Clinical Psychiatry News

TOPLINE:

The Strong African American Families (SAAF) prevention program reduces depressive symptoms related to racial discrimination in Black adolescents, results of a post hoc analysis of a randomized controlled trial show.

METHODOLOGY:

• SAAF is a 7-week family skills training program delivered at local community centers that targets effective parenting behavior, adolescent self-regulation, and Black pride.
• In the original trial, 472 Black children aged 11-12 years were randomly allocated to SAAF or no treatment control.
• The post hoc analysis investigated changes in adolescent-reported depressive symptoms from age 13 to 14 years using the 20-item Center for Epidemiologic Studies Depression Scale for Children.

TAKEAWAY:

• Exposure to racial discrimination at age 13 years correlated with increased depressive symptoms at age 14 years (P < .001).
• Participation in the SAAF program significantly attenuated the association of racial discrimination at age 13 with increases in depressive symptoms at age 14 (P = .01).
• Racial discrimination was significantly associated with increases in depressive symptoms in the control group (P < .001) but not in the SAAF group.
• This moderating effect was observed using intent-to-treat design; the investigators accounted for family socioeconomic disadvantage and youth gender.

IN PRACTICE:

The findings add to other evidence suggesting that “prevention programs targeting aspects of racial identity, racial socialization processes, and parenting behavior may, to some extent, mitigate the mental health effects associated with racial discrimination. These processes appear to increase positive coping in the aftermath of discrimination, and prevent adolescents internalization of toxic messages regarding racial inferiority,” the authors wrote.

SOURCE:

The study, with first author Steven M. Kogan, PhD, University of Georgia in Athens, was published online in JAMA Network Open with a commentary by Kevin M. Simon, MD, MPH, with Boston Children’s Hospital.

LIMITATIONS:

This was a post hoc analysis of trial data. The sample consisted of Black adolescents from rural areas of Georgia, and the results may not be generalizable to Black adolescents from urban areas or adolescents from other racial groups. Because of the study’s focus on individual-level racial discrimination, the potential for SAAF to buffer the effects of structural and institutional forms of racism is unknown.

DISCLOSURES:

The study had no specific funding. The authors have disclosed no relevant conflicts of interest.

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

TOPLINE:

The Strong African American Families (SAAF) prevention program reduces depressive symptoms related to racial discrimination in Black adolescents, results of a post hoc analysis of a randomized controlled trial show.

METHODOLOGY:

• SAAF is a 7-week family skills training program delivered at local community centers that targets effective parenting behavior, adolescent self-regulation, and Black pride.
• In the original trial, 472 Black children aged 11-12 years were randomly allocated to SAAF or no treatment control.
• The post hoc analysis investigated changes in adolescent-reported depressive symptoms from age 13 to 14 years using the 20-item Center for Epidemiologic Studies Depression Scale for Children.

TAKEAWAY:

• Exposure to racial discrimination at age 13 years correlated with increased depressive symptoms at age 14 years (P < .001).
• Participation in the SAAF program significantly attenuated the association of racial discrimination at age 13 with increases in depressive symptoms at age 14 (P = .01).
• Racial discrimination was significantly associated with increases in depressive symptoms in the control group (P < .001) but not in the SAAF group.
• This moderating effect was observed using intent-to-treat design; the investigators accounted for family socioeconomic disadvantage and youth gender.

IN PRACTICE:

The findings add to other evidence suggesting that “prevention programs targeting aspects of racial identity, racial socialization processes, and parenting behavior may, to some extent, mitigate the mental health effects associated with racial discrimination. These processes appear to increase positive coping in the aftermath of discrimination, and prevent adolescents internalization of toxic messages regarding racial inferiority,” the authors wrote.

SOURCE:

The study, with first author Steven M. Kogan, PhD, University of Georgia in Athens, was published online in JAMA Network Open with a commentary by Kevin M. Simon, MD, MPH, with Boston Children’s Hospital.

LIMITATIONS:

This was a post hoc analysis of trial data. The sample consisted of Black adolescents from rural areas of Georgia, and the results may not be generalizable to Black adolescents from urban areas or adolescents from other racial groups. Because of the study’s focus on individual-level racial discrimination, the potential for SAAF to buffer the effects of structural and institutional forms of racism is unknown.

DISCLOSURES:

The study had no specific funding. The authors have disclosed no relevant conflicts of interest.

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

TOPLINE:

The Strong African American Families (SAAF) prevention program reduces depressive symptoms related to racial discrimination in Black adolescents, results of a post hoc analysis of a randomized controlled trial show.

METHODOLOGY:

• SAAF is a 7-week family skills training program delivered at local community centers that targets effective parenting behavior, adolescent self-regulation, and Black pride.
• In the original trial, 472 Black children aged 11-12 years were randomly allocated to SAAF or no treatment control.
• The post hoc analysis investigated changes in adolescent-reported depressive symptoms from age 13 to 14 years using the 20-item Center for Epidemiologic Studies Depression Scale for Children.

TAKEAWAY:

• Exposure to racial discrimination at age 13 years correlated with increased depressive symptoms at age 14 years (P < .001).
• Participation in the SAAF program significantly attenuated the association of racial discrimination at age 13 with increases in depressive symptoms at age 14 (P = .01).
• Racial discrimination was significantly associated with increases in depressive symptoms in the control group (P < .001) but not in the SAAF group.
• This moderating effect was observed using intent-to-treat design; the investigators accounted for family socioeconomic disadvantage and youth gender.

IN PRACTICE:

The findings add to other evidence suggesting that “prevention programs targeting aspects of racial identity, racial socialization processes, and parenting behavior may, to some extent, mitigate the mental health effects associated with racial discrimination. These processes appear to increase positive coping in the aftermath of discrimination, and prevent adolescents internalization of toxic messages regarding racial inferiority,” the authors wrote.

SOURCE:

The study, with first author Steven M. Kogan, PhD, University of Georgia in Athens, was published online in JAMA Network Open with a commentary by Kevin M. Simon, MD, MPH, with Boston Children’s Hospital.

LIMITATIONS:

This was a post hoc analysis of trial data. The sample consisted of Black adolescents from rural areas of Georgia, and the results may not be generalizable to Black adolescents from urban areas or adolescents from other racial groups. Because of the study’s focus on individual-level racial discrimination, the potential for SAAF to buffer the effects of structural and institutional forms of racism is unknown.

DISCLOSURES:

The study had no specific funding. The authors have disclosed no relevant conflicts of interest.

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

TOPLINE:

Among children with urine drug screens that are positive for cannabinoids, confirmatory testing based on liquid chromatography–mass spectrometry (LC-MS) may be negative despite detectable concentrations of a cannabis metabolite, according to a research letter published online in JAMA Pediatrics.

METHODOLOGY:

• After a laboratory changed its reporting threshold for the metabolite 11-nor-9-carboxy-Δ9-tetrahydrocannabinol (THC-COOH) from 5 ng/mL to 15 ng/mL in 2019 to match federal standards, researchers examined the rate of false positives for the initial urine drug screen and the false-negative rate with LC-MS.
• Their study focused on 976 cannabinoid-positive drug screens conducted at a pediatric hospital between Nov. 18, 2019, and May 31, 2021, that had confirmatory LC-MS to rule out false-positive results.
• Patients had a median age of 16 years.

TAKEAWAY:

• The false-positive rate was 10.1% based on the 15 ng/mL threshold compared with 2% based on the 5 ng/mL limit of quantification.
• About 81% of samples with negative LC-MS reports had detectable concentrations of THC-COOH.

IN PRACTICE:

“Confirming THC-COOH in children’s and adolescents’ urine may be relevant at concentrations less than 15 ng/mL, particularly if child protection is pertinent,” according to the study authors.

“Confirmatory testing should be reserved for select cases and must be interpreted with caution,” they added. “Laboratories should report down to the limit of quantification on request.”

SOURCE:

Christopher J. Watson, MD, emergency medicine physician, Maine Medical Center, Portland, is the study’s corresponding author.

LIMITATIONS:

The researchers lacked information about the clinical context in which patients underwent drug screening.

DISCLOSURES:

A coauthor disclosed royalties from UpToDate outside of the study.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Among children with urine drug screens that are positive for cannabinoids, confirmatory testing based on liquid chromatography–mass spectrometry (LC-MS) may be negative despite detectable concentrations of a cannabis metabolite, according to a research letter published online in JAMA Pediatrics.

METHODOLOGY:

• After a laboratory changed its reporting threshold for the metabolite 11-nor-9-carboxy-Δ9-tetrahydrocannabinol (THC-COOH) from 5 ng/mL to 15 ng/mL in 2019 to match federal standards, researchers examined the rate of false positives for the initial urine drug screen and the false-negative rate with LC-MS.
• Their study focused on 976 cannabinoid-positive drug screens conducted at a pediatric hospital between Nov. 18, 2019, and May 31, 2021, that had confirmatory LC-MS to rule out false-positive results.
• Patients had a median age of 16 years.

TAKEAWAY:

• The false-positive rate was 10.1% based on the 15 ng/mL threshold compared with 2% based on the 5 ng/mL limit of quantification.
• About 81% of samples with negative LC-MS reports had detectable concentrations of THC-COOH.

IN PRACTICE:

“Confirming THC-COOH in children’s and adolescents’ urine may be relevant at concentrations less than 15 ng/mL, particularly if child protection is pertinent,” according to the study authors.

“Confirmatory testing should be reserved for select cases and must be interpreted with caution,” they added. “Laboratories should report down to the limit of quantification on request.”

SOURCE:

Christopher J. Watson, MD, emergency medicine physician, Maine Medical Center, Portland, is the study’s corresponding author.

LIMITATIONS:

The researchers lacked information about the clinical context in which patients underwent drug screening.

DISCLOSURES:

A coauthor disclosed royalties from UpToDate outside of the study.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Among children with urine drug screens that are positive for cannabinoids, confirmatory testing based on liquid chromatography–mass spectrometry (LC-MS) may be negative despite detectable concentrations of a cannabis metabolite, according to a research letter published online in JAMA Pediatrics.

METHODOLOGY:

• After a laboratory changed its reporting threshold for the metabolite 11-nor-9-carboxy-Δ9-tetrahydrocannabinol (THC-COOH) from 5 ng/mL to 15 ng/mL in 2019 to match federal standards, researchers examined the rate of false positives for the initial urine drug screen and the false-negative rate with LC-MS.
• Their study focused on 976 cannabinoid-positive drug screens conducted at a pediatric hospital between Nov. 18, 2019, and May 31, 2021, that had confirmatory LC-MS to rule out false-positive results.
• Patients had a median age of 16 years.

TAKEAWAY:

• The false-positive rate was 10.1% based on the 15 ng/mL threshold compared with 2% based on the 5 ng/mL limit of quantification.
• About 81% of samples with negative LC-MS reports had detectable concentrations of THC-COOH.

IN PRACTICE:

“Confirming THC-COOH in children’s and adolescents’ urine may be relevant at concentrations less than 15 ng/mL, particularly if child protection is pertinent,” according to the study authors.

“Confirmatory testing should be reserved for select cases and must be interpreted with caution,” they added. “Laboratories should report down to the limit of quantification on request.”

SOURCE:

Christopher J. Watson, MD, emergency medicine physician, Maine Medical Center, Portland, is the study’s corresponding author.

LIMITATIONS:

The researchers lacked information about the clinical context in which patients underwent drug screening.

DISCLOSURES:

A coauthor disclosed royalties from UpToDate outside of the study.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Posttraumatic stress disorder (PTSD) symptoms are associated with poorer cardiovascular and neurocognitive health among midlife women, particularly those who are APOEε4 carriers, new research suggests.

METHODOLOGY:

• Researchers conducted a cross-sectional study of 274 women (mean age, 59 years) participating in the MsBrain study of menopause and brain health.
• As part of the study, the women completed the PTSD Checklist–Civilian Version and underwent physical and neuropsychological testing, as well as carotid artery ultrasonography and brain MRI.
• Outcomes of interest were associations of PTSD symptoms with carotid intima media thickness (IMT), brain white matter hyperintensity volume (WMHV), and cognition, assessed in linear regression models.
• Interactions by APOEε4 were assessed; covariates included age, race/ethnicity, education, and CVD risk factors.

TAKEAWAY:

• Higher PTSD symptoms were associated with greater carotid IMT (P = .03); associations of PTSD symptoms with neurocognitive outcomes varied significantly by APOEε4 status.
• Among APOEε4 carriers, PTSD symptoms were associated with greater whole-brain WMHV (P = .009), periventricular WMHV (P = .02), deep WMHV (P = .01), and frontal WMHV (P = .04) in multivariable models.
• APOEε4 carriers with PTSD symptoms also had poorer cognition, specifically attention and working memory (P = .02), semantic fluency (P = .01), perceptual speed (P = .002) and processing speed (P = .002), in multivariable models.

IN PRACTICE:

“This study sheds important insight on the implications of PTSD symptoms to women’s cardiovascular and neurocognitive health. Our findings indicate that the APOEε4 genotype may identify a group of women with PTSD symptoms at particular risk for poor neurocognitive health,” the authors wrote.

SOURCE:

The study, with first author Rebecca Thurston, PhD, of the department of psychiatry, University of Pittsburgh, was published online  in JAMA Network Open.

