Clinical Psychiatry News

BARCELONA – Running therapy rivals antidepressant medication for the treatment of depression and anxiety, results of a new study show. However, running provides greater physical health benefits while adherence is greater with drug treatment.

“Both interventions helped with the depression to around the same extent,” study presenter Brenda W.J.H. Penninx, PhD, professor of psychiatric epidemiology at the VU University Medical Center in Amsterdam said in a release.

However, medication “generally had worse impact on body weight, heart rate variability, and blood pressure, whereas running therapy led to improved effect on general fitness and heart rate,” Dr. Penninx added.

The findings were presented at the annual congress of the European College of Neuropsychopharmacology and recently published in the Journal of Affective Disorders.
 

Research gap

Previous research suggests exercise interventions can have a therapeutic effect equivalent to antidepressants, but their impact on physical health has been “poorly examined in a psychiatric population, the investigators note.

The authors note that depressive and anxiety disorders “cause immense suffering by compromising both mental and physical health,” and the need for effective treatments is “pressing.”

Although antidepressant medication is considered a “standard first-line treatment” alongside psychotherapy, the drugs are “not effective for all and [are] often associated with side effects.”

The Mood Treatment with Antidepressant or Running (MOTAR) study was a partially randomized pragmatic trial in adults with depression and/or anxiety disorder, as determined using the DSM-IV algorithms with the Composite International Diagnostic Interview (CIDI).

The 16-week intervention study included 141 patients with depression and/or anxiety. The mean age was 38.2 years and 58% were women. Participants were offered a choice of treatment: 16 weeks of treatment with the selective serotonin reuptake inhibitor (SSRI) escitalopram (Lexapro) or a 16-week group-based running therapy.

Patients without a strong preference for treatment allocation were randomly assigned to either antidepressant medication or running therapy, while those unwilling to be randomized were allocated to their preferred intervention.

A total of 22 patients were randomly assigned to receive antidepressant treatment and 13 to running therapy. A total of 36 participants chose antidepressant treatment, while 83 chose the running therapy.

Running therapy involved 16 weeks of supervised 45-minute outdoor running sessions to a target of two to three sessions per week, in line with U.S. Centers for Disease Control and Prevention/American College of Sports Medicine recommendations.
 

Physical health benefits

Treatment adherence in the antidepressant group, defined as still using treatment at the posttreatment assessment, was 82.2% vs. 52.1% among running therapy participants, where adherence was specified as completing more than 22 sessions.

Remission was defined as no longer meeting the criteria of a current depressive or anxiety disorder via CIDI at week 16.

On intention-to-treat analysis, this requirement was met by 44.8% of patients taking antidepressants and 43.3% of those in the running therapy group (P = .88).

However, running therapy patients showed significant improvements in weight (P = .001), waist circumference (P = .011), systolic and diastolic blood pressure (P = .011 and P = .002, respectively), heart rate (P = .033), and heart rate variability (P = .006).

The investigators note the more favorable physical health changes in the running therapy group were attributable to “larger improvements in the running therapy group but also due to larger deterioration in the antidepressant group.”

Antidepressants are generally safe and effective and work for most people, said Dr. Penninx. She also noted that untreated depression leads to worse outcomes, so “antidepressants are generally a good choice.”

Nevertheless, she said, “we need to extend our treatment arsenal as not all patients respond to antidepressants or are willing to take them.”

The study’s results, she added, suggest that “implementing exercise therapy is something we should take much more seriously, as it could be a good, and maybe even better, choice for some of our patients.”

Francesca Cirulli, PhD, senior researcher and group leader at the National Institute of Health, Rome, said in an interview that the study is notable because it is one of the first to prospectively measure the effects of antidepressants and running on physical health.

Dr. Cirulli suggested that running therapy could be tried ahead of treatment with antidepressants if patients prefer physical exercise and can adhere to it. However, she said, the findings also suggest that an increase in physical activity should accompany treatment with antidepressant medications.

Overall, Dr. Cirulli said “the message should not be that everyone can be helped by running and antidepressants are bad,” but rather “these are both helpful, but not excellent, interventions against depression.”
 

‘Important limitations’

In a comment, Eduard Vieta, MD, PhD, chair of the department of psychiatry and psychology at the University of Barcelona Hospital Clinic, noted the study has “very important limitations.”

Among the limitations: the inclusion of nonrandomized patients who received the treatment of their choice, causing obvious bias and the “lack of binding and power issues” over the number of patients enrolled. 

Dr. Vieta also said that the results “seem obvious, because it is known that exercise improves physical health.”

The trial therefore shows, “if you can find people who are able to do exercise while depressed and adhere to it, those would benefit from that practice,” he noted.

Also commenting on the research, Eric Ruhe, MD, PhD, Radboud University Medical Center, Nijmegen, the Netherlands, said the results are confirmatory and “again show physical health can influence mental health.”

However, Dr. Ruhe underlined, while it is “common practice” to allow patients to follow their treatment preference and is “understandable from a pragmatic point of view,” the group comparison may be “biased,” compared with a “truly randomized study.”

“For example, patients in the antidepressant group were more depressed, which might be associated with less chance of persisting engagement in the exercises,” he said. “So, we have to be careful not to overinterpret the comparisons between groups, which the authors acknowledge properly.”

Turning to the difference in adherence between the two interventions, Dr. Ruhe said the results show adopting, and adhering to, a lifestyle habit is more difficult than taking a pill.

“This is not exclusively found in psychiatry, indicating that we also have to focus on how to improve compliance to healthy behavior. This could have tremendous impact on health care more generally, but also on psychiatric diseases,” Dr. Ruhe said.

The MOTAR study was funded by a NWO-VICI grant. Funding for the inflammatory markers was provided by ZonMw: The Netherlands Organization for Health Research and Development. The study authors and clinicians interviewed for this story declared no relevant financial relationships.

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

BARCELONA – Running therapy rivals antidepressant medication for the treatment of depression and anxiety, results of a new study show. However, running provides greater physical health benefits while adherence is greater with drug treatment.

“Both interventions helped with the depression to around the same extent,” study presenter Brenda W.J.H. Penninx, PhD, professor of psychiatric epidemiology at the VU University Medical Center in Amsterdam said in a release.

However, medication “generally had worse impact on body weight, heart rate variability, and blood pressure, whereas running therapy led to improved effect on general fitness and heart rate,” Dr. Penninx added.

The findings were presented at the annual congress of the European College of Neuropsychopharmacology and recently published in the Journal of Affective Disorders.
 

Research gap

Previous research suggests exercise interventions can have a therapeutic effect equivalent to antidepressants, but their impact on physical health has been “poorly examined in a psychiatric population, the investigators note.

The authors note that depressive and anxiety disorders “cause immense suffering by compromising both mental and physical health,” and the need for effective treatments is “pressing.”

Although antidepressant medication is considered a “standard first-line treatment” alongside psychotherapy, the drugs are “not effective for all and [are] often associated with side effects.”

The Mood Treatment with Antidepressant or Running (MOTAR) study was a partially randomized pragmatic trial in adults with depression and/or anxiety disorder, as determined using the DSM-IV algorithms with the Composite International Diagnostic Interview (CIDI).

The 16-week intervention study included 141 patients with depression and/or anxiety. The mean age was 38.2 years and 58% were women. Participants were offered a choice of treatment: 16 weeks of treatment with the selective serotonin reuptake inhibitor (SSRI) escitalopram (Lexapro) or a 16-week group-based running therapy.

Patients without a strong preference for treatment allocation were randomly assigned to either antidepressant medication or running therapy, while those unwilling to be randomized were allocated to their preferred intervention.

A total of 22 patients were randomly assigned to receive antidepressant treatment and 13 to running therapy. A total of 36 participants chose antidepressant treatment, while 83 chose the running therapy.

Running therapy involved 16 weeks of supervised 45-minute outdoor running sessions to a target of two to three sessions per week, in line with U.S. Centers for Disease Control and Prevention/American College of Sports Medicine recommendations.
 

Physical health benefits

Treatment adherence in the antidepressant group, defined as still using treatment at the posttreatment assessment, was 82.2% vs. 52.1% among running therapy participants, where adherence was specified as completing more than 22 sessions.

Remission was defined as no longer meeting the criteria of a current depressive or anxiety disorder via CIDI at week 16.

On intention-to-treat analysis, this requirement was met by 44.8% of patients taking antidepressants and 43.3% of those in the running therapy group (P = .88).

However, running therapy patients showed significant improvements in weight (P = .001), waist circumference (P = .011), systolic and diastolic blood pressure (P = .011 and P = .002, respectively), heart rate (P = .033), and heart rate variability (P = .006).

The investigators note the more favorable physical health changes in the running therapy group were attributable to “larger improvements in the running therapy group but also due to larger deterioration in the antidepressant group.”

Antidepressants are generally safe and effective and work for most people, said Dr. Penninx. She also noted that untreated depression leads to worse outcomes, so “antidepressants are generally a good choice.”

Nevertheless, she said, “we need to extend our treatment arsenal as not all patients respond to antidepressants or are willing to take them.”

The study’s results, she added, suggest that “implementing exercise therapy is something we should take much more seriously, as it could be a good, and maybe even better, choice for some of our patients.”

Francesca Cirulli, PhD, senior researcher and group leader at the National Institute of Health, Rome, said in an interview that the study is notable because it is one of the first to prospectively measure the effects of antidepressants and running on physical health.

Dr. Cirulli suggested that running therapy could be tried ahead of treatment with antidepressants if patients prefer physical exercise and can adhere to it. However, she said, the findings also suggest that an increase in physical activity should accompany treatment with antidepressant medications.

Overall, Dr. Cirulli said “the message should not be that everyone can be helped by running and antidepressants are bad,” but rather “these are both helpful, but not excellent, interventions against depression.”
 

‘Important limitations’

In a comment, Eduard Vieta, MD, PhD, chair of the department of psychiatry and psychology at the University of Barcelona Hospital Clinic, noted the study has “very important limitations.”

Among the limitations: the inclusion of nonrandomized patients who received the treatment of their choice, causing obvious bias and the “lack of binding and power issues” over the number of patients enrolled. 

Dr. Vieta also said that the results “seem obvious, because it is known that exercise improves physical health.”

The trial therefore shows, “if you can find people who are able to do exercise while depressed and adhere to it, those would benefit from that practice,” he noted.

Also commenting on the research, Eric Ruhe, MD, PhD, Radboud University Medical Center, Nijmegen, the Netherlands, said the results are confirmatory and “again show physical health can influence mental health.”

However, Dr. Ruhe underlined, while it is “common practice” to allow patients to follow their treatment preference and is “understandable from a pragmatic point of view,” the group comparison may be “biased,” compared with a “truly randomized study.”

“For example, patients in the antidepressant group were more depressed, which might be associated with less chance of persisting engagement in the exercises,” he said. “So, we have to be careful not to overinterpret the comparisons between groups, which the authors acknowledge properly.”

Turning to the difference in adherence between the two interventions, Dr. Ruhe said the results show adopting, and adhering to, a lifestyle habit is more difficult than taking a pill.

“This is not exclusively found in psychiatry, indicating that we also have to focus on how to improve compliance to healthy behavior. This could have tremendous impact on health care more generally, but also on psychiatric diseases,” Dr. Ruhe said.

The MOTAR study was funded by a NWO-VICI grant. Funding for the inflammatory markers was provided by ZonMw: The Netherlands Organization for Health Research and Development. The study authors and clinicians interviewed for this story declared no relevant financial relationships.

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

BARCELONA – Running therapy rivals antidepressant medication for the treatment of depression and anxiety, results of a new study show. However, running provides greater physical health benefits while adherence is greater with drug treatment.

“Both interventions helped with the depression to around the same extent,” study presenter Brenda W.J.H. Penninx, PhD, professor of psychiatric epidemiology at the VU University Medical Center in Amsterdam said in a release.

However, medication “generally had worse impact on body weight, heart rate variability, and blood pressure, whereas running therapy led to improved effect on general fitness and heart rate,” Dr. Penninx added.

The findings were presented at the annual congress of the European College of Neuropsychopharmacology and recently published in the Journal of Affective Disorders.
 

Research gap

Previous research suggests exercise interventions can have a therapeutic effect equivalent to antidepressants, but their impact on physical health has been “poorly examined in a psychiatric population, the investigators note.

