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A New and Early Predictor of Dementia?
, in new findings that may provide a potential opportunity to identify high-risk populations for targeted enrollment in clinical trials of dementia prevention and treatment.
Results of an international study assessing frailty trajectories showed frailty levels notably increased in the 4-9 years before dementia diagnosis. Even among study participants whose baseline frailty measurement was taken prior to that acceleration period, frailty was still positively associated with dementia risk, the investigators noted.
“We found that with every four to five additional health problems, there is on average a 40% higher risk of developing dementia, while the risk is lower for people who are more physically fit,” said study investigator David Ward, PhD, of the Centre for Health Services Research, The University of Queensland, Brisbane, Australia.
The findings were published online in JAMA Neurology.
A Promising Biomarker
An accessible biomarker for both biologic age and dementia risk is essential for advancing dementia prevention and treatment strategies, the investigators noted, adding that growing evidence suggests frailty may be a promising candidate for this role.
To learn more about the association between frailty and dementia, Ward and his team analyzed data on 29,849 participants aged 60 years or above (mean age, 71.6 years; 62% women) who participated in four cohort studies: the English Longitudinal Study of Ageing (ELSA; n = 6771), the Health and Retirement Study (HRS; n = 9045), the Rush Memory and Aging Project (MAP; n = 1451), and the National Alzheimer’s Coordinating Center (NACC; n = 12,582).
The primary outcome was all-cause dementia. Depending on the cohort, dementia diagnoses were determined through cognitive testing, self- or family report of physician diagnosis, or a diagnosis by the study physician. Participants were excluded if they had cognitive impairment at baseline.
Investigators retrospectively determined frailty index scores by gathering information on health and functional outcomes for participants from each cohort. Only participants with frailty data on at least 30 deficits were included.
Commonly included deficits included high blood pressure, cancer, and chronic pain, as well as functional problems such as hearing impairment, difficulty with mobility, and challenges managing finances.
Investigators conducted follow-up visits with participants until they developed dementia or until the study ended, with follow-up periods varying across cohorts.
After adjustment for potential confounders, frailty scores were modeled using backward time scales.
Among participants who developed incident dementia (n = 3154), covariate-adjusted expected frailty index scores were, on average, higher in women than in men by 18.5% in ELSA, 20.9% in HRS, and 16.2% in MAP. There were no differences in frailty scores between sexes in the NACC cohort.
When measured on a timeline, as compared with those who didn’t develop dementia, frailty scores were significantly and consistently higher in the dementia groups 8-20 before dementia onset (20 years in HRS; 13 in MAP; 12 in ELSA; 8 in NACC).
Increases in the rates of frailty index scores began accelerating 4-9 years before dementia onset for the various cohorts, investigators noted.
In all four cohorts, each 0.1 increase in frailty scores was positively associated with increased dementia risk.
Adjusted hazard ratios [aHRs] ranged from 1.18 in the HRS cohort to 1.73 in the NACC cohort, which showed the strongest association.
In participants whose baseline frailty measurement was conducted before the predementia acceleration period began, the association of frailty scores and dementia risk was positive. These aHRs ranged from 1.18 in the HRS cohort to 1.43 in the NACC cohort.
The ‘Four Pillars’ of Prevention
The good news, investigators said, is that the long trajectory of frailty symptoms preceding dementia onset provides plenty of opportunity for intervention.
To slow the development of frailty, Ward suggested adhering to the “four pillars of frailty prevention and management,” which include good nutrition with plenty of protein, exercise, optimizing medications for chronic conditions, and maintaining a strong social network.
Ward suggested neurologists track frailty in their patients and pointed to a recent article focused on helping neurologists use frailty measures to influence care planning.
Study limitations include the possibility of reverse causality and the fact that investigators could not adjust for genetic risk for dementia.
Unclear Pathway
Commenting on the findings, Lycia Neumann, PhD, senior director of Health Services Research at the Alzheimer’s Association, noted that many studies over the years have shown a link between frailty and dementia. However, she cautioned that a link does not imply causation.
The pathway from frailty to dementia is not 100% clear, and both are complex conditions, said Neumann, who was not part of the study.
“Adopting healthy lifestyle behaviors early and consistently can help decrease the risk of — or postpone the onset of — both frailty and cognitive decline,” she said. Neumann added that physical activity, a healthy diet, social engagement, and controlling diabetes and blood pressure can also reduce the risk for dementia as well as cardiovascular disease.
The study was funded in part by the Deep Dementia Phenotyping Network through the Frailty and Dementia Special Interest Group. Ward and Neumann reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
, in new findings that may provide a potential opportunity to identify high-risk populations for targeted enrollment in clinical trials of dementia prevention and treatment.
Results of an international study assessing frailty trajectories showed frailty levels notably increased in the 4-9 years before dementia diagnosis. Even among study participants whose baseline frailty measurement was taken prior to that acceleration period, frailty was still positively associated with dementia risk, the investigators noted.
“We found that with every four to five additional health problems, there is on average a 40% higher risk of developing dementia, while the risk is lower for people who are more physically fit,” said study investigator David Ward, PhD, of the Centre for Health Services Research, The University of Queensland, Brisbane, Australia.
The findings were published online in JAMA Neurology.
A Promising Biomarker
An accessible biomarker for both biologic age and dementia risk is essential for advancing dementia prevention and treatment strategies, the investigators noted, adding that growing evidence suggests frailty may be a promising candidate for this role.
To learn more about the association between frailty and dementia, Ward and his team analyzed data on 29,849 participants aged 60 years or above (mean age, 71.6 years; 62% women) who participated in four cohort studies: the English Longitudinal Study of Ageing (ELSA; n = 6771), the Health and Retirement Study (HRS; n = 9045), the Rush Memory and Aging Project (MAP; n = 1451), and the National Alzheimer’s Coordinating Center (NACC; n = 12,582).
The primary outcome was all-cause dementia. Depending on the cohort, dementia diagnoses were determined through cognitive testing, self- or family report of physician diagnosis, or a diagnosis by the study physician. Participants were excluded if they had cognitive impairment at baseline.
Investigators retrospectively determined frailty index scores by gathering information on health and functional outcomes for participants from each cohort. Only participants with frailty data on at least 30 deficits were included.
Commonly included deficits included high blood pressure, cancer, and chronic pain, as well as functional problems such as hearing impairment, difficulty with mobility, and challenges managing finances.
Investigators conducted follow-up visits with participants until they developed dementia or until the study ended, with follow-up periods varying across cohorts.
After adjustment for potential confounders, frailty scores were modeled using backward time scales.
Among participants who developed incident dementia (n = 3154), covariate-adjusted expected frailty index scores were, on average, higher in women than in men by 18.5% in ELSA, 20.9% in HRS, and 16.2% in MAP. There were no differences in frailty scores between sexes in the NACC cohort.
When measured on a timeline, as compared with those who didn’t develop dementia, frailty scores were significantly and consistently higher in the dementia groups 8-20 before dementia onset (20 years in HRS; 13 in MAP; 12 in ELSA; 8 in NACC).
Increases in the rates of frailty index scores began accelerating 4-9 years before dementia onset for the various cohorts, investigators noted.
In all four cohorts, each 0.1 increase in frailty scores was positively associated with increased dementia risk.
Adjusted hazard ratios [aHRs] ranged from 1.18 in the HRS cohort to 1.73 in the NACC cohort, which showed the strongest association.
In participants whose baseline frailty measurement was conducted before the predementia acceleration period began, the association of frailty scores and dementia risk was positive. These aHRs ranged from 1.18 in the HRS cohort to 1.43 in the NACC cohort.
The ‘Four Pillars’ of Prevention
The good news, investigators said, is that the long trajectory of frailty symptoms preceding dementia onset provides plenty of opportunity for intervention.
To slow the development of frailty, Ward suggested adhering to the “four pillars of frailty prevention and management,” which include good nutrition with plenty of protein, exercise, optimizing medications for chronic conditions, and maintaining a strong social network.
Ward suggested neurologists track frailty in their patients and pointed to a recent article focused on helping neurologists use frailty measures to influence care planning.
Study limitations include the possibility of reverse causality and the fact that investigators could not adjust for genetic risk for dementia.
Unclear Pathway
Commenting on the findings, Lycia Neumann, PhD, senior director of Health Services Research at the Alzheimer’s Association, noted that many studies over the years have shown a link between frailty and dementia. However, she cautioned that a link does not imply causation.
The pathway from frailty to dementia is not 100% clear, and both are complex conditions, said Neumann, who was not part of the study.
“Adopting healthy lifestyle behaviors early and consistently can help decrease the risk of — or postpone the onset of — both frailty and cognitive decline,” she said. Neumann added that physical activity, a healthy diet, social engagement, and controlling diabetes and blood pressure can also reduce the risk for dementia as well as cardiovascular disease.
The study was funded in part by the Deep Dementia Phenotyping Network through the Frailty and Dementia Special Interest Group. Ward and Neumann reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
, in new findings that may provide a potential opportunity to identify high-risk populations for targeted enrollment in clinical trials of dementia prevention and treatment.
Results of an international study assessing frailty trajectories showed frailty levels notably increased in the 4-9 years before dementia diagnosis. Even among study participants whose baseline frailty measurement was taken prior to that acceleration period, frailty was still positively associated with dementia risk, the investigators noted.
“We found that with every four to five additional health problems, there is on average a 40% higher risk of developing dementia, while the risk is lower for people who are more physically fit,” said study investigator David Ward, PhD, of the Centre for Health Services Research, The University of Queensland, Brisbane, Australia.
The findings were published online in JAMA Neurology.
A Promising Biomarker
An accessible biomarker for both biologic age and dementia risk is essential for advancing dementia prevention and treatment strategies, the investigators noted, adding that growing evidence suggests frailty may be a promising candidate for this role.
To learn more about the association between frailty and dementia, Ward and his team analyzed data on 29,849 participants aged 60 years or above (mean age, 71.6 years; 62% women) who participated in four cohort studies: the English Longitudinal Study of Ageing (ELSA; n = 6771), the Health and Retirement Study (HRS; n = 9045), the Rush Memory and Aging Project (MAP; n = 1451), and the National Alzheimer’s Coordinating Center (NACC; n = 12,582).
The primary outcome was all-cause dementia. Depending on the cohort, dementia diagnoses were determined through cognitive testing, self- or family report of physician diagnosis, or a diagnosis by the study physician. Participants were excluded if they had cognitive impairment at baseline.
Investigators retrospectively determined frailty index scores by gathering information on health and functional outcomes for participants from each cohort. Only participants with frailty data on at least 30 deficits were included.
Commonly included deficits included high blood pressure, cancer, and chronic pain, as well as functional problems such as hearing impairment, difficulty with mobility, and challenges managing finances.
Investigators conducted follow-up visits with participants until they developed dementia or until the study ended, with follow-up periods varying across cohorts.
After adjustment for potential confounders, frailty scores were modeled using backward time scales.
Among participants who developed incident dementia (n = 3154), covariate-adjusted expected frailty index scores were, on average, higher in women than in men by 18.5% in ELSA, 20.9% in HRS, and 16.2% in MAP. There were no differences in frailty scores between sexes in the NACC cohort.
When measured on a timeline, as compared with those who didn’t develop dementia, frailty scores were significantly and consistently higher in the dementia groups 8-20 before dementia onset (20 years in HRS; 13 in MAP; 12 in ELSA; 8 in NACC).
Increases in the rates of frailty index scores began accelerating 4-9 years before dementia onset for the various cohorts, investigators noted.
In all four cohorts, each 0.1 increase in frailty scores was positively associated with increased dementia risk.
Adjusted hazard ratios [aHRs] ranged from 1.18 in the HRS cohort to 1.73 in the NACC cohort, which showed the strongest association.
In participants whose baseline frailty measurement was conducted before the predementia acceleration period began, the association of frailty scores and dementia risk was positive. These aHRs ranged from 1.18 in the HRS cohort to 1.43 in the NACC cohort.
The ‘Four Pillars’ of Prevention
The good news, investigators said, is that the long trajectory of frailty symptoms preceding dementia onset provides plenty of opportunity for intervention.
To slow the development of frailty, Ward suggested adhering to the “four pillars of frailty prevention and management,” which include good nutrition with plenty of protein, exercise, optimizing medications for chronic conditions, and maintaining a strong social network.
Ward suggested neurologists track frailty in their patients and pointed to a recent article focused on helping neurologists use frailty measures to influence care planning.
Study limitations include the possibility of reverse causality and the fact that investigators could not adjust for genetic risk for dementia.
Unclear Pathway
Commenting on the findings, Lycia Neumann, PhD, senior director of Health Services Research at the Alzheimer’s Association, noted that many studies over the years have shown a link between frailty and dementia. However, she cautioned that a link does not imply causation.
The pathway from frailty to dementia is not 100% clear, and both are complex conditions, said Neumann, who was not part of the study.
“Adopting healthy lifestyle behaviors early and consistently can help decrease the risk of — or postpone the onset of — both frailty and cognitive decline,” she said. Neumann added that physical activity, a healthy diet, social engagement, and controlling diabetes and blood pressure can also reduce the risk for dementia as well as cardiovascular disease.
The study was funded in part by the Deep Dementia Phenotyping Network through the Frailty and Dementia Special Interest Group. Ward and Neumann reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
Semaglutide a Potential Treatment Option for Opioid Use Disorder?
Semaglutide (Ozempic, Novo Nordisk) is associated with a significantly lower risk for overdose in individuals with opioid use disorder (OUD), new research shows.
The findings suggest that the drug may be a promising treatment option for OUD, adding to the growing evidence of the potential psychiatric benefits of glucagon-like peptide 1 (GLP-1) inhibitors.
“Our study provided real-world evidence suggesting that semaglutide could have benefits in preventing opioid overdose and treating opioid use disorder,” co–lead author Rong Xu, PhD, director of the Center for Artificial Intelligence in Drug Discovery at Case Western Reserve University School of Medicine, Cleveland, Ohio, said in an interview.
However, Xu cautioned that this evidence is preliminary and randomized clinical trials are required to confirm these findings.
The study published online in a research letter on September 25 in JAMA Network Open.
New Addiction Meds an Urgent Priority
Investigators analyzed electronic medical records from 33,006 patients with type 2 diabetes and OUD who were prescribed one of eight antidiabetic medications between 2017 and 2023.
Drugs included in the study were semaglutide, insulin, metformin, albiglutide, dulaglutide, exenatide, liraglutide, lixisenatide, dipeptidyl peptidase–4 inhibitors, sodium-glucose cotransporter-2 inhibitors, sulfonylureas, and thiazolidinediones.
Participants in the semaglutide and each comparison group were matched for certain covariates at baseline, such as socioeconomic status and OUD medications.
After 1 year, semaglutide was associated with a 42%-68% lower risk for opioid overdose than other antidiabetic medications, including other GLP-1s (range of hazard ratio [HR]: HR, 0.32; 95% CI, 0.12-0.89; to HR, 0.58; 95%CI, 0.38-0.87).
Xu noted a number of study limitations including the effect of possible confounders and sole reliance on prescription data.
However, the findings are in line with those of prior studies showing that semaglutide may be associated with lower rates of alcohol and nicotine use, she said.
Earlier this year, Xu, along with National Institute on Drug Abuse Director Nora Volkow, MD, and colleagues, published a retrospective cohort study of nearly 84,000 patients with obesity. That analysis showed that semaglutide was associated with a significantly lower risk of new alcohol use disorder diagnoses.