LIMITATIONS:

No diagnostic clinical interviews were conducted, and PTSD treatment was not assessed. All participants identified as cisgender, and most were non-Hispanic Black or White. The study was observational and cross-sectional, precluding assertions about directionality or causality.

DISCLOSURES:

The study was funded by the National Institutes of Health, the University of Pittsburgh Clinical and Translational Science Institute, and the University of Pittsburgh Small Molecule Biomarker Core. Dr. Thurston reported receiving personal fees from Astellas Pharma, Bayer, Hello Therapeutics, Vira Health, and Happify Health outside the submitted work.

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

TOPLINE:

Posttraumatic stress disorder (PTSD) symptoms are associated with poorer cardiovascular and neurocognitive health among midlife women, particularly those who are APOEε4 carriers, new research suggests.

METHODOLOGY:

• Researchers conducted a cross-sectional study of 274 women (mean age, 59 years) participating in the MsBrain study of menopause and brain health.
• As part of the study, the women completed the PTSD Checklist–Civilian Version and underwent physical and neuropsychological testing, as well as carotid artery ultrasonography and brain MRI.
• Outcomes of interest were associations of PTSD symptoms with carotid intima media thickness (IMT), brain white matter hyperintensity volume (WMHV), and cognition, assessed in linear regression models.
• Interactions by APOEε4 were assessed; covariates included age, race/ethnicity, education, and CVD risk factors.

TAKEAWAY:

• Higher PTSD symptoms were associated with greater carotid IMT (P = .03); associations of PTSD symptoms with neurocognitive outcomes varied significantly by APOEε4 status.
• Among APOEε4 carriers, PTSD symptoms were associated with greater whole-brain WMHV (P = .009), periventricular WMHV (P = .02), deep WMHV (P = .01), and frontal WMHV (P = .04) in multivariable models.
• APOEε4 carriers with PTSD symptoms also had poorer cognition, specifically attention and working memory (P = .02), semantic fluency (P = .01), perceptual speed (P = .002) and processing speed (P = .002), in multivariable models.

IN PRACTICE:

“This study sheds important insight on the implications of PTSD symptoms to women’s cardiovascular and neurocognitive health. Our findings indicate that the APOEε4 genotype may identify a group of women with PTSD symptoms at particular risk for poor neurocognitive health,” the authors wrote.

SOURCE:

The study, with first author Rebecca Thurston, PhD, of the department of psychiatry, University of Pittsburgh, was published online  in JAMA Network Open.

LIMITATIONS:

No diagnostic clinical interviews were conducted, and PTSD treatment was not assessed. All participants identified as cisgender, and most were non-Hispanic Black or White. The study was observational and cross-sectional, precluding assertions about directionality or causality.

DISCLOSURES:

The study was funded by the National Institutes of Health, the University of Pittsburgh Clinical and Translational Science Institute, and the University of Pittsburgh Small Molecule Biomarker Core. Dr. Thurston reported receiving personal fees from Astellas Pharma, Bayer, Hello Therapeutics, Vira Health, and Happify Health outside the submitted work.

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

TOPLINE:

Posttraumatic stress disorder (PTSD) symptoms are associated with poorer cardiovascular and neurocognitive health among midlife women, particularly those who are APOEε4 carriers, new research suggests.

METHODOLOGY:

• Researchers conducted a cross-sectional study of 274 women (mean age, 59 years) participating in the MsBrain study of menopause and brain health.
• As part of the study, the women completed the PTSD Checklist–Civilian Version and underwent physical and neuropsychological testing, as well as carotid artery ultrasonography and brain MRI.
• Outcomes of interest were associations of PTSD symptoms with carotid intima media thickness (IMT), brain white matter hyperintensity volume (WMHV), and cognition, assessed in linear regression models.
• Interactions by APOEε4 were assessed; covariates included age, race/ethnicity, education, and CVD risk factors.

TAKEAWAY:

• Higher PTSD symptoms were associated with greater carotid IMT (P = .03); associations of PTSD symptoms with neurocognitive outcomes varied significantly by APOEε4 status.
• Among APOEε4 carriers, PTSD symptoms were associated with greater whole-brain WMHV (P = .009), periventricular WMHV (P = .02), deep WMHV (P = .01), and frontal WMHV (P = .04) in multivariable models.
• APOEε4 carriers with PTSD symptoms also had poorer cognition, specifically attention and working memory (P = .02), semantic fluency (P = .01), perceptual speed (P = .002) and processing speed (P = .002), in multivariable models.

IN PRACTICE:

“This study sheds important insight on the implications of PTSD symptoms to women’s cardiovascular and neurocognitive health. Our findings indicate that the APOEε4 genotype may identify a group of women with PTSD symptoms at particular risk for poor neurocognitive health,” the authors wrote.

SOURCE:

The study, with first author Rebecca Thurston, PhD, of the department of psychiatry, University of Pittsburgh, was published online  in JAMA Network Open.

LIMITATIONS:

No diagnostic clinical interviews were conducted, and PTSD treatment was not assessed. All participants identified as cisgender, and most were non-Hispanic Black or White. The study was observational and cross-sectional, precluding assertions about directionality or causality.

DISCLOSURES:

The study was funded by the National Institutes of Health, the University of Pittsburgh Clinical and Translational Science Institute, and the University of Pittsburgh Small Molecule Biomarker Core. Dr. Thurston reported receiving personal fees from Astellas Pharma, Bayer, Hello Therapeutics, Vira Health, and Happify Health outside the submitted work.

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

Adults with Parkinson’s disease are twice as likely to engage in suicidal behavior as the general population, results of a large meta-analysis show.

Given that up to half of patients with PD suffer from depression and anxiety, physicians should maintain a “high index of suspicion” for early recognition and management of suicidality, write the investigators, led by Eng-King Tan, MD, of Duke-NUS Medical School, Singapore.

“Management of both medical, such as sleep disorders, and psychosocial risk factors, such as feelings of loneliness, hopelessness, and depressed mood, could be useful in lowering suicide risk in patients with PD,” they add.

The study was published online  in JAMA Neurology.
 

Suicide risk neglected in PD?

The analysis included 505,950 patients with PD across 28 cross-sectional, case-control, and cohort studies.

Across 14 studies, the prevalence of suicidal ideation in patients with PD was 22.2% (95% confidence interval, 14.6-32.3). In a sensitivity analysis excluding three outliers, the prevalence of suicidal ideation was higher at 24% (95% CI, 19.1-29.7).

Across 21 studies, the prevalence of suicidal behavior was “substantial” at 1.25% (95% CI, 0.64-2.41), the authors report. The prevalence of suicidal behavior was significantly higher in prospective studies (1.75%; 95% CI, 1.03-2.95) than retrospective studies (0.50%; 95% CI, 0.24 to 1.01).

Across 10 studies, the likelihood of suicidal behavior was about twofold higher among patients with PD than general population controls (odds ratio, 2.15; 95% CI, 1.22-3.78; P = .01). Across nine studies, the hazard ratio for suicidal behavior was 1.73 (95% CI, 1.40-2.14; P < .001).

There was no evidence of sex-related differences in suicidal behavior, although the analysis was limited by the paucity of data, the researchers note. 

They note the quality of included studies was generally high, although eight of them did not explicitly identify and adjust for confounders.
 

Higher rate of mood, anxiety disorders

Paul Nestadt, MD, with Johns Hopkins Bloomberg School of Public Health, Baltimore, said this analysis reiterates what several reviews have found over the past few years, including his own.

“In general, rates of mood and anxiety disorders are much higher in PD than in other dementias, such as Alzheimer’s disease. This is reason enough to allocate resources to the mental health care of those diagnosed with PD and to pay special attention to at risk periods, such as early in the diagnosis, when suicide rates seem to be higher in dementias in general,” said Dr. Nestadt, who wasn’t involved in the study.

He noted that research has shown that suicides among people with PD are more likely to involve a firearm – likely because people with PD are more likely to be over age 65 and to be male – “both huge risk factors for firearm suicide.”

“Therefore, it is essential that caregivers be aware of the risks posed by firearms in the homes of people suffering from Parkinson’s or other dementias. It is the clinician’s responsibility to inform families of this risk, but it is all too often neglected,” Dr. Nestadt said.

Support for the study was provided in part by the National Medical Research Council. Dr. Tan reported honoraria from Eisai and Elsevier outside the submitted work. Dr. Nestadt reports no relevant financial relationships.

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

Adults with Parkinson’s disease are twice as likely to engage in suicidal behavior as the general population, results of a large meta-analysis show.

Given that up to half of patients with PD suffer from depression and anxiety, physicians should maintain a “high index of suspicion” for early recognition and management of suicidality, write the investigators, led by Eng-King Tan, MD, of Duke-NUS Medical School, Singapore.

“Management of both medical, such as sleep disorders, and psychosocial risk factors, such as feelings of loneliness, hopelessness, and depressed mood, could be useful in lowering suicide risk in patients with PD,” they add.

The study was published online  in JAMA Neurology.
 

Suicide risk neglected in PD?

The analysis included 505,950 patients with PD across 28 cross-sectional, case-control, and cohort studies.

Across 14 studies, the prevalence of suicidal ideation in patients with PD was 22.2% (95% confidence interval, 14.6-32.3). In a sensitivity analysis excluding three outliers, the prevalence of suicidal ideation was higher at 24% (95% CI, 19.1-29.7).

Across 21 studies, the prevalence of suicidal behavior was “substantial” at 1.25% (95% CI, 0.64-2.41), the authors report. The prevalence of suicidal behavior was significantly higher in prospective studies (1.75%; 95% CI, 1.03-2.95) than retrospective studies (0.50%; 95% CI, 0.24 to 1.01).

Across 10 studies, the likelihood of suicidal behavior was about twofold higher among patients with PD than general population controls (odds ratio, 2.15; 95% CI, 1.22-3.78; P = .01). Across nine studies, the hazard ratio for suicidal behavior was 1.73 (95% CI, 1.40-2.14; P < .001).

There was no evidence of sex-related differences in suicidal behavior, although the analysis was limited by the paucity of data, the researchers note. 

They note the quality of included studies was generally high, although eight of them did not explicitly identify and adjust for confounders.
 

Higher rate of mood, anxiety disorders

Paul Nestadt, MD, with Johns Hopkins Bloomberg School of Public Health, Baltimore, said this analysis reiterates what several reviews have found over the past few years, including his own.

“In general, rates of mood and anxiety disorders are much higher in PD than in other dementias, such as Alzheimer’s disease. This is reason enough to allocate resources to the mental health care of those diagnosed with PD and to pay special attention to at risk periods, such as early in the diagnosis, when suicide rates seem to be higher in dementias in general,” said Dr. Nestadt, who wasn’t involved in the study.

He noted that research has shown that suicides among people with PD are more likely to involve a firearm – likely because people with PD are more likely to be over age 65 and to be male – “both huge risk factors for firearm suicide.”

“Therefore, it is essential that caregivers be aware of the risks posed by firearms in the homes of people suffering from Parkinson’s or other dementias. It is the clinician’s responsibility to inform families of this risk, but it is all too often neglected,” Dr. Nestadt said.

Support for the study was provided in part by the National Medical Research Council. Dr. Tan reported honoraria from Eisai and Elsevier outside the submitted work. Dr. Nestadt reports no relevant financial relationships.

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

Adults with Parkinson’s disease are twice as likely to engage in suicidal behavior as the general population, results of a large meta-analysis show.

Given that up to half of patients with PD suffer from depression and anxiety, physicians should maintain a “high index of suspicion” for early recognition and management of suicidality, write the investigators, led by Eng-King Tan, MD, of Duke-NUS Medical School, Singapore.

“Management of both medical, such as sleep disorders, and psychosocial risk factors, such as feelings of loneliness, hopelessness, and depressed mood, could be useful in lowering suicide risk in patients with PD,” they add.

The study was published online  in JAMA Neurology.
 

Suicide risk neglected in PD?

The analysis included 505,950 patients with PD across 28 cross-sectional, case-control, and cohort studies.

Across 14 studies, the prevalence of suicidal ideation in patients with PD was 22.2% (95% confidence interval, 14.6-32.3). In a sensitivity analysis excluding three outliers, the prevalence of suicidal ideation was higher at 24% (95% CI, 19.1-29.7).

Across 21 studies, the prevalence of suicidal behavior was “substantial” at 1.25% (95% CI, 0.64-2.41), the authors report. The prevalence of suicidal behavior was significantly higher in prospective studies (1.75%; 95% CI, 1.03-2.95) than retrospective studies (0.50%; 95% CI, 0.24 to 1.01).

Across 10 studies, the likelihood of suicidal behavior was about twofold higher among patients with PD than general population controls (odds ratio, 2.15; 95% CI, 1.22-3.78; P = .01). Across nine studies, the hazard ratio for suicidal behavior was 1.73 (95% CI, 1.40-2.14; P < .001).

There was no evidence of sex-related differences in suicidal behavior, although the analysis was limited by the paucity of data, the researchers note. 

They note the quality of included studies was generally high, although eight of them did not explicitly identify and adjust for confounders.
 

Higher rate of mood, anxiety disorders

Paul Nestadt, MD, with Johns Hopkins Bloomberg School of Public Health, Baltimore, said this analysis reiterates what several reviews have found over the past few years, including his own.