The authors note that depressive and anxiety disorders “cause immense suffering by compromising both mental and physical health,” and the need for effective treatments is “pressing.”

Although antidepressant medication is considered a “standard first-line treatment” alongside psychotherapy, the drugs are “not effective for all and [are] often associated with side effects.”

The Mood Treatment with Antidepressant or Running (MOTAR) study was a partially randomized pragmatic trial in adults with depression and/or anxiety disorder, as determined using the DSM-IV algorithms with the Composite International Diagnostic Interview (CIDI).

The 16-week intervention study included 141 patients with depression and/or anxiety. The mean age was 38.2 years and 58% were women. Participants were offered a choice of treatment: 16 weeks of treatment with the selective serotonin reuptake inhibitor (SSRI) escitalopram (Lexapro) or a 16-week group-based running therapy.

Patients without a strong preference for treatment allocation were randomly assigned to either antidepressant medication or running therapy, while those unwilling to be randomized were allocated to their preferred intervention.

A total of 22 patients were randomly assigned to receive antidepressant treatment and 13 to running therapy. A total of 36 participants chose antidepressant treatment, while 83 chose the running therapy.

Running therapy involved 16 weeks of supervised 45-minute outdoor running sessions to a target of two to three sessions per week, in line with U.S. Centers for Disease Control and Prevention/American College of Sports Medicine recommendations.
 

Physical health benefits

Treatment adherence in the antidepressant group, defined as still using treatment at the posttreatment assessment, was 82.2% vs. 52.1% among running therapy participants, where adherence was specified as completing more than 22 sessions.

Remission was defined as no longer meeting the criteria of a current depressive or anxiety disorder via CIDI at week 16.

On intention-to-treat analysis, this requirement was met by 44.8% of patients taking antidepressants and 43.3% of those in the running therapy group (P = .88).

However, running therapy patients showed significant improvements in weight (P = .001), waist circumference (P = .011), systolic and diastolic blood pressure (P = .011 and P = .002, respectively), heart rate (P = .033), and heart rate variability (P = .006).

The investigators note the more favorable physical health changes in the running therapy group were attributable to “larger improvements in the running therapy group but also due to larger deterioration in the antidepressant group.”

Antidepressants are generally safe and effective and work for most people, said Dr. Penninx. She also noted that untreated depression leads to worse outcomes, so “antidepressants are generally a good choice.”

Nevertheless, she said, “we need to extend our treatment arsenal as not all patients respond to antidepressants or are willing to take them.”

The study’s results, she added, suggest that “implementing exercise therapy is something we should take much more seriously, as it could be a good, and maybe even better, choice for some of our patients.”

Francesca Cirulli, PhD, senior researcher and group leader at the National Institute of Health, Rome, said in an interview that the study is notable because it is one of the first to prospectively measure the effects of antidepressants and running on physical health.

Dr. Cirulli suggested that running therapy could be tried ahead of treatment with antidepressants if patients prefer physical exercise and can adhere to it. However, she said, the findings also suggest that an increase in physical activity should accompany treatment with antidepressant medications.

Overall, Dr. Cirulli said “the message should not be that everyone can be helped by running and antidepressants are bad,” but rather “these are both helpful, but not excellent, interventions against depression.”
 

‘Important limitations’

In a comment, Eduard Vieta, MD, PhD, chair of the department of psychiatry and psychology at the University of Barcelona Hospital Clinic, noted the study has “very important limitations.”

Among the limitations: the inclusion of nonrandomized patients who received the treatment of their choice, causing obvious bias and the “lack of binding and power issues” over the number of patients enrolled. 

Dr. Vieta also said that the results “seem obvious, because it is known that exercise improves physical health.”

The trial therefore shows, “if you can find people who are able to do exercise while depressed and adhere to it, those would benefit from that practice,” he noted.

Also commenting on the research, Eric Ruhe, MD, PhD, Radboud University Medical Center, Nijmegen, the Netherlands, said the results are confirmatory and “again show physical health can influence mental health.”

However, Dr. Ruhe underlined, while it is “common practice” to allow patients to follow their treatment preference and is “understandable from a pragmatic point of view,” the group comparison may be “biased,” compared with a “truly randomized study.”

“For example, patients in the antidepressant group were more depressed, which might be associated with less chance of persisting engagement in the exercises,” he said. “So, we have to be careful not to overinterpret the comparisons between groups, which the authors acknowledge properly.”

Turning to the difference in adherence between the two interventions, Dr. Ruhe said the results show adopting, and adhering to, a lifestyle habit is more difficult than taking a pill.

“This is not exclusively found in psychiatry, indicating that we also have to focus on how to improve compliance to healthy behavior. This could have tremendous impact on health care more generally, but also on psychiatric diseases,” Dr. Ruhe said.

The MOTAR study was funded by a NWO-VICI grant. Funding for the inflammatory markers was provided by ZonMw: The Netherlands Organization for Health Research and Development. The study authors and clinicians interviewed for this story declared no relevant financial relationships.

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

TOPLINE:

The risk for dementia before age 90 years was significantly higher among people with a history of proton pump inhibitor (PPI) use and was highest among those diagnosed before age 70 years regardless of when PPI treatment was initiated.

METHODOLOGY:

• Researchers used four Danish registries to collect data on dementia diagnoses and prescription PPI use among 1,983,785 individuals aged 60-75 years between 2000 and 2018.
• The median follow-up time was 10.3 years.

TAKEAWAY:

• There were 99,384 (5.0%) cases of all-cause dementia during follow-up, with a median age of diagnosis of 79 years.
• Twenty-one-point-two percent of dementia cases and 18.9% of controls reported a history of PPI use.
• Risk for all-cause dementia before age 90 years was 36% higher with PPI use in people aged 60-69 years at baseline (adjusted incidence rate ratio, 1.36; 95% confidence interval, 1.29-1.43) and 6% higher in those who were age 80-89 years at baseline (aIRR, 1.06; 95% CI, 1.03-1.09).
• Investigators found significant increased dementia risk before age 90 years with PPI use regardless of when PPI treatment began and found no link between PPI use and dementia diagnoses after age 90 years.

IN PRACTICE:

“The association between PPI use and dementia was unambiguously largest among the youngest cases of dementia, potentially suggestive of a critical window of exposure where midlife PPI use affects dementia risk to a larger degree compared to late-life use,” the authors wrote. “Further, the finding could signify a declining impact of individual risk factors with advancing age owing to lengthy ongoing neuropathological processes.”

SOURCE:

Lead author of the study was Nelsan Pourhadi, MD, Danish Dementia Research Centre, department of neurology, Copenhagen University Hospital–Rigshospitalet. It was published online in Alzheimer’s and Dementia.

LIMITATIONS:

The study did not include data on PPI prescriptions before 1995, over-the-counter PPI use, and in-hospital intravenous use of PPI during the study period.

DISCLOSURES:

The study was funded by the Danish Ministry of Health. The authors reported no relevant conflicts.

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

TOPLINE:

The risk for dementia before age 90 years was significantly higher among people with a history of proton pump inhibitor (PPI) use and was highest among those diagnosed before age 70 years regardless of when PPI treatment was initiated.

METHODOLOGY:

• Researchers used four Danish registries to collect data on dementia diagnoses and prescription PPI use among 1,983,785 individuals aged 60-75 years between 2000 and 2018.
• The median follow-up time was 10.3 years.

TAKEAWAY:

• There were 99,384 (5.0%) cases of all-cause dementia during follow-up, with a median age of diagnosis of 79 years.
• Twenty-one-point-two percent of dementia cases and 18.9% of controls reported a history of PPI use.
• Risk for all-cause dementia before age 90 years was 36% higher with PPI use in people aged 60-69 years at baseline (adjusted incidence rate ratio, 1.36; 95% confidence interval, 1.29-1.43) and 6% higher in those who were age 80-89 years at baseline (aIRR, 1.06; 95% CI, 1.03-1.09).
• Investigators found significant increased dementia risk before age 90 years with PPI use regardless of when PPI treatment began and found no link between PPI use and dementia diagnoses after age 90 years.

IN PRACTICE:

“The association between PPI use and dementia was unambiguously largest among the youngest cases of dementia, potentially suggestive of a critical window of exposure where midlife PPI use affects dementia risk to a larger degree compared to late-life use,” the authors wrote. “Further, the finding could signify a declining impact of individual risk factors with advancing age owing to lengthy ongoing neuropathological processes.”

SOURCE:

Lead author of the study was Nelsan Pourhadi, MD, Danish Dementia Research Centre, department of neurology, Copenhagen University Hospital–Rigshospitalet. It was published online in Alzheimer’s and Dementia.

LIMITATIONS:

The study did not include data on PPI prescriptions before 1995, over-the-counter PPI use, and in-hospital intravenous use of PPI during the study period.

DISCLOSURES:

The study was funded by the Danish Ministry of Health. The authors reported no relevant conflicts.

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

TOPLINE:

The risk for dementia before age 90 years was significantly higher among people with a history of proton pump inhibitor (PPI) use and was highest among those diagnosed before age 70 years regardless of when PPI treatment was initiated.

METHODOLOGY:

• Researchers used four Danish registries to collect data on dementia diagnoses and prescription PPI use among 1,983,785 individuals aged 60-75 years between 2000 and 2018.
• The median follow-up time was 10.3 years.

TAKEAWAY:

• There were 99,384 (5.0%) cases of all-cause dementia during follow-up, with a median age of diagnosis of 79 years.
• Twenty-one-point-two percent of dementia cases and 18.9% of controls reported a history of PPI use.
• Risk for all-cause dementia before age 90 years was 36% higher with PPI use in people aged 60-69 years at baseline (adjusted incidence rate ratio, 1.36; 95% confidence interval, 1.29-1.43) and 6% higher in those who were age 80-89 years at baseline (aIRR, 1.06; 95% CI, 1.03-1.09).
• Investigators found significant increased dementia risk before age 90 years with PPI use regardless of when PPI treatment began and found no link between PPI use and dementia diagnoses after age 90 years.

IN PRACTICE:

“The association between PPI use and dementia was unambiguously largest among the youngest cases of dementia, potentially suggestive of a critical window of exposure where midlife PPI use affects dementia risk to a larger degree compared to late-life use,” the authors wrote. “Further, the finding could signify a declining impact of individual risk factors with advancing age owing to lengthy ongoing neuropathological processes.”

SOURCE:

Lead author of the study was Nelsan Pourhadi, MD, Danish Dementia Research Centre, department of neurology, Copenhagen University Hospital–Rigshospitalet. It was published online in Alzheimer’s and Dementia.

LIMITATIONS:

The study did not include data on PPI prescriptions before 1995, over-the-counter PPI use, and in-hospital intravenous use of PPI during the study period.

DISCLOSURES:

The study was funded by the Danish Ministry of Health. The authors reported no relevant conflicts.

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

TOPLINE:

While the prevalence of attention-deficit/hyperactivity disorder in U.S. children increased from the late 1990s to 2016, more recent data show rates remained steady at around 10% from 2017 to 2022.

METHODOLOGY:

• Based on prior data, the prevalence of ADHD in children rose from 6.1% in 1997-1998 to 10.2% in 2015-2016, with a 42.0% increase from 2003 to 2011. The new report provides updated prevalence data for 2017-2022.
• The cross-sectional analysis used data from the National Health Interview Survey (NHIS) from 2017 to 2022 for more than 37,609 U.S. children and adolescents 4-17 years old (52% male, 53% non-Hispanic White, 24% Hispanic, 11% non-Hispanic Black, and 12% non-Hispanic other race).
• Information on health care provider–diagnosed ADHD was reported by a parent or guardian.

TAKEAWAY:

• A total of 4,098 children and adolescents (10.9%) were reported to have an ADHD diagnosis during the study period.
• The weighted prevalence of ADHD ranged from 10.08% to 10.47% from 2017 to 2022, which is similar to the prevalence in 2015-2016 (10.20%).
• There was no significant change on an annual basis or in all subgroups evaluated. Notably, the estimated prevalence of ADHD among U.S. children and adolescents was higher than worldwide estimates (5.3%) in earlier years (1978-2005).
• The prevalence of ADHD in U.S. children differed significantly by age, sex, race/ethnicity, and family income, in line with previous findings, with higher rates in those 12-17 years (vs. 4-11 years), males, non-Hispanic populations, and those with higher family income.

