Clinical Psychiatry News

Hormone replacement therapy (HRT) introduced early during the menopausal transition may protect against Alzheimer’s dementia in women carrying the APOE4 gene, new research suggests.

Results from a cohort study of almost 1,200 women showed that use of HRT was associated with higher delayed memory scores and larger entorhinal and hippocampal brain volumes – areas that are affected early by Alzheimer’s disease (AD) pathology.

HRT was also found to be most effective, as seen by larger hippocampal volume, when introduced during early perimenopause.

“Clinicians are very much aware of the susceptibility of women to cognitive disturbances during menopause,” lead author Rasha Saleh, MD, senior research associate, University of East Anglia (England), said in an interview.

“Identifying the at-risk APOE4 women and early HRT introduction can be of benefit. Confirming our findings in a clinical trial would be the next step forward,” Dr. Saleh said.

The findings were published online in Alzheimer’s Research and Therapy.
 

Personalized approaches

Dr. Saleh noted that estrogen receptors are localized in various areas of the brain, including cognition-related areas. Estrogen regulates such things as neuroinflammatory status, glucose utilization, and lipid metabolism.

“The decline of estrogen during menopause can lead to disturbance in these functions, which can accelerate AD-related pathology,” she said.

HRT during the menopausal transition and afterward is “being considered as a strategy to mitigate cognitive decline,” the investigators wrote. Early observational studies have suggested that oral estrogen “may be protective against dementia,” but results of clinical trials have been inconsistent, and some have even shown “harmful effects.”

The current researchers were “interested in the personalized approaches in the prevention of AD,” Dr. Saleh said. Preclinical and pilot data from her group have shown that women with APOE4 have “better cognitive test scores with nutritional and hormonal interventions.”

This led Dr. Saleh to hypothesize that HRT would be of more cognitive benefit for those with versus without APOE4, particularly when introduced early during the menopausal transition.

To investigate this hypothesis, the researchers analyzed baseline data from participants in the European Prevention of Alzheimer’s Dementia (EPAD) cohort. This project was initiated in 2015 with the aim of developing longitudinal models over the entire course of AD prior to dementia clinical diagnosis.

Participants were recruited from 10 European countries. All were required to be at least 50 years old, to have not been diagnosed with dementia at baseline, and to have no medical or psychiatric illness that could potentially exclude them from further research.

The current study included 1,178 women (mean age, 65.1 years), who were divided by genotype into non-APOE4 and APOE4 groups. HRT treatment for current or previous users included estrogen alone or estrogen plus progestogens via oral or transdermal administration routes, and at different doses.

The four tests used to assess cognition were the Mini-Mental State Examination dot counting to evaluate verbal working memory, the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) total score, the Four Mountain Test, and the supermarket trolley virtual reality test.

Brain MRI data were collected. The researchers focused on the medial temporal lobe as the “main brain region regulating cognition and memory processing.” This lobe includes the hippocampus, the parahippocampus, the entorhinal cortex, and the amygdala.
 

‘Critical window’

The researchers found a “trend” toward an APOE-HRT interaction (P-interaction = .097) for the total RBANS score. In particular, it was significant for the RBANS delayed memory index, where scores were consistently higher for women with APOE4 who had received HRT, compared with all other groups (P-interaction = .009).

Within-genotype group comparisons showed that HRT users had a higher RBANS total scale score and delayed memory index (P = .045 and P = .002, respectively), but only among APOE4 carriers. Effect size analyses showed a large effect of HRT use on the Four Mountain Test score and the supermarket trolley virtual reality test score (Cohen’s d = 0.988 and 1.2, respectively).

“This large effect was found only in APOE4 carriers,” the investigators noted.

Similarly, a moderate to large effect of HRT on the left entorhinal volume was observed in APOE4 carriers (Cohen’s d = 0.63).

In members of the APOE4 group who received HRT, the left entorhinal and left and right amygdala volumes were larger, compared with both no-APOE4 and non-HRT users (P-interaction = .002, .003, and .005, respectively). Similar trends were observed for the right entorhinal volume (P = .074).

In addition, among HRT users, the left entorhinal volume was larger (P = .03); the right and left anterior cingulate gyrus volumes were smaller (P = .003 and .062, respectively); and the left superior frontal gyrus volume was larger (P = .009) in comparison with women who did not receive HRT, independently of their APOE genotype.

Early use of HRT among APOE4 carriers was associated with larger right and left hippocampal volume (P = .035 and P = .028, respectively) – an association not found in non-APOE4 carriers. The association was also not significant when participants were not stratified by APOE genotype.

“The key important point here is the timing, or the ‘critical window,’ when HRT can be of most benefit,” Dr. Saleh said. “This is most beneficial when introduced early, before the neuropathology becomes irreversible.”

Study limitations include its cross-sectional design, which precludes the establishment of a causal relationship, and the fact that information regarding the type and dose of estrogen was not available for all participants.

HRT is not without risk, Dr. Saleh noted. She recommended that clinicians “carry out various screening tests to make sure that a woman is eligible for HRT and not at risk of hypercoagulability, for instance.”
 

Risk-benefit ratio

In a comment, Howard Fillit, MD, cofounder and chief science officer at the Alzheimer’s Drug Discovery Foundation, called the study “exactly the kind of work that needs to be done.”

Dr. Fillit, who was not involved with the current research, is a clinical professor of geriatric medicine, palliative care medicine, and neuroscience at Mount Sinai Hospital, New York.

He compared the process with that of osteoporosis. “We know that if women are treated [with HRT] at the time of the menopause, you can prevent the rapid bone loss that occurs with rapid estrogen loss. But if you wait 5, 10 years out, once the bone loss has occurred, the HRT doesn’t really have any impact on osteoporosis risk because the horse is already out of the barn,” he said.

Although HRT carries risks, “they can clearly be managed; and if it’s proven that estrogen or hormone replacement around the time of the menopause can be protective [against AD], the risk-benefit ratio of HRT could be in favor of treatment,” Dr. Fillit added.

The study was conducted as part of the Medical Research Council NuBrain Consortium. The investigators and Dr. Fillit reported no relevant financial relationships.

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

Hormone replacement therapy (HRT) introduced early during the menopausal transition may protect against Alzheimer’s dementia in women carrying the APOE4 gene, new research suggests.

Results from a cohort study of almost 1,200 women showed that use of HRT was associated with higher delayed memory scores and larger entorhinal and hippocampal brain volumes – areas that are affected early by Alzheimer’s disease (AD) pathology.

HRT was also found to be most effective, as seen by larger hippocampal volume, when introduced during early perimenopause.

“Clinicians are very much aware of the susceptibility of women to cognitive disturbances during menopause,” lead author Rasha Saleh, MD, senior research associate, University of East Anglia (England), said in an interview.

“Identifying the at-risk APOE4 women and early HRT introduction can be of benefit. Confirming our findings in a clinical trial would be the next step forward,” Dr. Saleh said.

The findings were published online in Alzheimer’s Research and Therapy.
 

Personalized approaches

Dr. Saleh noted that estrogen receptors are localized in various areas of the brain, including cognition-related areas. Estrogen regulates such things as neuroinflammatory status, glucose utilization, and lipid metabolism.

“The decline of estrogen during menopause can lead to disturbance in these functions, which can accelerate AD-related pathology,” she said.

HRT during the menopausal transition and afterward is “being considered as a strategy to mitigate cognitive decline,” the investigators wrote. Early observational studies have suggested that oral estrogen “may be protective against dementia,” but results of clinical trials have been inconsistent, and some have even shown “harmful effects.”

The current researchers were “interested in the personalized approaches in the prevention of AD,” Dr. Saleh said. Preclinical and pilot data from her group have shown that women with APOE4 have “better cognitive test scores with nutritional and hormonal interventions.”

This led Dr. Saleh to hypothesize that HRT would be of more cognitive benefit for those with versus without APOE4, particularly when introduced early during the menopausal transition.

To investigate this hypothesis, the researchers analyzed baseline data from participants in the European Prevention of Alzheimer’s Dementia (EPAD) cohort. This project was initiated in 2015 with the aim of developing longitudinal models over the entire course of AD prior to dementia clinical diagnosis.

Participants were recruited from 10 European countries. All were required to be at least 50 years old, to have not been diagnosed with dementia at baseline, and to have no medical or psychiatric illness that could potentially exclude them from further research.

The current study included 1,178 women (mean age, 65.1 years), who were divided by genotype into non-APOE4 and APOE4 groups. HRT treatment for current or previous users included estrogen alone or estrogen plus progestogens via oral or transdermal administration routes, and at different doses.

The four tests used to assess cognition were the Mini-Mental State Examination dot counting to evaluate verbal working memory, the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) total score, the Four Mountain Test, and the supermarket trolley virtual reality test.

Brain MRI data were collected. The researchers focused on the medial temporal lobe as the “main brain region regulating cognition and memory processing.” This lobe includes the hippocampus, the parahippocampus, the entorhinal cortex, and the amygdala.
 

‘Critical window’

The researchers found a “trend” toward an APOE-HRT interaction (P-interaction = .097) for the total RBANS score. In particular, it was significant for the RBANS delayed memory index, where scores were consistently higher for women with APOE4 who had received HRT, compared with all other groups (P-interaction = .009).

Within-genotype group comparisons showed that HRT users had a higher RBANS total scale score and delayed memory index (P = .045 and P = .002, respectively), but only among APOE4 carriers. Effect size analyses showed a large effect of HRT use on the Four Mountain Test score and the supermarket trolley virtual reality test score (Cohen’s d = 0.988 and 1.2, respectively).

“This large effect was found only in APOE4 carriers,” the investigators noted.

Similarly, a moderate to large effect of HRT on the left entorhinal volume was observed in APOE4 carriers (Cohen’s d = 0.63).

In members of the APOE4 group who received HRT, the left entorhinal and left and right amygdala volumes were larger, compared with both no-APOE4 and non-HRT users (P-interaction = .002, .003, and .005, respectively). Similar trends were observed for the right entorhinal volume (P = .074).

In addition, among HRT users, the left entorhinal volume was larger (P = .03); the right and left anterior cingulate gyrus volumes were smaller (P = .003 and .062, respectively); and the left superior frontal gyrus volume was larger (P = .009) in comparison with women who did not receive HRT, independently of their APOE genotype.

Early use of HRT among APOE4 carriers was associated with larger right and left hippocampal volume (P = .035 and P = .028, respectively) – an association not found in non-APOE4 carriers. The association was also not significant when participants were not stratified by APOE genotype.

“The key important point here is the timing, or the ‘critical window,’ when HRT can be of most benefit,” Dr. Saleh said. “This is most beneficial when introduced early, before the neuropathology becomes irreversible.”

Study limitations include its cross-sectional design, which precludes the establishment of a causal relationship, and the fact that information regarding the type and dose of estrogen was not available for all participants.

HRT is not without risk, Dr. Saleh noted. She recommended that clinicians “carry out various screening tests to make sure that a woman is eligible for HRT and not at risk of hypercoagulability, for instance.”
 

Risk-benefit ratio

In a comment, Howard Fillit, MD, cofounder and chief science officer at the Alzheimer’s Drug Discovery Foundation, called the study “exactly the kind of work that needs to be done.”

Dr. Fillit, who was not involved with the current research, is a clinical professor of geriatric medicine, palliative care medicine, and neuroscience at Mount Sinai Hospital, New York.

He compared the process with that of osteoporosis. “We know that if women are treated [with HRT] at the time of the menopause, you can prevent the rapid bone loss that occurs with rapid estrogen loss. But if you wait 5, 10 years out, once the bone loss has occurred, the HRT doesn’t really have any impact on osteoporosis risk because the horse is already out of the barn,” he said.

Although HRT carries risks, “they can clearly be managed; and if it’s proven that estrogen or hormone replacement around the time of the menopause can be protective [against AD], the risk-benefit ratio of HRT could be in favor of treatment,” Dr. Fillit added.

The study was conducted as part of the Medical Research Council NuBrain Consortium. The investigators and Dr. Fillit reported no relevant financial relationships.

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

Hormone replacement therapy (HRT) introduced early during the menopausal transition may protect against Alzheimer’s dementia in women carrying the APOE4 gene, new research suggests.

Results from a cohort study of almost 1,200 women showed that use of HRT was associated with higher delayed memory scores and larger entorhinal and hippocampal brain volumes – areas that are affected early by Alzheimer’s disease (AD) pathology.

HRT was also found to be most effective, as seen by larger hippocampal volume, when introduced during early perimenopause.

“Clinicians are very much aware of the susceptibility of women to cognitive disturbances during menopause,” lead author Rasha Saleh, MD, senior research associate, University of East Anglia (England), said in an interview.

“Identifying the at-risk APOE4 women and early HRT introduction can be of benefit. Confirming our findings in a clinical trial would be the next step forward,” Dr. Saleh said.

The findings were published online in Alzheimer’s Research and Therapy.
 

Personalized approaches

Dr. Saleh noted that estrogen receptors are localized in various areas of the brain, including cognition-related areas. Estrogen regulates such things as neuroinflammatory status, glucose utilization, and lipid metabolism.

“The decline of estrogen during menopause can lead to disturbance in these functions, which can accelerate AD-related pathology,” she said.

HRT during the menopausal transition and afterward is “being considered as a strategy to mitigate cognitive decline,” the investigators wrote. Early observational studies have suggested that oral estrogen “may be protective against dementia,” but results of clinical trials have been inconsistent, and some have even shown “harmful effects.”

The current researchers were “interested in the personalized approaches in the prevention of AD,” Dr. Saleh said. Preclinical and pilot data from her group have shown that women with APOE4 have “better cognitive test scores with nutritional and hormonal interventions.”

This led Dr. Saleh to hypothesize that HRT would be of more cognitive benefit for those with versus without APOE4, particularly when introduced early during the menopausal transition.

To investigate this hypothesis, the researchers analyzed baseline data from participants in the European Prevention of Alzheimer’s Dementia (EPAD) cohort. This project was initiated in 2015 with the aim of developing longitudinal models over the entire course of AD prior to dementia clinical diagnosis.

Participants were recruited from 10 European countries. All were required to be at least 50 years old, to have not been diagnosed with dementia at baseline, and to have no medical or psychiatric illness that could potentially exclude them from further research.

The current study included 1,178 women (mean age, 65.1 years), who were divided by genotype into non-APOE4 and APOE4 groups. HRT treatment for current or previous users included estrogen alone or estrogen plus progestogens via oral or transdermal administration routes, and at different doses.

The four tests used to assess cognition were the Mini-Mental State Examination dot counting to evaluate verbal working memory, the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) total score, the Four Mountain Test, and the supermarket trolley virtual reality test.

Brain MRI data were collected. The researchers focused on the medial temporal lobe as the “main brain region regulating cognition and memory processing.” This lobe includes the hippocampus, the parahippocampus, the entorhinal cortex, and the amygdala.
 

‘Critical window’

The researchers found a “trend” toward an APOE-HRT interaction (P-interaction = .097) for the total RBANS score. In particular, it was significant for the RBANS delayed memory index, where scores were consistently higher for women with APOE4 who had received HRT, compared with all other groups (P-interaction = .009).

Within-genotype group comparisons showed that HRT users had a higher RBANS total scale score and delayed memory index (P = .045 and P = .002, respectively), but only among APOE4 carriers. Effect size analyses showed a large effect of HRT use on the Four Mountain Test score and the supermarket trolley virtual reality test score (Cohen’s d = 0.988 and 1.2, respectively).

“This large effect was found only in APOE4 carriers,” the investigators noted.

Similarly, a moderate to large effect of HRT on the left entorhinal volume was observed in APOE4 carriers (Cohen’s d = 0.63).

In members of the APOE4 group who received HRT, the left entorhinal and left and right amygdala volumes were larger, compared with both no-APOE4 and non-HRT users (P-interaction = .002, .003, and .005, respectively). Similar trends were observed for the right entorhinal volume (P = .074).

In addition, among HRT users, the left entorhinal volume was larger (P = .03); the right and left anterior cingulate gyrus volumes were smaller (P = .003 and .062, respectively); and the left superior frontal gyrus volume was larger (P = .009) in comparison with women who did not receive HRT, independently of their APOE genotype.

Early use of HRT among APOE4 carriers was associated with larger right and left hippocampal volume (P = .035 and P = .028, respectively) – an association not found in non-APOE4 carriers. The association was also not significant when participants were not stratified by APOE genotype.

“The key important point here is the timing, or the ‘critical window,’ when HRT can be of most benefit,” Dr. Saleh said. “This is most beneficial when introduced early, before the neuropathology becomes irreversible.”

