and one comprising patients with PH with or without HIV and heart failure. In the HIV/heart failure group, PH without social adversity was associated with a nearly threefold increase in all-cause mortality (hazard ratio [HR], 2.83; P = .004), whereas PH with social adversity was linked to a more than sevenfold increase in all-cause mortality (HR, 7.14; P < .001). Social adversity without PA was associated with a more than fourfold increase (HR, 4.47; P < .001).

Within the PH cohort, social adversity was associated with lower survival (P < .001). When the researchers broke down the results by types of social adversity, they found statistically significant relationships between greater mortality risk and economic instability within the HIV+ population (HR, 2.59; P = .040), transportation issues within the HIV– population (HR, 12.8; P < .001), and lack of social or family support within both the HIV– (HR, 5.49; P < .001) and the HIV+ population (HR, 2.03; P = .028). 

The research has prompted interventions, which are now being studied at the institution, according to Dr. Biavati. “We have a policy of giving medications in bags when we discharge a patient with a social adversity. We literally go to the pharmacy, bring up the bag of medication, and we [put it] in their hands before they leave the hospital. They get a 1- or 3-month supply, depending on the medication, and then we usually discharge them with a clinical appointment already scheduled with either a pulmonary or primary care provider, and we usually call them before every appointment to confirm that they’re coming. That increases the chances of some success, but there’s still a very long way to go,” said Dr. Biavati.

Dr. Biavati was blinded to the results of the intervention, so he could not report on whether it was working. “But I can tell you that I’ve had busier clinics, so hopefully that means that they’re showing up more,” he said.

The problem is complex, according to Sandeep Jain, MD, who moderated the session. “Social adversity means lack of education. Lack of education means lack of compliance. Lack of compliance means what can you do if people are not taking medications? So it’s all matched together. It’s all lack of education and lack of money, lack of family support. And these drugs they have to take every single day. It’s not that easy. It’s very easy for us to say I had antiretroviral treatment for 6 months. It is almost impossible to continue regular treatment for that long [for a patient with social adversity]. You can’t blame them if they aren’t taking treatments. It’s very difficult for them,” said Dr. Jain.

That underscores the need for interventions that can address the needs of patients with social adversity. “We have to [practice] medicine considering the social situation of the patient and not just the medicine that we study in books. That’s kind of what we are faced with every day. We have therapies, and then life happens. It’s much harder to care for those patients,” said Dr. Biavati.

Dr. Biavati and Dr. Jain reported no relevant financial relationships.
 

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

TOPLINE: 

Virtual yoga classes significantly reduced chronic low back pain intensity and improved back-related function in health system employees. Improvements were sustained at 24 weeks, with reduced pain medication use and better sleep quality.

METHODOLOGY:

• A single-blinded, 24-week, 2-arm, randomized clinical trial was conducted from May 3, 2022, through May 23, 2023, comparing live-streamed yoga classes with a wait-list control among adults with chronic low back pain.
• A total of 140 participants aged 18-64 years with chronic low back pain were recruited from the Cleveland Clinic Employee Health Plan.
• Inclusion criteria included a mean low back pain intensity score of at least 4 on an 11-point numerical rating scale and daily back pain interference about half or more of the days.
• The intervention consisted of 12 consecutive weekly, 60-minute, virtual, live-streamed hatha yoga group classes.

Coprimary outcomes were mean pain intensity in the previous week on the 11-point numerical rating scale and back-related function as assessed using the 23-point modified Roland Morris Disability Questionnaire at 12 weeks.

TAKEAWAY:

• Participants in the virtual yoga group showed greater reductions in mean pain intensity at 12 weeks (mean change, –1.5 points; P < .001) and 24 weeks (mean change, –2.3 points; P < .001) compared to the wait-list control group.
• Back-related function improved significantly in the virtual yoga group at 12 weeks (mean change, –2.8 points; P < .001) and 24 weeks (mean change, –4.6 points; P < .001), compared with the control group.
• Virtual yoga participants reported 21.2 percentage points less use of any analgesic medication during the past week at 24 weeks, compared with the control group.
• Sleep quality improved more in the virtual yoga group at 12 weeks (mean change, 0.4 points; P = .008) and 24 weeks (mean change, 0.4 points; P = .005), compared with the control group.

IN PRACTICE:

“Given the demonstrated noninferiority of yoga to physical therapy, structured virtual yoga programs and physical therapy are reasonable choices for patients with [chronic low back pain] depending on accessibility, cost, and patient preference. These findings support the call by the National Academy of Medicine for increased evidenced-based pain treatments that can be disseminated via technology-based platforms,” wrote the authors of the study.

SOURCE:

The study was led by Hallie Tankha, PhD, Cleveland Clinic in Ohio. It was published online on November 1, 2024, in JAMA Network Open.

LIMITATIONS: 

The study had a low adherence rate, with only 36.6% of participants attending at least 50% of the yoga classes. There was also a higher rate of missing data in the yoga group compared to the control group. The study did not include a longer-term follow-up assessment beyond 24 weeks.

DISCLOSURES:

This study was supported by grants from Cleveland Clinic Healthcare Delivery and Implementation Science Center. One coauthor disclosed receiving personal fees from the Blue Cross Blue Shield Association. Eric Roseen, DC, PhD, reported receiving grants from the National Institutes of Health National Center for Complementary and Integrative Health. One coauthor disclosed receiving personal fees from UpToDate and grants from NCCIH related to yoga and tai chi for treatment of pain. Additional disclosures are noted 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 appeared on Medscape.com.

TOPLINE: 

Virtual yoga classes significantly reduced chronic low back pain intensity and improved back-related function in health system employees. Improvements were sustained at 24 weeks, with reduced pain medication use and better sleep quality.

METHODOLOGY:

• A single-blinded, 24-week, 2-arm, randomized clinical trial was conducted from May 3, 2022, through May 23, 2023, comparing live-streamed yoga classes with a wait-list control among adults with chronic low back pain.
• A total of 140 participants aged 18-64 years with chronic low back pain were recruited from the Cleveland Clinic Employee Health Plan.
• Inclusion criteria included a mean low back pain intensity score of at least 4 on an 11-point numerical rating scale and daily back pain interference about half or more of the days.
• The intervention consisted of 12 consecutive weekly, 60-minute, virtual, live-streamed hatha yoga group classes.

Coprimary outcomes were mean pain intensity in the previous week on the 11-point numerical rating scale and back-related function as assessed using the 23-point modified Roland Morris Disability Questionnaire at 12 weeks.

TAKEAWAY:

• Participants in the virtual yoga group showed greater reductions in mean pain intensity at 12 weeks (mean change, –1.5 points; P < .001) and 24 weeks (mean change, –2.3 points; P < .001) compared to the wait-list control group.
• Back-related function improved significantly in the virtual yoga group at 12 weeks (mean change, –2.8 points; P < .001) and 24 weeks (mean change, –4.6 points; P < .001), compared with the control group.
• Virtual yoga participants reported 21.2 percentage points less use of any analgesic medication during the past week at 24 weeks, compared with the control group.
• Sleep quality improved more in the virtual yoga group at 12 weeks (mean change, 0.4 points; P = .008) and 24 weeks (mean change, 0.4 points; P = .005), compared with the control group.

IN PRACTICE:

“Given the demonstrated noninferiority of yoga to physical therapy, structured virtual yoga programs and physical therapy are reasonable choices for patients with [chronic low back pain] depending on accessibility, cost, and patient preference. These findings support the call by the National Academy of Medicine for increased evidenced-based pain treatments that can be disseminated via technology-based platforms,” wrote the authors of the study.

SOURCE:

The study was led by Hallie Tankha, PhD, Cleveland Clinic in Ohio. It was published online on November 1, 2024, in JAMA Network Open.

LIMITATIONS: 

The study had a low adherence rate, with only 36.6% of participants attending at least 50% of the yoga classes. There was also a higher rate of missing data in the yoga group compared to the control group. The study did not include a longer-term follow-up assessment beyond 24 weeks.

DISCLOSURES:

This study was supported by grants from Cleveland Clinic Healthcare Delivery and Implementation Science Center. One coauthor disclosed receiving personal fees from the Blue Cross Blue Shield Association. Eric Roseen, DC, PhD, reported receiving grants from the National Institutes of Health National Center for Complementary and Integrative Health. One coauthor disclosed receiving personal fees from UpToDate and grants from NCCIH related to yoga and tai chi for treatment of pain. Additional disclosures are noted 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 appeared on Medscape.com.

TOPLINE: 

Virtual yoga classes significantly reduced chronic low back pain intensity and improved back-related function in health system employees. Improvements were sustained at 24 weeks, with reduced pain medication use and better sleep quality.

METHODOLOGY:

• A single-blinded, 24-week, 2-arm, randomized clinical trial was conducted from May 3, 2022, through May 23, 2023, comparing live-streamed yoga classes with a wait-list control among adults with chronic low back pain.
• A total of 140 participants aged 18-64 years with chronic low back pain were recruited from the Cleveland Clinic Employee Health Plan.
• Inclusion criteria included a mean low back pain intensity score of at least 4 on an 11-point numerical rating scale and daily back pain interference about half or more of the days.
• The intervention consisted of 12 consecutive weekly, 60-minute, virtual, live-streamed hatha yoga group classes.

Coprimary outcomes were mean pain intensity in the previous week on the 11-point numerical rating scale and back-related function as assessed using the 23-point modified Roland Morris Disability Questionnaire at 12 weeks.

TAKEAWAY:

• Participants in the virtual yoga group showed greater reductions in mean pain intensity at 12 weeks (mean change, –1.5 points; P < .001) and 24 weeks (mean change, –2.3 points; P < .001) compared to the wait-list control group.
• Back-related function improved significantly in the virtual yoga group at 12 weeks (mean change, –2.8 points; P < .001) and 24 weeks (mean change, –4.6 points; P < .001), compared with the control group.
• Virtual yoga participants reported 21.2 percentage points less use of any analgesic medication during the past week at 24 weeks, compared with the control group.
• Sleep quality improved more in the virtual yoga group at 12 weeks (mean change, 0.4 points; P = .008) and 24 weeks (mean change, 0.4 points; P = .005), compared with the control group.

IN PRACTICE:

“Given the demonstrated noninferiority of yoga to physical therapy, structured virtual yoga programs and physical therapy are reasonable choices for patients with [chronic low back pain] depending on accessibility, cost, and patient preference. These findings support the call by the National Academy of Medicine for increased evidenced-based pain treatments that can be disseminated via technology-based platforms,” wrote the authors of the study.

SOURCE:

The study was led by Hallie Tankha, PhD, Cleveland Clinic in Ohio. It was published online on November 1, 2024, in JAMA Network Open.

LIMITATIONS: 

The study had a low adherence rate, with only 36.6% of participants attending at least 50% of the yoga classes. There was also a higher rate of missing data in the yoga group compared to the control group. The study did not include a longer-term follow-up assessment beyond 24 weeks.

DISCLOSURES:

This study was supported by grants from Cleveland Clinic Healthcare Delivery and Implementation Science Center. One coauthor disclosed receiving personal fees from the Blue Cross Blue Shield Association. Eric Roseen, DC, PhD, reported receiving grants from the National Institutes of Health National Center for Complementary and Integrative Health. One coauthor disclosed receiving personal fees from UpToDate and grants from NCCIH related to yoga and tai chi for treatment of pain. Additional disclosures are noted 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 appeared on Medscape.com.

Approximately one third of parents of children with atopic dermatitis reported little or no improvement with elimination diets, and nearly 80% reintroduced the eliminated foods, based on survey data from nearly 300 parents.

Although atopic dermatitis can be associated with an increased risk for food allergies, major allergy organizations do not currently recommend elimination diets as a treatment for atopic dermatitis, said Nadia Makkoukdji, MD, a pediatrician at Jackson Memorial Hospital, Miami, in a presentation at the American College of Allergy, Asthma, and Immunology (ACAAI) Annual Scientific Meeting.

“A fear of drastic dietary changes often prevents families from seeking the care their children need,” Makkoukdji said in an interview. In the clinical setting, Makkoukdji noted that she has seen many patients who have started food elimination diets on their own or as recommended by other doctors, and that these diets can lead to dangers such as the development of immunoglobulin E–mediated food allergies on reintroduction of eliminated foods and malnutrition. They can also produce “emotional stress in children and anxiety or depression, while also adding stress to parents and the entire family.”

Makkoukdji conducted the study to explore parents’ perceptions of these diets in management of their children’s atopic dermatitis, she said.

In the study, Makkoukdji and colleagues sought to understand parents’ perceptions of the role of diet in atopic dermatitis in their children. The researchers reviewed surveys from 298 parents of children with atopic dermatitis who were seen at a single academic center. Parents completed the surveys in the emergency department or in an allergy, dermatology, and general pediatrics clinic.

Overall, 42% of parents identified food triggers for their child’s atopic dermatitis. The most commonly identified triggers were milk (32%), tree nuts/seeds/peanuts (16%), and eggs (11%).

Of the parents who reported food triggers, 23% removed the suspected trigger food from the child’s diet completely, 20% removed suspected trigger foods from their own diets while breastfeeding, and 19% changed their infant’s formula.

In the wake of the elimination diets, 38% of the parents reported no improvement in their child’s atopic dermatitis, 35% reported a 25% improvement, and 9% reported complete resolution. The majority (79%) reintroduced eliminated foods and reported no recurrence of atopic dermatitis symptoms.

