Eve Bender

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.

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.

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.

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.

TOPLINE:

US fentanyl seizures increased by more than 1700% between 2017 and 2023, new data showed. 

METHODOLOGY:

• Investigators analyzed data from the High Intensity Drug Trafficking Areas (HIDTA) program from 2017 through 2023.
• To assess trends in illicit fentanyl availability, investigators used eight indicators of potential shifts in illicit fentanyl supply, including total seizures, powder seizures, pill seizures, and the total weight of seizures.

TAKEAWAY:

• A total of 66,303 fentanyl seizures were identified. Of the total number of seizures, 67% were in powder form and 33% were pills.
• The total number of seizures during the study period increased by > 1700% — from 74,663 in 2017 to 115,221 in 2023.
• In 2023, the greatest number of fentanyl seizures was in Florida (n = 2,089), followed by Arizona (n = 1783) and California (n = 1440).Western United States experienced the greatest increase in seizures, particularly in pill form, suggesting a significant regional shift in fentanyl distribution. California had the greatest number of pills seized (n = 38.6 million) and also the greatest weight of powder seized (4315 kg).
• The findings highlight the rapidly changing nature of the illicit fentanyl market, with an increasing prevalence of fentanyl pills.
• Western United States experienced the greatest increase in seizures, particularly in pill form, suggesting a significant regional shift in fentanyl distribution. California had the greatest number of pills seized (n = 38.6 million) and also the greatest weight of powder seized (4315 kg).

The findings highlight the rapidly changing nature of the illicit fentanyl market, with an increasing prevalence of fentanyl pills.

IN PRACTICE:

“About half of seized fentanyl is now in pill form, suggesting that the illicit drug landscape has rapidly changed,” Joseph J. Palamar, PhD, MPH, of NYU Langone Health, New York, said in a press release. “The study’s findings underscore the evolving challenge of fentanyl in the illicit drug market, emphasizing the need for healthcare professionals to be vigilant in recognizing and responding to the risks associated with fentanyl, especially in pill form,” he added.

SOURCE:

Dr. Palamar led the study, which was published online on May 13, 2024, in the International Journal of Drug Policy. 

LIMITATIONS:

One limitation of the study is the inability to differentiate whether seizures were solely fentanyl, fentanyl combined with other drugs, or fentanyl analogs. Additionally, the reliance on HIDTA data may not fully represent the extent of illicit fentanyl availability.

DISCLOSURES:

Dr. Palamar reports a consulting or advisory relationship with the Washington Baltimore High Intensity Drug Trafficking Area. The study was supported by the National Institute on Drug Abuse.

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

TOPLINE:

US fentanyl seizures increased by more than 1700% between 2017 and 2023, new data showed. 

METHODOLOGY:

• Investigators analyzed data from the High Intensity Drug Trafficking Areas (HIDTA) program from 2017 through 2023.
• To assess trends in illicit fentanyl availability, investigators used eight indicators of potential shifts in illicit fentanyl supply, including total seizures, powder seizures, pill seizures, and the total weight of seizures.

TAKEAWAY:

• A total of 66,303 fentanyl seizures were identified. Of the total number of seizures, 67% were in powder form and 33% were pills.
• The total number of seizures during the study period increased by > 1700% — from 74,663 in 2017 to 115,221 in 2023.
• In 2023, the greatest number of fentanyl seizures was in Florida (n = 2,089), followed by Arizona (n = 1783) and California (n = 1440).Western United States experienced the greatest increase in seizures, particularly in pill form, suggesting a significant regional shift in fentanyl distribution. California had the greatest number of pills seized (n = 38.6 million) and also the greatest weight of powder seized (4315 kg).
• The findings highlight the rapidly changing nature of the illicit fentanyl market, with an increasing prevalence of fentanyl pills.
• Western United States experienced the greatest increase in seizures, particularly in pill form, suggesting a significant regional shift in fentanyl distribution. California had the greatest number of pills seized (n = 38.6 million) and also the greatest weight of powder seized (4315 kg).

The findings highlight the rapidly changing nature of the illicit fentanyl market, with an increasing prevalence of fentanyl pills.

IN PRACTICE:

“About half of seized fentanyl is now in pill form, suggesting that the illicit drug landscape has rapidly changed,” Joseph J. Palamar, PhD, MPH, of NYU Langone Health, New York, said in a press release. “The study’s findings underscore the evolving challenge of fentanyl in the illicit drug market, emphasizing the need for healthcare professionals to be vigilant in recognizing and responding to the risks associated with fentanyl, especially in pill form,” he added.

SOURCE:

Dr. Palamar led the study, which was published online on May 13, 2024, in the International Journal of Drug Policy. 

LIMITATIONS:

One limitation of the study is the inability to differentiate whether seizures were solely fentanyl, fentanyl combined with other drugs, or fentanyl analogs. Additionally, the reliance on HIDTA data may not fully represent the extent of illicit fentanyl availability.

DISCLOSURES:

Dr. Palamar reports a consulting or advisory relationship with the Washington Baltimore High Intensity Drug Trafficking Area. The study was supported by the National Institute on Drug Abuse.

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

TOPLINE:

US fentanyl seizures increased by more than 1700% between 2017 and 2023, new data showed. 

METHODOLOGY:

• Investigators analyzed data from the High Intensity Drug Trafficking Areas (HIDTA) program from 2017 through 2023.
• To assess trends in illicit fentanyl availability, investigators used eight indicators of potential shifts in illicit fentanyl supply, including total seizures, powder seizures, pill seizures, and the total weight of seizures.

TAKEAWAY:

• A total of 66,303 fentanyl seizures were identified. Of the total number of seizures, 67% were in powder form and 33% were pills.
• The total number of seizures during the study period increased by > 1700% — from 74,663 in 2017 to 115,221 in 2023.
• In 2023, the greatest number of fentanyl seizures was in Florida (n = 2,089), followed by Arizona (n = 1783) and California (n = 1440).Western United States experienced the greatest increase in seizures, particularly in pill form, suggesting a significant regional shift in fentanyl distribution. California had the greatest number of pills seized (n = 38.6 million) and also the greatest weight of powder seized (4315 kg).
• The findings highlight the rapidly changing nature of the illicit fentanyl market, with an increasing prevalence of fentanyl pills.
• Western United States experienced the greatest increase in seizures, particularly in pill form, suggesting a significant regional shift in fentanyl distribution. California had the greatest number of pills seized (n = 38.6 million) and also the greatest weight of powder seized (4315 kg).

The findings highlight the rapidly changing nature of the illicit fentanyl market, with an increasing prevalence of fentanyl pills.

IN PRACTICE:

“About half of seized fentanyl is now in pill form, suggesting that the illicit drug landscape has rapidly changed,” Joseph J. Palamar, PhD, MPH, of NYU Langone Health, New York, said in a press release. “The study’s findings underscore the evolving challenge of fentanyl in the illicit drug market, emphasizing the need for healthcare professionals to be vigilant in recognizing and responding to the risks associated with fentanyl, especially in pill form,” he added.

SOURCE:

Dr. Palamar led the study, which was published online on May 13, 2024, in the International Journal of Drug Policy. 