IN PRACTICE:

The estimated ADHD prevalence remains “high” and “further investigation is warranted to assess potentially modifiable risk factors and provide adequate resources for treatment of individuals with ADHD in the future,” the authors write.

SOURCE:

The study, with first author Yanmei Li, Guangdong Pharmaceutical University, Guangzhou, China, was published online in JAMA Network Open.

LIMITATIONS:

Information on ADHD relied on parent-reported diagnosis, which may lead to misreporting and recall bias. The NHIS underwent a major redesign in 2019, which may affect comparability with prior years, and the COVID-19 pandemic affected collection in 2020.

DISCLOSURES:

The study had no specific funding. The authors reported no relevant financial relationships.

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

TOPLINE:

While the prevalence of attention-deficit/hyperactivity disorder in U.S. children increased from the late 1990s to 2016, more recent data show rates remained steady at around 10% from 2017 to 2022.

METHODOLOGY:

• Based on prior data, the prevalence of ADHD in children rose from 6.1% in 1997-1998 to 10.2% in 2015-2016, with a 42.0% increase from 2003 to 2011. The new report provides updated prevalence data for 2017-2022.
• The cross-sectional analysis used data from the National Health Interview Survey (NHIS) from 2017 to 2022 for more than 37,609 U.S. children and adolescents 4-17 years old (52% male, 53% non-Hispanic White, 24% Hispanic, 11% non-Hispanic Black, and 12% non-Hispanic other race).
• Information on health care provider–diagnosed ADHD was reported by a parent or guardian.

TAKEAWAY:

• A total of 4,098 children and adolescents (10.9%) were reported to have an ADHD diagnosis during the study period.
• The weighted prevalence of ADHD ranged from 10.08% to 10.47% from 2017 to 2022, which is similar to the prevalence in 2015-2016 (10.20%).
• There was no significant change on an annual basis or in all subgroups evaluated. Notably, the estimated prevalence of ADHD among U.S. children and adolescents was higher than worldwide estimates (5.3%) in earlier years (1978-2005).
• The prevalence of ADHD in U.S. children differed significantly by age, sex, race/ethnicity, and family income, in line with previous findings, with higher rates in those 12-17 years (vs. 4-11 years), males, non-Hispanic populations, and those with higher family income.

IN PRACTICE:

The estimated ADHD prevalence remains “high” and “further investigation is warranted to assess potentially modifiable risk factors and provide adequate resources for treatment of individuals with ADHD in the future,” the authors write.

SOURCE:

The study, with first author Yanmei Li, Guangdong Pharmaceutical University, Guangzhou, China, was published online in JAMA Network Open.

LIMITATIONS:

Information on ADHD relied on parent-reported diagnosis, which may lead to misreporting and recall bias. The NHIS underwent a major redesign in 2019, which may affect comparability with prior years, and the COVID-19 pandemic affected collection in 2020.

DISCLOSURES:

The study had no specific funding. The authors reported no relevant financial relationships.

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

TOPLINE:

While the prevalence of attention-deficit/hyperactivity disorder in U.S. children increased from the late 1990s to 2016, more recent data show rates remained steady at around 10% from 2017 to 2022.

METHODOLOGY:

• Based on prior data, the prevalence of ADHD in children rose from 6.1% in 1997-1998 to 10.2% in 2015-2016, with a 42.0% increase from 2003 to 2011. The new report provides updated prevalence data for 2017-2022.
• The cross-sectional analysis used data from the National Health Interview Survey (NHIS) from 2017 to 2022 for more than 37,609 U.S. children and adolescents 4-17 years old (52% male, 53% non-Hispanic White, 24% Hispanic, 11% non-Hispanic Black, and 12% non-Hispanic other race).
• Information on health care provider–diagnosed ADHD was reported by a parent or guardian.

TAKEAWAY:

• A total of 4,098 children and adolescents (10.9%) were reported to have an ADHD diagnosis during the study period.
• The weighted prevalence of ADHD ranged from 10.08% to 10.47% from 2017 to 2022, which is similar to the prevalence in 2015-2016 (10.20%).
• There was no significant change on an annual basis or in all subgroups evaluated. Notably, the estimated prevalence of ADHD among U.S. children and adolescents was higher than worldwide estimates (5.3%) in earlier years (1978-2005).
• The prevalence of ADHD in U.S. children differed significantly by age, sex, race/ethnicity, and family income, in line with previous findings, with higher rates in those 12-17 years (vs. 4-11 years), males, non-Hispanic populations, and those with higher family income.

IN PRACTICE:

The estimated ADHD prevalence remains “high” and “further investigation is warranted to assess potentially modifiable risk factors and provide adequate resources for treatment of individuals with ADHD in the future,” the authors write.

SOURCE:

The study, with first author Yanmei Li, Guangdong Pharmaceutical University, Guangzhou, China, was published online in JAMA Network Open.

LIMITATIONS:

Information on ADHD relied on parent-reported diagnosis, which may lead to misreporting and recall bias. The NHIS underwent a major redesign in 2019, which may affect comparability with prior years, and the COVID-19 pandemic affected collection in 2020.

DISCLOSURES:

The study had no specific funding. The authors reported no relevant financial relationships.

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

The widening threat of the animal tranquilizer xylazine, otherwise known as tranq, which has been found in illegally manufactured fentanyl, necessitates wider testing, a better understanding of its effects, and more research on treatment options, according to a narrative review published in the Annals of Internal Medicine.

“A lot of doctors and providers are asking about this drug,” said Joseph D’Orazio, MD, an addiction medicine specialist and medical toxicologist at Cooper University Healthcare, Camden, N.J., who led the review.

Xylazine is believed to prolong or intensify the effects of opioids, making it a popular additive to illegally produced opioids, particularly fentanyl, according to the Drug Enforcement Administration. Users end up in a zombie-like state with slowed breathing, and they sometimes develop skin ulcers. Because xylazine is not an opioid, common antidotes such as naloxone are ineffective. The White House has called the fentanyl-xylazine combo an “emerging threat.”

“Xylazine is making the deadliest drug threat our country has ever faced, fentanyl, even deadlier,” said DEA administrator Anne Milgram, in a statement on the agency’s website. “DEA has seized xylazine and fentanyl mixtures in 48 of 50 States. The DEA Laboratory System is reporting that in 2022 approximately 23% of fentanyl powder and 7% of fentanyl pills seized by the DEA contained xylazine.”

Dr. D’Orazio paired clinical experience with available research to provide guidance on the care of patients exposed to xylazine.

He and his team issued a call for more research on the drug’s effects, including more details on dependency and withdrawal.

Testing a patient who may have been exposed to xylazine requires forensic lab capabilities, which makes testing complicated and costly. The review found no evidence of the origin of the drug or why it causes open sores.

The review calls for more education of providers, including primary care physicians, on the treatment and care of patients who have used xylazine and fentanyl. The authors also call for expanding standard urine analysis to test for xylazine and for intensifying surveillance of the drug supply and distribution of xylazine test strips.

The authors of an editorial that accompanied the journal article urged the health care community to get ahead of xylazine before the crisis worsens.

“Not testing for xylazine in current unaffected areas and populations may lead to delays in responding if and when the drug becomes prevalent in the drug supply,” the authors wrote.

Xylazine was detected in 90% of street opioid samples tested in Philadelphia in 2021, and a toxic surveillance study of drug paraphernalia in Maryland found xylazine in 80% of samples tested between 2021 and 2022.

Dr. D’Orazio stressed that although Narcan is ineffective in treating xylazine, because the sedative is almost always mixed with fentanyl or another opiate, the opioid antagonist should still be used in emergencies.

Angelique Campen, MD, an emergency medicine physician at Providence St. Joseph Medical Center, Burbank, Calif., said she has seen an increase in patients entering the emergency department under the influence of what seems like fentanyl or heroin, but standard treatments such as Narcan have a limited effect. These patients remain in a prolonged period of sedation.

Recently, she admitted to her hospital’s intensive care unit a patient suspected of a xylazine overdose who was not responding to treatment.

Dr. Campen said that patients are screened for fentanyl, but because no test is available for xylazine, she presumed xylazine was causing the complication.

“It makes perfect medical sense to me that that’s what was going on,” Dr. Campen, who has worked at St. Joseph’s for 25 years, said. “I’m hoping with physicians being more aware of it that we can have that part of our regular urine drug screen.”

Dr. Campen also said she hopes an antidote is soon developed.

“If we can just keep delivering that message, hopefully, [to] more and more people, it will get through to them,” she said. “Every time you’re taking this, even though you may have taken it a week before and been fine, you never know: The next dose you take may be the lethal dose.”

A review author reports being awarded $1,000 to cover travel cost for Best Overall Abstract at the American Society of Addiction Medicine 2023 Annual Meeting. Another author reports receiving payments for training conducted as part of a NJDMAHS training grant to educate on substance use disorders. Dr. D’Orazio reports a $500 honorarium for a one-time lecture on xylazine at Yale; and a $500 honorarium for speaking one to three times per year on various topics regarding opioid use disorder at the Health Federation of Philadelphia. No other disclosures were reported.

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

The widening threat of the animal tranquilizer xylazine, otherwise known as tranq, which has been found in illegally manufactured fentanyl, necessitates wider testing, a better understanding of its effects, and more research on treatment options, according to a narrative review published in the Annals of Internal Medicine.

“A lot of doctors and providers are asking about this drug,” said Joseph D’Orazio, MD, an addiction medicine specialist and medical toxicologist at Cooper University Healthcare, Camden, N.J., who led the review.

Xylazine is believed to prolong or intensify the effects of opioids, making it a popular additive to illegally produced opioids, particularly fentanyl, according to the Drug Enforcement Administration. Users end up in a zombie-like state with slowed breathing, and they sometimes develop skin ulcers. Because xylazine is not an opioid, common antidotes such as naloxone are ineffective. The White House has called the fentanyl-xylazine combo an “emerging threat.”

“Xylazine is making the deadliest drug threat our country has ever faced, fentanyl, even deadlier,” said DEA administrator Anne Milgram, in a statement on the agency’s website. “DEA has seized xylazine and fentanyl mixtures in 48 of 50 States. The DEA Laboratory System is reporting that in 2022 approximately 23% of fentanyl powder and 7% of fentanyl pills seized by the DEA contained xylazine.”

Dr. D’Orazio paired clinical experience with available research to provide guidance on the care of patients exposed to xylazine.

He and his team issued a call for more research on the drug’s effects, including more details on dependency and withdrawal.

Testing a patient who may have been exposed to xylazine requires forensic lab capabilities, which makes testing complicated and costly. The review found no evidence of the origin of the drug or why it causes open sores.

The review calls for more education of providers, including primary care physicians, on the treatment and care of patients who have used xylazine and fentanyl. The authors also call for expanding standard urine analysis to test for xylazine and for intensifying surveillance of the drug supply and distribution of xylazine test strips.

The authors of an editorial that accompanied the journal article urged the health care community to get ahead of xylazine before the crisis worsens.

“Not testing for xylazine in current unaffected areas and populations may lead to delays in responding if and when the drug becomes prevalent in the drug supply,” the authors wrote.

Xylazine was detected in 90% of street opioid samples tested in Philadelphia in 2021, and a toxic surveillance study of drug paraphernalia in Maryland found xylazine in 80% of samples tested between 2021 and 2022.

Dr. D’Orazio stressed that although Narcan is ineffective in treating xylazine, because the sedative is almost always mixed with fentanyl or another opiate, the opioid antagonist should still be used in emergencies.

Angelique Campen, MD, an emergency medicine physician at Providence St. Joseph Medical Center, Burbank, Calif., said she has seen an increase in patients entering the emergency department under the influence of what seems like fentanyl or heroin, but standard treatments such as Narcan have a limited effect. These patients remain in a prolonged period of sedation.

Recently, she admitted to her hospital’s intensive care unit a patient suspected of a xylazine overdose who was not responding to treatment.

Dr. Campen said that patients are screened for fentanyl, but because no test is available for xylazine, she presumed xylazine was causing the complication.

“It makes perfect medical sense to me that that’s what was going on,” Dr. Campen, who has worked at St. Joseph’s for 25 years, said. “I’m hoping with physicians being more aware of it that we can have that part of our regular urine drug screen.”

Dr. Campen also said she hopes an antidote is soon developed.