The researchers were surprised by how many parents changed their child’s diet in the belief that certain foods exacerbated their child’s atopic dermatitis, “although this perception aligns with the common concern that food allergens can trigger or worsen atopic dermatitis flares,” Makkoukdji said.

The current study highlights the need for more awareness of the limited impact of dietary modifications on atopic dermatitis in the absence of confirmed food allergies, Makkoukdji said. “Our study shows that food elimination diets are still commonly being used by parents in the local Miami population.”

The findings were limited by several factors, including the use of data from a single center and the focus only on pediatric patients, but the primary goal was to assess parental perceptions of AD flares in relation to dietary choices, said Makkoukdji. “Future studies that include larger and more diverse populations would be valuable for the field.”
 

Dietary Modifications Don’t Live Up to Hype

“Food continues to be one of the most discussed aspects of atopic dermatitis,” Peter Lio, MD, clinical assistant professor of dermatology and pediatrics at Northwestern University Feinberg School of Medicine, Chicago, Illinois, said in an interview.

“Almost all of my patients and families ask about dietary modifications, even though almost all of them have experimented with it to some degree,” said Lio. In his experience, diet plays a small role, if any, in the day-to-day management of atopic dermatitis.

This lack of effect of dietary changes is often frustrating to patients because of the persistent “common wisdom” that points to diet as a root cause of atopic dermatitis, Lio said. “Many practitioners continue to recommend excluding foods such as gluten or dairy from the diet, but generally these are only of modest help,” and although patients wish that dietary changes would fix the problem, most are left wondering why these changes didn’t help them.

The current study findings “reflect my own experience after nearly 20 years of being deeply immersed in the world of atopic dermatitis,” Lio said. Although the takeaway message does not argue against eating healthy foods, some foods do seem to make AD worse in some patients and may have nonallergic pro-inflammatory effects.

“In those cases, it is reasonable to limit or avoid those foods. However, it is extremely difficult to tell what food or foods are driving flare-ups when things are out of control, so dietary modification is generally not the best place to start,” he said.

True food allergies are much more common in patients with atopic dermatitis compared with individuals without atopic dermatitis, but the current study is not addressing these types of allergies, Lio emphasized. “If someone has true allergy to peanuts, for example, they should not be eating them; we also know that they are not ‘cheating’ because these patients would not merely have an eczema flare; they would have urticaria, angioedema, or anaphylaxis. There is tremendous confusion around this point and lots of confusion around allergy testing and its limitations.”

In addition, patients with atopic dermatitis are more likely than those without atopic dermatitis to have abnormalities in the gut microbiome and gut barrier, Lio said.

Abnormalities in the gut microbiome are different from the concept of allergy and may fall into the more complex category of barrier and microbiome disruptors, he said. Therefore, “the food category may not be nearly as important as the specific preparation of the food along with the additives (such as preservatives and emulsifiers) that may actually be driving the problem.”

Although in the past many clinicians advised patients to try cutting out certain foods to see whether atopic dermatitis symptoms improved, this strategy is not without risk, said Lio. “There have been incredible advancements in understanding the role of the gut in tolerization to foods.” Recent research has shown that by eating foods regularly, particularly those such as peanuts that seem to have more allergic potential, the body becomes tolerant, and this prevents the development of true food allergies.

As for additional research, many questions remain about the effects of types of foods, processing methods, and timing of introduction of foods on atopic dermatitis, Lio noted.

“Atopic dermatitis is a systemic condition with the immune system, with the skin/gut/respiratory barriers and microbiome involved; I think we now have a broader view of how big and complex the landscape really is,” he said.

The study received no outside funding. The researchers had no financial conflicts to disclose. Lio had no disclosures relevant to elimination diets but disclosed serving on the speakers bureau for AbbVie, Arcutis Biotherapeutics, Eli Lilly, Galderma, Hyphens Pharma, Incyte, La Roche–Posay/L’Oréal, Pfizer, Pierre Fabre Dermatologie, Regeneron/Sanofi Genzyme, and Verrica Pharmaceuticals; serving on consulting/advisory boards; or having stock options for many pharmaceutical companies. Lio also disclosed a patent pending for a Theraplex product with royalties paid and is a board member and Scientific Advisory Committee member emeritus of the National Eczema Association.

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

Approximately one third of parents of children with atopic dermatitis reported little or no improvement with elimination diets, and nearly 80% reintroduced the eliminated foods, based on survey data from nearly 300 parents.

Although atopic dermatitis can be associated with an increased risk for food allergies, major allergy organizations do not currently recommend elimination diets as a treatment for atopic dermatitis, said Nadia Makkoukdji, MD, a pediatrician at Jackson Memorial Hospital, Miami, in a presentation at the American College of Allergy, Asthma, and Immunology (ACAAI) Annual Scientific Meeting.

“A fear of drastic dietary changes often prevents families from seeking the care their children need,” Makkoukdji said in an interview. In the clinical setting, Makkoukdji noted that she has seen many patients who have started food elimination diets on their own or as recommended by other doctors, and that these diets can lead to dangers such as the development of immunoglobulin E–mediated food allergies on reintroduction of eliminated foods and malnutrition. They can also produce “emotional stress in children and anxiety or depression, while also adding stress to parents and the entire family.”

Makkoukdji conducted the study to explore parents’ perceptions of these diets in management of their children’s atopic dermatitis, she said.

In the study, Makkoukdji and colleagues sought to understand parents’ perceptions of the role of diet in atopic dermatitis in their children. The researchers reviewed surveys from 298 parents of children with atopic dermatitis who were seen at a single academic center. Parents completed the surveys in the emergency department or in an allergy, dermatology, and general pediatrics clinic.

Overall, 42% of parents identified food triggers for their child’s atopic dermatitis. The most commonly identified triggers were milk (32%), tree nuts/seeds/peanuts (16%), and eggs (11%).

Of the parents who reported food triggers, 23% removed the suspected trigger food from the child’s diet completely, 20% removed suspected trigger foods from their own diets while breastfeeding, and 19% changed their infant’s formula.

In the wake of the elimination diets, 38% of the parents reported no improvement in their child’s atopic dermatitis, 35% reported a 25% improvement, and 9% reported complete resolution. The majority (79%) reintroduced eliminated foods and reported no recurrence of atopic dermatitis symptoms.

The researchers were surprised by how many parents changed their child’s diet in the belief that certain foods exacerbated their child’s atopic dermatitis, “although this perception aligns with the common concern that food allergens can trigger or worsen atopic dermatitis flares,” Makkoukdji said.

The current study highlights the need for more awareness of the limited impact of dietary modifications on atopic dermatitis in the absence of confirmed food allergies, Makkoukdji said. “Our study shows that food elimination diets are still commonly being used by parents in the local Miami population.”

The findings were limited by several factors, including the use of data from a single center and the focus only on pediatric patients, but the primary goal was to assess parental perceptions of AD flares in relation to dietary choices, said Makkoukdji. “Future studies that include larger and more diverse populations would be valuable for the field.”
 

Dietary Modifications Don’t Live Up to Hype

“Food continues to be one of the most discussed aspects of atopic dermatitis,” Peter Lio, MD, clinical assistant professor of dermatology and pediatrics at Northwestern University Feinberg School of Medicine, Chicago, Illinois, said in an interview.

“Almost all of my patients and families ask about dietary modifications, even though almost all of them have experimented with it to some degree,” said Lio. In his experience, diet plays a small role, if any, in the day-to-day management of atopic dermatitis.

This lack of effect of dietary changes is often frustrating to patients because of the persistent “common wisdom” that points to diet as a root cause of atopic dermatitis, Lio said. “Many practitioners continue to recommend excluding foods such as gluten or dairy from the diet, but generally these are only of modest help,” and although patients wish that dietary changes would fix the problem, most are left wondering why these changes didn’t help them.

The current study findings “reflect my own experience after nearly 20 years of being deeply immersed in the world of atopic dermatitis,” Lio said. Although the takeaway message does not argue against eating healthy foods, some foods do seem to make AD worse in some patients and may have nonallergic pro-inflammatory effects.

“In those cases, it is reasonable to limit or avoid those foods. However, it is extremely difficult to tell what food or foods are driving flare-ups when things are out of control, so dietary modification is generally not the best place to start,” he said.

True food allergies are much more common in patients with atopic dermatitis compared with individuals without atopic dermatitis, but the current study is not addressing these types of allergies, Lio emphasized. “If someone has true allergy to peanuts, for example, they should not be eating them; we also know that they are not ‘cheating’ because these patients would not merely have an eczema flare; they would have urticaria, angioedema, or anaphylaxis. There is tremendous confusion around this point and lots of confusion around allergy testing and its limitations.”

In addition, patients with atopic dermatitis are more likely than those without atopic dermatitis to have abnormalities in the gut microbiome and gut barrier, Lio said.

Abnormalities in the gut microbiome are different from the concept of allergy and may fall into the more complex category of barrier and microbiome disruptors, he said. Therefore, “the food category may not be nearly as important as the specific preparation of the food along with the additives (such as preservatives and emulsifiers) that may actually be driving the problem.”

Although in the past many clinicians advised patients to try cutting out certain foods to see whether atopic dermatitis symptoms improved, this strategy is not without risk, said Lio. “There have been incredible advancements in understanding the role of the gut in tolerization to foods.” Recent research has shown that by eating foods regularly, particularly those such as peanuts that seem to have more allergic potential, the body becomes tolerant, and this prevents the development of true food allergies.

As for additional research, many questions remain about the effects of types of foods, processing methods, and timing of introduction of foods on atopic dermatitis, Lio noted.

“Atopic dermatitis is a systemic condition with the immune system, with the skin/gut/respiratory barriers and microbiome involved; I think we now have a broader view of how big and complex the landscape really is,” he said.

The study received no outside funding. The researchers had no financial conflicts to disclose. Lio had no disclosures relevant to elimination diets but disclosed serving on the speakers bureau for AbbVie, Arcutis Biotherapeutics, Eli Lilly, Galderma, Hyphens Pharma, Incyte, La Roche–Posay/L’Oréal, Pfizer, Pierre Fabre Dermatologie, Regeneron/Sanofi Genzyme, and Verrica Pharmaceuticals; serving on consulting/advisory boards; or having stock options for many pharmaceutical companies. Lio also disclosed a patent pending for a Theraplex product with royalties paid and is a board member and Scientific Advisory Committee member emeritus of the National Eczema Association.

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

Approximately one third of parents of children with atopic dermatitis reported little or no improvement with elimination diets, and nearly 80% reintroduced the eliminated foods, based on survey data from nearly 300 parents.

Although atopic dermatitis can be associated with an increased risk for food allergies, major allergy organizations do not currently recommend elimination diets as a treatment for atopic dermatitis, said Nadia Makkoukdji, MD, a pediatrician at Jackson Memorial Hospital, Miami, in a presentation at the American College of Allergy, Asthma, and Immunology (ACAAI) Annual Scientific Meeting.

“A fear of drastic dietary changes often prevents families from seeking the care their children need,” Makkoukdji said in an interview. In the clinical setting, Makkoukdji noted that she has seen many patients who have started food elimination diets on their own or as recommended by other doctors, and that these diets can lead to dangers such as the development of immunoglobulin E–mediated food allergies on reintroduction of eliminated foods and malnutrition. They can also produce “emotional stress in children and anxiety or depression, while also adding stress to parents and the entire family.”

Makkoukdji conducted the study to explore parents’ perceptions of these diets in management of their children’s atopic dermatitis, she said.

In the study, Makkoukdji and colleagues sought to understand parents’ perceptions of the role of diet in atopic dermatitis in their children. The researchers reviewed surveys from 298 parents of children with atopic dermatitis who were seen at a single academic center. Parents completed the surveys in the emergency department or in an allergy, dermatology, and general pediatrics clinic.

Overall, 42% of parents identified food triggers for their child’s atopic dermatitis. The most commonly identified triggers were milk (32%), tree nuts/seeds/peanuts (16%), and eggs (11%).

Of the parents who reported food triggers, 23% removed the suspected trigger food from the child’s diet completely, 20% removed suspected trigger foods from their own diets while breastfeeding, and 19% changed their infant’s formula.

In the wake of the elimination diets, 38% of the parents reported no improvement in their child’s atopic dermatitis, 35% reported a 25% improvement, and 9% reported complete resolution. The majority (79%) reintroduced eliminated foods and reported no recurrence of atopic dermatitis symptoms.

The researchers were surprised by how many parents changed their child’s diet in the belief that certain foods exacerbated their child’s atopic dermatitis, “although this perception aligns with the common concern that food allergens can trigger or worsen atopic dermatitis flares,” Makkoukdji said.

The current study highlights the need for more awareness of the limited impact of dietary modifications on atopic dermatitis in the absence of confirmed food allergies, Makkoukdji said. “Our study shows that food elimination diets are still commonly being used by parents in the local Miami population.”

The findings were limited by several factors, including the use of data from a single center and the focus only on pediatric patients, but the primary goal was to assess parental perceptions of AD flares in relation to dietary choices, said Makkoukdji. “Future studies that include larger and more diverse populations would be valuable for the field.”
 