LIMITATIONS:

One limitation of the study is the inability to differentiate whether seizures were solely fentanyl, fentanyl combined with other drugs, or fentanyl analogs. Additionally, the reliance on HIDTA data may not fully represent the extent of illicit fentanyl availability.

DISCLOSURES:

Dr. Palamar reports a consulting or advisory relationship with the Washington Baltimore High Intensity Drug Trafficking Area. The study was supported by the National Institute on Drug Abuse.

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

Serious mental illness (SMI), including bipolar disorder or schizophrenia spectrum disorders, is associated with a twofold increased risk for comorbid physical illness, results of a new meta-analysis showed.

“Although treatment of physical and mental health remains siloed in many health services globally, the high prevalence of physical multimorbidity attests to the urgent need for integrated care models that address both physical and mental health outcomes in people with severe mental illness,” the authors, led by Sean Halstead, MD, of The University of Queensland Medical School in Brisbane, Australia, wrote.

The findings were published online in The Lancet Psychiatry.
 

Shorter Lifespan?

SMI is associated with reduced life expectancy, and experts speculate that additional chronic illnesses — whether physical or psychiatric — may underlie this association.

While previous research has paired SMI with comorbid physical illnesses, the researchers noted that this study is the first to focus on both physical and psychiatric multimorbidity in individuals with SMI.

The investigators conducted a meta-analysis of 82 observational studies comprising 1.6 million individuals with SMI and 13.2 million control subjects to determine the risk for physical or psychiatric multimorbidity.

Studies were included if participants were diagnosed with either a schizophrenia spectrum disorder or bipolar disorder, and the study assessed either physical multimorbidity (at least two physical health conditions) or psychiatric multimorbidity (at least three psychiatric conditions), including the initial SMI.

Investigators found that individuals with SMI had more than a twofold increased risk for physical multimorbidity than those without SMI (odds ratio [OR], 2.40; 95% CI, 1.57-3.65; P = .0009).

Physical multimorbidity, which included cardiovascular, endocrine, neurological rental, gastrointestinal, musculoskeletal, and infectious disorders, was prevalent at similar rates in both schizophrenia spectrum disorder and bipolar disorder.

The ratio of physical multimorbidity was about four times higher in younger populations with SMI (mean age ≤ 40; OR, 3.99; 95% CI, 1.43-11.10) than in older populations (mean age > 40; OR, 1.55; 95% CI, 0.96-2.51; subgroup differences, P = .0013).

In terms of absolute prevalence, 25% of those with SMI had a physical multimorbidity, and 14% had a psychiatric multimorbidity, which were primarily anxiety and substance use disorders.

Investigators speculated that physical multimorbidity in SMI could stem from side effects of psychotropic medications, which are known to cause rapid cardiometabolic changes, including weight gain. In addition, lifestyle factors or nonmodifiable risk factors could also contribute to physical multimorbidity.

The study’s limitations included its small sample sizes for subgroup analyses and insufficient analysis for significant covariates, including smoking rates and symptom severity.

“While health services and treatment guidelines often operate on the assumption that individuals have a single principal diagnosis, these results attest to the clinical complexity many people with severe mental illness face in relation to burden of chronic disease,” the investigators wrote. They added that a greater understanding of the epidemiological manifestations of multimorbidity in SMI is “imperative.”

There was no source of funding for this study. Dr. Halstead is supported by the Australian Research Training Program scholarship. Other disclosures were noted in the original article.

A version of this article appeared on Medscape.com .

Serious mental illness (SMI), including bipolar disorder or schizophrenia spectrum disorders, is associated with a twofold increased risk for comorbid physical illness, results of a new meta-analysis showed.

“Although treatment of physical and mental health remains siloed in many health services globally, the high prevalence of physical multimorbidity attests to the urgent need for integrated care models that address both physical and mental health outcomes in people with severe mental illness,” the authors, led by Sean Halstead, MD, of The University of Queensland Medical School in Brisbane, Australia, wrote.

The findings were published online in The Lancet Psychiatry.
 

Shorter Lifespan?

SMI is associated with reduced life expectancy, and experts speculate that additional chronic illnesses — whether physical or psychiatric — may underlie this association.

While previous research has paired SMI with comorbid physical illnesses, the researchers noted that this study is the first to focus on both physical and psychiatric multimorbidity in individuals with SMI.

The investigators conducted a meta-analysis of 82 observational studies comprising 1.6 million individuals with SMI and 13.2 million control subjects to determine the risk for physical or psychiatric multimorbidity.

Studies were included if participants were diagnosed with either a schizophrenia spectrum disorder or bipolar disorder, and the study assessed either physical multimorbidity (at least two physical health conditions) or psychiatric multimorbidity (at least three psychiatric conditions), including the initial SMI.

Investigators found that individuals with SMI had more than a twofold increased risk for physical multimorbidity than those without SMI (odds ratio [OR], 2.40; 95% CI, 1.57-3.65; P = .0009).

Physical multimorbidity, which included cardiovascular, endocrine, neurological rental, gastrointestinal, musculoskeletal, and infectious disorders, was prevalent at similar rates in both schizophrenia spectrum disorder and bipolar disorder.

The ratio of physical multimorbidity was about four times higher in younger populations with SMI (mean age ≤ 40; OR, 3.99; 95% CI, 1.43-11.10) than in older populations (mean age > 40; OR, 1.55; 95% CI, 0.96-2.51; subgroup differences, P = .0013).

In terms of absolute prevalence, 25% of those with SMI had a physical multimorbidity, and 14% had a psychiatric multimorbidity, which were primarily anxiety and substance use disorders.

Investigators speculated that physical multimorbidity in SMI could stem from side effects of psychotropic medications, which are known to cause rapid cardiometabolic changes, including weight gain. In addition, lifestyle factors or nonmodifiable risk factors could also contribute to physical multimorbidity.

The study’s limitations included its small sample sizes for subgroup analyses and insufficient analysis for significant covariates, including smoking rates and symptom severity.

“While health services and treatment guidelines often operate on the assumption that individuals have a single principal diagnosis, these results attest to the clinical complexity many people with severe mental illness face in relation to burden of chronic disease,” the investigators wrote. They added that a greater understanding of the epidemiological manifestations of multimorbidity in SMI is “imperative.”

There was no source of funding for this study. Dr. Halstead is supported by the Australian Research Training Program scholarship. Other disclosures were noted in the original article.

A version of this article appeared on Medscape.com .

Serious mental illness (SMI), including bipolar disorder or schizophrenia spectrum disorders, is associated with a twofold increased risk for comorbid physical illness, results of a new meta-analysis showed.

“Although treatment of physical and mental health remains siloed in many health services globally, the high prevalence of physical multimorbidity attests to the urgent need for integrated care models that address both physical and mental health outcomes in people with severe mental illness,” the authors, led by Sean Halstead, MD, of The University of Queensland Medical School in Brisbane, Australia, wrote.

The findings were published online in The Lancet Psychiatry.
 

Shorter Lifespan?

SMI is associated with reduced life expectancy, and experts speculate that additional chronic illnesses — whether physical or psychiatric — may underlie this association.