In a previous editorial by Xu and Volkow that summarized the research to-date on GLP-1s for nicotine, alcohol, and substance use disorders, they note that “closing the addiction treatment gap and discovering new, more effective addiction medications are urgent priorities. In this regard, investigating the potential of GLP-1 analogue medications to treat substance use disorder deserves fast and rigorous testing.”
Caution Warranted
Commenting on the study, Riccardo De Giorgi, MD, PhD, department of psychiatry, University of Oxford in England, said at this point, “we have to be very careful about how we interpret these data.”
In August, De Giorgi published a study showing that semaglutide was associated with reduced risk for several neurologic and psychiatric outcomes including dementia and nicotine misuse.
While there is enough observational evidence linking GLP-1 medications with reduced SUD risk, he noted that “now is the time to move on and conduct some randomized clinical trials, specifically testing our hypothesis in people who have psychiatric disorders.”
De Giorgi also called for mechanistic studies of semaglutide and other so that researchers could learn more about how it works to reduce cravings. “Instead of going from bench to bed, we need to go back to the bench,” he said.
As previously reported, De Giorgi recently called on experts in the field to actively explore the potential of GLP-1 inhibitors for mental illness.
The study was funded by National Institute on Alcohol Abuse and Alcoholism, National Institute on Aging, the National Center for Advancing Translational Sciences, and the Intramural Research Program of the National Institutes of Health. Xu reported no relevant financial relationships. De Giorgi reported receiving funding from the National Institute for Health Research Oxford Health Biomedical Research Centre.
A version of this article first appeared on Medscape.com.
Semaglutide (Ozempic, Novo Nordisk) is associated with a significantly lower risk for overdose in individuals with opioid use disorder (OUD), new research shows.
The findings suggest that the drug may be a promising treatment option for OUD, adding to the growing evidence of the potential psychiatric benefits of glucagon-like peptide 1 (GLP-1) inhibitors.
“Our study provided real-world evidence suggesting that semaglutide could have benefits in preventing opioid overdose and treating opioid use disorder,” co–lead author Rong Xu, PhD, director of the Center for Artificial Intelligence in Drug Discovery at Case Western Reserve University School of Medicine, Cleveland, Ohio, said in an interview.
However, Xu cautioned that this evidence is preliminary and randomized clinical trials are required to confirm these findings.
The study published online in a research letter on September 25 in JAMA Network Open.
New Addiction Meds an Urgent Priority
Investigators analyzed electronic medical records from 33,006 patients with type 2 diabetes and OUD who were prescribed one of eight antidiabetic medications between 2017 and 2023.
Drugs included in the study were semaglutide, insulin, metformin, albiglutide, dulaglutide, exenatide, liraglutide, lixisenatide, dipeptidyl peptidase–4 inhibitors, sodium-glucose cotransporter-2 inhibitors, sulfonylureas, and thiazolidinediones.
Participants in the semaglutide and each comparison group were matched for certain covariates at baseline, such as socioeconomic status and OUD medications.
After 1 year, semaglutide was associated with a 42%-68% lower risk for opioid overdose than other antidiabetic medications, including other GLP-1s (range of hazard ratio [HR]: HR, 0.32; 95% CI, 0.12-0.89; to HR, 0.58; 95%CI, 0.38-0.87).
Xu noted a number of study limitations including the effect of possible confounders and sole reliance on prescription data.
However, the findings are in line with those of prior studies showing that semaglutide may be associated with lower rates of alcohol and nicotine use, she said.
Earlier this year, Xu, along with National Institute on Drug Abuse Director Nora Volkow, MD, and colleagues, published a retrospective cohort study of nearly 84,000 patients with obesity. That analysis showed that semaglutide was associated with a significantly lower risk of new alcohol use disorder diagnoses.
In a previous editorial by Xu and Volkow that summarized the research to-date on GLP-1s for nicotine, alcohol, and substance use disorders, they note that “closing the addiction treatment gap and discovering new, more effective addiction medications are urgent priorities. In this regard, investigating the potential of GLP-1 analogue medications to treat substance use disorder deserves fast and rigorous testing.”
Caution Warranted
Commenting on the study, Riccardo De Giorgi, MD, PhD, department of psychiatry, University of Oxford in England, said at this point, “we have to be very careful about how we interpret these data.”
In August, De Giorgi published a study showing that semaglutide was associated with reduced risk for several neurologic and psychiatric outcomes including dementia and nicotine misuse.
While there is enough observational evidence linking GLP-1 medications with reduced SUD risk, he noted that “now is the time to move on and conduct some randomized clinical trials, specifically testing our hypothesis in people who have psychiatric disorders.”
De Giorgi also called for mechanistic studies of semaglutide and other so that researchers could learn more about how it works to reduce cravings. “Instead of going from bench to bed, we need to go back to the bench,” he said.
As previously reported, De Giorgi recently called on experts in the field to actively explore the potential of GLP-1 inhibitors for mental illness.
The study was funded by National Institute on Alcohol Abuse and Alcoholism, National Institute on Aging, the National Center for Advancing Translational Sciences, and the Intramural Research Program of the National Institutes of Health. Xu reported no relevant financial relationships. De Giorgi reported receiving funding from the National Institute for Health Research Oxford Health Biomedical Research Centre.
A version of this article first appeared on Medscape.com.
Semaglutide (Ozempic, Novo Nordisk) is associated with a significantly lower risk for overdose in individuals with opioid use disorder (OUD), new research shows.
The findings suggest that the drug may be a promising treatment option for OUD, adding to the growing evidence of the potential psychiatric benefits of glucagon-like peptide 1 (GLP-1) inhibitors.
“Our study provided real-world evidence suggesting that semaglutide could have benefits in preventing opioid overdose and treating opioid use disorder,” co–lead author Rong Xu, PhD, director of the Center for Artificial Intelligence in Drug Discovery at Case Western Reserve University School of Medicine, Cleveland, Ohio, said in an interview.
However, Xu cautioned that this evidence is preliminary and randomized clinical trials are required to confirm these findings.
The study published online in a research letter on September 25 in JAMA Network Open.
New Addiction Meds an Urgent Priority
Investigators analyzed electronic medical records from 33,006 patients with type 2 diabetes and OUD who were prescribed one of eight antidiabetic medications between 2017 and 2023.
Drugs included in the study were semaglutide, insulin, metformin, albiglutide, dulaglutide, exenatide, liraglutide, lixisenatide, dipeptidyl peptidase–4 inhibitors, sodium-glucose cotransporter-2 inhibitors, sulfonylureas, and thiazolidinediones.
Participants in the semaglutide and each comparison group were matched for certain covariates at baseline, such as socioeconomic status and OUD medications.
After 1 year, semaglutide was associated with a 42%-68% lower risk for opioid overdose than other antidiabetic medications, including other GLP-1s (range of hazard ratio [HR]: HR, 0.32; 95% CI, 0.12-0.89; to HR, 0.58; 95%CI, 0.38-0.87).
Xu noted a number of study limitations including the effect of possible confounders and sole reliance on prescription data.
However, the findings are in line with those of prior studies showing that semaglutide may be associated with lower rates of alcohol and nicotine use, she said.
Earlier this year, Xu, along with National Institute on Drug Abuse Director Nora Volkow, MD, and colleagues, published a retrospective cohort study of nearly 84,000 patients with obesity. That analysis showed that semaglutide was associated with a significantly lower risk of new alcohol use disorder diagnoses.
In a previous editorial by Xu and Volkow that summarized the research to-date on GLP-1s for nicotine, alcohol, and substance use disorders, they note that “closing the addiction treatment gap and discovering new, more effective addiction medications are urgent priorities. In this regard, investigating the potential of GLP-1 analogue medications to treat substance use disorder deserves fast and rigorous testing.”
Caution Warranted
Commenting on the study, Riccardo De Giorgi, MD, PhD, department of psychiatry, University of Oxford in England, said at this point, “we have to be very careful about how we interpret these data.”
In August, De Giorgi published a study showing that semaglutide was associated with reduced risk for several neurologic and psychiatric outcomes including dementia and nicotine misuse.
While there is enough observational evidence linking GLP-1 medications with reduced SUD risk, he noted that “now is the time to move on and conduct some randomized clinical trials, specifically testing our hypothesis in people who have psychiatric disorders.”
De Giorgi also called for mechanistic studies of semaglutide and other so that researchers could learn more about how it works to reduce cravings. “Instead of going from bench to bed, we need to go back to the bench,” he said.
As previously reported, De Giorgi recently called on experts in the field to actively explore the potential of GLP-1 inhibitors for mental illness.
The study was funded by National Institute on Alcohol Abuse and Alcoholism, National Institute on Aging, the National Center for Advancing Translational Sciences, and the Intramural Research Program of the National Institutes of Health. Xu reported no relevant financial relationships. De Giorgi reported receiving funding from the National Institute for Health Research Oxford Health Biomedical Research Centre.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN
Is It Time for Universal Suicide Screening?
US suicide rates have reached alarming levels, with data from Centers for Disease Control and Prevention (CDC) showing a 37% increase from 2000 to 2022. Nearly 49,000 people died by suicide in 2022 alone, translating to one death every 11 minutes.
The increase in suicide rates has prompted calls for expansion of universal suicide screening, in which all individuals in medical or mental health care settings are screened for suicide risk, regardless of the purpose for their visit. But the psychiatric field is split on the issue, with some experts citing false positives and a lack of mental health care resources for those deemed at risk.
In 2022, when the US Preventative Services Task Force released its recommendations on suicide prevention, first in children and adolescents, and then in adults, the authors said there was insufficient evidence to support universal suicide screening.
Proponents of the practice pushed back on that finding, arguing that universal suicide screening could help identify those at high risk who might otherwise go undiagnosed, leading to earlier, potentially lifesaving, intervention.
So, what is the case for — and against — universal screening?
Sounding an Alert
The introduction of universal screening was driven by a confluence of factors that began with a 1999 report by then-US Surgeon General David Satcher, MD. This was followed by a report in 2016 from the Joint Commission on Detecting and Treating Suicidal Ideation that called for healthcare organizations to improve detection and treatment of suicidal ideation in all healthcare care settings.
Data from the alert showed that a significant number of people who died by suicide had a healthcare visit before their death. Half had seen a clinician a month before their death; nearly 30% had a medical visit just the week before — all with no detection of increased suicide risk.
It was that sort of finding that led Parkland Health and Hospital System in Dallas to become the first US hospital to implement universal suicide screening. Since the program launched in 2015, the system has screened more than 4.3 million patients in its emergency department, inpatient units, and 20 primary care clinics.
“Since the program began, we’ve completed between 40,000 to 50,000 screenings per month,” said Kimberly Roaten, PhD, associate chief quality and safety officer for behavioral health at Parkland Health.
Clinicians at Parkland use the five-item Ask Suicide-Screening Questions to assess suicidal intent, a commonly used tool that was originally developed for use in pediatric emergency rooms (ERs). The tool, which takes about 20 seconds to administer, has since been validated in both children and adults.
Based on a patient’s response, a clinical decision support system integrated into the electronic health record classifies suicide risk as none, moderate, or high.
Patients identified as moderate risk are offered a more in-depth assessment with a mental health clinician, though participation is not mandatory, said Dr. Roaten. Those at high risk receive a more thorough evaluation.
The proportion of ER patients at Parkland who screen positive for any suicidal intent has consistently remained at about 7%, and at 2% in the primary care clinics, she said.
To better understand what the program may have had on suicide prevention, Dr. Roaten is leading a National Institute of Mental Health–funded study to link a decade of mortality data from the state of Texas to patient data from Parkland Health. Investigators will analyze information about patients identified at risk for suicide, those patients’ characteristics, and who dies by suicide.
Universal Screening Expands
Other health systems have adopted universal suicide screening including the Indian Health Service and the US Veterans Health Administration. Universal suicide screening is also in place in a growing number of primary care practices and hospitals throughout the United States and will be mandatory for patients aged 12 years and older in all acute care hospitals in California beginning in 2025.
There is also a push for universal screening to be coordinated through local, state, and federal government, nonprofit, and private sectors. The National Action Alliance for Suicide Prevention is charged with advancing the White House’s 2024 National Strategy for Suicide Prevention, a 10-year plan to address gaps in suicide prevention in the United States.
Sarah Brummett, JD, director of the National Action Alliance for Suicide Prevention’s executive committee, said that universal suicide screening is part of the 2024 strategy. “We know there are barriers to universal screening, and so it’s important to recognize what they are so we can address them,” said Ms. Brummett.
Barriers may include adequate staffing, or a system in place to triage patients who screen positive.
At Parkland, cost and workload have been minimal, Dr. Roaten said. “We built a model that only dedicates our highest-value resources to the most at-risk patients.”
She also noted that relief may be on the horizon for health systems where cost is an obstacle to universal screening and subsequent intervention. “There are efforts at the federal level to increase funding for suicide assessment and crisis response,” she said.
Pushback on Universal Screening
Universal suicide screening has its detractors, including critics who say expansion is unlikely to reduce suicide rates.
“The issue with suicidal ideation is that it is very dynamic. Suicidal ideation changes very quickly — sometimes within hours,” said Craig Bryan, PsyD, professor of psychiatry and behavioral health at Ohio State University in Columbus, Ohio.
Universal screening can also lead to false positives, where a patient who screens positive for suicidal ideation has no actual intention of attempting suicide, potentially creating unnecessary concern and burden on health care resources, Dr. Bryan noted.
“What do you do with everyone who screens positive?” Dr. Bryan said. “I’ve spoken with leaders of many health systems in the United States, and there is pushback against universal screening because they don’t have enough mental health resources to handle all of the referrals.”
Suicide screening also doesn’t predict who will die by suicide, Dr. Bryan added. It only identifies those willing to disclose suicidal thoughts. There is a significant number of people without mental illness who may never seek medical care, so “the warning signs we’re teaching people to recognize — depression, anxiety, and substance abuse — might not be evident in these individuals,” he said.
“Life sideswipes them suddenly, and they go from 0 to 60 ... and they may have access to a highly lethal method [of suicide] which weaponizes that moment of despair,” said Dr. Bryan. No amount of screening could possibly predict those types of suicides, he added.
Paul Nestadt, MD, associate professor of psychiatry and behavioral sciences at Johns Hopkins School of Medicine, agrees with Dr. Bryan and noted there isn’t a strong correlation between suicidal ideation and death by suicide.
“Suicidal thoughts are very common, but suicide is a rare event,” he said.
He cited a study that showed that two thirds of individuals who died by suicide had denied experiencing suicidal thoughts when asked, and half of them died within 2 days of this denial. Other research suggests that as many as 98% of people who express suicidal ideation do not die by suicide, Dr. Nestadt said.
A Public Health Issue
If universal screening is not the answer to predicting and preventing suicide, what is? One way would be to approach suicide as a public health issue, Dr. Nestadt said.
“How did we reduce the rate of motor vehicle deaths? We didn’t test each driver’s reaction time behind the wheel,” he said. “Instead, we passed seatbelt and airbag legislation, implemented federal speed limits, and as a result, the number of motor vehicle fatalities decreased.”
Dr. Nestadt is an advocate for stronger gun safety legislation, which has proven effective in reducing suicide rates. A study published this year showed that states with child access prevention laws, negligent storage laws, and mandatory waiting periods for gun purchases reported fewer suicide deaths than those without that legislation.
Other measures might be applied in cases of extreme individual suicide risk, including extreme risk protection orders, also known as “red flag” laws, he added. This type of legislation provides a pathway for law enforcement to temporarily remove firearms from individuals who pose a risk to themselves or others.