Dietary Modifications Don’t Live Up to Hype

“Food continues to be one of the most discussed aspects of atopic dermatitis,” Peter Lio, MD, clinical assistant professor of dermatology and pediatrics at Northwestern University Feinberg School of Medicine, Chicago, Illinois, said in an interview.

“Almost all of my patients and families ask about dietary modifications, even though almost all of them have experimented with it to some degree,” said Lio. In his experience, diet plays a small role, if any, in the day-to-day management of atopic dermatitis.

This lack of effect of dietary changes is often frustrating to patients because of the persistent “common wisdom” that points to diet as a root cause of atopic dermatitis, Lio said. “Many practitioners continue to recommend excluding foods such as gluten or dairy from the diet, but generally these are only of modest help,” and although patients wish that dietary changes would fix the problem, most are left wondering why these changes didn’t help them.

The current study findings “reflect my own experience after nearly 20 years of being deeply immersed in the world of atopic dermatitis,” Lio said. Although the takeaway message does not argue against eating healthy foods, some foods do seem to make AD worse in some patients and may have nonallergic pro-inflammatory effects.

“In those cases, it is reasonable to limit or avoid those foods. However, it is extremely difficult to tell what food or foods are driving flare-ups when things are out of control, so dietary modification is generally not the best place to start,” he said.

True food allergies are much more common in patients with atopic dermatitis compared with individuals without atopic dermatitis, but the current study is not addressing these types of allergies, Lio emphasized. “If someone has true allergy to peanuts, for example, they should not be eating them; we also know that they are not ‘cheating’ because these patients would not merely have an eczema flare; they would have urticaria, angioedema, or anaphylaxis. There is tremendous confusion around this point and lots of confusion around allergy testing and its limitations.”

In addition, patients with atopic dermatitis are more likely than those without atopic dermatitis to have abnormalities in the gut microbiome and gut barrier, Lio said.

Abnormalities in the gut microbiome are different from the concept of allergy and may fall into the more complex category of barrier and microbiome disruptors, he said. Therefore, “the food category may not be nearly as important as the specific preparation of the food along with the additives (such as preservatives and emulsifiers) that may actually be driving the problem.”

Although in the past many clinicians advised patients to try cutting out certain foods to see whether atopic dermatitis symptoms improved, this strategy is not without risk, said Lio. “There have been incredible advancements in understanding the role of the gut in tolerization to foods.” Recent research has shown that by eating foods regularly, particularly those such as peanuts that seem to have more allergic potential, the body becomes tolerant, and this prevents the development of true food allergies.

As for additional research, many questions remain about the effects of types of foods, processing methods, and timing of introduction of foods on atopic dermatitis, Lio noted.

“Atopic dermatitis is a systemic condition with the immune system, with the skin/gut/respiratory barriers and microbiome involved; I think we now have a broader view of how big and complex the landscape really is,” he said.

The study received no outside funding. The researchers had no financial conflicts to disclose. Lio had no disclosures relevant to elimination diets but disclosed serving on the speakers bureau for AbbVie, Arcutis Biotherapeutics, Eli Lilly, Galderma, Hyphens Pharma, Incyte, La Roche–Posay/L’Oréal, Pfizer, Pierre Fabre Dermatologie, Regeneron/Sanofi Genzyme, and Verrica Pharmaceuticals; serving on consulting/advisory boards; or having stock options for many pharmaceutical companies. Lio also disclosed a patent pending for a Theraplex product with royalties paid and is a board member and Scientific Advisory Committee member emeritus of the National Eczema Association.

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

Many people with rheumatologic diseases try supplements for symptom relief. Here’s what you need to know about some common picks.

Dietary supplements were a $159 billion business in the United States in 2023, and many people with rheumatologic diseases are buying in. Research suggests more than 6 in 10 people with fibromyalgia, nearly 8 in 10 people with Sjögren’s disease, and more than 8 in 10 people with rheumatoid arthritis (RA) take dietary supplements.

Whatever the symptom — pain, swelling, or fatigue — you can probably find a supplement purporting to relieve it. But do these supplements work, and are they safe? A study review in RMD Open comprising 24 systematic reviews and 150 original articles suggests more high-quality research is needed on the effects of dietary supplements on rheumatologic diseases. Most studies have focused on RA or osteoarthritis (OA), where the evidence level is moderate at best.

Dr. Janet Funk

“The studies in this space are usually not very high quality because there’s no money to support them, among other things, plus the products are disparate,” said Janet Funk, MD, MS, professor in the School of Nutritional Sciences and Wellness at the University of Arizona, Tucson. She recommended brushing up on supplements and finding out what patients are taking so you can offer advice and watch for drug-supplement interactions.

When asked for a medication list, many patients forget to report supplements, Funk said. “You have to prompt them specifically. I think some physicians have very negative views about supplements because so little data is known, and patients might pick up on that and decide not to report their use.” She recommended saying something like: “To give you the best possible care, I want to know everything you’re taking, including supplements. The things I’m prescribing could maybe interact with the things you’re taking, so I want to make sure I know about all of it so that together we can figure out if the combination of things is safe.”

The quality of dietary supplements varies, and they aren’t regulated like drugs by the Food and Drug Administration. Funk recommended selecting products verified by NSF or ConsumerLab. They test supplements to ensure the label reflects what’s inside.

This news organization scoured the literature and asked experts to weigh in on the evidence behind popular supplements in rheumatology today.
 

The Essential Nutrients

Vitamin supplements are a staple in many homes — but are they helpful? “Individual vitamin supplements will not provide any benefit unless the person is deficient in a specific vitamin or mineral,” according to Elena Philippou, PhD, RD, associate professor of nutrition-dietetics at the University of Nicosia in Cyprus, and Elena Nikiphorou, MBBS, a rheumatologist at King’s College London in England. For some patients, deficiency is a reality. A retrospective cohort study in The Journal of Clinical Medicine found that people with RA were 17% more likely than age-matched control individuals to have nutrient deficiencies, perhaps because symptoms like fatigue, pain, and nausea affect their eating habits. Here’s what the science says about common vitamin supplements.

Dr. Elena Philippou

Vitamin D. This hormone-like vitamin, which attaches to receptors on immune cells to tamp down inflammation, was the most popular dietary supplement among rheumatology patients in a recent study from the United Kingdom. Vitamin D deficiency is common in people with RA, lupus, Sjögren’s disease, ankylosing spondylitis, systemic sclerosis, and fibromyalgia. In some cases, vitamin D levels track with disease activity, research suggests. Corticosteroids can also make vitamin D deficiency more likely. Can supplements help?

In RA, evidence points to small improvements. A systematic review of 11 studies including 3049 patients published in Nutrition Reviews showed that vitamin D supplements significantly reduced patients’ pain and Disease Activity Score in 28 joints (DAS28) using both C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR).

The research is mixed on the benefits of vitamin D supplementation for fibromyalgia symptoms, according to a study review in SN Comprehensive Clinical Medicine that included two studies and 80 patients on supplementation. However, researchers said it’s still worth discussing the potential benefits of taking vitamin D.

“Vitamin D supplementation is important in the context of various rheumatic diseases to prevent or treat bone disease,” said Philippou and Nikiphorou. “People with rheumatic disease should speak to their healthcare provider and ask to check their blood vitamin D concentration.” The results can help you recommend a dose.

Folate. Patients on methotrexate should take folic acid supplements under the guidance of a healthcare provider, said Philippou and Nikiphorou. The reason: Methotrexate can deplete folic acid levels, increasing the risk for side effects. An analysis of adverse event reports published showed that methotrexate users who took folic acid (or tumor necrosis factor–alpha inhibitors) had a reduced risk for hepatotoxicity or myelosuppression. A commonly recommended dose is 1 mg/d.

Vitamin B12. In a 2024 perspective paper in Rheumatology International, researchers said physicians should assess vitamin B12 levels early in the diagnostic process of rheumatologic diseases. One reason: Many symptoms of pernicious anemia, like fatigue, mimic symptoms of rheumatologic diseases. The gastrointestinal (GI) effects of systemic sclerosis could bring on vitamin B12 deficiency. In a small study in The Journal of Clinical Rheumatology, 44 of 62 patients with systemic sclerosis had low vitamin B12 levels.

Vitamin E. Vitamin E deficiency is rare in healthy adults. However, some medical conditions, like inflammatory bowel disease and malabsorption disorders, can make vitamin E deficiency more likely. In RA, a vitamin E supplement could help reduce joint swelling and sensitivity, according to a systematic review of nine studies including 39,845 patients in The European Journal of Clinical Nutrition. Researchers credit the nutrient’s role in aiding intestinal repair. Use with caution, as this supplement can increase bleeding risk in doses over 1000 mg/d.

Vitamin A. Like vitamin E, vitamin A deficiency is rare in the United States. The risk of oversupplementing is higher than undersupplementing. However, vitamin A deficiency can happen in people with chronic pancreatic, liver, or GI problems. In people with deficiency, a vitamin A supplement can help relieve dry eye symptoms common in Sjögren’s disease, suggests a narrative review published in Nutrients. Vitamin A might help reduce ocular surface changes by supporting the production of proteins that protect the outermost surfaces of the eyes. The recommended daily allowance for vitamin A is 900 μg. High-dose supplements can cause toxicity, resulting in GI symptoms and problems like lethargy, drowsiness, increased intracranial pressure, and skin changes.
 

The Replacements

These substances are similar to naturally occurring compounds in our bodies. The question is whether ingesting them yields benefits.

Glucosamine and chondroitin. Glucosamine and chondroitin occur naturally in our bodies and help us form and protect connective tissues. In pill form, this combo is the most popular dietary supplement for OA, according to research in the journal Maturitas. But studies of its effectiveness yield mixed results. A systematic review of 25 studies published in Inflammopharmacology showed that, in patients with knee OA, supplementation with about 1500 mg of glucosamine per day reduced tibiofemoral joint space narrowing, while supplementation with about 800 mg/d of chondroitin reduced pain intensity and improved physical function, compared with placebo. The duo of glucosamine and chondroitin did not bring significant benefits, perhaps because more studies are needed. Most side effects were mild, but some literature points to the potential for glucosamine to increase warfarin’s blood-thinning effects.

Omega-3 fatty acids. Fish oil is a top-selling supplement, and it might be helpful in inflammatory rheumatologic diseases. A systematic review of 30 studies including 710 patients published in Arthritis Research & Therapy showed that omega-3 fatty acid supplements can improve pain, swollen and tender joint count, DAS28 scores, and Health Assessment Questionnaire scores in patients with RA, psoriatic arthritis, or ankylosing spondylitis. In patients with lupus, a study review that included five studies and 284 patients in The International Journal of Environmental Research and Public Health suggested omega-3 fatty acid supplements could improve ESR, CRP, disease activity, inflammatory markers, oxidative stress, lipid levels, and endothelial function.

Omega-3 fatty acids have anti-inflammatory effects that might explain their benefits. In patients with RA, for example, fish oil supplementation was associated with elevated blood levels of resolvins and protectins, which help quell inflammation, according to a study in Prostaglandins, Leukotrienes and Essential Fatty Acids.

Philippou and Nikiphorou recommended combining food and supplements: Eat oily fish at least twice a week, regularly consume plant-based sources of omega-3s — like chia seeds, flaxseeds, or walnuts — and consider a daily supplement that contains 2 g of omega-3s from docosahexaenoic acid and eicosapentaenoic acid. Most fish oil side effects are mild, like heartburn and bad breath. Fish oil can have blood-thinning effects at high doses, so special attention is needed for patients on anticoagulants.

Probiotics. Building up the good bacteria in your gut might help you fight the effects of rheumatologic diseases. A systematic review of 80 randomized controlled trials in BMC Medicine suggested that therapies targeting the gut microbiota might improve the symptoms or inflammatory factors in celiac disease, lupus, juvenile idiopathic arthritis, psoriasis, Sjögren’s disease, multiple sclerosis, systemic sclerosis, Crohn’s disease, and ulcerative colitis. Probiotics were also shown to relieve pain in fibromyalgia, but they didn’t affect scores on the Fibromyalgia Impact Questionnaire. Probiotics were not helpful in spondyloarthritis or RA. There were no adverse events. By improving the balance of bacteria in the gut, probiotics might inhibit pro-inflammatory factors and signaling pathways and regulate CD4+ T-cell differentiation, the researchers wrote.

Not all probiotic supplements are created equal. Effects can vary by microorganism and dose. Until more high-quality studies are published, Philippou and Nikiphorou recommend daily consumption of probiotic food sources such as yogurt, kefir, sauerkraut, kimchi, tempeh, miso, and kombucha, along with prebiotic food sources such as bananas, onion, artichokes, asparagus, oats, leeks, and garlic.

Collagen. An increasingly popular supplement for hair, skin, and nails, some collagen peptide or hydrolyzed collagen supplements come with claims about joint health, too. Inside our bodies, collagen helps build joints. As a supplement, the jury is still out. A systematic review of 19 studies in The International Journal of Rheumatic Diseases suggested more research is needed to determine whether collagen supplements are harmful or helpful in OA or RA. Studies haven’t shown adverse events, and doses typically range from 2.5 to 15 g/d.

Coenzyme Q10 (CoQ10). This antioxidant occurs naturally in our cells and is produced through microbial fermentation for use in dietary supplements. A study review of 20 articles including 483 patients in Clinical Nutrition ESPEN concluded that CoQ10 supplementation up to 300 mg/d was beneficial in RA, fibromyalgia, or antiphospholipid syndrome (APS).

