Eve Bender

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.

Attention-deficit/hyperactivity disorder (ADHD) in adults is independently associated with an increased risk for dementia with Lewy bodies (DLB), dementia, and nonamnestic mild cognitive impairment (naMCI), results of a new study showed.

“Determining whether there is an association between ADHD and subsequent conversion to a specific type of dementia is important. This information could generate opportunities for prevention and early treatment, as well as initiate research into the pathophysiological processes involved in understanding the process of cognitive decline,” the researchers, led by Ángel Golimstok, MD, of Hospital Italiano, Buenos Aires, Argentina, wrote.

The findings were published online in The American Journal of Geriatric Psychiatry.
 

Seeking Confirmation

The researchers first identified a link between DLB and ADHD in 2011. Since then, there have been eight additional studies from other groups also showing a possible link between ADHD and DLB.

To confirm the relationship, the researchers recruited 270 individuals between the ages of 45 and 70 years between 2007 and 2012. Of these, 161 had ADHD, and 109 were healthy controls.

Participants with ADHD met the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, text revision criteria for a diagnosis in the past and had a chronic course of ADHD symptoms from adolescence to adulthood that caused mild to severe impairment.

Investigators excluded participants who had been taking ADHD medications for 6 months or more, those with MCI at study initiation, and those with other comorbid psychiatric disorders.

At baseline, all participants received a physical exam, an MRI, and a neuropsychological exam to test for any type of dementia-related impairment.

Study participants were followed for an average of 12 years. A total of 27 individuals with ADHD developed dementia versus four patients in the control group (17% vs 4%, respectively), and 19 of those also had DLB (P = .002 for both).

Of those who developed any type of dementia, 87% were from the ADHD group. The most frequent type of dementia was DLB, 95% of which occurred in the ADHD group. Overall, DLB represented 70% of the dementia cases among participants with ADHD.

A total of 108 participants with ADHD were subsequently diagnosed with naMCI versus 19 healthy controls (67% vs 17%; P < .001).

“Although this pattern of deficits is reasonably expected in early DLB, these results should be interpreted with caution because they may be related to the overlap of symptoms and cognitive deficits between ADHD and naMCI, which may lead to an overestimation of the degenerative phenomenon. Thus, our cases of naMCI could correspond to the natural aging of ADHD patients and not to pathological deterioration,” the authors wrote.

The researchers pointed out that the sample of patients with ADHD originally sought evaluation because of a cognitive complaint or their own motivation. Therefore, the study results are not generalizable to all patients with ADHD. Another limitation was the relatively small number of patients included in the sample.

There was no reported source of funding, and there were no relevant disclosures reported.

A version of this article appeared on Medscape.com.

Attention-deficit/hyperactivity disorder (ADHD) in adults is independently associated with an increased risk for dementia with Lewy bodies (DLB), dementia, and nonamnestic mild cognitive impairment (naMCI), results of a new study showed.

“Determining whether there is an association between ADHD and subsequent conversion to a specific type of dementia is important. This information could generate opportunities for prevention and early treatment, as well as initiate research into the pathophysiological processes involved in understanding the process of cognitive decline,” the researchers, led by Ángel Golimstok, MD, of Hospital Italiano, Buenos Aires, Argentina, wrote.

The findings were published online in The American Journal of Geriatric Psychiatry.
 

Seeking Confirmation

The researchers first identified a link between DLB and ADHD in 2011. Since then, there have been eight additional studies from other groups also showing a possible link between ADHD and DLB.

To confirm the relationship, the researchers recruited 270 individuals between the ages of 45 and 70 years between 2007 and 2012. Of these, 161 had ADHD, and 109 were healthy controls.

Participants with ADHD met the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, text revision criteria for a diagnosis in the past and had a chronic course of ADHD symptoms from adolescence to adulthood that caused mild to severe impairment.

Investigators excluded participants who had been taking ADHD medications for 6 months or more, those with MCI at study initiation, and those with other comorbid psychiatric disorders.

At baseline, all participants received a physical exam, an MRI, and a neuropsychological exam to test for any type of dementia-related impairment.

Study participants were followed for an average of 12 years. A total of 27 individuals with ADHD developed dementia versus four patients in the control group (17% vs 4%, respectively), and 19 of those also had DLB (P = .002 for both).

Of those who developed any type of dementia, 87% were from the ADHD group. The most frequent type of dementia was DLB, 95% of which occurred in the ADHD group. Overall, DLB represented 70% of the dementia cases among participants with ADHD.

