Mental Health

In the first study of its kind, U.K. and French researchers reported that exercise positively affected physical and cognitive health in persons with Down syndrome. “The findings are significant and offer a crucial challenge to the [Down syndrome] and wider societies,” wrote a team led by Dan Gordon, PhD, associate professor of cardiorespiratory exercise physiology at Anglia Ruskin University in Cambridge, England. “Impact of Prescribed Exercise on the Physical and Cognitive Health of Adults with Down Syndrome: The MinDSets Study” was published in the International Journal of Environmental Research and Public Health.

“Through the simple application of walking, a form of exercise which requires little to no equipment or expense, there were significant increases in cognitive and executive function, reflecting improved capabilities in key attributes of information processing, vigilance, and selective attention,” the researchers wrote.

Dr. Gordon

“Increased cognitive function will help foster increased societal integration and quality of life, which, given that this is the first generation of those with [Down syndrome] to outlive their parents and caregivers, is of importance,” they wrote.

For example, those in an exercise-only intervention arm had an 11.4% improvement on the distance covered in the Six-Minute Walk Test, going from a mean of 498.8 meters before intervention to 522.1 meters afterward. Those in a group that combined group exercise with cognitive training increased the distance walked by 9.9%, or 49.2 meters. Groups that got cognitive training only or no intervention showed no significant changes.

In measures of cognitive function, the exercise group showed a 38% increase in selective attention, with the cognitive and combined groups showing changes for the same measure of 16.5% and 55.3%, respectively. The changes for concentration in the exercise-alone group was 31.5%, while those receiving cognitive training alone or combined exercise plus cognitive training showed improvements in concentration of 21% and 15%, respectively.

Asked why a combination intervention was not superior to exercise alone, Dr. Gordon said in an interview, “Something we’re looking at in the data but can’t fully confirm is that the combined group started to become fatigued due to the double dose of the intervention, and this prevented them in the final tests from doing quite so well as the exercise-alone group. Irrespective of the magnitude of change, any cognitive adaptation observed will be beneficial to this population.”

The evidence for the benefits of exercise on both physical and cognitive health in a non–Down syndrome population are well established, he said, but there were few data on its effect on the Down syndrome population.

One small study showed physical and neurocognitive benefits with resistance training.

“The evidence from previous studies showed increased levels of inactivity and sitting time in Down syndrome individuals compared with non–[Down syndrome] controls, so we hypothesized that exercise, albeit small amounts, would increase their physical fitness,” Dr. Gordon said.

His team also hypothesized that walking would stimulate cognitive development since it requires heightened cognitive engagement compared with inactivity. “What surprised us was the degree of improvement,” Dr. Gordon said.

The process of walking requires the brain to interpret information on a real-time basis from both internal and external cues, he continued. “For most of us this process requires low-level cognitive engagement. However, in the [Down syndrome] population, where motor control is impaired and accompanied by poor muscle tone, walking imposes a heightened cognitive load.” It requires them to concentrate on the action, be aware of their surroundings, and make the right decisions, all of which stimulate areas of the brain that control these functions.
 

Study details

Eighty-three adult participants were available for final analysis – 67 from North America, 8 from Europe, 5 from Africa, 2 from Asia, and 1 from Australia. The mean age of participants was 27.1 years, 40 were female, and all had caregiver support during the study.

Those unable to visualize information on computer and mobile/tablet screens or to listen to instructions/auditory cues were excluded. All were provided with instructions and a mobile monitoring tool set to record steps completed, distances covered, speeds, and heart rate.

Each was assigned to one of four groups. Exercise intervention-only consisted of 8 weeks of cardiorespiratory exercise defined as either walking or jogging three times a week for 30 minutes. Cognitive training included eight levels (about 20 minutes) of cognitive and executive function exercises six times per week. The combined group completed both the cardiorespiratory and cognitive interventions, while the fourth group acted as controls with no intervention.

According to the authors, the study offers a real-life scenario that can be readily adopted within the Down syndrome community.

This study was commissioned by the Canadian Down Syndrome Society. The authors had no conflicts of interest to declare.

In the first study of its kind, U.K. and French researchers reported that exercise positively affected physical and cognitive health in persons with Down syndrome. “The findings are significant and offer a crucial challenge to the [Down syndrome] and wider societies,” wrote a team led by Dan Gordon, PhD, associate professor of cardiorespiratory exercise physiology at Anglia Ruskin University in Cambridge, England. “Impact of Prescribed Exercise on the Physical and Cognitive Health of Adults with Down Syndrome: The MinDSets Study” was published in the International Journal of Environmental Research and Public Health.

“Through the simple application of walking, a form of exercise which requires little to no equipment or expense, there were significant increases in cognitive and executive function, reflecting improved capabilities in key attributes of information processing, vigilance, and selective attention,” the researchers wrote.

Dr. Gordon

“Increased cognitive function will help foster increased societal integration and quality of life, which, given that this is the first generation of those with [Down syndrome] to outlive their parents and caregivers, is of importance,” they wrote.

For example, those in an exercise-only intervention arm had an 11.4% improvement on the distance covered in the Six-Minute Walk Test, going from a mean of 498.8 meters before intervention to 522.1 meters afterward. Those in a group that combined group exercise with cognitive training increased the distance walked by 9.9%, or 49.2 meters. Groups that got cognitive training only or no intervention showed no significant changes.

In measures of cognitive function, the exercise group showed a 38% increase in selective attention, with the cognitive and combined groups showing changes for the same measure of 16.5% and 55.3%, respectively. The changes for concentration in the exercise-alone group was 31.5%, while those receiving cognitive training alone or combined exercise plus cognitive training showed improvements in concentration of 21% and 15%, respectively.

Asked why a combination intervention was not superior to exercise alone, Dr. Gordon said in an interview, “Something we’re looking at in the data but can’t fully confirm is that the combined group started to become fatigued due to the double dose of the intervention, and this prevented them in the final tests from doing quite so well as the exercise-alone group. Irrespective of the magnitude of change, any cognitive adaptation observed will be beneficial to this population.”

The evidence for the benefits of exercise on both physical and cognitive health in a non–Down syndrome population are well established, he said, but there were few data on its effect on the Down syndrome population.

One small study showed physical and neurocognitive benefits with resistance training.

“The evidence from previous studies showed increased levels of inactivity and sitting time in Down syndrome individuals compared with non–[Down syndrome] controls, so we hypothesized that exercise, albeit small amounts, would increase their physical fitness,” Dr. Gordon said.

His team also hypothesized that walking would stimulate cognitive development since it requires heightened cognitive engagement compared with inactivity. “What surprised us was the degree of improvement,” Dr. Gordon said.

The process of walking requires the brain to interpret information on a real-time basis from both internal and external cues, he continued. “For most of us this process requires low-level cognitive engagement. However, in the [Down syndrome] population, where motor control is impaired and accompanied by poor muscle tone, walking imposes a heightened cognitive load.” It requires them to concentrate on the action, be aware of their surroundings, and make the right decisions, all of which stimulate areas of the brain that control these functions.
 

Study details

Eighty-three adult participants were available for final analysis – 67 from North America, 8 from Europe, 5 from Africa, 2 from Asia, and 1 from Australia. The mean age of participants was 27.1 years, 40 were female, and all had caregiver support during the study.

Those unable to visualize information on computer and mobile/tablet screens or to listen to instructions/auditory cues were excluded. All were provided with instructions and a mobile monitoring tool set to record steps completed, distances covered, speeds, and heart rate.

Each was assigned to one of four groups. Exercise intervention-only consisted of 8 weeks of cardiorespiratory exercise defined as either walking or jogging three times a week for 30 minutes. Cognitive training included eight levels (about 20 minutes) of cognitive and executive function exercises six times per week. The combined group completed both the cardiorespiratory and cognitive interventions, while the fourth group acted as controls with no intervention.

According to the authors, the study offers a real-life scenario that can be readily adopted within the Down syndrome community.

This study was commissioned by the Canadian Down Syndrome Society. The authors had no conflicts of interest to declare.

In the first study of its kind, U.K. and French researchers reported that exercise positively affected physical and cognitive health in persons with Down syndrome. “The findings are significant and offer a crucial challenge to the [Down syndrome] and wider societies,” wrote a team led by Dan Gordon, PhD, associate professor of cardiorespiratory exercise physiology at Anglia Ruskin University in Cambridge, England. “Impact of Prescribed Exercise on the Physical and Cognitive Health of Adults with Down Syndrome: The MinDSets Study” was published in the International Journal of Environmental Research and Public Health.

“Through the simple application of walking, a form of exercise which requires little to no equipment or expense, there were significant increases in cognitive and executive function, reflecting improved capabilities in key attributes of information processing, vigilance, and selective attention,” the researchers wrote.

Dr. Gordon

“Increased cognitive function will help foster increased societal integration and quality of life, which, given that this is the first generation of those with [Down syndrome] to outlive their parents and caregivers, is of importance,” they wrote.

For example, those in an exercise-only intervention arm had an 11.4% improvement on the distance covered in the Six-Minute Walk Test, going from a mean of 498.8 meters before intervention to 522.1 meters afterward. Those in a group that combined group exercise with cognitive training increased the distance walked by 9.9%, or 49.2 meters. Groups that got cognitive training only or no intervention showed no significant changes.

In measures of cognitive function, the exercise group showed a 38% increase in selective attention, with the cognitive and combined groups showing changes for the same measure of 16.5% and 55.3%, respectively. The changes for concentration in the exercise-alone group was 31.5%, while those receiving cognitive training alone or combined exercise plus cognitive training showed improvements in concentration of 21% and 15%, respectively.

Asked why a combination intervention was not superior to exercise alone, Dr. Gordon said in an interview, “Something we’re looking at in the data but can’t fully confirm is that the combined group started to become fatigued due to the double dose of the intervention, and this prevented them in the final tests from doing quite so well as the exercise-alone group. Irrespective of the magnitude of change, any cognitive adaptation observed will be beneficial to this population.”

The evidence for the benefits of exercise on both physical and cognitive health in a non–Down syndrome population are well established, he said, but there were few data on its effect on the Down syndrome population.

One small study showed physical and neurocognitive benefits with resistance training.

“The evidence from previous studies showed increased levels of inactivity and sitting time in Down syndrome individuals compared with non–[Down syndrome] controls, so we hypothesized that exercise, albeit small amounts, would increase their physical fitness,” Dr. Gordon said.

His team also hypothesized that walking would stimulate cognitive development since it requires heightened cognitive engagement compared with inactivity. “What surprised us was the degree of improvement,” Dr. Gordon said.