In RA, CoQ10 supplementation improved disease activity index, ESR, and cytokine levels and decreased malondialdehyde. CoQ10 might protect against the overproduction of reactive oxygen species that can promote inflammation and joint damage, the researchers said. In fibromyalgia, CoQ10 was linked with improvements in pain, fatigue, sleep, tender points count, mood disorders, and scores on the Fibromyalgia Impact Questionnaire in most of the included studies. CoQ10 might help in fibromyalgia by improving mitochondrial dysfunction. In APS, CoQ10 improved endothelial function and decreased prothrombotic and pro-inflammatory mediators. CoQ10 might change the expression of genes that promote atherosclerosis. A few patients had GI side effects like nausea and diarrhea, but the supplements were generally well tolerated.

Melatonin. Commonly touted as a sleep aid, this hormone has immune and anti-inflammatory activities that could benefit people with rheumatologic diseases. A study review of 13 articles including 533 patients in Clinical Nutrition ESPEN concluded that melatonin can help improve sleep, pain, and mood in fibromyalgia, OA, and osteoporosis but not in RA. Side effects were minimal, but a few people experienced nausea, drowsiness, nightmares, or headaches. Doses of 5-6 mg/d are likely safe for most adults.
 

The Plant-Derived Antioxidants

Many supplements used in rheumatology are antioxidants derived from herbs, spices, or other plants. When plants encounter stressors, like temperature changes or hungry insects, their secondary metabolism revs up and creates compounds with biological properties. Some of these substances influence inflammatory pathways in the human body, said Luís Silva, PhD, a medicinal chemistry researcher at the Polytechnic Institute of Guarda in Portugal. “If it is possible to reduce these kinds of anti-inflammatory processes, it is also possible that we could help people with inflammatory diseases to a good life, or a better life.”

Dr. Luís Silva

Turmeric and curcumin. You might see this supplement labeled as turmeric, a golden spice in curry powder, or curcumin, an antioxidant compound known as a curcuminoid in turmeric. Curcuminoids might reduce inflammation by scavenging free radicals and inhibiting enzymes that make prostaglandins, Silva said.

Turmeric is the most popular herbal supplement for people with RA, according to Funk’s research. A study review of six publications including 539 patients in Frontiers in Immunology showed that curcumin supplements improved RA patients’ ESR, DAS, swollen joint count, and tender joint count. Turmeric could help patients with OA, too. Patients with OA who took 1000 mg/d of curcumin improved their pain and function, according to a systematic review including 12 studies and 1438 participants in the journal Nutrients. In lupus, small studies are promising but inconclusive, suggested a study review in Frontiers in Immunology.

Watch patients taking turmeric and methotrexate closely, Funk said. Both have been associated with liver problems. Some users also experience GI symptoms like diarrhea because turmeric doesn’t absorb well in the GI tract.

Milk thistle (silymarin). This flowering plant is often marketed as a liver-supporting supplement, but research also suggests promise in RA and OA. A systematic review of 12 studies in Current Rheumatology Reviews suggested that silymarin supplements might help relieve pain, reduce inflammation, and protect the cartilage matrix, synovial membrane, and cartilage cells in joints. This supplement might help via immunomodulatory, anti-inflammatory, antioxidant, and anti-apoptotic properties, the researchers said. Doses of 250-750 mg appear to be safe. Side effects such as gastroenteritis, diarrhea, bloating, and headache can occur.

Boswellia serrata. Sourced from the resin of a tree that grows in dry, mountainous regions of Asia and Africa, Boswellia serrata can help relieve joint pain and stiffness and improve joint function in OA, suggested a systematic review of seven trials involving 545 patients in BMC Complementary Medicine and Therapies. Users saw benefits when taking 100-250 mg/d for 4 weeks or more. Compounds in Boswellia serrata may inhibit 5-lipoxygenase, an enzyme involved in producing inflammatory leukotrienes. No adverse events were reported. In some studies, users have reported GI side effects.

Ginger. Ginger is a popular herbal supplement among people with RA, Funk’s research suggested. One small clinical trial involving 70 patients with RA in the journal Gene showed that taking 1500 mg/d of ginger for 12 weeks improved their DAS and boosted their expression of FoxP3 genes, which are linked with the function of regulatory T cells. A meta-analysis including three studies with 330 patients taking ginger published in the journal Nutrients suggested ginger can reduce pain and systemic inflammation in people with OA. Preclinical studies suggested phenolic compounds in this spicy root, such as gingerols, reduce inflammation through multiple mechanisms.

Funk’s research revealed wide variation in the quality of ginger supplements, reinforcing the importance of selecting an independently verified product. Research suggested a safe dose is up to 2-2.5 g/kg body weight.

Resveratrol. Found in red grapes and red wine, this compound is particularly good at blocking COX-2 enzymes, an important step in the inflammatory cascade, Silva said. “Because of their chemical structure, they have great affinity to these enzymes to lead to their inhibition,” he said. A study review of five articles including 481 patients in The European Journal of Rheumatology showed that people with OA, RA, or Takayasu arteritis who took 250-1000 mg/d of resveratrol saw improvements in pain, function, disease activity, joint swelling, and inflammation, with no side effects.

Cinnamon. This warming spice is gaining popularity as a supplement, reported the American Botanical Council. Cinnamon is often marketed as lowering blood sugar and supporting bone health. In a small study of 36 women with RA published in The Journal of the American College of Nutrition, participants who consumed 2 g/d of cinnamon powder had reduced DASs along with reduced pain and tender and swollen joint counts. Cinnamon may reduce pain by inhibiting prostaglandin and blunt inflammation by reducing the release of arachidonic acid from cell membranes, according to a study review in Frontiers in Pharmacology. GI problems and allergic reactions are among the most common side effects.

Funk, Nikiphorou, Philippou, and Silva all had no relevant disclosures.

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

Many people with rheumatologic diseases try supplements for symptom relief. Here’s what you need to know about some common picks.

Dietary supplements were a $159 billion business in the United States in 2023, and many people with rheumatologic diseases are buying in. Research suggests more than 6 in 10 people with fibromyalgia, nearly 8 in 10 people with Sjögren’s disease, and more than 8 in 10 people with rheumatoid arthritis (RA) take dietary supplements.

Whatever the symptom — pain, swelling, or fatigue — you can probably find a supplement purporting to relieve it. But do these supplements work, and are they safe? A study review in RMD Open comprising 24 systematic reviews and 150 original articles suggests more high-quality research is needed on the effects of dietary supplements on rheumatologic diseases. Most studies have focused on RA or osteoarthritis (OA), where the evidence level is moderate at best.

Dr. Janet Funk

“The studies in this space are usually not very high quality because there’s no money to support them, among other things, plus the products are disparate,” said Janet Funk, MD, MS, professor in the School of Nutritional Sciences and Wellness at the University of Arizona, Tucson. She recommended brushing up on supplements and finding out what patients are taking so you can offer advice and watch for drug-supplement interactions.

When asked for a medication list, many patients forget to report supplements, Funk said. “You have to prompt them specifically. I think some physicians have very negative views about supplements because so little data is known, and patients might pick up on that and decide not to report their use.” She recommended saying something like: “To give you the best possible care, I want to know everything you’re taking, including supplements. The things I’m prescribing could maybe interact with the things you’re taking, so I want to make sure I know about all of it so that together we can figure out if the combination of things is safe.”

The quality of dietary supplements varies, and they aren’t regulated like drugs by the Food and Drug Administration. Funk recommended selecting products verified by NSF or ConsumerLab. They test supplements to ensure the label reflects what’s inside.

This news organization scoured the literature and asked experts to weigh in on the evidence behind popular supplements in rheumatology today.
 

The Essential Nutrients

Vitamin supplements are a staple in many homes — but are they helpful? “Individual vitamin supplements will not provide any benefit unless the person is deficient in a specific vitamin or mineral,” according to Elena Philippou, PhD, RD, associate professor of nutrition-dietetics at the University of Nicosia in Cyprus, and Elena Nikiphorou, MBBS, a rheumatologist at King’s College London in England. For some patients, deficiency is a reality. A retrospective cohort study in The Journal of Clinical Medicine found that people with RA were 17% more likely than age-matched control individuals to have nutrient deficiencies, perhaps because symptoms like fatigue, pain, and nausea affect their eating habits. Here’s what the science says about common vitamin supplements.

Dr. Elena Philippou

Vitamin D. This hormone-like vitamin, which attaches to receptors on immune cells to tamp down inflammation, was the most popular dietary supplement among rheumatology patients in a recent study from the United Kingdom. Vitamin D deficiency is common in people with RA, lupus, Sjögren’s disease, ankylosing spondylitis, systemic sclerosis, and fibromyalgia. In some cases, vitamin D levels track with disease activity, research suggests. Corticosteroids can also make vitamin D deficiency more likely. Can supplements help?

In RA, evidence points to small improvements. A systematic review of 11 studies including 3049 patients published in Nutrition Reviews showed that vitamin D supplements significantly reduced patients’ pain and Disease Activity Score in 28 joints (DAS28) using both C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR).

The research is mixed on the benefits of vitamin D supplementation for fibromyalgia symptoms, according to a study review in SN Comprehensive Clinical Medicine that included two studies and 80 patients on supplementation. However, researchers said it’s still worth discussing the potential benefits of taking vitamin D.

“Vitamin D supplementation is important in the context of various rheumatic diseases to prevent or treat bone disease,” said Philippou and Nikiphorou. “People with rheumatic disease should speak to their healthcare provider and ask to check their blood vitamin D concentration.” The results can help you recommend a dose.

Folate. Patients on methotrexate should take folic acid supplements under the guidance of a healthcare provider, said Philippou and Nikiphorou. The reason: Methotrexate can deplete folic acid levels, increasing the risk for side effects. An analysis of adverse event reports published showed that methotrexate users who took folic acid (or tumor necrosis factor–alpha inhibitors) had a reduced risk for hepatotoxicity or myelosuppression. A commonly recommended dose is 1 mg/d.

Vitamin B12. In a 2024 perspective paper in Rheumatology International, researchers said physicians should assess vitamin B12 levels early in the diagnostic process of rheumatologic diseases. One reason: Many symptoms of pernicious anemia, like fatigue, mimic symptoms of rheumatologic diseases. The gastrointestinal (GI) effects of systemic sclerosis could bring on vitamin B12 deficiency. In a small study in The Journal of Clinical Rheumatology, 44 of 62 patients with systemic sclerosis had low vitamin B12 levels.

Vitamin E. Vitamin E deficiency is rare in healthy adults. However, some medical conditions, like inflammatory bowel disease and malabsorption disorders, can make vitamin E deficiency more likely. In RA, a vitamin E supplement could help reduce joint swelling and sensitivity, according to a systematic review of nine studies including 39,845 patients in The European Journal of Clinical Nutrition. Researchers credit the nutrient’s role in aiding intestinal repair. Use with caution, as this supplement can increase bleeding risk in doses over 1000 mg/d.

Vitamin A. Like vitamin E, vitamin A deficiency is rare in the United States. The risk of oversupplementing is higher than undersupplementing. However, vitamin A deficiency can happen in people with chronic pancreatic, liver, or GI problems. In people with deficiency, a vitamin A supplement can help relieve dry eye symptoms common in Sjögren’s disease, suggests a narrative review published in Nutrients. Vitamin A might help reduce ocular surface changes by supporting the production of proteins that protect the outermost surfaces of the eyes. The recommended daily allowance for vitamin A is 900 μg. High-dose supplements can cause toxicity, resulting in GI symptoms and problems like lethargy, drowsiness, increased intracranial pressure, and skin changes.
 

The Replacements

These substances are similar to naturally occurring compounds in our bodies. The question is whether ingesting them yields benefits.

Glucosamine and chondroitin. Glucosamine and chondroitin occur naturally in our bodies and help us form and protect connective tissues. In pill form, this combo is the most popular dietary supplement for OA, according to research in the journal Maturitas. But studies of its effectiveness yield mixed results. A systematic review of 25 studies published in Inflammopharmacology showed that, in patients with knee OA, supplementation with about 1500 mg of glucosamine per day reduced tibiofemoral joint space narrowing, while supplementation with about 800 mg/d of chondroitin reduced pain intensity and improved physical function, compared with placebo. The duo of glucosamine and chondroitin did not bring significant benefits, perhaps because more studies are needed. Most side effects were mild, but some literature points to the potential for glucosamine to increase warfarin’s blood-thinning effects.

Omega-3 fatty acids. Fish oil is a top-selling supplement, and it might be helpful in inflammatory rheumatologic diseases. A systematic review of 30 studies including 710 patients published in Arthritis Research & Therapy showed that omega-3 fatty acid supplements can improve pain, swollen and tender joint count, DAS28 scores, and Health Assessment Questionnaire scores in patients with RA, psoriatic arthritis, or ankylosing spondylitis. In patients with lupus, a study review that included five studies and 284 patients in The International Journal of Environmental Research and Public Health suggested omega-3 fatty acid supplements could improve ESR, CRP, disease activity, inflammatory markers, oxidative stress, lipid levels, and endothelial function.

Omega-3 fatty acids have anti-inflammatory effects that might explain their benefits. In patients with RA, for example, fish oil supplementation was associated with elevated blood levels of resolvins and protectins, which help quell inflammation, according to a study in Prostaglandins, Leukotrienes and Essential Fatty Acids.