Study limitations include its cross-sectional design, which precludes the establishment of a causal relationship, and the fact that information regarding the type and dose of estrogen was not available for all participants.

HRT is not without risk, Dr. Saleh noted. She recommended that clinicians “carry out various screening tests to make sure that a woman is eligible for HRT and not at risk of hypercoagulability, for instance.”
 

Risk-benefit ratio

In a comment, Howard Fillit, MD, cofounder and chief science officer at the Alzheimer’s Drug Discovery Foundation, called the study “exactly the kind of work that needs to be done.”

Dr. Fillit, who was not involved with the current research, is a clinical professor of geriatric medicine, palliative care medicine, and neuroscience at Mount Sinai Hospital, New York.

He compared the process with that of osteoporosis. “We know that if women are treated [with HRT] at the time of the menopause, you can prevent the rapid bone loss that occurs with rapid estrogen loss. But if you wait 5, 10 years out, once the bone loss has occurred, the HRT doesn’t really have any impact on osteoporosis risk because the horse is already out of the barn,” he said.

Although HRT carries risks, “they can clearly be managed; and if it’s proven that estrogen or hormone replacement around the time of the menopause can be protective [against AD], the risk-benefit ratio of HRT could be in favor of treatment,” Dr. Fillit added.

The study was conducted as part of the Medical Research Council NuBrain Consortium. The investigators and Dr. Fillit reported no relevant financial relationships.

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

Nearly half of older adults with dementia experience falls, suggests new research that also identifies multiple risk factors for these falls.

In a study of more than 5,500 participants, 45.5% of those with dementia experienced one or more falls, compared with 30.9% of their peers without dementia.

Vision impairment and living with a spouse were among the strongest predictors of future fall risk among participants living with dementia. Interestingly, high neighborhood social deprivation, which is reflected by such things as income and education, was associated with lower odds of falling.

Overall, the results highlight the need for a multidisciplinary approach to preventing falls among elderly individuals with dementia, said lead author Safiyyah M. Okoye, PhD, assistant professor, College of Nursing and Health Professions, Drexel University, Philadelphia.

“We need to consider different dimensions and figure out how we can try to go beyond the clinic in our interactions,” she said.

Dr. Okoye noted that in addition to reviewing medications that may contribute to falls and screening for vision problems, clinicians might also consider resources to improve the home environment and ensure that families have appropriate caregiving.

The findings were published online  in Alzheimer’s and Dementia: The Journal of the Alzheimer’s Association.
 

No ‘silver bullet’

Every year, falls cause millions of injuries in older adults, and those with dementia are especially vulnerable. This population has twice the risk of falling and up to three times the risk of incurring serious fall-related injuries, such as fractures, the researchers noted.

Falls are a leading cause of hospitalization among those with dementia. Previous evidence has shown that persons with dementia are more likely to experience negative health consequences, such as delirium, while in hospital, compared with those without dementia. Even minor fall-related injuries are associated with the patient’s being discharged to a nursing home rather than returning home.

Dr. Okoye stressed that many factors contribute to falls, including health status; function, such as the ability to walk and balance; medications; home environment; and activity level.

“There are multidimensional aspects, and we can’t just find one silver bullet to address falls. It should be addressed comprehensively,” she said.

Existing studies “overwhelmingly” focus on factors related to health and function that could be addressed in the doctor’s office or with a referral, rather than on environmental and social factors, Dr. Okoye noted.

And even though the risk of falling is high among community-dwelling seniors with dementia, very few studies have addressed the risk of falls among these adults, she added.

The new analysis included a nationally representative sample of 5,581 community-dwelling adults who participated in both the 2015 and 2016 National Health and Aging Trends Study (NHATS). The NHATS is a population-based survey of health and disability trends and trajectories among Americans aged 65 years and older.

During interviews, participants were asked, personally or by proxy, about falls during the previous 12 months. Having fallen at baseline was evaluated as a possible predictor of falls in the subsequent 12 months.

To determine probable dementia, researchers asked whether a doctor had ever told the participants that they had dementia or Alzheimer’s disease. They also used a dementia screening questionnaire and neuropsychological tests of memory, orientation, and executive function.

Of the total sample, most (n = 5,093) did not have dementia.

Physical environmental factors that were assessed included conditions at home, such as clutter, tripping hazards, and structural issues, as well as neighborhood social and economic deprivation – such as income, education levels, and employment status.
 

Fall rates and counterintuitive findings

Results showed that significantly more of those with dementia than without experienced one or more falls (45.5% vs. 30.9%; P < .001).

In addition, a history of falling was significantly associated with subsequent falls among those with dementia (odds ratio, 6.20; 95% confidence interval, 3.81-10.09), as was vision impairment (OR, 2.22; 95% CI, 1.12-4.40) and living with a spouse versus alone (OR, 2.43; 95% CI, 1.09-5.43).

A possible explanation for higher fall risk among those living with a partner is that those living alone usually have better functioning, the investigators noted. Also, live-in partners tend to be of a similar age as the person with dementia and may have challenges of their own.

Interestingly, high neighborhood social deprivation was associated with lower odds of falling (OR, 0.55 for the highest deprivation scores; 95% CI, 0.31-0.98), a finding Dr. Okoye said was “counterintuitive.”

This result could be related to the social environment, she noted. “Maybe there are more people around in the house, more people with eyes on the person, or more people in the community who know the person. Despite the low economic resources, there could be social resources there,” she said.

The new findings underscore the idea that falling is a multidimensional phenomenon among older adults with dementia as well as those without dementia, Dr. Okoye noted.

Doctors can play a role in reducing falls among patients with dementia by asking about falls, possibly eliminating medications that are associated with risk of falling, and screening for and correcting vision and hearing impairments, she suggested.

They may also help determine household hazards for a patient, such as clutter and poor lighting, and ensure that these are addressed, Dr. Okoye added.
 

No surprise

Commenting on the study, David S. Knopman, MD, a clinical neurologist at Mayo Clinic, Rochester, Minn., said the finding that visual impairment and a prior history of falling are predictive of subsequent falls “comes as no surprise.”

Dr. Knopman, whose research focuses on late-life cognitive disorders, was not involved with the current study.

Risk reduction is “of course” a key management goal, he said. “Vigilance and optimizing the patient’s living space to reduce fall risks are the major strategies,” he added.

Dr. Knopman reiterated that falls among those with dementia are associated with higher mortality and often lead to loss of the capacity to live outside of an institution.

The study was supported by the National Institute on Aging. The investigators and Dr. Knopman report no relevant financial relationships.

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

Nearly half of older adults with dementia experience falls, suggests new research that also identifies multiple risk factors for these falls.

In a study of more than 5,500 participants, 45.5% of those with dementia experienced one or more falls, compared with 30.9% of their peers without dementia.

Vision impairment and living with a spouse were among the strongest predictors of future fall risk among participants living with dementia. Interestingly, high neighborhood social deprivation, which is reflected by such things as income and education, was associated with lower odds of falling.

Overall, the results highlight the need for a multidisciplinary approach to preventing falls among elderly individuals with dementia, said lead author Safiyyah M. Okoye, PhD, assistant professor, College of Nursing and Health Professions, Drexel University, Philadelphia.

“We need to consider different dimensions and figure out how we can try to go beyond the clinic in our interactions,” she said.

Dr. Okoye noted that in addition to reviewing medications that may contribute to falls and screening for vision problems, clinicians might also consider resources to improve the home environment and ensure that families have appropriate caregiving.

The findings were published online  in Alzheimer’s and Dementia: The Journal of the Alzheimer’s Association.
 

No ‘silver bullet’

Every year, falls cause millions of injuries in older adults, and those with dementia are especially vulnerable. This population has twice the risk of falling and up to three times the risk of incurring serious fall-related injuries, such as fractures, the researchers noted.

Falls are a leading cause of hospitalization among those with dementia. Previous evidence has shown that persons with dementia are more likely to experience negative health consequences, such as delirium, while in hospital, compared with those without dementia. Even minor fall-related injuries are associated with the patient’s being discharged to a nursing home rather than returning home.

Dr. Okoye stressed that many factors contribute to falls, including health status; function, such as the ability to walk and balance; medications; home environment; and activity level.

“There are multidimensional aspects, and we can’t just find one silver bullet to address falls. It should be addressed comprehensively,” she said.

Existing studies “overwhelmingly” focus on factors related to health and function that could be addressed in the doctor’s office or with a referral, rather than on environmental and social factors, Dr. Okoye noted.

And even though the risk of falling is high among community-dwelling seniors with dementia, very few studies have addressed the risk of falls among these adults, she added.

The new analysis included a nationally representative sample of 5,581 community-dwelling adults who participated in both the 2015 and 2016 National Health and Aging Trends Study (NHATS). The NHATS is a population-based survey of health and disability trends and trajectories among Americans aged 65 years and older.

During interviews, participants were asked, personally or by proxy, about falls during the previous 12 months. Having fallen at baseline was evaluated as a possible predictor of falls in the subsequent 12 months.

To determine probable dementia, researchers asked whether a doctor had ever told the participants that they had dementia or Alzheimer’s disease. They also used a dementia screening questionnaire and neuropsychological tests of memory, orientation, and executive function.

Of the total sample, most (n = 5,093) did not have dementia.

Physical environmental factors that were assessed included conditions at home, such as clutter, tripping hazards, and structural issues, as well as neighborhood social and economic deprivation – such as income, education levels, and employment status.
 

Fall rates and counterintuitive findings

Results showed that significantly more of those with dementia than without experienced one or more falls (45.5% vs. 30.9%; P < .001).

In addition, a history of falling was significantly associated with subsequent falls among those with dementia (odds ratio, 6.20; 95% confidence interval, 3.81-10.09), as was vision impairment (OR, 2.22; 95% CI, 1.12-4.40) and living with a spouse versus alone (OR, 2.43; 95% CI, 1.09-5.43).

A possible explanation for higher fall risk among those living with a partner is that those living alone usually have better functioning, the investigators noted. Also, live-in partners tend to be of a similar age as the person with dementia and may have challenges of their own.

Interestingly, high neighborhood social deprivation was associated with lower odds of falling (OR, 0.55 for the highest deprivation scores; 95% CI, 0.31-0.98), a finding Dr. Okoye said was “counterintuitive.”

This result could be related to the social environment, she noted. “Maybe there are more people around in the house, more people with eyes on the person, or more people in the community who know the person. Despite the low economic resources, there could be social resources there,” she said.

The new findings underscore the idea that falling is a multidimensional phenomenon among older adults with dementia as well as those without dementia, Dr. Okoye noted.

Doctors can play a role in reducing falls among patients with dementia by asking about falls, possibly eliminating medications that are associated with risk of falling, and screening for and correcting vision and hearing impairments, she suggested.

They may also help determine household hazards for a patient, such as clutter and poor lighting, and ensure that these are addressed, Dr. Okoye added.
 

No surprise

Commenting on the study, David S. Knopman, MD, a clinical neurologist at Mayo Clinic, Rochester, Minn., said the finding that visual impairment and a prior history of falling are predictive of subsequent falls “comes as no surprise.”

Dr. Knopman, whose research focuses on late-life cognitive disorders, was not involved with the current study.

Risk reduction is “of course” a key management goal, he said. “Vigilance and optimizing the patient’s living space to reduce fall risks are the major strategies,” he added.

Dr. Knopman reiterated that falls among those with dementia are associated with higher mortality and often lead to loss of the capacity to live outside of an institution.

The study was supported by the National Institute on Aging. The investigators and Dr. Knopman report no relevant financial relationships.

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

Nearly half of older adults with dementia experience falls, suggests new research that also identifies multiple risk factors for these falls.

In a study of more than 5,500 participants, 45.5% of those with dementia experienced one or more falls, compared with 30.9% of their peers without dementia.

Vision impairment and living with a spouse were among the strongest predictors of future fall risk among participants living with dementia. Interestingly, high neighborhood social deprivation, which is reflected by such things as income and education, was associated with lower odds of falling.

Overall, the results highlight the need for a multidisciplinary approach to preventing falls among elderly individuals with dementia, said lead author Safiyyah M. Okoye, PhD, assistant professor, College of Nursing and Health Professions, Drexel University, Philadelphia.

“We need to consider different dimensions and figure out how we can try to go beyond the clinic in our interactions,” she said.

Dr. Okoye noted that in addition to reviewing medications that may contribute to falls and screening for vision problems, clinicians might also consider resources to improve the home environment and ensure that families have appropriate caregiving.

The findings were published online  in Alzheimer’s and Dementia: The Journal of the Alzheimer’s Association.
 

No ‘silver bullet’

Every year, falls cause millions of injuries in older adults, and those with dementia are especially vulnerable. This population has twice the risk of falling and up to three times the risk of incurring serious fall-related injuries, such as fractures, the researchers noted.

Falls are a leading cause of hospitalization among those with dementia. Previous evidence has shown that persons with dementia are more likely to experience negative health consequences, such as delirium, while in hospital, compared with those without dementia. Even minor fall-related injuries are associated with the patient’s being discharged to a nursing home rather than returning home.

Dr. Okoye stressed that many factors contribute to falls, including health status; function, such as the ability to walk and balance; medications; home environment; and activity level.

“There are multidimensional aspects, and we can’t just find one silver bullet to address falls. It should be addressed comprehensively,” she said.

Existing studies “overwhelmingly” focus on factors related to health and function that could be addressed in the doctor’s office or with a referral, rather than on environmental and social factors, Dr. Okoye noted.

And even though the risk of falling is high among community-dwelling seniors with dementia, very few studies have addressed the risk of falls among these adults, she added.

The new analysis included a nationally representative sample of 5,581 community-dwelling adults who participated in both the 2015 and 2016 National Health and Aging Trends Study (NHATS). The NHATS is a population-based survey of health and disability trends and trajectories among Americans aged 65 years and older.

During interviews, participants were asked, personally or by proxy, about falls during the previous 12 months. Having fallen at baseline was evaluated as a possible predictor of falls in the subsequent 12 months.

To determine probable dementia, researchers asked whether a doctor had ever told the participants that they had dementia or Alzheimer’s disease. They also used a dementia screening questionnaire and neuropsychological tests of memory, orientation, and executive function.

Of the total sample, most (n = 5,093) did not have dementia.

Physical environmental factors that were assessed included conditions at home, such as clutter, tripping hazards, and structural issues, as well as neighborhood social and economic deprivation – such as income, education levels, and employment status.
 

Fall rates and counterintuitive findings

Results showed that significantly more of those with dementia than without experienced one or more falls (45.5% vs. 30.9%; P < .001).

In addition, a history of falling was significantly associated with subsequent falls among those with dementia (odds ratio, 6.20; 95% confidence interval, 3.81-10.09), as was vision impairment (OR, 2.22; 95% CI, 1.12-4.40) and living with a spouse versus alone (OR, 2.43; 95% CI, 1.09-5.43).

A possible explanation for higher fall risk among those living with a partner is that those living alone usually have better functioning, the investigators noted. Also, live-in partners tend to be of a similar age as the person with dementia and may have challenges of their own.

Interestingly, high neighborhood social deprivation was associated with lower odds of falling (OR, 0.55 for the highest deprivation scores; 95% CI, 0.31-0.98), a finding Dr. Okoye said was “counterintuitive.”

This result could be related to the social environment, she noted. “Maybe there are more people around in the house, more people with eyes on the person, or more people in the community who know the person. Despite the low economic resources, there could be social resources there,” she said.

The new findings underscore the idea that falling is a multidimensional phenomenon among older adults with dementia as well as those without dementia, Dr. Okoye noted.

Doctors can play a role in reducing falls among patients with dementia by asking about falls, possibly eliminating medications that are associated with risk of falling, and screening for and correcting vision and hearing impairments, she suggested.

They may also help determine household hazards for a patient, such as clutter and poor lighting, and ensure that these are addressed, Dr. Okoye added.
 

No surprise

Commenting on the study, David S. Knopman, MD, a clinical neurologist at Mayo Clinic, Rochester, Minn., said the finding that visual impairment and a prior history of falling are predictive of subsequent falls “comes as no surprise.”

Dr. Knopman, whose research focuses on late-life cognitive disorders, was not involved with the current study.

Risk reduction is “of course” a key management goal, he said. “Vigilance and optimizing the patient’s living space to reduce fall risks are the major strategies,” he added.

Dr. Knopman reiterated that falls among those with dementia are associated with higher mortality and often lead to loss of the capacity to live outside of an institution.