The process of walking requires the brain to interpret information on a real-time basis from both internal and external cues, he continued. “For most of us this process requires low-level cognitive engagement. However, in the [Down syndrome] population, where motor control is impaired and accompanied by poor muscle tone, walking imposes a heightened cognitive load.” It requires them to concentrate on the action, be aware of their surroundings, and make the right decisions, all of which stimulate areas of the brain that control these functions.
 

Study details

Eighty-three adult participants were available for final analysis – 67 from North America, 8 from Europe, 5 from Africa, 2 from Asia, and 1 from Australia. The mean age of participants was 27.1 years, 40 were female, and all had caregiver support during the study.

Those unable to visualize information on computer and mobile/tablet screens or to listen to instructions/auditory cues were excluded. All were provided with instructions and a mobile monitoring tool set to record steps completed, distances covered, speeds, and heart rate.

Each was assigned to one of four groups. Exercise intervention-only consisted of 8 weeks of cardiorespiratory exercise defined as either walking or jogging three times a week for 30 minutes. Cognitive training included eight levels (about 20 minutes) of cognitive and executive function exercises six times per week. The combined group completed both the cardiorespiratory and cognitive interventions, while the fourth group acted as controls with no intervention.

According to the authors, the study offers a real-life scenario that can be readily adopted within the Down syndrome community.

This study was commissioned by the Canadian Down Syndrome Society. The authors had no conflicts of interest to declare.

TOPLINE:

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

METHODOLOGY:

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

TAKEAWAY:

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

IN PRACTICE:

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

SOURCE:

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

LIMITATIONS:

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

DISCLOSURES:

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

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

TOPLINE:

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

METHODOLOGY:

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

TAKEAWAY:

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

IN PRACTICE:

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

SOURCE:

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

LIMITATIONS:

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

DISCLOSURES:

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

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

TOPLINE:

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

METHODOLOGY:

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

TAKEAWAY:

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

IN PRACTICE:

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

SOURCE:

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

LIMITATIONS:

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

DISCLOSURES:

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

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

TOPLINE:

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

METHODOLOGY:

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

TAKEAWAY:

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

IN PRACTICE:

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

SOURCE:

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

LIMITATIONS:

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

DISCLOSURES:

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

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

TOPLINE:

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

METHODOLOGY:

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

TAKEAWAY:

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

IN PRACTICE:

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

SOURCE:

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

LIMITATIONS:

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

DISCLOSURES:

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

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

TOPLINE:

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

METHODOLOGY:

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

TAKEAWAY:

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

IN PRACTICE:

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

SOURCE:

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

LIMITATIONS:

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

DISCLOSURES:

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

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

TOPLINE:

A 3-month yoga program that integrates deep breathing, meditation, and positive affirmations is associated with a significant reduction in seizure frequency, anxiety, and self-perceived feelings of stigma in people with epilepsy, a new study shows.

AlenaPaulus/E+/Getty Images

METHODOLOGY:

• Investigators included participants aged 18-60 years with epilepsy who scored ≥ 4 on the Kilifi Stigma Scale of Epilepsy. A score greater than the 66th percentile indicates the presence of strongly felt stigma.
• Patients (n = 160) had an average of one seizure per week, and most took at least two antiseizure medications.
• The intervention group (n = 80) participated in a yoga module with muscle-loosening exercises, slow and synchronized breathing, meditation, and positive affirmations. The control group (n = 80) participated in sham yoga sessions with no instructions on the breathing exercises or attention to the body movements and sensations during practice.
• Both groups participated in seven 1-hour supervised group yoga sessions over 3 months, were asked to practice the interventions at home five times per week, and received a psychoeducation module on epilepsy.

TAKEAWAY:

• Participants practicing the intervention module had significant reductions in self-perceived stigma, compared with those in the control group (P = .01).
• The proportion of participants in the intervention group who had a more than 50% seizure reduction (odds ratio, 4.11; P = .01) and complete seizure remission (OR, 7.4; P = .005) at the end of the 6-month follow-up was significantly higher than in the control group.
• Compared with those in the control group, there were also significant improvements in anxiety (P = .032) and quality of life (P < .001) in the intervention group.
• The intervention group also experienced significant improvement in mindfulness (P < .001) and cognitive impairment, compared with the control group (P < .004).

IN PRACTICE:

“This stigma can affect a person’s life in many ways, including treatment, emergency department visits, and poor mental health,” study investigator Majari Tripathi, MD, of All India Institute of Medical Sciences, New Delhi, said in a press release. “Our study showed that doing yoga can alleviate the burden of epilepsy and improve the overall quality of life by reducing this perceived stigma.”

SOURCE:

Dr. Tripathi and Kirandeep Kaur, MD, also of All India Institute of Medical Sciences, conducted the study with their colleagues. It was published online in Neurology.

LIMITATIONS:

There was no passive control or treatment as usual group, which would indicate the effect size of the intervention. In addition, there was no monitoring of seizure frequency before the study began, which may have biased the change of seizure frequency as an outcome.

DISCLOSURES:

The study investigators reported no study funding or reported disclosures.

A version of this article appeared on Medscape.com.

TOPLINE:

A 3-month yoga program that integrates deep breathing, meditation, and positive affirmations is associated with a significant reduction in seizure frequency, anxiety, and self-perceived feelings of stigma in people with epilepsy, a new study shows.

AlenaPaulus/E+/Getty Images

METHODOLOGY:

• Investigators included participants aged 18-60 years with epilepsy who scored ≥ 4 on the Kilifi Stigma Scale of Epilepsy. A score greater than the 66th percentile indicates the presence of strongly felt stigma.
• Patients (n = 160) had an average of one seizure per week, and most took at least two antiseizure medications.
• The intervention group (n = 80) participated in a yoga module with muscle-loosening exercises, slow and synchronized breathing, meditation, and positive affirmations. The control group (n = 80) participated in sham yoga sessions with no instructions on the breathing exercises or attention to the body movements and sensations during practice.
• Both groups participated in seven 1-hour supervised group yoga sessions over 3 months, were asked to practice the interventions at home five times per week, and received a psychoeducation module on epilepsy.

TAKEAWAY:

• Participants practicing the intervention module had significant reductions in self-perceived stigma, compared with those in the control group (P = .01).
• The proportion of participants in the intervention group who had a more than 50% seizure reduction (odds ratio, 4.11; P = .01) and complete seizure remission (OR, 7.4; P = .005) at the end of the 6-month follow-up was significantly higher than in the control group.
• Compared with those in the control group, there were also significant improvements in anxiety (P = .032) and quality of life (P < .001) in the intervention group.
• The intervention group also experienced significant improvement in mindfulness (P < .001) and cognitive impairment, compared with the control group (P < .004).

IN PRACTICE:

“This stigma can affect a person’s life in many ways, including treatment, emergency department visits, and poor mental health,” study investigator Majari Tripathi, MD, of All India Institute of Medical Sciences, New Delhi, said in a press release. “Our study showed that doing yoga can alleviate the burden of epilepsy and improve the overall quality of life by reducing this perceived stigma.”

SOURCE:

Dr. Tripathi and Kirandeep Kaur, MD, also of All India Institute of Medical Sciences, conducted the study with their colleagues. It was published online in Neurology.

LIMITATIONS:

There was no passive control or treatment as usual group, which would indicate the effect size of the intervention. In addition, there was no monitoring of seizure frequency before the study began, which may have biased the change of seizure frequency as an outcome.

DISCLOSURES:

The study investigators reported no study funding or reported disclosures.

A version of this article appeared on Medscape.com.

TOPLINE:

A 3-month yoga program that integrates deep breathing, meditation, and positive affirmations is associated with a significant reduction in seizure frequency, anxiety, and self-perceived feelings of stigma in people with epilepsy, a new study shows.

AlenaPaulus/E+/Getty Images

METHODOLOGY:

• Investigators included participants aged 18-60 years with epilepsy who scored ≥ 4 on the Kilifi Stigma Scale of Epilepsy. A score greater than the 66th percentile indicates the presence of strongly felt stigma.
• Patients (n = 160) had an average of one seizure per week, and most took at least two antiseizure medications.
• The intervention group (n = 80) participated in a yoga module with muscle-loosening exercises, slow and synchronized breathing, meditation, and positive affirmations. The control group (n = 80) participated in sham yoga sessions with no instructions on the breathing exercises or attention to the body movements and sensations during practice.
• Both groups participated in seven 1-hour supervised group yoga sessions over 3 months, were asked to practice the interventions at home five times per week, and received a psychoeducation module on epilepsy.

TAKEAWAY:

• Participants practicing the intervention module had significant reductions in self-perceived stigma, compared with those in the control group (P = .01).
• The proportion of participants in the intervention group who had a more than 50% seizure reduction (odds ratio, 4.11; P = .01) and complete seizure remission (OR, 7.4; P = .005) at the end of the 6-month follow-up was significantly higher than in the control group.
• Compared with those in the control group, there were also significant improvements in anxiety (P = .032) and quality of life (P < .001) in the intervention group.
• The intervention group also experienced significant improvement in mindfulness (P < .001) and cognitive impairment, compared with the control group (P < .004).

IN PRACTICE:

“This stigma can affect a person’s life in many ways, including treatment, emergency department visits, and poor mental health,” study investigator Majari Tripathi, MD, of All India Institute of Medical Sciences, New Delhi, said in a press release. “Our study showed that doing yoga can alleviate the burden of epilepsy and improve the overall quality of life by reducing this perceived stigma.”

SOURCE:

Dr. Tripathi and Kirandeep Kaur, MD, also of All India Institute of Medical Sciences, conducted the study with their colleagues. It was published online in Neurology.

LIMITATIONS:

There was no passive control or treatment as usual group, which would indicate the effect size of the intervention. In addition, there was no monitoring of seizure frequency before the study began, which may have biased the change of seizure frequency as an outcome.

DISCLOSURES:

The study investigators reported no study funding or reported disclosures.

A version of this article appeared on Medscape.com.

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

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

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

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

The study was published online in JAMA Psychiatry

Filling in the research gaps

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

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

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

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

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

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

Stimulants confer greatest risk

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

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

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

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

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

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

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

‘Tricky trade-offs’

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

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

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

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

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

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

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

A version of this article appeared on Medscape.com.

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

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

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

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

The study was published online in JAMA Psychiatry

Filling in the research gaps

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

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

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

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

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

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

Stimulants confer greatest risk

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

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

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

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

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

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

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

‘Tricky trade-offs’

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

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

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

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

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

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

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

A version of this article appeared on Medscape.com.

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

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

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

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

The study was published online in JAMA Psychiatry

Filling in the research gaps

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

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

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

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

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

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

Stimulants confer greatest risk

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

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

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

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

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

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

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

‘Tricky trade-offs’

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

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

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

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

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

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

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

A version of this article appeared on Medscape.com.

Adam Boggon, MBChB, was working at the Royal Free Hospital in North London during the city’s second wave of COVID-19. “I was effectively living in the hospital,” he recalled. “It felt like I was going 10,000 miles per hour, trying to corral hundreds of medical students and doctors.”