Philippou and Nikiphorou recommended combining food and supplements: Eat oily fish at least twice a week, regularly consume plant-based sources of omega-3s — like chia seeds, flaxseeds, or walnuts — and consider a daily supplement that contains 2 g of omega-3s from docosahexaenoic acid and eicosapentaenoic acid. Most fish oil side effects are mild, like heartburn and bad breath. Fish oil can have blood-thinning effects at high doses, so special attention is needed for patients on anticoagulants.

Probiotics. Building up the good bacteria in your gut might help you fight the effects of rheumatologic diseases. A systematic review of 80 randomized controlled trials in BMC Medicine suggested that therapies targeting the gut microbiota might improve the symptoms or inflammatory factors in celiac disease, lupus, juvenile idiopathic arthritis, psoriasis, Sjögren’s disease, multiple sclerosis, systemic sclerosis, Crohn’s disease, and ulcerative colitis. Probiotics were also shown to relieve pain in fibromyalgia, but they didn’t affect scores on the Fibromyalgia Impact Questionnaire. Probiotics were not helpful in spondyloarthritis or RA. There were no adverse events. By improving the balance of bacteria in the gut, probiotics might inhibit pro-inflammatory factors and signaling pathways and regulate CD4+ T-cell differentiation, the researchers wrote.

Not all probiotic supplements are created equal. Effects can vary by microorganism and dose. Until more high-quality studies are published, Philippou and Nikiphorou recommend daily consumption of probiotic food sources such as yogurt, kefir, sauerkraut, kimchi, tempeh, miso, and kombucha, along with prebiotic food sources such as bananas, onion, artichokes, asparagus, oats, leeks, and garlic.

Collagen. An increasingly popular supplement for hair, skin, and nails, some collagen peptide or hydrolyzed collagen supplements come with claims about joint health, too. Inside our bodies, collagen helps build joints. As a supplement, the jury is still out. A systematic review of 19 studies in The International Journal of Rheumatic Diseases suggested more research is needed to determine whether collagen supplements are harmful or helpful in OA or RA. Studies haven’t shown adverse events, and doses typically range from 2.5 to 15 g/d.

Coenzyme Q10 (CoQ10). This antioxidant occurs naturally in our cells and is produced through microbial fermentation for use in dietary supplements. A study review of 20 articles including 483 patients in Clinical Nutrition ESPEN concluded that CoQ10 supplementation up to 300 mg/d was beneficial in RA, fibromyalgia, or antiphospholipid syndrome (APS).

In RA, CoQ10 supplementation improved disease activity index, ESR, and cytokine levels and decreased malondialdehyde. CoQ10 might protect against the overproduction of reactive oxygen species that can promote inflammation and joint damage, the researchers said. In fibromyalgia, CoQ10 was linked with improvements in pain, fatigue, sleep, tender points count, mood disorders, and scores on the Fibromyalgia Impact Questionnaire in most of the included studies. CoQ10 might help in fibromyalgia by improving mitochondrial dysfunction. In APS, CoQ10 improved endothelial function and decreased prothrombotic and pro-inflammatory mediators. CoQ10 might change the expression of genes that promote atherosclerosis. A few patients had GI side effects like nausea and diarrhea, but the supplements were generally well tolerated.

Melatonin. Commonly touted as a sleep aid, this hormone has immune and anti-inflammatory activities that could benefit people with rheumatologic diseases. A study review of 13 articles including 533 patients in Clinical Nutrition ESPEN concluded that melatonin can help improve sleep, pain, and mood in fibromyalgia, OA, and osteoporosis but not in RA. Side effects were minimal, but a few people experienced nausea, drowsiness, nightmares, or headaches. Doses of 5-6 mg/d are likely safe for most adults.
 

The Plant-Derived Antioxidants

Many supplements used in rheumatology are antioxidants derived from herbs, spices, or other plants. When plants encounter stressors, like temperature changes or hungry insects, their secondary metabolism revs up and creates compounds with biological properties. Some of these substances influence inflammatory pathways in the human body, said Luís Silva, PhD, a medicinal chemistry researcher at the Polytechnic Institute of Guarda in Portugal. “If it is possible to reduce these kinds of anti-inflammatory processes, it is also possible that we could help people with inflammatory diseases to a good life, or a better life.”

Dr. Luís Silva

Turmeric and curcumin. You might see this supplement labeled as turmeric, a golden spice in curry powder, or curcumin, an antioxidant compound known as a curcuminoid in turmeric. Curcuminoids might reduce inflammation by scavenging free radicals and inhibiting enzymes that make prostaglandins, Silva said.

Turmeric is the most popular herbal supplement for people with RA, according to Funk’s research. A study review of six publications including 539 patients in Frontiers in Immunology showed that curcumin supplements improved RA patients’ ESR, DAS, swollen joint count, and tender joint count. Turmeric could help patients with OA, too. Patients with OA who took 1000 mg/d of curcumin improved their pain and function, according to a systematic review including 12 studies and 1438 participants in the journal Nutrients. In lupus, small studies are promising but inconclusive, suggested a study review in Frontiers in Immunology.

Watch patients taking turmeric and methotrexate closely, Funk said. Both have been associated with liver problems. Some users also experience GI symptoms like diarrhea because turmeric doesn’t absorb well in the GI tract.

Milk thistle (silymarin). This flowering plant is often marketed as a liver-supporting supplement, but research also suggests promise in RA and OA. A systematic review of 12 studies in Current Rheumatology Reviews suggested that silymarin supplements might help relieve pain, reduce inflammation, and protect the cartilage matrix, synovial membrane, and cartilage cells in joints. This supplement might help via immunomodulatory, anti-inflammatory, antioxidant, and anti-apoptotic properties, the researchers said. Doses of 250-750 mg appear to be safe. Side effects such as gastroenteritis, diarrhea, bloating, and headache can occur.

Boswellia serrata. Sourced from the resin of a tree that grows in dry, mountainous regions of Asia and Africa, Boswellia serrata can help relieve joint pain and stiffness and improve joint function in OA, suggested a systematic review of seven trials involving 545 patients in BMC Complementary Medicine and Therapies. Users saw benefits when taking 100-250 mg/d for 4 weeks or more. Compounds in Boswellia serrata may inhibit 5-lipoxygenase, an enzyme involved in producing inflammatory leukotrienes. No adverse events were reported. In some studies, users have reported GI side effects.

Ginger. Ginger is a popular herbal supplement among people with RA, Funk’s research suggested. One small clinical trial involving 70 patients with RA in the journal Gene showed that taking 1500 mg/d of ginger for 12 weeks improved their DAS and boosted their expression of FoxP3 genes, which are linked with the function of regulatory T cells. A meta-analysis including three studies with 330 patients taking ginger published in the journal Nutrients suggested ginger can reduce pain and systemic inflammation in people with OA. Preclinical studies suggested phenolic compounds in this spicy root, such as gingerols, reduce inflammation through multiple mechanisms.

Funk’s research revealed wide variation in the quality of ginger supplements, reinforcing the importance of selecting an independently verified product. Research suggested a safe dose is up to 2-2.5 g/kg body weight.

Resveratrol. Found in red grapes and red wine, this compound is particularly good at blocking COX-2 enzymes, an important step in the inflammatory cascade, Silva said. “Because of their chemical structure, they have great affinity to these enzymes to lead to their inhibition,” he said. A study review of five articles including 481 patients in The European Journal of Rheumatology showed that people with OA, RA, or Takayasu arteritis who took 250-1000 mg/d of resveratrol saw improvements in pain, function, disease activity, joint swelling, and inflammation, with no side effects.

Cinnamon. This warming spice is gaining popularity as a supplement, reported the American Botanical Council. Cinnamon is often marketed as lowering blood sugar and supporting bone health. In a small study of 36 women with RA published in The Journal of the American College of Nutrition, participants who consumed 2 g/d of cinnamon powder had reduced DASs along with reduced pain and tender and swollen joint counts. Cinnamon may reduce pain by inhibiting prostaglandin and blunt inflammation by reducing the release of arachidonic acid from cell membranes, according to a study review in Frontiers in Pharmacology. GI problems and allergic reactions are among the most common side effects.

Funk, Nikiphorou, Philippou, and Silva all had no relevant disclosures.

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

Many people with rheumatologic diseases try supplements for symptom relief. Here’s what you need to know about some common picks.

Dietary supplements were a $159 billion business in the United States in 2023, and many people with rheumatologic diseases are buying in. Research suggests more than 6 in 10 people with fibromyalgia, nearly 8 in 10 people with Sjögren’s disease, and more than 8 in 10 people with rheumatoid arthritis (RA) take dietary supplements.

Whatever the symptom — pain, swelling, or fatigue — you can probably find a supplement purporting to relieve it. But do these supplements work, and are they safe? A study review in RMD Open comprising 24 systematic reviews and 150 original articles suggests more high-quality research is needed on the effects of dietary supplements on rheumatologic diseases. Most studies have focused on RA or osteoarthritis (OA), where the evidence level is moderate at best.

Dr. Janet Funk

“The studies in this space are usually not very high quality because there’s no money to support them, among other things, plus the products are disparate,” said Janet Funk, MD, MS, professor in the School of Nutritional Sciences and Wellness at the University of Arizona, Tucson. She recommended brushing up on supplements and finding out what patients are taking so you can offer advice and watch for drug-supplement interactions.

When asked for a medication list, many patients forget to report supplements, Funk said. “You have to prompt them specifically. I think some physicians have very negative views about supplements because so little data is known, and patients might pick up on that and decide not to report their use.” She recommended saying something like: “To give you the best possible care, I want to know everything you’re taking, including supplements. The things I’m prescribing could maybe interact with the things you’re taking, so I want to make sure I know about all of it so that together we can figure out if the combination of things is safe.”

The quality of dietary supplements varies, and they aren’t regulated like drugs by the Food and Drug Administration. Funk recommended selecting products verified by NSF or ConsumerLab. They test supplements to ensure the label reflects what’s inside.

This news organization scoured the literature and asked experts to weigh in on the evidence behind popular supplements in rheumatology today.
 

The Essential Nutrients

Vitamin supplements are a staple in many homes — but are they helpful? “Individual vitamin supplements will not provide any benefit unless the person is deficient in a specific vitamin or mineral,” according to Elena Philippou, PhD, RD, associate professor of nutrition-dietetics at the University of Nicosia in Cyprus, and Elena Nikiphorou, MBBS, a rheumatologist at King’s College London in England. For some patients, deficiency is a reality. A retrospective cohort study in The Journal of Clinical Medicine found that people with RA were 17% more likely than age-matched control individuals to have nutrient deficiencies, perhaps because symptoms like fatigue, pain, and nausea affect their eating habits. Here’s what the science says about common vitamin supplements.

Dr. Elena Philippou

Vitamin D. This hormone-like vitamin, which attaches to receptors on immune cells to tamp down inflammation, was the most popular dietary supplement among rheumatology patients in a recent study from the United Kingdom. Vitamin D deficiency is common in people with RA, lupus, Sjögren’s disease, ankylosing spondylitis, systemic sclerosis, and fibromyalgia. In some cases, vitamin D levels track with disease activity, research suggests. Corticosteroids can also make vitamin D deficiency more likely. Can supplements help?

In RA, evidence points to small improvements. A systematic review of 11 studies including 3049 patients published in Nutrition Reviews showed that vitamin D supplements significantly reduced patients’ pain and Disease Activity Score in 28 joints (DAS28) using both C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR).

The research is mixed on the benefits of vitamin D supplementation for fibromyalgia symptoms, according to a study review in SN Comprehensive Clinical Medicine that included two studies and 80 patients on supplementation. However, researchers said it’s still worth discussing the potential benefits of taking vitamin D.

“Vitamin D supplementation is important in the context of various rheumatic diseases to prevent or treat bone disease,” said Philippou and Nikiphorou. “People with rheumatic disease should speak to their healthcare provider and ask to check their blood vitamin D concentration.” The results can help you recommend a dose.

Folate. Patients on methotrexate should take folic acid supplements under the guidance of a healthcare provider, said Philippou and Nikiphorou. The reason: Methotrexate can deplete folic acid levels, increasing the risk for side effects. An analysis of adverse event reports published showed that methotrexate users who took folic acid (or tumor necrosis factor–alpha inhibitors) had a reduced risk for hepatotoxicity or myelosuppression. A commonly recommended dose is 1 mg/d.

Vitamin B12. In a 2024 perspective paper in Rheumatology International, researchers said physicians should assess vitamin B12 levels early in the diagnostic process of rheumatologic diseases. One reason: Many symptoms of pernicious anemia, like fatigue, mimic symptoms of rheumatologic diseases. The gastrointestinal (GI) effects of systemic sclerosis could bring on vitamin B12 deficiency. In a small study in The Journal of Clinical Rheumatology, 44 of 62 patients with systemic sclerosis had low vitamin B12 levels.

Vitamin E. Vitamin E deficiency is rare in healthy adults. However, some medical conditions, like inflammatory bowel disease and malabsorption disorders, can make vitamin E deficiency more likely. In RA, a vitamin E supplement could help reduce joint swelling and sensitivity, according to a systematic review of nine studies including 39,845 patients in The European Journal of Clinical Nutrition. Researchers credit the nutrient’s role in aiding intestinal repair. Use with caution, as this supplement can increase bleeding risk in doses over 1000 mg/d.