The study was supported by the National Institute on Aging. The investigators and Dr. Knopman report no relevant financial relationships.

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

Dementia prevalence is 61% higher among older people with moderate to severe hearing loss compared with those with normal hearing, new national data show. Investigators also found that even mild hearing loss was associated with increased dementia risk, although it was not statistically significant, and that hearing aid use was tied to a 32% decrease in dementia prevalence.

“Every 10-decibel increase in hearing loss was associated with 16% greater prevalence of dementia, such that prevalence of dementia in older adults with moderate or greater hearing loss was 61% higher than prevalence in those with normal hearing,” said lead investigator Alison Huang, PhD, senior research associate in epidemiology at Johns Hopkins Bloomberg School of Public Health and core faculty in the Cochlear Center for Hearing and Public Health, Baltimore.

The findings were published online in JAMA.
 

Dose dependent effect

For their study, researchers analyzed data on 2,413 community-dwelling participants in the National Health and Aging Trends Study, a nationally representative, continuous panel study of U.S. Medicare beneficiaries aged 65 and older.

Data from the study was collected during in-home interviews, setting it apart from previous work that relied on data collected in a clinical setting, Dr. Huang said.

“This study was able to capture more vulnerable populations, such as the oldest old and older adults with disabilities, typically excluded from prior epidemiologic studies of the hearing loss–dementia association that use clinic-based data collection, which only captures people who have the ability and means to get to clinics,” Dr. Huang said.

Weighted hearing loss prevalence was 36.7% for mild and 29.8% for moderate to severe hearing loss, and weighted prevalence of dementia was 10.3%.

Those with moderate to severe hearing loss were 61% more likely to have dementia than were those with normal hearing (prevalence ratio, 1.61; 95% confidence interval [CI], 1.09-2.38).

Dementia prevalence increased with increasing severity of hearing loss: Normal hearing: 6.19% (95% CI, 4.31-8.80); mild hearing loss: 8.93% (95% CI, 6.99-11.34); moderate to severe hearing loss: 16.52% (95% CI, 13.81-19.64). But only moderate to severe hearing loss showed a statistically significant association with dementia (P = .02).

Dementia prevalence increased 16% per 10-decibel increase in hearing loss (prevalence ratio 1.16; P < .001).

Among the 853 individuals in the study with moderate to severe hearing loss, those who used hearing aids (n = 414) had a 32% lower risk of dementia compared with those who didn’t use assisted devices (prevalence ratio, 0.68; 95% CI, 0.47-1.00). Similar data were published in JAMA Neurology, suggesting that hearing aids reduce dementia risk.

“With this study, we were able to refine our understanding of the strength of the hearing loss–dementia association in a study more representative of older adults in the United States,” said Dr. Huang.
 

Robust association

Commenting on the findings, Justin S. Golub, MD, associate professor in the department of otolaryngology–head and neck surgery at Columbia University, New York, said the study supports earlier research and suggests a “robust” association between hearing loss and dementia.

“The particular advantage of this study was that it was high quality and nationally representative,” Dr. Golub said. “It is also among a smaller set of studies that have shown hearing aid use to be associated with lower risk of dementia.”

Although not statistically significant, researchers did find increasing prevalence of dementia among people with only mild hearing loss, and clinicians should take note, said Dr. Golub, who was not involved with this study.

“We would expect the relationship between mild hearing loss and dementia to be weaker than severe hearing loss and dementia and, as a result, it might take more participants to show an association among the mild group,” Dr. Golub said.

“Even though this particular study did not specifically find a relationship between mild hearing loss and dementia, I would still recommend people to start treating their hearing loss when it is early,” Dr. Golub added.

The study was funded by the National Institute on Aging. Dr. Golub reports no relevant financial relationships. Full disclosures for study authors are included in the original article.

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

Dementia prevalence is 61% higher among older people with moderate to severe hearing loss compared with those with normal hearing, new national data show. Investigators also found that even mild hearing loss was associated with increased dementia risk, although it was not statistically significant, and that hearing aid use was tied to a 32% decrease in dementia prevalence.

“Every 10-decibel increase in hearing loss was associated with 16% greater prevalence of dementia, such that prevalence of dementia in older adults with moderate or greater hearing loss was 61% higher than prevalence in those with normal hearing,” said lead investigator Alison Huang, PhD, senior research associate in epidemiology at Johns Hopkins Bloomberg School of Public Health and core faculty in the Cochlear Center for Hearing and Public Health, Baltimore.

The findings were published online in JAMA.
 

Dose dependent effect

For their study, researchers analyzed data on 2,413 community-dwelling participants in the National Health and Aging Trends Study, a nationally representative, continuous panel study of U.S. Medicare beneficiaries aged 65 and older.

Data from the study was collected during in-home interviews, setting it apart from previous work that relied on data collected in a clinical setting, Dr. Huang said.

“This study was able to capture more vulnerable populations, such as the oldest old and older adults with disabilities, typically excluded from prior epidemiologic studies of the hearing loss–dementia association that use clinic-based data collection, which only captures people who have the ability and means to get to clinics,” Dr. Huang said.

Weighted hearing loss prevalence was 36.7% for mild and 29.8% for moderate to severe hearing loss, and weighted prevalence of dementia was 10.3%.

Those with moderate to severe hearing loss were 61% more likely to have dementia than were those with normal hearing (prevalence ratio, 1.61; 95% confidence interval [CI], 1.09-2.38).

Dementia prevalence increased with increasing severity of hearing loss: Normal hearing: 6.19% (95% CI, 4.31-8.80); mild hearing loss: 8.93% (95% CI, 6.99-11.34); moderate to severe hearing loss: 16.52% (95% CI, 13.81-19.64). But only moderate to severe hearing loss showed a statistically significant association with dementia (P = .02).

Dementia prevalence increased 16% per 10-decibel increase in hearing loss (prevalence ratio 1.16; P < .001).

Among the 853 individuals in the study with moderate to severe hearing loss, those who used hearing aids (n = 414) had a 32% lower risk of dementia compared with those who didn’t use assisted devices (prevalence ratio, 0.68; 95% CI, 0.47-1.00). Similar data were published in JAMA Neurology, suggesting that hearing aids reduce dementia risk.

“With this study, we were able to refine our understanding of the strength of the hearing loss–dementia association in a study more representative of older adults in the United States,” said Dr. Huang.
 

Robust association

Commenting on the findings, Justin S. Golub, MD, associate professor in the department of otolaryngology–head and neck surgery at Columbia University, New York, said the study supports earlier research and suggests a “robust” association between hearing loss and dementia.

“The particular advantage of this study was that it was high quality and nationally representative,” Dr. Golub said. “It is also among a smaller set of studies that have shown hearing aid use to be associated with lower risk of dementia.”

Although not statistically significant, researchers did find increasing prevalence of dementia among people with only mild hearing loss, and clinicians should take note, said Dr. Golub, who was not involved with this study.

“We would expect the relationship between mild hearing loss and dementia to be weaker than severe hearing loss and dementia and, as a result, it might take more participants to show an association among the mild group,” Dr. Golub said.

“Even though this particular study did not specifically find a relationship between mild hearing loss and dementia, I would still recommend people to start treating their hearing loss when it is early,” Dr. Golub added.

The study was funded by the National Institute on Aging. Dr. Golub reports no relevant financial relationships. Full disclosures for study authors are included in the original article.

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

Dementia prevalence is 61% higher among older people with moderate to severe hearing loss compared with those with normal hearing, new national data show. Investigators also found that even mild hearing loss was associated with increased dementia risk, although it was not statistically significant, and that hearing aid use was tied to a 32% decrease in dementia prevalence.

“Every 10-decibel increase in hearing loss was associated with 16% greater prevalence of dementia, such that prevalence of dementia in older adults with moderate or greater hearing loss was 61% higher than prevalence in those with normal hearing,” said lead investigator Alison Huang, PhD, senior research associate in epidemiology at Johns Hopkins Bloomberg School of Public Health and core faculty in the Cochlear Center for Hearing and Public Health, Baltimore.

The findings were published online in JAMA.
 

Dose dependent effect

For their study, researchers analyzed data on 2,413 community-dwelling participants in the National Health and Aging Trends Study, a nationally representative, continuous panel study of U.S. Medicare beneficiaries aged 65 and older.

Data from the study was collected during in-home interviews, setting it apart from previous work that relied on data collected in a clinical setting, Dr. Huang said.

“This study was able to capture more vulnerable populations, such as the oldest old and older adults with disabilities, typically excluded from prior epidemiologic studies of the hearing loss–dementia association that use clinic-based data collection, which only captures people who have the ability and means to get to clinics,” Dr. Huang said.

Weighted hearing loss prevalence was 36.7% for mild and 29.8% for moderate to severe hearing loss, and weighted prevalence of dementia was 10.3%.

Those with moderate to severe hearing loss were 61% more likely to have dementia than were those with normal hearing (prevalence ratio, 1.61; 95% confidence interval [CI], 1.09-2.38).

Dementia prevalence increased with increasing severity of hearing loss: Normal hearing: 6.19% (95% CI, 4.31-8.80); mild hearing loss: 8.93% (95% CI, 6.99-11.34); moderate to severe hearing loss: 16.52% (95% CI, 13.81-19.64). But only moderate to severe hearing loss showed a statistically significant association with dementia (P = .02).

Dementia prevalence increased 16% per 10-decibel increase in hearing loss (prevalence ratio 1.16; P < .001).

Among the 853 individuals in the study with moderate to severe hearing loss, those who used hearing aids (n = 414) had a 32% lower risk of dementia compared with those who didn’t use assisted devices (prevalence ratio, 0.68; 95% CI, 0.47-1.00). Similar data were published in JAMA Neurology, suggesting that hearing aids reduce dementia risk.

“With this study, we were able to refine our understanding of the strength of the hearing loss–dementia association in a study more representative of older adults in the United States,” said Dr. Huang.
 

Robust association

Commenting on the findings, Justin S. Golub, MD, associate professor in the department of otolaryngology–head and neck surgery at Columbia University, New York, said the study supports earlier research and suggests a “robust” association between hearing loss and dementia.

“The particular advantage of this study was that it was high quality and nationally representative,” Dr. Golub said. “It is also among a smaller set of studies that have shown hearing aid use to be associated with lower risk of dementia.”

Although not statistically significant, researchers did find increasing prevalence of dementia among people with only mild hearing loss, and clinicians should take note, said Dr. Golub, who was not involved with this study.

“We would expect the relationship between mild hearing loss and dementia to be weaker than severe hearing loss and dementia and, as a result, it might take more participants to show an association among the mild group,” Dr. Golub said.

“Even though this particular study did not specifically find a relationship between mild hearing loss and dementia, I would still recommend people to start treating their hearing loss when it is early,” Dr. Golub added.

The study was funded by the National Institute on Aging. Dr. Golub reports no relevant financial relationships. Full disclosures for study authors are included in the original article.

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

Physicians and other clinicians could more easily exit contracts and change jobs under the Federal Trade Commission’s new proposed rule that would block companies from limiting employees’ ability to work for a rival.

The proposed rule seeks to ban companies from enforcing noncompete clauses in employment contracts, a practice that represents an “unfair method of competition” with “exploitative and widespread” impacts, including suppression of wages, innovation, and entrepreneurial spirit, the FTC said. The public has 60 days to submit comments on the proposal before the FTC issues the final rule.

Employers often include noncompete clauses in physician contracts because they want to avoid having patients leave their health care system and follow a doctor to a competitor. A 2018 survey of primary care physicians found that about half of office-based physicians and 37% of physicians employed at hospitals or freestanding care centers were bound by restrictive covenants.

“A federal ban on noncompete agreements will ensure that physicians nationwide can finally change jobs without fear of being sued,” Erik B. Smith, MD, JD, clinical assistant professor of anesthesiology at the University of Southern California, Los Angeles, said in an interview.

Many doctors would like to see noncompete agreements vanish, but some physicians still favor them.

“As a small-practice owner, I am personally against this. The noncompete helps me take a risk and hire a physician. It typically takes 2-3 years for me to break even. I think this will further consolidate employment with large hospital systems unfortunately,” Texas cardiologist Rishin Shah, MD, recently tweeted in response to the FTC announcement.

Dr. Smith, who has advocated for noncompete reform, said about half of states currently allow the controversial clauses.

However, several states have recently passed laws restricting their use. California, North Dakota, and Oklahoma ban noncompetes, although some narrowly defined exceptions, such as the sale of a business, remain.

Other states, like Colorado, Illinois, and Oregon, broadly ban noncompete clauses, except for workers earning above a certain threshold. For example, in Colorado, noncompete agreements are permitted for highly compensated employees earning more than $101,250.

Despite additional restrictions on noncompete agreements for workers in the District of Columbia, the new legislation does not apply to physicians earning total compensation of $250,000 or more. However, their employers must define the geographic parameters of the noncompete and limit postemployment restrictions to 2 years.

Restrictive covenants are “uniquely challenging to family medicine’s emphasis on longitudinal care and the patient-physician relationship,” said Tochi Iroku-Malize, MD, MPH, president of the American Academy of Family Physicians. The limitations imposed by noncompete agreements “potentially reduce patient choice, lower the quality of care for patients, and ultimately harm the foundation of family medicine – our relationships with our patients.”

Although the proposed rule aligns with President Biden’s executive order promoting economic competition, Dr. Smith said a national ban on noncompete agreements may push the limits of FTC authority.

“This new rule will certainly result in a ‘major questions doctrine’ Supreme Court challenge,” said Dr. Smith, and possibly be struck down if the court determines an administrative overstep into areas of “vast economic or political significance.”
 

A controversial policy

The American Medical Association’s code of ethics discourages covenants that “unreasonably restrict” the ability of physicians to practice following contract termination. And in 2022, the AMA cited “overly broad” noncompete language as a red flag young physicians should watch out for during contract negotiations.

But in 2020, the AMA asked the FTC not to use its rulemaking authority to regulate noncompete clauses in physician employment contracts, and instead, relegate enforcement of such agreements to each state. The American Hospital Association expressed similar views.

Still, the FTC said that eliminating noncompete clauses will increase annual wages by $300 billion, allow 30 million Americans to pursue better job opportunities, and encourage hiring competition among employers. It will also save consumers up to $148 billion in health care costs annually.

“Noncompetes block workers from freely switching jobs, depriving them of higher wages and better working conditions, and depriving businesses of a talent pool that they need to build and expand,” Lina M. Khan, FTC chair, said in a press release about the proposal.

A national ban on noncompetes would keep more physicians in the industry and practicing in their communities, a win for patients and providers, said Dr. Smith. It could also compel employers to offer more competitive employment packages, including fair wages, better work conditions, and a culture of well-being and patient safety.

“Whatever the final rule is, I’m certain it will be legally challenged,” said Dr. Smith, adding that the nation’s most prominent business lobbying group, the Chamber of Commerce, has already issued a statement calling the rule “blatantly unlawful."

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

Physicians and other clinicians could more easily exit contracts and change jobs under the Federal Trade Commission’s new proposed rule that would block companies from limiting employees’ ability to work for a rival.

The proposed rule seeks to ban companies from enforcing noncompete clauses in employment contracts, a practice that represents an “unfair method of competition” with “exploitative and widespread” impacts, including suppression of wages, innovation, and entrepreneurial spirit, the FTC said. The public has 60 days to submit comments on the proposal before the FTC issues the final rule.

Employers often include noncompete clauses in physician contracts because they want to avoid having patients leave their health care system and follow a doctor to a competitor. A 2018 survey of primary care physicians found that about half of office-based physicians and 37% of physicians employed at hospitals or freestanding care centers were bound by restrictive covenants.

“A federal ban on noncompete agreements will ensure that physicians nationwide can finally change jobs without fear of being sued,” Erik B. Smith, MD, JD, clinical assistant professor of anesthesiology at the University of Southern California, Los Angeles, said in an interview.

Many doctors would like to see noncompete agreements vanish, but some physicians still favor them.

“As a small-practice owner, I am personally against this. The noncompete helps me take a risk and hire a physician. It typically takes 2-3 years for me to break even. I think this will further consolidate employment with large hospital systems unfortunately,” Texas cardiologist Rishin Shah, MD, recently tweeted in response to the FTC announcement.

Dr. Smith, who has advocated for noncompete reform, said about half of states currently allow the controversial clauses.

However, several states have recently passed laws restricting their use. California, North Dakota, and Oklahoma ban noncompetes, although some narrowly defined exceptions, such as the sale of a business, remain.