While previous research has paired SMI with comorbid physical illnesses, the researchers noted that this study is the first to focus on both physical and psychiatric multimorbidity in individuals with SMI.

The investigators conducted a meta-analysis of 82 observational studies comprising 1.6 million individuals with SMI and 13.2 million control subjects to determine the risk for physical or psychiatric multimorbidity.

Studies were included if participants were diagnosed with either a schizophrenia spectrum disorder or bipolar disorder, and the study assessed either physical multimorbidity (at least two physical health conditions) or psychiatric multimorbidity (at least three psychiatric conditions), including the initial SMI.

Investigators found that individuals with SMI had more than a twofold increased risk for physical multimorbidity than those without SMI (odds ratio [OR], 2.40; 95% CI, 1.57-3.65; P = .0009).

Physical multimorbidity, which included cardiovascular, endocrine, neurological rental, gastrointestinal, musculoskeletal, and infectious disorders, was prevalent at similar rates in both schizophrenia spectrum disorder and bipolar disorder.

The ratio of physical multimorbidity was about four times higher in younger populations with SMI (mean age ≤ 40; OR, 3.99; 95% CI, 1.43-11.10) than in older populations (mean age > 40; OR, 1.55; 95% CI, 0.96-2.51; subgroup differences, P = .0013).

In terms of absolute prevalence, 25% of those with SMI had a physical multimorbidity, and 14% had a psychiatric multimorbidity, which were primarily anxiety and substance use disorders.

Investigators speculated that physical multimorbidity in SMI could stem from side effects of psychotropic medications, which are known to cause rapid cardiometabolic changes, including weight gain. In addition, lifestyle factors or nonmodifiable risk factors could also contribute to physical multimorbidity.

The study’s limitations included its small sample sizes for subgroup analyses and insufficient analysis for significant covariates, including smoking rates and symptom severity.

“While health services and treatment guidelines often operate on the assumption that individuals have a single principal diagnosis, these results attest to the clinical complexity many people with severe mental illness face in relation to burden of chronic disease,” the investigators wrote. They added that a greater understanding of the epidemiological manifestations of multimorbidity in SMI is “imperative.”

There was no source of funding for this study. Dr. Halstead is supported by the Australian Research Training Program scholarship. Other disclosures were noted in the original article.

A version of this article appeared on Medscape.com .

Racial discrimination in Black Americans is associated with an increased risk of developing Alzheimer’s disease (AD) in later life, new findings showed.

Researchers found that Black Americans who experience racism in their 40s and 50s are more likely to have increased serum levels of AD biomarkers p-tau181 and neurofilament light (NfL) more than a decade later.

“We know that Black Americans are at an elevated risk of Alzheimer’s disease and other dementias compared to non-Hispanic White Americans, but we don’t fully understand all the factors that contribute to this disproportionate risk,” Michelle Mielke, PhD, co-author and professor of epidemiology and prevention at Wake Forest University School of Medicine, Winston-Salem, North Carolina, said in a press release.

Recent data show AD is twice as prevalent in Black Americans as in Whites, at 18.6% and 10%, respectively. Dr. Mielke said this level of disparity cannot be attributed solely to genetic differences, and evidence suggests that racism and its related stress may play a role.

The findings were published online in Alzheimer’s and Dementia.
 

AD Biomarker Testing

To further explore a possible link between exposure to racism and AD risk, investigators analyzed data from the Family and Community Health Study, a multisite, longitudinal investigation that included more than 800 families in the United States.

Blood samples and information on racial discrimination were collected from 255 middle-aged Black Americans between 2002 and 2005.

Blood samples were tested for serum phosphorylated tau181 (p-Tau181), a marker of AD pathology; NfL, a nonspecific marker of neurodegeneration; and glial fibrillary acidic protein (GFAP), a marker of brain inflammation.

Participants answered questions about racial discrimination, which included whether they have been subjected to disrespectful treatment including racial slurs, harassment from law enforcement, or if they had ever been excluded from social activities because of their race.

The sample included 212 females and 43 males with a mean age of 46. Most participants (70%) lived in urban areas.
 

Stress-Related?

Investigators found no correlation between racial discrimination and increased levels of AD blood biomarkers in 2008 when participants were a mean age of 46 years. However, 11 years later, when participants were roughly 57 years old, investigators found experiencing racism in middle age was significantly correlated with higher levels of both p-Tau181 (r = 0.158; P ≤ .012) and NfL (r = 0.143; P ≤ .023). There was no significant association between reported discrimination and GFAP.

“These findings support the hypothesis that unique life stressors encountered by Black Americans in midlife become biologically embedded and contribute to AD pathology and neurodegeneration later in life,” the authors wrote.

Investigators speculated based on previous research that the stress related to discrimination may be associated with reductions in hippocampal and prefrontal cortex volumes and neurodegeneration in general.

Dr. Mielke also said it’s clear that future studies should focus on racism experienced by Black Americans to further understand their risk for dementia.

“This research can help inform policies and interventions to reduce racial disparities and reduce dementia risk,” she said.

Study limitations include the absence of amyloid biomarkers. Investigators noted that participants had non-detectable levels of amyloid, likely due to the use of serum vs cerebrospinal fluid.

The study was funded by the National Institute on Aging and the National Heart, Lung, and Blood Institute. Mielke reported serving on scientific advisory boards and/or having consulted for Acadia, Biogen, Eisai, LabCorp, Lilly, Merck, PeerView Institute, Roche, Siemens Healthineers, and Sunbird Bio.

A version of this article appeared on Medscape.com.

Racial discrimination in Black Americans is associated with an increased risk of developing Alzheimer’s disease (AD) in later life, new findings showed.

Researchers found that Black Americans who experience racism in their 40s and 50s are more likely to have increased serum levels of AD biomarkers p-tau181 and neurofilament light (NfL) more than a decade later.

“We know that Black Americans are at an elevated risk of Alzheimer’s disease and other dementias compared to non-Hispanic White Americans, but we don’t fully understand all the factors that contribute to this disproportionate risk,” Michelle Mielke, PhD, co-author and professor of epidemiology and prevention at Wake Forest University School of Medicine, Winston-Salem, North Carolina, said in a press release.

Recent data show AD is twice as prevalent in Black Americans as in Whites, at 18.6% and 10%, respectively. Dr. Mielke said this level of disparity cannot be attributed solely to genetic differences, and evidence suggests that racism and its related stress may play a role.

The findings were published online in Alzheimer’s and Dementia.
 

AD Biomarker Testing

To further explore a possible link between exposure to racism and AD risk, investigators analyzed data from the Family and Community Health Study, a multisite, longitudinal investigation that included more than 800 families in the United States.

Blood samples and information on racial discrimination were collected from 255 middle-aged Black Americans between 2002 and 2005.

Blood samples were tested for serum phosphorylated tau181 (p-Tau181), a marker of AD pathology; NfL, a nonspecific marker of neurodegeneration; and glial fibrillary acidic protein (GFAP), a marker of brain inflammation.

Participants answered questions about racial discrimination, which included whether they have been subjected to disrespectful treatment including racial slurs, harassment from law enforcement, or if they had ever been excluded from social activities because of their race.