Vitamin A. Like vitamin E, vitamin A deficiency is rare in the United States. The risk of oversupplementing is higher than undersupplementing. However, vitamin A deficiency can happen in people with chronic pancreatic, liver, or GI problems. In people with deficiency, a vitamin A supplement can help relieve dry eye symptoms common in Sjögren’s disease, suggests a narrative review published in Nutrients. Vitamin A might help reduce ocular surface changes by supporting the production of proteins that protect the outermost surfaces of the eyes. The recommended daily allowance for vitamin A is 900 μg. High-dose supplements can cause toxicity, resulting in GI symptoms and problems like lethargy, drowsiness, increased intracranial pressure, and skin changes.
 

The Replacements

These substances are similar to naturally occurring compounds in our bodies. The question is whether ingesting them yields benefits.

Glucosamine and chondroitin. Glucosamine and chondroitin occur naturally in our bodies and help us form and protect connective tissues. In pill form, this combo is the most popular dietary supplement for OA, according to research in the journal Maturitas. But studies of its effectiveness yield mixed results. A systematic review of 25 studies published in Inflammopharmacology showed that, in patients with knee OA, supplementation with about 1500 mg of glucosamine per day reduced tibiofemoral joint space narrowing, while supplementation with about 800 mg/d of chondroitin reduced pain intensity and improved physical function, compared with placebo. The duo of glucosamine and chondroitin did not bring significant benefits, perhaps because more studies are needed. Most side effects were mild, but some literature points to the potential for glucosamine to increase warfarin’s blood-thinning effects.

Omega-3 fatty acids. Fish oil is a top-selling supplement, and it might be helpful in inflammatory rheumatologic diseases. A systematic review of 30 studies including 710 patients published in Arthritis Research & Therapy showed that omega-3 fatty acid supplements can improve pain, swollen and tender joint count, DAS28 scores, and Health Assessment Questionnaire scores in patients with RA, psoriatic arthritis, or ankylosing spondylitis. In patients with lupus, a study review that included five studies and 284 patients in The International Journal of Environmental Research and Public Health suggested omega-3 fatty acid supplements could improve ESR, CRP, disease activity, inflammatory markers, oxidative stress, lipid levels, and endothelial function.

Omega-3 fatty acids have anti-inflammatory effects that might explain their benefits. In patients with RA, for example, fish oil supplementation was associated with elevated blood levels of resolvins and protectins, which help quell inflammation, according to a study in Prostaglandins, Leukotrienes and Essential Fatty Acids.

Philippou and Nikiphorou recommended combining food and supplements: Eat oily fish at least twice a week, regularly consume plant-based sources of omega-3s — like chia seeds, flaxseeds, or walnuts — and consider a daily supplement that contains 2 g of omega-3s from docosahexaenoic acid and eicosapentaenoic acid. Most fish oil side effects are mild, like heartburn and bad breath. Fish oil can have blood-thinning effects at high doses, so special attention is needed for patients on anticoagulants.

Probiotics. Building up the good bacteria in your gut might help you fight the effects of rheumatologic diseases. A systematic review of 80 randomized controlled trials in BMC Medicine suggested that therapies targeting the gut microbiota might improve the symptoms or inflammatory factors in celiac disease, lupus, juvenile idiopathic arthritis, psoriasis, Sjögren’s disease, multiple sclerosis, systemic sclerosis, Crohn’s disease, and ulcerative colitis. Probiotics were also shown to relieve pain in fibromyalgia, but they didn’t affect scores on the Fibromyalgia Impact Questionnaire. Probiotics were not helpful in spondyloarthritis or RA. There were no adverse events. By improving the balance of bacteria in the gut, probiotics might inhibit pro-inflammatory factors and signaling pathways and regulate CD4+ T-cell differentiation, the researchers wrote.

Not all probiotic supplements are created equal. Effects can vary by microorganism and dose. Until more high-quality studies are published, Philippou and Nikiphorou recommend daily consumption of probiotic food sources such as yogurt, kefir, sauerkraut, kimchi, tempeh, miso, and kombucha, along with prebiotic food sources such as bananas, onion, artichokes, asparagus, oats, leeks, and garlic.

Collagen. An increasingly popular supplement for hair, skin, and nails, some collagen peptide or hydrolyzed collagen supplements come with claims about joint health, too. Inside our bodies, collagen helps build joints. As a supplement, the jury is still out. A systematic review of 19 studies in The International Journal of Rheumatic Diseases suggested more research is needed to determine whether collagen supplements are harmful or helpful in OA or RA. Studies haven’t shown adverse events, and doses typically range from 2.5 to 15 g/d.

Coenzyme Q10 (CoQ10). This antioxidant occurs naturally in our cells and is produced through microbial fermentation for use in dietary supplements. A study review of 20 articles including 483 patients in Clinical Nutrition ESPEN concluded that CoQ10 supplementation up to 300 mg/d was beneficial in RA, fibromyalgia, or antiphospholipid syndrome (APS).

In RA, CoQ10 supplementation improved disease activity index, ESR, and cytokine levels and decreased malondialdehyde. CoQ10 might protect against the overproduction of reactive oxygen species that can promote inflammation and joint damage, the researchers said. In fibromyalgia, CoQ10 was linked with improvements in pain, fatigue, sleep, tender points count, mood disorders, and scores on the Fibromyalgia Impact Questionnaire in most of the included studies. CoQ10 might help in fibromyalgia by improving mitochondrial dysfunction. In APS, CoQ10 improved endothelial function and decreased prothrombotic and pro-inflammatory mediators. CoQ10 might change the expression of genes that promote atherosclerosis. A few patients had GI side effects like nausea and diarrhea, but the supplements were generally well tolerated.

Melatonin. Commonly touted as a sleep aid, this hormone has immune and anti-inflammatory activities that could benefit people with rheumatologic diseases. A study review of 13 articles including 533 patients in Clinical Nutrition ESPEN concluded that melatonin can help improve sleep, pain, and mood in fibromyalgia, OA, and osteoporosis but not in RA. Side effects were minimal, but a few people experienced nausea, drowsiness, nightmares, or headaches. Doses of 5-6 mg/d are likely safe for most adults.
 

The Plant-Derived Antioxidants

Many supplements used in rheumatology are antioxidants derived from herbs, spices, or other plants. When plants encounter stressors, like temperature changes or hungry insects, their secondary metabolism revs up and creates compounds with biological properties. Some of these substances influence inflammatory pathways in the human body, said Luís Silva, PhD, a medicinal chemistry researcher at the Polytechnic Institute of Guarda in Portugal. “If it is possible to reduce these kinds of anti-inflammatory processes, it is also possible that we could help people with inflammatory diseases to a good life, or a better life.”

Dr. Luís Silva

Turmeric and curcumin. You might see this supplement labeled as turmeric, a golden spice in curry powder, or curcumin, an antioxidant compound known as a curcuminoid in turmeric. Curcuminoids might reduce inflammation by scavenging free radicals and inhibiting enzymes that make prostaglandins, Silva said.

Turmeric is the most popular herbal supplement for people with RA, according to Funk’s research. A study review of six publications including 539 patients in Frontiers in Immunology showed that curcumin supplements improved RA patients’ ESR, DAS, swollen joint count, and tender joint count. Turmeric could help patients with OA, too. Patients with OA who took 1000 mg/d of curcumin improved their pain and function, according to a systematic review including 12 studies and 1438 participants in the journal Nutrients. In lupus, small studies are promising but inconclusive, suggested a study review in Frontiers in Immunology.

Watch patients taking turmeric and methotrexate closely, Funk said. Both have been associated with liver problems. Some users also experience GI symptoms like diarrhea because turmeric doesn’t absorb well in the GI tract.

Milk thistle (silymarin). This flowering plant is often marketed as a liver-supporting supplement, but research also suggests promise in RA and OA. A systematic review of 12 studies in Current Rheumatology Reviews suggested that silymarin supplements might help relieve pain, reduce inflammation, and protect the cartilage matrix, synovial membrane, and cartilage cells in joints. This supplement might help via immunomodulatory, anti-inflammatory, antioxidant, and anti-apoptotic properties, the researchers said. Doses of 250-750 mg appear to be safe. Side effects such as gastroenteritis, diarrhea, bloating, and headache can occur.

Boswellia serrata. Sourced from the resin of a tree that grows in dry, mountainous regions of Asia and Africa, Boswellia serrata can help relieve joint pain and stiffness and improve joint function in OA, suggested a systematic review of seven trials involving 545 patients in BMC Complementary Medicine and Therapies. Users saw benefits when taking 100-250 mg/d for 4 weeks or more. Compounds in Boswellia serrata may inhibit 5-lipoxygenase, an enzyme involved in producing inflammatory leukotrienes. No adverse events were reported. In some studies, users have reported GI side effects.

Ginger. Ginger is a popular herbal supplement among people with RA, Funk’s research suggested. One small clinical trial involving 70 patients with RA in the journal Gene showed that taking 1500 mg/d of ginger for 12 weeks improved their DAS and boosted their expression of FoxP3 genes, which are linked with the function of regulatory T cells. A meta-analysis including three studies with 330 patients taking ginger published in the journal Nutrients suggested ginger can reduce pain and systemic inflammation in people with OA. Preclinical studies suggested phenolic compounds in this spicy root, such as gingerols, reduce inflammation through multiple mechanisms.

Funk’s research revealed wide variation in the quality of ginger supplements, reinforcing the importance of selecting an independently verified product. Research suggested a safe dose is up to 2-2.5 g/kg body weight.

Resveratrol. Found in red grapes and red wine, this compound is particularly good at blocking COX-2 enzymes, an important step in the inflammatory cascade, Silva said. “Because of their chemical structure, they have great affinity to these enzymes to lead to their inhibition,” he said. A study review of five articles including 481 patients in The European Journal of Rheumatology showed that people with OA, RA, or Takayasu arteritis who took 250-1000 mg/d of resveratrol saw improvements in pain, function, disease activity, joint swelling, and inflammation, with no side effects.

Cinnamon. This warming spice is gaining popularity as a supplement, reported the American Botanical Council. Cinnamon is often marketed as lowering blood sugar and supporting bone health. In a small study of 36 women with RA published in The Journal of the American College of Nutrition, participants who consumed 2 g/d of cinnamon powder had reduced DASs along with reduced pain and tender and swollen joint counts. Cinnamon may reduce pain by inhibiting prostaglandin and blunt inflammation by reducing the release of arachidonic acid from cell membranes, according to a study review in Frontiers in Pharmacology. GI problems and allergic reactions are among the most common side effects.

Funk, Nikiphorou, Philippou, and Silva all had no relevant disclosures.

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

LOS ANGELES — Metformin prescribed within a week of SARS-CoV-2 infection was associated with a 53% reduction in long COVID or death over 6 months in people without diabetes or prediabetes, according to data presented at the Infectious Disease Week (IDWeek) 2024 Annual Meeting.

Long COVID was determined by using the diagnostic code U09.9 or a computable phenotype based on symptoms and conditions. Most participants in this study were infected with the Omicron variant.

Researchers, led by Carolyn Bramante, MD, MPH, an internist, pediatrician, and obesity medicine specialist at the University of Minnesota Medical School in Minneapolis, simulated a randomized controlled trial of metformin vs control using the National COVID Cohort Collaborative (N3C) Electronic Health Record Database.

The intervention was a prescription for metformin within 6 days of SARS-CoV-2 infection. Those in the control group, which was designed to mimic placebo, had a prescription for fluvoxamine, fluticasone, ivermectin, or montelukast (all drugs that have been used off-label for COVID but have shown no effect on acute COVID outcomes in clinical trials). Exclusions included anyone with a previous metformin prescription or a comparator prescription; any indication for chronic metformin use; or a contraindication for metformin.
 

Why Study Metformin for Long COVID?

Dr. Bramante led a previous randomized controlled trial, COVID-OUT, with 1323 people that indicated metformin showed possible benefit for preventing the more severe components of COVID-19. She also led a 2020 review, in which she examined electronic health records from adults with type 2 diabetes or obesity. The researchers found that women taking metformin before they developed COVID-19 were significantly less likely to die after being hospitalized — although men didn’t see the same protective effect. Another randomized trial of 20 people found that 60% of those taking metformin vs 100% of those given a placebo had detectable SARS-CoV-2 viral load by day 4.

Other trials have highlighted the anti-inflammatory and antiviral properties of metformin. The existing evidence coupled with metformin’s well-established safety profile, led Dr. Bramante’s team to conduct the current simulated trial in people without diabetes or prediabetes. Dr. Bramante noted that metformin’s only US Food and Drug Administration–approved indication is for diabetes.

The current study featured a similar racial/ethnic makeup in the metformin and control groups: 16% and 17% were Black and 16% and 13% were Hispanic, respectively. Within 6 months, 4.0% in the metformin group developed long COVID or died compared with 8.5% in the control group (Relative Risk [RR], 0.47; 95% CI, 0.25-0.89). For prescriptions made on days 0-1 relative to infection, the RR was 0.39 (95% CI, 0.12-1.24). When metformin was prescribed on days 0-14, the RR was 0.75 (95% CI, 0.52-1.08).

The reason it’s important to have an active comparator is to control for things that can’t be measured, such as engagement in healthcare and the placebo effect, Dr. Bramante said.