“If we can just keep delivering that message, hopefully, [to] more and more people, it will get through to them,” she said. “Every time you’re taking this, even though you may have taken it a week before and been fine, you never know: The next dose you take may be the lethal dose.”

A review author reports being awarded $1,000 to cover travel cost for Best Overall Abstract at the American Society of Addiction Medicine 2023 Annual Meeting. Another author reports receiving payments for training conducted as part of a NJDMAHS training grant to educate on substance use disorders. Dr. D’Orazio reports a $500 honorarium for a one-time lecture on xylazine at Yale; and a $500 honorarium for speaking one to three times per year on various topics regarding opioid use disorder at the Health Federation of Philadelphia. No other disclosures were reported.

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

The widening threat of the animal tranquilizer xylazine, otherwise known as tranq, which has been found in illegally manufactured fentanyl, necessitates wider testing, a better understanding of its effects, and more research on treatment options, according to a narrative review published in the Annals of Internal Medicine.

“A lot of doctors and providers are asking about this drug,” said Joseph D’Orazio, MD, an addiction medicine specialist and medical toxicologist at Cooper University Healthcare, Camden, N.J., who led the review.

Xylazine is believed to prolong or intensify the effects of opioids, making it a popular additive to illegally produced opioids, particularly fentanyl, according to the Drug Enforcement Administration. Users end up in a zombie-like state with slowed breathing, and they sometimes develop skin ulcers. Because xylazine is not an opioid, common antidotes such as naloxone are ineffective. The White House has called the fentanyl-xylazine combo an “emerging threat.”

“Xylazine is making the deadliest drug threat our country has ever faced, fentanyl, even deadlier,” said DEA administrator Anne Milgram, in a statement on the agency’s website. “DEA has seized xylazine and fentanyl mixtures in 48 of 50 States. The DEA Laboratory System is reporting that in 2022 approximately 23% of fentanyl powder and 7% of fentanyl pills seized by the DEA contained xylazine.”

Dr. D’Orazio paired clinical experience with available research to provide guidance on the care of patients exposed to xylazine.

He and his team issued a call for more research on the drug’s effects, including more details on dependency and withdrawal.

Testing a patient who may have been exposed to xylazine requires forensic lab capabilities, which makes testing complicated and costly. The review found no evidence of the origin of the drug or why it causes open sores.

The review calls for more education of providers, including primary care physicians, on the treatment and care of patients who have used xylazine and fentanyl. The authors also call for expanding standard urine analysis to test for xylazine and for intensifying surveillance of the drug supply and distribution of xylazine test strips.

The authors of an editorial that accompanied the journal article urged the health care community to get ahead of xylazine before the crisis worsens.

“Not testing for xylazine in current unaffected areas and populations may lead to delays in responding if and when the drug becomes prevalent in the drug supply,” the authors wrote.

Xylazine was detected in 90% of street opioid samples tested in Philadelphia in 2021, and a toxic surveillance study of drug paraphernalia in Maryland found xylazine in 80% of samples tested between 2021 and 2022.

Dr. D’Orazio stressed that although Narcan is ineffective in treating xylazine, because the sedative is almost always mixed with fentanyl or another opiate, the opioid antagonist should still be used in emergencies.

Angelique Campen, MD, an emergency medicine physician at Providence St. Joseph Medical Center, Burbank, Calif., said she has seen an increase in patients entering the emergency department under the influence of what seems like fentanyl or heroin, but standard treatments such as Narcan have a limited effect. These patients remain in a prolonged period of sedation.

Recently, she admitted to her hospital’s intensive care unit a patient suspected of a xylazine overdose who was not responding to treatment.

Dr. Campen said that patients are screened for fentanyl, but because no test is available for xylazine, she presumed xylazine was causing the complication.

“It makes perfect medical sense to me that that’s what was going on,” Dr. Campen, who has worked at St. Joseph’s for 25 years, said. “I’m hoping with physicians being more aware of it that we can have that part of our regular urine drug screen.”

Dr. Campen also said she hopes an antidote is soon developed.

“If we can just keep delivering that message, hopefully, [to] more and more people, it will get through to them,” she said. “Every time you’re taking this, even though you may have taken it a week before and been fine, you never know: The next dose you take may be the lethal dose.”

A review author reports being awarded $1,000 to cover travel cost for Best Overall Abstract at the American Society of Addiction Medicine 2023 Annual Meeting. Another author reports receiving payments for training conducted as part of a NJDMAHS training grant to educate on substance use disorders. Dr. D’Orazio reports a $500 honorarium for a one-time lecture on xylazine at Yale; and a $500 honorarium for speaking one to three times per year on various topics regarding opioid use disorder at the Health Federation of Philadelphia. No other disclosures were reported.

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

The poster child for a burned-out physician is a young woman practicing in primary care, according to a new study of more than 1,300 clinicians.

The study, published in JAMA Network Open. investigated patterns in physician burnout among 1,373 physicians at Massachusetts General Physicians Organization, a hospital-owned group practice. It assessed burnout in 3 years: 2017, 2019, and 2021.

Rates of burnout appear to be worsening; they increased from 44% to 50% between 2017 and 2021. Respondents were queried about their satisfaction with their career and compensation, as well as their well-being, administrative workload, and leadership and diversity.

Female physicians exhibited a higher burnout rate than male physicians (odds ratio, 1.47; 95% confidence interval, 1.02-2.12), while among primary care physicians (PCPs), the burnout rate was almost three times higher than among those in internal medicine (OR, 2.82; 95% CI, 1.76-4.50). Among physicians with 30 or more years of experience, the burnout rate was lower than among those with 10 years of experience or less (OR, 0.21; 95% CI, 0.13-0.35).

The fact that burnout disproportionately affects female physicians could reflect the additional household and family obligations women are often expected to handle, as well as their desire to form relationships with their patients, according to Timothy Hoff, PhD, a professor of management, healthcare systems, and health policy at Northeastern University, Boston.

“Female physicians tend to practice differently than their male counterparts,” said Dr. Hoff, who studies primary care. “They may focus more on the relational aspects of care, and that could lead to a higher rate of burnout.”

The study used the Maslach Burnout Inventory and three burnout subscales: exhaustion, cynicism, and reduced personal efficacy. The cohort was composed of 50% men, 67% White respondents, and 87% non-Hispanic respondents. A little over two-thirds of physicians had from 11 to 20 years of experience.

About 93% of those surveyed responded; by comparison, response rates were between 27% and 32% in previous analyses of physician burnout, the study authors say. They attribute this high participation rate to the fact that they compensated each participant with $850, more than is usually offered.

Hilton Gomes, MD, a partner at a concierge primary care practice in Miami – who has been practicing medicine for more than 15 years – said the increased rates of burnout among his younger colleagues are partly the result of a recent shift in what is considered the ideal work-life balance.

“Younger generations of doctors enter the profession with a strong desire for a better work-life balance. Unfortunately, medicine does not typically lend itself to achieving this balance,” he said.

Dr. Gomes recalled a time in medical school when he tried to visit his former pediatrician, who couldn’t be found at home.

“His wife informed me that he was tending to an urgent sick visit at the hospital, while his wife had to deal with their own grandson’s fracture being treated at urgent care,” Dr. Gomes said. “This illustrates, in my experience, how older generations of physicians accepted the demands of the profession as part of their commitment, and this often involved putting our own families second.”

Dr. Gomes, like many other PCPs who have converted to concierge medicine, previously worked at a practice where he saw nearly two dozen patients a day for a maximum of 15 minutes each.

“The structure of managed care often results in primary care physicians spending less time with patients and more time on paperwork, which is not the reason why physicians enter the field of medicine,” Dr. Gomes said.

Physicians are not alone in their feelings of physical and mental exhaustion. In the Medscape Physician Assistant Burnout Report 2023, 16% of respondents said the burnout they experienced was so severe that they were thinking of leaving medicine.

In 2022, PCP burnout cost the United States $260 million in excess health care expenditures. Burnout has also increased rates of physician suicide over the past 50 years and has led to a rise in medical errors.

Physicians say that programs that teach them to perform yoga and take deep breaths – which are offered by their employers – are not the solution.

“We sort of know what the realities of physician burnout are now; the imperative is to address it,” Dr. Hoff said. “We need studies that focus on the concepts of sustainability.”

The study was funded by the Massachusetts General Physicians Organization. A coauthor reports receiving a grant from the American Heart Association. No other disclosures were reported.

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

The poster child for a burned-out physician is a young woman practicing in primary care, according to a new study of more than 1,300 clinicians.

The study, published in JAMA Network Open. investigated patterns in physician burnout among 1,373 physicians at Massachusetts General Physicians Organization, a hospital-owned group practice. It assessed burnout in 3 years: 2017, 2019, and 2021.

Rates of burnout appear to be worsening; they increased from 44% to 50% between 2017 and 2021. Respondents were queried about their satisfaction with their career and compensation, as well as their well-being, administrative workload, and leadership and diversity.

Female physicians exhibited a higher burnout rate than male physicians (odds ratio, 1.47; 95% confidence interval, 1.02-2.12), while among primary care physicians (PCPs), the burnout rate was almost three times higher than among those in internal medicine (OR, 2.82; 95% CI, 1.76-4.50). Among physicians with 30 or more years of experience, the burnout rate was lower than among those with 10 years of experience or less (OR, 0.21; 95% CI, 0.13-0.35).

The fact that burnout disproportionately affects female physicians could reflect the additional household and family obligations women are often expected to handle, as well as their desire to form relationships with their patients, according to Timothy Hoff, PhD, a professor of management, healthcare systems, and health policy at Northeastern University, Boston.

“Female physicians tend to practice differently than their male counterparts,” said Dr. Hoff, who studies primary care. “They may focus more on the relational aspects of care, and that could lead to a higher rate of burnout.”

The study used the Maslach Burnout Inventory and three burnout subscales: exhaustion, cynicism, and reduced personal efficacy. The cohort was composed of 50% men, 67% White respondents, and 87% non-Hispanic respondents. A little over two-thirds of physicians had from 11 to 20 years of experience.

About 93% of those surveyed responded; by comparison, response rates were between 27% and 32% in previous analyses of physician burnout, the study authors say. They attribute this high participation rate to the fact that they compensated each participant with $850, more than is usually offered.

Hilton Gomes, MD, a partner at a concierge primary care practice in Miami – who has been practicing medicine for more than 15 years – said the increased rates of burnout among his younger colleagues are partly the result of a recent shift in what is considered the ideal work-life balance.

“Younger generations of doctors enter the profession with a strong desire for a better work-life balance. Unfortunately, medicine does not typically lend itself to achieving this balance,” he said.

Dr. Gomes recalled a time in medical school when he tried to visit his former pediatrician, who couldn’t be found at home.

“His wife informed me that he was tending to an urgent sick visit at the hospital, while his wife had to deal with their own grandson’s fracture being treated at urgent care,” Dr. Gomes said. “This illustrates, in my experience, how older generations of physicians accepted the demands of the profession as part of their commitment, and this often involved putting our own families second.”

Dr. Gomes, like many other PCPs who have converted to concierge medicine, previously worked at a practice where he saw nearly two dozen patients a day for a maximum of 15 minutes each.

“The structure of managed care often results in primary care physicians spending less time with patients and more time on paperwork, which is not the reason why physicians enter the field of medicine,” Dr. Gomes said.

Physicians are not alone in their feelings of physical and mental exhaustion. In the Medscape Physician Assistant Burnout Report 2023, 16% of respondents said the burnout they experienced was so severe that they were thinking of leaving medicine.

In 2022, PCP burnout cost the United States $260 million in excess health care expenditures. Burnout has also increased rates of physician suicide over the past 50 years and has led to a rise in medical errors.

Physicians say that programs that teach them to perform yoga and take deep breaths – which are offered by their employers – are not the solution.

“We sort of know what the realities of physician burnout are now; the imperative is to address it,” Dr. Hoff said. “We need studies that focus on the concepts of sustainability.”

The study was funded by the Massachusetts General Physicians Organization. A coauthor reports receiving a grant from the American Heart Association. No other disclosures were reported.

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

The poster child for a burned-out physician is a young woman practicing in primary care, according to a new study of more than 1,300 clinicians.

The study, published in JAMA Network Open. investigated patterns in physician burnout among 1,373 physicians at Massachusetts General Physicians Organization, a hospital-owned group practice. It assessed burnout in 3 years: 2017, 2019, and 2021.