Other states, like Colorado, Illinois, and Oregon, broadly ban noncompete clauses, except for workers earning above a certain threshold. For example, in Colorado, noncompete agreements are permitted for highly compensated employees earning more than $101,250.

Despite additional restrictions on noncompete agreements for workers in the District of Columbia, the new legislation does not apply to physicians earning total compensation of $250,000 or more. However, their employers must define the geographic parameters of the noncompete and limit postemployment restrictions to 2 years.

Restrictive covenants are “uniquely challenging to family medicine’s emphasis on longitudinal care and the patient-physician relationship,” said Tochi Iroku-Malize, MD, MPH, president of the American Academy of Family Physicians. The limitations imposed by noncompete agreements “potentially reduce patient choice, lower the quality of care for patients, and ultimately harm the foundation of family medicine – our relationships with our patients.”

Although the proposed rule aligns with President Biden’s executive order promoting economic competition, Dr. Smith said a national ban on noncompete agreements may push the limits of FTC authority.

“This new rule will certainly result in a ‘major questions doctrine’ Supreme Court challenge,” said Dr. Smith, and possibly be struck down if the court determines an administrative overstep into areas of “vast economic or political significance.”
 

A controversial policy

The American Medical Association’s code of ethics discourages covenants that “unreasonably restrict” the ability of physicians to practice following contract termination. And in 2022, the AMA cited “overly broad” noncompete language as a red flag young physicians should watch out for during contract negotiations.

But in 2020, the AMA asked the FTC not to use its rulemaking authority to regulate noncompete clauses in physician employment contracts, and instead, relegate enforcement of such agreements to each state. The American Hospital Association expressed similar views.

Still, the FTC said that eliminating noncompete clauses will increase annual wages by $300 billion, allow 30 million Americans to pursue better job opportunities, and encourage hiring competition among employers. It will also save consumers up to $148 billion in health care costs annually.

“Noncompetes block workers from freely switching jobs, depriving them of higher wages and better working conditions, and depriving businesses of a talent pool that they need to build and expand,” Lina M. Khan, FTC chair, said in a press release about the proposal.

A national ban on noncompetes would keep more physicians in the industry and practicing in their communities, a win for patients and providers, said Dr. Smith. It could also compel employers to offer more competitive employment packages, including fair wages, better work conditions, and a culture of well-being and patient safety.

“Whatever the final rule is, I’m certain it will be legally challenged,” said Dr. Smith, adding that the nation’s most prominent business lobbying group, the Chamber of Commerce, has already issued a statement calling the rule “blatantly unlawful."

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

Physicians and other clinicians could more easily exit contracts and change jobs under the Federal Trade Commission’s new proposed rule that would block companies from limiting employees’ ability to work for a rival.

The proposed rule seeks to ban companies from enforcing noncompete clauses in employment contracts, a practice that represents an “unfair method of competition” with “exploitative and widespread” impacts, including suppression of wages, innovation, and entrepreneurial spirit, the FTC said. The public has 60 days to submit comments on the proposal before the FTC issues the final rule.

Employers often include noncompete clauses in physician contracts because they want to avoid having patients leave their health care system and follow a doctor to a competitor. A 2018 survey of primary care physicians found that about half of office-based physicians and 37% of physicians employed at hospitals or freestanding care centers were bound by restrictive covenants.

“A federal ban on noncompete agreements will ensure that physicians nationwide can finally change jobs without fear of being sued,” Erik B. Smith, MD, JD, clinical assistant professor of anesthesiology at the University of Southern California, Los Angeles, said in an interview.

Many doctors would like to see noncompete agreements vanish, but some physicians still favor them.

“As a small-practice owner, I am personally against this. The noncompete helps me take a risk and hire a physician. It typically takes 2-3 years for me to break even. I think this will further consolidate employment with large hospital systems unfortunately,” Texas cardiologist Rishin Shah, MD, recently tweeted in response to the FTC announcement.

Dr. Smith, who has advocated for noncompete reform, said about half of states currently allow the controversial clauses.

However, several states have recently passed laws restricting their use. California, North Dakota, and Oklahoma ban noncompetes, although some narrowly defined exceptions, such as the sale of a business, remain.

Other states, like Colorado, Illinois, and Oregon, broadly ban noncompete clauses, except for workers earning above a certain threshold. For example, in Colorado, noncompete agreements are permitted for highly compensated employees earning more than $101,250.

Despite additional restrictions on noncompete agreements for workers in the District of Columbia, the new legislation does not apply to physicians earning total compensation of $250,000 or more. However, their employers must define the geographic parameters of the noncompete and limit postemployment restrictions to 2 years.

Restrictive covenants are “uniquely challenging to family medicine’s emphasis on longitudinal care and the patient-physician relationship,” said Tochi Iroku-Malize, MD, MPH, president of the American Academy of Family Physicians. The limitations imposed by noncompete agreements “potentially reduce patient choice, lower the quality of care for patients, and ultimately harm the foundation of family medicine – our relationships with our patients.”

Although the proposed rule aligns with President Biden’s executive order promoting economic competition, Dr. Smith said a national ban on noncompete agreements may push the limits of FTC authority.

“This new rule will certainly result in a ‘major questions doctrine’ Supreme Court challenge,” said Dr. Smith, and possibly be struck down if the court determines an administrative overstep into areas of “vast economic or political significance.”
 

A controversial policy

The American Medical Association’s code of ethics discourages covenants that “unreasonably restrict” the ability of physicians to practice following contract termination. And in 2022, the AMA cited “overly broad” noncompete language as a red flag young physicians should watch out for during contract negotiations.

But in 2020, the AMA asked the FTC not to use its rulemaking authority to regulate noncompete clauses in physician employment contracts, and instead, relegate enforcement of such agreements to each state. The American Hospital Association expressed similar views.

Still, the FTC said that eliminating noncompete clauses will increase annual wages by $300 billion, allow 30 million Americans to pursue better job opportunities, and encourage hiring competition among employers. It will also save consumers up to $148 billion in health care costs annually.

“Noncompetes block workers from freely switching jobs, depriving them of higher wages and better working conditions, and depriving businesses of a talent pool that they need to build and expand,” Lina M. Khan, FTC chair, said in a press release about the proposal.

A national ban on noncompetes would keep more physicians in the industry and practicing in their communities, a win for patients and providers, said Dr. Smith. It could also compel employers to offer more competitive employment packages, including fair wages, better work conditions, and a culture of well-being and patient safety.

“Whatever the final rule is, I’m certain it will be legally challenged,” said Dr. Smith, adding that the nation’s most prominent business lobbying group, the Chamber of Commerce, has already issued a statement calling the rule “blatantly unlawful."

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

While psychiatry has been the subject of many films, video games are not a medium commonly known for examining mental illness.¹ There have been PC games over the years with psychiatric themes, such as Sanitarium (1998), Depression Quest (2013), Fran Bow (2015), and Night in the Woods (2017). Now for perhaps the first time a game has been developed with the practice of psychiatry as its primary focus.

Freud’s Bones is a 2022 game developed by independent Italian game studio Fortuna Imperatore. The result of a successful Kickstarter crowdfunding campaign, Freud’s Bones is advertised as “the first point & click narrative-drive game to pay homage to the birth of psychoanalysis and its founder, addressing the themes of sexuality and neuroses filled with existential doubts.”

In Freud’s Bones, you take control of Sigmund Freud and guide him through his daily tasks. Gameplay is of the simple point-and-click variety, modeled after classic LucasArts-style adventure games of the 1990s such as The Secret of Monkey Island or Day of the Tentacle. Prior to seeing your first patient, the game provides several documents the player can peruse to become familiar with basic concepts of psychoanalysis. Although the game was originally written in Italian (and translation gaffes occasionally arise), generally the English wording is easy to read. However, some players may feel intimidated or bored by the sheer quantity of text the game provides. All in-game text, including books and spoken words, are written and there is no recorded voice acting. Audio consists largely of unintrusive background music and occasional sound effects. The graphical style is simple and cartoonish but pleasant.

Freud’s personal life is a major focus of the game. His real life dog Jofi is a constant presence in Freud’s office. At various times the player will witness Freud’s dreams, act as a voice inside his head, and attempt to interpret mystical Egyptian messages he receives. Players are also tasked with managing Freud’s reputation in the scientific community. This is apparently intended as a reflection of in-game clinical acumen, but it was sometimes difficult to tell what direct influence my actions had on Freud’s reputation.

Freud’s energy may flag at various points during the game, and the player may choose to give him a cigar or a dose of cocaine to stimulate him. These options sound interesting on the surface, but I found the effect of these substances on the game’s actual outcome to be minimal. Some tasks are presented in a less than user-friendly manner. For example, on my initial playthrough I could not figure out how to complete several optional errands such as shopping for more tobacco or selecting a cover for Freud’s books. The player is also given the opportunity to make choices that affect Freud’s personal life, such as whether to pursue an extramarital affair. The game does have a few narrative surprises, including appearances from some of Freud’s well-known contemporaries. One particularly vivid sequence late in the game involves navigating Freud through a hallucination with some bizarre, but very Freudian, imagery.

By far the most interesting and enjoyable part of the game is the psychoanalysis sessions. The player guides Freud through multiple sessions with four different patients. Each of them has a unique story and associated symptoms, and the player can choose a variety of responses. For example, will you take a comforting, paternalistic approach to the patient uncomfortable with her first appointment? Or will you take the more stoic, quiet approach of the analyst and allow the patient to speak without prompting? Part of the player’s quest in guiding Freud through these sessions is to help patients bring their unconscious thoughts to conscious awareness. This is depicted graphically as the thought moves vertically through images representing the id, superego, and ego. Skillful questioning can bring these thoughts to the surface, but poor choices can leave valuable insights buried in the unconscious.

These therapy sessions were unique and engaging, and I wish they constituted a larger portion of the gameplay in Freud’s Bones. More patients, more sessions with each patient, and longer sessions would all have been welcome additions. These analytic sessions eventually culminate in an opportunity to offer a diagnosis, and the player’s accuracy in treatment can result in divergent outcomes for each patient. The game is not lengthy, as it can be played in its entirety in roughly 5-6 hours. Selecting different options for Freud’s personal life and the analysis sessions provides some replay value for subsequent playthroughs.

Overall, Freud’s Bones is a worthy effort for being uniquely designed as interactive entertainment simulating psychoanalysis. It provides an experience of interest to psychiatrists but is also accessible to the general public. While the game has flaws in that it can be overly text-heavy and goals are not always clear, it shines in the moments where it allows the player to participate directly in the process of psychoanalysis. Freud’s Bones is available for purchase on Steam (currently priced at $13.99) and can be played on Windows PCs.

Dr. Weber is a psychiatrist at Intermountain Logan Regional Hospital in Logan, Utah. He disclosed no relevant financial relationships.

References

1. See, for example, Gabbard GO, Gabbard K. Psychiatry and the Cinema, 2nd ed. American Psychiatric Press, Inc.; 1999.

While psychiatry has been the subject of many films, video games are not a medium commonly known for examining mental illness.¹ There have been PC games over the years with psychiatric themes, such as Sanitarium (1998), Depression Quest (2013), Fran Bow (2015), and Night in the Woods (2017). Now for perhaps the first time a game has been developed with the practice of psychiatry as its primary focus.

Freud’s Bones is a 2022 game developed by independent Italian game studio Fortuna Imperatore. The result of a successful Kickstarter crowdfunding campaign, Freud’s Bones is advertised as “the first point & click narrative-drive game to pay homage to the birth of psychoanalysis and its founder, addressing the themes of sexuality and neuroses filled with existential doubts.”

In Freud’s Bones, you take control of Sigmund Freud and guide him through his daily tasks. Gameplay is of the simple point-and-click variety, modeled after classic LucasArts-style adventure games of the 1990s such as The Secret of Monkey Island or Day of the Tentacle. Prior to seeing your first patient, the game provides several documents the player can peruse to become familiar with basic concepts of psychoanalysis. Although the game was originally written in Italian (and translation gaffes occasionally arise), generally the English wording is easy to read. However, some players may feel intimidated or bored by the sheer quantity of text the game provides. All in-game text, including books and spoken words, are written and there is no recorded voice acting. Audio consists largely of unintrusive background music and occasional sound effects. The graphical style is simple and cartoonish but pleasant.

Freud’s personal life is a major focus of the game. His real life dog Jofi is a constant presence in Freud’s office. At various times the player will witness Freud’s dreams, act as a voice inside his head, and attempt to interpret mystical Egyptian messages he receives. Players are also tasked with managing Freud’s reputation in the scientific community. This is apparently intended as a reflection of in-game clinical acumen, but it was sometimes difficult to tell what direct influence my actions had on Freud’s reputation.

Freud’s energy may flag at various points during the game, and the player may choose to give him a cigar or a dose of cocaine to stimulate him. These options sound interesting on the surface, but I found the effect of these substances on the game’s actual outcome to be minimal. Some tasks are presented in a less than user-friendly manner. For example, on my initial playthrough I could not figure out how to complete several optional errands such as shopping for more tobacco or selecting a cover for Freud’s books. The player is also given the opportunity to make choices that affect Freud’s personal life, such as whether to pursue an extramarital affair. The game does have a few narrative surprises, including appearances from some of Freud’s well-known contemporaries. One particularly vivid sequence late in the game involves navigating Freud through a hallucination with some bizarre, but very Freudian, imagery.

By far the most interesting and enjoyable part of the game is the psychoanalysis sessions. The player guides Freud through multiple sessions with four different patients. Each of them has a unique story and associated symptoms, and the player can choose a variety of responses. For example, will you take a comforting, paternalistic approach to the patient uncomfortable with her first appointment? Or will you take the more stoic, quiet approach of the analyst and allow the patient to speak without prompting? Part of the player’s quest in guiding Freud through these sessions is to help patients bring their unconscious thoughts to conscious awareness. This is depicted graphically as the thought moves vertically through images representing the id, superego, and ego. Skillful questioning can bring these thoughts to the surface, but poor choices can leave valuable insights buried in the unconscious.

These therapy sessions were unique and engaging, and I wish they constituted a larger portion of the gameplay in Freud’s Bones. More patients, more sessions with each patient, and longer sessions would all have been welcome additions. These analytic sessions eventually culminate in an opportunity to offer a diagnosis, and the player’s accuracy in treatment can result in divergent outcomes for each patient. The game is not lengthy, as it can be played in its entirety in roughly 5-6 hours. Selecting different options for Freud’s personal life and the analysis sessions provides some replay value for subsequent playthroughs.

Overall, Freud’s Bones is a worthy effort for being uniquely designed as interactive entertainment simulating psychoanalysis. It provides an experience of interest to psychiatrists but is also accessible to the general public. While the game has flaws in that it can be overly text-heavy and goals are not always clear, it shines in the moments where it allows the player to participate directly in the process of psychoanalysis. Freud’s Bones is available for purchase on Steam (currently priced at $13.99) and can be played on Windows PCs.

Dr. Weber is a psychiatrist at Intermountain Logan Regional Hospital in Logan, Utah. He disclosed no relevant financial relationships.

References

1. See, for example, Gabbard GO, Gabbard K. Psychiatry and the Cinema, 2nd ed. American Psychiatric Press, Inc.; 1999.

While psychiatry has been the subject of many films, video games are not a medium commonly known for examining mental illness.¹ There have been PC games over the years with psychiatric themes, such as Sanitarium (1998), Depression Quest (2013), Fran Bow (2015), and Night in the Woods (2017). Now for perhaps the first time a game has been developed with the practice of psychiatry as its primary focus.

Freud’s Bones is a 2022 game developed by independent Italian game studio Fortuna Imperatore. The result of a successful Kickstarter crowdfunding campaign, Freud’s Bones is advertised as “the first point & click narrative-drive game to pay homage to the birth of psychoanalysis and its founder, addressing the themes of sexuality and neuroses filled with existential doubts.”

In Freud’s Bones, you take control of Sigmund Freud and guide him through his daily tasks. Gameplay is of the simple point-and-click variety, modeled after classic LucasArts-style adventure games of the 1990s such as The Secret of Monkey Island or Day of the Tentacle. Prior to seeing your first patient, the game provides several documents the player can peruse to become familiar with basic concepts of psychoanalysis. Although the game was originally written in Italian (and translation gaffes occasionally arise), generally the English wording is easy to read. However, some players may feel intimidated or bored by the sheer quantity of text the game provides. All in-game text, including books and spoken words, are written and there is no recorded voice acting. Audio consists largely of unintrusive background music and occasional sound effects. The graphical style is simple and cartoonish but pleasant.

