Eve Bender

Short-term and cyclical use of estrogen and progestin therapy for menopausal symptoms is linked to an increased risk of dementia, results of a large observational study show.

Investigators found that women in their 50s who took hormone therapy (HT) for menopausal symptoms had a 24% increased risk of developing dementia and Alzheimer’s disease (AD) 20 years later, compared with those who didn’t use HT. The risk was present even in women who used HT for brief periods at menopause onset.

However, both the investigators and experts not involved in the research caution that further studies are needed to explore whether the increased risk of dementia stems from HT use or whether women in need of HT have other underlying dementia risk factors.

“We cannot guarantee that our findings illustrate a causal relationship or if they represent underlying disposition to dementia in women in need of [HT],” lead investigator Nelsan Pourhadi, MD, from the Danish Dementia Research Centre at Copenhagen University Hospital Rigshospitalet, told this news organization.

Still, he added, the findings supported evidence from the Women’s Health Initiative Memory Study (WHIMS), the largest randomized trial on menopausal hormone therapy and dementia.

The findings were published online in BMJ.
 

Conflicting findings

Before WHIMS was published in 2003, HT was widely prescribed to relieve menopausal symptoms. However, WHIMS, which included more than 4,000 women aged 65 years or older, revealed that HT was associated with a twofold increased risk of dementia.

Studies published since then have yielded mixed results, adding to the controversy surrounding the safety of HT.

To discover whether age of initiation or length of duration of HT affects health outcomes, Dr. Pourhadi and his team undertook the observational study.

Between 2000 and 2018, the researchers tracked more than 60,000 Danish women aged 50-60 years using diagnosis and prescription information from Denmark’s National Registry of Patients.

The registry records showed that nearly 5,600 women developed dementia and 56,000 did not develop dementia. Of the 5,600 women with dementia, 1,460 had a diagnosis of AD.

Nearly 18,000 participants in the study sample received HT – 1,790 (29%) in the dementia group and 16,150 (32%) in the control group. Half started treatment before age 53 years and half stopped within 4 years. Roughly 90% used oral medications, which included a combination of estrogen and progestin.

The median age at which participants started HT was 53 years for both cases and controls, and the median duration of use was 4 years.
 

Longer use equals greater risk

Compared with those who did not use HT, those who used estrogen-progestin therapy had a 24% increased risk of developing all-cause dementia (hazard ratio, 1.24; 95% confidence interval, 1.17-1.44).

The increased dementia risk was similar between continuous (estrogen and progestin taken daily) and cyclic (daily estrogen with progestin taken 10-14 days a month) treatment regimens.

Longer durations of HT use were associated with increased risk, ranging from a 21% increased risk (HR, 1.21; 95% CI, 1.09-1.35) for those who used it for 1 year or less to a 74% increased risk (HR, 1.74; 95% CI, 1.45-2.10) for use lasting 12 years or more.

Women who started HT between the age of 45 and 50 had a 26% increased risk of developing all-cause dementia (HR, 1.26; 95% CI, 1.13-1.41) while women who initiated HT between age 51 and 60 had a 21% greater risk (HR, 1.21; 95% CI, 1.12-1.29).

Progestin-only or vaginal-estrogen-only therapy was not associated with the development of dementia.

The investigators noted that because this is an observational study, “further studies are warranted to explore if the observed association in this study between menopausal hormone therapy use and increased risk of dementia illustrates a causal effect.”
 

No causal relationship

In an accompanying editorial, Kejal Kantarci, MD, a professor of radiology at the Mayo Clinic, Rochester, Minn., noted that three clinical trials, including the WHIMS of Younger Women (WHIMS-Y) in 2013, did not show a link between cognitive function and HT.

“Although [Dr.] Pourhadi and colleagues’ study was done carefully using national registries, the observed associations could be artefactual and should not be used to infer a causal relationship between hormone therapy and dementia risk. These findings cannot inform shared decision-making about use of hormone therapy for menopausal symptoms,” she states in the editorial.

Also commenting on the findings, Amanda Heslegrave, PhD, a senior research fellow at the U.K. Dementia Research Institute, London, said in a release from the U.K.’s Science Media Centre that while the study “may cause alarm for women taking [HT], it highlights just how much we still don’t know about the effects of hormones on women’s brain health, and with promising treatments on the horizon, it should be a call to action to make this a priority area of research.”