A total of 108 participants with ADHD were subsequently diagnosed with naMCI versus 19 healthy controls (67% vs 17%; P < .001).

“Although this pattern of deficits is reasonably expected in early DLB, these results should be interpreted with caution because they may be related to the overlap of symptoms and cognitive deficits between ADHD and naMCI, which may lead to an overestimation of the degenerative phenomenon. Thus, our cases of naMCI could correspond to the natural aging of ADHD patients and not to pathological deterioration,” the authors wrote.

The researchers pointed out that the sample of patients with ADHD originally sought evaluation because of a cognitive complaint or their own motivation. Therefore, the study results are not generalizable to all patients with ADHD. Another limitation was the relatively small number of patients included in the sample.

There was no reported source of funding, and there were no relevant disclosures reported.

A version of this article appeared on Medscape.com.

Attention-deficit/hyperactivity disorder (ADHD) in adults is independently associated with an increased risk for dementia with Lewy bodies (DLB), dementia, and nonamnestic mild cognitive impairment (naMCI), results of a new study showed.

“Determining whether there is an association between ADHD and subsequent conversion to a specific type of dementia is important. This information could generate opportunities for prevention and early treatment, as well as initiate research into the pathophysiological processes involved in understanding the process of cognitive decline,” the researchers, led by Ángel Golimstok, MD, of Hospital Italiano, Buenos Aires, Argentina, wrote.

The findings were published online in The American Journal of Geriatric Psychiatry.
 

Seeking Confirmation

The researchers first identified a link between DLB and ADHD in 2011. Since then, there have been eight additional studies from other groups also showing a possible link between ADHD and DLB.

To confirm the relationship, the researchers recruited 270 individuals between the ages of 45 and 70 years between 2007 and 2012. Of these, 161 had ADHD, and 109 were healthy controls.

Participants with ADHD met the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, text revision criteria for a diagnosis in the past and had a chronic course of ADHD symptoms from adolescence to adulthood that caused mild to severe impairment.

Investigators excluded participants who had been taking ADHD medications for 6 months or more, those with MCI at study initiation, and those with other comorbid psychiatric disorders.

At baseline, all participants received a physical exam, an MRI, and a neuropsychological exam to test for any type of dementia-related impairment.

Study participants were followed for an average of 12 years. A total of 27 individuals with ADHD developed dementia versus four patients in the control group (17% vs 4%, respectively), and 19 of those also had DLB (P = .002 for both).

Of those who developed any type of dementia, 87% were from the ADHD group. The most frequent type of dementia was DLB, 95% of which occurred in the ADHD group. Overall, DLB represented 70% of the dementia cases among participants with ADHD.

A total of 108 participants with ADHD were subsequently diagnosed with naMCI versus 19 healthy controls (67% vs 17%; P < .001).

“Although this pattern of deficits is reasonably expected in early DLB, these results should be interpreted with caution because they may be related to the overlap of symptoms and cognitive deficits between ADHD and naMCI, which may lead to an overestimation of the degenerative phenomenon. Thus, our cases of naMCI could correspond to the natural aging of ADHD patients and not to pathological deterioration,” the authors wrote.

The researchers pointed out that the sample of patients with ADHD originally sought evaluation because of a cognitive complaint or their own motivation. Therefore, the study results are not generalizable to all patients with ADHD. Another limitation was the relatively small number of patients included in the sample.

There was no reported source of funding, and there were no relevant disclosures reported.

A version of this article appeared on Medscape.com.

Proton pump inhibitors (PPIs), which are used to control acid reflux, are associated with an increased risk for migraine and other severe headache types, new research showed. 

Using data from the National Health and Nutrition Examination Survey (NHANES), investigators conducted a cross-sectional analysis and found all types of acid-suppression therapy were associated with an increased risk for severe headache including migraine but that PPIs conferred the greatest risk.

“It’s important to note that many people do need acid-reducing medications to manage acid reflux or other conditions, and people with migraine or severe headache who are taking these drugs or supplements should talk with their doctors about whether they should continue,” lead author Margaret Slavin, PhD, of the University of Maryland in College Park, said in a press release. 

The findings were published online  in Neurology Clinical Practice. 
 

New Look at Old Data

Previous research has shown that headache is listed among the most common adverse reactions in adults taking PPIs and histamine receptor agonists (H2RAs), which include cimetidine, famotidine, and nizatidine.

Other large studies of health databases have shown increased headache risk within a week of PPI exposure.