During a national lockdown, there were few places Dr. Boggon could escape to, but the Hampstead Heath swimming ponds mostly remained open. He swam there regularly to exercise and recharge even in winter.

“Swimming in cold water takes you out of yourself,” Dr. Boggon said. “It was such a release for someone who grew up in a rural place and had access to green space, even though the water is murky.” It also hovers around 50 °F (10 °C).

Jumping into cold water, well, kind of stinks. So why do it? It’s not only for bragging rights. A growing number of studies suggest significant mental and physical health benefits to swimming in cold water, specifically to improve depression symptoms and even ease inflammatory conditions.

And a lot of that research is driven by medical pros who love to do it themselves.

For Dr. Boggon, swimming in frigid water is uncomfortable, but he feels that a sensation of calmness follows that makes the plunge more than worth it. Now a Fulbright Scholar at Harvard, where he studies public health and health management, Dr. Boggon is able to frequent the fabled Walden Pond just outside of Boston.

As Thoreau himself said, “You can never have enough of nature.”

Yes, even if it’s really, really cold.
 

Taking a deeper dive

Heather Massey, PhD, a senior lecturer in Sport, Health, and Exercise Science at University of Portsmouth, blames her father, a dinghy sailor, for her affinity for cold-water swimming.

And she’s done more than most, including an epic 16-hour crossing of the English Channel. The water temperature was in the upper-50s °F, and she swam without a wetsuit. “Time just seemed to collapse,” she has shared about the experience.

While working on her PhD and studying the effects of environmental physiology, in particular what happens to the body when it gets hot or cold, Dr. Massey’s hobby and studies seemed to coalesce.

Her research initially focused on the hazards around being in cold open water. But she also noticed a growing trend of people claiming health benefits from the practice. “People started to talk about experiencing improved symptoms of depression or improved mental health from their activities in the water,” she said.

She partnered with another outdoor swimming enthusiast, Hannah Denton, a counseling psychologist working for the National Health Service in the United Kingdom. Ms. Denton was publishing papers on the potential impact that outdoor swimming may have on people with depression and how it could improve mental health in general. She also regularly engages in cold-water swims to boost feelings of mindfulness and peace.

“Having the experience of being so close to nature, as well as the strong sensory experience of being in cold water, does really encourage you to be in the moment,” Ms. Denton wrote in an article for the Sussex Mindfulness Centre. “My experiences of sea swimming and mindfulness support each other. Both have made me feel more comfortable with my body, to have more of a present moment focus, to pay attention to my breathing, and to gain distance from difficult thoughts.”

Over the past few years, Dr. Massey and Ms. Denton have moved from fairly small-scale studies with no real controls to today, completing a randomized controlled trial and looking at the impact that outdoor swimming may have on people living with mild to moderate depression.

“At first, people sort of thought our idea was a bit wacky,” said Dr. Massey. “Now, the popularity of open-water swimming has really blossomed, and so has this area of research. We’re starting to build more rigor into the work.”

Like all the researchers and physicians interviewed for this article, Dr. Massey hesitates to claim that cold-water swimming is a “cure” that should be medicalized.

“It’s not about prescribing it or forcing people to do it,” said Dr. Massey. “This is not something that a doctor should write on a prescription and say you should go and have eight 1-hour sessions of swimming.”
 

(Not yet) a common cure

Enter into the conversation Mark Harper, MD, PhD, consultant anesthetist at Sussex University Hospitals in the United Kingdom and Kristiansand, Norway. Dr. Harper is the author of the 2022 book, Chill: The Cold Water Swim Cure – A Transformative Guide to Renew Your Body and Mind.

Dr. Harper grew up swimming in pools, and it wasn’t until his pool closed for 2 weeks that he ventured into the sea. He recalled walking up the beach afterward, thinking, God, this feels good, and from that moment on, he became hooked on outdoor swimming and curious about its therapeutic potential.

The “cure” in the book’s title, Dr. Harper explained, is being used in the historical sense of “treatment,” as in the first medical book about sea-bathing written over 250 years ago. Dr. Harper acknowledged that the connection to health is still speculative. “However, the circumstantial evidence, the feedback from participants and early study data for its benefits are now very strong,” he said.

In a small study published in 2022, Dr. Harper and colleagues took 59 people with anxiety and depression and put them through a sea-swimming course. Afterward, 80% showed a clinically significant improvement in their mental health.

More recently, Dr. Harper and his team of researchers released a survey to determine how many people were using cold-water swimming as a treatment for a mental or physical ailment. “We thought 30 or 40 people would respond, but we ended up with over 700,” he said. “The majority were using it for mental health but also included inflammation-related conditions.”

Over 2 decades, Dr. Harper has seen dramatic success stories. In his book, he recalled a good friend who, in his early 20s, suffered from Crohn’s disease so badly he couldn’t walk up the steps to his parents’ house. The friend turned to outdoor cold swimming as a low-impact workout and began noticing the symptoms of his disease were improving. Within months, he was able to go off his medications. In 2022, he completed 52 triathlons: one per week for the entire year.
 

How cold exposure may play with your brain

Vaibhav Diwadkar, PhD, professor of psychiatry and behavioral neurosciences at Wayne State University, in Detroit, is studying how human brain networks respond to cold exposure. Dr. Diwadkar and his colleague, Otto Muzik, PhD, began by putting volunteers in a rubber suit with thin tubing and infusing the tubing with temperature-controlled water. Meanwhile, they collected functional brain imaging data to analyze which parts of the brain were responding as body temperature changed.

The data showed that the cold exposure made certain areas of the brain very active, including some that have been associated with the regulation of mood.

Dr. Diwadkar posits that controlled exposure to cold serves as a low-level stressor that knocks different systems within the brain and body out of homeostasis. Once the stress is removed, the brain responds by releasing neurotransmitters that enhance mood, frequently leading to feelings of euphoria in participants.

“We don’t have direct evidence of such a mechanism, but it’s a reasonable speculation,” said Dr. Diwadkar.

However, he pointed out that science writers in the media often portray topics such as this one in black and white, which is “oversimplifying the scientific complexity of biology.”

Clearly, more research needs to be done on the potential therapeutic benefits of cold-water swimming. But for those suffering from anxiety, depression, or chronic illness, if taking a cold dip makes you feel better, the why and how might be beside the point.

Plus, as Dr. Harper pointed out, it’s an easy and accessible therapy.

“All you need is some water – enough to submerge your entire body in – that’s less than 68 °F (20 °C),” he said. “If you stay long enough to get over that initial shock, which is just 2 or 3 minutes, then you’ve got the effect. If you get out and want to go back in again, then you’ve done it right.”
 

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

Adam Boggon, MBChB, was working at the Royal Free Hospital in North London during the city’s second wave of COVID-19. “I was effectively living in the hospital,” he recalled. “It felt like I was going 10,000 miles per hour, trying to corral hundreds of medical students and doctors.”

During a national lockdown, there were few places Dr. Boggon could escape to, but the Hampstead Heath swimming ponds mostly remained open. He swam there regularly to exercise and recharge even in winter.

“Swimming in cold water takes you out of yourself,” Dr. Boggon said. “It was such a release for someone who grew up in a rural place and had access to green space, even though the water is murky.” It also hovers around 50 °F (10 °C).

Jumping into cold water, well, kind of stinks. So why do it? It’s not only for bragging rights. A growing number of studies suggest significant mental and physical health benefits to swimming in cold water, specifically to improve depression symptoms and even ease inflammatory conditions.

And a lot of that research is driven by medical pros who love to do it themselves.

For Dr. Boggon, swimming in frigid water is uncomfortable, but he feels that a sensation of calmness follows that makes the plunge more than worth it. Now a Fulbright Scholar at Harvard, where he studies public health and health management, Dr. Boggon is able to frequent the fabled Walden Pond just outside of Boston.

As Thoreau himself said, “You can never have enough of nature.”

Yes, even if it’s really, really cold.
 

Taking a deeper dive

Heather Massey, PhD, a senior lecturer in Sport, Health, and Exercise Science at University of Portsmouth, blames her father, a dinghy sailor, for her affinity for cold-water swimming.

And she’s done more than most, including an epic 16-hour crossing of the English Channel. The water temperature was in the upper-50s °F, and she swam without a wetsuit. “Time just seemed to collapse,” she has shared about the experience.

While working on her PhD and studying the effects of environmental physiology, in particular what happens to the body when it gets hot or cold, Dr. Massey’s hobby and studies seemed to coalesce.

Her research initially focused on the hazards around being in cold open water. But she also noticed a growing trend of people claiming health benefits from the practice. “People started to talk about experiencing improved symptoms of depression or improved mental health from their activities in the water,” she said.

She partnered with another outdoor swimming enthusiast, Hannah Denton, a counseling psychologist working for the National Health Service in the United Kingdom. Ms. Denton was publishing papers on the potential impact that outdoor swimming may have on people with depression and how it could improve mental health in general. She also regularly engages in cold-water swims to boost feelings of mindfulness and peace.

“Having the experience of being so close to nature, as well as the strong sensory experience of being in cold water, does really encourage you to be in the moment,” Ms. Denton wrote in an article for the Sussex Mindfulness Centre. “My experiences of sea swimming and mindfulness support each other. Both have made me feel more comfortable with my body, to have more of a present moment focus, to pay attention to my breathing, and to gain distance from difficult thoughts.”

Over the past few years, Dr. Massey and Ms. Denton have moved from fairly small-scale studies with no real controls to today, completing a randomized controlled trial and looking at the impact that outdoor swimming may have on people living with mild to moderate depression.

“At first, people sort of thought our idea was a bit wacky,” said Dr. Massey. “Now, the popularity of open-water swimming has really blossomed, and so has this area of research. We’re starting to build more rigor into the work.”

Like all the researchers and physicians interviewed for this article, Dr. Massey hesitates to claim that cold-water swimming is a “cure” that should be medicalized.

“It’s not about prescribing it or forcing people to do it,” said Dr. Massey. “This is not something that a doctor should write on a prescription and say you should go and have eight 1-hour sessions of swimming.”
 

(Not yet) a common cure

Enter into the conversation Mark Harper, MD, PhD, consultant anesthetist at Sussex University Hospitals in the United Kingdom and Kristiansand, Norway. Dr. Harper is the author of the 2022 book, Chill: The Cold Water Swim Cure – A Transformative Guide to Renew Your Body and Mind.

Dr. Harper grew up swimming in pools, and it wasn’t until his pool closed for 2 weeks that he ventured into the sea. He recalled walking up the beach afterward, thinking, God, this feels good, and from that moment on, he became hooked on outdoor swimming and curious about its therapeutic potential.