There was no specific funding for the study. Dr. Kantarci reported working on an unpaid educational activity on Alzheimer’s disease for Biogen and is the PI on a study of a PET imaging ligand for Alzheimer’s disease, to which Eli Lilly and Avid Radiopharmaceuticals donated supplies.

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

Short-term and cyclical use of estrogen and progestin therapy for menopausal symptoms is linked to an increased risk of dementia, results of a large observational study show.

Investigators found that women in their 50s who took hormone therapy (HT) for menopausal symptoms had a 24% increased risk of developing dementia and Alzheimer’s disease (AD) 20 years later, compared with those who didn’t use HT. The risk was present even in women who used HT for brief periods at menopause onset.

However, both the investigators and experts not involved in the research caution that further studies are needed to explore whether the increased risk of dementia stems from HT use or whether women in need of HT have other underlying dementia risk factors.

“We cannot guarantee that our findings illustrate a causal relationship or if they represent underlying disposition to dementia in women in need of [HT],” lead investigator Nelsan Pourhadi, MD, from the Danish Dementia Research Centre at Copenhagen University Hospital Rigshospitalet, told this news organization.

Still, he added, the findings supported evidence from the Women’s Health Initiative Memory Study (WHIMS), the largest randomized trial on menopausal hormone therapy and dementia.

The findings were published online in BMJ.
 

Conflicting findings

Before WHIMS was published in 2003, HT was widely prescribed to relieve menopausal symptoms. However, WHIMS, which included more than 4,000 women aged 65 years or older, revealed that HT was associated with a twofold increased risk of dementia.

Studies published since then have yielded mixed results, adding to the controversy surrounding the safety of HT.

To discover whether age of initiation or length of duration of HT affects health outcomes, Dr. Pourhadi and his team undertook the observational study.

Between 2000 and 2018, the researchers tracked more than 60,000 Danish women aged 50-60 years using diagnosis and prescription information from Denmark’s National Registry of Patients.

The registry records showed that nearly 5,600 women developed dementia and 56,000 did not develop dementia. Of the 5,600 women with dementia, 1,460 had a diagnosis of AD.

Nearly 18,000 participants in the study sample received HT – 1,790 (29%) in the dementia group and 16,150 (32%) in the control group. Half started treatment before age 53 years and half stopped within 4 years. Roughly 90% used oral medications, which included a combination of estrogen and progestin.

The median age at which participants started HT was 53 years for both cases and controls, and the median duration of use was 4 years.
 

Longer use equals greater risk

Compared with those who did not use HT, those who used estrogen-progestin therapy had a 24% increased risk of developing all-cause dementia (hazard ratio, 1.24; 95% confidence interval, 1.17-1.44).

The increased dementia risk was similar between continuous (estrogen and progestin taken daily) and cyclic (daily estrogen with progestin taken 10-14 days a month) treatment regimens.

Longer durations of HT use were associated with increased risk, ranging from a 21% increased risk (HR, 1.21; 95% CI, 1.09-1.35) for those who used it for 1 year or less to a 74% increased risk (HR, 1.74; 95% CI, 1.45-2.10) for use lasting 12 years or more.

Women who started HT between the age of 45 and 50 had a 26% increased risk of developing all-cause dementia (HR, 1.26; 95% CI, 1.13-1.41) while women who initiated HT between age 51 and 60 had a 21% greater risk (HR, 1.21; 95% CI, 1.12-1.29).

Progestin-only or vaginal-estrogen-only therapy was not associated with the development of dementia.

The investigators noted that because this is an observational study, “further studies are warranted to explore if the observed association in this study between menopausal hormone therapy use and increased risk of dementia illustrates a causal effect.”
 

No causal relationship

In an accompanying editorial, Kejal Kantarci, MD, a professor of radiology at the Mayo Clinic, Rochester, Minn., noted that three clinical trials, including the WHIMS of Younger Women (WHIMS-Y) in 2013, did not show a link between cognitive function and HT.