“These have been shown to be very effective in saving lives,” Dr. Nestadt said.
Dr. Nestadt and others are also using machine learning models to predict suicide risk. Those identified as high-risk may be flagged on their electronic medical record. Ideally, when the algorithm becomes more accurate at predicting suicide, anyone treating this patient can then decide if action is needed, said Dr. Nestadt.
In his work with suicidal military personnel, Dr. Bryan and his colleagues established a brief form of cognitive behavioral therapy (BCBT) to help participants challenge cognitive distortions and build coping strategies to deal with feel with intense feelings of distress. Data show that BCBT reduced suicide attempts among active-duty soldiers by 60% compared with standard mental health treatment. It has since been shown to work in civilians as well.
Dr. Bryan is also researching fluctuations in the wish to live versus the wish to die relative to one another and mapping the trajectory of risk states along the way.
The goal is that these and other suicide prevention strategies currently under study by his team and others will help stem the rise in suicide deaths.
“Overall, we need to train mental health providers to implement suicide prevention therapies and establish suicide risk programs,” Dr. Bryan said. “But until we build one of these suicide prevention interventions to scale, we’re putting the cart before the horse.”
Dr. Roaten, Ms. Brummett, Dr. Bryan, and Dr. Nestadt reported no relevant disclosures.
A version of this article appeared on Medscape.com.
US suicide rates have reached alarming levels, with data from Centers for Disease Control and Prevention (CDC) showing a 37% increase from 2000 to 2022. Nearly 49,000 people died by suicide in 2022 alone, translating to one death every 11 minutes.
The increase in suicide rates has prompted calls for expansion of universal suicide screening, in which all individuals in medical or mental health care settings are screened for suicide risk, regardless of the purpose for their visit. But the psychiatric field is split on the issue, with some experts citing false positives and a lack of mental health care resources for those deemed at risk.
In 2022, when the US Preventative Services Task Force released its recommendations on suicide prevention, first in children and adolescents, and then in adults, the authors said there was insufficient evidence to support universal suicide screening.
Proponents of the practice pushed back on that finding, arguing that universal suicide screening could help identify those at high risk who might otherwise go undiagnosed, leading to earlier, potentially lifesaving, intervention.
So, what is the case for — and against — universal screening?
Sounding an Alert
The introduction of universal screening was driven by a confluence of factors that began with a 1999 report by then-US Surgeon General David Satcher, MD. This was followed by a report in 2016 from the Joint Commission on Detecting and Treating Suicidal Ideation that called for healthcare organizations to improve detection and treatment of suicidal ideation in all healthcare care settings.
Data from the alert showed that a significant number of people who died by suicide had a healthcare visit before their death. Half had seen a clinician a month before their death; nearly 30% had a medical visit just the week before — all with no detection of increased suicide risk.
It was that sort of finding that led Parkland Health and Hospital System in Dallas to become the first US hospital to implement universal suicide screening. Since the program launched in 2015, the system has screened more than 4.3 million patients in its emergency department, inpatient units, and 20 primary care clinics.
“Since the program began, we’ve completed between 40,000 to 50,000 screenings per month,” said Kimberly Roaten, PhD, associate chief quality and safety officer for behavioral health at Parkland Health.
Clinicians at Parkland use the five-item Ask Suicide-Screening Questions to assess suicidal intent, a commonly used tool that was originally developed for use in pediatric emergency rooms (ERs). The tool, which takes about 20 seconds to administer, has since been validated in both children and adults.
Based on a patient’s response, a clinical decision support system integrated into the electronic health record classifies suicide risk as none, moderate, or high.
Patients identified as moderate risk are offered a more in-depth assessment with a mental health clinician, though participation is not mandatory, said Dr. Roaten. Those at high risk receive a more thorough evaluation.
The proportion of ER patients at Parkland who screen positive for any suicidal intent has consistently remained at about 7%, and at 2% in the primary care clinics, she said.
To better understand what the program may have had on suicide prevention, Dr. Roaten is leading a National Institute of Mental Health–funded study to link a decade of mortality data from the state of Texas to patient data from Parkland Health. Investigators will analyze information about patients identified at risk for suicide, those patients’ characteristics, and who dies by suicide.
Universal Screening Expands
Other health systems have adopted universal suicide screening including the Indian Health Service and the US Veterans Health Administration. Universal suicide screening is also in place in a growing number of primary care practices and hospitals throughout the United States and will be mandatory for patients aged 12 years and older in all acute care hospitals in California beginning in 2025.
There is also a push for universal screening to be coordinated through local, state, and federal government, nonprofit, and private sectors. The National Action Alliance for Suicide Prevention is charged with advancing the White House’s 2024 National Strategy for Suicide Prevention, a 10-year plan to address gaps in suicide prevention in the United States.
Sarah Brummett, JD, director of the National Action Alliance for Suicide Prevention’s executive committee, said that universal suicide screening is part of the 2024 strategy. “We know there are barriers to universal screening, and so it’s important to recognize what they are so we can address them,” said Ms. Brummett.
Barriers may include adequate staffing, or a system in place to triage patients who screen positive.
At Parkland, cost and workload have been minimal, Dr. Roaten said. “We built a model that only dedicates our highest-value resources to the most at-risk patients.”
She also noted that relief may be on the horizon for health systems where cost is an obstacle to universal screening and subsequent intervention. “There are efforts at the federal level to increase funding for suicide assessment and crisis response,” she said.
Pushback on Universal Screening
Universal suicide screening has its detractors, including critics who say expansion is unlikely to reduce suicide rates.
“The issue with suicidal ideation is that it is very dynamic. Suicidal ideation changes very quickly — sometimes within hours,” said Craig Bryan, PsyD, professor of psychiatry and behavioral health at Ohio State University in Columbus, Ohio.
Universal screening can also lead to false positives, where a patient who screens positive for suicidal ideation has no actual intention of attempting suicide, potentially creating unnecessary concern and burden on health care resources, Dr. Bryan noted.
“What do you do with everyone who screens positive?” Dr. Bryan said. “I’ve spoken with leaders of many health systems in the United States, and there is pushback against universal screening because they don’t have enough mental health resources to handle all of the referrals.”
Suicide screening also doesn’t predict who will die by suicide, Dr. Bryan added. It only identifies those willing to disclose suicidal thoughts. There is a significant number of people without mental illness who may never seek medical care, so “the warning signs we’re teaching people to recognize — depression, anxiety, and substance abuse — might not be evident in these individuals,” he said.
“Life sideswipes them suddenly, and they go from 0 to 60 ... and they may have access to a highly lethal method [of suicide] which weaponizes that moment of despair,” said Dr. Bryan. No amount of screening could possibly predict those types of suicides, he added.
Paul Nestadt, MD, associate professor of psychiatry and behavioral sciences at Johns Hopkins School of Medicine, agrees with Dr. Bryan and noted there isn’t a strong correlation between suicidal ideation and death by suicide.
“Suicidal thoughts are very common, but suicide is a rare event,” he said.
He cited a study that showed that two thirds of individuals who died by suicide had denied experiencing suicidal thoughts when asked, and half of them died within 2 days of this denial. Other research suggests that as many as 98% of people who express suicidal ideation do not die by suicide, Dr. Nestadt said.
A Public Health Issue
If universal screening is not the answer to predicting and preventing suicide, what is? One way would be to approach suicide as a public health issue, Dr. Nestadt said.
“How did we reduce the rate of motor vehicle deaths? We didn’t test each driver’s reaction time behind the wheel,” he said. “Instead, we passed seatbelt and airbag legislation, implemented federal speed limits, and as a result, the number of motor vehicle fatalities decreased.”
Dr. Nestadt is an advocate for stronger gun safety legislation, which has proven effective in reducing suicide rates. A study published this year showed that states with child access prevention laws, negligent storage laws, and mandatory waiting periods for gun purchases reported fewer suicide deaths than those without that legislation.
Other measures might be applied in cases of extreme individual suicide risk, including extreme risk protection orders, also known as “red flag” laws, he added. This type of legislation provides a pathway for law enforcement to temporarily remove firearms from individuals who pose a risk to themselves or others.
“These have been shown to be very effective in saving lives,” Dr. Nestadt said.
Dr. Nestadt and others are also using machine learning models to predict suicide risk. Those identified as high-risk may be flagged on their electronic medical record. Ideally, when the algorithm becomes more accurate at predicting suicide, anyone treating this patient can then decide if action is needed, said Dr. Nestadt.
In his work with suicidal military personnel, Dr. Bryan and his colleagues established a brief form of cognitive behavioral therapy (BCBT) to help participants challenge cognitive distortions and build coping strategies to deal with feel with intense feelings of distress. Data show that BCBT reduced suicide attempts among active-duty soldiers by 60% compared with standard mental health treatment. It has since been shown to work in civilians as well.
Dr. Bryan is also researching fluctuations in the wish to live versus the wish to die relative to one another and mapping the trajectory of risk states along the way.
The goal is that these and other suicide prevention strategies currently under study by his team and others will help stem the rise in suicide deaths.
“Overall, we need to train mental health providers to implement suicide prevention therapies and establish suicide risk programs,” Dr. Bryan said. “But until we build one of these suicide prevention interventions to scale, we’re putting the cart before the horse.”
Dr. Roaten, Ms. Brummett, Dr. Bryan, and Dr. Nestadt reported no relevant disclosures.
A version of this article appeared on Medscape.com.
US suicide rates have reached alarming levels, with data from Centers for Disease Control and Prevention (CDC) showing a 37% increase from 2000 to 2022. Nearly 49,000 people died by suicide in 2022 alone, translating to one death every 11 minutes.
The increase in suicide rates has prompted calls for expansion of universal suicide screening, in which all individuals in medical or mental health care settings are screened for suicide risk, regardless of the purpose for their visit. But the psychiatric field is split on the issue, with some experts citing false positives and a lack of mental health care resources for those deemed at risk.
In 2022, when the US Preventative Services Task Force released its recommendations on suicide prevention, first in children and adolescents, and then in adults, the authors said there was insufficient evidence to support universal suicide screening.
Proponents of the practice pushed back on that finding, arguing that universal suicide screening could help identify those at high risk who might otherwise go undiagnosed, leading to earlier, potentially lifesaving, intervention.
So, what is the case for — and against — universal screening?
Sounding an Alert
The introduction of universal screening was driven by a confluence of factors that began with a 1999 report by then-US Surgeon General David Satcher, MD. This was followed by a report in 2016 from the Joint Commission on Detecting and Treating Suicidal Ideation that called for healthcare organizations to improve detection and treatment of suicidal ideation in all healthcare care settings.
Data from the alert showed that a significant number of people who died by suicide had a healthcare visit before their death. Half had seen a clinician a month before their death; nearly 30% had a medical visit just the week before — all with no detection of increased suicide risk.
It was that sort of finding that led Parkland Health and Hospital System in Dallas to become the first US hospital to implement universal suicide screening. Since the program launched in 2015, the system has screened more than 4.3 million patients in its emergency department, inpatient units, and 20 primary care clinics.
“Since the program began, we’ve completed between 40,000 to 50,000 screenings per month,” said Kimberly Roaten, PhD, associate chief quality and safety officer for behavioral health at Parkland Health.
Clinicians at Parkland use the five-item Ask Suicide-Screening Questions to assess suicidal intent, a commonly used tool that was originally developed for use in pediatric emergency rooms (ERs). The tool, which takes about 20 seconds to administer, has since been validated in both children and adults.
Based on a patient’s response, a clinical decision support system integrated into the electronic health record classifies suicide risk as none, moderate, or high.
Patients identified as moderate risk are offered a more in-depth assessment with a mental health clinician, though participation is not mandatory, said Dr. Roaten. Those at high risk receive a more thorough evaluation.
The proportion of ER patients at Parkland who screen positive for any suicidal intent has consistently remained at about 7%, and at 2% in the primary care clinics, she said.
To better understand what the program may have had on suicide prevention, Dr. Roaten is leading a National Institute of Mental Health–funded study to link a decade of mortality data from the state of Texas to patient data from Parkland Health. Investigators will analyze information about patients identified at risk for suicide, those patients’ characteristics, and who dies by suicide.
Universal Screening Expands
Other health systems have adopted universal suicide screening including the Indian Health Service and the US Veterans Health Administration. Universal suicide screening is also in place in a growing number of primary care practices and hospitals throughout the United States and will be mandatory for patients aged 12 years and older in all acute care hospitals in California beginning in 2025.
There is also a push for universal screening to be coordinated through local, state, and federal government, nonprofit, and private sectors. The National Action Alliance for Suicide Prevention is charged with advancing the White House’s 2024 National Strategy for Suicide Prevention, a 10-year plan to address gaps in suicide prevention in the United States.
Sarah Brummett, JD, director of the National Action Alliance for Suicide Prevention’s executive committee, said that universal suicide screening is part of the 2024 strategy. “We know there are barriers to universal screening, and so it’s important to recognize what they are so we can address them,” said Ms. Brummett.
Barriers may include adequate staffing, or a system in place to triage patients who screen positive.
At Parkland, cost and workload have been minimal, Dr. Roaten said. “We built a model that only dedicates our highest-value resources to the most at-risk patients.”
She also noted that relief may be on the horizon for health systems where cost is an obstacle to universal screening and subsequent intervention. “There are efforts at the federal level to increase funding for suicide assessment and crisis response,” she said.
Pushback on Universal Screening
Universal suicide screening has its detractors, including critics who say expansion is unlikely to reduce suicide rates.
“The issue with suicidal ideation is that it is very dynamic. Suicidal ideation changes very quickly — sometimes within hours,” said Craig Bryan, PsyD, professor of psychiatry and behavioral health at Ohio State University in Columbus, Ohio.
Universal screening can also lead to false positives, where a patient who screens positive for suicidal ideation has no actual intention of attempting suicide, potentially creating unnecessary concern and burden on health care resources, Dr. Bryan noted.
“What do you do with everyone who screens positive?” Dr. Bryan said. “I’ve spoken with leaders of many health systems in the United States, and there is pushback against universal screening because they don’t have enough mental health resources to handle all of the referrals.”
Suicide screening also doesn’t predict who will die by suicide, Dr. Bryan added. It only identifies those willing to disclose suicidal thoughts. There is a significant number of people without mental illness who may never seek medical care, so “the warning signs we’re teaching people to recognize — depression, anxiety, and substance abuse — might not be evident in these individuals,” he said.
“Life sideswipes them suddenly, and they go from 0 to 60 ... and they may have access to a highly lethal method [of suicide] which weaponizes that moment of despair,” said Dr. Bryan. No amount of screening could possibly predict those types of suicides, he added.
Paul Nestadt, MD, associate professor of psychiatry and behavioral sciences at Johns Hopkins School of Medicine, agrees with Dr. Bryan and noted there isn’t a strong correlation between suicidal ideation and death by suicide.
“Suicidal thoughts are very common, but suicide is a rare event,” he said.
He cited a study that showed that two thirds of individuals who died by suicide had denied experiencing suicidal thoughts when asked, and half of them died within 2 days of this denial. Other research suggests that as many as 98% of people who express suicidal ideation do not die by suicide, Dr. Nestadt said.
A Public Health Issue
If universal screening is not the answer to predicting and preventing suicide, what is? One way would be to approach suicide as a public health issue, Dr. Nestadt said.