The “cure” in the book’s title, Dr. Harper explained, is being used in the historical sense of “treatment,” as in the first medical book about sea-bathing written over 250 years ago. Dr. Harper acknowledged that the connection to health is still speculative. “However, the circumstantial evidence, the feedback from participants and early study data for its benefits are now very strong,” he said.

In a small study published in 2022, Dr. Harper and colleagues took 59 people with anxiety and depression and put them through a sea-swimming course. Afterward, 80% showed a clinically significant improvement in their mental health.

More recently, Dr. Harper and his team of researchers released a survey to determine how many people were using cold-water swimming as a treatment for a mental or physical ailment. “We thought 30 or 40 people would respond, but we ended up with over 700,” he said. “The majority were using it for mental health but also included inflammation-related conditions.”

Over 2 decades, Dr. Harper has seen dramatic success stories. In his book, he recalled a good friend who, in his early 20s, suffered from Crohn’s disease so badly he couldn’t walk up the steps to his parents’ house. The friend turned to outdoor cold swimming as a low-impact workout and began noticing the symptoms of his disease were improving. Within months, he was able to go off his medications. In 2022, he completed 52 triathlons: one per week for the entire year.
 

How cold exposure may play with your brain

Vaibhav Diwadkar, PhD, professor of psychiatry and behavioral neurosciences at Wayne State University, in Detroit, is studying how human brain networks respond to cold exposure. Dr. Diwadkar and his colleague, Otto Muzik, PhD, began by putting volunteers in a rubber suit with thin tubing and infusing the tubing with temperature-controlled water. Meanwhile, they collected functional brain imaging data to analyze which parts of the brain were responding as body temperature changed.

The data showed that the cold exposure made certain areas of the brain very active, including some that have been associated with the regulation of mood.

Dr. Diwadkar posits that controlled exposure to cold serves as a low-level stressor that knocks different systems within the brain and body out of homeostasis. Once the stress is removed, the brain responds by releasing neurotransmitters that enhance mood, frequently leading to feelings of euphoria in participants.

“We don’t have direct evidence of such a mechanism, but it’s a reasonable speculation,” said Dr. Diwadkar.

However, he pointed out that science writers in the media often portray topics such as this one in black and white, which is “oversimplifying the scientific complexity of biology.”

Clearly, more research needs to be done on the potential therapeutic benefits of cold-water swimming. But for those suffering from anxiety, depression, or chronic illness, if taking a cold dip makes you feel better, the why and how might be beside the point.

Plus, as Dr. Harper pointed out, it’s an easy and accessible therapy.

“All you need is some water – enough to submerge your entire body in – that’s less than 68 °F (20 °C),” he said. “If you stay long enough to get over that initial shock, which is just 2 or 3 minutes, then you’ve got the effect. If you get out and want to go back in again, then you’ve done it right.”
 

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

Adam Boggon, MBChB, was working at the Royal Free Hospital in North London during the city’s second wave of COVID-19. “I was effectively living in the hospital,” he recalled. “It felt like I was going 10,000 miles per hour, trying to corral hundreds of medical students and doctors.”

During a national lockdown, there were few places Dr. Boggon could escape to, but the Hampstead Heath swimming ponds mostly remained open. He swam there regularly to exercise and recharge even in winter.

“Swimming in cold water takes you out of yourself,” Dr. Boggon said. “It was such a release for someone who grew up in a rural place and had access to green space, even though the water is murky.” It also hovers around 50 °F (10 °C).

Jumping into cold water, well, kind of stinks. So why do it? It’s not only for bragging rights. A growing number of studies suggest significant mental and physical health benefits to swimming in cold water, specifically to improve depression symptoms and even ease inflammatory conditions.

And a lot of that research is driven by medical pros who love to do it themselves.

For Dr. Boggon, swimming in frigid water is uncomfortable, but he feels that a sensation of calmness follows that makes the plunge more than worth it. Now a Fulbright Scholar at Harvard, where he studies public health and health management, Dr. Boggon is able to frequent the fabled Walden Pond just outside of Boston.

As Thoreau himself said, “You can never have enough of nature.”

Yes, even if it’s really, really cold.
 

Taking a deeper dive

Heather Massey, PhD, a senior lecturer in Sport, Health, and Exercise Science at University of Portsmouth, blames her father, a dinghy sailor, for her affinity for cold-water swimming.

And she’s done more than most, including an epic 16-hour crossing of the English Channel. The water temperature was in the upper-50s °F, and she swam without a wetsuit. “Time just seemed to collapse,” she has shared about the experience.

While working on her PhD and studying the effects of environmental physiology, in particular what happens to the body when it gets hot or cold, Dr. Massey’s hobby and studies seemed to coalesce.

Her research initially focused on the hazards around being in cold open water. But she also noticed a growing trend of people claiming health benefits from the practice. “People started to talk about experiencing improved symptoms of depression or improved mental health from their activities in the water,” she said.

She partnered with another outdoor swimming enthusiast, Hannah Denton, a counseling psychologist working for the National Health Service in the United Kingdom. Ms. Denton was publishing papers on the potential impact that outdoor swimming may have on people with depression and how it could improve mental health in general. She also regularly engages in cold-water swims to boost feelings of mindfulness and peace.

“Having the experience of being so close to nature, as well as the strong sensory experience of being in cold water, does really encourage you to be in the moment,” Ms. Denton wrote in an article for the Sussex Mindfulness Centre. “My experiences of sea swimming and mindfulness support each other. Both have made me feel more comfortable with my body, to have more of a present moment focus, to pay attention to my breathing, and to gain distance from difficult thoughts.”

Over the past few years, Dr. Massey and Ms. Denton have moved from fairly small-scale studies with no real controls to today, completing a randomized controlled trial and looking at the impact that outdoor swimming may have on people living with mild to moderate depression.

“At first, people sort of thought our idea was a bit wacky,” said Dr. Massey. “Now, the popularity of open-water swimming has really blossomed, and so has this area of research. We’re starting to build more rigor into the work.”

Like all the researchers and physicians interviewed for this article, Dr. Massey hesitates to claim that cold-water swimming is a “cure” that should be medicalized.

“It’s not about prescribing it or forcing people to do it,” said Dr. Massey. “This is not something that a doctor should write on a prescription and say you should go and have eight 1-hour sessions of swimming.”
 

(Not yet) a common cure

Enter into the conversation Mark Harper, MD, PhD, consultant anesthetist at Sussex University Hospitals in the United Kingdom and Kristiansand, Norway. Dr. Harper is the author of the 2022 book, Chill: The Cold Water Swim Cure – A Transformative Guide to Renew Your Body and Mind.

Dr. Harper grew up swimming in pools, and it wasn’t until his pool closed for 2 weeks that he ventured into the sea. He recalled walking up the beach afterward, thinking, God, this feels good, and from that moment on, he became hooked on outdoor swimming and curious about its therapeutic potential.

The “cure” in the book’s title, Dr. Harper explained, is being used in the historical sense of “treatment,” as in the first medical book about sea-bathing written over 250 years ago. Dr. Harper acknowledged that the connection to health is still speculative. “However, the circumstantial evidence, the feedback from participants and early study data for its benefits are now very strong,” he said.

In a small study published in 2022, Dr. Harper and colleagues took 59 people with anxiety and depression and put them through a sea-swimming course. Afterward, 80% showed a clinically significant improvement in their mental health.

More recently, Dr. Harper and his team of researchers released a survey to determine how many people were using cold-water swimming as a treatment for a mental or physical ailment. “We thought 30 or 40 people would respond, but we ended up with over 700,” he said. “The majority were using it for mental health but also included inflammation-related conditions.”

Over 2 decades, Dr. Harper has seen dramatic success stories. In his book, he recalled a good friend who, in his early 20s, suffered from Crohn’s disease so badly he couldn’t walk up the steps to his parents’ house. The friend turned to outdoor cold swimming as a low-impact workout and began noticing the symptoms of his disease were improving. Within months, he was able to go off his medications. In 2022, he completed 52 triathlons: one per week for the entire year.
 

How cold exposure may play with your brain

Vaibhav Diwadkar, PhD, professor of psychiatry and behavioral neurosciences at Wayne State University, in Detroit, is studying how human brain networks respond to cold exposure. Dr. Diwadkar and his colleague, Otto Muzik, PhD, began by putting volunteers in a rubber suit with thin tubing and infusing the tubing with temperature-controlled water. Meanwhile, they collected functional brain imaging data to analyze which parts of the brain were responding as body temperature changed.

The data showed that the cold exposure made certain areas of the brain very active, including some that have been associated with the regulation of mood.

Dr. Diwadkar posits that controlled exposure to cold serves as a low-level stressor that knocks different systems within the brain and body out of homeostasis. Once the stress is removed, the brain responds by releasing neurotransmitters that enhance mood, frequently leading to feelings of euphoria in participants.

“We don’t have direct evidence of such a mechanism, but it’s a reasonable speculation,” said Dr. Diwadkar.

However, he pointed out that science writers in the media often portray topics such as this one in black and white, which is “oversimplifying the scientific complexity of biology.”

Clearly, more research needs to be done on the potential therapeutic benefits of cold-water swimming. But for those suffering from anxiety, depression, or chronic illness, if taking a cold dip makes you feel better, the why and how might be beside the point.

Plus, as Dr. Harper pointed out, it’s an easy and accessible therapy.

“All you need is some water – enough to submerge your entire body in – that’s less than 68 °F (20 °C),” he said. “If you stay long enough to get over that initial shock, which is just 2 or 3 minutes, then you’ve got the effect. If you get out and want to go back in again, then you’ve done it right.”
 

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

Pharmacogenomic testing for antidepressants could help reduce the time and cost it takes to find the most effective medication for a patient, according to a new study.

Scientists developed a microsimulation model to evaluate the effectiveness of pharmacogenomic testing for adult patients in British Columbia, with newly diagnosed moderate to severe major depressive disorder (MDD). The model predicted that testing could result in 37% fewer patients developing refractory depression, 15% more time of patients feeling well, and a health system cost-savings of $956 million CAD over 20 years.

“Our study shows that, if pharmacogenomic testing guides the prescription of an effective antidepressant, it can reduce the lengthy trial-and-error process many patients experience and dramatically reduce the financial burden on the health care system,” Shahzad Ghanbarian, PhD, the lead author and a research analyst at the University of British Columbia’s Centre for Clinical Epidemiology and Evaluation, Vancouver, said in an interview.

“The next step should be developing implementation strategies and identifying the most suitable health care professionals to provide pharmacogenomic-guided care,” she said.

The study was published online on in the Canadian Medical Association Journal.
 

Developing a model

The World Health Organization has predicted that depression will be the leading cause of disability worldwide by 2030. However, about half of patients don’t respond to the antidepressant that they are initially prescribed, and more than one-quarter report adverse effects. Previous studies have found that up to 42% of the lack in response stems from genetic factors that affect medication metabolism.