“Although [Dr.] Pourhadi and colleagues’ study was done carefully using national registries, the observed associations could be artefactual and should not be used to infer a causal relationship between hormone therapy and dementia risk. These findings cannot inform shared decision-making about use of hormone therapy for menopausal symptoms,” she states in the editorial.

Also commenting on the findings, Amanda Heslegrave, PhD, a senior research fellow at the U.K. Dementia Research Institute, London, said in a release from the U.K.’s Science Media Centre that while the study “may cause alarm for women taking [HT], it highlights just how much we still don’t know about the effects of hormones on women’s brain health, and with promising treatments on the horizon, it should be a call to action to make this a priority area of research.”

There was no specific funding for the study. Dr. Kantarci reported working on an unpaid educational activity on Alzheimer’s disease for Biogen and is the PI on a study of a PET imaging ligand for Alzheimer’s disease, to which Eli Lilly and Avid Radiopharmaceuticals donated supplies.

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

Short-term and cyclical use of estrogen and progestin therapy for menopausal symptoms is linked to an increased risk of dementia, results of a large observational study show.

Investigators found that women in their 50s who took hormone therapy (HT) for menopausal symptoms had a 24% increased risk of developing dementia and Alzheimer’s disease (AD) 20 years later, compared with those who didn’t use HT. The risk was present even in women who used HT for brief periods at menopause onset.

However, both the investigators and experts not involved in the research caution that further studies are needed to explore whether the increased risk of dementia stems from HT use or whether women in need of HT have other underlying dementia risk factors.

“We cannot guarantee that our findings illustrate a causal relationship or if they represent underlying disposition to dementia in women in need of [HT],” lead investigator Nelsan Pourhadi, MD, from the Danish Dementia Research Centre at Copenhagen University Hospital Rigshospitalet, told this news organization.

Still, he added, the findings supported evidence from the Women’s Health Initiative Memory Study (WHIMS), the largest randomized trial on menopausal hormone therapy and dementia.

The findings were published online in BMJ.
 

Conflicting findings

Before WHIMS was published in 2003, HT was widely prescribed to relieve menopausal symptoms. However, WHIMS, which included more than 4,000 women aged 65 years or older, revealed that HT was associated with a twofold increased risk of dementia.

Studies published since then have yielded mixed results, adding to the controversy surrounding the safety of HT.

To discover whether age of initiation or length of duration of HT affects health outcomes, Dr. Pourhadi and his team undertook the observational study.

Between 2000 and 2018, the researchers tracked more than 60,000 Danish women aged 50-60 years using diagnosis and prescription information from Denmark’s National Registry of Patients.

The registry records showed that nearly 5,600 women developed dementia and 56,000 did not develop dementia. Of the 5,600 women with dementia, 1,460 had a diagnosis of AD.

Nearly 18,000 participants in the study sample received HT – 1,790 (29%) in the dementia group and 16,150 (32%) in the control group. Half started treatment before age 53 years and half stopped within 4 years. Roughly 90% used oral medications, which included a combination of estrogen and progestin.

The median age at which participants started HT was 53 years for both cases and controls, and the median duration of use was 4 years.
 

Longer use equals greater risk

Compared with those who did not use HT, those who used estrogen-progestin therapy had a 24% increased risk of developing all-cause dementia (hazard ratio, 1.24; 95% confidence interval, 1.17-1.44).

The increased dementia risk was similar between continuous (estrogen and progestin taken daily) and cyclic (daily estrogen with progestin taken 10-14 days a month) treatment regimens.

Longer durations of HT use were associated with increased risk, ranging from a 21% increased risk (HR, 1.21; 95% CI, 1.09-1.35) for those who used it for 1 year or less to a 74% increased risk (HR, 1.74; 95% CI, 1.45-2.10) for use lasting 12 years or more.

Women who started HT between the age of 45 and 50 had a 26% increased risk of developing all-cause dementia (HR, 1.26; 95% CI, 1.13-1.41) while women who initiated HT between age 51 and 60 had a 21% greater risk (HR, 1.21; 95% CI, 1.12-1.29).

Progestin-only or vaginal-estrogen-only therapy was not associated with the development of dementia.

The investigators noted that because this is an observational study, “further studies are warranted to explore if the observed association in this study between menopausal hormone therapy use and increased risk of dementia illustrates a causal effect.”
 