The sample included 212 females and 43 males with a mean age of 46. Most participants (70%) lived in urban areas.
 

Stress-Related?

Investigators found no correlation between racial discrimination and increased levels of AD blood biomarkers in 2008 when participants were a mean age of 46 years. However, 11 years later, when participants were roughly 57 years old, investigators found experiencing racism in middle age was significantly correlated with higher levels of both p-Tau181 (r = 0.158; P ≤ .012) and NfL (r = 0.143; P ≤ .023). There was no significant association between reported discrimination and GFAP.

“These findings support the hypothesis that unique life stressors encountered by Black Americans in midlife become biologically embedded and contribute to AD pathology and neurodegeneration later in life,” the authors wrote.

Investigators speculated based on previous research that the stress related to discrimination may be associated with reductions in hippocampal and prefrontal cortex volumes and neurodegeneration in general.

Dr. Mielke also said it’s clear that future studies should focus on racism experienced by Black Americans to further understand their risk for dementia.

“This research can help inform policies and interventions to reduce racial disparities and reduce dementia risk,” she said.

Study limitations include the absence of amyloid biomarkers. Investigators noted that participants had non-detectable levels of amyloid, likely due to the use of serum vs cerebrospinal fluid.

The study was funded by the National Institute on Aging and the National Heart, Lung, and Blood Institute. Mielke reported serving on scientific advisory boards and/or having consulted for Acadia, Biogen, Eisai, LabCorp, Lilly, Merck, PeerView Institute, Roche, Siemens Healthineers, and Sunbird Bio.

A version of this article appeared on Medscape.com.

Racial discrimination in Black Americans is associated with an increased risk of developing Alzheimer’s disease (AD) in later life, new findings showed.

Researchers found that Black Americans who experience racism in their 40s and 50s are more likely to have increased serum levels of AD biomarkers p-tau181 and neurofilament light (NfL) more than a decade later.

“We know that Black Americans are at an elevated risk of Alzheimer’s disease and other dementias compared to non-Hispanic White Americans, but we don’t fully understand all the factors that contribute to this disproportionate risk,” Michelle Mielke, PhD, co-author and professor of epidemiology and prevention at Wake Forest University School of Medicine, Winston-Salem, North Carolina, said in a press release.

Recent data show AD is twice as prevalent in Black Americans as in Whites, at 18.6% and 10%, respectively. Dr. Mielke said this level of disparity cannot be attributed solely to genetic differences, and evidence suggests that racism and its related stress may play a role.

The findings were published online in Alzheimer’s and Dementia.
 

AD Biomarker Testing

To further explore a possible link between exposure to racism and AD risk, investigators analyzed data from the Family and Community Health Study, a multisite, longitudinal investigation that included more than 800 families in the United States.

Blood samples and information on racial discrimination were collected from 255 middle-aged Black Americans between 2002 and 2005.

Blood samples were tested for serum phosphorylated tau181 (p-Tau181), a marker of AD pathology; NfL, a nonspecific marker of neurodegeneration; and glial fibrillary acidic protein (GFAP), a marker of brain inflammation.

Participants answered questions about racial discrimination, which included whether they have been subjected to disrespectful treatment including racial slurs, harassment from law enforcement, or if they had ever been excluded from social activities because of their race.

The sample included 212 females and 43 males with a mean age of 46. Most participants (70%) lived in urban areas.
 

Stress-Related?

Investigators found no correlation between racial discrimination and increased levels of AD blood biomarkers in 2008 when participants were a mean age of 46 years. However, 11 years later, when participants were roughly 57 years old, investigators found experiencing racism in middle age was significantly correlated with higher levels of both p-Tau181 (r = 0.158; P ≤ .012) and NfL (r = 0.143; P ≤ .023). There was no significant association between reported discrimination and GFAP.

“These findings support the hypothesis that unique life stressors encountered by Black Americans in midlife become biologically embedded and contribute to AD pathology and neurodegeneration later in life,” the authors wrote.

Investigators speculated based on previous research that the stress related to discrimination may be associated with reductions in hippocampal and prefrontal cortex volumes and neurodegeneration in general.

Dr. Mielke also said it’s clear that future studies should focus on racism experienced by Black Americans to further understand their risk for dementia.

“This research can help inform policies and interventions to reduce racial disparities and reduce dementia risk,” she said.

Study limitations include the absence of amyloid biomarkers. Investigators noted that participants had non-detectable levels of amyloid, likely due to the use of serum vs cerebrospinal fluid.

The study was funded by the National Institute on Aging and the National Heart, Lung, and Blood Institute. Mielke reported serving on scientific advisory boards and/or having consulted for Acadia, Biogen, Eisai, LabCorp, Lilly, Merck, PeerView Institute, Roche, Siemens Healthineers, and Sunbird Bio.

A version of this article appeared on Medscape.com.

Cognitive-behavioral therapy (CBT) is superior to mindfulness-based cognitive therapy (MT) for reducing symptom severity in patients with prolonged grief disorder, results from a randomized trial showed.

While patients receiving grief-focused CBT had a superior response compared with those receiving MT, participants in both groups experienced a significant reduction in symptoms 6 months after treatment.

“We emphasize that these results do not suggest that mindfulness-based therapy was not effective in treating grief-focused CBT, but rather that grief-focused CBT was relatively more effective in reducing prolonged grief disorder, depression, and grief-related cognitions than mindfulness-based cognitive therapy,” investigators, led by Richard Bryant, PhD, of the University of New South Wales, Sydney, Australia, wrote.

The findings were published online in JAMA Psychiatry.

Barrier to Treatment

Prolonged grief disorder can affect up to 10% of bereaved individuals and is associated with increased suicide risk, cancer, immunological dysfunction, cardiac events, and functional impairment.

One barrier to treatment for individuals with prolonged grief disorder is that the treatment process can be emotionally painful. Between 15% and 25% of patients with prolonged grief offered grief-focused CBT decline to participate because they are reluctant to focus on painful emotions surrounding the death of their loved one.

To compare grief-focused CBT with mindfulness-based CT, another psychotherapeutic treatment, investigators recruited 100 adults aged 18-70 years between 2012 and 2022.

Participants who met the criteria for prolonged grief disorder were randomized on a 1:1 basis to receive either grief-focused CBT (n = 50) or CT (n = 50). All assessors were blinded to the treatment condition.

Therapy in both groups included 11 weekly 90-minute individual sessions.

Participants were assessed posttreatment at the 6-month mark for prolonged grief disorder symptom severity with the Prolonged Grief (PG)-13 Scale. They were also assessed for symptoms of depression, anxiety, and self-reported quality of life.

Grief-focused CBT entailed education on prolonged grief disorder, monitoring of daily thoughts, revisiting the death memory for several sessions, reframing maladaptive grief-related thoughts, writing a letter to the deceased loved one, relapse prevention strategies, and goal setting.

Mindfulness-based CT was adapted to problematic grief and began with psychoeducation about prolonged grief disorder. The additional sessions entailed mindfulness-orienting exercises, meditation, body scans, and how mindfulness practices can be used to tolerate aversive emotions and thoughts or to manage grief reactions.