Pharmacogenomic testing, which uses a blood, saliva, or buccal swab sample, could help identify genetic variants involved in drug metabolism and response as well as guide prescribing and reduce adverse effects, the authors wrote.

Dr. Ghanbarian and colleagues developed a microsimulation model in collaboration with patient partners, clinicians, and the health system to evaluate the effectiveness and cost-effectiveness of pharmacogenomic testing for adult patients with MDD in British Columbia. The model included unique patient characteristics, such as metabolizer phenotypes, and followed the experience of patients through diagnosis, treatment, and recurrence.

According to British Columbia administrative data from 2015 to 2020, the model simulated a population of 194,149 adults and incorporated 40 different antidepressants and other treatments, including electroconvulsive therapy (ECT) and psychotherapy. The research team compared treatment pathways for patients with and without pharmacogenomic testing over 20 years.

Overall, the model showed that pharmacogenomic-guided treatment resulted in higher remission rates and lower discontinuation rates, with 23,216 (37%) fewer patients developing refractory depression and decreased use of resource-intensive treatment options such as ECT and psychotherapy (by 28% and 22%, respectively). According to the model, these reductions would save the British Columbia health system $4,926 CAD per patient, or about $56 million CAD over 20 years.

These findings provide a solid economic justification for clinical implementation of pharmacogenomic-guided depression treatment in Canada.

In addition, the model found that patients who underwent pharmacogenomic testing spent 15% more time in the “well” state without depression symptoms and 18% less time in the MDD state with recurrent episodes or refractory depression. In turn, this would mean 1,869 fewer deaths and 21,346 fewer all-cause hospital admissions over 20 years.

Pharmacogenomic testing also led to gains of 0.064 life-years and 0.381 quality-adjusted life-years per patient, or 12,436 life-years and 74,023 QALYs for all of British Columbia over 20 years.

From a cost perspective, the $121 million CAD cost of pharmacogenomic testing and $524 million CAD increase in episodic care were offset by a decrease in the cost of refractory MDD care. In sensitivity analyses, up-front investment in pharmacogenomic testing was typically offset after 2 years through lower direct medical costs, and it was also considered a cost-saving measure from that point forward.

“By incorporating the perspectives of patients with lived and living experience into this model, alongside robust data sets, we were able to carefully simulate the treatment journey of people with major depression,” Dr. Ghanbarian said. “The simulation model is designed to be flexible and could be applied to other jurisdictions beyond British Columbia, where we might expect to see similar benefits, particularly within a comparable Canadian context.”
 

Implementing the model

Now, Dr. Ghanbarian and colleagues are interested in potential implementation strategies at a system-wide level. For now, pharmacogenomic tests aren’t offered through the public health systems across Canada, but patients can pay for them through private companies.

“These findings provide a solid economic justification for clinical implementation of pharmacogenomic-guided depression treatment in Canada,” Chad Bousman, PhD, associate professor of physiology and pharmacology at the University of Calgary (Alta.), said in an interview.

Dr. Bousman, who was not involved with this study, coauthored the Clinical Pharmacogenetics Implementation Consortium guideline for several genotypes and serotonin reuptake inhibitor antidepressants. He and colleagues have also developed and evaluated web-based tools that translate pharmacogenetic data into evidence-based prescribing recommendations.

“The hope is that this work will facilitate investment in the establishment of the necessary infrastructure to ensure Canadians have equitable access to pharmacogenomic testing and ultimately improve mental health outcomes,” he said.

The study was funded by Genome BC, Genome Canada, and Michael Smith Health Research British Columbia. Dr. Ghanbarian and Dr. Bousman reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

Pharmacogenomic testing for antidepressants could help reduce the time and cost it takes to find the most effective medication for a patient, according to a new study.

Scientists developed a microsimulation model to evaluate the effectiveness of pharmacogenomic testing for adult patients in British Columbia, with newly diagnosed moderate to severe major depressive disorder (MDD). The model predicted that testing could result in 37% fewer patients developing refractory depression, 15% more time of patients feeling well, and a health system cost-savings of $956 million CAD over 20 years.

“Our study shows that, if pharmacogenomic testing guides the prescription of an effective antidepressant, it can reduce the lengthy trial-and-error process many patients experience and dramatically reduce the financial burden on the health care system,” Shahzad Ghanbarian, PhD, the lead author and a research analyst at the University of British Columbia’s Centre for Clinical Epidemiology and Evaluation, Vancouver, said in an interview.

“The next step should be developing implementation strategies and identifying the most suitable health care professionals to provide pharmacogenomic-guided care,” she said.

The study was published online on in the Canadian Medical Association Journal.
 

Developing a model

The World Health Organization has predicted that depression will be the leading cause of disability worldwide by 2030. However, about half of patients don’t respond to the antidepressant that they are initially prescribed, and more than one-quarter report adverse effects. Previous studies have found that up to 42% of the lack in response stems from genetic factors that affect medication metabolism.

Pharmacogenomic testing, which uses a blood, saliva, or buccal swab sample, could help identify genetic variants involved in drug metabolism and response as well as guide prescribing and reduce adverse effects, the authors wrote.

Dr. Ghanbarian and colleagues developed a microsimulation model in collaboration with patient partners, clinicians, and the health system to evaluate the effectiveness and cost-effectiveness of pharmacogenomic testing for adult patients with MDD in British Columbia. The model included unique patient characteristics, such as metabolizer phenotypes, and followed the experience of patients through diagnosis, treatment, and recurrence.

According to British Columbia administrative data from 2015 to 2020, the model simulated a population of 194,149 adults and incorporated 40 different antidepressants and other treatments, including electroconvulsive therapy (ECT) and psychotherapy. The research team compared treatment pathways for patients with and without pharmacogenomic testing over 20 years.

Overall, the model showed that pharmacogenomic-guided treatment resulted in higher remission rates and lower discontinuation rates, with 23,216 (37%) fewer patients developing refractory depression and decreased use of resource-intensive treatment options such as ECT and psychotherapy (by 28% and 22%, respectively). According to the model, these reductions would save the British Columbia health system $4,926 CAD per patient, or about $56 million CAD over 20 years.

These findings provide a solid economic justification for clinical implementation of pharmacogenomic-guided depression treatment in Canada.

In addition, the model found that patients who underwent pharmacogenomic testing spent 15% more time in the “well” state without depression symptoms and 18% less time in the MDD state with recurrent episodes or refractory depression. In turn, this would mean 1,869 fewer deaths and 21,346 fewer all-cause hospital admissions over 20 years.

Pharmacogenomic testing also led to gains of 0.064 life-years and 0.381 quality-adjusted life-years per patient, or 12,436 life-years and 74,023 QALYs for all of British Columbia over 20 years.

From a cost perspective, the $121 million CAD cost of pharmacogenomic testing and $524 million CAD increase in episodic care were offset by a decrease in the cost of refractory MDD care. In sensitivity analyses, up-front investment in pharmacogenomic testing was typically offset after 2 years through lower direct medical costs, and it was also considered a cost-saving measure from that point forward.

“By incorporating the perspectives of patients with lived and living experience into this model, alongside robust data sets, we were able to carefully simulate the treatment journey of people with major depression,” Dr. Ghanbarian said. “The simulation model is designed to be flexible and could be applied to other jurisdictions beyond British Columbia, where we might expect to see similar benefits, particularly within a comparable Canadian context.”
 

Implementing the model

Now, Dr. Ghanbarian and colleagues are interested in potential implementation strategies at a system-wide level. For now, pharmacogenomic tests aren’t offered through the public health systems across Canada, but patients can pay for them through private companies.

“These findings provide a solid economic justification for clinical implementation of pharmacogenomic-guided depression treatment in Canada,” Chad Bousman, PhD, associate professor of physiology and pharmacology at the University of Calgary (Alta.), said in an interview.

Dr. Bousman, who was not involved with this study, coauthored the Clinical Pharmacogenetics Implementation Consortium guideline for several genotypes and serotonin reuptake inhibitor antidepressants. He and colleagues have also developed and evaluated web-based tools that translate pharmacogenetic data into evidence-based prescribing recommendations.

“The hope is that this work will facilitate investment in the establishment of the necessary infrastructure to ensure Canadians have equitable access to pharmacogenomic testing and ultimately improve mental health outcomes,” he said.

The study was funded by Genome BC, Genome Canada, and Michael Smith Health Research British Columbia. Dr. Ghanbarian and Dr. Bousman reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

Pharmacogenomic testing for antidepressants could help reduce the time and cost it takes to find the most effective medication for a patient, according to a new study.

Scientists developed a microsimulation model to evaluate the effectiveness of pharmacogenomic testing for adult patients in British Columbia, with newly diagnosed moderate to severe major depressive disorder (MDD). The model predicted that testing could result in 37% fewer patients developing refractory depression, 15% more time of patients feeling well, and a health system cost-savings of $956 million CAD over 20 years.

“Our study shows that, if pharmacogenomic testing guides the prescription of an effective antidepressant, it can reduce the lengthy trial-and-error process many patients experience and dramatically reduce the financial burden on the health care system,” Shahzad Ghanbarian, PhD, the lead author and a research analyst at the University of British Columbia’s Centre for Clinical Epidemiology and Evaluation, Vancouver, said in an interview.

“The next step should be developing implementation strategies and identifying the most suitable health care professionals to provide pharmacogenomic-guided care,” she said.

The study was published online on in the Canadian Medical Association Journal.
 

Developing a model

The World Health Organization has predicted that depression will be the leading cause of disability worldwide by 2030. However, about half of patients don’t respond to the antidepressant that they are initially prescribed, and more than one-quarter report adverse effects. Previous studies have found that up to 42% of the lack in response stems from genetic factors that affect medication metabolism.

Pharmacogenomic testing, which uses a blood, saliva, or buccal swab sample, could help identify genetic variants involved in drug metabolism and response as well as guide prescribing and reduce adverse effects, the authors wrote.

Dr. Ghanbarian and colleagues developed a microsimulation model in collaboration with patient partners, clinicians, and the health system to evaluate the effectiveness and cost-effectiveness of pharmacogenomic testing for adult patients with MDD in British Columbia. The model included unique patient characteristics, such as metabolizer phenotypes, and followed the experience of patients through diagnosis, treatment, and recurrence.

According to British Columbia administrative data from 2015 to 2020, the model simulated a population of 194,149 adults and incorporated 40 different antidepressants and other treatments, including electroconvulsive therapy (ECT) and psychotherapy. The research team compared treatment pathways for patients with and without pharmacogenomic testing over 20 years.