Rates of burnout appear to be worsening; they increased from 44% to 50% between 2017 and 2021. Respondents were queried about their satisfaction with their career and compensation, as well as their well-being, administrative workload, and leadership and diversity.

Female physicians exhibited a higher burnout rate than male physicians (odds ratio, 1.47; 95% confidence interval, 1.02-2.12), while among primary care physicians (PCPs), the burnout rate was almost three times higher than among those in internal medicine (OR, 2.82; 95% CI, 1.76-4.50). Among physicians with 30 or more years of experience, the burnout rate was lower than among those with 10 years of experience or less (OR, 0.21; 95% CI, 0.13-0.35).

The fact that burnout disproportionately affects female physicians could reflect the additional household and family obligations women are often expected to handle, as well as their desire to form relationships with their patients, according to Timothy Hoff, PhD, a professor of management, healthcare systems, and health policy at Northeastern University, Boston.

“Female physicians tend to practice differently than their male counterparts,” said Dr. Hoff, who studies primary care. “They may focus more on the relational aspects of care, and that could lead to a higher rate of burnout.”

The study used the Maslach Burnout Inventory and three burnout subscales: exhaustion, cynicism, and reduced personal efficacy. The cohort was composed of 50% men, 67% White respondents, and 87% non-Hispanic respondents. A little over two-thirds of physicians had from 11 to 20 years of experience.

About 93% of those surveyed responded; by comparison, response rates were between 27% and 32% in previous analyses of physician burnout, the study authors say. They attribute this high participation rate to the fact that they compensated each participant with $850, more than is usually offered.

Hilton Gomes, MD, a partner at a concierge primary care practice in Miami – who has been practicing medicine for more than 15 years – said the increased rates of burnout among his younger colleagues are partly the result of a recent shift in what is considered the ideal work-life balance.

“Younger generations of doctors enter the profession with a strong desire for a better work-life balance. Unfortunately, medicine does not typically lend itself to achieving this balance,” he said.

Dr. Gomes recalled a time in medical school when he tried to visit his former pediatrician, who couldn’t be found at home.

“His wife informed me that he was tending to an urgent sick visit at the hospital, while his wife had to deal with their own grandson’s fracture being treated at urgent care,” Dr. Gomes said. “This illustrates, in my experience, how older generations of physicians accepted the demands of the profession as part of their commitment, and this often involved putting our own families second.”

Dr. Gomes, like many other PCPs who have converted to concierge medicine, previously worked at a practice where he saw nearly two dozen patients a day for a maximum of 15 minutes each.

“The structure of managed care often results in primary care physicians spending less time with patients and more time on paperwork, which is not the reason why physicians enter the field of medicine,” Dr. Gomes said.

Physicians are not alone in their feelings of physical and mental exhaustion. In the Medscape Physician Assistant Burnout Report 2023, 16% of respondents said the burnout they experienced was so severe that they were thinking of leaving medicine.

In 2022, PCP burnout cost the United States $260 million in excess health care expenditures. Burnout has also increased rates of physician suicide over the past 50 years and has led to a rise in medical errors.

Physicians say that programs that teach them to perform yoga and take deep breaths – which are offered by their employers – are not the solution.

“We sort of know what the realities of physician burnout are now; the imperative is to address it,” Dr. Hoff said. “We need studies that focus on the concepts of sustainability.”

The study was funded by the Massachusetts General Physicians Organization. A coauthor reports receiving a grant from the American Heart Association. No other disclosures were reported.

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

Damaged mitochondrial DNA (mtDNA) initiates and spreads Parkinson’s disease (PD) pathology, potentially opening new avenues for early diagnosis, disease monitoring, and drug development.

While defects in mitochondrial functions and in mitochondrial DNA have been implicated in PD in the past, the current study demonstrates “for the first time how damaged mitochondrial DNA can underlie the mechanisms of PD initiation and spread in brain,” lead investigator Shohreh Issazadeh-Navikas, PhD, with the University of Copenhagen, told this news organization.

“This has direct implication for clinical diagnosis” – if damaged mtDNA can be detected in blood, it could serve as an early biomarker for disease, she explained.

The study was published online in Molecular Psychiatry.
 

“Infectious-like” spread of PD pathology

In earlier work, the researchers identified dysregulated interferon-beta (IFN-beta) signaling as a “top candidate pathway” associated with sporadic PD and its progression to PD with dementia (PDD).

In mice PD models that were deficient in IFN-beta signaling, the investigators showed that neuronal IFN-beta is required to maintain mitochondrial homeostasis and metabolism.

Lack of neuronal IFN-beta or disruption of its downstream signaling causes the accumulation of damaged mitochondria with excessive oxidative stress and insufficient adenosine triphosphate production.

In the current study, using postmortem brain tissue samples from patients with sporadic PD, they confirmed that there were deletions of mtDNA in the medial frontal gyrus, a region implicated in cognitive impairments in PD, suggesting a potential role of damaged mtDNA in disease pathophysiology.

They also identified mtDNA deletions in a “hotspot” in complex I respiratory chain subunits that were associated with dysregulation of oxidative stress and DNA damage response pathways in cohorts with sporadic PD and PDD.

They confirmed the contribution of mtDNA damage to PD pathology in the PD mouse models. They showed that lack of neuronal IFN-beta signaling leads to oxidative damage and mutations in mtDNA in neurons, which are subsequently released outside the neurons.

Injecting damaged mtDNA into mouse brain induced PDD-like behavioral symptoms, including neuropsychiatric, motor, and cognitive impairments. It also caused neurodegeneration in brain regions distant from the injection site, suggesting that damaged mtDNA triggers spread of PDD characteristics in an “infectious-like” manner, the researchers report.

Further study revealed that the mechanism through which damaged mtDNA causes pathology in healthy neurons involves dual activation of Toll-like receptor (TLR) 9 and 4 pathways, leading to increased oxidative stress and neuronal cell death, respectively.

“Our proteomic analysis of extracellular vesicles containing damaged mtDNA identified the TLR4 activator, ribosomal protein S3, as a key protein involved in recognizing and extruding damaged mtDNA,” the investigators write.

In the future they plan to investigate how mtDNA damage can serve as a predictive marker for different disease stages and progression and to explore potential therapeutic strategies aimed at restoring normal mitochondrial function to rectify the mitochondrial dysfunctions implicated in PD.
 

Making a comeback?

Commenting on the research for this news organization, James Beck, PhD, chief scientific officer at the Parkinson’s Foundation, noted that the role of mitochondria in PD is “like a starlet that burst onto the scene in the 80s, faded into obscurity, and through diligence and continued research has moved beyond being a solid character actor and is reemerging as a force to reckon with.

“This paper only adds to the allure that mitochondria may have in contributing to PD by providing evidence of a novel process by which mitochondria may be not only contributing to PD and loss of dopamine neurons but may play a larger role in the subsequent effects that many people with PD experience – dementia,” Dr. Beck said.

He noted that the authors identified several proteins as facilitating the neurodegeneration that is wrought by damaged mitochondrial DNA.

“These could be potential targets for future drug development. In addition, this work implicates alterations in immune signaling and drugs in development to target inflammatory responses may also bring ancillary benefit,” Dr. Beck said.

However, he said, “while very interesting findings, this is really the first effort that demonstrates how damaged mitochondrial DNA may contribute to neurodegeneration in the context of PD and PD dementia. Further work needs to validate these findings as well as to elucidate mechanisms underlying the propagation of the mitochondrial DNA from cell to cell.”

Funding for this research was provided by the European Union’s Horizon 2020 Research and Innovation Program, the Lundbeck Foundation, and the Danish Council for Independent Research–Medicine. Dr. Issazadeh-Navikas and Dr. Beck have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Damaged mitochondrial DNA (mtDNA) initiates and spreads Parkinson’s disease (PD) pathology, potentially opening new avenues for early diagnosis, disease monitoring, and drug development.

While defects in mitochondrial functions and in mitochondrial DNA have been implicated in PD in the past, the current study demonstrates “for the first time how damaged mitochondrial DNA can underlie the mechanisms of PD initiation and spread in brain,” lead investigator Shohreh Issazadeh-Navikas, PhD, with the University of Copenhagen, told this news organization.

“This has direct implication for clinical diagnosis” – if damaged mtDNA can be detected in blood, it could serve as an early biomarker for disease, she explained.

The study was published online in Molecular Psychiatry.
 

“Infectious-like” spread of PD pathology

In earlier work, the researchers identified dysregulated interferon-beta (IFN-beta) signaling as a “top candidate pathway” associated with sporadic PD and its progression to PD with dementia (PDD).

In mice PD models that were deficient in IFN-beta signaling, the investigators showed that neuronal IFN-beta is required to maintain mitochondrial homeostasis and metabolism.

Lack of neuronal IFN-beta or disruption of its downstream signaling causes the accumulation of damaged mitochondria with excessive oxidative stress and insufficient adenosine triphosphate production.

In the current study, using postmortem brain tissue samples from patients with sporadic PD, they confirmed that there were deletions of mtDNA in the medial frontal gyrus, a region implicated in cognitive impairments in PD, suggesting a potential role of damaged mtDNA in disease pathophysiology.

They also identified mtDNA deletions in a “hotspot” in complex I respiratory chain subunits that were associated with dysregulation of oxidative stress and DNA damage response pathways in cohorts with sporadic PD and PDD.

They confirmed the contribution of mtDNA damage to PD pathology in the PD mouse models. They showed that lack of neuronal IFN-beta signaling leads to oxidative damage and mutations in mtDNA in neurons, which are subsequently released outside the neurons.

Injecting damaged mtDNA into mouse brain induced PDD-like behavioral symptoms, including neuropsychiatric, motor, and cognitive impairments. It also caused neurodegeneration in brain regions distant from the injection site, suggesting that damaged mtDNA triggers spread of PDD characteristics in an “infectious-like” manner, the researchers report.

Further study revealed that the mechanism through which damaged mtDNA causes pathology in healthy neurons involves dual activation of Toll-like receptor (TLR) 9 and 4 pathways, leading to increased oxidative stress and neuronal cell death, respectively.

“Our proteomic analysis of extracellular vesicles containing damaged mtDNA identified the TLR4 activator, ribosomal protein S3, as a key protein involved in recognizing and extruding damaged mtDNA,” the investigators write.

In the future they plan to investigate how mtDNA damage can serve as a predictive marker for different disease stages and progression and to explore potential therapeutic strategies aimed at restoring normal mitochondrial function to rectify the mitochondrial dysfunctions implicated in PD.
 

Making a comeback?

Commenting on the research for this news organization, James Beck, PhD, chief scientific officer at the Parkinson’s Foundation, noted that the role of mitochondria in PD is “like a starlet that burst onto the scene in the 80s, faded into obscurity, and through diligence and continued research has moved beyond being a solid character actor and is reemerging as a force to reckon with.

“This paper only adds to the allure that mitochondria may have in contributing to PD by providing evidence of a novel process by which mitochondria may be not only contributing to PD and loss of dopamine neurons but may play a larger role in the subsequent effects that many people with PD experience – dementia,” Dr. Beck said.

He noted that the authors identified several proteins as facilitating the neurodegeneration that is wrought by damaged mitochondrial DNA.

“These could be potential targets for future drug development. In addition, this work implicates alterations in immune signaling and drugs in development to target inflammatory responses may also bring ancillary benefit,” Dr. Beck said.

However, he said, “while very interesting findings, this is really the first effort that demonstrates how damaged mitochondrial DNA may contribute to neurodegeneration in the context of PD and PD dementia. Further work needs to validate these findings as well as to elucidate mechanisms underlying the propagation of the mitochondrial DNA from cell to cell.”

Funding for this research was provided by the European Union’s Horizon 2020 Research and Innovation Program, the Lundbeck Foundation, and the Danish Council for Independent Research–Medicine. Dr. Issazadeh-Navikas and Dr. Beck have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Damaged mitochondrial DNA (mtDNA) initiates and spreads Parkinson’s disease (PD) pathology, potentially opening new avenues for early diagnosis, disease monitoring, and drug development.

While defects in mitochondrial functions and in mitochondrial DNA have been implicated in PD in the past, the current study demonstrates “for the first time how damaged mitochondrial DNA can underlie the mechanisms of PD initiation and spread in brain,” lead investigator Shohreh Issazadeh-Navikas, PhD, with the University of Copenhagen, told this news organization.