“In general, rates of mood and anxiety disorders are much higher in PD than in other dementias, such as Alzheimer’s disease. This is reason enough to allocate resources to the mental health care of those diagnosed with PD and to pay special attention to at risk periods, such as early in the diagnosis, when suicide rates seem to be higher in dementias in general,” said Dr. Nestadt, who wasn’t involved in the study.

He noted that research has shown that suicides among people with PD are more likely to involve a firearm – likely because people with PD are more likely to be over age 65 and to be male – “both huge risk factors for firearm suicide.”

“Therefore, it is essential that caregivers be aware of the risks posed by firearms in the homes of people suffering from Parkinson’s or other dementias. It is the clinician’s responsibility to inform families of this risk, but it is all too often neglected,” Dr. Nestadt said.

Support for the study was provided in part by the National Medical Research Council. Dr. Tan reported honoraria from Eisai and Elsevier outside the submitted work. Dr. Nestadt reports no relevant financial relationships.

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

Melatonin usage has become increasingly common among children in the United States, with almost one in five kids over the age of 5 having taken the sleep aid in the past 30 days, according to a recent study.

These findings should prompt clinicians to discuss with parents the various factors that could be driving sleep disturbances, and potential safety issues associated with melatonin usage, lead author Lauren E. Hartstein, PhD, a postdoctoral fellow in the Sleep and Development Lab at the University of Colorado, Boulder, and colleagues reported.

Writing in JAMA Pediatrics, the investigators noted that melatonin products are notorious for mislabeling, with active ingredient quantities as much as three times higher than the labeled amount. This issue is particularly concerning, they added, as calls to poison control for melatonin ingestion jumped more than fivefold from 2012 to 2021, with most cases involving children younger than 5 years. Meanwhile, scant evidence is available to characterize intentional usage in the same population.

“Current data are lacking on the prevalence of melatonin use and the frequency, dosing, and timing of melatonin administration in U.S. youth,” Dr. Hartstein and colleagues wrote.

To address this knowledge gap, the investigators conducted an online survey of parents with children and adolescents aged 1.0-13.9 years. The survey asked parents to report any melatonin usage in their children in the past 30 days.

Parents reporting melatonin usage were asked about frequency, dose, timing of administration before bedtime, and duration of use.

Findings were reported within three age groups: preschool (1-4 years), school aged (5-9 years), and preteen (10-13 years).

The survey revealed that almost one in five children in the older age groups were using melatonin, with a rate of 18.5% in the school-aged group and 19.4% in the preteen group. In comparison, 5.6% of preschool children had received melatonin for sleep in the past 30 days.
 

A significant uptick in usage

These findings point to a significant uptick in usage, according to Dr. Hartstein and colleagues, who cited a 2017-2018 study that found just 1.3% of U.S. children had taken melatonin in the past 30 days.

In the present study, melatonin was typically administered 30 minutes before bedtime, most often as a gummy (64.3%) or chewable tablet (27.0%).

Frequency of administration was similar between age groups and trended toward a bimodal pattern, with melatonin often given either 1 day per week or 7 days per week.

Median dose increased significantly with age, from 0.5 mg in the preschool group to 1.0 mg in the school-aged group and 2.0 mg in the preteen group. Median duration also showed a significant upward trend, with 12-month, 18-month, and 21-month durations, respectively, for ascending age groups.

The investigators concluded that melatonin usage among U.S. adolescents and children is “exceedingly common,” despite a lack of evidence to support long-term safety or guide optimal dosing.
 

Is melatonin use masking other sleep issues?

“Widespread melatonin use across developmental stages may suggest a high prevalence of sleep disruption, which deserves accurate diagnosis and effective treatment,” Dr. Hartstein and colleagues wrote. “Dissemination of information regarding safety concerns, such as overdose and supplement mislabeling, is necessary. Clinicians should discuss with parents the factors associated with sleep difficulties and effective behavioral strategies.”

Large-scale, long-term studies are needed, they added, to generate relevant safety and efficacy data, and to characterize the factors driving melatonin administration by parents.

courtesy UCLA

“Studies like these add to our knowledge base and give us insight into what patients or parents may be doing that can impact overall health,” said Alfonso J. Padilla, MD, assistant clinical professor of sleep medicine at the University of California, Los Angeles, in a written comment. “Often, in normal encounters with our patients we may not be able to gather this information easily. It may help open conversations about sleep issues that are not being addressed.”

Dr. Padilla suggested that parents may believe that melatonin is safe because it is not regulated by the Food and Drug Administration, when in fact they could be negatively impacting their children’s sleep. He noted that short-term risks include altered circadian rhythm and vivid dreams or nightmares, while long-term safety remains unclear.

“As a sleep physician, I use melatonin for specific indications only,” Dr. Padilla said. “I may use it in small children that are having difficulty falling asleep, especially in children with autism or special needs. I also use it for help in adjustment in circadian rhythm, especially in adolescents.”

He recommends melatonin, he added, if he has a complete case history, and melatonin is suitable for that patient.

Typically, it’s not.

“Most often a medication is not the answer for the sleep concern that parents are having about their child,” he said.

The investigators disclosed grants from the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the Colorado Clinical and Translational Science Award Program of the National Center for Advancing Translational Sciences of the National Institutes of Health. They reported no conflicts of interest.

Melatonin usage has become increasingly common among children in the United States, with almost one in five kids over the age of 5 having taken the sleep aid in the past 30 days, according to a recent study.

These findings should prompt clinicians to discuss with parents the various factors that could be driving sleep disturbances, and potential safety issues associated with melatonin usage, lead author Lauren E. Hartstein, PhD, a postdoctoral fellow in the Sleep and Development Lab at the University of Colorado, Boulder, and colleagues reported.

Writing in JAMA Pediatrics, the investigators noted that melatonin products are notorious for mislabeling, with active ingredient quantities as much as three times higher than the labeled amount. This issue is particularly concerning, they added, as calls to poison control for melatonin ingestion jumped more than fivefold from 2012 to 2021, with most cases involving children younger than 5 years. Meanwhile, scant evidence is available to characterize intentional usage in the same population.

“Current data are lacking on the prevalence of melatonin use and the frequency, dosing, and timing of melatonin administration in U.S. youth,” Dr. Hartstein and colleagues wrote.

To address this knowledge gap, the investigators conducted an online survey of parents with children and adolescents aged 1.0-13.9 years. The survey asked parents to report any melatonin usage in their children in the past 30 days.

Parents reporting melatonin usage were asked about frequency, dose, timing of administration before bedtime, and duration of use.

Findings were reported within three age groups: preschool (1-4 years), school aged (5-9 years), and preteen (10-13 years).

The survey revealed that almost one in five children in the older age groups were using melatonin, with a rate of 18.5% in the school-aged group and 19.4% in the preteen group. In comparison, 5.6% of preschool children had received melatonin for sleep in the past 30 days.
 

A significant uptick in usage

These findings point to a significant uptick in usage, according to Dr. Hartstein and colleagues, who cited a 2017-2018 study that found just 1.3% of U.S. children had taken melatonin in the past 30 days.

In the present study, melatonin was typically administered 30 minutes before bedtime, most often as a gummy (64.3%) or chewable tablet (27.0%).

Frequency of administration was similar between age groups and trended toward a bimodal pattern, with melatonin often given either 1 day per week or 7 days per week.

Median dose increased significantly with age, from 0.5 mg in the preschool group to 1.0 mg in the school-aged group and 2.0 mg in the preteen group. Median duration also showed a significant upward trend, with 12-month, 18-month, and 21-month durations, respectively, for ascending age groups.

The investigators concluded that melatonin usage among U.S. adolescents and children is “exceedingly common,” despite a lack of evidence to support long-term safety or guide optimal dosing.
 

Is melatonin use masking other sleep issues?

“Widespread melatonin use across developmental stages may suggest a high prevalence of sleep disruption, which deserves accurate diagnosis and effective treatment,” Dr. Hartstein and colleagues wrote. “Dissemination of information regarding safety concerns, such as overdose and supplement mislabeling, is necessary. Clinicians should discuss with parents the factors associated with sleep difficulties and effective behavioral strategies.”

Large-scale, long-term studies are needed, they added, to generate relevant safety and efficacy data, and to characterize the factors driving melatonin administration by parents.

courtesy UCLA

“Studies like these add to our knowledge base and give us insight into what patients or parents may be doing that can impact overall health,” said Alfonso J. Padilla, MD, assistant clinical professor of sleep medicine at the University of California, Los Angeles, in a written comment. “Often, in normal encounters with our patients we may not be able to gather this information easily. It may help open conversations about sleep issues that are not being addressed.”

Dr. Padilla suggested that parents may believe that melatonin is safe because it is not regulated by the Food and Drug Administration, when in fact they could be negatively impacting their children’s sleep. He noted that short-term risks include altered circadian rhythm and vivid dreams or nightmares, while long-term safety remains unclear.

“As a sleep physician, I use melatonin for specific indications only,” Dr. Padilla said. “I may use it in small children that are having difficulty falling asleep, especially in children with autism or special needs. I also use it for help in adjustment in circadian rhythm, especially in adolescents.”

He recommends melatonin, he added, if he has a complete case history, and melatonin is suitable for that patient.

Typically, it’s not.

“Most often a medication is not the answer for the sleep concern that parents are having about their child,” he said.

The investigators disclosed grants from the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the Colorado Clinical and Translational Science Award Program of the National Center for Advancing Translational Sciences of the National Institutes of Health. They reported no conflicts of interest.

Melatonin usage has become increasingly common among children in the United States, with almost one in five kids over the age of 5 having taken the sleep aid in the past 30 days, according to a recent study.

These findings should prompt clinicians to discuss with parents the various factors that could be driving sleep disturbances, and potential safety issues associated with melatonin usage, lead author Lauren E. Hartstein, PhD, a postdoctoral fellow in the Sleep and Development Lab at the University of Colorado, Boulder, and colleagues reported.

Writing in JAMA Pediatrics, the investigators noted that melatonin products are notorious for mislabeling, with active ingredient quantities as much as three times higher than the labeled amount. This issue is particularly concerning, they added, as calls to poison control for melatonin ingestion jumped more than fivefold from 2012 to 2021, with most cases involving children younger than 5 years. Meanwhile, scant evidence is available to characterize intentional usage in the same population.

“Current data are lacking on the prevalence of melatonin use and the frequency, dosing, and timing of melatonin administration in U.S. youth,” Dr. Hartstein and colleagues wrote.

To address this knowledge gap, the investigators conducted an online survey of parents with children and adolescents aged 1.0-13.9 years. The survey asked parents to report any melatonin usage in their children in the past 30 days.

Parents reporting melatonin usage were asked about frequency, dose, timing of administration before bedtime, and duration of use.

Findings were reported within three age groups: preschool (1-4 years), school aged (5-9 years), and preteen (10-13 years).

The survey revealed that almost one in five children in the older age groups were using melatonin, with a rate of 18.5% in the school-aged group and 19.4% in the preteen group. In comparison, 5.6% of preschool children had received melatonin for sleep in the past 30 days.
 

A significant uptick in usage

These findings point to a significant uptick in usage, according to Dr. Hartstein and colleagues, who cited a 2017-2018 study that found just 1.3% of U.S. children had taken melatonin in the past 30 days.

In the present study, melatonin was typically administered 30 minutes before bedtime, most often as a gummy (64.3%) or chewable tablet (27.0%).

Frequency of administration was similar between age groups and trended toward a bimodal pattern, with melatonin often given either 1 day per week or 7 days per week.

Median dose increased significantly with age, from 0.5 mg in the preschool group to 1.0 mg in the school-aged group and 2.0 mg in the preteen group. Median duration also showed a significant upward trend, with 12-month, 18-month, and 21-month durations, respectively, for ascending age groups.

The investigators concluded that melatonin usage among U.S. adolescents and children is “exceedingly common,” despite a lack of evidence to support long-term safety or guide optimal dosing.
 

Is melatonin use masking other sleep issues?

“Widespread melatonin use across developmental stages may suggest a high prevalence of sleep disruption, which deserves accurate diagnosis and effective treatment,” Dr. Hartstein and colleagues wrote. “Dissemination of information regarding safety concerns, such as overdose and supplement mislabeling, is necessary. Clinicians should discuss with parents the factors associated with sleep difficulties and effective behavioral strategies.”

Large-scale, long-term studies are needed, they added, to generate relevant safety and efficacy data, and to characterize the factors driving melatonin administration by parents.

courtesy UCLA

“Studies like these add to our knowledge base and give us insight into what patients or parents may be doing that can impact overall health,” said Alfonso J. Padilla, MD, assistant clinical professor of sleep medicine at the University of California, Los Angeles, in a written comment. “Often, in normal encounters with our patients we may not be able to gather this information easily. It may help open conversations about sleep issues that are not being addressed.”

Dr. Padilla suggested that parents may believe that melatonin is safe because it is not regulated by the Food and Drug Administration, when in fact they could be negatively impacting their children’s sleep. He noted that short-term risks include altered circadian rhythm and vivid dreams or nightmares, while long-term safety remains unclear.

“As a sleep physician, I use melatonin for specific indications only,” Dr. Padilla said. “I may use it in small children that are having difficulty falling asleep, especially in children with autism or special needs. I also use it for help in adjustment in circadian rhythm, especially in adolescents.”

He recommends melatonin, he added, if he has a complete case history, and melatonin is suitable for that patient.

Typically, it’s not.

“Most often a medication is not the answer for the sleep concern that parents are having about their child,” he said.