To compare the risk from PPIs versus H2RAs and other generics, researchers analyzed data from the NHANES for those who used PPIs, H2RAs, and generic antacids to learn more about the potential link between acid-suppression therapy and headache.

They used survey data from 1999 to 2004, the only years the NHANES included a question about migraine and other headache during the past 3 months. 

Investigators analyzed data for 11,800 participants aged 20 years or older who used prescription drugs, over-the-counter medications, and nutritional supplements during the past month. 

Participants who used acid-suppressing medications had an increased risk for migraine or severe headache versus those who did not use these agents. Investigators found PPIs were tied to a 70% increased risk, while H2RAs and antacids were associated with 40% and 30% higher risks, respectively. Use of any type of acid-suppression therapy was tied to a 47% increased risk for severe headache.
 

Magnesium a Risk Factor?

While magnesium supplements are sometimes prescribed as a “natural” headache prevention therapy to prevent migraine and other headache types, the investigators noted they were surprised to find individuals taking H2RAs who met the dietary reference intake for magnesium had a nearly threefold increased risk for migraine or severe headache (odds ratio, 2.80; 95% CI, 1.02-1.45; P = .025).

However, there was no association between magnesium and the other acid-reducing medications. 

The study’s limitations included the use of a single question to identify migraine or severe headache, which may have resulted in some misclassification of the outcome. The authors also pointed out that dietary and drug-intake data may be subject to recall bias. 

“These results suggest that there is a need for more intentionally designed prospective work to inform the extent to which associations between migraine and acid-suppression therapy are merely detecting comorbidities or to what extent migraine is an adverse event associated with the medications,” the authors wrote. 

There was no targeted funding. Disclosures are noted in the original article.

A version of this article appeared on Medscape.com.

Proton pump inhibitors (PPIs), which are used to control acid reflux, are associated with an increased risk for migraine and other severe headache types, new research showed. 

Using data from the National Health and Nutrition Examination Survey (NHANES), investigators conducted a cross-sectional analysis and found all types of acid-suppression therapy were associated with an increased risk for severe headache including migraine but that PPIs conferred the greatest risk.

“It’s important to note that many people do need acid-reducing medications to manage acid reflux or other conditions, and people with migraine or severe headache who are taking these drugs or supplements should talk with their doctors about whether they should continue,” lead author Margaret Slavin, PhD, of the University of Maryland in College Park, said in a press release. 

The findings were published online  in Neurology Clinical Practice. 
 

New Look at Old Data

Previous research has shown that headache is listed among the most common adverse reactions in adults taking PPIs and histamine receptor agonists (H2RAs), which include cimetidine, famotidine, and nizatidine.

Other large studies of health databases have shown increased headache risk within a week of PPI exposure.

To compare the risk from PPIs versus H2RAs and other generics, researchers analyzed data from the NHANES for those who used PPIs, H2RAs, and generic antacids to learn more about the potential link between acid-suppression therapy and headache.

They used survey data from 1999 to 2004, the only years the NHANES included a question about migraine and other headache during the past 3 months. 

Investigators analyzed data for 11,800 participants aged 20 years or older who used prescription drugs, over-the-counter medications, and nutritional supplements during the past month. 

Participants who used acid-suppressing medications had an increased risk for migraine or severe headache versus those who did not use these agents. Investigators found PPIs were tied to a 70% increased risk, while H2RAs and antacids were associated with 40% and 30% higher risks, respectively. Use of any type of acid-suppression therapy was tied to a 47% increased risk for severe headache.
 

Magnesium a Risk Factor?

While magnesium supplements are sometimes prescribed as a “natural” headache prevention therapy to prevent migraine and other headache types, the investigators noted they were surprised to find individuals taking H2RAs who met the dietary reference intake for magnesium had a nearly threefold increased risk for migraine or severe headache (odds ratio, 2.80; 95% CI, 1.02-1.45; P = .025).

However, there was no association between magnesium and the other acid-reducing medications. 

The study’s limitations included the use of a single question to identify migraine or severe headache, which may have resulted in some misclassification of the outcome. The authors also pointed out that dietary and drug-intake data may be subject to recall bias. 

“These results suggest that there is a need for more intentionally designed prospective work to inform the extent to which associations between migraine and acid-suppression therapy are merely detecting comorbidities or to what extent migraine is an adverse event associated with the medications,” the authors wrote. 

There was no targeted funding. Disclosures are noted in the original article.

A version of this article appeared on Medscape.com.