“This has direct implication for clinical diagnosis” – if damaged mtDNA can be detected in blood, it could serve as an early biomarker for disease, she explained.

The study was published online in Molecular Psychiatry.
 

“Infectious-like” spread of PD pathology

In earlier work, the researchers identified dysregulated interferon-beta (IFN-beta) signaling as a “top candidate pathway” associated with sporadic PD and its progression to PD with dementia (PDD).

In mice PD models that were deficient in IFN-beta signaling, the investigators showed that neuronal IFN-beta is required to maintain mitochondrial homeostasis and metabolism.

Lack of neuronal IFN-beta or disruption of its downstream signaling causes the accumulation of damaged mitochondria with excessive oxidative stress and insufficient adenosine triphosphate production.

In the current study, using postmortem brain tissue samples from patients with sporadic PD, they confirmed that there were deletions of mtDNA in the medial frontal gyrus, a region implicated in cognitive impairments in PD, suggesting a potential role of damaged mtDNA in disease pathophysiology.

They also identified mtDNA deletions in a “hotspot” in complex I respiratory chain subunits that were associated with dysregulation of oxidative stress and DNA damage response pathways in cohorts with sporadic PD and PDD.

They confirmed the contribution of mtDNA damage to PD pathology in the PD mouse models. They showed that lack of neuronal IFN-beta signaling leads to oxidative damage and mutations in mtDNA in neurons, which are subsequently released outside the neurons.

Injecting damaged mtDNA into mouse brain induced PDD-like behavioral symptoms, including neuropsychiatric, motor, and cognitive impairments. It also caused neurodegeneration in brain regions distant from the injection site, suggesting that damaged mtDNA triggers spread of PDD characteristics in an “infectious-like” manner, the researchers report.

Further study revealed that the mechanism through which damaged mtDNA causes pathology in healthy neurons involves dual activation of Toll-like receptor (TLR) 9 and 4 pathways, leading to increased oxidative stress and neuronal cell death, respectively.

“Our proteomic analysis of extracellular vesicles containing damaged mtDNA identified the TLR4 activator, ribosomal protein S3, as a key protein involved in recognizing and extruding damaged mtDNA,” the investigators write.

In the future they plan to investigate how mtDNA damage can serve as a predictive marker for different disease stages and progression and to explore potential therapeutic strategies aimed at restoring normal mitochondrial function to rectify the mitochondrial dysfunctions implicated in PD.
 

Making a comeback?

Commenting on the research for this news organization, James Beck, PhD, chief scientific officer at the Parkinson’s Foundation, noted that the role of mitochondria in PD is “like a starlet that burst onto the scene in the 80s, faded into obscurity, and through diligence and continued research has moved beyond being a solid character actor and is reemerging as a force to reckon with.

“This paper only adds to the allure that mitochondria may have in contributing to PD by providing evidence of a novel process by which mitochondria may be not only contributing to PD and loss of dopamine neurons but may play a larger role in the subsequent effects that many people with PD experience – dementia,” Dr. Beck said.

He noted that the authors identified several proteins as facilitating the neurodegeneration that is wrought by damaged mitochondrial DNA.

“These could be potential targets for future drug development. In addition, this work implicates alterations in immune signaling and drugs in development to target inflammatory responses may also bring ancillary benefit,” Dr. Beck said.

However, he said, “while very interesting findings, this is really the first effort that demonstrates how damaged mitochondrial DNA may contribute to neurodegeneration in the context of PD and PD dementia. Further work needs to validate these findings as well as to elucidate mechanisms underlying the propagation of the mitochondrial DNA from cell to cell.”

Funding for this research was provided by the European Union’s Horizon 2020 Research and Innovation Program, the Lundbeck Foundation, and the Danish Council for Independent Research–Medicine. Dr. Issazadeh-Navikas and Dr. Beck have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

TOPLINE:

People with a history of depression or stress were significantly more likely to be diagnosed with mild cognitive impairment (MCI) or Alzheimer’s disease (AD) later in life compared with those without either condition, a new study found.

METHODOLOGY:

• Longitudinal cohort study of 1,362,548 people with records in the Region Stockholm administrative health care database with a diagnosis of stress-induced exhaustion disorder (SED), depression, or both between 2012 and 2013.
• Cohort followed for diagnosis of MCI or AD between 2014 and 2022.

TAKEAWAY:

• SED diagnosed in 0.3%, depression in 2.9% and both SED and depression in 0.1%
• Compared with people without SED or depression, AD risk was more than double in patients with SED (adjusted odds ratio [aOR], 2.45; 99% confidence interval [CI], 1.22-4.91) or depression (aOR, 2.32; 99% CI, 1.85-2.90) and four times higher in patients with both SED and depression (aOR, 4.00; 99% CI, 1.67-9.58)
• Risk for MCI was also higher in people with SED (aOR, 1.87; 99% CI,1.20-2.91), depression (aOR, 2.85; 99% CI, 2.53-3.22) or both SED and depression (aOR, 3.87; 99% CI, 2.39-6.27) vs patients with no history of SED or depression.
• Only patients with depression had a higher risk for another dementia type (aOR, 2.39; 99% CI, 1.92-2.96).

IN PRACTICE:

“Future studies should examine the possibility that symptoms of depression and/or chronic stress could be prodromal symptoms of dementia rather than risk factors,” study authors wrote.

SOURCE:

The study was conducted by Johanna Wallensten, doctoral student, department of clinical sciences, Danderyd Hospital, Stockholm, and colleagues and funded by the Karolinska Institute. It was published online in Alzheimer’s Research and Therapy.

LIMITATIONS:

Use of a health care registry could have led to over- or underestimation of depression, MCI and AD. The study probably captures most people with depression but not most people with depressive symptoms.

DISCLOSURES:

The authors reported no relevant conflicts.

A version of this article appeared on Medscape.com.

TOPLINE:

People with a history of depression or stress were significantly more likely to be diagnosed with mild cognitive impairment (MCI) or Alzheimer’s disease (AD) later in life compared with those without either condition, a new study found.

METHODOLOGY:

• Longitudinal cohort study of 1,362,548 people with records in the Region Stockholm administrative health care database with a diagnosis of stress-induced exhaustion disorder (SED), depression, or both between 2012 and 2013.
• Cohort followed for diagnosis of MCI or AD between 2014 and 2022.

TAKEAWAY:

• SED diagnosed in 0.3%, depression in 2.9% and both SED and depression in 0.1%
• Compared with people without SED or depression, AD risk was more than double in patients with SED (adjusted odds ratio [aOR], 2.45; 99% confidence interval [CI], 1.22-4.91) or depression (aOR, 2.32; 99% CI, 1.85-2.90) and four times higher in patients with both SED and depression (aOR, 4.00; 99% CI, 1.67-9.58)
• Risk for MCI was also higher in people with SED (aOR, 1.87; 99% CI,1.20-2.91), depression (aOR, 2.85; 99% CI, 2.53-3.22) or both SED and depression (aOR, 3.87; 99% CI, 2.39-6.27) vs patients with no history of SED or depression.
• Only patients with depression had a higher risk for another dementia type (aOR, 2.39; 99% CI, 1.92-2.96).

IN PRACTICE:

“Future studies should examine the possibility that symptoms of depression and/or chronic stress could be prodromal symptoms of dementia rather than risk factors,” study authors wrote.

SOURCE:

The study was conducted by Johanna Wallensten, doctoral student, department of clinical sciences, Danderyd Hospital, Stockholm, and colleagues and funded by the Karolinska Institute. It was published online in Alzheimer’s Research and Therapy.

LIMITATIONS:

Use of a health care registry could have led to over- or underestimation of depression, MCI and AD. The study probably captures most people with depression but not most people with depressive symptoms.

DISCLOSURES:

The authors reported no relevant conflicts.

A version of this article appeared on Medscape.com.

TOPLINE:

People with a history of depression or stress were significantly more likely to be diagnosed with mild cognitive impairment (MCI) or Alzheimer’s disease (AD) later in life compared with those without either condition, a new study found.

METHODOLOGY:

• Longitudinal cohort study of 1,362,548 people with records in the Region Stockholm administrative health care database with a diagnosis of stress-induced exhaustion disorder (SED), depression, or both between 2012 and 2013.
• Cohort followed for diagnosis of MCI or AD between 2014 and 2022.

TAKEAWAY:

• SED diagnosed in 0.3%, depression in 2.9% and both SED and depression in 0.1%
• Compared with people without SED or depression, AD risk was more than double in patients with SED (adjusted odds ratio [aOR], 2.45; 99% confidence interval [CI], 1.22-4.91) or depression (aOR, 2.32; 99% CI, 1.85-2.90) and four times higher in patients with both SED and depression (aOR, 4.00; 99% CI, 1.67-9.58)
• Risk for MCI was also higher in people with SED (aOR, 1.87; 99% CI,1.20-2.91), depression (aOR, 2.85; 99% CI, 2.53-3.22) or both SED and depression (aOR, 3.87; 99% CI, 2.39-6.27) vs patients with no history of SED or depression.
• Only patients with depression had a higher risk for another dementia type (aOR, 2.39; 99% CI, 1.92-2.96).

IN PRACTICE:

“Future studies should examine the possibility that symptoms of depression and/or chronic stress could be prodromal symptoms of dementia rather than risk factors,” study authors wrote.

SOURCE:

The study was conducted by Johanna Wallensten, doctoral student, department of clinical sciences, Danderyd Hospital, Stockholm, and colleagues and funded by the Karolinska Institute. It was published online in Alzheimer’s Research and Therapy.

LIMITATIONS:

Use of a health care registry could have led to over- or underestimation of depression, MCI and AD. The study probably captures most people with depression but not most people with depressive symptoms.

DISCLOSURES:

The authors reported no relevant conflicts.

A version of this article appeared on Medscape.com.

In a large prospective study, a graded higher risk of all-cause mortality and mortality from cardiovascular disease (CVD) and ischemic heart disease (IHD) emerged in adults with moderate to severe depressive symptoms, compared with those with no such symptoms.

Participants with mild depressive symptoms had a 35%-49% higher risk of all-cause and CVD mortality, respectively, while for those with moderate to severe depressive symptoms, the risk of all-cause, CVD, and IHD mortality was 62%, 79%, and 121% higher, respectively.

Dr. Zefeng Zhang, CDC

“This information highlights the importance for clinicians to identify patients with depressive symptoms and help them engage in treatment,” lead author Zefeng Zhang, MD, PhD, of the division for heart disease and stroke prevention at the U.S. Centers for Disease Control and Prevention, Atlanta, said in an interview.

The study appears in JAMA Network Open.

A nonclassic risk factor for CVD death

This graded positive association between depressive symptoms and CVD death was observed in data from the National Health and Nutrition Examination Survey 2005-2018, which were linked with the National Death Index through 2019 for adults aged 20 and older. Data analysis occurred from March 1 to May 26, 2023. According to the authors, their analyses extend findings from previous research by assessing these associations in a large, diverse, and nationally representative sample. Using more nuanced CVD-related causes of death, depressive symptoms emerged as a nontraditional risk factor for CVD mortality.

The study

In a total cohort of 23,694, about half male, mean overall age 44.7 years, prevalences of mild and moderate to severe depression were 14.9% and 7.2%, respectively, with depressive symptoms assessed by the nine-item Patient Health Questionnaire asking about symptoms over the past 2 weeks.

Adults with depression had significantly lower CV health scores in six of the American Heart Association Life’s Essential 8 metrics for heart health. For all-cause mortality, hazard ratios were 1.35 (95% confidence interval, 1.07-1.72) for mild depressive symptoms vs. none and 1.62 (95% CI, 1.24-2.12) for moderate to severe depressive symptoms vs. none.

The corresponding hazard ratios were 1.49 (95% CI, 1.11-2.0) and 1.79 (95% CI,1.22-2.62) for CVD mortality and 0.96 (95% CI, 0.58-1.60) and 2.21 (95% CI, 1.24-3.91) for IHD death, with associations largely consistent across subgroups.

At the highest severity of depressive symptoms (almost daily for past 2 weeks), feeling tired or having little energy, poor appetite or overeating, and having little interest in doing things were significantly associated with all-cause and CVD mortality after adjusting for potential confounders.