The investigators disclosed grants from the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the Colorado Clinical and Translational Science Award Program of the National Center for Advancing Translational Sciences of the National Institutes of Health. They reported no conflicts of interest.

Longer cumulative use of medication to treat attention-deficit/hyperactivity disorder (ADHD) is associated with a small, but statistically significant, increased risk for cardiovascular disease (CVD), results of a large Swedish nested case-control study suggest.

The increased risk was evident only for hypertension and arterial disease, was dose dependent, and was higher for stimulant than nonstimulant ADHD medications.

“Clinicians should be vigilant in monitoring signs and symptoms of cardiovascular diseases, particularly among those receiving higher doses,” Zheng Chang, PhD, principal researcher, department of medical epidemiology and biostatistics, Karolinska Institutet, Stockholm, said in an interview.

“Treatment decisions, as always, should be based on careful weighing of potential benefits and risks at individual patient level, rather than simple one-size-fits-all recommendations,” Dr. Chang added.

The study was published online in JAMA Psychiatry

Filling in the research gaps

The use of medications to treat ADHD has increased markedly over the past decades in both children and adults. The potential risk for CVD associated with long-term ADHD medication use remains unclear. Most “longitudinal” studies that have looked at the association have an average follow-up time of no more than 2 years, the authors note.

In contrast, the Swedish study assessed the association between cumulative use of ADHD medication in children and adults followed for up to 14 years and also looked at whether associations differ across types of medication and dosages, types of CVD, gender, and age.

Among 278,027 individuals aged 6-64 years diagnosed with ADHD or dispensed ADHD medication, 10,388 with CVD were identified and matched to 51,672 controls without CVD.

Longer cumulative duration of ADHD medication use was associated with a statistically significant increased risk for CVD, compared with no use.

When the risk for specific CVDs was examined, long-term use of ADHD medication (compared with no use) was associated with an increased risk for hypertension and arterial disease but not arrhythmias, heart failure, ischemic heart disease, thromboembolic disease, or cerebrovascular disease.

For hypertension, the adjusted odds ratio was 1.72 (95% confidence interval, 1.51-1.97) for 3 to ≤ 5 years and 1.80 (95% CI, 1.55-2.08) for > 5 years of medication use. For arterial disease, the AOR was 1.65 (95% CI, 1.11-2.45) for 3 to ≤ 5 years and 1.49 (95% CI, 0.96-2.32) for > 5 years of use.
 

Stimulants confer greatest risk

Across the 14-year follow-up period, each additional year of ADHD medication use was associated with an average 4% increased CVD risk, with a larger 8% increased risk in the first 3 years of cumulative use, followed by stable risk over the remaining follow-up.

Similar risks were observed in children and adults, as well as in females and males.

When focusing on specific ADHD medications, compared with no use, long-term use of the stimulant methylphenidate was associated with an increased risk for CVD (AOR, 1.20 [95% CI, 1.10-1.31] for 3 to ≤ 5 years and 1.19 [95% CI, 1.08-1.31] for > 5 years).

The same was true for long-term use of the stimulant lisdexamfetamine (AOR, 1.23 [95% CI, 1.05-1.44] for 2 to ≤ 3 years and 1.17 [95% CI, 0.98-1.40] for > 3 years).

In contrast, use of the nonstimulant atomoxetine was associated with elevated CVD risk only for the first year of use (AOR, 1.07; 95% CI, 1.01-1.13).

The increased risk for CVD occurred only above certain average daily doses: 45 mg for methylphenidate and lisdexamfetamine, 22.5 mg for amphetamines, and 120 mg for atomoxetine.

The authors note that, although they accounted for a wide range of potential confounding variables, considering the observational nature of the study and the possibility of residual confounding, they could not prove causality.

‘Tricky trade-offs’

The coauthors of an editorial in JAMA Psychiatry (2023 Nov 22. doi: 10.1001/jamapsychiatry.2023.4126) note that the study “should remind us that clinical decision-making is often based on tricky trade-offs that should be considered at the individual patient level.”

Given that hypertension is the leading cause of CV morbidity and mortality worldwide, the increased likelihood of hypertension with long-term use of ADHD medications “cannot be disregarded,” write Samuele Cortese, MD, PhD, and Cristiano Fava, MD, PhD, with University of Southampton (England).

“These findings are especially relevant given the reported association between ADHD and physical conditions, such as obesity, which further contribute to increased cardiovascular risk,” they add.

Dr. Cortese and Dr. Fava say that the increased CV risk – averaging 4% per year and stabilizing after 3 years of treatment – “should be carefully weighed against the established benefits, on a case-by-case basis.”

“Importantly,” they write, “large real-world self-controlled studies have shown that individuals with ADHD experience significantly fewer unintentional physical injuries, motor vehicle crashes, substance use disorders, and criminal acts, as well as improved academic functioning, during periods when they are taking, compared with periods when they are not taking, methylphenidate.”

The risk-benefit ratio, however, may be lower in people with preexisting heart conditions. However, more evidence and precise recommendations are needed in relation to the treatment of individuals with ADHD and preexisting CV conditions, the editorial writers say.

This study was supported by grants from the Swedish Research Council for Health, Working Life, and Welfare and the European Union’s Horizon 2020 research and innovation program. The authors and editorial writers have no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

Longer cumulative use of medication to treat attention-deficit/hyperactivity disorder (ADHD) is associated with a small, but statistically significant, increased risk for cardiovascular disease (CVD), results of a large Swedish nested case-control study suggest.

The increased risk was evident only for hypertension and arterial disease, was dose dependent, and was higher for stimulant than nonstimulant ADHD medications.

“Clinicians should be vigilant in monitoring signs and symptoms of cardiovascular diseases, particularly among those receiving higher doses,” Zheng Chang, PhD, principal researcher, department of medical epidemiology and biostatistics, Karolinska Institutet, Stockholm, said in an interview.

“Treatment decisions, as always, should be based on careful weighing of potential benefits and risks at individual patient level, rather than simple one-size-fits-all recommendations,” Dr. Chang added.

The study was published online in JAMA Psychiatry

Filling in the research gaps

The use of medications to treat ADHD has increased markedly over the past decades in both children and adults. The potential risk for CVD associated with long-term ADHD medication use remains unclear. Most “longitudinal” studies that have looked at the association have an average follow-up time of no more than 2 years, the authors note.

In contrast, the Swedish study assessed the association between cumulative use of ADHD medication in children and adults followed for up to 14 years and also looked at whether associations differ across types of medication and dosages, types of CVD, gender, and age.

Among 278,027 individuals aged 6-64 years diagnosed with ADHD or dispensed ADHD medication, 10,388 with CVD were identified and matched to 51,672 controls without CVD.

Longer cumulative duration of ADHD medication use was associated with a statistically significant increased risk for CVD, compared with no use.

When the risk for specific CVDs was examined, long-term use of ADHD medication (compared with no use) was associated with an increased risk for hypertension and arterial disease but not arrhythmias, heart failure, ischemic heart disease, thromboembolic disease, or cerebrovascular disease.

For hypertension, the adjusted odds ratio was 1.72 (95% confidence interval, 1.51-1.97) for 3 to ≤ 5 years and 1.80 (95% CI, 1.55-2.08) for > 5 years of medication use. For arterial disease, the AOR was 1.65 (95% CI, 1.11-2.45) for 3 to ≤ 5 years and 1.49 (95% CI, 0.96-2.32) for > 5 years of use.
 

Stimulants confer greatest risk

Across the 14-year follow-up period, each additional year of ADHD medication use was associated with an average 4% increased CVD risk, with a larger 8% increased risk in the first 3 years of cumulative use, followed by stable risk over the remaining follow-up.

Similar risks were observed in children and adults, as well as in females and males.

When focusing on specific ADHD medications, compared with no use, long-term use of the stimulant methylphenidate was associated with an increased risk for CVD (AOR, 1.20 [95% CI, 1.10-1.31] for 3 to ≤ 5 years and 1.19 [95% CI, 1.08-1.31] for > 5 years).

The same was true for long-term use of the stimulant lisdexamfetamine (AOR, 1.23 [95% CI, 1.05-1.44] for 2 to ≤ 3 years and 1.17 [95% CI, 0.98-1.40] for > 3 years).

In contrast, use of the nonstimulant atomoxetine was associated with elevated CVD risk only for the first year of use (AOR, 1.07; 95% CI, 1.01-1.13).

The increased risk for CVD occurred only above certain average daily doses: 45 mg for methylphenidate and lisdexamfetamine, 22.5 mg for amphetamines, and 120 mg for atomoxetine.

The authors note that, although they accounted for a wide range of potential confounding variables, considering the observational nature of the study and the possibility of residual confounding, they could not prove causality.

‘Tricky trade-offs’

The coauthors of an editorial in JAMA Psychiatry (2023 Nov 22. doi: 10.1001/jamapsychiatry.2023.4126) note that the study “should remind us that clinical decision-making is often based on tricky trade-offs that should be considered at the individual patient level.”

Given that hypertension is the leading cause of CV morbidity and mortality worldwide, the increased likelihood of hypertension with long-term use of ADHD medications “cannot be disregarded,” write Samuele Cortese, MD, PhD, and Cristiano Fava, MD, PhD, with University of Southampton (England).

“These findings are especially relevant given the reported association between ADHD and physical conditions, such as obesity, which further contribute to increased cardiovascular risk,” they add.

Dr. Cortese and Dr. Fava say that the increased CV risk – averaging 4% per year and stabilizing after 3 years of treatment – “should be carefully weighed against the established benefits, on a case-by-case basis.”

“Importantly,” they write, “large real-world self-controlled studies have shown that individuals with ADHD experience significantly fewer unintentional physical injuries, motor vehicle crashes, substance use disorders, and criminal acts, as well as improved academic functioning, during periods when they are taking, compared with periods when they are not taking, methylphenidate.”

The risk-benefit ratio, however, may be lower in people with preexisting heart conditions. However, more evidence and precise recommendations are needed in relation to the treatment of individuals with ADHD and preexisting CV conditions, the editorial writers say.

This study was supported by grants from the Swedish Research Council for Health, Working Life, and Welfare and the European Union’s Horizon 2020 research and innovation program. The authors and editorial writers have no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

Longer cumulative use of medication to treat attention-deficit/hyperactivity disorder (ADHD) is associated with a small, but statistically significant, increased risk for cardiovascular disease (CVD), results of a large Swedish nested case-control study suggest.

The increased risk was evident only for hypertension and arterial disease, was dose dependent, and was higher for stimulant than nonstimulant ADHD medications.

“Clinicians should be vigilant in monitoring signs and symptoms of cardiovascular diseases, particularly among those receiving higher doses,” Zheng Chang, PhD, principal researcher, department of medical epidemiology and biostatistics, Karolinska Institutet, Stockholm, said in an interview.

“Treatment decisions, as always, should be based on careful weighing of potential benefits and risks at individual patient level, rather than simple one-size-fits-all recommendations,” Dr. Chang added.

The study was published online in JAMA Psychiatry

Filling in the research gaps

The use of medications to treat ADHD has increased markedly over the past decades in both children and adults. The potential risk for CVD associated with long-term ADHD medication use remains unclear. Most “longitudinal” studies that have looked at the association have an average follow-up time of no more than 2 years, the authors note.

In contrast, the Swedish study assessed the association between cumulative use of ADHD medication in children and adults followed for up to 14 years and also looked at whether associations differ across types of medication and dosages, types of CVD, gender, and age.

Among 278,027 individuals aged 6-64 years diagnosed with ADHD or dispensed ADHD medication, 10,388 with CVD were identified and matched to 51,672 controls without CVD.

Longer cumulative duration of ADHD medication use was associated with a statistically significant increased risk for CVD, compared with no use.

When the risk for specific CVDs was examined, long-term use of ADHD medication (compared with no use) was associated with an increased risk for hypertension and arterial disease but not arrhythmias, heart failure, ischemic heart disease, thromboembolic disease, or cerebrovascular disease.

For hypertension, the adjusted odds ratio was 1.72 (95% confidence interval, 1.51-1.97) for 3 to ≤ 5 years and 1.80 (95% CI, 1.55-2.08) for > 5 years of medication use. For arterial disease, the AOR was 1.65 (95% CI, 1.11-2.45) for 3 to ≤ 5 years and 1.49 (95% CI, 0.96-2.32) for > 5 years of use.
 

Stimulants confer greatest risk

Across the 14-year follow-up period, each additional year of ADHD medication use was associated with an average 4% increased CVD risk, with a larger 8% increased risk in the first 3 years of cumulative use, followed by stable risk over the remaining follow-up.

Similar risks were observed in children and adults, as well as in females and males.

When focusing on specific ADHD medications, compared with no use, long-term use of the stimulant methylphenidate was associated with an increased risk for CVD (AOR, 1.20 [95% CI, 1.10-1.31] for 3 to ≤ 5 years and 1.19 [95% CI, 1.08-1.31] for > 5 years).

The same was true for long-term use of the stimulant lisdexamfetamine (AOR, 1.23 [95% CI, 1.05-1.44] for 2 to ≤ 3 years and 1.17 [95% CI, 0.98-1.40] for > 3 years).

In contrast, use of the nonstimulant atomoxetine was associated with elevated CVD risk only for the first year of use (AOR, 1.07; 95% CI, 1.01-1.13).