Overall, the model showed that pharmacogenomic-guided treatment resulted in higher remission rates and lower discontinuation rates, with 23,216 (37%) fewer patients developing refractory depression and decreased use of resource-intensive treatment options such as ECT and psychotherapy (by 28% and 22%, respectively). According to the model, these reductions would save the British Columbia health system $4,926 CAD per patient, or about $56 million CAD over 20 years.

These findings provide a solid economic justification for clinical implementation of pharmacogenomic-guided depression treatment in Canada.

In addition, the model found that patients who underwent pharmacogenomic testing spent 15% more time in the “well” state without depression symptoms and 18% less time in the MDD state with recurrent episodes or refractory depression. In turn, this would mean 1,869 fewer deaths and 21,346 fewer all-cause hospital admissions over 20 years.

Pharmacogenomic testing also led to gains of 0.064 life-years and 0.381 quality-adjusted life-years per patient, or 12,436 life-years and 74,023 QALYs for all of British Columbia over 20 years.

From a cost perspective, the $121 million CAD cost of pharmacogenomic testing and $524 million CAD increase in episodic care were offset by a decrease in the cost of refractory MDD care. In sensitivity analyses, up-front investment in pharmacogenomic testing was typically offset after 2 years through lower direct medical costs, and it was also considered a cost-saving measure from that point forward.

“By incorporating the perspectives of patients with lived and living experience into this model, alongside robust data sets, we were able to carefully simulate the treatment journey of people with major depression,” Dr. Ghanbarian said. “The simulation model is designed to be flexible and could be applied to other jurisdictions beyond British Columbia, where we might expect to see similar benefits, particularly within a comparable Canadian context.”
 

Implementing the model

Now, Dr. Ghanbarian and colleagues are interested in potential implementation strategies at a system-wide level. For now, pharmacogenomic tests aren’t offered through the public health systems across Canada, but patients can pay for them through private companies.

“These findings provide a solid economic justification for clinical implementation of pharmacogenomic-guided depression treatment in Canada,” Chad Bousman, PhD, associate professor of physiology and pharmacology at the University of Calgary (Alta.), said in an interview.

Dr. Bousman, who was not involved with this study, coauthored the Clinical Pharmacogenetics Implementation Consortium guideline for several genotypes and serotonin reuptake inhibitor antidepressants. He and colleagues have also developed and evaluated web-based tools that translate pharmacogenetic data into evidence-based prescribing recommendations.

“The hope is that this work will facilitate investment in the establishment of the necessary infrastructure to ensure Canadians have equitable access to pharmacogenomic testing and ultimately improve mental health outcomes,” he said.

The study was funded by Genome BC, Genome Canada, and Michael Smith Health Research British Columbia. Dr. Ghanbarian and Dr. Bousman reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

Maternal depressive symptoms probably start at or before pregnancy, with trajectories that remain stable across the perinatal into the postnatal period, new research suggests.

The analysis of more than 11,000 pregnant women with depressive symptoms from seven prospective cohorts in Canada, the United Kingdom, and Singapore suggests that depressive symptoms (low, mild, or high levels) start sooner and last longer than is commonly thought.

The term “postnatal depression” is “at odds with existing scientific literature and the experience of clinicians who treat mental disorders in the context of obstetric practice,” said Michael J. Meaney, PhD, professor at McGill University, Montreal, and director of the Translational Neuroscience Program at the Agency for Science, Technology and Research (A*STAR), Singapore. 

“Although we anticipated that the prenatal period would be the primary time of onset and that symptom levels would be largely stable, I was nevertheless surprised at how this pattern was so universal across so many studies,” he said in an interview. “In truth, we saw very little evidence for a postnatal onset.”

This suggests that depressive symptoms start earlier than previously thought, and “that the relevant clinical settings for prevention are those treating women in routine health care, including family medicine,” he added.
 

Start screening sooner 

The investigators examined the course and stability of self-reported depressive symptoms at multiple time points across the perinatal period among 11,563 pregnant women in seven cohorts from the United Kingdom, Canada, and Singapore. Participants’ mean age was 29 years; 87.6% were White, 4.9% were East Asian, and 2.6% were Southeast Asian. 

The analysis tracked depressive symptoms from preconception through pregnancy to 2 years after childbirth. Three groups of mothers were identified in each cohort on the basis of their level of depressive symptoms (low, mild, or high) as assessed by the Edinburgh Postnatal Depression Scale (EPDS) or the Center for Epidemiological Studies Depression (CES-D).

The team found that all mothers within and across all cohorts had stable trajectories of maternal depressive symptoms from pregnancy onward. Trajectories for mothers who passed clinically validated cutoffs for “probable” depression also showed stable trajectories from pregnancy into the postnatal period.

“Taken together, these findings suggest that maternal depressive symptom levels in community-based cohort studies are apparent during pregnancy and remain stable into the postnatal period,” the authors write. “The results point to the early antenatal period as a timepoint for the identification of stable trajectories of maternal depressive symptoms. Public health policies should emphasize the early antenatal period as the optimal timing for interventions targeting maternal depressive symptoms.”

The findings, they note, “underscore the American Psychiatric Association’s recent approach in renaming postpartum depression as peripartum depression.”

Furthermore, a recent paper of the group’s findings details that depressive symptoms may often predate conception. 

“Our findings should serve to universally align practice to prenatal screening,” even though depression screening often takes place in a mid-gestational visit during the second trimester, Dr. Meaney said. “Our findings and those on the effects on child development strongly suggest the timing of the screening must be advanced into the first confirmation of pregnancy.” 
 

Depression is likely worse in the United States

Catherine Monk, PhD, chief of the Division of Women’s Mental Health and professor of medical psychology at Columbia University, Vagelos College of Physicians and Surgeons, New York, said in an interview that the results of the study “amplify similar research findings and the experience of most perinatal clinicians: Depression is stable from pregnancy onwards.”

John Abbott/Columbia University

Dr. Monk, who was not involved in the research, said that “as the authors note, the common focus on postpartum depression misses the months of prior suffering and an opportunity for earlier intervention.” Dr. Monk said she would have liked the results to have been examined further by race and ethnicity and socioeconomic factors. “Also, the combined sample does not include a U.S. cohort. This is significant as the U.S. has the highest maternal morbidity and mortality rate of developed nations, and some reports identify mental health factors as the number-one cause of maternal mortality.”

“Given the tremendous economic, racial, and ethnic inequities in health care – the lack of any kind of health justice – it is quite possible that in the U.S., depression that starts in pregnancy worsens over time, at least for some demographic groups,” Dr. Monk said. “Rates of depression, levels of depression, and the course of it during the peripartum period may be even more dire [in the U.S.] than what is represented in this article.” “What should be practice-changing about this article, and so many others demonstrating the persistent and often high levels of life-threatening depression during pregnancy, is the need for mental health providers to advocate for changes to the low rates of insurance reimbursement that push providers away from accepting insurance and into private practice, making access to affordable mental care nearly impossible for most,” she concluded. 

This study was supported by the Singapore Institute for Clinical Sciences, Agency for Science, Technology, and Research; the Toxic Stress Network of the JPB Foundation; the Hope for Depression Research Foundation; and the Jacob’s Foundation. Dr. Meaney and Dr. Monk report no conflicts of interest.

A version of this article appeared on Medscape.com.

Maternal depressive symptoms probably start at or before pregnancy, with trajectories that remain stable across the perinatal into the postnatal period, new research suggests.

The analysis of more than 11,000 pregnant women with depressive symptoms from seven prospective cohorts in Canada, the United Kingdom, and Singapore suggests that depressive symptoms (low, mild, or high levels) start sooner and last longer than is commonly thought.

The term “postnatal depression” is “at odds with existing scientific literature and the experience of clinicians who treat mental disorders in the context of obstetric practice,” said Michael J. Meaney, PhD, professor at McGill University, Montreal, and director of the Translational Neuroscience Program at the Agency for Science, Technology and Research (A*STAR), Singapore. 

“Although we anticipated that the prenatal period would be the primary time of onset and that symptom levels would be largely stable, I was nevertheless surprised at how this pattern was so universal across so many studies,” he said in an interview. “In truth, we saw very little evidence for a postnatal onset.”

This suggests that depressive symptoms start earlier than previously thought, and “that the relevant clinical settings for prevention are those treating women in routine health care, including family medicine,” he added.
 

Start screening sooner 

The investigators examined the course and stability of self-reported depressive symptoms at multiple time points across the perinatal period among 11,563 pregnant women in seven cohorts from the United Kingdom, Canada, and Singapore. Participants’ mean age was 29 years; 87.6% were White, 4.9% were East Asian, and 2.6% were Southeast Asian. 

The analysis tracked depressive symptoms from preconception through pregnancy to 2 years after childbirth. Three groups of mothers were identified in each cohort on the basis of their level of depressive symptoms (low, mild, or high) as assessed by the Edinburgh Postnatal Depression Scale (EPDS) or the Center for Epidemiological Studies Depression (CES-D).

The team found that all mothers within and across all cohorts had stable trajectories of maternal depressive symptoms from pregnancy onward. Trajectories for mothers who passed clinically validated cutoffs for “probable” depression also showed stable trajectories from pregnancy into the postnatal period.

“Taken together, these findings suggest that maternal depressive symptom levels in community-based cohort studies are apparent during pregnancy and remain stable into the postnatal period,” the authors write. “The results point to the early antenatal period as a timepoint for the identification of stable trajectories of maternal depressive symptoms. Public health policies should emphasize the early antenatal period as the optimal timing for interventions targeting maternal depressive symptoms.”

The findings, they note, “underscore the American Psychiatric Association’s recent approach in renaming postpartum depression as peripartum depression.”

Furthermore, a recent paper of the group’s findings details that depressive symptoms may often predate conception. 

“Our findings should serve to universally align practice to prenatal screening,” even though depression screening often takes place in a mid-gestational visit during the second trimester, Dr. Meaney said. “Our findings and those on the effects on child development strongly suggest the timing of the screening must be advanced into the first confirmation of pregnancy.” 
 

Depression is likely worse in the United States

Catherine Monk, PhD, chief of the Division of Women’s Mental Health and professor of medical psychology at Columbia University, Vagelos College of Physicians and Surgeons, New York, said in an interview that the results of the study “amplify similar research findings and the experience of most perinatal clinicians: Depression is stable from pregnancy onwards.”

John Abbott/Columbia University

Dr. Monk, who was not involved in the research, said that “as the authors note, the common focus on postpartum depression misses the months of prior suffering and an opportunity for earlier intervention.” Dr. Monk said she would have liked the results to have been examined further by race and ethnicity and socioeconomic factors. “Also, the combined sample does not include a U.S. cohort. This is significant as the U.S. has the highest maternal morbidity and mortality rate of developed nations, and some reports identify mental health factors as the number-one cause of maternal mortality.”