Approximately 11%-16% of the positive associations could be explained by lifestyle factors such as excess alcohol consumption, overeating, and inactivity as per the AHA’s Life’s Essential 8 metrics.

“Taken together with the body of literature on associations between depression and CVD mortality, these findings can support public health efforts to develop a comprehensive, nationwide strategy to improve well-being, including both mental and cardiovascular health,” Dr. Zhang and associates wrote.

This research was funded by the U.S. Centers for Disease Control and Prevention. The authors had no conflicts of interest to disclose.

In a large prospective study, a graded higher risk of all-cause mortality and mortality from cardiovascular disease (CVD) and ischemic heart disease (IHD) emerged in adults with moderate to severe depressive symptoms, compared with those with no such symptoms.

Participants with mild depressive symptoms had a 35%-49% higher risk of all-cause and CVD mortality, respectively, while for those with moderate to severe depressive symptoms, the risk of all-cause, CVD, and IHD mortality was 62%, 79%, and 121% higher, respectively.

Dr. Zefeng Zhang, CDC

“This information highlights the importance for clinicians to identify patients with depressive symptoms and help them engage in treatment,” lead author Zefeng Zhang, MD, PhD, of the division for heart disease and stroke prevention at the U.S. Centers for Disease Control and Prevention, Atlanta, said in an interview.

The study appears in JAMA Network Open.

A nonclassic risk factor for CVD death

This graded positive association between depressive symptoms and CVD death was observed in data from the National Health and Nutrition Examination Survey 2005-2018, which were linked with the National Death Index through 2019 for adults aged 20 and older. Data analysis occurred from March 1 to May 26, 2023. According to the authors, their analyses extend findings from previous research by assessing these associations in a large, diverse, and nationally representative sample. Using more nuanced CVD-related causes of death, depressive symptoms emerged as a nontraditional risk factor for CVD mortality.

The study

In a total cohort of 23,694, about half male, mean overall age 44.7 years, prevalences of mild and moderate to severe depression were 14.9% and 7.2%, respectively, with depressive symptoms assessed by the nine-item Patient Health Questionnaire asking about symptoms over the past 2 weeks.

Adults with depression had significantly lower CV health scores in six of the American Heart Association Life’s Essential 8 metrics for heart health. For all-cause mortality, hazard ratios were 1.35 (95% confidence interval, 1.07-1.72) for mild depressive symptoms vs. none and 1.62 (95% CI, 1.24-2.12) for moderate to severe depressive symptoms vs. none.

The corresponding hazard ratios were 1.49 (95% CI, 1.11-2.0) and 1.79 (95% CI,1.22-2.62) for CVD mortality and 0.96 (95% CI, 0.58-1.60) and 2.21 (95% CI, 1.24-3.91) for IHD death, with associations largely consistent across subgroups.

At the highest severity of depressive symptoms (almost daily for past 2 weeks), feeling tired or having little energy, poor appetite or overeating, and having little interest in doing things were significantly associated with all-cause and CVD mortality after adjusting for potential confounders.

Approximately 11%-16% of the positive associations could be explained by lifestyle factors such as excess alcohol consumption, overeating, and inactivity as per the AHA’s Life’s Essential 8 metrics.

“Taken together with the body of literature on associations between depression and CVD mortality, these findings can support public health efforts to develop a comprehensive, nationwide strategy to improve well-being, including both mental and cardiovascular health,” Dr. Zhang and associates wrote.

This research was funded by the U.S. Centers for Disease Control and Prevention. The authors had no conflicts of interest to disclose.

In a large prospective study, a graded higher risk of all-cause mortality and mortality from cardiovascular disease (CVD) and ischemic heart disease (IHD) emerged in adults with moderate to severe depressive symptoms, compared with those with no such symptoms.

Participants with mild depressive symptoms had a 35%-49% higher risk of all-cause and CVD mortality, respectively, while for those with moderate to severe depressive symptoms, the risk of all-cause, CVD, and IHD mortality was 62%, 79%, and 121% higher, respectively.

Dr. Zefeng Zhang, CDC

“This information highlights the importance for clinicians to identify patients with depressive symptoms and help them engage in treatment,” lead author Zefeng Zhang, MD, PhD, of the division for heart disease and stroke prevention at the U.S. Centers for Disease Control and Prevention, Atlanta, said in an interview.

The study appears in JAMA Network Open.

A nonclassic risk factor for CVD death

This graded positive association between depressive symptoms and CVD death was observed in data from the National Health and Nutrition Examination Survey 2005-2018, which were linked with the National Death Index through 2019 for adults aged 20 and older. Data analysis occurred from March 1 to May 26, 2023. According to the authors, their analyses extend findings from previous research by assessing these associations in a large, diverse, and nationally representative sample. Using more nuanced CVD-related causes of death, depressive symptoms emerged as a nontraditional risk factor for CVD mortality.

The study

In a total cohort of 23,694, about half male, mean overall age 44.7 years, prevalences of mild and moderate to severe depression were 14.9% and 7.2%, respectively, with depressive symptoms assessed by the nine-item Patient Health Questionnaire asking about symptoms over the past 2 weeks.

Adults with depression had significantly lower CV health scores in six of the American Heart Association Life’s Essential 8 metrics for heart health. For all-cause mortality, hazard ratios were 1.35 (95% confidence interval, 1.07-1.72) for mild depressive symptoms vs. none and 1.62 (95% CI, 1.24-2.12) for moderate to severe depressive symptoms vs. none.

The corresponding hazard ratios were 1.49 (95% CI, 1.11-2.0) and 1.79 (95% CI,1.22-2.62) for CVD mortality and 0.96 (95% CI, 0.58-1.60) and 2.21 (95% CI, 1.24-3.91) for IHD death, with associations largely consistent across subgroups.

At the highest severity of depressive symptoms (almost daily for past 2 weeks), feeling tired or having little energy, poor appetite or overeating, and having little interest in doing things were significantly associated with all-cause and CVD mortality after adjusting for potential confounders.

Approximately 11%-16% of the positive associations could be explained by lifestyle factors such as excess alcohol consumption, overeating, and inactivity as per the AHA’s Life’s Essential 8 metrics.

“Taken together with the body of literature on associations between depression and CVD mortality, these findings can support public health efforts to develop a comprehensive, nationwide strategy to improve well-being, including both mental and cardiovascular health,” Dr. Zhang and associates wrote.

This research was funded by the U.S. Centers for Disease Control and Prevention. The authors had no conflicts of interest to disclose.

Evaluation of temperament in mental health outpatients showed a significant association between the irritable temperament type and a diagnosis of bipolar I and bipolar II disorders, based on data from more than 1,700 individuals.

When German psychiatrist Emil Kraepelin (1856-1926) studied emotions in patients with affective disorders, he identified four temperaments: the depressive (DT), the hyperthymic (HT), the irritable (IT), and the cyclothymic (CT). Subsequent researchers later identified an anxious temperament (AT).

“The notion that temperaments can be useful in predicting bipolar disorders sparked a plethora of research,” wrote Elie G. Karam, MD, of Saint George Hospital, Beirut, and colleagues. In particular, the cyclothymic (CT) and irritable (IT) temperament types have been targeted in studies of patients with bipolar disorders, but previous studies of temperament and bipolar have been limited by methodological issues, they said.

In a study published in European Psychiatry, the researchers reviewed data from 1,723 consecutive adult outpatients who presented to a university-based mental health clinic with various symptoms between January 2014 and September 2019.

Patients were assessed using the Hypomania Checklist-32 (HCL-32) and the Temperament Evaluation of Memphis, Pisa, Paris, and San Diego-Auto-questionnaire (TEMPS-A), then were diagnosed by psychiatrists using DSM-5 criteria. Patients with any bipolar types as defined by the DSM-5 underwent simple and multiple binary logistic regression analyses. The analysis included continuous scores and categorical normalized z-scores.

A total of 369 patients had confirmed DSM-5 diagnosis of bipolar disorder (52 with type I, 176 with type II, 102 with other specified bipolar and related disorder, and 39 with substance- or medication-induced bipolar disorder. The mean age of the participants was 38 years, and 54% were female.

In a bivariate analysis, all continuous temperament scores were significant predictors of bipolar disorder; all except AT remained significant in multivariate analysis. Increasing scores of IT, CT, and HT were associated with bipolar disorder, but increasing scores of DT were reflective of lower chance of bipolar disorder, the researchers noted.

In multivariate analysis of categorical normalized z-scores, IT and CT were significant predictors of bipolar disorder. At the highest point, CT was the stronger predictor, compared with IT (odds ratio, 3.84 vs. 2.55); having a higher DT score significantly reduced the odds of bipolar disorder (OR, 0.50).

However, “after adjusting for the presence of all temperaments as well as age and gender, only IT remained a significant predictor of patients with bipolar I disorder with adjusted OR of 1.19,” the researchers wrote.

“Correlations among temperaments were solid whether looking at patients with bipolarity or not, further emphasizing the necessity of controlling for them,” the researchers wrote in their discussion.

The findings were limited by several factors including the lack of structured interviews, the use of an outpatient-only sample, and the small number of bipolar I patients, the researchers noted.

However, the result suggest that IT can serve as a predictor of bipolar I and bipolar II disorders they said. Given the underdiagnosis of bipolar disorder in many studies, the incorporation of temperaments into the assessment of patients and research participants alike is likely to help us detect the presence of bipolarity more readily and quite importantly help us in our quest to understand their genesis,” they concluded.

The study was supported in part by anonymous private unrestricted donations to IDRAAC, Lebanon, and by Eli Lilly. The researchers had no financial conflicts to disclose.

Evaluation of temperament in mental health outpatients showed a significant association between the irritable temperament type and a diagnosis of bipolar I and bipolar II disorders, based on data from more than 1,700 individuals.

When German psychiatrist Emil Kraepelin (1856-1926) studied emotions in patients with affective disorders, he identified four temperaments: the depressive (DT), the hyperthymic (HT), the irritable (IT), and the cyclothymic (CT). Subsequent researchers later identified an anxious temperament (AT).

“The notion that temperaments can be useful in predicting bipolar disorders sparked a plethora of research,” wrote Elie G. Karam, MD, of Saint George Hospital, Beirut, and colleagues. In particular, the cyclothymic (CT) and irritable (IT) temperament types have been targeted in studies of patients with bipolar disorders, but previous studies of temperament and bipolar have been limited by methodological issues, they said.

In a study published in European Psychiatry, the researchers reviewed data from 1,723 consecutive adult outpatients who presented to a university-based mental health clinic with various symptoms between January 2014 and September 2019.

Patients were assessed using the Hypomania Checklist-32 (HCL-32) and the Temperament Evaluation of Memphis, Pisa, Paris, and San Diego-Auto-questionnaire (TEMPS-A), then were diagnosed by psychiatrists using DSM-5 criteria. Patients with any bipolar types as defined by the DSM-5 underwent simple and multiple binary logistic regression analyses. The analysis included continuous scores and categorical normalized z-scores.

A total of 369 patients had confirmed DSM-5 diagnosis of bipolar disorder (52 with type I, 176 with type II, 102 with other specified bipolar and related disorder, and 39 with substance- or medication-induced bipolar disorder. The mean age of the participants was 38 years, and 54% were female.

In a bivariate analysis, all continuous temperament scores were significant predictors of bipolar disorder; all except AT remained significant in multivariate analysis. Increasing scores of IT, CT, and HT were associated with bipolar disorder, but increasing scores of DT were reflective of lower chance of bipolar disorder, the researchers noted.

In multivariate analysis of categorical normalized z-scores, IT and CT were significant predictors of bipolar disorder. At the highest point, CT was the stronger predictor, compared with IT (odds ratio, 3.84 vs. 2.55); having a higher DT score significantly reduced the odds of bipolar disorder (OR, 0.50).

However, “after adjusting for the presence of all temperaments as well as age and gender, only IT remained a significant predictor of patients with bipolar I disorder with adjusted OR of 1.19,” the researchers wrote.

“Correlations among temperaments were solid whether looking at patients with bipolarity or not, further emphasizing the necessity of controlling for them,” the researchers wrote in their discussion.

The findings were limited by several factors including the lack of structured interviews, the use of an outpatient-only sample, and the small number of bipolar I patients, the researchers noted.