“How did we reduce the rate of motor vehicle deaths? We didn’t test each driver’s reaction time behind the wheel,” he said. “Instead, we passed seatbelt and airbag legislation, implemented federal speed limits, and as a result, the number of motor vehicle fatalities decreased.”
Dr. Nestadt is an advocate for stronger gun safety legislation, which has proven effective in reducing suicide rates. A study published this year showed that states with child access prevention laws, negligent storage laws, and mandatory waiting periods for gun purchases reported fewer suicide deaths than those without that legislation.
Other measures might be applied in cases of extreme individual suicide risk, including extreme risk protection orders, also known as “red flag” laws, he added. This type of legislation provides a pathway for law enforcement to temporarily remove firearms from individuals who pose a risk to themselves or others.
“These have been shown to be very effective in saving lives,” Dr. Nestadt said.
Dr. Nestadt and others are also using machine learning models to predict suicide risk. Those identified as high-risk may be flagged on their electronic medical record. Ideally, when the algorithm becomes more accurate at predicting suicide, anyone treating this patient can then decide if action is needed, said Dr. Nestadt.
In his work with suicidal military personnel, Dr. Bryan and his colleagues established a brief form of cognitive behavioral therapy (BCBT) to help participants challenge cognitive distortions and build coping strategies to deal with feel with intense feelings of distress. Data show that BCBT reduced suicide attempts among active-duty soldiers by 60% compared with standard mental health treatment. It has since been shown to work in civilians as well.
Dr. Bryan is also researching fluctuations in the wish to live versus the wish to die relative to one another and mapping the trajectory of risk states along the way.
The goal is that these and other suicide prevention strategies currently under study by his team and others will help stem the rise in suicide deaths.
“Overall, we need to train mental health providers to implement suicide prevention therapies and establish suicide risk programs,” Dr. Bryan said. “But until we build one of these suicide prevention interventions to scale, we’re putting the cart before the horse.”
Dr. Roaten, Ms. Brummett, Dr. Bryan, and Dr. Nestadt reported no relevant disclosures.
A version of this article appeared on Medscape.com.
Brain Structure Differs in Youth With Conduct Disorder
Youth with conduct disorder (CD) have extensive brain structure differences, new research showed.
“We know very little about this disorder even though it can carry a high burden for families and societies,” co–lead author Yidian Gao, PhD, of the University of Birmingham, Birmingham, England, said in a press release.
“The sample included in our study is 10-20 times larger than previous studies and contains data on children from North America, Europe, and Asia. It provides the most compelling evidence to date that CD is associated with widespread structural brain differences,” he added.
The findings were published online in The Lancet Psychiatry.
An Understudied Disorder
In the largest study of its kind, researchers at the Universities of Bath and Birmingham, both in England, collaborated with research teams across Europe, North America, and Asia, as part of the Enhancing NeuroImaging Genetics through Meta-Analysis–Antisocial Behavior Working Group to learn more about one of the “least researched psychiatric disorders,” they wrote.
The investigators used MRI to examine the brain structure of 1185 children with a clinical diagnosis of CD and 1253 typically developing children from 17-21 across 15 international study cohorts.
After adjusting for total intracranial volume investigators found that youth with CD (29% women; mean age, 13.7 years) had lower total surface area and lower regional surface area in 26 of the 34 cortical regions, spanning all four lobes of the brain, compared with their typically developing counterparts (35.6% women; mean age, 13.5 years).
Youth with CD also showed greater cortical thickness in the caudal anterior cingulate cortex (P = .0001) and lower cortical thickness in the banks of the superior temporal sulcus vs those without CD (P = .0010).
In addition, the CD group also had lower volume in the thalamus (P = .0009), amygdala (P = .0014), hippocampus (P = .0031), and nucleus accumbens (P = .0052).
Most findings remained significant after adjusting for intelligence quotient, psychiatric comorbidities, and psychotropic medication use. Of note, group difference in cortical thickness, 22 of 27 differences in surface area. In addition, three of four subcortical differences remained robust after adjusting for co-occurring attention-deficit/hyperactivity disorder, the most frequent comorbidity.
When the investigators divided individuals with CD into two subgroups — those with high vs low levels of callous-unemotional traits — they found limited overall differences. However, those with high callous-unemotional traits had lower surface area in the superior temporal and superior frontal gyri vs those with low callous-unemotional traits and the typically developing group.
Investigators also found that individuals with childhood-onset CD had greater cortical thickness in the caudal anterior cingulate cortex compared with those with adolescent-onset CD.
Study limitations include comparison of different cohorts with differing protocols that could affect the validity of the findings. In addition, subgroup samples were small and had lower statistical power.
“Our finding of robust brain alterations in conduct disorder — similar to those in more widely recognized and widely treated disorders such as ADHD — emphasize the need for a greater focus on conduct disorder in research, treatment, and public policy,” the authors noted.
Seven study authors reported conflicts of interest with various pharmaceutical companies and other organizations.
A version of this article first appeared on Medscape.com.
Youth with conduct disorder (CD) have extensive brain structure differences, new research showed.
“We know very little about this disorder even though it can carry a high burden for families and societies,” co–lead author Yidian Gao, PhD, of the University of Birmingham, Birmingham, England, said in a press release.
“The sample included in our study is 10-20 times larger than previous studies and contains data on children from North America, Europe, and Asia. It provides the most compelling evidence to date that CD is associated with widespread structural brain differences,” he added.
The findings were published online in The Lancet Psychiatry.
An Understudied Disorder
In the largest study of its kind, researchers at the Universities of Bath and Birmingham, both in England, collaborated with research teams across Europe, North America, and Asia, as part of the Enhancing NeuroImaging Genetics through Meta-Analysis–Antisocial Behavior Working Group to learn more about one of the “least researched psychiatric disorders,” they wrote.
The investigators used MRI to examine the brain structure of 1185 children with a clinical diagnosis of CD and 1253 typically developing children from 17-21 across 15 international study cohorts.
After adjusting for total intracranial volume investigators found that youth with CD (29% women; mean age, 13.7 years) had lower total surface area and lower regional surface area in 26 of the 34 cortical regions, spanning all four lobes of the brain, compared with their typically developing counterparts (35.6% women; mean age, 13.5 years).
Youth with CD also showed greater cortical thickness in the caudal anterior cingulate cortex (P = .0001) and lower cortical thickness in the banks of the superior temporal sulcus vs those without CD (P = .0010).
In addition, the CD group also had lower volume in the thalamus (P = .0009), amygdala (P = .0014), hippocampus (P = .0031), and nucleus accumbens (P = .0052).
Most findings remained significant after adjusting for intelligence quotient, psychiatric comorbidities, and psychotropic medication use. Of note, group difference in cortical thickness, 22 of 27 differences in surface area. In addition, three of four subcortical differences remained robust after adjusting for co-occurring attention-deficit/hyperactivity disorder, the most frequent comorbidity.
When the investigators divided individuals with CD into two subgroups — those with high vs low levels of callous-unemotional traits — they found limited overall differences. However, those with high callous-unemotional traits had lower surface area in the superior temporal and superior frontal gyri vs those with low callous-unemotional traits and the typically developing group.
Investigators also found that individuals with childhood-onset CD had greater cortical thickness in the caudal anterior cingulate cortex compared with those with adolescent-onset CD.
Study limitations include comparison of different cohorts with differing protocols that could affect the validity of the findings. In addition, subgroup samples were small and had lower statistical power.
“Our finding of robust brain alterations in conduct disorder — similar to those in more widely recognized and widely treated disorders such as ADHD — emphasize the need for a greater focus on conduct disorder in research, treatment, and public policy,” the authors noted.
Seven study authors reported conflicts of interest with various pharmaceutical companies and other organizations.
A version of this article first appeared on Medscape.com.
Youth with conduct disorder (CD) have extensive brain structure differences, new research showed.
“We know very little about this disorder even though it can carry a high burden for families and societies,” co–lead author Yidian Gao, PhD, of the University of Birmingham, Birmingham, England, said in a press release.
“The sample included in our study is 10-20 times larger than previous studies and contains data on children from North America, Europe, and Asia. It provides the most compelling evidence to date that CD is associated with widespread structural brain differences,” he added.
The findings were published online in The Lancet Psychiatry.
An Understudied Disorder
In the largest study of its kind, researchers at the Universities of Bath and Birmingham, both in England, collaborated with research teams across Europe, North America, and Asia, as part of the Enhancing NeuroImaging Genetics through Meta-Analysis–Antisocial Behavior Working Group to learn more about one of the “least researched psychiatric disorders,” they wrote.
The investigators used MRI to examine the brain structure of 1185 children with a clinical diagnosis of CD and 1253 typically developing children from 17-21 across 15 international study cohorts.
After adjusting for total intracranial volume investigators found that youth with CD (29% women; mean age, 13.7 years) had lower total surface area and lower regional surface area in 26 of the 34 cortical regions, spanning all four lobes of the brain, compared with their typically developing counterparts (35.6% women; mean age, 13.5 years).
Youth with CD also showed greater cortical thickness in the caudal anterior cingulate cortex (P = .0001) and lower cortical thickness in the banks of the superior temporal sulcus vs those without CD (P = .0010).
In addition, the CD group also had lower volume in the thalamus (P = .0009), amygdala (P = .0014), hippocampus (P = .0031), and nucleus accumbens (P = .0052).
Most findings remained significant after adjusting for intelligence quotient, psychiatric comorbidities, and psychotropic medication use. Of note, group difference in cortical thickness, 22 of 27 differences in surface area. In addition, three of four subcortical differences remained robust after adjusting for co-occurring attention-deficit/hyperactivity disorder, the most frequent comorbidity.
When the investigators divided individuals with CD into two subgroups — those with high vs low levels of callous-unemotional traits — they found limited overall differences. However, those with high callous-unemotional traits had lower surface area in the superior temporal and superior frontal gyri vs those with low callous-unemotional traits and the typically developing group.
Investigators also found that individuals with childhood-onset CD had greater cortical thickness in the caudal anterior cingulate cortex compared with those with adolescent-onset CD.
Study limitations include comparison of different cohorts with differing protocols that could affect the validity of the findings. In addition, subgroup samples were small and had lower statistical power.
“Our finding of robust brain alterations in conduct disorder — similar to those in more widely recognized and widely treated disorders such as ADHD — emphasize the need for a greater focus on conduct disorder in research, treatment, and public policy,” the authors noted.
Seven study authors reported conflicts of interest with various pharmaceutical companies and other organizations.
A version of this article first appeared on Medscape.com.
FROM THE LANCET PSYCHIATRY
Moderate Exercise in Midlife Linked to Lower Risk for ALS
Moderate exercise in midlife is associated with a reduced risk for amyotrophic lateral sclerosis (ALS) later in life, but this benefit appears to be limited to men, findings from a large prospective study showed.
Men who reported moderate levels of physical activity had a 29% lower risk for ALS, whereas those with high levels of physical activity had a 41% lower risk for the disease.
The findings were published online in Neurology.
Conflicting Findings
Several famous athletes have died of ALS, including the baseball player Lou Gehrig (for whom the disease is named), football players Dwight Clark, Steve Gleason, and Kevin Turner, and the boxer Ezzard Charles. This has led some scientists to speculate that intense physical activity may play a role in the development of the disease.
Anders M. Vaage, MD, noted there have been conflicting findings in previous studies on the topic, with results showing both increased and reduced ALS risks with increasing levels of physical activity.
In one study, researchers followed more than 212,000 Swedish cross-country skiers and more than 500,000 Swedish individuals in the general population for 20 years and found that strenuous cross-country skiing was associated with a higher risk for ALS but only among the best skiers; recreational skiers appeared to have a reduced risk.
“Our study does not necessarily contradict previous studies with findings of an increased ALS risk with extreme or intense levels of physical activity in athletes, as this study reflects more moderate levels of physical activity and fitness in the total population,” said Dr. Vaage.
To further explore the association, the researchers followed 373,700 individuals who participated in a cardiovascular health survey for an average of 27 years. When the survey began, most participants were 40-42 years old.
Participants were followed until the date of ALS diagnosis, ALS death, death from other causes, emigration, or the end of study in August 2021.
Participants answered questions about physical activity levels, smoking status, and other issues relating to cardiovascular health, and participants’ resting heart rate was measured and divided into quartiles of 31-65 beats per minute (BPM), 66-74 BPM, 75-81 BPM, or 82-100 BPM.
Participants self-reported their physical activity over the past year, classifying it into one of four categories: Sedentary, at least 4 hours per week of walking or cycling, at least 4 hours per week of recreational sports or heavy gardening, or regular participation in intense training or sports competitions several times per week.
Only a few participants reported the highest level of physical activity, so researchers combined the third and fourth categories into a single high-activity group.
Of the total study cohort, 504 participants developed ALS. Of those who developed the disease, 59% were men.
Researchers found that of the 41,898 male participants with the highest level of physical activity, 63 developed ALS. In comparison, of the 76,769 male participants who reported an intermediate level of physical activity, 131 developed ALS. Among the 29,468 male participants who reported the lowest level of physical activity, 68 developed ALS.
No Link in Women?
After adjusting for smoking, body mass index, and other risk factors, investigators found that men with moderate physical activity levels had a 29% lower risk for ALS compared with those with low physical activity levels, whereas those with the highest activity levels had a 41% lower risk.
In addition, men in the lowest of the four categories of resting heart rate had a 32% reduced risk for ALS compared with men with a higher resting heart rate.
Investigators are unclear why there was a lack of association between physical activity and resting heart rate and ALS risk in women.
“There are known sex differences in ALS, which includes a sex ratio with male preponderance, and there are also sex differences in response to physical exercise. Perhaps underlying mechanisms herein can explain the difference observed between males and females in the study,” Dr. Vaage said. He noted that future research should explore this difference.
Study limitations included the absence of data on physical trauma and head trauma, which have been linked with increased ALS risk. In addition, there were no data on genotype.
In an accompanying editorial, Pamela Shaw, MD, and Johnathan Cooper-Knock, BMBCh, PhD, of the University of Sheffield, Sheffield, England, described the research as a “valuable contribution to the field and potentially provides some reassurance that mild/moderate levels of physical activity in middle age do not increase the risk for ALS but may instead have a beneficial protective effect.”
Future research on exercise in ALS, they add, should consider sex differences, capture the most extreme physical activity levels, and identify any genetic factors that may mediate the association between intense exercise and ALS.
No targeted funding was reported. Dr. Vaage reported receiving funding from ALS Laboratory Group Norway.
A version of this article first appeared on Medscape.com.
Moderate exercise in midlife is associated with a reduced risk for amyotrophic lateral sclerosis (ALS) later in life, but this benefit appears to be limited to men, findings from a large prospective study showed.
Men who reported moderate levels of physical activity had a 29% lower risk for ALS, whereas those with high levels of physical activity had a 41% lower risk for the disease.
The findings were published online in Neurology.
Conflicting Findings
Several famous athletes have died of ALS, including the baseball player Lou Gehrig (for whom the disease is named), football players Dwight Clark, Steve Gleason, and Kevin Turner, and the boxer Ezzard Charles. This has led some scientists to speculate that intense physical activity may play a role in the development of the disease.
Anders M. Vaage, MD, noted there have been conflicting findings in previous studies on the topic, with results showing both increased and reduced ALS risks with increasing levels of physical activity.
In one study, researchers followed more than 212,000 Swedish cross-country skiers and more than 500,000 Swedish individuals in the general population for 20 years and found that strenuous cross-country skiing was associated with a higher risk for ALS but only among the best skiers; recreational skiers appeared to have a reduced risk.