“Given the tremendous economic, racial, and ethnic inequities in health care – the lack of any kind of health justice – it is quite possible that in the U.S., depression that starts in pregnancy worsens over time, at least for some demographic groups,” Dr. Monk said. “Rates of depression, levels of depression, and the course of it during the peripartum period may be even more dire [in the U.S.] than what is represented in this article.” “What should be practice-changing about this article, and so many others demonstrating the persistent and often high levels of life-threatening depression during pregnancy, is the need for mental health providers to advocate for changes to the low rates of insurance reimbursement that push providers away from accepting insurance and into private practice, making access to affordable mental care nearly impossible for most,” she concluded. 

This study was supported by the Singapore Institute for Clinical Sciences, Agency for Science, Technology, and Research; the Toxic Stress Network of the JPB Foundation; the Hope for Depression Research Foundation; and the Jacob’s Foundation. Dr. Meaney and Dr. Monk report no conflicts of interest.

A version of this article appeared on Medscape.com.

Maternal depressive symptoms probably start at or before pregnancy, with trajectories that remain stable across the perinatal into the postnatal period, new research suggests.

The analysis of more than 11,000 pregnant women with depressive symptoms from seven prospective cohorts in Canada, the United Kingdom, and Singapore suggests that depressive symptoms (low, mild, or high levels) start sooner and last longer than is commonly thought.

The term “postnatal depression” is “at odds with existing scientific literature and the experience of clinicians who treat mental disorders in the context of obstetric practice,” said Michael J. Meaney, PhD, professor at McGill University, Montreal, and director of the Translational Neuroscience Program at the Agency for Science, Technology and Research (A*STAR), Singapore. 

“Although we anticipated that the prenatal period would be the primary time of onset and that symptom levels would be largely stable, I was nevertheless surprised at how this pattern was so universal across so many studies,” he said in an interview. “In truth, we saw very little evidence for a postnatal onset.”

This suggests that depressive symptoms start earlier than previously thought, and “that the relevant clinical settings for prevention are those treating women in routine health care, including family medicine,” he added.
 

Start screening sooner 

The investigators examined the course and stability of self-reported depressive symptoms at multiple time points across the perinatal period among 11,563 pregnant women in seven cohorts from the United Kingdom, Canada, and Singapore. Participants’ mean age was 29 years; 87.6% were White, 4.9% were East Asian, and 2.6% were Southeast Asian. 

The analysis tracked depressive symptoms from preconception through pregnancy to 2 years after childbirth. Three groups of mothers were identified in each cohort on the basis of their level of depressive symptoms (low, mild, or high) as assessed by the Edinburgh Postnatal Depression Scale (EPDS) or the Center for Epidemiological Studies Depression (CES-D).

The team found that all mothers within and across all cohorts had stable trajectories of maternal depressive symptoms from pregnancy onward. Trajectories for mothers who passed clinically validated cutoffs for “probable” depression also showed stable trajectories from pregnancy into the postnatal period.

“Taken together, these findings suggest that maternal depressive symptom levels in community-based cohort studies are apparent during pregnancy and remain stable into the postnatal period,” the authors write. “The results point to the early antenatal period as a timepoint for the identification of stable trajectories of maternal depressive symptoms. Public health policies should emphasize the early antenatal period as the optimal timing for interventions targeting maternal depressive symptoms.”

The findings, they note, “underscore the American Psychiatric Association’s recent approach in renaming postpartum depression as peripartum depression.”

Furthermore, a recent paper of the group’s findings details that depressive symptoms may often predate conception. 

“Our findings should serve to universally align practice to prenatal screening,” even though depression screening often takes place in a mid-gestational visit during the second trimester, Dr. Meaney said. “Our findings and those on the effects on child development strongly suggest the timing of the screening must be advanced into the first confirmation of pregnancy.” 
 

Depression is likely worse in the United States

Catherine Monk, PhD, chief of the Division of Women’s Mental Health and professor of medical psychology at Columbia University, Vagelos College of Physicians and Surgeons, New York, said in an interview that the results of the study “amplify similar research findings and the experience of most perinatal clinicians: Depression is stable from pregnancy onwards.”

John Abbott/Columbia University

Dr. Monk, who was not involved in the research, said that “as the authors note, the common focus on postpartum depression misses the months of prior suffering and an opportunity for earlier intervention.” Dr. Monk said she would have liked the results to have been examined further by race and ethnicity and socioeconomic factors. “Also, the combined sample does not include a U.S. cohort. This is significant as the U.S. has the highest maternal morbidity and mortality rate of developed nations, and some reports identify mental health factors as the number-one cause of maternal mortality.”

“Given the tremendous economic, racial, and ethnic inequities in health care – the lack of any kind of health justice – it is quite possible that in the U.S., depression that starts in pregnancy worsens over time, at least for some demographic groups,” Dr. Monk said. “Rates of depression, levels of depression, and the course of it during the peripartum period may be even more dire [in the U.S.] than what is represented in this article.” “What should be practice-changing about this article, and so many others demonstrating the persistent and often high levels of life-threatening depression during pregnancy, is the need for mental health providers to advocate for changes to the low rates of insurance reimbursement that push providers away from accepting insurance and into private practice, making access to affordable mental care nearly impossible for most,” she concluded. 

This study was supported by the Singapore Institute for Clinical Sciences, Agency for Science, Technology, and Research; the Toxic Stress Network of the JPB Foundation; the Hope for Depression Research Foundation; and the Jacob’s Foundation. Dr. Meaney and Dr. Monk report no conflicts of interest.

A version of this article appeared on Medscape.com.

Women with bipolar disorder were three times more likely than were healthy controls to experience polycystic ovarian syndrome, based on data from nearly 250 individuals.

Previous studies suggest that the prevalence of polycystic ovarian syndrome (PCOS) is higher in bipolar disorder (BD) patients compared with individuals not diagnosed with BD, wrote Jieyu Liu, PhD, of the Second Xiangya Hospital of Central South University, Hunan, China, and colleagues.

However, studies have been limited to drug-treated BD patients, and data on the effects of BD on the development of PCOS are limited, they said. Data from previous studies also indicate that serum testosterone levels, serum androstenedione levels, and polycystic ovarian morphology (PCOM) are increased in BD patients compared with women without BD.

In a study published in the Journal of Affective Disorders, the researchers recruited 72 BD patients on long-term medication, 72 drug-naive patients, and 98 healthy controls between March 2022 and November 2022.

PCOM was assessed using ≥ 8 MHz transvaginal transducers to determine the number of follicles and ovarian volume. PCOS was then defined using the Rotterdam criteria, in which patients met two of three qualifications: oligoovulation or anovulation; hyperandrogenemia; or PCOM (excluding other endocrine diseases).

In a multivariate analysis, drug-naive women with BD had significantly higher rates of PCOS compared with healthy controls (odds ratio 3.02). The drug-naive BD patients also had a greater prevalence of oligoamenorrhea compared with healthy controls (36.36% vs. 12.12%) and higher levels of anti-mullerian hormone, luteinizing hormone, and follicle stimulating hormone compared to the controls.

A further regression analysis showed that those on long-term valproate treatment had the highest risk (OR 3.89) and the prevalence of PCOS was significantly higher among patients treated with valproate compared with drug-naive patients (53.3% vs. 30.6%). Younger age and the presence of insulin resistance also were associated with increased risk of PCOS (OR 0.37 and OR 1.73, respectively).

“Unexpectedly, no significant differences in serum androgen levels, including TT, FAI, androstenedione, and [dehydroepiandrosterone sulfate] levels, were observed between drug-naive BD patients and the HCs,” the researchers wrote in their discussion. This difference may stem from multiple causes including demographic variables, inclusion of PCOM as a diagnostic criterion, and the impact of genetic and environmental factors, they said.

The findings were limited by several factors including the small study population, which prevented conclusions of causality and comparison of the effects of different mood stabilizers on PCOS, the researchers noted. Other limitations included the relatively homogeneous population from a single region in China, and the inability to account for the effects of diet and lifestyle.

More research is needed to explore the impact of mediations, but the results suggest that BD patients are susceptible to PCOS; therefore, they should evaluate their reproductive health before starting any medication, and review reproductive health regularly, the researchers concluded.

The study was supported by the National Natural Science Foundation of China. The researchers had no financial conflicts to disclose.

Women with bipolar disorder were three times more likely than were healthy controls to experience polycystic ovarian syndrome, based on data from nearly 250 individuals.

Previous studies suggest that the prevalence of polycystic ovarian syndrome (PCOS) is higher in bipolar disorder (BD) patients compared with individuals not diagnosed with BD, wrote Jieyu Liu, PhD, of the Second Xiangya Hospital of Central South University, Hunan, China, and colleagues.

However, studies have been limited to drug-treated BD patients, and data on the effects of BD on the development of PCOS are limited, they said. Data from previous studies also indicate that serum testosterone levels, serum androstenedione levels, and polycystic ovarian morphology (PCOM) are increased in BD patients compared with women without BD.

In a study published in the Journal of Affective Disorders, the researchers recruited 72 BD patients on long-term medication, 72 drug-naive patients, and 98 healthy controls between March 2022 and November 2022.

PCOM was assessed using ≥ 8 MHz transvaginal transducers to determine the number of follicles and ovarian volume. PCOS was then defined using the Rotterdam criteria, in which patients met two of three qualifications: oligoovulation or anovulation; hyperandrogenemia; or PCOM (excluding other endocrine diseases).

In a multivariate analysis, drug-naive women with BD had significantly higher rates of PCOS compared with healthy controls (odds ratio 3.02). The drug-naive BD patients also had a greater prevalence of oligoamenorrhea compared with healthy controls (36.36% vs. 12.12%) and higher levels of anti-mullerian hormone, luteinizing hormone, and follicle stimulating hormone compared to the controls.

A further regression analysis showed that those on long-term valproate treatment had the highest risk (OR 3.89) and the prevalence of PCOS was significantly higher among patients treated with valproate compared with drug-naive patients (53.3% vs. 30.6%). Younger age and the presence of insulin resistance also were associated with increased risk of PCOS (OR 0.37 and OR 1.73, respectively).

“Unexpectedly, no significant differences in serum androgen levels, including TT, FAI, androstenedione, and [dehydroepiandrosterone sulfate] levels, were observed between drug-naive BD patients and the HCs,” the researchers wrote in their discussion. This difference may stem from multiple causes including demographic variables, inclusion of PCOM as a diagnostic criterion, and the impact of genetic and environmental factors, they said.

The findings were limited by several factors including the small study population, which prevented conclusions of causality and comparison of the effects of different mood stabilizers on PCOS, the researchers noted. Other limitations included the relatively homogeneous population from a single region in China, and the inability to account for the effects of diet and lifestyle.