Participants were assessed at the end of their treatment and had a mean age of 47 years, and 87% were female. The majority (71%) were White, and 21% were African, Indigenous Australian, and Pacific Islander.

While participants in both groups had similar outcomes posttreatment, at the 6-month follow-up, grief-focused CBT led to more significant reductions in scores on the PG-13 scale compared with mindfulness-based CT (mean difference, 7.1 points; 95% CI, 1.6-12.5; P = .01) with a large between-group effect size (0.8; 95% CI, 0.2-1.3).

PG-13 scores range from 11 to 55, with higher scores indicating greater prolonged grief disorder severity.

Of note, both treatment groups had a significant reduction in prolonged grief disorder symptoms (mean difference, 11.3; 95% CI, 8.6-14.1; P < .001), with a large effect size (1.2; 95% CI, 0.9-1.5).

Grief-focused CBT also led to greater reductions in depression at 6 months as measured by the Beck Depression Inventory (mean difference, 6.6; 95% CI, 0.5-12.9; P = .04). Investigators noted that this finding was unexpected and “suggests that the greater reduction of depression in participants receiving grief-focused cognitive behavior therapy may be attributed to the superior reductions in prolonged grief disorder severity, thereby leading to downstream decreases in depression.”

The investigators noted several study limitations. Most participants were White, which limits the generalizability of the results to other races and ethnicities. Therapists were not blinded to treatment conditions, and investigators did not monitor participants’ therapeutic exercises that were to be practiced posttreatment until the 6-month mark.

The study was funded by the National Health and Medical Research Council. Dr. Bryant served on the ICD Eleventh Revision Working Group on the Classification of Stress-Related Disorders. No other disclosures were reported.

A version of this article appeared on Medscape.com .

Cognitive-behavioral therapy (CBT) is superior to mindfulness-based cognitive therapy (MT) for reducing symptom severity in patients with prolonged grief disorder, results from a randomized trial showed.

While patients receiving grief-focused CBT had a superior response compared with those receiving MT, participants in both groups experienced a significant reduction in symptoms 6 months after treatment.

“We emphasize that these results do not suggest that mindfulness-based therapy was not effective in treating grief-focused CBT, but rather that grief-focused CBT was relatively more effective in reducing prolonged grief disorder, depression, and grief-related cognitions than mindfulness-based cognitive therapy,” investigators, led by Richard Bryant, PhD, of the University of New South Wales, Sydney, Australia, wrote.

The findings were published online in JAMA Psychiatry.

Barrier to Treatment

Prolonged grief disorder can affect up to 10% of bereaved individuals and is associated with increased suicide risk, cancer, immunological dysfunction, cardiac events, and functional impairment.

One barrier to treatment for individuals with prolonged grief disorder is that the treatment process can be emotionally painful. Between 15% and 25% of patients with prolonged grief offered grief-focused CBT decline to participate because they are reluctant to focus on painful emotions surrounding the death of their loved one.

To compare grief-focused CBT with mindfulness-based CT, another psychotherapeutic treatment, investigators recruited 100 adults aged 18-70 years between 2012 and 2022.

Participants who met the criteria for prolonged grief disorder were randomized on a 1:1 basis to receive either grief-focused CBT (n = 50) or CT (n = 50). All assessors were blinded to the treatment condition.

Therapy in both groups included 11 weekly 90-minute individual sessions.

Participants were assessed posttreatment at the 6-month mark for prolonged grief disorder symptom severity with the Prolonged Grief (PG)-13 Scale. They were also assessed for symptoms of depression, anxiety, and self-reported quality of life.

Grief-focused CBT entailed education on prolonged grief disorder, monitoring of daily thoughts, revisiting the death memory for several sessions, reframing maladaptive grief-related thoughts, writing a letter to the deceased loved one, relapse prevention strategies, and goal setting.

Mindfulness-based CT was adapted to problematic grief and began with psychoeducation about prolonged grief disorder. The additional sessions entailed mindfulness-orienting exercises, meditation, body scans, and how mindfulness practices can be used to tolerate aversive emotions and thoughts or to manage grief reactions.

Participants were assessed at the end of their treatment and had a mean age of 47 years, and 87% were female. The majority (71%) were White, and 21% were African, Indigenous Australian, and Pacific Islander.

While participants in both groups had similar outcomes posttreatment, at the 6-month follow-up, grief-focused CBT led to more significant reductions in scores on the PG-13 scale compared with mindfulness-based CT (mean difference, 7.1 points; 95% CI, 1.6-12.5; P = .01) with a large between-group effect size (0.8; 95% CI, 0.2-1.3).

PG-13 scores range from 11 to 55, with higher scores indicating greater prolonged grief disorder severity.

Of note, both treatment groups had a significant reduction in prolonged grief disorder symptoms (mean difference, 11.3; 95% CI, 8.6-14.1; P < .001), with a large effect size (1.2; 95% CI, 0.9-1.5).

Grief-focused CBT also led to greater reductions in depression at 6 months as measured by the Beck Depression Inventory (mean difference, 6.6; 95% CI, 0.5-12.9; P = .04). Investigators noted that this finding was unexpected and “suggests that the greater reduction of depression in participants receiving grief-focused cognitive behavior therapy may be attributed to the superior reductions in prolonged grief disorder severity, thereby leading to downstream decreases in depression.”

The investigators noted several study limitations. Most participants were White, which limits the generalizability of the results to other races and ethnicities. Therapists were not blinded to treatment conditions, and investigators did not monitor participants’ therapeutic exercises that were to be practiced posttreatment until the 6-month mark.

The study was funded by the National Health and Medical Research Council. Dr. Bryant served on the ICD Eleventh Revision Working Group on the Classification of Stress-Related Disorders. No other disclosures were reported.

A version of this article appeared on Medscape.com .

Cognitive-behavioral therapy (CBT) is superior to mindfulness-based cognitive therapy (MT) for reducing symptom severity in patients with prolonged grief disorder, results from a randomized trial showed.

While patients receiving grief-focused CBT had a superior response compared with those receiving MT, participants in both groups experienced a significant reduction in symptoms 6 months after treatment.

“We emphasize that these results do not suggest that mindfulness-based therapy was not effective in treating grief-focused CBT, but rather that grief-focused CBT was relatively more effective in reducing prolonged grief disorder, depression, and grief-related cognitions than mindfulness-based cognitive therapy,” investigators, led by Richard Bryant, PhD, of the University of New South Wales, Sydney, Australia, wrote.

The findings were published online in JAMA Psychiatry.

Barrier to Treatment

Prolonged grief disorder can affect up to 10% of bereaved individuals and is associated with increased suicide risk, cancer, immunological dysfunction, cardiac events, and functional impairment.

One barrier to treatment for individuals with prolonged grief disorder is that the treatment process can be emotionally painful. Between 15% and 25% of patients with prolonged grief offered grief-focused CBT decline to participate because they are reluctant to focus on painful emotions surrounding the death of their loved one.

To compare grief-focused CBT with mindfulness-based CT, another psychotherapeutic treatment, investigators recruited 100 adults aged 18-70 years between 2012 and 2022.