Proton pump inhibitors (PPIs), which are used to control acid reflux, are associated with an increased risk for migraine and other severe headache types, new research showed. 

Using data from the National Health and Nutrition Examination Survey (NHANES), investigators conducted a cross-sectional analysis and found all types of acid-suppression therapy were associated with an increased risk for severe headache including migraine but that PPIs conferred the greatest risk.

“It’s important to note that many people do need acid-reducing medications to manage acid reflux or other conditions, and people with migraine or severe headache who are taking these drugs or supplements should talk with their doctors about whether they should continue,” lead author Margaret Slavin, PhD, of the University of Maryland in College Park, said in a press release. 

The findings were published online  in Neurology Clinical Practice. 
 

New Look at Old Data

Previous research has shown that headache is listed among the most common adverse reactions in adults taking PPIs and histamine receptor agonists (H2RAs), which include cimetidine, famotidine, and nizatidine.

Other large studies of health databases have shown increased headache risk within a week of PPI exposure.

To compare the risk from PPIs versus H2RAs and other generics, researchers analyzed data from the NHANES for those who used PPIs, H2RAs, and generic antacids to learn more about the potential link between acid-suppression therapy and headache.

They used survey data from 1999 to 2004, the only years the NHANES included a question about migraine and other headache during the past 3 months. 

Investigators analyzed data for 11,800 participants aged 20 years or older who used prescription drugs, over-the-counter medications, and nutritional supplements during the past month. 

Participants who used acid-suppressing medications had an increased risk for migraine or severe headache versus those who did not use these agents. Investigators found PPIs were tied to a 70% increased risk, while H2RAs and antacids were associated with 40% and 30% higher risks, respectively. Use of any type of acid-suppression therapy was tied to a 47% increased risk for severe headache.
 

Magnesium a Risk Factor?

While magnesium supplements are sometimes prescribed as a “natural” headache prevention therapy to prevent migraine and other headache types, the investigators noted they were surprised to find individuals taking H2RAs who met the dietary reference intake for magnesium had a nearly threefold increased risk for migraine or severe headache (odds ratio, 2.80; 95% CI, 1.02-1.45; P = .025).

However, there was no association between magnesium and the other acid-reducing medications. 

The study’s limitations included the use of a single question to identify migraine or severe headache, which may have resulted in some misclassification of the outcome. The authors also pointed out that dietary and drug-intake data may be subject to recall bias. 

“These results suggest that there is a need for more intentionally designed prospective work to inform the extent to which associations between migraine and acid-suppression therapy are merely detecting comorbidities or to what extent migraine is an adverse event associated with the medications,” the authors wrote. 

There was no targeted funding. Disclosures are noted in the original article.

A version of this article appeared on Medscape.com.

A new genetic variant in individuals who are APOE4 carriers is linked to a 70% reduction in the risk for Alzheimer’s disease, new research suggests.

The variant occurs on the fibronectin 1 (FN1) gene, which expresses fibronectin, an adhesive glycoprotein that lines the blood vessels at the blood-brain barrier and controls substances that move in and out of the brain.

While fibronectin is normally present in the blood-brain barrier in small amounts, individuals with Alzheimer’s disease tend to have it in excess. Normally, patients with Alzheimer’s disease have amyloid deposits that collect in the brain, but those with the FN1 variant appear to have the ability to amyloid from the brain before symptoms begin.

The researchers estimate that 1%-3% of APOE4 carriers in the United States — roughly 200,000-620,000 people — may have the protective mutation.

“Alzheimer’s disease may get started with amyloid deposits in the brain, but the disease manifestations are the result of changes that happen after the deposits appear,” Caghan Kizil, PhD, of Columbia University Vagelos College of Physicians and Surgeons in New York City, and a co-leader of the study, said in a press release.

The findings were published online in Acta Neuropathologica,
 

Combing Genetic Data

To find potentially protective Alzheimer’s disease variants, the investigators sequenced the genomes of more than 3500 APOE4 carriers older than 70 years with and without Alzheimer’s disease from various ethnic backgrounds.

They identified two variants on the FN1 gene, rs116558455 and rs140926439, present in healthy APOE4 carriers, that protected the APOE4 carriers against Alzheimer’s disease.

After Dr. Kizil and colleagues published their findings in a preprint, another research group that included investigators from Stanford and Washington Universities replicated the Columbia results in an independent sample of more than 7000 APOE4 carriers aged 60 years who were of European descent and identified the same FN1 variant.