The increased risk for CVD occurred only above certain average daily doses: 45 mg for methylphenidate and lisdexamfetamine, 22.5 mg for amphetamines, and 120 mg for atomoxetine.

The authors note that, although they accounted for a wide range of potential confounding variables, considering the observational nature of the study and the possibility of residual confounding, they could not prove causality.

‘Tricky trade-offs’

The coauthors of an editorial in JAMA Psychiatry (2023 Nov 22. doi: 10.1001/jamapsychiatry.2023.4126) note that the study “should remind us that clinical decision-making is often based on tricky trade-offs that should be considered at the individual patient level.”

Given that hypertension is the leading cause of CV morbidity and mortality worldwide, the increased likelihood of hypertension with long-term use of ADHD medications “cannot be disregarded,” write Samuele Cortese, MD, PhD, and Cristiano Fava, MD, PhD, with University of Southampton (England).

“These findings are especially relevant given the reported association between ADHD and physical conditions, such as obesity, which further contribute to increased cardiovascular risk,” they add.

Dr. Cortese and Dr. Fava say that the increased CV risk – averaging 4% per year and stabilizing after 3 years of treatment – “should be carefully weighed against the established benefits, on a case-by-case basis.”

“Importantly,” they write, “large real-world self-controlled studies have shown that individuals with ADHD experience significantly fewer unintentional physical injuries, motor vehicle crashes, substance use disorders, and criminal acts, as well as improved academic functioning, during periods when they are taking, compared with periods when they are not taking, methylphenidate.”

The risk-benefit ratio, however, may be lower in people with preexisting heart conditions. However, more evidence and precise recommendations are needed in relation to the treatment of individuals with ADHD and preexisting CV conditions, the editorial writers say.

This study was supported by grants from the Swedish Research Council for Health, Working Life, and Welfare and the European Union’s Horizon 2020 research and innovation program. The authors and editorial writers have no relevant conflicts of interest.

A version of this article appeared on Medscape.com.

In the pursuit of optimal health, regular physical activity (PA) is recommended to protect against dementia, cardiovascular disease (CVD), cancer, and other noncommunicable diseases. A significant body of research suggests the benefits of PA are positively correlated with higher frequency and intensity – with more often deemed better. This research has spawned a focus on increasing step counts and investing in standing desks and other interventions aimed at keeping people active.

But for many people, PA is a work requirement over which they have little control, and emerging evidence suggests that these workers not only do not reap the benefits associated with leisure-time PA, but they also actually experience an increased risk for the very conditions that PA is intended to prevent.

A study published recently in The Lancet Regional Health – Europe used registry data from more than 7,000 adults in Norway, following them from age 33 to 65 years, to assess PA trajectories and risks for later-life mild cognitive impairment (MCI) and dementia at age 70 or older.

“Incorporating a life-course perspective gives a broader picture of how participants’ occupational histories relate to cognitive impairment later in life,” principal investigator Vegard Skirbekk, PhD, Columbia University Mailman School of Public Health, New York, said in an interview. Other studies typically have assessed occupational PA at a single time point, often close to the end of an individual’s career, and largely relied on self-report, he said.

Study participants worked in more than 300 different occupations. General physical activities performed on the included jobs required “considerable” use of arms and legs and moving the whole body, such as climbing, lifting, balancing, walking, stooping, and handling of materials.

Dr. Skirbekk and colleagues grouped participants into four PA trajectories over the 44-year study period: stable low, increasing then decreasing, stable intermediate, and stable high.

A total of 902 individuals were diagnosed with dementia and 2,407 with MCI at age 70 years or older. After adjustment, risks for MCI and dementia were 15.5% for those with higher occupational PA scores in the latter part of their working life and 9% for those with lower physical demands. The researchers concluded that “consistently working in an occupation with intermediate or high occupational PA was linked to an increased risk of cognitive impairment.”

The findings support those of the Copenhagen Male Study. Published in 2020, this longitudinal study compared leisure-time and occupational PA among more than 4,000 men in Denmark aged 40-59 at baseline in 1970-1971 and followed them until they turned 60. After adjustment, participants with high occupational PA had a 55% greater risk of developing dementia compared with those doing sedentary work.
 

Good vs. bad PA

“[T]he WHO [World Health Organization] guide to preventing dementia and disease on the whole mentions physical activity as an important factor. But our study suggests that it must be a ‘good’ form of physical activity, which hard physical work is not,” said Kirsten Nabe-Nielsen, PhD, lead author of this study

Beyond dementia, another recent study adds to a wealth of data on associations between occupational PA and cardiovascular risks. The cross-sectional analysis of U.S. data from the National Institute for Occupational Safety and Health showed that odds of CVD were higher when participants were “always” performing total occupational activity (odds ratio [OR], 1.99), occupational exertion (OR, 2.15), or occupational standing and walking around (OR, 1.84) compared with “never” engaging in these activities.

The contrasting effects of leisure-time vs. occupational PA constitute the “physical activity paradox” hypothesis. Starting in 2011, multiple studies by Andreas Holtermann, PhD, of the National Research Centre for the Working Environment lend support to the PA paradox theory, as do subsequent studies by others.

Although only “marginally considered” until a few years ago, recent large cohort studies seem to confirm the paradox, Pier Luigi Temporelli, MD wrote in a recent editorial.

In separate interviews, Dr. Skirbekk and lead author Tyler Quinn, PhD, MS, West Virginia University, Morgantown, pointed to the PA paradox as an explanation for their own recent findings, suggesting that the mechanisms that underlie it probably are responsible for the associated deleterious effects of occupational PA on the brain and heart, and even mortality.

“It’s well established that PA in your leisure time can be positive, but in the workplace, the results are quite the opposite,” Dr. Skirbekk said. “The specific mechanisms for why occupational PA is associated with elevated dementia risk are still not well understood and we need more knowledge. But we know that higher occupational physical demands have been linked to smaller hippocampal volume and poorer memory performance.”

Furthermore, he said, individuals working in jobs with high demands, both psychological and physical, combined with low job control perform more poorly on cognitive testing later in life.

“We looked mainly at professions where people have heavy workloads and you have much less autonomy, such as nursing assistants, office cleaners, childcare workers, and other personal care workers,” he said. “You cannot sit. You have somebody relying on you. It’s not all pleasure, and it can be very hard. That’s where we find the associations.”
 

Lack of autonomy

Specific characteristics indirectly associated with high occupational PA jobs – low cognitive stimuli, lifestyle factors, and socioeconomic influences – as well as factors directly related to high occupational PA, such as long hours, repetitive tasks, low levels of control, and stress, could also adversely affect cognitive trajectories, Dr. Skirbekk explained.

“By contrast, leisure-time physical activities tend to be of much shorter duration; are associated with socialization, play, [and] positive emotions; and [include] the opportunity to take breaks or shift to other types of activities if one prefers,” he said. “It may also be that too little or too much PA could be adversely related to cognitive outcomes – hence moderate activity levels, for example 10,000 steps a day, are still likely beneficial for cognitive functioning.”

Dr. Quinn said most of the CVD risk linked to occupational PA has to do with long periods of exertion such as lifting and carrying objects. While occupational standing and walking all day are also linked to CVD risk, they’re not as risky as lifting and carrying, he said.

Like Dr. Skirbekk, Dr. Quinn noted that individuals can take a break from leisure-time PA when they are tired, but occupational PA doesn’t have that same autonomy to allow for recovery.

“So, in many cases, individuals are not getting the recovery their body needs to actually experience PA benefits, because those benefits come during rest,” Dr. Quinn said.

“We’ve shown that PA at work raises acute cardiovascular responses, which are related to cardiovascular risk. For example, 24-hour and waking heart rate and diastolic blood pressure, as well as nonwork diastolic blood pressure, all were significantly higher on workdays versus non-workdays,” he said.

Dr. Quinn also said that psychological stress at work amplifies risk. “A person who does PA at work and is stressed is likely to be at greater risk than someone who has a physically active job but doesn’t have psychological stress combined with it.”
 

Research gaps

However, Dr. Skirbekk noted that there are strategies that can reduce the risk for MCI and dementia despite high levels of occupational PA. “It is often difficult to change professions, and even if you do, it won’t immediately affect cognition. But altering one’s lifestyle is likely to have effects on cognitive development across the life cycle.

“Many clinicians say they always advise lifestyle changes, but nothing happens. But it makes sense to emphasize that these changes – stopping smoking, eating well, getting proper sleep, etc. – affect not only cardiovascular risk but also cognition. And I think clinicians should also take a patient’s occupation into account during any evaluation,” Dr. Skirbekk noted.

Dr. Quinn said it isn’t realistic to expect workers to come up with solutions to the PA paradox because many don’t have the autonomy to be able to mitigate their occupational risk.

“I think administrative controls and policy changes eventually will be the levers of change. We’re not quite there yet, but those are the types of things we should do when we’re trying to reduce loads in some way, or reduce the time that people spend doing certain tasks we know are potentially bad,” he said.

However, not everyone agrees that occupational PA doesn’t confer the same benefits of leisure-time PA, at least with respect to cardiovascular risk. For example, the Prospective Urban Rural Epidemiology (PURE) study, which includes a cohort of 130,000 people from 17 high-income, middle-income, and low-income countries, concluded that both higher recreational and nonrecreational PA were associated with a lower risk for mortality and CVD events.

What additional research is needed to clarify the effects of occupational and leisure-time activity and to address conflicting findings?

“Even studies coming out now regarding the effects of occupational PA have mainly used older data,” Dr. Skirbekk noted. “Labor markets and job demands have changed over time. There are different types of tasks and skills required now than there were 20 or 40 years ago. And of course, working from home is a recent phenomenon that’s happened on a large scale and might affect daily routines, sleep patterns, and also cognition. We need a better understanding of what the consequences might be.”
 

Health inequity issue

More research is also necessary to understand the social determinants of cognitive decline, impairment, and dementia, he said. “Many of the studies we see today are based on self-report of what someone has done in the past, which is particularly problematic for individuals who are impaired or who give interviews with others, which can induce biases.”

Dr. Quinn suggests that PA guidelines may need to differentiate between occupational and leisure-time PA to better reflect current research findings.

Meanwhile, Dr. Skirbekk and Dr. Quinn both point to the toll that occupational PA takes on the brain and body in lower-income workers as an important health equity issue.

“Our national guidelines for PA include occupational activity,” said Dr. Quinn. “But it’s clear that a lot of people who are getting a lot of occupational PA, particularly socioeconomic and racial/ethnic minorities, are not benefiting from it.”

Dr. Holtermann, who has arguably done the most research to date on the PA paradox, noted in a recent editorial that the majority of workers with high occupational PA have a low socioeconomic position and therefore “improving our understanding of the underlying mechanisms behind the PA health paradox and identifying new intervention targets along those pathways will be an important step to reduce socioeconomic health inequalities across the globe.”
 

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

In the pursuit of optimal health, regular physical activity (PA) is recommended to protect against dementia, cardiovascular disease (CVD), cancer, and other noncommunicable diseases. A significant body of research suggests the benefits of PA are positively correlated with higher frequency and intensity – with more often deemed better. This research has spawned a focus on increasing step counts and investing in standing desks and other interventions aimed at keeping people active.

But for many people, PA is a work requirement over which they have little control, and emerging evidence suggests that these workers not only do not reap the benefits associated with leisure-time PA, but they also actually experience an increased risk for the very conditions that PA is intended to prevent.

A study published recently in The Lancet Regional Health – Europe used registry data from more than 7,000 adults in Norway, following them from age 33 to 65 years, to assess PA trajectories and risks for later-life mild cognitive impairment (MCI) and dementia at age 70 or older.

“Incorporating a life-course perspective gives a broader picture of how participants’ occupational histories relate to cognitive impairment later in life,” principal investigator Vegard Skirbekk, PhD, Columbia University Mailman School of Public Health, New York, said in an interview. Other studies typically have assessed occupational PA at a single time point, often close to the end of an individual’s career, and largely relied on self-report, he said.

Study participants worked in more than 300 different occupations. General physical activities performed on the included jobs required “considerable” use of arms and legs and moving the whole body, such as climbing, lifting, balancing, walking, stooping, and handling of materials.

Dr. Skirbekk and colleagues grouped participants into four PA trajectories over the 44-year study period: stable low, increasing then decreasing, stable intermediate, and stable high.

A total of 902 individuals were diagnosed with dementia and 2,407 with MCI at age 70 years or older. After adjustment, risks for MCI and dementia were 15.5% for those with higher occupational PA scores in the latter part of their working life and 9% for those with lower physical demands. The researchers concluded that “consistently working in an occupation with intermediate or high occupational PA was linked to an increased risk of cognitive impairment.”

The findings support those of the Copenhagen Male Study. Published in 2020, this longitudinal study compared leisure-time and occupational PA among more than 4,000 men in Denmark aged 40-59 at baseline in 1970-1971 and followed them until they turned 60. After adjustment, participants with high occupational PA had a 55% greater risk of developing dementia compared with those doing sedentary work.
 