Participants who met the criteria for prolonged grief disorder were randomized on a 1:1 basis to receive either grief-focused CBT (n = 50) or CT (n = 50). All assessors were blinded to the treatment condition.

Therapy in both groups included 11 weekly 90-minute individual sessions.

Participants were assessed posttreatment at the 6-month mark for prolonged grief disorder symptom severity with the Prolonged Grief (PG)-13 Scale. They were also assessed for symptoms of depression, anxiety, and self-reported quality of life.

Grief-focused CBT entailed education on prolonged grief disorder, monitoring of daily thoughts, revisiting the death memory for several sessions, reframing maladaptive grief-related thoughts, writing a letter to the deceased loved one, relapse prevention strategies, and goal setting.

Mindfulness-based CT was adapted to problematic grief and began with psychoeducation about prolonged grief disorder. The additional sessions entailed mindfulness-orienting exercises, meditation, body scans, and how mindfulness practices can be used to tolerate aversive emotions and thoughts or to manage grief reactions.

Participants were assessed at the end of their treatment and had a mean age of 47 years, and 87% were female. The majority (71%) were White, and 21% were African, Indigenous Australian, and Pacific Islander.

While participants in both groups had similar outcomes posttreatment, at the 6-month follow-up, grief-focused CBT led to more significant reductions in scores on the PG-13 scale compared with mindfulness-based CT (mean difference, 7.1 points; 95% CI, 1.6-12.5; P = .01) with a large between-group effect size (0.8; 95% CI, 0.2-1.3).

PG-13 scores range from 11 to 55, with higher scores indicating greater prolonged grief disorder severity.

Of note, both treatment groups had a significant reduction in prolonged grief disorder symptoms (mean difference, 11.3; 95% CI, 8.6-14.1; P < .001), with a large effect size (1.2; 95% CI, 0.9-1.5).

Grief-focused CBT also led to greater reductions in depression at 6 months as measured by the Beck Depression Inventory (mean difference, 6.6; 95% CI, 0.5-12.9; P = .04). Investigators noted that this finding was unexpected and “suggests that the greater reduction of depression in participants receiving grief-focused cognitive behavior therapy may be attributed to the superior reductions in prolonged grief disorder severity, thereby leading to downstream decreases in depression.”

The investigators noted several study limitations. Most participants were White, which limits the generalizability of the results to other races and ethnicities. Therapists were not blinded to treatment conditions, and investigators did not monitor participants’ therapeutic exercises that were to be practiced posttreatment until the 6-month mark.

The study was funded by the National Health and Medical Research Council. Dr. Bryant served on the ICD Eleventh Revision Working Group on the Classification of Stress-Related Disorders. No other disclosures were reported.

A version of this article appeared on Medscape.com .

There is no association between the SARS-CoV-2 vaccine and the risk for new-onset seizure, data from a new meta-analysis of six randomized, placebo-controlled clinical trials (RCTs) showed.

Results of the pooled analysis that included 63,500 individuals vaccinated with SARS-CoV-2 and 55,000 who received a placebo vaccine showed there was no significant difference between the two groups with respect to new-onset seizures at 28- or 43-day follow-up.

Regarding new-onset seizures in the general population, there was no statistically significant difference in risk for seizure incidence among vaccinated individuals vs placebo recipients, according to our meta-analysis, wrote the investigators, led by Ali Rafati, MD, MPH, Iran University of Medical Sciences in Tehran.

The findings were published online in JAMA Neurology.

Mixed Results

Results from previous research have been mixed regarding the link between the SARS-CoV-2 vaccination and new-onset seizures, with some showing an association.

To learn more about the possible association between the vaccines and new-onset seizures, the researchers conducted a literature review and identified six RCTs that measured adverse events following SARS-CoV-2 vaccinations (including messenger RNA, viral vector, and inactivated virus) vs placebo or other vaccines.

While five of the studies defined new-onset seizures according to the Medical Dictionary for Regulatory Activities, trial investigators in the sixth RCT assessed and determined new-onset seizures in participants.

Participants received two vaccinations 28 days apart in five RCTs and only one vaccine in the sixth trial.

The research team searched the data for new-onset seizure in the 28 days following one or both COVID vaccinations.

No Link Found

After comparing the incidence of new-onset seizure between the 63,500 vaccine (nine new-onset seizures, 0.014%) and 55,000 placebo recipients (one new-onset seizure, 0.002%), investigators found no significant difference between the two groups (odds ratio [OR], 2.70; 95% CI, 0.76-9.57; P = .12)

Investigators also sliced the data several ways to see if it would yield different results. When they analyzed data by vaccine platform (viral vector) and age group (children), they didn’t observe significant differences in new-onset data.

The researchers also searched for data beyond the month following the injection to encompass the entire blinded phase, so they analyzed the results of three RCTs that reported adverse events up to 162 days after the vaccine.

After pooling the results from the three studies, investigators found no statistical difference between the vaccine and placebo groups in terms of the new-onset seizure (OR, 2.31; 95% CI, 0.86%-3.23; P > .99)

Study limitations included the missing information on vaccine doses or risk factors for the development of seizures. Also, the RCTs included in the meta-analysis were conducted at different times, so the SARS-CoV-2 vaccines may have differed in their composition and efficacy.

“The global vaccination drive against SARS-CoV-2 has been a monumental effort in combating the pandemic. SARS-CoV-2 vaccinations that are now available appear safe and appropriate,” the authors wrote.

There were no study funding sources or disclosures reported.

A version of this article appeared on Medscape.com.

There is no association between the SARS-CoV-2 vaccine and the risk for new-onset seizure, data from a new meta-analysis of six randomized, placebo-controlled clinical trials (RCTs) showed.

Results of the pooled analysis that included 63,500 individuals vaccinated with SARS-CoV-2 and 55,000 who received a placebo vaccine showed there was no significant difference between the two groups with respect to new-onset seizures at 28- or 43-day follow-up.

Regarding new-onset seizures in the general population, there was no statistically significant difference in risk for seizure incidence among vaccinated individuals vs placebo recipients, according to our meta-analysis, wrote the investigators, led by Ali Rafati, MD, MPH, Iran University of Medical Sciences in Tehran.

The findings were published online in JAMA Neurology.

Mixed Results

Results from previous research have been mixed regarding the link between the SARS-CoV-2 vaccination and new-onset seizures, with some showing an association.

To learn more about the possible association between the vaccines and new-onset seizures, the researchers conducted a literature review and identified six RCTs that measured adverse events following SARS-CoV-2 vaccinations (including messenger RNA, viral vector, and inactivated virus) vs placebo or other vaccines.

While five of the studies defined new-onset seizures according to the Medical Dictionary for Regulatory Activities, trial investigators in the sixth RCT assessed and determined new-onset seizures in participants.

Participants received two vaccinations 28 days apart in five RCTs and only one vaccine in the sixth trial.

The research team searched the data for new-onset seizure in the 28 days following one or both COVID vaccinations.

No Link Found

After comparing the incidence of new-onset seizure between the 63,500 vaccine (nine new-onset seizures, 0.014%) and 55,000 placebo recipients (one new-onset seizure, 0.002%), investigators found no significant difference between the two groups (odds ratio [OR], 2.70; 95% CI, 0.76-9.57; P = .12)

Investigators also sliced the data several ways to see if it would yield different results. When they analyzed data by vaccine platform (viral vector) and age group (children), they didn’t observe significant differences in new-onset data.