However, the result suggest that IT can serve as a predictor of bipolar I and bipolar II disorders they said. Given the underdiagnosis of bipolar disorder in many studies, the incorporation of temperaments into the assessment of patients and research participants alike is likely to help us detect the presence of bipolarity more readily and quite importantly help us in our quest to understand their genesis,” they concluded.

The study was supported in part by anonymous private unrestricted donations to IDRAAC, Lebanon, and by Eli Lilly. The researchers had no financial conflicts to disclose.

Evaluation of temperament in mental health outpatients showed a significant association between the irritable temperament type and a diagnosis of bipolar I and bipolar II disorders, based on data from more than 1,700 individuals.

When German psychiatrist Emil Kraepelin (1856-1926) studied emotions in patients with affective disorders, he identified four temperaments: the depressive (DT), the hyperthymic (HT), the irritable (IT), and the cyclothymic (CT). Subsequent researchers later identified an anxious temperament (AT).

“The notion that temperaments can be useful in predicting bipolar disorders sparked a plethora of research,” wrote Elie G. Karam, MD, of Saint George Hospital, Beirut, and colleagues. In particular, the cyclothymic (CT) and irritable (IT) temperament types have been targeted in studies of patients with bipolar disorders, but previous studies of temperament and bipolar have been limited by methodological issues, they said.

In a study published in European Psychiatry, the researchers reviewed data from 1,723 consecutive adult outpatients who presented to a university-based mental health clinic with various symptoms between January 2014 and September 2019.

Patients were assessed using the Hypomania Checklist-32 (HCL-32) and the Temperament Evaluation of Memphis, Pisa, Paris, and San Diego-Auto-questionnaire (TEMPS-A), then were diagnosed by psychiatrists using DSM-5 criteria. Patients with any bipolar types as defined by the DSM-5 underwent simple and multiple binary logistic regression analyses. The analysis included continuous scores and categorical normalized z-scores.

A total of 369 patients had confirmed DSM-5 diagnosis of bipolar disorder (52 with type I, 176 with type II, 102 with other specified bipolar and related disorder, and 39 with substance- or medication-induced bipolar disorder. The mean age of the participants was 38 years, and 54% were female.

In a bivariate analysis, all continuous temperament scores were significant predictors of bipolar disorder; all except AT remained significant in multivariate analysis. Increasing scores of IT, CT, and HT were associated with bipolar disorder, but increasing scores of DT were reflective of lower chance of bipolar disorder, the researchers noted.

In multivariate analysis of categorical normalized z-scores, IT and CT were significant predictors of bipolar disorder. At the highest point, CT was the stronger predictor, compared with IT (odds ratio, 3.84 vs. 2.55); having a higher DT score significantly reduced the odds of bipolar disorder (OR, 0.50).

However, “after adjusting for the presence of all temperaments as well as age and gender, only IT remained a significant predictor of patients with bipolar I disorder with adjusted OR of 1.19,” the researchers wrote.

“Correlations among temperaments were solid whether looking at patients with bipolarity or not, further emphasizing the necessity of controlling for them,” the researchers wrote in their discussion.

The findings were limited by several factors including the lack of structured interviews, the use of an outpatient-only sample, and the small number of bipolar I patients, the researchers noted.

However, the result suggest that IT can serve as a predictor of bipolar I and bipolar II disorders they said. Given the underdiagnosis of bipolar disorder in many studies, the incorporation of temperaments into the assessment of patients and research participants alike is likely to help us detect the presence of bipolarity more readily and quite importantly help us in our quest to understand their genesis,” they concluded.

The study was supported in part by anonymous private unrestricted donations to IDRAAC, Lebanon, and by Eli Lilly. The researchers had no financial conflicts to disclose.

TOPLINE:

Individuals who visited the ER for substance-induced psychosis had a 160% greater risk of developing a schizophrenia spectrum disorder (SSD), compared with the general population, new research shows. Three years after an initial ER visit, 18.5% of those with substance-induced psychosis were diagnosed with an SSD. Cannabis-induced psychosis was associated with the greatest risk.

METHODOLOGY:

• In this retrospective, population-based cohort study, investigators evaluated the risk of transition to a diagnosis of SSD for individuals with an ER visit for substance use versus the general population.
• Investigators at The Ottawa Hospital and the Institute for Clinical Evaluative Sciences, both in Ontario, analyzed data from six linked databases containing health information on nearly 10 million Ontario residents aged 14-65 years eligible for medical coverage.
• Investigators collected the health data between January 2008 and March 2022 on residents with substance use–related ER visits with, and without, psychosis.

TAKEAWAY:

• There were nearly 408,000 individuals with an ER visit for substance use, of which 13,800 (3.4%) of the visits were for substance-induced psychosis.
• Individuals with substance-induced psychosis were at a 163-fold (age- and sex-adjusted hazard ratio, 163.2; 95% confidence interval, 156.1-170.5) increased risk of transitioning to an SSD, relative to the general population (3-year risk, 18.5% vs. 0.1%).
• Individuals with an ER visit for substance use without psychosis had a lower relative risk of transitioning (aHR, 9.8; 95% CI, 9.5-10.2; 3-year risk, 1.4%) but incurred more than three times the absolute number of transitions (9,969 vs. 3,029).
• ER visits related to cannabis use had the highest transition risk among visits with psychosis (aHR, 241.6; 95% CI, 225.5-258.9) and the third-highest risk among visits without psychosis (aHR, 14.3; 95% CI, 13.5-15.2).
• Younger age and male sex were associated with a higher risk of transition, and the risk of male sex was greater in younger, compared with older, individuals particularly for cannabis use.

IN PRACTICE:

“Primary prevention efforts aimed at reducing substance use and substance use disorders could substantially reduce the population-level burden of chronic psychoses,” the investigators write. “Our findings also highlight the need for targeted secondary prevention providing early intervention and reducing substance use in the highest-risk groups, which may delay or prevent transition to schizophrenia spectrum disorders.”

SOURCE:

Daniel T. Myran, MD, MPH, of the Ottawa Hospital Research Institute, led the study, which was funded by the Canadian Institutes of Health Research and the University of Ottawa department of family medicine. The study was published online in JAMA Psychiatry.

LIMITATIONS:

Investigators did not have access to detailed data on substance-related outpatient visits or patterns of substance use, which could provide additional prognostic information.

DISCLOSURES:

Dr. Myran reported receiving grants from the Canadian Institutes of Health Research during the conduct of the study. Dr. Solmi reported receiving honoraria for participation on advisory boards or presentations from AbbVie, Angelini, Lundbeck, and Otsuka outside the submitted work. The remaining authors have disclosed no relevant financial relationships.

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

TOPLINE:

Individuals who visited the ER for substance-induced psychosis had a 160% greater risk of developing a schizophrenia spectrum disorder (SSD), compared with the general population, new research shows. Three years after an initial ER visit, 18.5% of those with substance-induced psychosis were diagnosed with an SSD. Cannabis-induced psychosis was associated with the greatest risk.

METHODOLOGY:

• In this retrospective, population-based cohort study, investigators evaluated the risk of transition to a diagnosis of SSD for individuals with an ER visit for substance use versus the general population.
• Investigators at The Ottawa Hospital and the Institute for Clinical Evaluative Sciences, both in Ontario, analyzed data from six linked databases containing health information on nearly 10 million Ontario residents aged 14-65 years eligible for medical coverage.
• Investigators collected the health data between January 2008 and March 2022 on residents with substance use–related ER visits with, and without, psychosis.

TAKEAWAY:

• There were nearly 408,000 individuals with an ER visit for substance use, of which 13,800 (3.4%) of the visits were for substance-induced psychosis.
• Individuals with substance-induced psychosis were at a 163-fold (age- and sex-adjusted hazard ratio, 163.2; 95% confidence interval, 156.1-170.5) increased risk of transitioning to an SSD, relative to the general population (3-year risk, 18.5% vs. 0.1%).
• Individuals with an ER visit for substance use without psychosis had a lower relative risk of transitioning (aHR, 9.8; 95% CI, 9.5-10.2; 3-year risk, 1.4%) but incurred more than three times the absolute number of transitions (9,969 vs. 3,029).
• ER visits related to cannabis use had the highest transition risk among visits with psychosis (aHR, 241.6; 95% CI, 225.5-258.9) and the third-highest risk among visits without psychosis (aHR, 14.3; 95% CI, 13.5-15.2).
• Younger age and male sex were associated with a higher risk of transition, and the risk of male sex was greater in younger, compared with older, individuals particularly for cannabis use.

IN PRACTICE:

“Primary prevention efforts aimed at reducing substance use and substance use disorders could substantially reduce the population-level burden of chronic psychoses,” the investigators write. “Our findings also highlight the need for targeted secondary prevention providing early intervention and reducing substance use in the highest-risk groups, which may delay or prevent transition to schizophrenia spectrum disorders.”

SOURCE:

Daniel T. Myran, MD, MPH, of the Ottawa Hospital Research Institute, led the study, which was funded by the Canadian Institutes of Health Research and the University of Ottawa department of family medicine. The study was published online in JAMA Psychiatry.

LIMITATIONS:

Investigators did not have access to detailed data on substance-related outpatient visits or patterns of substance use, which could provide additional prognostic information.

DISCLOSURES:

Dr. Myran reported receiving grants from the Canadian Institutes of Health Research during the conduct of the study. Dr. Solmi reported receiving honoraria for participation on advisory boards or presentations from AbbVie, Angelini, Lundbeck, and Otsuka outside the submitted work. The remaining authors have disclosed no relevant financial relationships.

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

TOPLINE:

Individuals who visited the ER for substance-induced psychosis had a 160% greater risk of developing a schizophrenia spectrum disorder (SSD), compared with the general population, new research shows. Three years after an initial ER visit, 18.5% of those with substance-induced psychosis were diagnosed with an SSD. Cannabis-induced psychosis was associated with the greatest risk.

METHODOLOGY:

• In this retrospective, population-based cohort study, investigators evaluated the risk of transition to a diagnosis of SSD for individuals with an ER visit for substance use versus the general population.
• Investigators at The Ottawa Hospital and the Institute for Clinical Evaluative Sciences, both in Ontario, analyzed data from six linked databases containing health information on nearly 10 million Ontario residents aged 14-65 years eligible for medical coverage.
• Investigators collected the health data between January 2008 and March 2022 on residents with substance use–related ER visits with, and without, psychosis.

TAKEAWAY:

• There were nearly 408,000 individuals with an ER visit for substance use, of which 13,800 (3.4%) of the visits were for substance-induced psychosis.
• Individuals with substance-induced psychosis were at a 163-fold (age- and sex-adjusted hazard ratio, 163.2; 95% confidence interval, 156.1-170.5) increased risk of transitioning to an SSD, relative to the general population (3-year risk, 18.5% vs. 0.1%).
• Individuals with an ER visit for substance use without psychosis had a lower relative risk of transitioning (aHR, 9.8; 95% CI, 9.5-10.2; 3-year risk, 1.4%) but incurred more than three times the absolute number of transitions (9,969 vs. 3,029).
• ER visits related to cannabis use had the highest transition risk among visits with psychosis (aHR, 241.6; 95% CI, 225.5-258.9) and the third-highest risk among visits without psychosis (aHR, 14.3; 95% CI, 13.5-15.2).
• Younger age and male sex were associated with a higher risk of transition, and the risk of male sex was greater in younger, compared with older, individuals particularly for cannabis use.

IN PRACTICE:

“Primary prevention efforts aimed at reducing substance use and substance use disorders could substantially reduce the population-level burden of chronic psychoses,” the investigators write. “Our findings also highlight the need for targeted secondary prevention providing early intervention and reducing substance use in the highest-risk groups, which may delay or prevent transition to schizophrenia spectrum disorders.”

SOURCE:

Daniel T. Myran, MD, MPH, of the Ottawa Hospital Research Institute, led the study, which was funded by the Canadian Institutes of Health Research and the University of Ottawa department of family medicine. The study was published online in JAMA Psychiatry.

LIMITATIONS:

Investigators did not have access to detailed data on substance-related outpatient visits or patterns of substance use, which could provide additional prognostic information.

DISCLOSURES:

Dr. Myran reported receiving grants from the Canadian Institutes of Health Research during the conduct of the study. Dr. Solmi reported receiving honoraria for participation on advisory boards or presentations from AbbVie, Angelini, Lundbeck, and Otsuka outside the submitted work. The remaining authors have disclosed no relevant financial relationships.

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