Emily Erbelding, MD, MPH, director of the Division of Microbiology and Infectious Diseases at the National Institute of Allergy and Infectious Diseases, who was not part of the study, noted the potential implications of the findings.
 

Proven Safety and Low Cost of Metformin 

“We don’t have therapies for long COVID, and we don’t know how to prevent it in people who have SARS-CoV-2 infections,” Dr. Erbelding noted. “This analysis points to metformin, a drug that millions of people have taken safely for their diabetes or their borderline diabetes. It’s licensed, it’s out there, and it’s inexpensive. The fact that we have data that point to this potentially being a therapy is important. I think that’s the power of this.”

Dr. Erbelding said a strength of the study is the size of the N3C Electronic Health Record Database (with data on nearly 9 million COVID cases) the researchers used to simulate the randomized controlled trial.

“(These results) gives us a reason to think about doing a large randomized controlled study with metformin,” she said. However, there are some limitations, she noted.

“The definition of long COVID may not have been applied exactly the same way across all the patients and you don’t know what led the prescribers to prescribe metformin. There might have been confounders that couldn’t be controlled for or weren’t evident in the way they approached the data.”

This study has “relatively rigorous methodology for an observational study,” Dr. Erbelding said. “It’s novel to try to simulate a randomized controlled trial through a large, observational, electronic record–based cohort. Maybe we should be doing more of this because these bioinformatic systems exist now. And we need to get all the public health use out of them that we can.” 

“The fact that they may be unlocking something new here that needs follow-up in a truly randomized controlled trial is important as well because there are a lot of people out there suffering from long COVID.”

Bramante and Erbelding disclosed no relevant financial relationships. This research was supported in part by the intramural/extramural research program of the National Center for Advancing Translational Science, National Institutes of Health.
 

A version of this article appeared on Medscape.com.

LOS ANGELES — Metformin prescribed within a week of SARS-CoV-2 infection was associated with a 53% reduction in long COVID or death over 6 months in people without diabetes or prediabetes, according to data presented at the Infectious Disease Week (IDWeek) 2024 Annual Meeting.

Long COVID was determined by using the diagnostic code U09.9 or a computable phenotype based on symptoms and conditions. Most participants in this study were infected with the Omicron variant.

Researchers, led by Carolyn Bramante, MD, MPH, an internist, pediatrician, and obesity medicine specialist at the University of Minnesota Medical School in Minneapolis, simulated a randomized controlled trial of metformin vs control using the National COVID Cohort Collaborative (N3C) Electronic Health Record Database.

The intervention was a prescription for metformin within 6 days of SARS-CoV-2 infection. Those in the control group, which was designed to mimic placebo, had a prescription for fluvoxamine, fluticasone, ivermectin, or montelukast (all drugs that have been used off-label for COVID but have shown no effect on acute COVID outcomes in clinical trials). Exclusions included anyone with a previous metformin prescription or a comparator prescription; any indication for chronic metformin use; or a contraindication for metformin.
 

Why Study Metformin for Long COVID?

Dr. Bramante led a previous randomized controlled trial, COVID-OUT, with 1323 people that indicated metformin showed possible benefit for preventing the more severe components of COVID-19. She also led a 2020 review, in which she examined electronic health records from adults with type 2 diabetes or obesity. The researchers found that women taking metformin before they developed COVID-19 were significantly less likely to die after being hospitalized — although men didn’t see the same protective effect. Another randomized trial of 20 people found that 60% of those taking metformin vs 100% of those given a placebo had detectable SARS-CoV-2 viral load by day 4.

Other trials have highlighted the anti-inflammatory and antiviral properties of metformin. The existing evidence coupled with metformin’s well-established safety profile, led Dr. Bramante’s team to conduct the current simulated trial in people without diabetes or prediabetes. Dr. Bramante noted that metformin’s only US Food and Drug Administration–approved indication is for diabetes.

The current study featured a similar racial/ethnic makeup in the metformin and control groups: 16% and 17% were Black and 16% and 13% were Hispanic, respectively. Within 6 months, 4.0% in the metformin group developed long COVID or died compared with 8.5% in the control group (Relative Risk [RR], 0.47; 95% CI, 0.25-0.89). For prescriptions made on days 0-1 relative to infection, the RR was 0.39 (95% CI, 0.12-1.24). When metformin was prescribed on days 0-14, the RR was 0.75 (95% CI, 0.52-1.08).

The reason it’s important to have an active comparator is to control for things that can’t be measured, such as engagement in healthcare and the placebo effect, Dr. Bramante said.

Emily Erbelding, MD, MPH, director of the Division of Microbiology and Infectious Diseases at the National Institute of Allergy and Infectious Diseases, who was not part of the study, noted the potential implications of the findings.
 

Proven Safety and Low Cost of Metformin 

“We don’t have therapies for long COVID, and we don’t know how to prevent it in people who have SARS-CoV-2 infections,” Dr. Erbelding noted. “This analysis points to metformin, a drug that millions of people have taken safely for their diabetes or their borderline diabetes. It’s licensed, it’s out there, and it’s inexpensive. The fact that we have data that point to this potentially being a therapy is important. I think that’s the power of this.”

Dr. Erbelding said a strength of the study is the size of the N3C Electronic Health Record Database (with data on nearly 9 million COVID cases) the researchers used to simulate the randomized controlled trial.

“(These results) gives us a reason to think about doing a large randomized controlled study with metformin,” she said. However, there are some limitations, she noted.

“The definition of long COVID may not have been applied exactly the same way across all the patients and you don’t know what led the prescribers to prescribe metformin. There might have been confounders that couldn’t be controlled for or weren’t evident in the way they approached the data.”

This study has “relatively rigorous methodology for an observational study,” Dr. Erbelding said. “It’s novel to try to simulate a randomized controlled trial through a large, observational, electronic record–based cohort. Maybe we should be doing more of this because these bioinformatic systems exist now. And we need to get all the public health use out of them that we can.” 

“The fact that they may be unlocking something new here that needs follow-up in a truly randomized controlled trial is important as well because there are a lot of people out there suffering from long COVID.”

Bramante and Erbelding disclosed no relevant financial relationships. This research was supported in part by the intramural/extramural research program of the National Center for Advancing Translational Science, National Institutes of Health.
 

A version of this article appeared on Medscape.com.

LOS ANGELES — Metformin prescribed within a week of SARS-CoV-2 infection was associated with a 53% reduction in long COVID or death over 6 months in people without diabetes or prediabetes, according to data presented at the Infectious Disease Week (IDWeek) 2024 Annual Meeting.

Long COVID was determined by using the diagnostic code U09.9 or a computable phenotype based on symptoms and conditions. Most participants in this study were infected with the Omicron variant.

Researchers, led by Carolyn Bramante, MD, MPH, an internist, pediatrician, and obesity medicine specialist at the University of Minnesota Medical School in Minneapolis, simulated a randomized controlled trial of metformin vs control using the National COVID Cohort Collaborative (N3C) Electronic Health Record Database.

The intervention was a prescription for metformin within 6 days of SARS-CoV-2 infection. Those in the control group, which was designed to mimic placebo, had a prescription for fluvoxamine, fluticasone, ivermectin, or montelukast (all drugs that have been used off-label for COVID but have shown no effect on acute COVID outcomes in clinical trials). Exclusions included anyone with a previous metformin prescription or a comparator prescription; any indication for chronic metformin use; or a contraindication for metformin.
 

Why Study Metformin for Long COVID?

Dr. Bramante led a previous randomized controlled trial, COVID-OUT, with 1323 people that indicated metformin showed possible benefit for preventing the more severe components of COVID-19. She also led a 2020 review, in which she examined electronic health records from adults with type 2 diabetes or obesity. The researchers found that women taking metformin before they developed COVID-19 were significantly less likely to die after being hospitalized — although men didn’t see the same protective effect. Another randomized trial of 20 people found that 60% of those taking metformin vs 100% of those given a placebo had detectable SARS-CoV-2 viral load by day 4.

Other trials have highlighted the anti-inflammatory and antiviral properties of metformin. The existing evidence coupled with metformin’s well-established safety profile, led Dr. Bramante’s team to conduct the current simulated trial in people without diabetes or prediabetes. Dr. Bramante noted that metformin’s only US Food and Drug Administration–approved indication is for diabetes.

The current study featured a similar racial/ethnic makeup in the metformin and control groups: 16% and 17% were Black and 16% and 13% were Hispanic, respectively. Within 6 months, 4.0% in the metformin group developed long COVID or died compared with 8.5% in the control group (Relative Risk [RR], 0.47; 95% CI, 0.25-0.89). For prescriptions made on days 0-1 relative to infection, the RR was 0.39 (95% CI, 0.12-1.24). When metformin was prescribed on days 0-14, the RR was 0.75 (95% CI, 0.52-1.08).

The reason it’s important to have an active comparator is to control for things that can’t be measured, such as engagement in healthcare and the placebo effect, Dr. Bramante said.

Emily Erbelding, MD, MPH, director of the Division of Microbiology and Infectious Diseases at the National Institute of Allergy and Infectious Diseases, who was not part of the study, noted the potential implications of the findings.
 

Proven Safety and Low Cost of Metformin 

“We don’t have therapies for long COVID, and we don’t know how to prevent it in people who have SARS-CoV-2 infections,” Dr. Erbelding noted. “This analysis points to metformin, a drug that millions of people have taken safely for their diabetes or their borderline diabetes. It’s licensed, it’s out there, and it’s inexpensive. The fact that we have data that point to this potentially being a therapy is important. I think that’s the power of this.”

Dr. Erbelding said a strength of the study is the size of the N3C Electronic Health Record Database (with data on nearly 9 million COVID cases) the researchers used to simulate the randomized controlled trial.

“(These results) gives us a reason to think about doing a large randomized controlled study with metformin,” she said. However, there are some limitations, she noted.

“The definition of long COVID may not have been applied exactly the same way across all the patients and you don’t know what led the prescribers to prescribe metformin. There might have been confounders that couldn’t be controlled for or weren’t evident in the way they approached the data.”

This study has “relatively rigorous methodology for an observational study,” Dr. Erbelding said. “It’s novel to try to simulate a randomized controlled trial through a large, observational, electronic record–based cohort. Maybe we should be doing more of this because these bioinformatic systems exist now. And we need to get all the public health use out of them that we can.” 

“The fact that they may be unlocking something new here that needs follow-up in a truly randomized controlled trial is important as well because there are a lot of people out there suffering from long COVID.”

Bramante and Erbelding disclosed no relevant financial relationships. This research was supported in part by the intramural/extramural research program of the National Center for Advancing Translational Science, National Institutes of Health.
 

A version of this article appeared on Medscape.com.

TOPLINE:

The use of newer biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs) for treating juvenile idiopathic arthritis (JIA) rose sharply from 2001 to 2022, while the use of conventional synthetic DMARDs (csDMARDs) plummeted, with adalimumab becoming the most commonly used b/tsDMARD.

METHODOLOGY:

• Researchers performed a serial cross-sectional study using Merative MarketScan Commercial Claims and Encounters data from 2000 to 2022 to describe recent trends in DMARD use for children with JIA in the United States.
• They identified 20,258 new episodes of DMARD use among 13,696 children with JIA (median age, 14 years; 67.5% girls) who newly initiated at least one DMARD.
• Participants were required to have ≥ 365 days of continuous healthcare and pharmacy eligibility prior to the index date, defined as the date of DMARD initiation.

TAKEAWAY:

• The use of csDMARDs declined from 89.5% to 43.2% between 2001 and 2022 (P < .001 for trend), whereas the use of bDMARDs increased from 10.5% to 50.0% over the same period (P < .001).
• Methotrexate was the most commonly used DMARD throughout the study period ; however, as with other csDMARDs, its use declined from 42.1% in 2001 to 21.5% in 2022 (P < .001 ).
• Use of the tumor necrosis factor inhibitor adalimumab doubled from 7% in 2007 to 14% in 2008 and increased further up to 20.5% by 2022; adalimumab also became the most predominantly used b/tsDMARD after csDMARD monotherapy, accounting for 77.8% of prescriptions following csDMARDs in 2022.
• Even though the use of individual TNF inhibitors increased, their overall popularity fell in recent years as the use of newer b/tsDMARDs, such as ustekinumab and secukinumab, increased.

IN PRACTICE:

“These real-world treatment patterns give us insight into how selection of therapies for JIA has evolved with increasing availability of effective agents and help prepare for future studies on comparative DMARD safety and effectiveness,” the authors wrote.

SOURCE:

The study was led by Priyanka Yalamanchili, PharmD, MS, Center for Pharmacoepidemiology and Treatment Science, Institute for Health, Rutgers University, New Brunswick, New Jersey, and was published online October 22, 2024, in Arthritis & Rheumatology.

LIMITATIONS: 

The dependence on commercial claims data may have limited the generalizability of the findings to other populations, such as those with public insurance or without insurance. The study did not have access to demographic data of the participants to investigate the presence of disparities in the use of DMARDs. Moreover, the lack of clinical details about the patients with JIA, including disease severity and specialty of prescribers, may have affected the interpretation of the results.

DISCLOSURES:

The study was supported by funding from the National Institute of Arthritis and Musculoskeletal and Skin Diseases and several other institutes of the National Institutes of Health, as well as the Rheumatology Research Foundation and the Juvenile Diabetes Research Foundation. No conflicts of interest were reported by the authors.