Good vs. bad PA

“[T]he WHO [World Health Organization] guide to preventing dementia and disease on the whole mentions physical activity as an important factor. But our study suggests that it must be a ‘good’ form of physical activity, which hard physical work is not,” said Kirsten Nabe-Nielsen, PhD, lead author of this study

Beyond dementia, another recent study adds to a wealth of data on associations between occupational PA and cardiovascular risks. The cross-sectional analysis of U.S. data from the National Institute for Occupational Safety and Health showed that odds of CVD were higher when participants were “always” performing total occupational activity (odds ratio [OR], 1.99), occupational exertion (OR, 2.15), or occupational standing and walking around (OR, 1.84) compared with “never” engaging in these activities.

The contrasting effects of leisure-time vs. occupational PA constitute the “physical activity paradox” hypothesis. Starting in 2011, multiple studies by Andreas Holtermann, PhD, of the National Research Centre for the Working Environment lend support to the PA paradox theory, as do subsequent studies by others.

Although only “marginally considered” until a few years ago, recent large cohort studies seem to confirm the paradox, Pier Luigi Temporelli, MD wrote in a recent editorial.

In separate interviews, Dr. Skirbekk and lead author Tyler Quinn, PhD, MS, West Virginia University, Morgantown, pointed to the PA paradox as an explanation for their own recent findings, suggesting that the mechanisms that underlie it probably are responsible for the associated deleterious effects of occupational PA on the brain and heart, and even mortality.

“It’s well established that PA in your leisure time can be positive, but in the workplace, the results are quite the opposite,” Dr. Skirbekk said. “The specific mechanisms for why occupational PA is associated with elevated dementia risk are still not well understood and we need more knowledge. But we know that higher occupational physical demands have been linked to smaller hippocampal volume and poorer memory performance.”

Furthermore, he said, individuals working in jobs with high demands, both psychological and physical, combined with low job control perform more poorly on cognitive testing later in life.

“We looked mainly at professions where people have heavy workloads and you have much less autonomy, such as nursing assistants, office cleaners, childcare workers, and other personal care workers,” he said. “You cannot sit. You have somebody relying on you. It’s not all pleasure, and it can be very hard. That’s where we find the associations.”
 

Lack of autonomy

Specific characteristics indirectly associated with high occupational PA jobs – low cognitive stimuli, lifestyle factors, and socioeconomic influences – as well as factors directly related to high occupational PA, such as long hours, repetitive tasks, low levels of control, and stress, could also adversely affect cognitive trajectories, Dr. Skirbekk explained.

“By contrast, leisure-time physical activities tend to be of much shorter duration; are associated with socialization, play, [and] positive emotions; and [include] the opportunity to take breaks or shift to other types of activities if one prefers,” he said. “It may also be that too little or too much PA could be adversely related to cognitive outcomes – hence moderate activity levels, for example 10,000 steps a day, are still likely beneficial for cognitive functioning.”

Dr. Quinn said most of the CVD risk linked to occupational PA has to do with long periods of exertion such as lifting and carrying objects. While occupational standing and walking all day are also linked to CVD risk, they’re not as risky as lifting and carrying, he said.

Like Dr. Skirbekk, Dr. Quinn noted that individuals can take a break from leisure-time PA when they are tired, but occupational PA doesn’t have that same autonomy to allow for recovery.

“So, in many cases, individuals are not getting the recovery their body needs to actually experience PA benefits, because those benefits come during rest,” Dr. Quinn said.

“We’ve shown that PA at work raises acute cardiovascular responses, which are related to cardiovascular risk. For example, 24-hour and waking heart rate and diastolic blood pressure, as well as nonwork diastolic blood pressure, all were significantly higher on workdays versus non-workdays,” he said.

Dr. Quinn also said that psychological stress at work amplifies risk. “A person who does PA at work and is stressed is likely to be at greater risk than someone who has a physically active job but doesn’t have psychological stress combined with it.”
 

Research gaps

However, Dr. Skirbekk noted that there are strategies that can reduce the risk for MCI and dementia despite high levels of occupational PA. “It is often difficult to change professions, and even if you do, it won’t immediately affect cognition. But altering one’s lifestyle is likely to have effects on cognitive development across the life cycle.

“Many clinicians say they always advise lifestyle changes, but nothing happens. But it makes sense to emphasize that these changes – stopping smoking, eating well, getting proper sleep, etc. – affect not only cardiovascular risk but also cognition. And I think clinicians should also take a patient’s occupation into account during any evaluation,” Dr. Skirbekk noted.

Dr. Quinn said it isn’t realistic to expect workers to come up with solutions to the PA paradox because many don’t have the autonomy to be able to mitigate their occupational risk.

“I think administrative controls and policy changes eventually will be the levers of change. We’re not quite there yet, but those are the types of things we should do when we’re trying to reduce loads in some way, or reduce the time that people spend doing certain tasks we know are potentially bad,” he said.

However, not everyone agrees that occupational PA doesn’t confer the same benefits of leisure-time PA, at least with respect to cardiovascular risk. For example, the Prospective Urban Rural Epidemiology (PURE) study, which includes a cohort of 130,000 people from 17 high-income, middle-income, and low-income countries, concluded that both higher recreational and nonrecreational PA were associated with a lower risk for mortality and CVD events.

What additional research is needed to clarify the effects of occupational and leisure-time activity and to address conflicting findings?

“Even studies coming out now regarding the effects of occupational PA have mainly used older data,” Dr. Skirbekk noted. “Labor markets and job demands have changed over time. There are different types of tasks and skills required now than there were 20 or 40 years ago. And of course, working from home is a recent phenomenon that’s happened on a large scale and might affect daily routines, sleep patterns, and also cognition. We need a better understanding of what the consequences might be.”
 

Health inequity issue

More research is also necessary to understand the social determinants of cognitive decline, impairment, and dementia, he said. “Many of the studies we see today are based on self-report of what someone has done in the past, which is particularly problematic for individuals who are impaired or who give interviews with others, which can induce biases.”

Dr. Quinn suggests that PA guidelines may need to differentiate between occupational and leisure-time PA to better reflect current research findings.

Meanwhile, Dr. Skirbekk and Dr. Quinn both point to the toll that occupational PA takes on the brain and body in lower-income workers as an important health equity issue.

“Our national guidelines for PA include occupational activity,” said Dr. Quinn. “But it’s clear that a lot of people who are getting a lot of occupational PA, particularly socioeconomic and racial/ethnic minorities, are not benefiting from it.”

Dr. Holtermann, who has arguably done the most research to date on the PA paradox, noted in a recent editorial that the majority of workers with high occupational PA have a low socioeconomic position and therefore “improving our understanding of the underlying mechanisms behind the PA health paradox and identifying new intervention targets along those pathways will be an important step to reduce socioeconomic health inequalities across the globe.”
 

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

In the pursuit of optimal health, regular physical activity (PA) is recommended to protect against dementia, cardiovascular disease (CVD), cancer, and other noncommunicable diseases. A significant body of research suggests the benefits of PA are positively correlated with higher frequency and intensity – with more often deemed better. This research has spawned a focus on increasing step counts and investing in standing desks and other interventions aimed at keeping people active.

But for many people, PA is a work requirement over which they have little control, and emerging evidence suggests that these workers not only do not reap the benefits associated with leisure-time PA, but they also actually experience an increased risk for the very conditions that PA is intended to prevent.

A study published recently in The Lancet Regional Health – Europe used registry data from more than 7,000 adults in Norway, following them from age 33 to 65 years, to assess PA trajectories and risks for later-life mild cognitive impairment (MCI) and dementia at age 70 or older.

“Incorporating a life-course perspective gives a broader picture of how participants’ occupational histories relate to cognitive impairment later in life,” principal investigator Vegard Skirbekk, PhD, Columbia University Mailman School of Public Health, New York, said in an interview. Other studies typically have assessed occupational PA at a single time point, often close to the end of an individual’s career, and largely relied on self-report, he said.

Study participants worked in more than 300 different occupations. General physical activities performed on the included jobs required “considerable” use of arms and legs and moving the whole body, such as climbing, lifting, balancing, walking, stooping, and handling of materials.

Dr. Skirbekk and colleagues grouped participants into four PA trajectories over the 44-year study period: stable low, increasing then decreasing, stable intermediate, and stable high.

A total of 902 individuals were diagnosed with dementia and 2,407 with MCI at age 70 years or older. After adjustment, risks for MCI and dementia were 15.5% for those with higher occupational PA scores in the latter part of their working life and 9% for those with lower physical demands. The researchers concluded that “consistently working in an occupation with intermediate or high occupational PA was linked to an increased risk of cognitive impairment.”

The findings support those of the Copenhagen Male Study. Published in 2020, this longitudinal study compared leisure-time and occupational PA among more than 4,000 men in Denmark aged 40-59 at baseline in 1970-1971 and followed them until they turned 60. After adjustment, participants with high occupational PA had a 55% greater risk of developing dementia compared with those doing sedentary work.
 

Good vs. bad PA

“[T]he WHO [World Health Organization] guide to preventing dementia and disease on the whole mentions physical activity as an important factor. But our study suggests that it must be a ‘good’ form of physical activity, which hard physical work is not,” said Kirsten Nabe-Nielsen, PhD, lead author of this study

Beyond dementia, another recent study adds to a wealth of data on associations between occupational PA and cardiovascular risks. The cross-sectional analysis of U.S. data from the National Institute for Occupational Safety and Health showed that odds of CVD were higher when participants were “always” performing total occupational activity (odds ratio [OR], 1.99), occupational exertion (OR, 2.15), or occupational standing and walking around (OR, 1.84) compared with “never” engaging in these activities.

The contrasting effects of leisure-time vs. occupational PA constitute the “physical activity paradox” hypothesis. Starting in 2011, multiple studies by Andreas Holtermann, PhD, of the National Research Centre for the Working Environment lend support to the PA paradox theory, as do subsequent studies by others.

Although only “marginally considered” until a few years ago, recent large cohort studies seem to confirm the paradox, Pier Luigi Temporelli, MD wrote in a recent editorial.

In separate interviews, Dr. Skirbekk and lead author Tyler Quinn, PhD, MS, West Virginia University, Morgantown, pointed to the PA paradox as an explanation for their own recent findings, suggesting that the mechanisms that underlie it probably are responsible for the associated deleterious effects of occupational PA on the brain and heart, and even mortality.

“It’s well established that PA in your leisure time can be positive, but in the workplace, the results are quite the opposite,” Dr. Skirbekk said. “The specific mechanisms for why occupational PA is associated with elevated dementia risk are still not well understood and we need more knowledge. But we know that higher occupational physical demands have been linked to smaller hippocampal volume and poorer memory performance.”

Furthermore, he said, individuals working in jobs with high demands, both psychological and physical, combined with low job control perform more poorly on cognitive testing later in life.

“We looked mainly at professions where people have heavy workloads and you have much less autonomy, such as nursing assistants, office cleaners, childcare workers, and other personal care workers,” he said. “You cannot sit. You have somebody relying on you. It’s not all pleasure, and it can be very hard. That’s where we find the associations.”
 

Lack of autonomy

Specific characteristics indirectly associated with high occupational PA jobs – low cognitive stimuli, lifestyle factors, and socioeconomic influences – as well as factors directly related to high occupational PA, such as long hours, repetitive tasks, low levels of control, and stress, could also adversely affect cognitive trajectories, Dr. Skirbekk explained.

“By contrast, leisure-time physical activities tend to be of much shorter duration; are associated with socialization, play, [and] positive emotions; and [include] the opportunity to take breaks or shift to other types of activities if one prefers,” he said. “It may also be that too little or too much PA could be adversely related to cognitive outcomes – hence moderate activity levels, for example 10,000 steps a day, are still likely beneficial for cognitive functioning.”

Dr. Quinn said most of the CVD risk linked to occupational PA has to do with long periods of exertion such as lifting and carrying objects. While occupational standing and walking all day are also linked to CVD risk, they’re not as risky as lifting and carrying, he said.

Like Dr. Skirbekk, Dr. Quinn noted that individuals can take a break from leisure-time PA when they are tired, but occupational PA doesn’t have that same autonomy to allow for recovery.

“So, in many cases, individuals are not getting the recovery their body needs to actually experience PA benefits, because those benefits come during rest,” Dr. Quinn said.

“We’ve shown that PA at work raises acute cardiovascular responses, which are related to cardiovascular risk. For example, 24-hour and waking heart rate and diastolic blood pressure, as well as nonwork diastolic blood pressure, all were significantly higher on workdays versus non-workdays,” he said.

Dr. Quinn also said that psychological stress at work amplifies risk. “A person who does PA at work and is stressed is likely to be at greater risk than someone who has a physically active job but doesn’t have psychological stress combined with it.”
 

Research gaps

However, Dr. Skirbekk noted that there are strategies that can reduce the risk for MCI and dementia despite high levels of occupational PA. “It is often difficult to change professions, and even if you do, it won’t immediately affect cognition. But altering one’s lifestyle is likely to have effects on cognitive development across the life cycle.

“Many clinicians say they always advise lifestyle changes, but nothing happens. But it makes sense to emphasize that these changes – stopping smoking, eating well, getting proper sleep, etc. – affect not only cardiovascular risk but also cognition. And I think clinicians should also take a patient’s occupation into account during any evaluation,” Dr. Skirbekk noted.

Dr. Quinn said it isn’t realistic to expect workers to come up with solutions to the PA paradox because many don’t have the autonomy to be able to mitigate their occupational risk.

“I think administrative controls and policy changes eventually will be the levers of change. We’re not quite there yet, but those are the types of things we should do when we’re trying to reduce loads in some way, or reduce the time that people spend doing certain tasks we know are potentially bad,” he said.