“Our study does not necessarily contradict previous studies with findings of an increased ALS risk with extreme or intense levels of physical activity in athletes, as this study reflects more moderate levels of physical activity and fitness in the total population,” said Dr. Vaage.
To further explore the association, the researchers followed 373,700 individuals who participated in a cardiovascular health survey for an average of 27 years. When the survey began, most participants were 40-42 years old.
Participants were followed until the date of ALS diagnosis, ALS death, death from other causes, emigration, or the end of study in August 2021.
Participants answered questions about physical activity levels, smoking status, and other issues relating to cardiovascular health, and participants’ resting heart rate was measured and divided into quartiles of 31-65 beats per minute (BPM), 66-74 BPM, 75-81 BPM, or 82-100 BPM.
Participants self-reported their physical activity over the past year, classifying it into one of four categories: Sedentary, at least 4 hours per week of walking or cycling, at least 4 hours per week of recreational sports or heavy gardening, or regular participation in intense training or sports competitions several times per week.
Only a few participants reported the highest level of physical activity, so researchers combined the third and fourth categories into a single high-activity group.
Of the total study cohort, 504 participants developed ALS. Of those who developed the disease, 59% were men.
Researchers found that of the 41,898 male participants with the highest level of physical activity, 63 developed ALS. In comparison, of the 76,769 male participants who reported an intermediate level of physical activity, 131 developed ALS. Among the 29,468 male participants who reported the lowest level of physical activity, 68 developed ALS.
No Link in Women?
After adjusting for smoking, body mass index, and other risk factors, investigators found that men with moderate physical activity levels had a 29% lower risk for ALS compared with those with low physical activity levels, whereas those with the highest activity levels had a 41% lower risk.
In addition, men in the lowest of the four categories of resting heart rate had a 32% reduced risk for ALS compared with men with a higher resting heart rate.
Investigators are unclear why there was a lack of association between physical activity and resting heart rate and ALS risk in women.
“There are known sex differences in ALS, which includes a sex ratio with male preponderance, and there are also sex differences in response to physical exercise. Perhaps underlying mechanisms herein can explain the difference observed between males and females in the study,” Dr. Vaage said. He noted that future research should explore this difference.
Study limitations included the absence of data on physical trauma and head trauma, which have been linked with increased ALS risk. In addition, there were no data on genotype.
In an accompanying editorial, Pamela Shaw, MD, and Johnathan Cooper-Knock, BMBCh, PhD, of the University of Sheffield, Sheffield, England, described the research as a “valuable contribution to the field and potentially provides some reassurance that mild/moderate levels of physical activity in middle age do not increase the risk for ALS but may instead have a beneficial protective effect.”
Future research on exercise in ALS, they add, should consider sex differences, capture the most extreme physical activity levels, and identify any genetic factors that may mediate the association between intense exercise and ALS.
No targeted funding was reported. Dr. Vaage reported receiving funding from ALS Laboratory Group Norway.
A version of this article first appeared on Medscape.com.
Moderate exercise in midlife is associated with a reduced risk for amyotrophic lateral sclerosis (ALS) later in life, but this benefit appears to be limited to men, findings from a large prospective study showed.
Men who reported moderate levels of physical activity had a 29% lower risk for ALS, whereas those with high levels of physical activity had a 41% lower risk for the disease.
The findings were published online in Neurology.
Conflicting Findings
Several famous athletes have died of ALS, including the baseball player Lou Gehrig (for whom the disease is named), football players Dwight Clark, Steve Gleason, and Kevin Turner, and the boxer Ezzard Charles. This has led some scientists to speculate that intense physical activity may play a role in the development of the disease.
Anders M. Vaage, MD, noted there have been conflicting findings in previous studies on the topic, with results showing both increased and reduced ALS risks with increasing levels of physical activity.
In one study, researchers followed more than 212,000 Swedish cross-country skiers and more than 500,000 Swedish individuals in the general population for 20 years and found that strenuous cross-country skiing was associated with a higher risk for ALS but only among the best skiers; recreational skiers appeared to have a reduced risk.
“Our study does not necessarily contradict previous studies with findings of an increased ALS risk with extreme or intense levels of physical activity in athletes, as this study reflects more moderate levels of physical activity and fitness in the total population,” said Dr. Vaage.
To further explore the association, the researchers followed 373,700 individuals who participated in a cardiovascular health survey for an average of 27 years. When the survey began, most participants were 40-42 years old.
Participants were followed until the date of ALS diagnosis, ALS death, death from other causes, emigration, or the end of study in August 2021.
Participants answered questions about physical activity levels, smoking status, and other issues relating to cardiovascular health, and participants’ resting heart rate was measured and divided into quartiles of 31-65 beats per minute (BPM), 66-74 BPM, 75-81 BPM, or 82-100 BPM.
Participants self-reported their physical activity over the past year, classifying it into one of four categories: Sedentary, at least 4 hours per week of walking or cycling, at least 4 hours per week of recreational sports or heavy gardening, or regular participation in intense training or sports competitions several times per week.
Only a few participants reported the highest level of physical activity, so researchers combined the third and fourth categories into a single high-activity group.
Of the total study cohort, 504 participants developed ALS. Of those who developed the disease, 59% were men.
Researchers found that of the 41,898 male participants with the highest level of physical activity, 63 developed ALS. In comparison, of the 76,769 male participants who reported an intermediate level of physical activity, 131 developed ALS. Among the 29,468 male participants who reported the lowest level of physical activity, 68 developed ALS.
No Link in Women?
After adjusting for smoking, body mass index, and other risk factors, investigators found that men with moderate physical activity levels had a 29% lower risk for ALS compared with those with low physical activity levels, whereas those with the highest activity levels had a 41% lower risk.
In addition, men in the lowest of the four categories of resting heart rate had a 32% reduced risk for ALS compared with men with a higher resting heart rate.
Investigators are unclear why there was a lack of association between physical activity and resting heart rate and ALS risk in women.
“There are known sex differences in ALS, which includes a sex ratio with male preponderance, and there are also sex differences in response to physical exercise. Perhaps underlying mechanisms herein can explain the difference observed between males and females in the study,” Dr. Vaage said. He noted that future research should explore this difference.
Study limitations included the absence of data on physical trauma and head trauma, which have been linked with increased ALS risk. In addition, there were no data on genotype.
In an accompanying editorial, Pamela Shaw, MD, and Johnathan Cooper-Knock, BMBCh, PhD, of the University of Sheffield, Sheffield, England, described the research as a “valuable contribution to the field and potentially provides some reassurance that mild/moderate levels of physical activity in middle age do not increase the risk for ALS but may instead have a beneficial protective effect.”
Future research on exercise in ALS, they add, should consider sex differences, capture the most extreme physical activity levels, and identify any genetic factors that may mediate the association between intense exercise and ALS.
No targeted funding was reported. Dr. Vaage reported receiving funding from ALS Laboratory Group Norway.
A version of this article first appeared on Medscape.com.
FROM NEUROLOGY
Common Antidepressants Ranked by Potential for Weight Gain
Eight commonly used antidepressants have been ranked by their weight gain potential.
Results of a large observational study showed small differences in short- and long-term weight change in patients prescribed one of eight antidepressants, with bupropion associated with the lowest weight gain and escitalopram, paroxetine, and duloxetine associated with the greatest.
Escitalopram, paroxetine, and duloxetine users were 10%-15% more likely to gain at least 5% of their baseline weight compared with those taking sertraline, which was used as a comparator.
“Patients and their clinicians often have several options when starting an antidepressant for the first time. This study provides important real-world evidence regarding the amount of weight gain that should be expected after starting some of the most common antidepressants,” lead author Joshua Petimar, ScD, assistant professor of population medicine in the Harvard Pilgrim Health Care Institute at Harvard Medical School, Boston, said in a press release.
The findings were published online in Annals of Internal Medicine.
Real-World Data
Though weight gain is a commonly reported side effect of antidepressant use and may lead to medication nonadherence and worse outcomes, there is a lack of real-world data about weight change across specific medications.
Investigators used electronic health records from eight health care systems across the United States spanning from 2010 to 2019. The analysis included information on 183,118 adults aged 20-80 years who were new users of one of eight common first-line antidepressants. Investigators measured their weight at baseline and at 6, 12, and 24 months after initiation to estimate intention-to-treat (ITT) effects of weight change.
At baseline, participants were randomly assigned to begin sertraline, citalopram, escitalopram, fluoxetine, paroxetine, bupropion, duloxetine, or venlafaxine.
The most common antidepressants prescribed were sertraline, citalopram, and bupropion. Approximately 36% of participants had a diagnosis of depression, and 39% were diagnosed with anxiety.
Among selective serotonin reuptake inhibitors (SSRIs), escitalopram and paroxetine were associated with the greatest 6-month weight gain, whereas bupropion was associated with the least weight gain across all analyses.
Using sertraline as a comparator, 6-month weight change was lower for bupropion (difference, 0.22 kg) and higher for escitalopram (difference, 0.41 kg), duloxetine (difference, 0.34 kg), paroxetine (difference, 0.37 kg), and venlafaxine (difference, 0.17 kg).
Escitalopram, paroxetine, and duloxetine users were 10%-15% more likely to gain at least 5% of their baseline weight compared with sertraline users.
Investigators noted little difference in adherence levels between medications during the study except at 6 months, when it was higher for those who took bupropion (41%) than for those taking other antidepressants (28%-36%).
The study included data only on prescriptions and investigators could not verify whether the medications were dispensed or taken as prescribed. Other limitations included missing weight information because most patients did not encounter the health system at exactly 6, 12, and 24 months; only 15%-30% had weight measurements in those months.
Finally, the low adherence rates made it difficult to attribute relative weight change at the 12- and 24-month time points to the specific medications of interest.
“Clinicians and patients could consider these differences when making decisions about specific antidepressants, especially given the complex relationships of obesity and depression with health, quality of life, and stigma,” the authors wrote.
The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases. Disclosures are noted in the original article.
A version of this article appeared on Medscape.com.
Eight commonly used antidepressants have been ranked by their weight gain potential.
Results of a large observational study showed small differences in short- and long-term weight change in patients prescribed one of eight antidepressants, with bupropion associated with the lowest weight gain and escitalopram, paroxetine, and duloxetine associated with the greatest.
Escitalopram, paroxetine, and duloxetine users were 10%-15% more likely to gain at least 5% of their baseline weight compared with those taking sertraline, which was used as a comparator.
“Patients and their clinicians often have several options when starting an antidepressant for the first time. This study provides important real-world evidence regarding the amount of weight gain that should be expected after starting some of the most common antidepressants,” lead author Joshua Petimar, ScD, assistant professor of population medicine in the Harvard Pilgrim Health Care Institute at Harvard Medical School, Boston, said in a press release.
The findings were published online in Annals of Internal Medicine.
Real-World Data
Though weight gain is a commonly reported side effect of antidepressant use and may lead to medication nonadherence and worse outcomes, there is a lack of real-world data about weight change across specific medications.
Investigators used electronic health records from eight health care systems across the United States spanning from 2010 to 2019. The analysis included information on 183,118 adults aged 20-80 years who were new users of one of eight common first-line antidepressants. Investigators measured their weight at baseline and at 6, 12, and 24 months after initiation to estimate intention-to-treat (ITT) effects of weight change.
At baseline, participants were randomly assigned to begin sertraline, citalopram, escitalopram, fluoxetine, paroxetine, bupropion, duloxetine, or venlafaxine.
The most common antidepressants prescribed were sertraline, citalopram, and bupropion. Approximately 36% of participants had a diagnosis of depression, and 39% were diagnosed with anxiety.
Among selective serotonin reuptake inhibitors (SSRIs), escitalopram and paroxetine were associated with the greatest 6-month weight gain, whereas bupropion was associated with the least weight gain across all analyses.
Using sertraline as a comparator, 6-month weight change was lower for bupropion (difference, 0.22 kg) and higher for escitalopram (difference, 0.41 kg), duloxetine (difference, 0.34 kg), paroxetine (difference, 0.37 kg), and venlafaxine (difference, 0.17 kg).
Escitalopram, paroxetine, and duloxetine users were 10%-15% more likely to gain at least 5% of their baseline weight compared with sertraline users.
Investigators noted little difference in adherence levels between medications during the study except at 6 months, when it was higher for those who took bupropion (41%) than for those taking other antidepressants (28%-36%).
The study included data only on prescriptions and investigators could not verify whether the medications were dispensed or taken as prescribed. Other limitations included missing weight information because most patients did not encounter the health system at exactly 6, 12, and 24 months; only 15%-30% had weight measurements in those months.
Finally, the low adherence rates made it difficult to attribute relative weight change at the 12- and 24-month time points to the specific medications of interest.
“Clinicians and patients could consider these differences when making decisions about specific antidepressants, especially given the complex relationships of obesity and depression with health, quality of life, and stigma,” the authors wrote.
The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases. Disclosures are noted in the original article.
A version of this article appeared on Medscape.com.
Eight commonly used antidepressants have been ranked by their weight gain potential.
Results of a large observational study showed small differences in short- and long-term weight change in patients prescribed one of eight antidepressants, with bupropion associated with the lowest weight gain and escitalopram, paroxetine, and duloxetine associated with the greatest.
Escitalopram, paroxetine, and duloxetine users were 10%-15% more likely to gain at least 5% of their baseline weight compared with those taking sertraline, which was used as a comparator.
“Patients and their clinicians often have several options when starting an antidepressant for the first time. This study provides important real-world evidence regarding the amount of weight gain that should be expected after starting some of the most common antidepressants,” lead author Joshua Petimar, ScD, assistant professor of population medicine in the Harvard Pilgrim Health Care Institute at Harvard Medical School, Boston, said in a press release.
The findings were published online in Annals of Internal Medicine.
Real-World Data
Though weight gain is a commonly reported side effect of antidepressant use and may lead to medication nonadherence and worse outcomes, there is a lack of real-world data about weight change across specific medications.
Investigators used electronic health records from eight health care systems across the United States spanning from 2010 to 2019. The analysis included information on 183,118 adults aged 20-80 years who were new users of one of eight common first-line antidepressants. Investigators measured their weight at baseline and at 6, 12, and 24 months after initiation to estimate intention-to-treat (ITT) effects of weight change.
At baseline, participants were randomly assigned to begin sertraline, citalopram, escitalopram, fluoxetine, paroxetine, bupropion, duloxetine, or venlafaxine.
The most common antidepressants prescribed were sertraline, citalopram, and bupropion. Approximately 36% of participants had a diagnosis of depression, and 39% were diagnosed with anxiety.
Among selective serotonin reuptake inhibitors (SSRIs), escitalopram and paroxetine were associated with the greatest 6-month weight gain, whereas bupropion was associated with the least weight gain across all analyses.
Using sertraline as a comparator, 6-month weight change was lower for bupropion (difference, 0.22 kg) and higher for escitalopram (difference, 0.41 kg), duloxetine (difference, 0.34 kg), paroxetine (difference, 0.37 kg), and venlafaxine (difference, 0.17 kg).
Escitalopram, paroxetine, and duloxetine users were 10%-15% more likely to gain at least 5% of their baseline weight compared with sertraline users.
Investigators noted little difference in adherence levels between medications during the study except at 6 months, when it was higher for those who took bupropion (41%) than for those taking other antidepressants (28%-36%).