More research is needed to explore the impact of mediations, but the results suggest that BD patients are susceptible to PCOS; therefore, they should evaluate their reproductive health before starting any medication, and review reproductive health regularly, the researchers concluded.

The study was supported by the National Natural Science Foundation of China. The researchers had no financial conflicts to disclose.

Women with bipolar disorder were three times more likely than were healthy controls to experience polycystic ovarian syndrome, based on data from nearly 250 individuals.

Previous studies suggest that the prevalence of polycystic ovarian syndrome (PCOS) is higher in bipolar disorder (BD) patients compared with individuals not diagnosed with BD, wrote Jieyu Liu, PhD, of the Second Xiangya Hospital of Central South University, Hunan, China, and colleagues.

However, studies have been limited to drug-treated BD patients, and data on the effects of BD on the development of PCOS are limited, they said. Data from previous studies also indicate that serum testosterone levels, serum androstenedione levels, and polycystic ovarian morphology (PCOM) are increased in BD patients compared with women without BD.

In a study published in the Journal of Affective Disorders, the researchers recruited 72 BD patients on long-term medication, 72 drug-naive patients, and 98 healthy controls between March 2022 and November 2022.

PCOM was assessed using ≥ 8 MHz transvaginal transducers to determine the number of follicles and ovarian volume. PCOS was then defined using the Rotterdam criteria, in which patients met two of three qualifications: oligoovulation or anovulation; hyperandrogenemia; or PCOM (excluding other endocrine diseases).

In a multivariate analysis, drug-naive women with BD had significantly higher rates of PCOS compared with healthy controls (odds ratio 3.02). The drug-naive BD patients also had a greater prevalence of oligoamenorrhea compared with healthy controls (36.36% vs. 12.12%) and higher levels of anti-mullerian hormone, luteinizing hormone, and follicle stimulating hormone compared to the controls.

A further regression analysis showed that those on long-term valproate treatment had the highest risk (OR 3.89) and the prevalence of PCOS was significantly higher among patients treated with valproate compared with drug-naive patients (53.3% vs. 30.6%). Younger age and the presence of insulin resistance also were associated with increased risk of PCOS (OR 0.37 and OR 1.73, respectively).

“Unexpectedly, no significant differences in serum androgen levels, including TT, FAI, androstenedione, and [dehydroepiandrosterone sulfate] levels, were observed between drug-naive BD patients and the HCs,” the researchers wrote in their discussion. This difference may stem from multiple causes including demographic variables, inclusion of PCOM as a diagnostic criterion, and the impact of genetic and environmental factors, they said.

The findings were limited by several factors including the small study population, which prevented conclusions of causality and comparison of the effects of different mood stabilizers on PCOS, the researchers noted. Other limitations included the relatively homogeneous population from a single region in China, and the inability to account for the effects of diet and lifestyle.

More research is needed to explore the impact of mediations, but the results suggest that BD patients are susceptible to PCOS; therefore, they should evaluate their reproductive health before starting any medication, and review reproductive health regularly, the researchers concluded.

The study was supported by the National Natural Science Foundation of China. The researchers had no financial conflicts to disclose.

TOPLINE:

Irritable bowel syndrome (IBS) is associated with increased odds of fibromyalgia and chronic fatigue syndrome (CFS), new research suggests.

METHODOLOGY:

• The authors conducted a retrospective cohort study to investigate the prevalence and predictors of fibromyalgia and CFS in patients hospitalized with IBS vs people without IBS.
• The researchers used ICD-10 codes to analyze U.S. National Inpatient Sample (NIS) data from 2016-2019.
• A subgroup analysis investigated associations with IBS-diarrhea (IBS-D), IBS-constipation (IBS-C), and IBS-mixed types.
• Variables included patient age, sex, ethnicity, race, household income, insurance status, and hospital-level characteristics (including location, bed size, and teaching status).

TAKEAWAY:

• Among 1.2 million patients with IBS included in the study, 10.7% also had fibromyalgia and 0.4% had CFS. The majority of fibromyalgia (96.5%) and CFS (89.9%) patients were female and White (86.5%). CFS prevalence also was highest among White persons (90.7%).
• The prevalence of fibromyalgia and CFS was significantly higher in patients with IBS compared to those without IBS (adjusted odds ratio [AOR], 5.33 for fibromyalgia and AOR, 5.4 for CFS).
• IBS-D, IBS-C, and IBS-mixed types were independently associated with increased odds of fibromyalgia and CFS.
• Independent predictors of increased odds of fibromyalgia and CFS, respectively, were increasing age (AOR, 1.02 for both), female sex (AOR, 11.2; AOR, 1.86) and White race (AOR, 2.04; AOR, 1.69).
• Overall, White race, lower socioeconomic status, smoking, alcohol use, obesity, and hyperlipidemia were associated with increased odds of fibromyalgia. For CFS, increased odds were associated with White race, higher socioeconomic status, smoking, obesity, and hyperlipidemia.

IN PRACTICE:

“In current clinical practice, there is a high risk of neglecting multi-syndromic patients. We as clinicians should integrate in our practice with regular screening for other somatic disorders in the IBS population and determine the need to consult other specialties like rheumatology and psychiatry to improve the overall health outcome in IBS patients,” the authors wrote.

SOURCE:

Zahid Ijaz Tarar, MD, University of Missouri, Columbia, led the study, which was published online in Biomedicines.

LIMITATIONS:

The retrospective design of the study can only show associations, not a causal relationship. Lack of blinding and randomization in the data creates bias. The NIS database does not provide medication and laboratory data, so the effect of pharmaceutical therapies cannot be measured.

DISCLOSURES:

The research received no external funding. The authors declare no potential conflict of interest with respect to the research, authorship, and/or publication of this article.

TOPLINE:

Irritable bowel syndrome (IBS) is associated with increased odds of fibromyalgia and chronic fatigue syndrome (CFS), new research suggests.

METHODOLOGY:

• The authors conducted a retrospective cohort study to investigate the prevalence and predictors of fibromyalgia and CFS in patients hospitalized with IBS vs people without IBS.
• The researchers used ICD-10 codes to analyze U.S. National Inpatient Sample (NIS) data from 2016-2019.
• A subgroup analysis investigated associations with IBS-diarrhea (IBS-D), IBS-constipation (IBS-C), and IBS-mixed types.
• Variables included patient age, sex, ethnicity, race, household income, insurance status, and hospital-level characteristics (including location, bed size, and teaching status).

TAKEAWAY:

• Among 1.2 million patients with IBS included in the study, 10.7% also had fibromyalgia and 0.4% had CFS. The majority of fibromyalgia (96.5%) and CFS (89.9%) patients were female and White (86.5%). CFS prevalence also was highest among White persons (90.7%).
• The prevalence of fibromyalgia and CFS was significantly higher in patients with IBS compared to those without IBS (adjusted odds ratio [AOR], 5.33 for fibromyalgia and AOR, 5.4 for CFS).
• IBS-D, IBS-C, and IBS-mixed types were independently associated with increased odds of fibromyalgia and CFS.
• Independent predictors of increased odds of fibromyalgia and CFS, respectively, were increasing age (AOR, 1.02 for both), female sex (AOR, 11.2; AOR, 1.86) and White race (AOR, 2.04; AOR, 1.69).
• Overall, White race, lower socioeconomic status, smoking, alcohol use, obesity, and hyperlipidemia were associated with increased odds of fibromyalgia. For CFS, increased odds were associated with White race, higher socioeconomic status, smoking, obesity, and hyperlipidemia.

IN PRACTICE:

“In current clinical practice, there is a high risk of neglecting multi-syndromic patients. We as clinicians should integrate in our practice with regular screening for other somatic disorders in the IBS population and determine the need to consult other specialties like rheumatology and psychiatry to improve the overall health outcome in IBS patients,” the authors wrote.

SOURCE:

Zahid Ijaz Tarar, MD, University of Missouri, Columbia, led the study, which was published online in Biomedicines.

LIMITATIONS:

The retrospective design of the study can only show associations, not a causal relationship. Lack of blinding and randomization in the data creates bias. The NIS database does not provide medication and laboratory data, so the effect of pharmaceutical therapies cannot be measured.

DISCLOSURES:

The research received no external funding. The authors declare no potential conflict of interest with respect to the research, authorship, and/or publication of this article.

TOPLINE:

Irritable bowel syndrome (IBS) is associated with increased odds of fibromyalgia and chronic fatigue syndrome (CFS), new research suggests.

METHODOLOGY:

• The authors conducted a retrospective cohort study to investigate the prevalence and predictors of fibromyalgia and CFS in patients hospitalized with IBS vs people without IBS.
• The researchers used ICD-10 codes to analyze U.S. National Inpatient Sample (NIS) data from 2016-2019.
• A subgroup analysis investigated associations with IBS-diarrhea (IBS-D), IBS-constipation (IBS-C), and IBS-mixed types.
• Variables included patient age, sex, ethnicity, race, household income, insurance status, and hospital-level characteristics (including location, bed size, and teaching status).

TAKEAWAY:

• Among 1.2 million patients with IBS included in the study, 10.7% also had fibromyalgia and 0.4% had CFS. The majority of fibromyalgia (96.5%) and CFS (89.9%) patients were female and White (86.5%). CFS prevalence also was highest among White persons (90.7%).
• The prevalence of fibromyalgia and CFS was significantly higher in patients with IBS compared to those without IBS (adjusted odds ratio [AOR], 5.33 for fibromyalgia and AOR, 5.4 for CFS).
• IBS-D, IBS-C, and IBS-mixed types were independently associated with increased odds of fibromyalgia and CFS.
• Independent predictors of increased odds of fibromyalgia and CFS, respectively, were increasing age (AOR, 1.02 for both), female sex (AOR, 11.2; AOR, 1.86) and White race (AOR, 2.04; AOR, 1.69).
• Overall, White race, lower socioeconomic status, smoking, alcohol use, obesity, and hyperlipidemia were associated with increased odds of fibromyalgia. For CFS, increased odds were associated with White race, higher socioeconomic status, smoking, obesity, and hyperlipidemia.

IN PRACTICE:

“In current clinical practice, there is a high risk of neglecting multi-syndromic patients. We as clinicians should integrate in our practice with regular screening for other somatic disorders in the IBS population and determine the need to consult other specialties like rheumatology and psychiatry to improve the overall health outcome in IBS patients,” the authors wrote.

SOURCE:

Zahid Ijaz Tarar, MD, University of Missouri, Columbia, led the study, which was published online in Biomedicines.

LIMITATIONS:

The retrospective design of the study can only show associations, not a causal relationship. Lack of blinding and randomization in the data creates bias. The NIS database does not provide medication and laboratory data, so the effect of pharmaceutical therapies cannot be measured.

DISCLOSURES:

The research received no external funding. The authors declare no potential conflict of interest with respect to the research, authorship, and/or publication of this article.