No causal relationship

In an accompanying editorial, Kejal Kantarci, MD, a professor of radiology at the Mayo Clinic, Rochester, Minn., noted that three clinical trials, including the WHIMS of Younger Women (WHIMS-Y) in 2013, did not show a link between cognitive function and HT.

“Although [Dr.] Pourhadi and colleagues’ study was done carefully using national registries, the observed associations could be artefactual and should not be used to infer a causal relationship between hormone therapy and dementia risk. These findings cannot inform shared decision-making about use of hormone therapy for menopausal symptoms,” she states in the editorial.

Also commenting on the findings, Amanda Heslegrave, PhD, a senior research fellow at the U.K. Dementia Research Institute, London, said in a release from the U.K.’s Science Media Centre that while the study “may cause alarm for women taking [HT], it highlights just how much we still don’t know about the effects of hormones on women’s brain health, and with promising treatments on the horizon, it should be a call to action to make this a priority area of research.”

There was no specific funding for the study. Dr. Kantarci reported working on an unpaid educational activity on Alzheimer’s disease for Biogen and is the PI on a study of a PET imaging ligand for Alzheimer’s disease, to which Eli Lilly and Avid Radiopharmaceuticals donated supplies.

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

An automated artificial intelligence (AI) model trained to read electroencephalograms (EEGs) in patients with suspected epilepsy is just as accurate as trained neurologists, new data suggest.

Known as SCORE-AI, the technology distinguishes between abnormal and normal EEG recordings and classifies irregular recordings into specific categories crucial for patient decision-making.

“SCORE-AI can be used in place of experts in underprivileged areas, where expertise is missing, or to help physicians to preselect or prescore recordings in areas where the workload is high – we can all benefit from AI,” study investigator Sándor Beniczky, MD, PhD, said in a JAMA Neurology podcast.

Dr. Beniczky is professor of clinical neurophysiology at Aarhus University in Denmark.

The findings were published online in JAMA Neurology.
 

Gaining a foothold

Increasingly, AI is gaining a foothold in medicine by credibly addressing patient queries and aiding radiologists.

To bring AI to EEG interpretation, the researchers developed and validated an AI model that was able to assess routine, clinical EEGs in patients with suspected epilepsy.

Beyond using AI to distinguish abnormal from normal EEG recordings, the researchers wanted to train the new system to classify abnormal recordings into the major categories that are most relevant for clinical decision-making in patients who may have epilepsy. The categories included epileptiform-focal, epileptiform-generalized, nonepileptiform-focal, and nonepileptiform-diffuse abnormalities.

The researchers trained the learning model using Standardized Computer-based Organized Reporting of EEG (SCORE) software.

In the development phase, the model was trained using more than 30,490 anonymized and highly annotated EEG recordings from 14,100 men (median age, 25 years) from a single center. The recordings had an average duration of 31 minutes and were interpreted by 17 neurologists using standardized criteria. If an EEG recording was abnormal, the physicians had to specify which abnormal features were present.

SCORE-AI then performed an analysis of the recordings based on input from the experts.

To validate the findings, investigators used two independent test datasets. The first dataset consisted of 100 representative routine EEGs from 61 men (median age, 26 years), evaluated by 11 neurologists from different centers.

The consensus of these evaluations served as the reference standard. The second dataset comprised nearly 10,000 EEGs from a single center (5,170 men; median age, 35 years), independently assessed by 14 neurologists.
 

Near-perfect accuracy

When compared with the experts, SCORE-AI had near-perfect accuracy with an area under the receiver operating characteristic (AUROC) curve for differentiating normal from abnormal EEG recordings of 0.95.

SCORE-AI also performed well at identifying generalized epileptiform abnormalities (AUROC, 0.96), focal epileptiform abnormalities (AUROC, 0.91), focal nonepileptiform abnormalities (AUROC, 0.89), and diffuse nonepileptiform abnormalities (AUROC, 0.93).

In addition, SCORE-AI had excellent agreement with clinicians – and sometimes agreed with individual experts more than the experts agreed with one another.

When Dr. Beniczky and team tested SCORE-AI against three previously published AI models, SCORE-AI demonstrated greater specificity than those models (90% vs. 3%-63%) but was not as sensitive (86.7%) as two of the models (96.7% and 100%).