The researchers also searched for data beyond the month following the injection to encompass the entire blinded phase, so they analyzed the results of three RCTs that reported adverse events up to 162 days after the vaccine.

After pooling the results from the three studies, investigators found no statistical difference between the vaccine and placebo groups in terms of the new-onset seizure (OR, 2.31; 95% CI, 0.86%-3.23; P > .99)

Study limitations included the missing information on vaccine doses or risk factors for the development of seizures. Also, the RCTs included in the meta-analysis were conducted at different times, so the SARS-CoV-2 vaccines may have differed in their composition and efficacy.

“The global vaccination drive against SARS-CoV-2 has been a monumental effort in combating the pandemic. SARS-CoV-2 vaccinations that are now available appear safe and appropriate,” the authors wrote.

There were no study funding sources or disclosures reported.

A version of this article appeared on Medscape.com.

There is no association between the SARS-CoV-2 vaccine and the risk for new-onset seizure, data from a new meta-analysis of six randomized, placebo-controlled clinical trials (RCTs) showed.

Results of the pooled analysis that included 63,500 individuals vaccinated with SARS-CoV-2 and 55,000 who received a placebo vaccine showed there was no significant difference between the two groups with respect to new-onset seizures at 28- or 43-day follow-up.

Regarding new-onset seizures in the general population, there was no statistically significant difference in risk for seizure incidence among vaccinated individuals vs placebo recipients, according to our meta-analysis, wrote the investigators, led by Ali Rafati, MD, MPH, Iran University of Medical Sciences in Tehran.

The findings were published online in JAMA Neurology.

Mixed Results

Results from previous research have been mixed regarding the link between the SARS-CoV-2 vaccination and new-onset seizures, with some showing an association.

To learn more about the possible association between the vaccines and new-onset seizures, the researchers conducted a literature review and identified six RCTs that measured adverse events following SARS-CoV-2 vaccinations (including messenger RNA, viral vector, and inactivated virus) vs placebo or other vaccines.

While five of the studies defined new-onset seizures according to the Medical Dictionary for Regulatory Activities, trial investigators in the sixth RCT assessed and determined new-onset seizures in participants.

Participants received two vaccinations 28 days apart in five RCTs and only one vaccine in the sixth trial.

The research team searched the data for new-onset seizure in the 28 days following one or both COVID vaccinations.

No Link Found

After comparing the incidence of new-onset seizure between the 63,500 vaccine (nine new-onset seizures, 0.014%) and 55,000 placebo recipients (one new-onset seizure, 0.002%), investigators found no significant difference between the two groups (odds ratio [OR], 2.70; 95% CI, 0.76-9.57; P = .12)

Investigators also sliced the data several ways to see if it would yield different results. When they analyzed data by vaccine platform (viral vector) and age group (children), they didn’t observe significant differences in new-onset data.

The researchers also searched for data beyond the month following the injection to encompass the entire blinded phase, so they analyzed the results of three RCTs that reported adverse events up to 162 days after the vaccine.

After pooling the results from the three studies, investigators found no statistical difference between the vaccine and placebo groups in terms of the new-onset seizure (OR, 2.31; 95% CI, 0.86%-3.23; P > .99)

Study limitations included the missing information on vaccine doses or risk factors for the development of seizures. Also, the RCTs included in the meta-analysis were conducted at different times, so the SARS-CoV-2 vaccines may have differed in their composition and efficacy.

“The global vaccination drive against SARS-CoV-2 has been a monumental effort in combating the pandemic. SARS-CoV-2 vaccinations that are now available appear safe and appropriate,” the authors wrote.

There were no study funding sources or disclosures reported.

A version of this article appeared on Medscape.com.

Deaths of despair — defined as midlife deaths from suicide, drug overdose, and alcoholic liver disease — among African Americans surpassed the rate in White Americans in 2022, new research showed. In addition, the study also revealed that Native Americans had more than double the rate of both their Black and White counterparts that year.

These new findings, the investigators noted, counter a nearly 10-year-old narrative that was sparked by a seminal 2015 study. It showed that from 1999 to 2013 deaths of despair predominantly affected White individuals at a rate of 72.15 per 100,000 population — twice that of Black Americans.

The investigators of the 2015 study posited that such deaths in the group were linked to declining social and economic conditions and a perceived loss of status especially in White individuals without a college degree. However, the investigators noted that data for Native Americans were not included in the 2015 study or in the many follow-up analyses the research triggered.

The study was published online in JAMA Psychiatry.
 

Racial Differences

The current investigators assessed trends by race and ethnicity in deaths of despair in the years following the 2015 study when an increase in racial and ethnic inequality were reported for numerous causes of death.

The cross-sectional study used publicly available records from the US Centers for Disease Control and Prevention database WONDER to calculate midlife mortality in the United States from January 1999 to December 2022 to determine deaths from suicide, drug overdose, and alcoholic liver disease for White, Black, and Native American individuals aged 45-55 years. The data were then analyzed by race and ethnicity.

Results showed that deaths of despair in Black Americans (103.81 per 100,000) surpassed that of White Americans (102.63 per 100,000) in 2022. Furthermore, the rate in Black Americans tripled from 2013 to 2022 (from 36.24 to 103.81 per 100,000), with a sharp increase in such deaths from 2015 onward.

The rate for Native American and Alaska Native populations was the highest at 241.7 per 100,000 population in 2022.

It has been posited that the increase in rates of deaths of despair among White people is associated with declining social and economic conditions and a perceived loss of status, especially among White individuals without a college degree, the authors noted. 

The initial seminal study became a focus of ongoing national discourse after results showed White individuals had the highest mortality rates from these causes at 72 per 100,000 people in 2013 — twice that of Black Americans.

They examined midlife mortality from suicide, drug overdose, and alcoholic liver disease between January 1999 and December 2022. The data were then analyzed by race and ethnicity.
 

The rate of midlife deaths from alcoholic liver disease among American Indian or Alaska Native individuals (109 per 100,000) was six times the rate of White individuals (18 per 100,000) in 2022. 

Rates of midlife suicide deaths in 2022 remained elevated among Native American or Alaska Native (28 per 100,000) and White (25 per 100,000) individuals compared with Black individuals (9 per 100,000).

Increases in deaths of despair among Black and Native Americans are associated with differential access to safety resources in the context of an increasingly toxic illicit drug supply, increased rates of polysubstance use, worsening economic precarity, and stark disparities in access to mental health and substance use treatment programs, the investigators noted.

“The findings reinforce the notion that we need to invest in services that can address these issues, and ultimately, we need much more comprehensive access to low-barrier mental health care and substance use treatment in the US,” study investigator Joseph Friedman, PhD, of the David Geffen School of Medicine at UCLA, Los Angeles, California, said in a press release. 

“We need to specifically make sure those treatments, services, and programs are implemented in a way that is accessible for communities of color and will actively work to address inequality,” Dr. Friedman added.