The two research groups then combined their data on 11,000 participants and found that the FN1 variant rs140926439 was associated with a significantly reduced risk for Alzheimer’s disease in APOE4 carriers (odds ratio, 0.29; P = .014). A secondary analysis showed that the variant delayed Alzheimer’s disease symptom onset by 3.4 years (P = .025).

The investigators hope to use these findings to develop therapies to protect APOE4 carriers against Alzheimer’s disease.

“Anything that reduces excess fibronectin should provide some protection, and a drug that does this could be a significant step forward in the fight against this debilitating condition,” Dr. Kizil said.

Study limitations included a lack of longitudinal data on the relationship between amyloid concentration and fibronectin and the fact that investigators conducted the studies in clinically assessed individuals. Given the rare occurrence of the FN1 mutation, researchers do not have neuropathological assessments of study participants with the variant.

The study was funded by the National Institute on Aging, the Schaefer Research Scholars Program Award, Taub Institute Grants for Emerging Research, the National Institute of General Medical Sciences, and the Thompson Family Foundation Program for Accelerated Medicine Exploration in Alzheimer’s Disease and Related Disorders of the Nervous System. There were no disclosures reported.

A version of this article appeared on Medscape.com.

A new genetic variant in individuals who are APOE4 carriers is linked to a 70% reduction in the risk for Alzheimer’s disease, new research suggests.

The variant occurs on the fibronectin 1 (FN1) gene, which expresses fibronectin, an adhesive glycoprotein that lines the blood vessels at the blood-brain barrier and controls substances that move in and out of the brain.

While fibronectin is normally present in the blood-brain barrier in small amounts, individuals with Alzheimer’s disease tend to have it in excess. Normally, patients with Alzheimer’s disease have amyloid deposits that collect in the brain, but those with the FN1 variant appear to have the ability to amyloid from the brain before symptoms begin.

The researchers estimate that 1%-3% of APOE4 carriers in the United States — roughly 200,000-620,000 people — may have the protective mutation.

“Alzheimer’s disease may get started with amyloid deposits in the brain, but the disease manifestations are the result of changes that happen after the deposits appear,” Caghan Kizil, PhD, of Columbia University Vagelos College of Physicians and Surgeons in New York City, and a co-leader of the study, said in a press release.

The findings were published online in Acta Neuropathologica,
 

Combing Genetic Data

To find potentially protective Alzheimer’s disease variants, the investigators sequenced the genomes of more than 3500 APOE4 carriers older than 70 years with and without Alzheimer’s disease from various ethnic backgrounds.

They identified two variants on the FN1 gene, rs116558455 and rs140926439, present in healthy APOE4 carriers, that protected the APOE4 carriers against Alzheimer’s disease.

After Dr. Kizil and colleagues published their findings in a preprint, another research group that included investigators from Stanford and Washington Universities replicated the Columbia results in an independent sample of more than 7000 APOE4 carriers aged 60 years who were of European descent and identified the same FN1 variant.

The two research groups then combined their data on 11,000 participants and found that the FN1 variant rs140926439 was associated with a significantly reduced risk for Alzheimer’s disease in APOE4 carriers (odds ratio, 0.29; P = .014). A secondary analysis showed that the variant delayed Alzheimer’s disease symptom onset by 3.4 years (P = .025).

The investigators hope to use these findings to develop therapies to protect APOE4 carriers against Alzheimer’s disease.

“Anything that reduces excess fibronectin should provide some protection, and a drug that does this could be a significant step forward in the fight against this debilitating condition,” Dr. Kizil said.

Study limitations included a lack of longitudinal data on the relationship between amyloid concentration and fibronectin and the fact that investigators conducted the studies in clinically assessed individuals. Given the rare occurrence of the FN1 mutation, researchers do not have neuropathological assessments of study participants with the variant.

The study was funded by the National Institute on Aging, the Schaefer Research Scholars Program Award, Taub Institute Grants for Emerging Research, the National Institute of General Medical Sciences, and the Thompson Family Foundation Program for Accelerated Medicine Exploration in Alzheimer’s Disease and Related Disorders of the Nervous System. There were no disclosures reported.

A version of this article appeared on Medscape.com.

A new genetic variant in individuals who are APOE4 carriers is linked to a 70% reduction in the risk for Alzheimer’s disease, new research suggests.

The variant occurs on the fibronectin 1 (FN1) gene, which expresses fibronectin, an adhesive glycoprotein that lines the blood vessels at the blood-brain barrier and controls substances that move in and out of the brain.