The study included data only on prescriptions and investigators could not verify whether the medications were dispensed or taken as prescribed. Other limitations included missing weight information because most patients did not encounter the health system at exactly 6, 12, and 24 months; only 15%-30% had weight measurements in those months.
Finally, the low adherence rates made it difficult to attribute relative weight change at the 12- and 24-month time points to the specific medications of interest.
“Clinicians and patients could consider these differences when making decisions about specific antidepressants, especially given the complex relationships of obesity and depression with health, quality of life, and stigma,” the authors wrote.
The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases. Disclosures are noted in the original article.
A version of this article appeared on Medscape.com.
Prostate Meds Tied to Reduced Risk for Lewy Body Dementia
Certain medications that are used to treat benign prostatic hyperplasia (BPH) are associated with a reduced risk for dementia with Lewy bodies (DLB), the second most common neurodegenerative type of dementia after Alzheimer’s disease.
Investigators found older men taking alpha-1 blockers terazosin, doxazosin, or alfuzosin (Tz/Dz/Az) were 40% less likely to develop DLB than those taking tamsulosin and 37% less likely than men taking the 5-alpha reductase inhibitors (5ARI) finasteride and dutasteride.
“These results are exciting because right now there are no drugs to prevent or treat dementia with Lewy bodies,” study investigator Jacob E. Simmering, PhD, of the University of Iowa in Iowa City, said in a press release. “If we can determine that an existing drug can offer protection against this debilitating disease, that has the potential to greatly reduce its effects.”
The findings were published online in Neurology.
Increasing ATP Neuroprotective?
In recent years, investigators have speculated that improving metabolic activity in the brain may reduce the risk for Parkinson’s disease (PD).
In previous studies, the use of Tz/Dz/Az resulted in the activation of phosphoglycerate kinase-1 (PKG1), which increases the availability of adenosine triphosphate (ATP).
There have been case reports of PD being linked to mutations affecting PGK1. Researchers speculate that increased ATP availability in neurons resulting from the activation of PKG1 allows cells to better adapt to aging and synuclein aggregation.
To investigate whether glycolysis-enhancing drugs might be neuroprotective in those with DLB, investigators conducted a retrospective cohort study using a commercial health insurance claims database and a Medicare supplemental health claims database to follow a sample of men aged > 40 years taking Tz, Dz, or Az (n = 126,313), tamsulosin (n = 437,035), or a 5ARI (n = 80,158) for BPH.
Tamsulosin and 5ARI medications do not activate PKG1, so investigators used them as comparators to Tz/Dz/Az. Participants were followed from the medication initiation date until the end of enrollment in the claims databases.
After following claimants for an average of 3 years, 195 participants developed DLB who were taking Tz, Dz, or Az, a rate of 5.21 cases per 10,000 people per year.
During the follow-up period, 1286 participants taking tamsulosin developed DLB, a rate of 10.8 per 10,000 people per year, and among those taking 5ARIs, 193 cases of DLB were reported, a rate of 7.8 per 10,000 people per year.
After matching the groups by age and other health conditions that may explain differences in rates of DLB, men taking Tz/Dz/Az had a 60% lower risk than those taking tamsulosin (P < .001) and a 37% lower risk for developing DLB than those taking the 5ARI medications (P = .012).
“This emerging evidence of a protective association across a spectrum of diseases suggests a broad neuroprotective effect for Tz/Dz/Az, consistent with our hypothesized mechanism that activation of PGK1 increases brain ATP and mitigates neurodegeneration,” the authors wrote.
Study limitations include excluding women from the study, so the findings cannot be generalized to women. Claims analyses were limited to administrative data that could have been incorrect, and the analyses did not include medication dosages.
No study funding or author disclosures were reported.
A version of this article first appeared on Medscape.com.
Certain medications that are used to treat benign prostatic hyperplasia (BPH) are associated with a reduced risk for dementia with Lewy bodies (DLB), the second most common neurodegenerative type of dementia after Alzheimer’s disease.
Investigators found older men taking alpha-1 blockers terazosin, doxazosin, or alfuzosin (Tz/Dz/Az) were 40% less likely to develop DLB than those taking tamsulosin and 37% less likely than men taking the 5-alpha reductase inhibitors (5ARI) finasteride and dutasteride.
“These results are exciting because right now there are no drugs to prevent or treat dementia with Lewy bodies,” study investigator Jacob E. Simmering, PhD, of the University of Iowa in Iowa City, said in a press release. “If we can determine that an existing drug can offer protection against this debilitating disease, that has the potential to greatly reduce its effects.”
The findings were published online in Neurology.
Increasing ATP Neuroprotective?
In recent years, investigators have speculated that improving metabolic activity in the brain may reduce the risk for Parkinson’s disease (PD).
In previous studies, the use of Tz/Dz/Az resulted in the activation of phosphoglycerate kinase-1 (PKG1), which increases the availability of adenosine triphosphate (ATP).
There have been case reports of PD being linked to mutations affecting PGK1. Researchers speculate that increased ATP availability in neurons resulting from the activation of PKG1 allows cells to better adapt to aging and synuclein aggregation.
To investigate whether glycolysis-enhancing drugs might be neuroprotective in those with DLB, investigators conducted a retrospective cohort study using a commercial health insurance claims database and a Medicare supplemental health claims database to follow a sample of men aged > 40 years taking Tz, Dz, or Az (n = 126,313), tamsulosin (n = 437,035), or a 5ARI (n = 80,158) for BPH.
Tamsulosin and 5ARI medications do not activate PKG1, so investigators used them as comparators to Tz/Dz/Az. Participants were followed from the medication initiation date until the end of enrollment in the claims databases.
After following claimants for an average of 3 years, 195 participants developed DLB who were taking Tz, Dz, or Az, a rate of 5.21 cases per 10,000 people per year.
During the follow-up period, 1286 participants taking tamsulosin developed DLB, a rate of 10.8 per 10,000 people per year, and among those taking 5ARIs, 193 cases of DLB were reported, a rate of 7.8 per 10,000 people per year.
After matching the groups by age and other health conditions that may explain differences in rates of DLB, men taking Tz/Dz/Az had a 60% lower risk than those taking tamsulosin (P < .001) and a 37% lower risk for developing DLB than those taking the 5ARI medications (P = .012).
“This emerging evidence of a protective association across a spectrum of diseases suggests a broad neuroprotective effect for Tz/Dz/Az, consistent with our hypothesized mechanism that activation of PGK1 increases brain ATP and mitigates neurodegeneration,” the authors wrote.
Study limitations include excluding women from the study, so the findings cannot be generalized to women. Claims analyses were limited to administrative data that could have been incorrect, and the analyses did not include medication dosages.
No study funding or author disclosures were reported.
A version of this article first appeared on Medscape.com.
Certain medications that are used to treat benign prostatic hyperplasia (BPH) are associated with a reduced risk for dementia with Lewy bodies (DLB), the second most common neurodegenerative type of dementia after Alzheimer’s disease.
Investigators found older men taking alpha-1 blockers terazosin, doxazosin, or alfuzosin (Tz/Dz/Az) were 40% less likely to develop DLB than those taking tamsulosin and 37% less likely than men taking the 5-alpha reductase inhibitors (5ARI) finasteride and dutasteride.
“These results are exciting because right now there are no drugs to prevent or treat dementia with Lewy bodies,” study investigator Jacob E. Simmering, PhD, of the University of Iowa in Iowa City, said in a press release. “If we can determine that an existing drug can offer protection against this debilitating disease, that has the potential to greatly reduce its effects.”
The findings were published online in Neurology.
Increasing ATP Neuroprotective?
In recent years, investigators have speculated that improving metabolic activity in the brain may reduce the risk for Parkinson’s disease (PD).
In previous studies, the use of Tz/Dz/Az resulted in the activation of phosphoglycerate kinase-1 (PKG1), which increases the availability of adenosine triphosphate (ATP).
There have been case reports of PD being linked to mutations affecting PGK1. Researchers speculate that increased ATP availability in neurons resulting from the activation of PKG1 allows cells to better adapt to aging and synuclein aggregation.
To investigate whether glycolysis-enhancing drugs might be neuroprotective in those with DLB, investigators conducted a retrospective cohort study using a commercial health insurance claims database and a Medicare supplemental health claims database to follow a sample of men aged > 40 years taking Tz, Dz, or Az (n = 126,313), tamsulosin (n = 437,035), or a 5ARI (n = 80,158) for BPH.
Tamsulosin and 5ARI medications do not activate PKG1, so investigators used them as comparators to Tz/Dz/Az. Participants were followed from the medication initiation date until the end of enrollment in the claims databases.
After following claimants for an average of 3 years, 195 participants developed DLB who were taking Tz, Dz, or Az, a rate of 5.21 cases per 10,000 people per year.
During the follow-up period, 1286 participants taking tamsulosin developed DLB, a rate of 10.8 per 10,000 people per year, and among those taking 5ARIs, 193 cases of DLB were reported, a rate of 7.8 per 10,000 people per year.
After matching the groups by age and other health conditions that may explain differences in rates of DLB, men taking Tz/Dz/Az had a 60% lower risk than those taking tamsulosin (P < .001) and a 37% lower risk for developing DLB than those taking the 5ARI medications (P = .012).
“This emerging evidence of a protective association across a spectrum of diseases suggests a broad neuroprotective effect for Tz/Dz/Az, consistent with our hypothesized mechanism that activation of PGK1 increases brain ATP and mitigates neurodegeneration,” the authors wrote.
Study limitations include excluding women from the study, so the findings cannot be generalized to women. Claims analyses were limited to administrative data that could have been incorrect, and the analyses did not include medication dosages.
No study funding or author disclosures were reported.
A version of this article first appeared on Medscape.com.
Chronic Loneliness Tied to Increased Stroke Risk
Adults older than 50 years who report experiencing persistently high levels of loneliness have a 56% increased risk for stroke, a new study showed.
The increased stroke risk did not apply to individuals who reported experiencing situational loneliness, a finding that investigators believe bolsters the hypothesis that chronic loneliness is driving the association.
“Our findings suggest that individuals who experience chronic loneliness are at higher risk for incident stroke,” lead investigator Yenee Soh, ScD, research associate of social and behavioral sciences in the Harvard T.H. Chan School of Public Health, Boston, told this news organization. “It is important to routinely assess loneliness, as the consequences may be worse if unidentified and/or ignored.”
The findings were published online in eClinicalMedicine.
Significant, Chronic Health Consequences
Exacerbated by the COVID-19 pandemic, loneliness is at an all-time high. A 2023 Surgeon General’s report highlighted the fact that loneliness and social isolation are linked to significant and chronic health consequences.
Previous research has linked loneliness to cardiovascular disease, yet few studies have examined the association between loneliness and stroke risk. The current study is one of the first to examine the association between changes in loneliness and stroke risk over time.
Using data from the 2006-2018 Health and Retirement Study, researchers assessed the link between loneliness and incident stroke over time. Between 2006 and 2008, 12,161 study participants, who were all older than 50 years with no history of stroke, responded to questions from the Revised UCLA Loneliness Scale. From these responses, researchers created summary loneliness scores.
Four years later, from 2010 to 2012, the 8936 remaining study participants responded to the same 20 questions again. Based on loneliness scores across the two time points, participants were divided into four groups:
- Consistently low (those who scored low on the loneliness scale at both baseline and follow-up).
- Remitting (those who scored high at baseline and low at follow-up).
- Recent onset (those who scored low at baseline and high at follow-up).
- Consistently high (those who scored high at both baseline and follow-up).
Incident stroke was determined by participant report and medical record data.
Among participants whose loneliness was measured at baseline only, 1237 strokes occurred during the 2006-2018 follow-up period. Among those who provided two loneliness assessments over time, 601 strokes occurred during the follow-up period.
Even after adjusting for social isolation, depressive symptoms, physical activity, body mass index, and other health conditions, investigators found that participants who reported being lonely at baseline only had a 25% increased stroke risk, compared with those who did not report being lonely at baseline (hazard ratio [HR], 1.25; 95% confidence interval (CI), 1.06-1.47).
Participants who reported having consistently high loneliness across both time points had a 56% increased risk for incident stroke vs those who did not report loneliness at both time points after adjusting for social isolation and depression (HR, 1.56; 95% CI, 1.11-2.18).
The researchers did not investigate any of the underlying issues that may contribute to the association between loneliness and stroke risk, but speculated there may be physiological factors at play. These could include inflammation caused by increased hypothalamic pituitary-adrenocortical activity, behavioral factors such as poor medication adherence, smoking and/or alcohol use, and psychosocial issues.
Those who experience chronic loneliness may represent individuals that are unable to develop or maintain satisfying social relationships, which may result in longer-term interpersonal difficulties, Dr. Soh noted.
“Since loneliness is a highly subjective experience, seeking help to address and intervene to address a patient’s specific personal needs is important. It’s important to distinguish loneliness from social isolation,” said Dr. Soh.
She added that “by screening for loneliness and providing care or referring patients to relevant behavioral healthcare providers, clinicians can play a crucial role in addressing loneliness and its associated health risks early on to help reduce the population burden of loneliness.”
Progressive Research
Commenting on the findings for this news organization, Elaine Jones, MD, medical director of Access TeleCare, who was not involved in the research, applauded the investigators for “advancing the topic by looking at the chronicity aspect of loneliness.”
She said more research is needed to investigate loneliness as a stroke risk factor and noted that there may be something inherently different among respondents who reported loneliness at both study time points.
“Personality types may play a role here. We know people with positive attitudes and outlooks can do better in challenging health situations than people who are negative in their attitudes, regardless of depression. Perhaps those who feel lonely initially decided to do something about it and join groups, take up a hobby, or re-engage with family or friends. Perhaps the people who are chronically lonely don’t, or can’t, do this,” Dr. Jones said.
Chronic loneliness can cause stress, she added, “and we know that stress chemicals and hormones can be harmful to health over long durations of time.”
The study was funded by the National Institute on Aging. There were no conflicts of interest noted.
A version of this article first appeared on Medscape.com.
Adults older than 50 years who report experiencing persistently high levels of loneliness have a 56% increased risk for stroke, a new study showed.
The increased stroke risk did not apply to individuals who reported experiencing situational loneliness, a finding that investigators believe bolsters the hypothesis that chronic loneliness is driving the association.
“Our findings suggest that individuals who experience chronic loneliness are at higher risk for incident stroke,” lead investigator Yenee Soh, ScD, research associate of social and behavioral sciences in the Harvard T.H. Chan School of Public Health, Boston, told this news organization. “It is important to routinely assess loneliness, as the consequences may be worse if unidentified and/or ignored.”
The findings were published online in eClinicalMedicine.
Significant, Chronic Health Consequences
Exacerbated by the COVID-19 pandemic, loneliness is at an all-time high. A 2023 Surgeon General’s report highlighted the fact that loneliness and social isolation are linked to significant and chronic health consequences.
Previous research has linked loneliness to cardiovascular disease, yet few studies have examined the association between loneliness and stroke risk. The current study is one of the first to examine the association between changes in loneliness and stroke risk over time.
Using data from the 2006-2018 Health and Retirement Study, researchers assessed the link between loneliness and incident stroke over time. Between 2006 and 2008, 12,161 study participants, who were all older than 50 years with no history of stroke, responded to questions from the Revised UCLA Loneliness Scale. From these responses, researchers created summary loneliness scores.
Four years later, from 2010 to 2012, the 8936 remaining study participants responded to the same 20 questions again. Based on loneliness scores across the two time points, participants were divided into four groups:
- Consistently low (those who scored low on the loneliness scale at both baseline and follow-up).