However, not everyone agrees that occupational PA doesn’t confer the same benefits of leisure-time PA, at least with respect to cardiovascular risk. For example, the Prospective Urban Rural Epidemiology (PURE) study, which includes a cohort of 130,000 people from 17 high-income, middle-income, and low-income countries, concluded that both higher recreational and nonrecreational PA were associated with a lower risk for mortality and CVD events.

What additional research is needed to clarify the effects of occupational and leisure-time activity and to address conflicting findings?

“Even studies coming out now regarding the effects of occupational PA have mainly used older data,” Dr. Skirbekk noted. “Labor markets and job demands have changed over time. There are different types of tasks and skills required now than there were 20 or 40 years ago. And of course, working from home is a recent phenomenon that’s happened on a large scale and might affect daily routines, sleep patterns, and also cognition. We need a better understanding of what the consequences might be.”
 

Health inequity issue

More research is also necessary to understand the social determinants of cognitive decline, impairment, and dementia, he said. “Many of the studies we see today are based on self-report of what someone has done in the past, which is particularly problematic for individuals who are impaired or who give interviews with others, which can induce biases.”

Dr. Quinn suggests that PA guidelines may need to differentiate between occupational and leisure-time PA to better reflect current research findings.

Meanwhile, Dr. Skirbekk and Dr. Quinn both point to the toll that occupational PA takes on the brain and body in lower-income workers as an important health equity issue.

“Our national guidelines for PA include occupational activity,” said Dr. Quinn. “But it’s clear that a lot of people who are getting a lot of occupational PA, particularly socioeconomic and racial/ethnic minorities, are not benefiting from it.”

Dr. Holtermann, who has arguably done the most research to date on the PA paradox, noted in a recent editorial that the majority of workers with high occupational PA have a low socioeconomic position and therefore “improving our understanding of the underlying mechanisms behind the PA health paradox and identifying new intervention targets along those pathways will be an important step to reduce socioeconomic health inequalities across the globe.”
 

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

Leading UK Alzheimer’s organizations have launched an ambitious plan to have a diagnostic Alzheimer’s disease (AD) blood test widely available within the next 5 years.

Alzheimer’s Research UK, the Alzheimer’s Society, and the National Institute for Health and Care Research (NIHR) are collaborating and leading AD researchers to bring a diagnostic blood test to the UK’s National Health Service (NHS).

“Dementia affects around 900,000 people in the UK today, and that number is expected to rise to 1.4 million by 2040. It is the UK’s biggest killer,” Fiona Carragher, with the Alzheimer’s Society, said during a media briefing announcing the project.

Yet, many people face a very long wait of up to 2-4 years to get a dementia diagnosis, and many cases remain undiagnosed, she noted.

A chief reason is lack of access to specialized diagnostic testing. Currently, only 2% of people in the United Kingdom have access to advanced diagnostic tests such as PET scans and lumbar punctures owing to limited availability.

“Getting an early and accurate diagnosis is the pivotal first step to getting help today and unlocking hope for the future” and blood biomarkers provide a “real opportunity to disrupt the diagnostic paradigm,” Ms. Carragher said. It also offers greater opportunities to participate in research and clinical trials, she added.
 

Attitude shift

Susan Kohlhaas, PhD, with Alzheimer’s Research UK, noted that attitudes toward dementia diagnosis have changed in the past few years. The days when people may have not wanted to know if they have dementia are gone.

Data from the latest wave of the Alzheimer’s Research UK Dementia Attitudes Monitor survey show that 9 in 10 people would seek a diagnosis from their provider. “That’s been driven by awareness of treatments and things that people can proactively do to try and slow disease progression,” Dr. Kohlhaas said.

“As new treatments for dementia become available there will to be a surge in people seeking a diagnosis. At the moment, we don’t have adequate infrastructure to cope with that demand,” Dr. Kohlhaas added.

She noted that blood tests are starting to show their potential as an effective part of the diagnosis and are widely used in research.

“In some cases, they are similar in sensitivity to gold-standard PET scans and lumbar punctures, and they’re less expensive and potentially more scalable on the NHS. What we need to do over the next several years is to understand how they fit into the clinical pathway,” Dr. Kohlhaas said.

The project will involve working with leading dementia researchers to pilot the implementation of potential blood tests in the NHS that can give an early and accurate diagnose of dementia.

The project, which kicks off in January 2024, will receive £5 million ($6.13 million) awarded by the UK Postcode Dream Fund. Specific details regarding the leadership team, participating centers, and specific blood biomarker tests to be trialed will be announced then.

Ms. Carragher and Dr. Kohlhaas reported no relevant financial conflicts of interest.
 

A version of this article appeared on Medscape.com.

Leading UK Alzheimer’s organizations have launched an ambitious plan to have a diagnostic Alzheimer’s disease (AD) blood test widely available within the next 5 years.

Alzheimer’s Research UK, the Alzheimer’s Society, and the National Institute for Health and Care Research (NIHR) are collaborating and leading AD researchers to bring a diagnostic blood test to the UK’s National Health Service (NHS).

“Dementia affects around 900,000 people in the UK today, and that number is expected to rise to 1.4 million by 2040. It is the UK’s biggest killer,” Fiona Carragher, with the Alzheimer’s Society, said during a media briefing announcing the project.

Yet, many people face a very long wait of up to 2-4 years to get a dementia diagnosis, and many cases remain undiagnosed, she noted.

A chief reason is lack of access to specialized diagnostic testing. Currently, only 2% of people in the United Kingdom have access to advanced diagnostic tests such as PET scans and lumbar punctures owing to limited availability.

“Getting an early and accurate diagnosis is the pivotal first step to getting help today and unlocking hope for the future” and blood biomarkers provide a “real opportunity to disrupt the diagnostic paradigm,” Ms. Carragher said. It also offers greater opportunities to participate in research and clinical trials, she added.
 

Attitude shift

Susan Kohlhaas, PhD, with Alzheimer’s Research UK, noted that attitudes toward dementia diagnosis have changed in the past few years. The days when people may have not wanted to know if they have dementia are gone.

Data from the latest wave of the Alzheimer’s Research UK Dementia Attitudes Monitor survey show that 9 in 10 people would seek a diagnosis from their provider. “That’s been driven by awareness of treatments and things that people can proactively do to try and slow disease progression,” Dr. Kohlhaas said.

“As new treatments for dementia become available there will to be a surge in people seeking a diagnosis. At the moment, we don’t have adequate infrastructure to cope with that demand,” Dr. Kohlhaas added.

She noted that blood tests are starting to show their potential as an effective part of the diagnosis and are widely used in research.

“In some cases, they are similar in sensitivity to gold-standard PET scans and lumbar punctures, and they’re less expensive and potentially more scalable on the NHS. What we need to do over the next several years is to understand how they fit into the clinical pathway,” Dr. Kohlhaas said.

The project will involve working with leading dementia researchers to pilot the implementation of potential blood tests in the NHS that can give an early and accurate diagnose of dementia.

The project, which kicks off in January 2024, will receive £5 million ($6.13 million) awarded by the UK Postcode Dream Fund. Specific details regarding the leadership team, participating centers, and specific blood biomarker tests to be trialed will be announced then.

Ms. Carragher and Dr. Kohlhaas reported no relevant financial conflicts of interest.
 

A version of this article appeared on Medscape.com.

Leading UK Alzheimer’s organizations have launched an ambitious plan to have a diagnostic Alzheimer’s disease (AD) blood test widely available within the next 5 years.

Alzheimer’s Research UK, the Alzheimer’s Society, and the National Institute for Health and Care Research (NIHR) are collaborating and leading AD researchers to bring a diagnostic blood test to the UK’s National Health Service (NHS).

“Dementia affects around 900,000 people in the UK today, and that number is expected to rise to 1.4 million by 2040. It is the UK’s biggest killer,” Fiona Carragher, with the Alzheimer’s Society, said during a media briefing announcing the project.

Yet, many people face a very long wait of up to 2-4 years to get a dementia diagnosis, and many cases remain undiagnosed, she noted.

A chief reason is lack of access to specialized diagnostic testing. Currently, only 2% of people in the United Kingdom have access to advanced diagnostic tests such as PET scans and lumbar punctures owing to limited availability.

“Getting an early and accurate diagnosis is the pivotal first step to getting help today and unlocking hope for the future” and blood biomarkers provide a “real opportunity to disrupt the diagnostic paradigm,” Ms. Carragher said. It also offers greater opportunities to participate in research and clinical trials, she added.
 

Attitude shift

Susan Kohlhaas, PhD, with Alzheimer’s Research UK, noted that attitudes toward dementia diagnosis have changed in the past few years. The days when people may have not wanted to know if they have dementia are gone.

Data from the latest wave of the Alzheimer’s Research UK Dementia Attitudes Monitor survey show that 9 in 10 people would seek a diagnosis from their provider. “That’s been driven by awareness of treatments and things that people can proactively do to try and slow disease progression,” Dr. Kohlhaas said.

“As new treatments for dementia become available there will to be a surge in people seeking a diagnosis. At the moment, we don’t have adequate infrastructure to cope with that demand,” Dr. Kohlhaas added.

She noted that blood tests are starting to show their potential as an effective part of the diagnosis and are widely used in research.

“In some cases, they are similar in sensitivity to gold-standard PET scans and lumbar punctures, and they’re less expensive and potentially more scalable on the NHS. What we need to do over the next several years is to understand how they fit into the clinical pathway,” Dr. Kohlhaas said.

The project will involve working with leading dementia researchers to pilot the implementation of potential blood tests in the NHS that can give an early and accurate diagnose of dementia.

The project, which kicks off in January 2024, will receive £5 million ($6.13 million) awarded by the UK Postcode Dream Fund. Specific details regarding the leadership team, participating centers, and specific blood biomarker tests to be trialed will be announced then.

Ms. Carragher and Dr. Kohlhaas reported no relevant financial conflicts of interest.
 

A version of this article appeared on Medscape.com.

TOPLINE:

A history of military service is associated with a 26% increased risk for amyloid plaque and 10% increased risk for elevated tau tangle levels, underscoring the urgent need for amyloid screening among veterans.

METHODOLOGY:

• The study included 597 male decedents who donated their brains to one of two Alzheimer’s Disease Research Center (ADRC) brain bank programs between 1986 and 2018.
• Researchers conducted public data tracing for historical information on military history, which included searching online commercial genealogical databases and paper archives.
• They evaluated tau tangles (using a B score of neurofibrillary tangle deposition in four stages: B0 [not present], B1 [transentorhinal stages], B2 [limbic stages], and B3 [isocortical stages]) and amyloid plaque pathology (using a C score that classifies neuritic amyloid plaque into four categories: no plaques, sparse, moderate, or frequent).
• The study involved three B score comparisons (1, 2, 3 vs. 0; 2, 3 vs. 0, 1; and 3 vs. 0, 1, 2) and two C score comparisons (sparse, moderate, or frequent vs. no plaques, and moderate or frequent vs. no plaque or sparse).

TAKEAWAY:

• Public record tracing determined that 60% of the sample of male decedents had a history of military service; the median year of birth was 1923 and the median year of death was 2007.
• After adjustment for age and year of death, those with a military service history had a 26% increased risk for a higher neuritic amyloid plaque C score compared with those without such history (odds ratio [OR], 1.26; 95% confidence interval [CI], 1.06-1.49), an increase that applied for both relevant comparisons.
• A history of military service was also associated with a 10% greater adjusted odds of a higher neurofibrillary tangle B score (OR, 1.10; 95% CI, 1.08-1.12), with the increase applying to all three comparisons.
• A sensitivity analysis that included both the male decedents and 556 female decedents (increasing the overall sample to 1,153) and was adjusted for sex in addition to age and year of death showed similar results to the male-only sample estimations for both B and C score comparisons.

IN PRACTICE:

Understanding how military service affects AD biological processes is “essential” from a research perspective, the investigators noted. These new findings “emphasize that targeted AD therapies in the veteran population are urgently needed.”

SOURCE:

The study was conducted by W. Ryan Powell, Center for Health Disparities Research and Department of Medicine, Geriatrics Division, University of Wisconsin School of Medicine and Public Health, and colleagues. It was published online in Alzheimer’s & Dementia.

LIMITATIONS:

Selection bias in brain donation is likely because ADRC cohorts are recruitment based. The study was unable to rigorously identify factors that may explain why individuals with military service are at greater risk of having amyloid and tau neuropathology (including the interplay between environmental and genetic risk factors such as apolipoprotein E status).

DISCLOSURES:

The study was supported by the National Institute on Aging. The authors reported no disclosures.

A version of this article appeared on Medscape.com.

TOPLINE:

A history of military service is associated with a 26% increased risk for amyloid plaque and 10% increased risk for elevated tau tangle levels, underscoring the urgent need for amyloid screening among veterans.

METHODOLOGY:

• The study included 597 male decedents who donated their brains to one of two Alzheimer’s Disease Research Center (ADRC) brain bank programs between 1986 and 2018.
• Researchers conducted public data tracing for historical information on military history, which included searching online commercial genealogical databases and paper archives.
• They evaluated tau tangles (using a B score of neurofibrillary tangle deposition in four stages: B0 [not present], B1 [transentorhinal stages], B2 [limbic stages], and B3 [isocortical stages]) and amyloid plaque pathology (using a C score that classifies neuritic amyloid plaque into four categories: no plaques, sparse, moderate, or frequent).
• The study involved three B score comparisons (1, 2, 3 vs. 0; 2, 3 vs. 0, 1; and 3 vs. 0, 1, 2) and two C score comparisons (sparse, moderate, or frequent vs. no plaques, and moderate or frequent vs. no plaque or sparse).