Freud’s personal life is a major focus of the game. His real life dog Jofi is a constant presence in Freud’s office. At various times the player will witness Freud’s dreams, act as a voice inside his head, and attempt to interpret mystical Egyptian messages he receives. Players are also tasked with managing Freud’s reputation in the scientific community. This is apparently intended as a reflection of in-game clinical acumen, but it was sometimes difficult to tell what direct influence my actions had on Freud’s reputation.

Freud’s energy may flag at various points during the game, and the player may choose to give him a cigar or a dose of cocaine to stimulate him. These options sound interesting on the surface, but I found the effect of these substances on the game’s actual outcome to be minimal. Some tasks are presented in a less than user-friendly manner. For example, on my initial playthrough I could not figure out how to complete several optional errands such as shopping for more tobacco or selecting a cover for Freud’s books. The player is also given the opportunity to make choices that affect Freud’s personal life, such as whether to pursue an extramarital affair. The game does have a few narrative surprises, including appearances from some of Freud’s well-known contemporaries. One particularly vivid sequence late in the game involves navigating Freud through a hallucination with some bizarre, but very Freudian, imagery.

By far the most interesting and enjoyable part of the game is the psychoanalysis sessions. The player guides Freud through multiple sessions with four different patients. Each of them has a unique story and associated symptoms, and the player can choose a variety of responses. For example, will you take a comforting, paternalistic approach to the patient uncomfortable with her first appointment? Or will you take the more stoic, quiet approach of the analyst and allow the patient to speak without prompting? Part of the player’s quest in guiding Freud through these sessions is to help patients bring their unconscious thoughts to conscious awareness. This is depicted graphically as the thought moves vertically through images representing the id, superego, and ego. Skillful questioning can bring these thoughts to the surface, but poor choices can leave valuable insights buried in the unconscious.

These therapy sessions were unique and engaging, and I wish they constituted a larger portion of the gameplay in Freud’s Bones. More patients, more sessions with each patient, and longer sessions would all have been welcome additions. These analytic sessions eventually culminate in an opportunity to offer a diagnosis, and the player’s accuracy in treatment can result in divergent outcomes for each patient. The game is not lengthy, as it can be played in its entirety in roughly 5-6 hours. Selecting different options for Freud’s personal life and the analysis sessions provides some replay value for subsequent playthroughs.

Overall, Freud’s Bones is a worthy effort for being uniquely designed as interactive entertainment simulating psychoanalysis. It provides an experience of interest to psychiatrists but is also accessible to the general public. While the game has flaws in that it can be overly text-heavy and goals are not always clear, it shines in the moments where it allows the player to participate directly in the process of psychoanalysis. Freud’s Bones is available for purchase on Steam (currently priced at $13.99) and can be played on Windows PCs.

Dr. Weber is a psychiatrist at Intermountain Logan Regional Hospital in Logan, Utah. He disclosed no relevant financial relationships.

References

1. See, for example, Gabbard GO, Gabbard K. Psychiatry and the Cinema, 2nd ed. American Psychiatric Press, Inc.; 1999.

Patients with borderline personality disorder and major depressive episodes had a longer time to depression remission than patients with major depressive disorder or bipolar disorder who had major depressive episodes, based on data from 95 individuals.

Major depressive episodes (MDEs) occur in major depressive disorder (MDD) and bipolar disorder (BD), John J. Söderholm, MD, of the University of Helsinki and colleagues wrote. Borderline personality disorder (BPD) includes an increased risk for depression, but data on the relationship between BPD symptoms and depressive illness are limited. In particular, they noted “a lack of studies prospectively comparing the presence of (hypo)manic symptoms over time during the recovery process from MDE between MDD, MDE/BD, and MDE/BPD patients.”

John J. Söderholm

In a cohort study published in the Journal of Affective Disorders, the researchers collected data from 39 adult MDE patients with MDD, 33 with BD, and 23 with BPD. The patients were diagnosed with MDE using the SCID-I/P and SCID-II interviews, mixed symptoms were identified using the Mix-MDE scale, and borderline symptoms were identified using the Borderline Personality Disorder Severity Index.

Over a 6-month follow-up period, the participants completed biweekly online assessments. The primary outcomes were time to first full remission of symptoms and duration and nature of mood episodes.

Overall, the mean number of distinct mood states was 5.75, and the median duration was 60.9 days. When identified by subcohorts, the median number of mood state periods for MDD, BD, and BPD was 4.49, 8.05, and 4.67, respectively. The median durations were 69.2 days, 40.30 days, and 75.6 days, respectively.

The rates of remission for depressive symptoms were similar for MDD, MDE/BD, and MDE/BPD patients. However, MDE/BD patients had a significantly shorter time to first remission (hazard ratio, 2.44). Patients in the BPD group had a significantly longer time to first remission (HR, 0.95).

“When the cohort was divided into quintiles according to BPD feature severity, there was an approximately 1-month difference in time to first period of remission between the first and third and between the third and fifth quintiles, with longer times seen in patients with more severe BPD symptoms,” the researchers wrote.

The study findings were limited by several factors including the small sample size and short follow-up period that prevented investigation of depressive recurrence, the researchers noted. Other limitations included the lack of diagnostic blinding and variation in patients’ treatment schedules.

However, the results were strengthened by the representative samples of subjects with various disorders, the prospective and multimodal assessment of affective states, and the comparison of three patient groups in a single study.

As BPD was associated with a longer time to remission from depressive symptoms, the results suggest that BPD severity may be an indicator of more severe disease in patients with MDD in the context of depression, the researchers concluded.

The study was supported by the Finska Lakaresallskapet, the City of Helsinki, the Hospital District of Helsinki and Uusimaa, and the Finnish Psychiatric Association. The researchers had no financial conflicts to disclose.

Patients with borderline personality disorder and major depressive episodes had a longer time to depression remission than patients with major depressive disorder or bipolar disorder who had major depressive episodes, based on data from 95 individuals.

Major depressive episodes (MDEs) occur in major depressive disorder (MDD) and bipolar disorder (BD), John J. Söderholm, MD, of the University of Helsinki and colleagues wrote. Borderline personality disorder (BPD) includes an increased risk for depression, but data on the relationship between BPD symptoms and depressive illness are limited. In particular, they noted “a lack of studies prospectively comparing the presence of (hypo)manic symptoms over time during the recovery process from MDE between MDD, MDE/BD, and MDE/BPD patients.”

John J. Söderholm

In a cohort study published in the Journal of Affective Disorders, the researchers collected data from 39 adult MDE patients with MDD, 33 with BD, and 23 with BPD. The patients were diagnosed with MDE using the SCID-I/P and SCID-II interviews, mixed symptoms were identified using the Mix-MDE scale, and borderline symptoms were identified using the Borderline Personality Disorder Severity Index.

Over a 6-month follow-up period, the participants completed biweekly online assessments. The primary outcomes were time to first full remission of symptoms and duration and nature of mood episodes.

Overall, the mean number of distinct mood states was 5.75, and the median duration was 60.9 days. When identified by subcohorts, the median number of mood state periods for MDD, BD, and BPD was 4.49, 8.05, and 4.67, respectively. The median durations were 69.2 days, 40.30 days, and 75.6 days, respectively.

The rates of remission for depressive symptoms were similar for MDD, MDE/BD, and MDE/BPD patients. However, MDE/BD patients had a significantly shorter time to first remission (hazard ratio, 2.44). Patients in the BPD group had a significantly longer time to first remission (HR, 0.95).

“When the cohort was divided into quintiles according to BPD feature severity, there was an approximately 1-month difference in time to first period of remission between the first and third and between the third and fifth quintiles, with longer times seen in patients with more severe BPD symptoms,” the researchers wrote.

The study findings were limited by several factors including the small sample size and short follow-up period that prevented investigation of depressive recurrence, the researchers noted. Other limitations included the lack of diagnostic blinding and variation in patients’ treatment schedules.

However, the results were strengthened by the representative samples of subjects with various disorders, the prospective and multimodal assessment of affective states, and the comparison of three patient groups in a single study.

As BPD was associated with a longer time to remission from depressive symptoms, the results suggest that BPD severity may be an indicator of more severe disease in patients with MDD in the context of depression, the researchers concluded.

The study was supported by the Finska Lakaresallskapet, the City of Helsinki, the Hospital District of Helsinki and Uusimaa, and the Finnish Psychiatric Association. The researchers had no financial conflicts to disclose.

Patients with borderline personality disorder and major depressive episodes had a longer time to depression remission than patients with major depressive disorder or bipolar disorder who had major depressive episodes, based on data from 95 individuals.

Major depressive episodes (MDEs) occur in major depressive disorder (MDD) and bipolar disorder (BD), John J. Söderholm, MD, of the University of Helsinki and colleagues wrote. Borderline personality disorder (BPD) includes an increased risk for depression, but data on the relationship between BPD symptoms and depressive illness are limited. In particular, they noted “a lack of studies prospectively comparing the presence of (hypo)manic symptoms over time during the recovery process from MDE between MDD, MDE/BD, and MDE/BPD patients.”

John J. Söderholm

In a cohort study published in the Journal of Affective Disorders, the researchers collected data from 39 adult MDE patients with MDD, 33 with BD, and 23 with BPD. The patients were diagnosed with MDE using the SCID-I/P and SCID-II interviews, mixed symptoms were identified using the Mix-MDE scale, and borderline symptoms were identified using the Borderline Personality Disorder Severity Index.

Over a 6-month follow-up period, the participants completed biweekly online assessments. The primary outcomes were time to first full remission of symptoms and duration and nature of mood episodes.

Overall, the mean number of distinct mood states was 5.75, and the median duration was 60.9 days. When identified by subcohorts, the median number of mood state periods for MDD, BD, and BPD was 4.49, 8.05, and 4.67, respectively. The median durations were 69.2 days, 40.30 days, and 75.6 days, respectively.

The rates of remission for depressive symptoms were similar for MDD, MDE/BD, and MDE/BPD patients. However, MDE/BD patients had a significantly shorter time to first remission (hazard ratio, 2.44). Patients in the BPD group had a significantly longer time to first remission (HR, 0.95).

“When the cohort was divided into quintiles according to BPD feature severity, there was an approximately 1-month difference in time to first period of remission between the first and third and between the third and fifth quintiles, with longer times seen in patients with more severe BPD symptoms,” the researchers wrote.

The study findings were limited by several factors including the small sample size and short follow-up period that prevented investigation of depressive recurrence, the researchers noted. Other limitations included the lack of diagnostic blinding and variation in patients’ treatment schedules.

However, the results were strengthened by the representative samples of subjects with various disorders, the prospective and multimodal assessment of affective states, and the comparison of three patient groups in a single study.

As BPD was associated with a longer time to remission from depressive symptoms, the results suggest that BPD severity may be an indicator of more severe disease in patients with MDD in the context of depression, the researchers concluded.

The study was supported by the Finska Lakaresallskapet, the City of Helsinki, the Hospital District of Helsinki and Uusimaa, and the Finnish Psychiatric Association. The researchers had no financial conflicts to disclose.

Short bouts of intense exercise may help protect the brain from age-related cognitive decline by increasing production of a key protein involved in neuroplasticity, learning, and memory, new research suggests.

In a small study of healthy adults, 6 minutes of high-intensity cycling increased circulating levels of brain-derived neurotrophic factor (BDNF) to a significantly greater extent than prolonged light cycling or fasting.

However, the data do not suggest that 6 minutes of high-intensity exercise “wards off dementia,” cautioned lead investigator Travis Gibbons, MSc, PhD candidate in environmental physiology at the University of Otago (New Zealand), Dunedin, and now postdoctoral fellow at the University of British Columbia – Okanagan, Kelowna.

“Like all science, this is just a small piece that supports a potential mechanistic role for how exercise might improve brain health,” Dr. Gibbons told this news organization.

The findings were published online in the Journal of Physiology.
 

Targeting BDNF

Both intermittent fasting and exercise have previously been shown to have potent neuroprotective effects; and an acute upregulation of BDNF appears to be a common mechanistic link.

To tease apart the influence of fasting and exercise on BDNF production, Dr. Gibbons and colleagues studied 12 aerobically fit, healthy men (n = 6) and women (n = 6) aged 20-40 years.

In a study that employed a repeated-measures crossover design, they assessed circulating BDNF levels after a 20-hour fast, prolonged (90-min) light cycling, short (6-min) high-intensity cycling, and combined fasting and exercise.

Six minutes of high-intensity exercise appeared to be the most efficient way to increase BDNF.

Fasting for 20 hours led to a ninefold increase in ketone body delivery to the brain but had no effect on any metric of BDNF in peripheral circulation at rest or during exercise.

Six minutes of high-intensity exercise increased every metric of circulating BDNF four to five times more than prolonged low-intensity exercise.

In addition, the increase in plasma-derived BDNF correlated with a sixfold increase in circulating lactate irrespective of feeding or fasting state.
 

Lactate delivery?

“My leading theory is that, during and following intense exercise, lactate produced by muscles is delivered and consumed by the brain,” Dr. Gibbons noted.

“It takes high-intensity exercise to provoke this ‘cerebral substrate switch’ from glucose to lactate. Critically, this cerebral substrate switch has been shown to contribute to the early processes that upregulate BDNF production in the brain,” he said.

However, “Whether this translates to ‘warding off dementia’ is not clear,” Dr. Gibbons added.

The study also suggests that increases in plasma volume and platelet concentration appear to play a role in concentrating BDNF in the circulation during exercise.

The investigators note that BDNF and other neurotrophic-based pharmaceutical therapies have shown “great promise” in slowing and even arresting neurodegenerative processes in animals, but attempts to harness the protective power of BDNF in human neurodegeneration have thus far failed.

“Whether episodically upregulating BDNF production with intense exercise is an effective strategy to curb age-related cognitive decline in humans is unknown, but animal models indicate that it is and that BDNF plays a primary role,” the researchers write.

Funding for the study was provided by the Healthcare Otago Charitable Trust. The investigators have reported no relevant financial relationships.

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

Short bouts of intense exercise may help protect the brain from age-related cognitive decline by increasing production of a key protein involved in neuroplasticity, learning, and memory, new research suggests.

In a small study of healthy adults, 6 minutes of high-intensity cycling increased circulating levels of brain-derived neurotrophic factor (BDNF) to a significantly greater extent than prolonged light cycling or fasting.

However, the data do not suggest that 6 minutes of high-intensity exercise “wards off dementia,” cautioned lead investigator Travis Gibbons, MSc, PhD candidate in environmental physiology at the University of Otago (New Zealand), Dunedin, and now postdoctoral fellow at the University of British Columbia – Okanagan, Kelowna.

“Like all science, this is just a small piece that supports a potential mechanistic role for how exercise might improve brain health,” Dr. Gibbons told this news organization.

The findings were published online in the Journal of Physiology.
 

Targeting BDNF

Both intermittent fasting and exercise have previously been shown to have potent neuroprotective effects; and an acute upregulation of BDNF appears to be a common mechanistic link.

To tease apart the influence of fasting and exercise on BDNF production, Dr. Gibbons and colleagues studied 12 aerobically fit, healthy men (n = 6) and women (n = 6) aged 20-40 years.

In a study that employed a repeated-measures crossover design, they assessed circulating BDNF levels after a 20-hour fast, prolonged (90-min) light cycling, short (6-min) high-intensity cycling, and combined fasting and exercise.

Six minutes of high-intensity exercise appeared to be the most efficient way to increase BDNF.

Fasting for 20 hours led to a ninefold increase in ketone body delivery to the brain but had no effect on any metric of BDNF in peripheral circulation at rest or during exercise.

Six minutes of high-intensity exercise increased every metric of circulating BDNF four to five times more than prolonged low-intensity exercise.

In addition, the increase in plasma-derived BDNF correlated with a sixfold increase in circulating lactate irrespective of feeding or fasting state.
 

Lactate delivery?

“My leading theory is that, during and following intense exercise, lactate produced by muscles is delivered and consumed by the brain,” Dr. Gibbons noted.

“It takes high-intensity exercise to provoke this ‘cerebral substrate switch’ from glucose to lactate. Critically, this cerebral substrate switch has been shown to contribute to the early processes that upregulate BDNF production in the brain,” he said.

However, “Whether this translates to ‘warding off dementia’ is not clear,” Dr. Gibbons added.

The study also suggests that increases in plasma volume and platelet concentration appear to play a role in concentrating BDNF in the circulation during exercise.