One of the study’s limitations was the fact that SCORE-AI was developed and validated on routine EEGs that excluded neonates and critically ill patients.

In the future, Dr. Beniczky said on the podcast, the team would like to train SCORE-AI to read EEGs with more granularity, and eventually use only one single channel to record EEGs. At present, SCORE-AI is being integrated with Natus Neuro, a widely used EEG equipment system, the investigators note.

In an accompanying editorial, Jonathan Kleen, MD, PhD, and Elan Guterman, MD, said, “The overall approach taken ... in developing and validating SCORE-AI sets a standard for this work going forward.”

Dr. Kleen and Dr. Guterman note that the technological gains brought about by SCORE-AI technology “could offer an exciting prospect to improve EEG availability and clinical care for the 50 million people with epilepsy worldwide.”
 

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

An automated artificial intelligence (AI) model trained to read electroencephalograms (EEGs) in patients with suspected epilepsy is just as accurate as trained neurologists, new data suggest.

Known as SCORE-AI, the technology distinguishes between abnormal and normal EEG recordings and classifies irregular recordings into specific categories crucial for patient decision-making.

“SCORE-AI can be used in place of experts in underprivileged areas, where expertise is missing, or to help physicians to preselect or prescore recordings in areas where the workload is high – we can all benefit from AI,” study investigator Sándor Beniczky, MD, PhD, said in a JAMA Neurology podcast.

Dr. Beniczky is professor of clinical neurophysiology at Aarhus University in Denmark.

The findings were published online in JAMA Neurology.
 

Gaining a foothold

Increasingly, AI is gaining a foothold in medicine by credibly addressing patient queries and aiding radiologists.

To bring AI to EEG interpretation, the researchers developed and validated an AI model that was able to assess routine, clinical EEGs in patients with suspected epilepsy.

Beyond using AI to distinguish abnormal from normal EEG recordings, the researchers wanted to train the new system to classify abnormal recordings into the major categories that are most relevant for clinical decision-making in patients who may have epilepsy. The categories included epileptiform-focal, epileptiform-generalized, nonepileptiform-focal, and nonepileptiform-diffuse abnormalities.

The researchers trained the learning model using Standardized Computer-based Organized Reporting of EEG (SCORE) software.

In the development phase, the model was trained using more than 30,490 anonymized and highly annotated EEG recordings from 14,100 men (median age, 25 years) from a single center. The recordings had an average duration of 31 minutes and were interpreted by 17 neurologists using standardized criteria. If an EEG recording was abnormal, the physicians had to specify which abnormal features were present.

SCORE-AI then performed an analysis of the recordings based on input from the experts.

To validate the findings, investigators used two independent test datasets. The first dataset consisted of 100 representative routine EEGs from 61 men (median age, 26 years), evaluated by 11 neurologists from different centers.

The consensus of these evaluations served as the reference standard. The second dataset comprised nearly 10,000 EEGs from a single center (5,170 men; median age, 35 years), independently assessed by 14 neurologists.
 

Near-perfect accuracy

When compared with the experts, SCORE-AI had near-perfect accuracy with an area under the receiver operating characteristic (AUROC) curve for differentiating normal from abnormal EEG recordings of 0.95.

SCORE-AI also performed well at identifying generalized epileptiform abnormalities (AUROC, 0.96), focal epileptiform abnormalities (AUROC, 0.91), focal nonepileptiform abnormalities (AUROC, 0.89), and diffuse nonepileptiform abnormalities (AUROC, 0.93).

In addition, SCORE-AI had excellent agreement with clinicians – and sometimes agreed with individual experts more than the experts agreed with one another.

When Dr. Beniczky and team tested SCORE-AI against three previously published AI models, SCORE-AI demonstrated greater specificity than those models (90% vs. 3%-63%) but was not as sensitive (86.7%) as two of the models (96.7% and 100%).

One of the study’s limitations was the fact that SCORE-AI was developed and validated on routine EEGs that excluded neonates and critically ill patients.

In the future, Dr. Beniczky said on the podcast, the team would like to train SCORE-AI to read EEGs with more granularity, and eventually use only one single channel to record EEGs. At present, SCORE-AI is being integrated with Natus Neuro, a widely used EEG equipment system, the investigators note.