Potential study limitations include possible misclassification of race and ethnicity, which could underestimate observed inequalities, and the ecological design that precludes measuring causality of underlying factors, the researchers noted.

The investigators reported no relevant financial conflicts of interest.

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

Deaths of despair — defined as midlife deaths from suicide, drug overdose, and alcoholic liver disease — among African Americans surpassed the rate in White Americans in 2022, new research showed. In addition, the study also revealed that Native Americans had more than double the rate of both their Black and White counterparts that year.

These new findings, the investigators noted, counter a nearly 10-year-old narrative that was sparked by a seminal 2015 study. It showed that from 1999 to 2013 deaths of despair predominantly affected White individuals at a rate of 72.15 per 100,000 population — twice that of Black Americans.

The investigators of the 2015 study posited that such deaths in the group were linked to declining social and economic conditions and a perceived loss of status especially in White individuals without a college degree. However, the investigators noted that data for Native Americans were not included in the 2015 study or in the many follow-up analyses the research triggered.

The study was published online in JAMA Psychiatry.
 

Racial Differences

The current investigators assessed trends by race and ethnicity in deaths of despair in the years following the 2015 study when an increase in racial and ethnic inequality were reported for numerous causes of death.

The cross-sectional study used publicly available records from the US Centers for Disease Control and Prevention database WONDER to calculate midlife mortality in the United States from January 1999 to December 2022 to determine deaths from suicide, drug overdose, and alcoholic liver disease for White, Black, and Native American individuals aged 45-55 years. The data were then analyzed by race and ethnicity.

Results showed that deaths of despair in Black Americans (103.81 per 100,000) surpassed that of White Americans (102.63 per 100,000) in 2022. Furthermore, the rate in Black Americans tripled from 2013 to 2022 (from 36.24 to 103.81 per 100,000), with a sharp increase in such deaths from 2015 onward.

The rate for Native American and Alaska Native populations was the highest at 241.7 per 100,000 population in 2022.

It has been posited that the increase in rates of deaths of despair among White people is associated with declining social and economic conditions and a perceived loss of status, especially among White individuals without a college degree, the authors noted. 

The initial seminal study became a focus of ongoing national discourse after results showed White individuals had the highest mortality rates from these causes at 72 per 100,000 people in 2013 — twice that of Black Americans.

They examined midlife mortality from suicide, drug overdose, and alcoholic liver disease between January 1999 and December 2022. The data were then analyzed by race and ethnicity.
 

The rate of midlife deaths from alcoholic liver disease among American Indian or Alaska Native individuals (109 per 100,000) was six times the rate of White individuals (18 per 100,000) in 2022. 

Rates of midlife suicide deaths in 2022 remained elevated among Native American or Alaska Native (28 per 100,000) and White (25 per 100,000) individuals compared with Black individuals (9 per 100,000).

Increases in deaths of despair among Black and Native Americans are associated with differential access to safety resources in the context of an increasingly toxic illicit drug supply, increased rates of polysubstance use, worsening economic precarity, and stark disparities in access to mental health and substance use treatment programs, the investigators noted.

“The findings reinforce the notion that we need to invest in services that can address these issues, and ultimately, we need much more comprehensive access to low-barrier mental health care and substance use treatment in the US,” study investigator Joseph Friedman, PhD, of the David Geffen School of Medicine at UCLA, Los Angeles, California, said in a press release. 

“We need to specifically make sure those treatments, services, and programs are implemented in a way that is accessible for communities of color and will actively work to address inequality,” Dr. Friedman added.

Potential study limitations include possible misclassification of race and ethnicity, which could underestimate observed inequalities, and the ecological design that precludes measuring causality of underlying factors, the researchers noted.

The investigators reported no relevant financial conflicts of interest.

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

Deaths of despair — defined as midlife deaths from suicide, drug overdose, and alcoholic liver disease — among African Americans surpassed the rate in White Americans in 2022, new research showed. In addition, the study also revealed that Native Americans had more than double the rate of both their Black and White counterparts that year.

These new findings, the investigators noted, counter a nearly 10-year-old narrative that was sparked by a seminal 2015 study. It showed that from 1999 to 2013 deaths of despair predominantly affected White individuals at a rate of 72.15 per 100,000 population — twice that of Black Americans.

The investigators of the 2015 study posited that such deaths in the group were linked to declining social and economic conditions and a perceived loss of status especially in White individuals without a college degree. However, the investigators noted that data for Native Americans were not included in the 2015 study or in the many follow-up analyses the research triggered.

The study was published online in JAMA Psychiatry.
 

Racial Differences

The current investigators assessed trends by race and ethnicity in deaths of despair in the years following the 2015 study when an increase in racial and ethnic inequality were reported for numerous causes of death.

The cross-sectional study used publicly available records from the US Centers for Disease Control and Prevention database WONDER to calculate midlife mortality in the United States from January 1999 to December 2022 to determine deaths from suicide, drug overdose, and alcoholic liver disease for White, Black, and Native American individuals aged 45-55 years. The data were then analyzed by race and ethnicity.

Results showed that deaths of despair in Black Americans (103.81 per 100,000) surpassed that of White Americans (102.63 per 100,000) in 2022. Furthermore, the rate in Black Americans tripled from 2013 to 2022 (from 36.24 to 103.81 per 100,000), with a sharp increase in such deaths from 2015 onward.

The rate for Native American and Alaska Native populations was the highest at 241.7 per 100,000 population in 2022.

It has been posited that the increase in rates of deaths of despair among White people is associated with declining social and economic conditions and a perceived loss of status, especially among White individuals without a college degree, the authors noted. 

The initial seminal study became a focus of ongoing national discourse after results showed White individuals had the highest mortality rates from these causes at 72 per 100,000 people in 2013 — twice that of Black Americans.

They examined midlife mortality from suicide, drug overdose, and alcoholic liver disease between January 1999 and December 2022. The data were then analyzed by race and ethnicity.
 

The rate of midlife deaths from alcoholic liver disease among American Indian or Alaska Native individuals (109 per 100,000) was six times the rate of White individuals (18 per 100,000) in 2022. 

Rates of midlife suicide deaths in 2022 remained elevated among Native American or Alaska Native (28 per 100,000) and White (25 per 100,000) individuals compared with Black individuals (9 per 100,000).

Increases in deaths of despair among Black and Native Americans are associated with differential access to safety resources in the context of an increasingly toxic illicit drug supply, increased rates of polysubstance use, worsening economic precarity, and stark disparities in access to mental health and substance use treatment programs, the investigators noted.

“The findings reinforce the notion that we need to invest in services that can address these issues, and ultimately, we need much more comprehensive access to low-barrier mental health care and substance use treatment in the US,” study investigator Joseph Friedman, PhD, of the David Geffen School of Medicine at UCLA, Los Angeles, California, said in a press release. 

“We need to specifically make sure those treatments, services, and programs are implemented in a way that is accessible for communities of color and will actively work to address inequality,” Dr. Friedman added.

Potential study limitations include possible misclassification of race and ethnicity, which could underestimate observed inequalities, and the ecological design that precludes measuring causality of underlying factors, the researchers noted.

The investigators reported no relevant financial conflicts of interest.

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