The investigators note that BDNF and other neurotrophic-based pharmaceutical therapies have shown “great promise” in slowing and even arresting neurodegenerative processes in animals, but attempts to harness the protective power of BDNF in human neurodegeneration have thus far failed.

“Whether episodically upregulating BDNF production with intense exercise is an effective strategy to curb age-related cognitive decline in humans is unknown, but animal models indicate that it is and that BDNF plays a primary role,” the researchers write.

Funding for the study was provided by the Healthcare Otago Charitable Trust. The investigators have reported no relevant financial relationships.

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

Short bouts of intense exercise may help protect the brain from age-related cognitive decline by increasing production of a key protein involved in neuroplasticity, learning, and memory, new research suggests.

In a small study of healthy adults, 6 minutes of high-intensity cycling increased circulating levels of brain-derived neurotrophic factor (BDNF) to a significantly greater extent than prolonged light cycling or fasting.

However, the data do not suggest that 6 minutes of high-intensity exercise “wards off dementia,” cautioned lead investigator Travis Gibbons, MSc, PhD candidate in environmental physiology at the University of Otago (New Zealand), Dunedin, and now postdoctoral fellow at the University of British Columbia – Okanagan, Kelowna.

“Like all science, this is just a small piece that supports a potential mechanistic role for how exercise might improve brain health,” Dr. Gibbons told this news organization.

The findings were published online in the Journal of Physiology.
 

Targeting BDNF

Both intermittent fasting and exercise have previously been shown to have potent neuroprotective effects; and an acute upregulation of BDNF appears to be a common mechanistic link.

To tease apart the influence of fasting and exercise on BDNF production, Dr. Gibbons and colleagues studied 12 aerobically fit, healthy men (n = 6) and women (n = 6) aged 20-40 years.

In a study that employed a repeated-measures crossover design, they assessed circulating BDNF levels after a 20-hour fast, prolonged (90-min) light cycling, short (6-min) high-intensity cycling, and combined fasting and exercise.

Six minutes of high-intensity exercise appeared to be the most efficient way to increase BDNF.

Fasting for 20 hours led to a ninefold increase in ketone body delivery to the brain but had no effect on any metric of BDNF in peripheral circulation at rest or during exercise.

Six minutes of high-intensity exercise increased every metric of circulating BDNF four to five times more than prolonged low-intensity exercise.

In addition, the increase in plasma-derived BDNF correlated with a sixfold increase in circulating lactate irrespective of feeding or fasting state.
 

Lactate delivery?

“My leading theory is that, during and following intense exercise, lactate produced by muscles is delivered and consumed by the brain,” Dr. Gibbons noted.

“It takes high-intensity exercise to provoke this ‘cerebral substrate switch’ from glucose to lactate. Critically, this cerebral substrate switch has been shown to contribute to the early processes that upregulate BDNF production in the brain,” he said.

However, “Whether this translates to ‘warding off dementia’ is not clear,” Dr. Gibbons added.

The study also suggests that increases in plasma volume and platelet concentration appear to play a role in concentrating BDNF in the circulation during exercise.

The investigators note that BDNF and other neurotrophic-based pharmaceutical therapies have shown “great promise” in slowing and even arresting neurodegenerative processes in animals, but attempts to harness the protective power of BDNF in human neurodegeneration have thus far failed.

“Whether episodically upregulating BDNF production with intense exercise is an effective strategy to curb age-related cognitive decline in humans is unknown, but animal models indicate that it is and that BDNF plays a primary role,” the researchers write.

Funding for the study was provided by the Healthcare Otago Charitable Trust. The investigators have reported no relevant financial relationships.

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

Low levels of serum lactate dehydrogenase were significantly associated with depression and suicide attempts in adults with major depressive disorder, based on data from more than 300 individuals.

The pathogenesis of depression is complex, and recent research has focused on the potential relationship between energy metabolism and depression, wrote Qian Yao, MD, of Wuhan University, Hubei, China, and colleagues.

Previous studies have suggested that serum lactate dehydrogenase (LDH) may be a biomarker for Parkinson’s disease, Huntington’s disease, and post-stroke depression, but the link between lactate metabolism and depression remains unclear, they said.

“We hypothesize that LDH may act as a potential biomarker for MDD, considering it represents a reduced energy metabolic status in depressive patients,” they explained.

In a study published in General Hospital Psychiatry, the researchers examined differences in serum LDH in 232 patients with major depressive disorder (MDD) and 110 healthy controls. They also examined whether LDH was predictive of suicide attempts in the MDD patients. Depression was assessed via the 24-item Hamilton Depression Scale (HAMD-24).

The mean age across both groups was 33 years; other clinical characteristics were similar between the groups.

The serum LDH level of the MDD group was significantly lower than the control group was (177.94 U/L vs. 196.50 U/L; P < .001). Analysis of blood lipid levels showed significantly lower levels of total cholesterol in the MDD group compared with controls, but no significant differences were noted in LDL cholesterol, HDL cholesterol, or triglycerides.

In a further analysis of subgroups of depression, the serum LDH in MDD patients who had attempted suicide was significantly lower compared to those without suicide attempts (169.96 vs. 181.25; P = .002), although the LDH level for the non-suicide MDD patients also was significantly lower than controls (181.25 vs. 196.50; P < .001). No significant correlation was noted between HAMD-24 score and suicide attempts.

Some gender differences also appeared. Both male and female MDD patients had significantly lower LDH levels compared with controls. However, in a regression analysis, a correlation between total cholesterol and LDL cholesterol as potential suicide markers was noted in female MDD patients, but not male MDD patients, which suggests an impact of gender on suicide risk in MDD, the researchers wrote in their discussion.

The findings were limited by several factors including the retrospective design, lack of investigation of changes in LDH isozymes in MDD patients, and lack of assessment of changes in LDH in cerebrospinal fluid, the researchers noted. However, the results “provide clear evidence that the concentration of LDH in serum is associated with early onset and clinical prognosis of depressive symptoms,” in MDD, which may inform diagnosis and guide clinical intervention, including early identification of suicide risk, they concluded.

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

Low levels of serum lactate dehydrogenase were significantly associated with depression and suicide attempts in adults with major depressive disorder, based on data from more than 300 individuals.

The pathogenesis of depression is complex, and recent research has focused on the potential relationship between energy metabolism and depression, wrote Qian Yao, MD, of Wuhan University, Hubei, China, and colleagues.

Previous studies have suggested that serum lactate dehydrogenase (LDH) may be a biomarker for Parkinson’s disease, Huntington’s disease, and post-stroke depression, but the link between lactate metabolism and depression remains unclear, they said.

“We hypothesize that LDH may act as a potential biomarker for MDD, considering it represents a reduced energy metabolic status in depressive patients,” they explained.

In a study published in General Hospital Psychiatry, the researchers examined differences in serum LDH in 232 patients with major depressive disorder (MDD) and 110 healthy controls. They also examined whether LDH was predictive of suicide attempts in the MDD patients. Depression was assessed via the 24-item Hamilton Depression Scale (HAMD-24).

The mean age across both groups was 33 years; other clinical characteristics were similar between the groups.

The serum LDH level of the MDD group was significantly lower than the control group was (177.94 U/L vs. 196.50 U/L; P < .001). Analysis of blood lipid levels showed significantly lower levels of total cholesterol in the MDD group compared with controls, but no significant differences were noted in LDL cholesterol, HDL cholesterol, or triglycerides.

In a further analysis of subgroups of depression, the serum LDH in MDD patients who had attempted suicide was significantly lower compared to those without suicide attempts (169.96 vs. 181.25; P = .002), although the LDH level for the non-suicide MDD patients also was significantly lower than controls (181.25 vs. 196.50; P < .001). No significant correlation was noted between HAMD-24 score and suicide attempts.

Some gender differences also appeared. Both male and female MDD patients had significantly lower LDH levels compared with controls. However, in a regression analysis, a correlation between total cholesterol and LDL cholesterol as potential suicide markers was noted in female MDD patients, but not male MDD patients, which suggests an impact of gender on suicide risk in MDD, the researchers wrote in their discussion.

The findings were limited by several factors including the retrospective design, lack of investigation of changes in LDH isozymes in MDD patients, and lack of assessment of changes in LDH in cerebrospinal fluid, the researchers noted. However, the results “provide clear evidence that the concentration of LDH in serum is associated with early onset and clinical prognosis of depressive symptoms,” in MDD, which may inform diagnosis and guide clinical intervention, including early identification of suicide risk, they concluded.

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

Low levels of serum lactate dehydrogenase were significantly associated with depression and suicide attempts in adults with major depressive disorder, based on data from more than 300 individuals.

The pathogenesis of depression is complex, and recent research has focused on the potential relationship between energy metabolism and depression, wrote Qian Yao, MD, of Wuhan University, Hubei, China, and colleagues.

Previous studies have suggested that serum lactate dehydrogenase (LDH) may be a biomarker for Parkinson’s disease, Huntington’s disease, and post-stroke depression, but the link between lactate metabolism and depression remains unclear, they said.

“We hypothesize that LDH may act as a potential biomarker for MDD, considering it represents a reduced energy metabolic status in depressive patients,” they explained.

In a study published in General Hospital Psychiatry, the researchers examined differences in serum LDH in 232 patients with major depressive disorder (MDD) and 110 healthy controls. They also examined whether LDH was predictive of suicide attempts in the MDD patients. Depression was assessed via the 24-item Hamilton Depression Scale (HAMD-24).

The mean age across both groups was 33 years; other clinical characteristics were similar between the groups.

The serum LDH level of the MDD group was significantly lower than the control group was (177.94 U/L vs. 196.50 U/L; P < .001). Analysis of blood lipid levels showed significantly lower levels of total cholesterol in the MDD group compared with controls, but no significant differences were noted in LDL cholesterol, HDL cholesterol, or triglycerides.

In a further analysis of subgroups of depression, the serum LDH in MDD patients who had attempted suicide was significantly lower compared to those without suicide attempts (169.96 vs. 181.25; P = .002), although the LDH level for the non-suicide MDD patients also was significantly lower than controls (181.25 vs. 196.50; P < .001). No significant correlation was noted between HAMD-24 score and suicide attempts.

Some gender differences also appeared. Both male and female MDD patients had significantly lower LDH levels compared with controls. However, in a regression analysis, a correlation between total cholesterol and LDL cholesterol as potential suicide markers was noted in female MDD patients, but not male MDD patients, which suggests an impact of gender on suicide risk in MDD, the researchers wrote in their discussion.

The findings were limited by several factors including the retrospective design, lack of investigation of changes in LDH isozymes in MDD patients, and lack of assessment of changes in LDH in cerebrospinal fluid, the researchers noted. However, the results “provide clear evidence that the concentration of LDH in serum is associated with early onset and clinical prognosis of depressive symptoms,” in MDD, which may inform diagnosis and guide clinical intervention, including early identification of suicide risk, they concluded.

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

The assessment and diagnosis of bipolar disorder in youth has a complicated and controversial history. I recall from my child and adolescent fellowship training that there was a thinly veiled faculty argument about the diagnosis itself with strong opinions on each side. To revisit this quandary, I reviewed the most up-to-date literature and outlined a case-based approach to the initial screening assessment. Certainly, the assessment by a child and adolescent psychiatrist would be the standard for diagnosis, but we do know that the pediatrician’s office may be the first setting for a child and parent to present with mood symptoms and concerns about bipolar disorder. What can you do to address this adolescent, Carrie, and her mother’s concerns?

Case

Carrie is a 17-year-old girl who has struggled through her childhood and adolescence with anxious and depressive symptoms which have ebbed and flowed with major life stressors, including her parent’s divorce. She has tried cognitive-behavioral therapy and selective serotonin reuptake inhibitors, but the SSRI seemed to cause feelings of anxiousness and agitation, so she stopped it within weeks.

Her mother presents to you concerned that Carrie has had a more persistently irritable mood toward her, often just wanting to be with her friends or otherwise isolate in her room when home to study.

Most concerning to her mother is that Carrie, as a straight A student, has also developed a pattern of staying up all night to study for tests and then “crashes” and sleeps through the weekend, avoiding her mother and only brightening with her friends.

To complicate matters, Carrie’s biological father had type 1 bipolar disorder and an addiction. Her mother comes to you with an initially nonparticipatory Carrie in tow and says: “My former husband began his manic episodes with a lack of sleep and Carrie is so irritable towards me. I feel like I am walking on eggshells all the time. Could this be bipolar disorder?”
 

Case discussion

First, it’s always useful to frame a visit stating that you will spend some time with the patient and some time with both the patient and parent. Emphasizing confidentiality about issues such as drug use, which can be comorbid with mood symptoms and go undetected in high-achieving students such as Carrie, is also important. Further emphasizing that information will not be reflexively shared with the parent unless the child presents a danger to herself or others is also paramount to receive an honest report of symptoms.

Second, there are many signs and symptoms of bipolar disorder that naturally overlap with other conditions such as distractibility with attention-deficit/hyperactivity disorder, or irritability in either a unipolar depression or disruptive mood dysregulation disorder.1 You are looking for an episodic (not chronic) course of symptoms with episodes that last over 5 days for hypomania and over the course of weeks for mania all while meeting all the classic criteria for bipolar disorder.

Note that the broadening of diagnostic criteria has been thought to contribute to an inflated sense of prevalence. The actual expert estimate of prevalence is around 0.8%-1.8% in pediatric populations, although there is a large published range depending on whether the criteria are modified or not.2 Use of the unmodified criteria from the DSM-5 is the recommended approach. Bipolar disorder is exceedingly rare in prepubertal children, and it would be more common for prodromal symptoms such as Carrie’s to emerge and escalate over the teenage years, culminating in a clearer diagnosis in the later teens or 20s.3

In my screening questions, I find the idea of an “infatiguable state” is the most pathognomonic one in considering mania in bipolar disorder.4 Carrie’s “crashing” after nights of studying shows that she clearly fatigues. Patients with bipolar disorder within episodes of hypomania or mania have a seismic shift in perceived energy and a matching lack of ability to sleep that can affect their thought processes, speech, and decision-making. At first blush, Carrie’s history does not indicate current symptoms of bipolar disorder.3
 

Case, continued

When you meet with Carrie alone she shares that she has been experimenting with prescribed stimulants from her older college-aged brother in order to study and ace her tests. She is also experimenting with alcohol and marijuana with her friends. You provide her the CRAFFT tool to deepen your screening of this issue.5

With her mother, you administer the Parent General Behavior Inventory6 and the and the Child Mania Rating Scale7. From these scales, you note that the irritability is more specific to Carrie’s family than pan-present in school and with friends. Her lack of sleep occurs at high-pressure and discreet times.

At this point, you reassure Carrie and her mother that Carrie does not present with symptoms of bipolar disorder but that certainly you will continue screening assessments over time, as they are a good means to track symptoms. You also recommend that Carrie consider mood tracking so she can develop insights into her mood and its relationship to sleep and other events as she prepares for college.8
 

Case discussion, continued

The strongest risk factor for bipolar disorder in youth is family history (specifically a parent) with bipolar disorder).9 If there is the chance to explore the parent’s illness with open-ended questions, you will want to hear about the parent’s age of symptom onset, course of treatment, any hospitalizations, and stabilizing medications because this has prognostic power for your patient. It is important to ensure that the parent indeed has a diagnosis of bipolar disorder and that it is not just being used colloquially to characterize an adult who has labile moods from hour to hour or day to day. This would give undue anticipatory anxiety to a youth about their risk, which is up to 8- to 10-fold greater with a parent with bipolar disorder.9

Even with a strong family history, we do not often see bipolar disorder emerge in prepubertal children.10,11 There may be still concerning prodromal symptoms in which a diagnosis of unipolar depression with more irritable features and mood lability seems more commonly complicated by substance use, as with Carrie.

Activation with an SSRI, as in Carrie’s case, even if not resulting in full mania or hypomania, can also be a soft sign of the serotonergic sensitivity present in bipolar disorder. However, if there are not additional symptoms of bipolar disorder and you are concerned based on family history alone, you do not want to withhold antidepressant treatment because fear of risk. You would want to consider a “dose low and go slow” titration process with more frequent monitoring.

A diagnostic interview with a child and adolescent psychiatrist and administration of scales such as the Young Mania Rating Scale and the Modified Child Depression Rating Scale are the standard means to assess for bipolar symptoms.12 Considering the dearth of child psychiatrists nationally, it would be useful to improve one’s screening in primary care so as to not inadvertently “refer out” all patients for whom mood dysregulation is a concern.