TAKEAWAY:

• Public record tracing determined that 60% of the sample of male decedents had a history of military service; the median year of birth was 1923 and the median year of death was 2007.
• After adjustment for age and year of death, those with a military service history had a 26% increased risk for a higher neuritic amyloid plaque C score compared with those without such history (odds ratio [OR], 1.26; 95% confidence interval [CI], 1.06-1.49), an increase that applied for both relevant comparisons.
• A history of military service was also associated with a 10% greater adjusted odds of a higher neurofibrillary tangle B score (OR, 1.10; 95% CI, 1.08-1.12), with the increase applying to all three comparisons.
• A sensitivity analysis that included both the male decedents and 556 female decedents (increasing the overall sample to 1,153) and was adjusted for sex in addition to age and year of death showed similar results to the male-only sample estimations for both B and C score comparisons.

IN PRACTICE:

Understanding how military service affects AD biological processes is “essential” from a research perspective, the investigators noted. These new findings “emphasize that targeted AD therapies in the veteran population are urgently needed.”

SOURCE:

The study was conducted by W. Ryan Powell, Center for Health Disparities Research and Department of Medicine, Geriatrics Division, University of Wisconsin School of Medicine and Public Health, and colleagues. It was published online in Alzheimer’s & Dementia.

LIMITATIONS:

Selection bias in brain donation is likely because ADRC cohorts are recruitment based. The study was unable to rigorously identify factors that may explain why individuals with military service are at greater risk of having amyloid and tau neuropathology (including the interplay between environmental and genetic risk factors such as apolipoprotein E status).

DISCLOSURES:

The study was supported by the National Institute on Aging. The authors reported no disclosures.

A version of this article appeared on Medscape.com.

TOPLINE:

A history of military service is associated with a 26% increased risk for amyloid plaque and 10% increased risk for elevated tau tangle levels, underscoring the urgent need for amyloid screening among veterans.

METHODOLOGY:

• The study included 597 male decedents who donated their brains to one of two Alzheimer’s Disease Research Center (ADRC) brain bank programs between 1986 and 2018.
• Researchers conducted public data tracing for historical information on military history, which included searching online commercial genealogical databases and paper archives.
• They evaluated tau tangles (using a B score of neurofibrillary tangle deposition in four stages: B0 [not present], B1 [transentorhinal stages], B2 [limbic stages], and B3 [isocortical stages]) and amyloid plaque pathology (using a C score that classifies neuritic amyloid plaque into four categories: no plaques, sparse, moderate, or frequent).
• The study involved three B score comparisons (1, 2, 3 vs. 0; 2, 3 vs. 0, 1; and 3 vs. 0, 1, 2) and two C score comparisons (sparse, moderate, or frequent vs. no plaques, and moderate or frequent vs. no plaque or sparse).

TAKEAWAY:

• Public record tracing determined that 60% of the sample of male decedents had a history of military service; the median year of birth was 1923 and the median year of death was 2007.
• After adjustment for age and year of death, those with a military service history had a 26% increased risk for a higher neuritic amyloid plaque C score compared with those without such history (odds ratio [OR], 1.26; 95% confidence interval [CI], 1.06-1.49), an increase that applied for both relevant comparisons.
• A history of military service was also associated with a 10% greater adjusted odds of a higher neurofibrillary tangle B score (OR, 1.10; 95% CI, 1.08-1.12), with the increase applying to all three comparisons.
• A sensitivity analysis that included both the male decedents and 556 female decedents (increasing the overall sample to 1,153) and was adjusted for sex in addition to age and year of death showed similar results to the male-only sample estimations for both B and C score comparisons.

IN PRACTICE:

Understanding how military service affects AD biological processes is “essential” from a research perspective, the investigators noted. These new findings “emphasize that targeted AD therapies in the veteran population are urgently needed.”

SOURCE:

The study was conducted by W. Ryan Powell, Center for Health Disparities Research and Department of Medicine, Geriatrics Division, University of Wisconsin School of Medicine and Public Health, and colleagues. It was published online in Alzheimer’s & Dementia.

LIMITATIONS:

Selection bias in brain donation is likely because ADRC cohorts are recruitment based. The study was unable to rigorously identify factors that may explain why individuals with military service are at greater risk of having amyloid and tau neuropathology (including the interplay between environmental and genetic risk factors such as apolipoprotein E status).

DISCLOSURES:

The study was supported by the National Institute on Aging. The authors reported no disclosures.

A version of this article appeared on Medscape.com.

TOPLINE:

In the first year of the COVID-19 pandemic, there was a significant drop in working memory and executive function in older individuals. This was attributed to an increase in known dementia risk factors, including increased alcohol use and a more sedentary lifestyle. This trend persisted into the second year of the pandemic, after social restrictions had eased.

METHODOLOGY:

• In total, 3,140 participants (54% women; mean age, 68 years) in the PROTECT study, a longitudinal aging study in the United Kingdom, completed annual cognitive assessments and self-reported questionnaires related to mental health and lifestyle.
• Investigators analyzed cognition across three time periods: during the year before the pandemic (March 2019 to February 2020), during pandemic year 1 (March 2020 to February 2021), and pandemic year 2 (March 2021 to February 2022).
• Investigators conducted a subanalysis on those with mild cognitive impairment and those with a history of COVID-19 (n = 752).

TAKEAWAY:

• During the first year of the pandemic, when there were societal lockdowns totaling 6 months, significant worsening of executive function and working memory was seen across the entire cohort (effect sizes, 0.15 and 0.51, respectively), in people with mild cognitive impairment (effect sizes, 0.13 and 0.40, respectively), and in those with a previous history of COVID-19 (effect sizes, 0.24 and 0.46, respectively).
• Worsening of working memory was sustained across the whole cohort in the second year of the pandemic after lockdowns were lifted (effect size, 0.47).
• Even after investigators removed data on people with mild cognitive impairment and COVID-19, the decline in executive function (effect size, 0.15; P < .0001) and working memory (effect size, 0.53; P < .0001) persisted.
• Cognitive decline was significantly associated with known risk factors for dementia, such as reduced exercise (P = .0049) and increased alcohol use (P = .049), across the whole cohort, as well as depression (P = .011) in those with a history of COVID-19 and loneliness (P = .0038) in those with mild cognitive impairment.

IN PRACTICE:

Investigators noted that these data add to existing knowledge of long-standing health consequences of COVID-19, especially for older people with memory problems. “On the positive note, there is evidence that lifestyle changes and improved health management can positively influence mental functioning,” study coauthor Dag Aarsland, MD, PhD, professor of old age psychiatry at the Institute of Psychiatry, Psychology & Neuroscience of King’s College London, said in a press release. “The current study underlines the importance of careful monitoring of people at risk during major events such as the pandemic.”

SOURCE:

The study was led by Anne Corbett, PhD, of University of Exeter, and was published online in The Lancet Healthy Longevity. The research was funded by the National Institute for Health and Care Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King’s College London and the NIHR Exeter Biomedical Research Centre.

LIMITATIONS:

The study relied on self-reported data. In addition, the PROTECT cohort is self-selected and may skew toward participants with higher education levels.

DISCLOSURES:

Dr. Corbett reported receiving funding from the NIHR and grants from Synexus, reMYND, and Novo Nordisk. Other disclosures are noted in the original article.
 

A version of this article appeared on Medscape.com.

TOPLINE:

In the first year of the COVID-19 pandemic, there was a significant drop in working memory and executive function in older individuals. This was attributed to an increase in known dementia risk factors, including increased alcohol use and a more sedentary lifestyle. This trend persisted into the second year of the pandemic, after social restrictions had eased.

METHODOLOGY:

• In total, 3,140 participants (54% women; mean age, 68 years) in the PROTECT study, a longitudinal aging study in the United Kingdom, completed annual cognitive assessments and self-reported questionnaires related to mental health and lifestyle.
• Investigators analyzed cognition across three time periods: during the year before the pandemic (March 2019 to February 2020), during pandemic year 1 (March 2020 to February 2021), and pandemic year 2 (March 2021 to February 2022).
• Investigators conducted a subanalysis on those with mild cognitive impairment and those with a history of COVID-19 (n = 752).

TAKEAWAY:

• During the first year of the pandemic, when there were societal lockdowns totaling 6 months, significant worsening of executive function and working memory was seen across the entire cohort (effect sizes, 0.15 and 0.51, respectively), in people with mild cognitive impairment (effect sizes, 0.13 and 0.40, respectively), and in those with a previous history of COVID-19 (effect sizes, 0.24 and 0.46, respectively).
• Worsening of working memory was sustained across the whole cohort in the second year of the pandemic after lockdowns were lifted (effect size, 0.47).
• Even after investigators removed data on people with mild cognitive impairment and COVID-19, the decline in executive function (effect size, 0.15; P < .0001) and working memory (effect size, 0.53; P < .0001) persisted.
• Cognitive decline was significantly associated with known risk factors for dementia, such as reduced exercise (P = .0049) and increased alcohol use (P = .049), across the whole cohort, as well as depression (P = .011) in those with a history of COVID-19 and loneliness (P = .0038) in those with mild cognitive impairment.

IN PRACTICE:

Investigators noted that these data add to existing knowledge of long-standing health consequences of COVID-19, especially for older people with memory problems. “On the positive note, there is evidence that lifestyle changes and improved health management can positively influence mental functioning,” study coauthor Dag Aarsland, MD, PhD, professor of old age psychiatry at the Institute of Psychiatry, Psychology & Neuroscience of King’s College London, said in a press release. “The current study underlines the importance of careful monitoring of people at risk during major events such as the pandemic.”

SOURCE:

The study was led by Anne Corbett, PhD, of University of Exeter, and was published online in The Lancet Healthy Longevity. The research was funded by the National Institute for Health and Care Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King’s College London and the NIHR Exeter Biomedical Research Centre.

LIMITATIONS:

The study relied on self-reported data. In addition, the PROTECT cohort is self-selected and may skew toward participants with higher education levels.

DISCLOSURES:

Dr. Corbett reported receiving funding from the NIHR and grants from Synexus, reMYND, and Novo Nordisk. Other disclosures are noted in the original article.
 

A version of this article appeared on Medscape.com.

TOPLINE:

In the first year of the COVID-19 pandemic, there was a significant drop in working memory and executive function in older individuals. This was attributed to an increase in known dementia risk factors, including increased alcohol use and a more sedentary lifestyle. This trend persisted into the second year of the pandemic, after social restrictions had eased.

METHODOLOGY:

• In total, 3,140 participants (54% women; mean age, 68 years) in the PROTECT study, a longitudinal aging study in the United Kingdom, completed annual cognitive assessments and self-reported questionnaires related to mental health and lifestyle.
• Investigators analyzed cognition across three time periods: during the year before the pandemic (March 2019 to February 2020), during pandemic year 1 (March 2020 to February 2021), and pandemic year 2 (March 2021 to February 2022).
• Investigators conducted a subanalysis on those with mild cognitive impairment and those with a history of COVID-19 (n = 752).

TAKEAWAY:

• During the first year of the pandemic, when there were societal lockdowns totaling 6 months, significant worsening of executive function and working memory was seen across the entire cohort (effect sizes, 0.15 and 0.51, respectively), in people with mild cognitive impairment (effect sizes, 0.13 and 0.40, respectively), and in those with a previous history of COVID-19 (effect sizes, 0.24 and 0.46, respectively).
• Worsening of working memory was sustained across the whole cohort in the second year of the pandemic after lockdowns were lifted (effect size, 0.47).
• Even after investigators removed data on people with mild cognitive impairment and COVID-19, the decline in executive function (effect size, 0.15; P < .0001) and working memory (effect size, 0.53; P < .0001) persisted.
• Cognitive decline was significantly associated with known risk factors for dementia, such as reduced exercise (P = .0049) and increased alcohol use (P = .049), across the whole cohort, as well as depression (P = .011) in those with a history of COVID-19 and loneliness (P = .0038) in those with mild cognitive impairment.

IN PRACTICE:

Investigators noted that these data add to existing knowledge of long-standing health consequences of COVID-19, especially for older people with memory problems. “On the positive note, there is evidence that lifestyle changes and improved health management can positively influence mental functioning,” study coauthor Dag Aarsland, MD, PhD, professor of old age psychiatry at the Institute of Psychiatry, Psychology & Neuroscience of King’s College London, said in a press release. “The current study underlines the importance of careful monitoring of people at risk during major events such as the pandemic.”

SOURCE:

The study was led by Anne Corbett, PhD, of University of Exeter, and was published online in The Lancet Healthy Longevity. The research was funded by the National Institute for Health and Care Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King’s College London and the NIHR Exeter Biomedical Research Centre.

LIMITATIONS:

The study relied on self-reported data. In addition, the PROTECT cohort is self-selected and may skew toward participants with higher education levels.

DISCLOSURES:

Dr. Corbett reported receiving funding from the NIHR and grants from Synexus, reMYND, and Novo Nordisk. Other disclosures are noted in the original article.
 

A version of this article appeared on Medscape.com.