In an accompanying editorial, Jonathan Kleen, MD, PhD, and Elan Guterman, MD, said, “The overall approach taken ... in developing and validating SCORE-AI sets a standard for this work going forward.”

Dr. Kleen and Dr. Guterman note that the technological gains brought about by SCORE-AI technology “could offer an exciting prospect to improve EEG availability and clinical care for the 50 million people with epilepsy worldwide.”
 

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

An automated artificial intelligence (AI) model trained to read electroencephalograms (EEGs) in patients with suspected epilepsy is just as accurate as trained neurologists, new data suggest.

Known as SCORE-AI, the technology distinguishes between abnormal and normal EEG recordings and classifies irregular recordings into specific categories crucial for patient decision-making.

“SCORE-AI can be used in place of experts in underprivileged areas, where expertise is missing, or to help physicians to preselect or prescore recordings in areas where the workload is high – we can all benefit from AI,” study investigator Sándor Beniczky, MD, PhD, said in a JAMA Neurology podcast.

Dr. Beniczky is professor of clinical neurophysiology at Aarhus University in Denmark.

The findings were published online in JAMA Neurology.
 

Gaining a foothold

Increasingly, AI is gaining a foothold in medicine by credibly addressing patient queries and aiding radiologists.

To bring AI to EEG interpretation, the researchers developed and validated an AI model that was able to assess routine, clinical EEGs in patients with suspected epilepsy.

Beyond using AI to distinguish abnormal from normal EEG recordings, the researchers wanted to train the new system to classify abnormal recordings into the major categories that are most relevant for clinical decision-making in patients who may have epilepsy. The categories included epileptiform-focal, epileptiform-generalized, nonepileptiform-focal, and nonepileptiform-diffuse abnormalities.

The researchers trained the learning model using Standardized Computer-based Organized Reporting of EEG (SCORE) software.

In the development phase, the model was trained using more than 30,490 anonymized and highly annotated EEG recordings from 14,100 men (median age, 25 years) from a single center. The recordings had an average duration of 31 minutes and were interpreted by 17 neurologists using standardized criteria. If an EEG recording was abnormal, the physicians had to specify which abnormal features were present.

SCORE-AI then performed an analysis of the recordings based on input from the experts.

To validate the findings, investigators used two independent test datasets. The first dataset consisted of 100 representative routine EEGs from 61 men (median age, 26 years), evaluated by 11 neurologists from different centers.

The consensus of these evaluations served as the reference standard. The second dataset comprised nearly 10,000 EEGs from a single center (5,170 men; median age, 35 years), independently assessed by 14 neurologists.
 

Near-perfect accuracy

When compared with the experts, SCORE-AI had near-perfect accuracy with an area under the receiver operating characteristic (AUROC) curve for differentiating normal from abnormal EEG recordings of 0.95.

SCORE-AI also performed well at identifying generalized epileptiform abnormalities (AUROC, 0.96), focal epileptiform abnormalities (AUROC, 0.91), focal nonepileptiform abnormalities (AUROC, 0.89), and diffuse nonepileptiform abnormalities (AUROC, 0.93).

In addition, SCORE-AI had excellent agreement with clinicians – and sometimes agreed with individual experts more than the experts agreed with one another.

When Dr. Beniczky and team tested SCORE-AI against three previously published AI models, SCORE-AI demonstrated greater specificity than those models (90% vs. 3%-63%) but was not as sensitive (86.7%) as two of the models (96.7% and 100%).

One of the study’s limitations was the fact that SCORE-AI was developed and validated on routine EEGs that excluded neonates and critically ill patients.

In the future, Dr. Beniczky said on the podcast, the team would like to train SCORE-AI to read EEGs with more granularity, and eventually use only one single channel to record EEGs. At present, SCORE-AI is being integrated with Natus Neuro, a widely used EEG equipment system, the investigators note.

In an accompanying editorial, Jonathan Kleen, MD, PhD, and Elan Guterman, MD, said, “The overall approach taken ... in developing and validating SCORE-AI sets a standard for this work going forward.”