There is also a more expanded tool that includes several scales integrated with clinical information (parent’s age of mood disorder onset, child’s age) which can culminate in a risk score.13

Lastly, I provide my patients with a handout of the Young Mania Rating Scale to take home as a reference and to complete before our next visit.14

You can repeat scales to monitor for more striking bipolar disorder signs and symptoms that emerge over the course of one’s longitudinal treatment of a pediatric patient. This can be an ongoing, episodic assessment since the emergence of bipolar disorder has been shown to range from the teenage years and beyond into the 20s and sometimes 30s.
 

Case, continued

Carrie presents to you again while in her first semester of college at the age of 19. She is taking a leave of absence after she began experimenting with cocaine at college and had a manic episode characterized by a lack of sleep without fatigue, persistent unabating energy, rapid and pressured speech, and ultimately, concern from her college friends. She was admitted to a psychiatric unit and stabilized on a second-generation antipsychotic, risperidone, which has solid evidence for mania, but she and you are now concerned about longer-term metabolic effects.15,16

You discuss monitoring her lipid profile and hemoglobin A1c, in addition to weight gain and waist circumference. She has connected with a therapist and psychiatrist through the college counseling center and hopes to return next semester with a fresh start and commitment to sobriety and social rhythms therapy known to be helpful for patients with bipolar disorder.17

While it is challenging to manage a chronic illness at her age, she feels hopeful that she can make better choices for her overall health with your support and the support of her family and mental health team.

Dr. Pawlowski is a child and adolescent consulting psychiatrist. She is a division chief at the University of Vermont Medical Center, Burlington, where she focuses on primary care mental health integration within primary care pediatrics, internal medicine, and family medicine.
 

References

1. Bipolar Disord. 2016 Jan 9 doi: 10.1111/bdi.12358.

2. Int J Bipolar Disord. 2021 Jun 25. doi: 10.1186/s40345-021-00225-5.

3. Am J Psychiatry. 2018 Dec 11. doi: 10.1176/appi.ajp.2018.18040461.

4. DSM-5 Changes: Implications for Child Serious Emotional Disturbance. Rockville, Md.: Substance Abuse and Mental Health Services Administration, 2016.

5. The CRAFFT tool.

6. General Behavior Inventory. Parent Version (P-GBI) Short Form – H/B (Revised Version, 2008).

7. Child Mania Rating Scale, Parent Version (CMRS-P).

8. https://www.moodtracker.com.

9. J Clin Psychiatry. 2000 Sep. doi: 10.4088/jcp.v61n0906.

10. Int J Bipolar Disord. 2020 Apr 20. doi: 10.1186/s40345-020-00185-2.

11. Int J Bipolar Disord. 2021 Jun 25. doi: 10.1186/s40345-021-00225-5.

12. Bipolar Disord. 2017 Sep 25. doi: 10.1111/bdi.12556.

13. www.cabsresearch.pitt.edu/bpriskcalculator/.

14. Parent Version of the Young Mania Rating Scale (PYMRS).

15. Arch Gen Psychiatry. 2012 Jan 2. doi: 10.1001/archgenpsychiatry.2011.1508.

16. The Carlat Child Psychiatry Report. “Bipolar Disorder” Newburyport, Mass.: Carlat Publishing, 2012.

17. https://www.ipsrt.org/.

The assessment and diagnosis of bipolar disorder in youth has a complicated and controversial history. I recall from my child and adolescent fellowship training that there was a thinly veiled faculty argument about the diagnosis itself with strong opinions on each side. To revisit this quandary, I reviewed the most up-to-date literature and outlined a case-based approach to the initial screening assessment. Certainly, the assessment by a child and adolescent psychiatrist would be the standard for diagnosis, but we do know that the pediatrician’s office may be the first setting for a child and parent to present with mood symptoms and concerns about bipolar disorder. What can you do to address this adolescent, Carrie, and her mother’s concerns?

Case

Carrie is a 17-year-old girl who has struggled through her childhood and adolescence with anxious and depressive symptoms which have ebbed and flowed with major life stressors, including her parent’s divorce. She has tried cognitive-behavioral therapy and selective serotonin reuptake inhibitors, but the SSRI seemed to cause feelings of anxiousness and agitation, so she stopped it within weeks.

Her mother presents to you concerned that Carrie has had a more persistently irritable mood toward her, often just wanting to be with her friends or otherwise isolate in her room when home to study.

Most concerning to her mother is that Carrie, as a straight A student, has also developed a pattern of staying up all night to study for tests and then “crashes” and sleeps through the weekend, avoiding her mother and only brightening with her friends.

To complicate matters, Carrie’s biological father had type 1 bipolar disorder and an addiction. Her mother comes to you with an initially nonparticipatory Carrie in tow and says: “My former husband began his manic episodes with a lack of sleep and Carrie is so irritable towards me. I feel like I am walking on eggshells all the time. Could this be bipolar disorder?”
 

Case discussion

First, it’s always useful to frame a visit stating that you will spend some time with the patient and some time with both the patient and parent. Emphasizing confidentiality about issues such as drug use, which can be comorbid with mood symptoms and go undetected in high-achieving students such as Carrie, is also important. Further emphasizing that information will not be reflexively shared with the parent unless the child presents a danger to herself or others is also paramount to receive an honest report of symptoms.

Second, there are many signs and symptoms of bipolar disorder that naturally overlap with other conditions such as distractibility with attention-deficit/hyperactivity disorder, or irritability in either a unipolar depression or disruptive mood dysregulation disorder.1 You are looking for an episodic (not chronic) course of symptoms with episodes that last over 5 days for hypomania and over the course of weeks for mania all while meeting all the classic criteria for bipolar disorder.

Note that the broadening of diagnostic criteria has been thought to contribute to an inflated sense of prevalence. The actual expert estimate of prevalence is around 0.8%-1.8% in pediatric populations, although there is a large published range depending on whether the criteria are modified or not.2 Use of the unmodified criteria from the DSM-5 is the recommended approach. Bipolar disorder is exceedingly rare in prepubertal children, and it would be more common for prodromal symptoms such as Carrie’s to emerge and escalate over the teenage years, culminating in a clearer diagnosis in the later teens or 20s.3

In my screening questions, I find the idea of an “infatiguable state” is the most pathognomonic one in considering mania in bipolar disorder.4 Carrie’s “crashing” after nights of studying shows that she clearly fatigues. Patients with bipolar disorder within episodes of hypomania or mania have a seismic shift in perceived energy and a matching lack of ability to sleep that can affect their thought processes, speech, and decision-making. At first blush, Carrie’s history does not indicate current symptoms of bipolar disorder.3
 

Case, continued

When you meet with Carrie alone she shares that she has been experimenting with prescribed stimulants from her older college-aged brother in order to study and ace her tests. She is also experimenting with alcohol and marijuana with her friends. You provide her the CRAFFT tool to deepen your screening of this issue.5

With her mother, you administer the Parent General Behavior Inventory6 and the and the Child Mania Rating Scale7. From these scales, you note that the irritability is more specific to Carrie’s family than pan-present in school and with friends. Her lack of sleep occurs at high-pressure and discreet times.

At this point, you reassure Carrie and her mother that Carrie does not present with symptoms of bipolar disorder but that certainly you will continue screening assessments over time, as they are a good means to track symptoms. You also recommend that Carrie consider mood tracking so she can develop insights into her mood and its relationship to sleep and other events as she prepares for college.8
 

Case discussion, continued

The strongest risk factor for bipolar disorder in youth is family history (specifically a parent) with bipolar disorder).9 If there is the chance to explore the parent’s illness with open-ended questions, you will want to hear about the parent’s age of symptom onset, course of treatment, any hospitalizations, and stabilizing medications because this has prognostic power for your patient. It is important to ensure that the parent indeed has a diagnosis of bipolar disorder and that it is not just being used colloquially to characterize an adult who has labile moods from hour to hour or day to day. This would give undue anticipatory anxiety to a youth about their risk, which is up to 8- to 10-fold greater with a parent with bipolar disorder.9

Even with a strong family history, we do not often see bipolar disorder emerge in prepubertal children.10,11 There may be still concerning prodromal symptoms in which a diagnosis of unipolar depression with more irritable features and mood lability seems more commonly complicated by substance use, as with Carrie.

Activation with an SSRI, as in Carrie’s case, even if not resulting in full mania or hypomania, can also be a soft sign of the serotonergic sensitivity present in bipolar disorder. However, if there are not additional symptoms of bipolar disorder and you are concerned based on family history alone, you do not want to withhold antidepressant treatment because fear of risk. You would want to consider a “dose low and go slow” titration process with more frequent monitoring.

A diagnostic interview with a child and adolescent psychiatrist and administration of scales such as the Young Mania Rating Scale and the Modified Child Depression Rating Scale are the standard means to assess for bipolar symptoms.12 Considering the dearth of child psychiatrists nationally, it would be useful to improve one’s screening in primary care so as to not inadvertently “refer out” all patients for whom mood dysregulation is a concern.

There is also a more expanded tool that includes several scales integrated with clinical information (parent’s age of mood disorder onset, child’s age) which can culminate in a risk score.13

Lastly, I provide my patients with a handout of the Young Mania Rating Scale to take home as a reference and to complete before our next visit.14

You can repeat scales to monitor for more striking bipolar disorder signs and symptoms that emerge over the course of one’s longitudinal treatment of a pediatric patient. This can be an ongoing, episodic assessment since the emergence of bipolar disorder has been shown to range from the teenage years and beyond into the 20s and sometimes 30s.
 

Case, continued

Carrie presents to you again while in her first semester of college at the age of 19. She is taking a leave of absence after she began experimenting with cocaine at college and had a manic episode characterized by a lack of sleep without fatigue, persistent unabating energy, rapid and pressured speech, and ultimately, concern from her college friends. She was admitted to a psychiatric unit and stabilized on a second-generation antipsychotic, risperidone, which has solid evidence for mania, but she and you are now concerned about longer-term metabolic effects.15,16

You discuss monitoring her lipid profile and hemoglobin A1c, in addition to weight gain and waist circumference. She has connected with a therapist and psychiatrist through the college counseling center and hopes to return next semester with a fresh start and commitment to sobriety and social rhythms therapy known to be helpful for patients with bipolar disorder.17

While it is challenging to manage a chronic illness at her age, she feels hopeful that she can make better choices for her overall health with your support and the support of her family and mental health team.

Dr. Pawlowski is a child and adolescent consulting psychiatrist. She is a division chief at the University of Vermont Medical Center, Burlington, where she focuses on primary care mental health integration within primary care pediatrics, internal medicine, and family medicine.
 

References

1. Bipolar Disord. 2016 Jan 9 doi: 10.1111/bdi.12358.

2. Int J Bipolar Disord. 2021 Jun 25. doi: 10.1186/s40345-021-00225-5.

3. Am J Psychiatry. 2018 Dec 11. doi: 10.1176/appi.ajp.2018.18040461.

4. DSM-5 Changes: Implications for Child Serious Emotional Disturbance. Rockville, Md.: Substance Abuse and Mental Health Services Administration, 2016.

5. The CRAFFT tool.

6. General Behavior Inventory. Parent Version (P-GBI) Short Form – H/B (Revised Version, 2008).

7. Child Mania Rating Scale, Parent Version (CMRS-P).

8. https://www.moodtracker.com.

9. J Clin Psychiatry. 2000 Sep. doi: 10.4088/jcp.v61n0906.

10. Int J Bipolar Disord. 2020 Apr 20. doi: 10.1186/s40345-020-00185-2.

11. Int J Bipolar Disord. 2021 Jun 25. doi: 10.1186/s40345-021-00225-5.

12. Bipolar Disord. 2017 Sep 25. doi: 10.1111/bdi.12556.

13. www.cabsresearch.pitt.edu/bpriskcalculator/.

14. Parent Version of the Young Mania Rating Scale (PYMRS).

15. Arch Gen Psychiatry. 2012 Jan 2. doi: 10.1001/archgenpsychiatry.2011.1508.

16. The Carlat Child Psychiatry Report. “Bipolar Disorder” Newburyport, Mass.: Carlat Publishing, 2012.

17. https://www.ipsrt.org/.

The assessment and diagnosis of bipolar disorder in youth has a complicated and controversial history. I recall from my child and adolescent fellowship training that there was a thinly veiled faculty argument about the diagnosis itself with strong opinions on each side. To revisit this quandary, I reviewed the most up-to-date literature and outlined a case-based approach to the initial screening assessment. Certainly, the assessment by a child and adolescent psychiatrist would be the standard for diagnosis, but we do know that the pediatrician’s office may be the first setting for a child and parent to present with mood symptoms and concerns about bipolar disorder. What can you do to address this adolescent, Carrie, and her mother’s concerns?

Case

Carrie is a 17-year-old girl who has struggled through her childhood and adolescence with anxious and depressive symptoms which have ebbed and flowed with major life stressors, including her parent’s divorce. She has tried cognitive-behavioral therapy and selective serotonin reuptake inhibitors, but the SSRI seemed to cause feelings of anxiousness and agitation, so she stopped it within weeks.

Her mother presents to you concerned that Carrie has had a more persistently irritable mood toward her, often just wanting to be with her friends or otherwise isolate in her room when home to study.

Most concerning to her mother is that Carrie, as a straight A student, has also developed a pattern of staying up all night to study for tests and then “crashes” and sleeps through the weekend, avoiding her mother and only brightening with her friends.

To complicate matters, Carrie’s biological father had type 1 bipolar disorder and an addiction. Her mother comes to you with an initially nonparticipatory Carrie in tow and says: “My former husband began his manic episodes with a lack of sleep and Carrie is so irritable towards me. I feel like I am walking on eggshells all the time. Could this be bipolar disorder?”
 

Case discussion

First, it’s always useful to frame a visit stating that you will spend some time with the patient and some time with both the patient and parent. Emphasizing confidentiality about issues such as drug use, which can be comorbid with mood symptoms and go undetected in high-achieving students such as Carrie, is also important. Further emphasizing that information will not be reflexively shared with the parent unless the child presents a danger to herself or others is also paramount to receive an honest report of symptoms.

Second, there are many signs and symptoms of bipolar disorder that naturally overlap with other conditions such as distractibility with attention-deficit/hyperactivity disorder, or irritability in either a unipolar depression or disruptive mood dysregulation disorder.1 You are looking for an episodic (not chronic) course of symptoms with episodes that last over 5 days for hypomania and over the course of weeks for mania all while meeting all the classic criteria for bipolar disorder.

Note that the broadening of diagnostic criteria has been thought to contribute to an inflated sense of prevalence. The actual expert estimate of prevalence is around 0.8%-1.8% in pediatric populations, although there is a large published range depending on whether the criteria are modified or not.2 Use of the unmodified criteria from the DSM-5 is the recommended approach. Bipolar disorder is exceedingly rare in prepubertal children, and it would be more common for prodromal symptoms such as Carrie’s to emerge and escalate over the teenage years, culminating in a clearer diagnosis in the later teens or 20s.3

In my screening questions, I find the idea of an “infatiguable state” is the most pathognomonic one in considering mania in bipolar disorder.4 Carrie’s “crashing” after nights of studying shows that she clearly fatigues. Patients with bipolar disorder within episodes of hypomania or mania have a seismic shift in perceived energy and a matching lack of ability to sleep that can affect their thought processes, speech, and decision-making. At first blush, Carrie’s history does not indicate current symptoms of bipolar disorder.3
 

Case, continued

When you meet with Carrie alone she shares that she has been experimenting with prescribed stimulants from her older college-aged brother in order to study and ace her tests. She is also experimenting with alcohol and marijuana with her friends. You provide her the CRAFFT tool to deepen your screening of this issue.5

With her mother, you administer the Parent General Behavior Inventory6 and the and the Child Mania Rating Scale7. From these scales, you note that the irritability is more specific to Carrie’s family than pan-present in school and with friends. Her lack of sleep occurs at high-pressure and discreet times.

At this point, you reassure Carrie and her mother that Carrie does not present with symptoms of bipolar disorder but that certainly you will continue screening assessments over time, as they are a good means to track symptoms. You also recommend that Carrie consider mood tracking so she can develop insights into her mood and its relationship to sleep and other events as she prepares for college.8
 

Case discussion, continued

The strongest risk factor for bipolar disorder in youth is family history (specifically a parent) with bipolar disorder).9 If there is the chance to explore the parent’s illness with open-ended questions, you will want to hear about the parent’s age of symptom onset, course of treatment, any hospitalizations, and stabilizing medications because this has prognostic power for your patient. It is important to ensure that the parent indeed has a diagnosis of bipolar disorder and that it is not just being used colloquially to characterize an adult who has labile moods from hour to hour or day to day. This would give undue anticipatory anxiety to a youth about their risk, which is up to 8- to 10-fold greater with a parent with bipolar disorder.9

Even with a strong family history, we do not often see bipolar disorder emerge in prepubertal children.10,11 There may be still concerning prodromal symptoms in which a diagnosis of unipolar depression with more irritable features and mood lability seems more commonly complicated by substance use, as with Carrie.