While fibronectin is normally present in the blood-brain barrier in small amounts, individuals with Alzheimer’s disease tend to have it in excess. Normally, patients with Alzheimer’s disease have amyloid deposits that collect in the brain, but those with the FN1 variant appear to have the ability to amyloid from the brain before symptoms begin.

The researchers estimate that 1%-3% of APOE4 carriers in the United States — roughly 200,000-620,000 people — may have the protective mutation.

“Alzheimer’s disease may get started with amyloid deposits in the brain, but the disease manifestations are the result of changes that happen after the deposits appear,” Caghan Kizil, PhD, of Columbia University Vagelos College of Physicians and Surgeons in New York City, and a co-leader of the study, said in a press release.

The findings were published online in Acta Neuropathologica,
 

Combing Genetic Data

To find potentially protective Alzheimer’s disease variants, the investigators sequenced the genomes of more than 3500 APOE4 carriers older than 70 years with and without Alzheimer’s disease from various ethnic backgrounds.

They identified two variants on the FN1 gene, rs116558455 and rs140926439, present in healthy APOE4 carriers, that protected the APOE4 carriers against Alzheimer’s disease.

After Dr. Kizil and colleagues published their findings in a preprint, another research group that included investigators from Stanford and Washington Universities replicated the Columbia results in an independent sample of more than 7000 APOE4 carriers aged 60 years who were of European descent and identified the same FN1 variant.

The two research groups then combined their data on 11,000 participants and found that the FN1 variant rs140926439 was associated with a significantly reduced risk for Alzheimer’s disease in APOE4 carriers (odds ratio, 0.29; P = .014). A secondary analysis showed that the variant delayed Alzheimer’s disease symptom onset by 3.4 years (P = .025).

The investigators hope to use these findings to develop therapies to protect APOE4 carriers against Alzheimer’s disease.

“Anything that reduces excess fibronectin should provide some protection, and a drug that does this could be a significant step forward in the fight against this debilitating condition,” Dr. Kizil said.

Study limitations included a lack of longitudinal data on the relationship between amyloid concentration and fibronectin and the fact that investigators conducted the studies in clinically assessed individuals. Given the rare occurrence of the FN1 mutation, researchers do not have neuropathological assessments of study participants with the variant.

The study was funded by the National Institute on Aging, the Schaefer Research Scholars Program Award, Taub Institute Grants for Emerging Research, the National Institute of General Medical Sciences, and the Thompson Family Foundation Program for Accelerated Medicine Exploration in Alzheimer’s Disease and Related Disorders of the Nervous System. There were no disclosures reported.

A version of this article appeared on Medscape.com.

The ketogenic diet shows promise in reducing the symptoms of bipolar disorder and schizophrenia and reversing metabolic syndrome, results of a new pilot study show. 

Participants who adhered to the high-fat, low-carb diet experienced a 30% reduction in psychiatric symptoms and an average 10% reduction in weight. 

“We’re seeing huge changes,” first author Shebani Sethi, MD, of Stanford University in Stanford, California said in a press release. “Even if you’re on antipsychotic drugs, we can still reverse the obesity, the metabolic syndrome, and the insulin resistance. I think that’s very encouraging for patients.”

The findings were published online in Psychiatric Research. 
 

Neuroprotective Effect? 

Recent research supports the hypothesis that psychiatric illness may stem, at least in part, from deficits in brain metabolism and that a keto diet may be neuroprotective by reducing inflammation and oxidative stress. 

The pilot study included 21 participants with schizophrenia (n = 5) or bipolar disorder (n = 16) who were aged 18-75 years. All were currently taking psychotropic medications. Participants were overweight (body mass index [BMI] ≥ 25) and had gained more than 5% of their body mass while taking psychotropic medication, or they had at least one metabolic abnormality, such as insulin resistance or dyslipidemia. 

At baseline, participants received a physical and psychiatric evaluation and 1 hour of instruction on how to implement the keto diet, which included 10% carbohydrate, 30% protein, and 60% fat. 

Investigators monitored blood ketone levels at least once a week and defined participants as keto-adherent if their levels were 0.5-5 mM for 80%-100% of the times they were measured.

Health coaches checked in with participants for about 5-10 minutes each week to answer diet-related questions.

Psychiatric assessments, which included mood rating and global functioning scales, were completed at baseline, 2 months, and at the end of the 4-month study. 

The research team tracked participants’ adherence to the diet by weekly measurement of blood ketone levels. 