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:

The use of newer biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs) for treating juvenile idiopathic arthritis (JIA) rose sharply from 2001 to 2022, while the use of conventional synthetic DMARDs (csDMARDs) plummeted, with adalimumab becoming the most commonly used b/tsDMARD.

METHODOLOGY:

• Researchers performed a serial cross-sectional study using Merative MarketScan Commercial Claims and Encounters data from 2000 to 2022 to describe recent trends in DMARD use for children with JIA in the United States.
• They identified 20,258 new episodes of DMARD use among 13,696 children with JIA (median age, 14 years; 67.5% girls) who newly initiated at least one DMARD.
• Participants were required to have ≥ 365 days of continuous healthcare and pharmacy eligibility prior to the index date, defined as the date of DMARD initiation.

TAKEAWAY:

• The use of csDMARDs declined from 89.5% to 43.2% between 2001 and 2022 (P < .001 for trend), whereas the use of bDMARDs increased from 10.5% to 50.0% over the same period (P < .001).
• Methotrexate was the most commonly used DMARD throughout the study period ; however, as with other csDMARDs, its use declined from 42.1% in 2001 to 21.5% in 2022 (P < .001 ).
• Use of the tumor necrosis factor inhibitor adalimumab doubled from 7% in 2007 to 14% in 2008 and increased further up to 20.5% by 2022; adalimumab also became the most predominantly used b/tsDMARD after csDMARD monotherapy, accounting for 77.8% of prescriptions following csDMARDs in 2022.
• Even though the use of individual TNF inhibitors increased, their overall popularity fell in recent years as the use of newer b/tsDMARDs, such as ustekinumab and secukinumab, increased.

IN PRACTICE:

“These real-world treatment patterns give us insight into how selection of therapies for JIA has evolved with increasing availability of effective agents and help prepare for future studies on comparative DMARD safety and effectiveness,” the authors wrote.

SOURCE:

The study was led by Priyanka Yalamanchili, PharmD, MS, Center for Pharmacoepidemiology and Treatment Science, Institute for Health, Rutgers University, New Brunswick, New Jersey, and was published online October 22, 2024, in Arthritis & Rheumatology.

LIMITATIONS: 

The dependence on commercial claims data may have limited the generalizability of the findings to other populations, such as those with public insurance or without insurance. The study did not have access to demographic data of the participants to investigate the presence of disparities in the use of DMARDs. Moreover, the lack of clinical details about the patients with JIA, including disease severity and specialty of prescribers, may have affected the interpretation of the results.

DISCLOSURES:

The study was supported by funding from the National Institute of Arthritis and Musculoskeletal and Skin Diseases and several other institutes of the National Institutes of Health, as well as the Rheumatology Research Foundation and the Juvenile Diabetes Research Foundation. No conflicts of interest were reported by the authors.

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:

The use of newer biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs) for treating juvenile idiopathic arthritis (JIA) rose sharply from 2001 to 2022, while the use of conventional synthetic DMARDs (csDMARDs) plummeted, with adalimumab becoming the most commonly used b/tsDMARD.

METHODOLOGY:

• Researchers performed a serial cross-sectional study using Merative MarketScan Commercial Claims and Encounters data from 2000 to 2022 to describe recent trends in DMARD use for children with JIA in the United States.
• They identified 20,258 new episodes of DMARD use among 13,696 children with JIA (median age, 14 years; 67.5% girls) who newly initiated at least one DMARD.
• Participants were required to have ≥ 365 days of continuous healthcare and pharmacy eligibility prior to the index date, defined as the date of DMARD initiation.

TAKEAWAY:

• The use of csDMARDs declined from 89.5% to 43.2% between 2001 and 2022 (P < .001 for trend), whereas the use of bDMARDs increased from 10.5% to 50.0% over the same period (P < .001).
• Methotrexate was the most commonly used DMARD throughout the study period ; however, as with other csDMARDs, its use declined from 42.1% in 2001 to 21.5% in 2022 (P < .001 ).
• Use of the tumor necrosis factor inhibitor adalimumab doubled from 7% in 2007 to 14% in 2008 and increased further up to 20.5% by 2022; adalimumab also became the most predominantly used b/tsDMARD after csDMARD monotherapy, accounting for 77.8% of prescriptions following csDMARDs in 2022.
• Even though the use of individual TNF inhibitors increased, their overall popularity fell in recent years as the use of newer b/tsDMARDs, such as ustekinumab and secukinumab, increased.

IN PRACTICE:

“These real-world treatment patterns give us insight into how selection of therapies for JIA has evolved with increasing availability of effective agents and help prepare for future studies on comparative DMARD safety and effectiveness,” the authors wrote.

SOURCE:

The study was led by Priyanka Yalamanchili, PharmD, MS, Center for Pharmacoepidemiology and Treatment Science, Institute for Health, Rutgers University, New Brunswick, New Jersey, and was published online October 22, 2024, in Arthritis & Rheumatology.

LIMITATIONS: 

The dependence on commercial claims data may have limited the generalizability of the findings to other populations, such as those with public insurance or without insurance. The study did not have access to demographic data of the participants to investigate the presence of disparities in the use of DMARDs. Moreover, the lack of clinical details about the patients with JIA, including disease severity and specialty of prescribers, may have affected the interpretation of the results.

DISCLOSURES:

The study was supported by funding from the National Institute of Arthritis and Musculoskeletal and Skin Diseases and several other institutes of the National Institutes of Health, as well as the Rheumatology Research Foundation and the Juvenile Diabetes Research Foundation. No conflicts of interest were reported by the authors.

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: 

In patients with giant cell arteritis (GCA), intravenous methylprednisolone compared with oral glucocorticoids alone does not improve visual acuity and increases the risk for diabetes within the first year. Survival rates do not differ with these two treatments.

METHODOLOGY:

• Researchers conducted a population-based retrospective study at three centers in Sweden to assess the clinical characteristics, treatment-related toxicity, and mortality in patients with GCA who were receiving high-dose intravenous methylprednisolone.
• A total of 419 patients with biopsy-confirmed GCA (mean age at diagnosis, 75 years; 69% women) diagnosed from 2004 to 2019 were included.
• Patients were treated with either intravenous methylprednisolone (n = 111) at a dose of 500-1000 mg per day for 3 consecutive days or oral glucocorticoids alone (n = 308).
• Ischemic visual complications considered to indicate visual involvement were confirmed by an ophthalmologist, and data on visual acuity were collected from ophthalmologic clinic records at initial consultations and follow-up at 3-18 months.

TAKEAWAY:

• Despite a tendency toward improvement, no significant difference in visual acuity was observed with intravenous methylprednisolone compared with oral glucocorticoids.
• Patients treated with intravenous methylprednisolone had a higher risk for newly diagnosed diabetes within a year of GCA diagnosis (odds ratio [OR], 2.59; P = .01).
• The risk for diabetes remained elevated even after adjustment for the cumulative oral glucocorticoid dose at 3 months (adjusted OR, 3.30; P = .01).
• Survival rates did not significantly differ between the treatment groups over a mean follow-up of 6.6 years.

IN PRACTICE:

“In this study on the use of intravenous methylprednisolone treatment in GCA, we found no evidence of a beneficial effect in improving visual acuity or enabling more rapid tapering of the oral glucocorticoid dose,” the authors wrote. “The use of IVMP [intravenous methylprednisolone] was associated with an increased risk of diabetes during the first year compared with oral GC [glucocorticoid], raising questions about the value of IVMP in GCA treatment.”

SOURCE:

The study, led by Hampus Henningson, Department of Clinical Sciences, Rheumatology, Lund University, Lund, Sweden, was published online in Rheumatology.

LIMITATIONS: 

The retrospective nature of the study may have resulted in missing data and difficulty in accurately quantifying the cumulative glucocorticoid doses. The study did not validate the diagnoses of comorbidities but relied solely on diagnostic codes.

DISCLOSURES:

This study was supported by the Swedish Research Council, Swedish Rheumatism Association, Swedish Medical Society, Alfred Österlund’s Foundation, and King Gustaf V’s 80-year foundation. The authors declared 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 first appeared on Medscape.com.

TOPLINE: 

In patients with giant cell arteritis (GCA), intravenous methylprednisolone compared with oral glucocorticoids alone does not improve visual acuity and increases the risk for diabetes within the first year. Survival rates do not differ with these two treatments.

METHODOLOGY:

• Researchers conducted a population-based retrospective study at three centers in Sweden to assess the clinical characteristics, treatment-related toxicity, and mortality in patients with GCA who were receiving high-dose intravenous methylprednisolone.
• A total of 419 patients with biopsy-confirmed GCA (mean age at diagnosis, 75 years; 69% women) diagnosed from 2004 to 2019 were included.
• Patients were treated with either intravenous methylprednisolone (n = 111) at a dose of 500-1000 mg per day for 3 consecutive days or oral glucocorticoids alone (n = 308).
• Ischemic visual complications considered to indicate visual involvement were confirmed by an ophthalmologist, and data on visual acuity were collected from ophthalmologic clinic records at initial consultations and follow-up at 3-18 months.

TAKEAWAY:

• Despite a tendency toward improvement, no significant difference in visual acuity was observed with intravenous methylprednisolone compared with oral glucocorticoids.
• Patients treated with intravenous methylprednisolone had a higher risk for newly diagnosed diabetes within a year of GCA diagnosis (odds ratio [OR], 2.59; P = .01).
• The risk for diabetes remained elevated even after adjustment for the cumulative oral glucocorticoid dose at 3 months (adjusted OR, 3.30; P = .01).
• Survival rates did not significantly differ between the treatment groups over a mean follow-up of 6.6 years.

IN PRACTICE:

“In this study on the use of intravenous methylprednisolone treatment in GCA, we found no evidence of a beneficial effect in improving visual acuity or enabling more rapid tapering of the oral glucocorticoid dose,” the authors wrote. “The use of IVMP [intravenous methylprednisolone] was associated with an increased risk of diabetes during the first year compared with oral GC [glucocorticoid], raising questions about the value of IVMP in GCA treatment.”

SOURCE:

The study, led by Hampus Henningson, Department of Clinical Sciences, Rheumatology, Lund University, Lund, Sweden, was published online in Rheumatology.

LIMITATIONS: 

The retrospective nature of the study may have resulted in missing data and difficulty in accurately quantifying the cumulative glucocorticoid doses. The study did not validate the diagnoses of comorbidities but relied solely on diagnostic codes.

DISCLOSURES:

This study was supported by the Swedish Research Council, Swedish Rheumatism Association, Swedish Medical Society, Alfred Österlund’s Foundation, and King Gustaf V’s 80-year foundation. The authors declared 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 first appeared on Medscape.com.

TOPLINE: 

In patients with giant cell arteritis (GCA), intravenous methylprednisolone compared with oral glucocorticoids alone does not improve visual acuity and increases the risk for diabetes within the first year. Survival rates do not differ with these two treatments.

METHODOLOGY:

• Researchers conducted a population-based retrospective study at three centers in Sweden to assess the clinical characteristics, treatment-related toxicity, and mortality in patients with GCA who were receiving high-dose intravenous methylprednisolone.
• A total of 419 patients with biopsy-confirmed GCA (mean age at diagnosis, 75 years; 69% women) diagnosed from 2004 to 2019 were included.
• Patients were treated with either intravenous methylprednisolone (n = 111) at a dose of 500-1000 mg per day for 3 consecutive days or oral glucocorticoids alone (n = 308).
• Ischemic visual complications considered to indicate visual involvement were confirmed by an ophthalmologist, and data on visual acuity were collected from ophthalmologic clinic records at initial consultations and follow-up at 3-18 months.

TAKEAWAY:

• Despite a tendency toward improvement, no significant difference in visual acuity was observed with intravenous methylprednisolone compared with oral glucocorticoids.
• Patients treated with intravenous methylprednisolone had a higher risk for newly diagnosed diabetes within a year of GCA diagnosis (odds ratio [OR], 2.59; P = .01).
• The risk for diabetes remained elevated even after adjustment for the cumulative oral glucocorticoid dose at 3 months (adjusted OR, 3.30; P = .01).
• Survival rates did not significantly differ between the treatment groups over a mean follow-up of 6.6 years.

IN PRACTICE:

“In this study on the use of intravenous methylprednisolone treatment in GCA, we found no evidence of a beneficial effect in improving visual acuity or enabling more rapid tapering of the oral glucocorticoid dose,” the authors wrote. “The use of IVMP [intravenous methylprednisolone] was associated with an increased risk of diabetes during the first year compared with oral GC [glucocorticoid], raising questions about the value of IVMP in GCA treatment.”

SOURCE:

The study, led by Hampus Henningson, Department of Clinical Sciences, Rheumatology, Lund University, Lund, Sweden, was published online in Rheumatology.

LIMITATIONS: 

The retrospective nature of the study may have resulted in missing data and difficulty in accurately quantifying the cumulative glucocorticoid doses. The study did not validate the diagnoses of comorbidities but relied solely on diagnostic codes.

DISCLOSURES:

This study was supported by the Swedish Research Council, Swedish Rheumatism Association, Swedish Medical Society, Alfred Österlund’s Foundation, and King Gustaf V’s 80-year foundation. The authors declared 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 first appeared on Medscape.com.