Activation with an SSRI, as in Carrie’s case, even if not resulting in full mania or hypomania, can also be a soft sign of the serotonergic sensitivity present in bipolar disorder. However, if there are not additional symptoms of bipolar disorder and you are concerned based on family history alone, you do not want to withhold antidepressant treatment because fear of risk. You would want to consider a “dose low and go slow” titration process with more frequent monitoring.

A diagnostic interview with a child and adolescent psychiatrist and administration of scales such as the Young Mania Rating Scale and the Modified Child Depression Rating Scale are the standard means to assess for bipolar symptoms.12 Considering the dearth of child psychiatrists nationally, it would be useful to improve one’s screening in primary care so as to not inadvertently “refer out” all patients for whom mood dysregulation is a concern.

There is also a more expanded tool that includes several scales integrated with clinical information (parent’s age of mood disorder onset, child’s age) which can culminate in a risk score.13

Lastly, I provide my patients with a handout of the Young Mania Rating Scale to take home as a reference and to complete before our next visit.14

You can repeat scales to monitor for more striking bipolar disorder signs and symptoms that emerge over the course of one’s longitudinal treatment of a pediatric patient. This can be an ongoing, episodic assessment since the emergence of bipolar disorder has been shown to range from the teenage years and beyond into the 20s and sometimes 30s.
 

Case, continued

Carrie presents to you again while in her first semester of college at the age of 19. She is taking a leave of absence after she began experimenting with cocaine at college and had a manic episode characterized by a lack of sleep without fatigue, persistent unabating energy, rapid and pressured speech, and ultimately, concern from her college friends. She was admitted to a psychiatric unit and stabilized on a second-generation antipsychotic, risperidone, which has solid evidence for mania, but she and you are now concerned about longer-term metabolic effects.15,16

You discuss monitoring her lipid profile and hemoglobin A1c, in addition to weight gain and waist circumference. She has connected with a therapist and psychiatrist through the college counseling center and hopes to return next semester with a fresh start and commitment to sobriety and social rhythms therapy known to be helpful for patients with bipolar disorder.17

While it is challenging to manage a chronic illness at her age, she feels hopeful that she can make better choices for her overall health with your support and the support of her family and mental health team.

Dr. Pawlowski is a child and adolescent consulting psychiatrist. She is a division chief at the University of Vermont Medical Center, Burlington, where she focuses on primary care mental health integration within primary care pediatrics, internal medicine, and family medicine.
 

References

1. Bipolar Disord. 2016 Jan 9 doi: 10.1111/bdi.12358.

2. Int J Bipolar Disord. 2021 Jun 25. doi: 10.1186/s40345-021-00225-5.

3. Am J Psychiatry. 2018 Dec 11. doi: 10.1176/appi.ajp.2018.18040461.

4. DSM-5 Changes: Implications for Child Serious Emotional Disturbance. Rockville, Md.: Substance Abuse and Mental Health Services Administration, 2016.

5. The CRAFFT tool.

6. General Behavior Inventory. Parent Version (P-GBI) Short Form – H/B (Revised Version, 2008).

7. Child Mania Rating Scale, Parent Version (CMRS-P).

8. https://www.moodtracker.com.

9. J Clin Psychiatry. 2000 Sep. doi: 10.4088/jcp.v61n0906.

10. Int J Bipolar Disord. 2020 Apr 20. doi: 10.1186/s40345-020-00185-2.

11. Int J Bipolar Disord. 2021 Jun 25. doi: 10.1186/s40345-021-00225-5.

12. Bipolar Disord. 2017 Sep 25. doi: 10.1111/bdi.12556.

13. www.cabsresearch.pitt.edu/bpriskcalculator/.

14. Parent Version of the Young Mania Rating Scale (PYMRS).

15. Arch Gen Psychiatry. 2012 Jan 2. doi: 10.1001/archgenpsychiatry.2011.1508.

16. The Carlat Child Psychiatry Report. “Bipolar Disorder” Newburyport, Mass.: Carlat Publishing, 2012.

17. https://www.ipsrt.org/.

A smartphone-based self-management intervention developed for patients with bipolar disorder (BD) can help decrease depressive symptoms and improve quality of life, new research suggests.

In a randomized clinical trial of usual care plus the experimental smartphone-based intervention known as LiveWell vs. usual care alone, participants in the smartphone group who were categorized as low-risk or in asymptomatic recovery at baseline also showed reduced manic symptom severity.

The results suggest that “apps for individuals with bipolar disorder will likely be useful for some people in managing medication use, sleep duration, routine, and monitoring for and managing signs and symptoms” of the disorder, coinvestigator Evan H. Goulding, MD, PhD, assistant professor of psychiatry and behavioral sciences, Northwestern University, Chicago, told this news organization.

Use of the app may also “lead to decreased recurrence of mood episodes, impact overall depressive and manic symptom levels, and improve some aspects of quality of life,” Dr. Goulding added.

The findings were published online in JAMA Psychiatry.
 

Daily check-ins

The researchers randomly assigned 205 patients with BD to receive either usual care (n = 81; 56% women; mean age, 39 years) or usual care plus the smartphone-based self-management intervention LiveWell (n = 124; 65% women; mean age, 43 years) between March 2017 and April 2020. To be included, participants could not be experiencing a current mood episode or suicidal ideation.

The smartphone intervention included a daily check-in to monitor medication adherence, sleep, and wellness levels; coach visits to support adherence to the app; six phone calls over 16 weeks; and support from mental health professionals whenever needed. Participants in this group were asked to engage their mental health providers in the intervention as well.

Each participant in the control group had a visit with a coach who facilitated self-management support.

Investigators assessed all participants every 8 weeks until week 48 to gather information on mood symptoms and severity over the past 2 weeks and on quality of life.

The patients were also stratified into high- and low-risk relapse groups. The low-risk group was in asymptomatic recovery, meaning that they experienced two or fewer moderate symptoms of mania or depression in the previous 8 weeks. In addition, they had no moderate symptoms of mania or depression at study enrollment.

Patients in the high-risk group were recovering from an episode of mania or depression. They also had two or fewer moderate symptoms, but for 8 weeks or less.
 

Low-risk group fares better

Results showed that the smartphone intervention was significantly associated with a reduction in depressive symptoms vs. usual care (P = .02), as well as improvement in one aspect of the World Health Organization Quality of Life Assessment that measures social relationships (P = .02).

When the investigators stratified participants into risk groups, they found that for those in the low-risk group the smartphone-based intervention was associated with lower episode-relapse rates, lower mean percentage time symptomatic, and decreased manic symptom severity.

Mean estimated relapse rates by 48 weeks for the low-risk group were 12% for those in the intervention group and 37.2% for those in the control group. No differences were noted for the high-risk group.

Low-risk patients in the intervention group also had lower mean percentage-time symptomatic (17.9%) than those in the control group (26.1%) (Cohen d = .31).

“Our results are consistent with literature emphasizing the identification and facilitation of management plans for early warning signs of mood episodes and using these plans as an important self-management technique for avoiding relapse,” Dr. Goulding said.

Study limitations included low engagement by mental health professionals and low data generalizability to other populations, as the sample was mostly White (84% of the app group and 81% of the control group).

“There is a fairly large literature on risk factors, longitudinal trajectories, and stages of diseases that suggest we should already be able to predict relapse risk for individuals,” Dr. Goulding said.

“However, moving from overall risk to individual risk is trickier and will require larger datasets with longer follow-up to better understand what types of help should be delivered when and to whom,” he added.
 

‘Requires commitment’

John Torous, MD, director of the division of digital psychiatry at Beth Israel Deaconess Medical Center, Boston, noted that mental health apps such as LiveWell require “time and energy devoted by both the patient and their clinician for maximal efficacy, which requires commitment from and training for both parties as well.

“But with such an investment in people, there is good evidence apps can help people with bipolar disorder even during the more severe periods of the illness,” added Dr. Torous, who was not involved with the research.

The study was funded by the National Institute of Mental Health.

Dr. Goulding reports having received honoraria from Otsuka. Dr. Torous has reported no relevant financial relationships.

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

A smartphone-based self-management intervention developed for patients with bipolar disorder (BD) can help decrease depressive symptoms and improve quality of life, new research suggests.

In a randomized clinical trial of usual care plus the experimental smartphone-based intervention known as LiveWell vs. usual care alone, participants in the smartphone group who were categorized as low-risk or in asymptomatic recovery at baseline also showed reduced manic symptom severity.

The results suggest that “apps for individuals with bipolar disorder will likely be useful for some people in managing medication use, sleep duration, routine, and monitoring for and managing signs and symptoms” of the disorder, coinvestigator Evan H. Goulding, MD, PhD, assistant professor of psychiatry and behavioral sciences, Northwestern University, Chicago, told this news organization.

Use of the app may also “lead to decreased recurrence of mood episodes, impact overall depressive and manic symptom levels, and improve some aspects of quality of life,” Dr. Goulding added.

The findings were published online in JAMA Psychiatry.
 

Daily check-ins

The researchers randomly assigned 205 patients with BD to receive either usual care (n = 81; 56% women; mean age, 39 years) or usual care plus the smartphone-based self-management intervention LiveWell (n = 124; 65% women; mean age, 43 years) between March 2017 and April 2020. To be included, participants could not be experiencing a current mood episode or suicidal ideation.

The smartphone intervention included a daily check-in to monitor medication adherence, sleep, and wellness levels; coach visits to support adherence to the app; six phone calls over 16 weeks; and support from mental health professionals whenever needed. Participants in this group were asked to engage their mental health providers in the intervention as well.

Each participant in the control group had a visit with a coach who facilitated self-management support.

Investigators assessed all participants every 8 weeks until week 48 to gather information on mood symptoms and severity over the past 2 weeks and on quality of life.

The patients were also stratified into high- and low-risk relapse groups. The low-risk group was in asymptomatic recovery, meaning that they experienced two or fewer moderate symptoms of mania or depression in the previous 8 weeks. In addition, they had no moderate symptoms of mania or depression at study enrollment.

Patients in the high-risk group were recovering from an episode of mania or depression. They also had two or fewer moderate symptoms, but for 8 weeks or less.
 

Low-risk group fares better

Results showed that the smartphone intervention was significantly associated with a reduction in depressive symptoms vs. usual care (P = .02), as well as improvement in one aspect of the World Health Organization Quality of Life Assessment that measures social relationships (P = .02).

When the investigators stratified participants into risk groups, they found that for those in the low-risk group the smartphone-based intervention was associated with lower episode-relapse rates, lower mean percentage time symptomatic, and decreased manic symptom severity.

Mean estimated relapse rates by 48 weeks for the low-risk group were 12% for those in the intervention group and 37.2% for those in the control group. No differences were noted for the high-risk group.

Low-risk patients in the intervention group also had lower mean percentage-time symptomatic (17.9%) than those in the control group (26.1%) (Cohen d = .31).

“Our results are consistent with literature emphasizing the identification and facilitation of management plans for early warning signs of mood episodes and using these plans as an important self-management technique for avoiding relapse,” Dr. Goulding said.

Study limitations included low engagement by mental health professionals and low data generalizability to other populations, as the sample was mostly White (84% of the app group and 81% of the control group).

“There is a fairly large literature on risk factors, longitudinal trajectories, and stages of diseases that suggest we should already be able to predict relapse risk for individuals,” Dr. Goulding said.

“However, moving from overall risk to individual risk is trickier and will require larger datasets with longer follow-up to better understand what types of help should be delivered when and to whom,” he added.
 

‘Requires commitment’

John Torous, MD, director of the division of digital psychiatry at Beth Israel Deaconess Medical Center, Boston, noted that mental health apps such as LiveWell require “time and energy devoted by both the patient and their clinician for maximal efficacy, which requires commitment from and training for both parties as well.

“But with such an investment in people, there is good evidence apps can help people with bipolar disorder even during the more severe periods of the illness,” added Dr. Torous, who was not involved with the research.

The study was funded by the National Institute of Mental Health.

Dr. Goulding reports having received honoraria from Otsuka. Dr. Torous has reported no relevant financial relationships.

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

A smartphone-based self-management intervention developed for patients with bipolar disorder (BD) can help decrease depressive symptoms and improve quality of life, new research suggests.

In a randomized clinical trial of usual care plus the experimental smartphone-based intervention known as LiveWell vs. usual care alone, participants in the smartphone group who were categorized as low-risk or in asymptomatic recovery at baseline also showed reduced manic symptom severity.

The results suggest that “apps for individuals with bipolar disorder will likely be useful for some people in managing medication use, sleep duration, routine, and monitoring for and managing signs and symptoms” of the disorder, coinvestigator Evan H. Goulding, MD, PhD, assistant professor of psychiatry and behavioral sciences, Northwestern University, Chicago, told this news organization.

Use of the app may also “lead to decreased recurrence of mood episodes, impact overall depressive and manic symptom levels, and improve some aspects of quality of life,” Dr. Goulding added.

The findings were published online in JAMA Psychiatry.
 

Daily check-ins

The researchers randomly assigned 205 patients with BD to receive either usual care (n = 81; 56% women; mean age, 39 years) or usual care plus the smartphone-based self-management intervention LiveWell (n = 124; 65% women; mean age, 43 years) between March 2017 and April 2020. To be included, participants could not be experiencing a current mood episode or suicidal ideation.

The smartphone intervention included a daily check-in to monitor medication adherence, sleep, and wellness levels; coach visits to support adherence to the app; six phone calls over 16 weeks; and support from mental health professionals whenever needed. Participants in this group were asked to engage their mental health providers in the intervention as well.

Each participant in the control group had a visit with a coach who facilitated self-management support.

Investigators assessed all participants every 8 weeks until week 48 to gather information on mood symptoms and severity over the past 2 weeks and on quality of life.

The patients were also stratified into high- and low-risk relapse groups. The low-risk group was in asymptomatic recovery, meaning that they experienced two or fewer moderate symptoms of mania or depression in the previous 8 weeks. In addition, they had no moderate symptoms of mania or depression at study enrollment.

Patients in the high-risk group were recovering from an episode of mania or depression. They also had two or fewer moderate symptoms, but for 8 weeks or less.
 

Low-risk group fares better

Results showed that the smartphone intervention was significantly associated with a reduction in depressive symptoms vs. usual care (P = .02), as well as improvement in one aspect of the World Health Organization Quality of Life Assessment that measures social relationships (P = .02).

When the investigators stratified participants into risk groups, they found that for those in the low-risk group the smartphone-based intervention was associated with lower episode-relapse rates, lower mean percentage time symptomatic, and decreased manic symptom severity.

Mean estimated relapse rates by 48 weeks for the low-risk group were 12% for those in the intervention group and 37.2% for those in the control group. No differences were noted for the high-risk group.

Low-risk patients in the intervention group also had lower mean percentage-time symptomatic (17.9%) than those in the control group (26.1%) (Cohen d = .31).

“Our results are consistent with literature emphasizing the identification and facilitation of management plans for early warning signs of mood episodes and using these plans as an important self-management technique for avoiding relapse,” Dr. Goulding said.

Study limitations included low engagement by mental health professionals and low data generalizability to other populations, as the sample was mostly White (84% of the app group and 81% of the control group).

“There is a fairly large literature on risk factors, longitudinal trajectories, and stages of diseases that suggest we should already be able to predict relapse risk for individuals,” Dr. Goulding said.

“However, moving from overall risk to individual risk is trickier and will require larger datasets with longer follow-up to better understand what types of help should be delivered when and to whom,” he added.
 

‘Requires commitment’

John Torous, MD, director of the division of digital psychiatry at Beth Israel Deaconess Medical Center, Boston, noted that mental health apps such as LiveWell require “time and energy devoted by both the patient and their clinician for maximal efficacy, which requires commitment from and training for both parties as well.

“But with such an investment in people, there is good evidence apps can help people with bipolar disorder even during the more severe periods of the illness,” added Dr. Torous, who was not involved with the research.

The study was funded by the National Institute of Mental Health.

Dr. Goulding reports having received honoraria from Otsuka. Dr. Torous has reported no relevant financial relationships.

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