By the end of the trial, 14 patients had been fully adherent with the diet, six had been semi-adherent, and only one had been nonadherent. Higher ketone levels, suggesting greater adherence, correlated with better metabolic health.

As measured by the Clinical Global Impression-Schizophrenia and Clinical Global Impression for Bipolar Disorder–Overall Severity, participants experienced a 31% reduction in symptom severity (P < .001). Overall, 43% (P < .02) of participants achieved recovery as defined by the Clinical Mood Monitoring Form criteria: 50% of the adherent group and 33% of those who were semi-adherent.
 

Metabolic Benefits

Initially, 29% of participants had metabolic syndrome and more than 85% had co-occurring medical conditions such as obesity, hyperlipidemia, or prediabetes. By the end of the study, none met criteria for metabolic syndrome.

On average, participants experienced a 10% reduction in weight and BMI. Waist circumference was reduced by 11%, fat mass index dropped by 17%, and systolic blood pressure decreased by 6%. In addition, metabolic markers including visceral fat, inflammation, A1c, and insulin resistance also improved. All outcomes were significant at P < .001 except for systolic blood pressure, at P < .005.

There was also a 20% reduction in triglycerides and a 21% increase in low-density lipoprotein cholesterol (both at P < .02). 

The study’s limitations include its small sample size, the lack of control arm, and short duration.

“Mental health and physical health are interconnected and addressing metabolic issues can complement psychiatric treatment to enhance overall well-being. Understanding the

mechanisms and potential synergies between psychiatric treatment and metabolic improvements can also inform the development of more effective interventions,” the researchers wrote. 

The study was funded by the Baszucki Group, Kuen Lau Fund, and the Obesity Treatment Foundation. The authors declare no competing interests.

A version of this article appeared on Medscape.com.

The ketogenic diet shows promise in reducing the symptoms of bipolar disorder and schizophrenia and reversing metabolic syndrome, results of a new pilot study show. 

Participants who adhered to the high-fat, low-carb diet experienced a 30% reduction in psychiatric symptoms and an average 10% reduction in weight. 

“We’re seeing huge changes,” first author Shebani Sethi, MD, of Stanford University in Stanford, California said in a press release. “Even if you’re on antipsychotic drugs, we can still reverse the obesity, the metabolic syndrome, and the insulin resistance. I think that’s very encouraging for patients.”

The findings were published online in Psychiatric Research. 
 

Neuroprotective Effect? 

Recent research supports the hypothesis that psychiatric illness may stem, at least in part, from deficits in brain metabolism and that a keto diet may be neuroprotective by reducing inflammation and oxidative stress. 

The pilot study included 21 participants with schizophrenia (n = 5) or bipolar disorder (n = 16) who were aged 18-75 years. All were currently taking psychotropic medications. Participants were overweight (body mass index [BMI] ≥ 25) and had gained more than 5% of their body mass while taking psychotropic medication, or they had at least one metabolic abnormality, such as insulin resistance or dyslipidemia. 

At baseline, participants received a physical and psychiatric evaluation and 1 hour of instruction on how to implement the keto diet, which included 10% carbohydrate, 30% protein, and 60% fat. 

Investigators monitored blood ketone levels at least once a week and defined participants as keto-adherent if their levels were 0.5-5 mM for 80%-100% of the times they were measured.

Health coaches checked in with participants for about 5-10 minutes each week to answer diet-related questions.

Psychiatric assessments, which included mood rating and global functioning scales, were completed at baseline, 2 months, and at the end of the 4-month study. 

The research team tracked participants’ adherence to the diet by weekly measurement of blood ketone levels. 

By the end of the trial, 14 patients had been fully adherent with the diet, six had been semi-adherent, and only one had been nonadherent. Higher ketone levels, suggesting greater adherence, correlated with better metabolic health.

As measured by the Clinical Global Impression-Schizophrenia and Clinical Global Impression for Bipolar Disorder–Overall Severity, participants experienced a 31% reduction in symptom severity (P < .001). Overall, 43% (P < .02) of participants achieved recovery as defined by the Clinical Mood Monitoring Form criteria: 50% of the adherent group and 33% of those who were semi-adherent.
 

Metabolic Benefits

Initially, 29% of participants had metabolic syndrome and more than 85% had co-occurring medical conditions such as obesity, hyperlipidemia, or prediabetes. By the end of the study, none met criteria for metabolic syndrome.