- Remitting (those who scored high at baseline and low at follow-up).
- Recent onset (those who scored low at baseline and high at follow-up).
- Consistently high (those who scored high at both baseline and follow-up).
Incident stroke was determined by participant report and medical record data.
Among participants whose loneliness was measured at baseline only, 1237 strokes occurred during the 2006-2018 follow-up period. Among those who provided two loneliness assessments over time, 601 strokes occurred during the follow-up period.
Even after adjusting for social isolation, depressive symptoms, physical activity, body mass index, and other health conditions, investigators found that participants who reported being lonely at baseline only had a 25% increased stroke risk, compared with those who did not report being lonely at baseline (hazard ratio [HR], 1.25; 95% confidence interval (CI), 1.06-1.47).
Participants who reported having consistently high loneliness across both time points had a 56% increased risk for incident stroke vs those who did not report loneliness at both time points after adjusting for social isolation and depression (HR, 1.56; 95% CI, 1.11-2.18).
The researchers did not investigate any of the underlying issues that may contribute to the association between loneliness and stroke risk, but speculated there may be physiological factors at play. These could include inflammation caused by increased hypothalamic pituitary-adrenocortical activity, behavioral factors such as poor medication adherence, smoking and/or alcohol use, and psychosocial issues.
Those who experience chronic loneliness may represent individuals that are unable to develop or maintain satisfying social relationships, which may result in longer-term interpersonal difficulties, Dr. Soh noted.
“Since loneliness is a highly subjective experience, seeking help to address and intervene to address a patient’s specific personal needs is important. It’s important to distinguish loneliness from social isolation,” said Dr. Soh.
She added that “by screening for loneliness and providing care or referring patients to relevant behavioral healthcare providers, clinicians can play a crucial role in addressing loneliness and its associated health risks early on to help reduce the population burden of loneliness.”
Progressive Research
Commenting on the findings for this news organization, Elaine Jones, MD, medical director of Access TeleCare, who was not involved in the research, applauded the investigators for “advancing the topic by looking at the chronicity aspect of loneliness.”
She said more research is needed to investigate loneliness as a stroke risk factor and noted that there may be something inherently different among respondents who reported loneliness at both study time points.
“Personality types may play a role here. We know people with positive attitudes and outlooks can do better in challenging health situations than people who are negative in their attitudes, regardless of depression. Perhaps those who feel lonely initially decided to do something about it and join groups, take up a hobby, or re-engage with family or friends. Perhaps the people who are chronically lonely don’t, or can’t, do this,” Dr. Jones said.
Chronic loneliness can cause stress, she added, “and we know that stress chemicals and hormones can be harmful to health over long durations of time.”
The study was funded by the National Institute on Aging. There were no conflicts of interest noted.
A version of this article first appeared on Medscape.com.
Adults older than 50 years who report experiencing persistently high levels of loneliness have a 56% increased risk for stroke, a new study showed.
The increased stroke risk did not apply to individuals who reported experiencing situational loneliness, a finding that investigators believe bolsters the hypothesis that chronic loneliness is driving the association.
“Our findings suggest that individuals who experience chronic loneliness are at higher risk for incident stroke,” lead investigator Yenee Soh, ScD, research associate of social and behavioral sciences in the Harvard T.H. Chan School of Public Health, Boston, told this news organization. “It is important to routinely assess loneliness, as the consequences may be worse if unidentified and/or ignored.”
The findings were published online in eClinicalMedicine.
Significant, Chronic Health Consequences
Exacerbated by the COVID-19 pandemic, loneliness is at an all-time high. A 2023 Surgeon General’s report highlighted the fact that loneliness and social isolation are linked to significant and chronic health consequences.
Previous research has linked loneliness to cardiovascular disease, yet few studies have examined the association between loneliness and stroke risk. The current study is one of the first to examine the association between changes in loneliness and stroke risk over time.
Using data from the 2006-2018 Health and Retirement Study, researchers assessed the link between loneliness and incident stroke over time. Between 2006 and 2008, 12,161 study participants, who were all older than 50 years with no history of stroke, responded to questions from the Revised UCLA Loneliness Scale. From these responses, researchers created summary loneliness scores.
Four years later, from 2010 to 2012, the 8936 remaining study participants responded to the same 20 questions again. Based on loneliness scores across the two time points, participants were divided into four groups:
- Consistently low (those who scored low on the loneliness scale at both baseline and follow-up).
- Remitting (those who scored high at baseline and low at follow-up).
- Recent onset (those who scored low at baseline and high at follow-up).
- Consistently high (those who scored high at both baseline and follow-up).
Incident stroke was determined by participant report and medical record data.
Among participants whose loneliness was measured at baseline only, 1237 strokes occurred during the 2006-2018 follow-up period. Among those who provided two loneliness assessments over time, 601 strokes occurred during the follow-up period.
Even after adjusting for social isolation, depressive symptoms, physical activity, body mass index, and other health conditions, investigators found that participants who reported being lonely at baseline only had a 25% increased stroke risk, compared with those who did not report being lonely at baseline (hazard ratio [HR], 1.25; 95% confidence interval (CI), 1.06-1.47).
Participants who reported having consistently high loneliness across both time points had a 56% increased risk for incident stroke vs those who did not report loneliness at both time points after adjusting for social isolation and depression (HR, 1.56; 95% CI, 1.11-2.18).
The researchers did not investigate any of the underlying issues that may contribute to the association between loneliness and stroke risk, but speculated there may be physiological factors at play. These could include inflammation caused by increased hypothalamic pituitary-adrenocortical activity, behavioral factors such as poor medication adherence, smoking and/or alcohol use, and psychosocial issues.
Those who experience chronic loneliness may represent individuals that are unable to develop or maintain satisfying social relationships, which may result in longer-term interpersonal difficulties, Dr. Soh noted.
“Since loneliness is a highly subjective experience, seeking help to address and intervene to address a patient’s specific personal needs is important. It’s important to distinguish loneliness from social isolation,” said Dr. Soh.
She added that “by screening for loneliness and providing care or referring patients to relevant behavioral healthcare providers, clinicians can play a crucial role in addressing loneliness and its associated health risks early on to help reduce the population burden of loneliness.”
Progressive Research
Commenting on the findings for this news organization, Elaine Jones, MD, medical director of Access TeleCare, who was not involved in the research, applauded the investigators for “advancing the topic by looking at the chronicity aspect of loneliness.”
She said more research is needed to investigate loneliness as a stroke risk factor and noted that there may be something inherently different among respondents who reported loneliness at both study time points.
“Personality types may play a role here. We know people with positive attitudes and outlooks can do better in challenging health situations than people who are negative in their attitudes, regardless of depression. Perhaps those who feel lonely initially decided to do something about it and join groups, take up a hobby, or re-engage with family or friends. Perhaps the people who are chronically lonely don’t, or can’t, do this,” Dr. Jones said.
Chronic loneliness can cause stress, she added, “and we know that stress chemicals and hormones can be harmful to health over long durations of time.”
The study was funded by the National Institute on Aging. There were no conflicts of interest noted.
A version of this article first appeared on Medscape.com.
New Blood Test for Large Vessel Stroke Could Be a ‘Game Changer’
When combined with clinical scores, a “game-changing” blood test can expedite the diagnosis and treatment of large vessel occlusion (LVO) stroke, potentially saving many lives, new data suggested.
Using cutoff levels of two blood biomarkers, glial fibrillary acidic protein (GFAP; 213 pg/mL) and D-dimer (600 ng/mL), and the field assessment stroke triage for emergency destination (FAST-ED) (score, > 2), investigators were able to detect LVOs with 81% sensitivity and 93% specificity less than 6 hours from the onset of symptoms.
GFAP has previously been linked to brain bleeds and traumatic brain injury.
The test also ruled out all patients with brain bleeds, and investigators noted that it could also be used to detect intracerebral hemorrhage.
“We have developed a game-changing, accessible tool that could help ensure that more people suffering from stroke are in the right place at the right time to receive critical, life-restoring care,” senior author Joshua Bernstock, MD, PhD, MPH, a clinical fellow in the department of neurosurgery at Brigham and Women’s Hospital in Boston, said in a press release.
The findings were published online on May 17 in Stroke: Vascular and Interventional Neurology.
Early Identification Crucial
Acute LVO stroke is one of the most treatable stroke types because of the availability of endovascular thrombectomy (EVT). However, EVT requires specialized equipment and teams that represent a small subset of accredited stroke centers and an even smaller subset of emergency medical facilities, so early identification of LVO is crucial, the investigators noted.
Dr. Bernstock and his team developed the TIME trial to assess the sensitivity and specificity of the blood biomarkers and scale cutoff values for identifying LVO vs non-LVO stroke.
As part of the observational prospective cohort trial, investigators included consecutive patients admitted to the Brandon Regional Hospital Emergency Department in Brandon, Florida, between May 2021 and August 2022 if they were referred for a suspected stroke and the time from symptom onset was under 18 hours.
Patients were excluded if they received thrombolytic therapy before blood was collected or if it was anticipated that blood collection would be difficult.
Investigators gathered information on patients’ clinical data, hematology results, time since last known well, and imaging findings to construct a clinical diagnosis (LVO, non-LVO, ischemic stroke, hemorrhagic stroke, or transient ischemic attack [TIA]).
In addition to the National Institutes of Health Stroke Scale, patients were assessed with the FAST-ED, the Rapid Arterial oCclusion Evaluation (RACE), the Cincinnati Stroke Triage Assessment Tool, and the Emergency Medical Stroke Assessment.
Of 323 patients in the final study sample, 29 (9%) had LVO ischemic stroke, and 48 (15%) had non-LVO ischemic stroke. Another 13 (4%) had hemorrhagic stroke, 12 had TIA (3.7%), and the largest proportion of patients had stroke mimic (n = 220; 68%), which included encephalopathy, hyperglycemia, hypertensive emergency, migraine, posterior reversible encephalopathy syndrome, and undetermined.
The Case for Biomarkers
When investigators looked at those with LVO ischemic stroke, they found the concentration of plasma D-dimer was significantly higher than that in patients with non-LVO suspected stroke (LVO suspected stroke, 1213 ng/mL; interquartile range [IQR], 733-1609 vs non-LVO suspected stroke, 617 ng/mL; IQR, 377-1345; P < .001).
In addition, GFAP was significantly increased in the plasma of patients with hemorrhagic stroke vs all other patients with suspected stroke (hemorrhagic stroke, 1464 pg/mL; IQR, 292-2580 vs nonhemorrhagic suspected stroke, 48 pg/mL; IQR, 12-98; P < .005).
Combinations of the blood biomarkers with the scales FAST-ED or RACE showed the best performance for LVO detection, with a specificity of 94% (for either scale combination) and a sensitivity of 71% for both scales.
When investigators analyzed data for just those patients identified within 6 hours of symptom onset, the combination of biomarkers plus FAST-ED resulted in a specificity of 93% and a sensitivity of 81%.
Given that clinical stroke scales in patients with hemorrhagic stroke frequently suggest LVO and that these patients are not candidates for EVT, a tool capable of ruling out hemorrhage and identifying only nonhemorrhagic ischemic LVO is essential, the investigators noted.
“In stroke care, time is brain,” Dr. Bernstock said. “The sooner a patient is put on the right care pathway, the better they are going to do. Whether that means ruling out bleeds or ruling in something that needs an intervention, being able to do this in a prehospital setting with the technology that we built is going to be truly transformative.”
The study was funded by the Innovate UK grant and private funding. Dr. Bernstock has positions and equity in Pockit Diagnostics Ltd. and Treovir Inc. and is on the boards of Centile Bio and NeuroX1. Other disclosures are noted in the original article.
A version of this article appeared on Medscape.com.
When combined with clinical scores, a “game-changing” blood test can expedite the diagnosis and treatment of large vessel occlusion (LVO) stroke, potentially saving many lives, new data suggested.
Using cutoff levels of two blood biomarkers, glial fibrillary acidic protein (GFAP; 213 pg/mL) and D-dimer (600 ng/mL), and the field assessment stroke triage for emergency destination (FAST-ED) (score, > 2), investigators were able to detect LVOs with 81% sensitivity and 93% specificity less than 6 hours from the onset of symptoms.
GFAP has previously been linked to brain bleeds and traumatic brain injury.
The test also ruled out all patients with brain bleeds, and investigators noted that it could also be used to detect intracerebral hemorrhage.
“We have developed a game-changing, accessible tool that could help ensure that more people suffering from stroke are in the right place at the right time to receive critical, life-restoring care,” senior author Joshua Bernstock, MD, PhD, MPH, a clinical fellow in the department of neurosurgery at Brigham and Women’s Hospital in Boston, said in a press release.
The findings were published online on May 17 in Stroke: Vascular and Interventional Neurology.
Early Identification Crucial
Acute LVO stroke is one of the most treatable stroke types because of the availability of endovascular thrombectomy (EVT). However, EVT requires specialized equipment and teams that represent a small subset of accredited stroke centers and an even smaller subset of emergency medical facilities, so early identification of LVO is crucial, the investigators noted.
Dr. Bernstock and his team developed the TIME trial to assess the sensitivity and specificity of the blood biomarkers and scale cutoff values for identifying LVO vs non-LVO stroke.
As part of the observational prospective cohort trial, investigators included consecutive patients admitted to the Brandon Regional Hospital Emergency Department in Brandon, Florida, between May 2021 and August 2022 if they were referred for a suspected stroke and the time from symptom onset was under 18 hours.
Patients were excluded if they received thrombolytic therapy before blood was collected or if it was anticipated that blood collection would be difficult.
Investigators gathered information on patients’ clinical data, hematology results, time since last known well, and imaging findings to construct a clinical diagnosis (LVO, non-LVO, ischemic stroke, hemorrhagic stroke, or transient ischemic attack [TIA]).
In addition to the National Institutes of Health Stroke Scale, patients were assessed with the FAST-ED, the Rapid Arterial oCclusion Evaluation (RACE), the Cincinnati Stroke Triage Assessment Tool, and the Emergency Medical Stroke Assessment.
Of 323 patients in the final study sample, 29 (9%) had LVO ischemic stroke, and 48 (15%) had non-LVO ischemic stroke. Another 13 (4%) had hemorrhagic stroke, 12 had TIA (3.7%), and the largest proportion of patients had stroke mimic (n = 220; 68%), which included encephalopathy, hyperglycemia, hypertensive emergency, migraine, posterior reversible encephalopathy syndrome, and undetermined.
The Case for Biomarkers
When investigators looked at those with LVO ischemic stroke, they found the concentration of plasma D-dimer was significantly higher than that in patients with non-LVO suspected stroke (LVO suspected stroke, 1213 ng/mL; interquartile range [IQR], 733-1609 vs non-LVO suspected stroke, 617 ng/mL; IQR, 377-1345; P < .001).
In addition, GFAP was significantly increased in the plasma of patients with hemorrhagic stroke vs all other patients with suspected stroke (hemorrhagic stroke, 1464 pg/mL; IQR, 292-2580 vs nonhemorrhagic suspected stroke, 48 pg/mL; IQR, 12-98; P < .005).
Combinations of the blood biomarkers with the scales FAST-ED or RACE showed the best performance for LVO detection, with a specificity of 94% (for either scale combination) and a sensitivity of 71% for both scales.
When investigators analyzed data for just those patients identified within 6 hours of symptom onset, the combination of biomarkers plus FAST-ED resulted in a specificity of 93% and a sensitivity of 81%.