On average, participants experienced a 10% reduction in weight and BMI. Waist circumference was reduced by 11%, fat mass index dropped by 17%, and systolic blood pressure decreased by 6%. In addition, metabolic markers including visceral fat, inflammation, A1c, and insulin resistance also improved. All outcomes were significant at P < .001 except for systolic blood pressure, at P < .005.

There was also a 20% reduction in triglycerides and a 21% increase in low-density lipoprotein cholesterol (both at P < .02). 

The study’s limitations include its small sample size, the lack of control arm, and short duration.

“Mental health and physical health are interconnected and addressing metabolic issues can complement psychiatric treatment to enhance overall well-being. Understanding the

mechanisms and potential synergies between psychiatric treatment and metabolic improvements can also inform the development of more effective interventions,” the researchers wrote. 

The study was funded by the Baszucki Group, Kuen Lau Fund, and the Obesity Treatment Foundation. The authors declare no competing interests.

A version of this article appeared on Medscape.com.

The ketogenic diet shows promise in reducing the symptoms of bipolar disorder and schizophrenia and reversing metabolic syndrome, results of a new pilot study show. 

Participants who adhered to the high-fat, low-carb diet experienced a 30% reduction in psychiatric symptoms and an average 10% reduction in weight. 

“We’re seeing huge changes,” first author Shebani Sethi, MD, of Stanford University in Stanford, California said in a press release. “Even if you’re on antipsychotic drugs, we can still reverse the obesity, the metabolic syndrome, and the insulin resistance. I think that’s very encouraging for patients.”

The findings were published online in Psychiatric Research. 
 

Neuroprotective Effect? 

Recent research supports the hypothesis that psychiatric illness may stem, at least in part, from deficits in brain metabolism and that a keto diet may be neuroprotective by reducing inflammation and oxidative stress. 

The pilot study included 21 participants with schizophrenia (n = 5) or bipolar disorder (n = 16) who were aged 18-75 years. All were currently taking psychotropic medications. Participants were overweight (body mass index [BMI] ≥ 25) and had gained more than 5% of their body mass while taking psychotropic medication, or they had at least one metabolic abnormality, such as insulin resistance or dyslipidemia. 

At baseline, participants received a physical and psychiatric evaluation and 1 hour of instruction on how to implement the keto diet, which included 10% carbohydrate, 30% protein, and 60% fat. 

Investigators monitored blood ketone levels at least once a week and defined participants as keto-adherent if their levels were 0.5-5 mM for 80%-100% of the times they were measured.

Health coaches checked in with participants for about 5-10 minutes each week to answer diet-related questions.

Psychiatric assessments, which included mood rating and global functioning scales, were completed at baseline, 2 months, and at the end of the 4-month study. 

The research team tracked participants’ adherence to the diet by weekly measurement of blood ketone levels. 

By the end of the trial, 14 patients had been fully adherent with the diet, six had been semi-adherent, and only one had been nonadherent. Higher ketone levels, suggesting greater adherence, correlated with better metabolic health.

As measured by the Clinical Global Impression-Schizophrenia and Clinical Global Impression for Bipolar Disorder–Overall Severity, participants experienced a 31% reduction in symptom severity (P < .001). Overall, 43% (P < .02) of participants achieved recovery as defined by the Clinical Mood Monitoring Form criteria: 50% of the adherent group and 33% of those who were semi-adherent.
 

Metabolic Benefits

Initially, 29% of participants had metabolic syndrome and more than 85% had co-occurring medical conditions such as obesity, hyperlipidemia, or prediabetes. By the end of the study, none met criteria for metabolic syndrome.

On average, participants experienced a 10% reduction in weight and BMI. Waist circumference was reduced by 11%, fat mass index dropped by 17%, and systolic blood pressure decreased by 6%. In addition, metabolic markers including visceral fat, inflammation, A1c, and insulin resistance also improved. All outcomes were significant at P < .001 except for systolic blood pressure, at P < .005.

There was also a 20% reduction in triglycerides and a 21% increase in low-density lipoprotein cholesterol (both at P < .02). 

The study’s limitations include its small sample size, the lack of control arm, and short duration.

“Mental health and physical health are interconnected and addressing metabolic issues can complement psychiatric treatment to enhance overall well-being. Understanding the

mechanisms and potential synergies between psychiatric treatment and metabolic improvements can also inform the development of more effective interventions,” the researchers wrote. 

The study was funded by the Baszucki Group, Kuen Lau Fund, and the Obesity Treatment Foundation. The authors declare no competing interests.

A version of this article appeared on Medscape.com.