Given that clinical stroke scales in patients with hemorrhagic stroke frequently suggest LVO and that these patients are not candidates for EVT, a tool capable of ruling out hemorrhage and identifying only nonhemorrhagic ischemic LVO is essential, the investigators noted.
“In stroke care, time is brain,” Dr. Bernstock said. “The sooner a patient is put on the right care pathway, the better they are going to do. Whether that means ruling out bleeds or ruling in something that needs an intervention, being able to do this in a prehospital setting with the technology that we built is going to be truly transformative.”
The study was funded by the Innovate UK grant and private funding. Dr. Bernstock has positions and equity in Pockit Diagnostics Ltd. and Treovir Inc. and is on the boards of Centile Bio and NeuroX1. Other disclosures are noted in the original article.
A version of this article appeared on Medscape.com.
When combined with clinical scores, a “game-changing” blood test can expedite the diagnosis and treatment of large vessel occlusion (LVO) stroke, potentially saving many lives, new data suggested.
Using cutoff levels of two blood biomarkers, glial fibrillary acidic protein (GFAP; 213 pg/mL) and D-dimer (600 ng/mL), and the field assessment stroke triage for emergency destination (FAST-ED) (score, > 2), investigators were able to detect LVOs with 81% sensitivity and 93% specificity less than 6 hours from the onset of symptoms.
GFAP has previously been linked to brain bleeds and traumatic brain injury.
The test also ruled out all patients with brain bleeds, and investigators noted that it could also be used to detect intracerebral hemorrhage.
“We have developed a game-changing, accessible tool that could help ensure that more people suffering from stroke are in the right place at the right time to receive critical, life-restoring care,” senior author Joshua Bernstock, MD, PhD, MPH, a clinical fellow in the department of neurosurgery at Brigham and Women’s Hospital in Boston, said in a press release.
The findings were published online on May 17 in Stroke: Vascular and Interventional Neurology.
Early Identification Crucial
Acute LVO stroke is one of the most treatable stroke types because of the availability of endovascular thrombectomy (EVT). However, EVT requires specialized equipment and teams that represent a small subset of accredited stroke centers and an even smaller subset of emergency medical facilities, so early identification of LVO is crucial, the investigators noted.
Dr. Bernstock and his team developed the TIME trial to assess the sensitivity and specificity of the blood biomarkers and scale cutoff values for identifying LVO vs non-LVO stroke.
As part of the observational prospective cohort trial, investigators included consecutive patients admitted to the Brandon Regional Hospital Emergency Department in Brandon, Florida, between May 2021 and August 2022 if they were referred for a suspected stroke and the time from symptom onset was under 18 hours.
Patients were excluded if they received thrombolytic therapy before blood was collected or if it was anticipated that blood collection would be difficult.
Investigators gathered information on patients’ clinical data, hematology results, time since last known well, and imaging findings to construct a clinical diagnosis (LVO, non-LVO, ischemic stroke, hemorrhagic stroke, or transient ischemic attack [TIA]).
In addition to the National Institutes of Health Stroke Scale, patients were assessed with the FAST-ED, the Rapid Arterial oCclusion Evaluation (RACE), the Cincinnati Stroke Triage Assessment Tool, and the Emergency Medical Stroke Assessment.
Of 323 patients in the final study sample, 29 (9%) had LVO ischemic stroke, and 48 (15%) had non-LVO ischemic stroke. Another 13 (4%) had hemorrhagic stroke, 12 had TIA (3.7%), and the largest proportion of patients had stroke mimic (n = 220; 68%), which included encephalopathy, hyperglycemia, hypertensive emergency, migraine, posterior reversible encephalopathy syndrome, and undetermined.
The Case for Biomarkers
When investigators looked at those with LVO ischemic stroke, they found the concentration of plasma D-dimer was significantly higher than that in patients with non-LVO suspected stroke (LVO suspected stroke, 1213 ng/mL; interquartile range [IQR], 733-1609 vs non-LVO suspected stroke, 617 ng/mL; IQR, 377-1345; P < .001).
In addition, GFAP was significantly increased in the plasma of patients with hemorrhagic stroke vs all other patients with suspected stroke (hemorrhagic stroke, 1464 pg/mL; IQR, 292-2580 vs nonhemorrhagic suspected stroke, 48 pg/mL; IQR, 12-98; P < .005).
Combinations of the blood biomarkers with the scales FAST-ED or RACE showed the best performance for LVO detection, with a specificity of 94% (for either scale combination) and a sensitivity of 71% for both scales.
When investigators analyzed data for just those patients identified within 6 hours of symptom onset, the combination of biomarkers plus FAST-ED resulted in a specificity of 93% and a sensitivity of 81%.
Given that clinical stroke scales in patients with hemorrhagic stroke frequently suggest LVO and that these patients are not candidates for EVT, a tool capable of ruling out hemorrhage and identifying only nonhemorrhagic ischemic LVO is essential, the investigators noted.
“In stroke care, time is brain,” Dr. Bernstock said. “The sooner a patient is put on the right care pathway, the better they are going to do. Whether that means ruling out bleeds or ruling in something that needs an intervention, being able to do this in a prehospital setting with the technology that we built is going to be truly transformative.”
The study was funded by the Innovate UK grant and private funding. Dr. Bernstock has positions and equity in Pockit Diagnostics Ltd. and Treovir Inc. and is on the boards of Centile Bio and NeuroX1. Other disclosures are noted in the original article.
A version of this article appeared on Medscape.com.
FROM STROKE: VASCULAR AND INTERVENTIONAL NEUROLOGY
Early-Life Exposure to Pollution Linked to Psychosis, Anxiety, Depression
Early-life exposure to air and noise pollution is associated with a higher risk for psychosis, depression, and anxiety in adolescence and early adulthood, results from a longitudinal birth cohort study showed.
While air pollution was associated primarily with psychotic experiences and depression, noise pollution was more likely to be associated with anxiety in adolescence and early adulthood.
“Early-life exposure could be detrimental to mental health given the extensive brain development and epigenetic processes that occur in utero and during infancy,” the researchers, led by Joanne Newbury, PhD, of Bristol Medical School, University of Bristol, England, wrote, adding that “the results of this cohort study provide novel evidence that early-life exposure to particulate matter is prospectively associated with the development of psychotic experiences and depression in youth.”
The findings were published online on May 28 in JAMA Network Open.
Large, Longitudinal Study
To learn more about how air and noise pollution may affect the brain from an early age, the investigators used data from the Avon Longitudinal Study of Parents and Children, an ongoing longitudinal birth cohort capturing data on new births in Southwest England from 1991 to 1992.
Investigators captured levels of air pollutants, which included nitrogen dioxide and fine particulate matter with a diameter smaller than 2.5 µm (PM2.5), in the areas where expectant mothers lived and where their children lived until age 12.
They also collected decibel levels of noise pollution in neighborhoods where expectant mothers and their children lived.
Participants were assessed for psychotic experiences, depression, and anxiety when they were 13, 18, and 24 years old.
Among the 9065 participants who had mental health data, 20% reported psychotic experiences, 11% reported depression, and 10% reported anxiety. About 60% of the participants had a family history of mental illness.
When they were age 13, 13.6% of participants reported psychotic experiences; 9.2% reported them at age 18, and 12.6% at age 24.
A lower number of participants reported feeling depressed and anxious at 13 years (5.6% for depression and 3.6% for anxiety) and 18 years (7.9% for depression and 5.7% for anxiety).
After adjusting for individual and family-level variables, including family psychiatric history, maternal social class, and neighborhood deprivation, elevated PM2.5 levels during pregnancy (P = .002) and childhood (P = .04) were associated with a significantly increased risk for psychotic experiences later in life. Pregnancy PM2.5 exposure was also associated with depression (P = .01).
Participants exposed to higher noise pollution in childhood and adolescence had an increased risk for anxiety (P = .03) as teenagers.
Vulnerability of the Developing Brain
The investigators noted that more information is needed to understand the underlying mechanisms behind these associations but noted that early-life exposure could be detrimental to mental health given “extensive brain development and epigenetic processes that occur in utero.”
They also noted that air pollution could lead to restricted fetal growth and premature birth, both of which are risk factors for psychopathology.
Martin Clift, PhD, of Swansea University in Swansea, Wales, who was not involved in the study, said that the paper highlights the need for more consideration of health consequences related to these exposures.
“As noted by the authors, this is an area that has received a lot of recent attention, yet there remains a large void of knowledge,” Dr. Clift said in a UK Science Media Centre release. “It highlights that some of the most dominant air pollutants can impact different mental health diagnoses, but that time-of-life is particularly important as to how each individual air pollutant may impact this diagnosis.”
Study limitations included limitations to generalizability of the data — the families in the study were more affluent and less diverse than the UK population overall.
The study was funded by the UK Medical Research Council, Wellcome Trust, and University of Bristol. Disclosures were noted in the original article.
A version of this article appeared on Medscape.com.
Early-life exposure to air and noise pollution is associated with a higher risk for psychosis, depression, and anxiety in adolescence and early adulthood, results from a longitudinal birth cohort study showed.
While air pollution was associated primarily with psychotic experiences and depression, noise pollution was more likely to be associated with anxiety in adolescence and early adulthood.
“Early-life exposure could be detrimental to mental health given the extensive brain development and epigenetic processes that occur in utero and during infancy,” the researchers, led by Joanne Newbury, PhD, of Bristol Medical School, University of Bristol, England, wrote, adding that “the results of this cohort study provide novel evidence that early-life exposure to particulate matter is prospectively associated with the development of psychotic experiences and depression in youth.”
The findings were published online on May 28 in JAMA Network Open.
Large, Longitudinal Study
To learn more about how air and noise pollution may affect the brain from an early age, the investigators used data from the Avon Longitudinal Study of Parents and Children, an ongoing longitudinal birth cohort capturing data on new births in Southwest England from 1991 to 1992.
Investigators captured levels of air pollutants, which included nitrogen dioxide and fine particulate matter with a diameter smaller than 2.5 µm (PM2.5), in the areas where expectant mothers lived and where their children lived until age 12.
They also collected decibel levels of noise pollution in neighborhoods where expectant mothers and their children lived.
Participants were assessed for psychotic experiences, depression, and anxiety when they were 13, 18, and 24 years old.
Among the 9065 participants who had mental health data, 20% reported psychotic experiences, 11% reported depression, and 10% reported anxiety. About 60% of the participants had a family history of mental illness.
When they were age 13, 13.6% of participants reported psychotic experiences; 9.2% reported them at age 18, and 12.6% at age 24.
A lower number of participants reported feeling depressed and anxious at 13 years (5.6% for depression and 3.6% for anxiety) and 18 years (7.9% for depression and 5.7% for anxiety).
After adjusting for individual and family-level variables, including family psychiatric history, maternal social class, and neighborhood deprivation, elevated PM2.5 levels during pregnancy (P = .002) and childhood (P = .04) were associated with a significantly increased risk for psychotic experiences later in life. Pregnancy PM2.5 exposure was also associated with depression (P = .01).
Participants exposed to higher noise pollution in childhood and adolescence had an increased risk for anxiety (P = .03) as teenagers.
Vulnerability of the Developing Brain
The investigators noted that more information is needed to understand the underlying mechanisms behind these associations but noted that early-life exposure could be detrimental to mental health given “extensive brain development and epigenetic processes that occur in utero.”
They also noted that air pollution could lead to restricted fetal growth and premature birth, both of which are risk factors for psychopathology.
Martin Clift, PhD, of Swansea University in Swansea, Wales, who was not involved in the study, said that the paper highlights the need for more consideration of health consequences related to these exposures.
“As noted by the authors, this is an area that has received a lot of recent attention, yet there remains a large void of knowledge,” Dr. Clift said in a UK Science Media Centre release. “It highlights that some of the most dominant air pollutants can impact different mental health diagnoses, but that time-of-life is particularly important as to how each individual air pollutant may impact this diagnosis.”
Study limitations included limitations to generalizability of the data — the families in the study were more affluent and less diverse than the UK population overall.
The study was funded by the UK Medical Research Council, Wellcome Trust, and University of Bristol. Disclosures were noted in the original article.
A version of this article appeared on Medscape.com.
Early-life exposure to air and noise pollution is associated with a higher risk for psychosis, depression, and anxiety in adolescence and early adulthood, results from a longitudinal birth cohort study showed.
While air pollution was associated primarily with psychotic experiences and depression, noise pollution was more likely to be associated with anxiety in adolescence and early adulthood.
“Early-life exposure could be detrimental to mental health given the extensive brain development and epigenetic processes that occur in utero and during infancy,” the researchers, led by Joanne Newbury, PhD, of Bristol Medical School, University of Bristol, England, wrote, adding that “the results of this cohort study provide novel evidence that early-life exposure to particulate matter is prospectively associated with the development of psychotic experiences and depression in youth.”
The findings were published online on May 28 in JAMA Network Open.
Large, Longitudinal Study
To learn more about how air and noise pollution may affect the brain from an early age, the investigators used data from the Avon Longitudinal Study of Parents and Children, an ongoing longitudinal birth cohort capturing data on new births in Southwest England from 1991 to 1992.
Investigators captured levels of air pollutants, which included nitrogen dioxide and fine particulate matter with a diameter smaller than 2.5 µm (PM2.5), in the areas where expectant mothers lived and where their children lived until age 12.
They also collected decibel levels of noise pollution in neighborhoods where expectant mothers and their children lived.
Participants were assessed for psychotic experiences, depression, and anxiety when they were 13, 18, and 24 years old.
Among the 9065 participants who had mental health data, 20% reported psychotic experiences, 11% reported depression, and 10% reported anxiety. About 60% of the participants had a family history of mental illness.
When they were age 13, 13.6% of participants reported psychotic experiences; 9.2% reported them at age 18, and 12.6% at age 24.
A lower number of participants reported feeling depressed and anxious at 13 years (5.6% for depression and 3.6% for anxiety) and 18 years (7.9% for depression and 5.7% for anxiety).
After adjusting for individual and family-level variables, including family psychiatric history, maternal social class, and neighborhood deprivation, elevated PM2.5 levels during pregnancy (P = .002) and childhood (P = .04) were associated with a significantly increased risk for psychotic experiences later in life. Pregnancy PM2.5 exposure was also associated with depression (P = .01).
Participants exposed to higher noise pollution in childhood and adolescence had an increased risk for anxiety (P = .03) as teenagers.
Vulnerability of the Developing Brain
The investigators noted that more information is needed to understand the underlying mechanisms behind these associations but noted that early-life exposure could be detrimental to mental health given “extensive brain development and epigenetic processes that occur in utero.”
They also noted that air pollution could lead to restricted fetal growth and premature birth, both of which are risk factors for psychopathology.
Martin Clift, PhD, of Swansea University in Swansea, Wales, who was not involved in the study, said that the paper highlights the need for more consideration of health consequences related to these exposures.
“As noted by the authors, this is an area that has received a lot of recent attention, yet there remains a large void of knowledge,” Dr. Clift said in a UK Science Media Centre release. “It highlights that some of the most dominant air pollutants can impact different mental health diagnoses, but that time-of-life is particularly important as to how each individual air pollutant may impact this diagnosis.”
Study limitations included limitations to generalizability of the data — the families in the study were more affluent and less diverse than the UK population overall.
The study was funded by the UK Medical Research Council, Wellcome Trust, and University of Bristol. Disclosures were noted in the original article.
A version of this article appeared on Medscape.com.