Dr. Kleen and Dr. Guterman note that the technological gains brought about by SCORE-AI technology “could offer an exciting prospect to improve EEG availability and clinical care for the 50 million people with epilepsy worldwide.”
 

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

Daily napping may help preserve brain health, new research suggests.

Investigators at University College London, and the University of the Republic of Uruguay, Montevideo, found individuals genetically predisposed to regular napping had larger total brain volume, a surrogate of better cognitive health.

“Our results suggest that napping may improve brain health,” first author Valentina Paz, MSc, a PhD candidate at the University of the Republic of Uruguay said in an interview. “Specifically, our work revealed a 15.8 cubic cm increase in total brain volume with more frequent daytime napping,” she said.

The findings were published online in Sleep Health.
 

Higher brain volume

Previous studies examining the potential link between napping and cognition in older adults have yielded conflicting results.

To clarify this association, Ms. Paz and colleagues used Mendelian randomization to study DNA samples, cognitive outcomes, and functional magnetic resonance imaging data in participants from the ongoing UK Biobank Study.  

Starting with data from 378,932 study participants (mean age 57), investigators compared measures of brain health and cognition of those who are more genetically programmed to nap with people who did not have these genetic variations.

More specifically, the investigators examined 97 sections of genetic code previously linked to the likelihood of regular napping and correlated these results with fMRI and cognitive outcomes between those genetically predisposed to take regular naps and those who weren’t.

Study outcomes included total brain volume, hippocampal volume, reaction time, and visual memory.

The final study sample included 35,080 with neuroimaging, cognitive assessment, and genotype data.

The researchers estimated that the average difference in brain volume between individuals genetically programmed to be habitual nappers and those who were not was equivalent to 15.8 cubic cm, or 2.6-6.5 years of aging.

However, there was no difference in the other three outcomes – hippocampal volume, reaction time, and visual processing – between the two study groups.

Since investigators did not have information on the length of time participants napped, Ms. Paz suggested that “taking a short nap in the early afternoon may help cognition in those needing it.”

However, she added, the study’s findings need to be replicated before any firm conclusions can be made.

“More work is needed to examine the associations between napping and cognition, and the replication of these findings using other datasets and methods,” she said.

The investigators note that the study’s findings augment the knowledge of the “impact of habitual daytime napping on brain health, which is essential to understanding cognitive impairment in the aging population. The lack of evidence for an association between napping and hippocampal volume and cognitive outcomes (for example, alertness) may be affected by habitual daytime napping and should be studied in the future.”
 

Strengths, limitations

Tara Spires-Jones, PhD, president of the British Neuroscience Association and group leader at the UK Dementia Research Institute, said, “the study shows a small but significant increase in brain volume in people who have a genetic signature associated with taking daytime naps.”

Dr. Spires-Jones, who was not involved in the research, noted that while the study is well-conducted, it has limitations. Because Mendelian randomization uses a genetic signature, she noted, outcomes depend on the accuracy of the signature. 

“The napping habits of UK Biobank participants were self-reported, which might not be entirely accurate, and the ‘napping’ signature overlapped substantially with the signature for cognitive outcomes in the study, which makes the causal link weaker,” she said.

“Even with those limitations, this study is interesting because it adds to the data indicating that sleep is important for brain health,” said Dr. Spires-Jones.

The study was supported by Diabetes UK, the British Heart Foundation, and the Diabetes Research and Wellness Foundation. In Uruguay, it was supported by Programa de Desarrollo de las Ciencias Básicas, Agencia Nacional de Investigación e Innovación, Comisión Sectorial de Investigación Científica, and Comisión Académica de Posgrado. In the United States it was supported by the National Heart, Lung, and Blood Institute. There were no disclosures reported.

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

Daily napping may help preserve brain health, new research suggests.

Investigators at University College London, and the University of the Republic of Uruguay, Montevideo, found individuals genetically predisposed to regular napping had larger total brain volume, a surrogate of better cognitive health.

“Our results suggest that napping may improve brain health,” first author Valentina Paz, MSc, a PhD candidate at the University of the Republic of Uruguay said in an interview. “Specifically, our work revealed a 15.8 cubic cm increase in total brain volume with more frequent daytime napping,” she said.

The findings were published online in Sleep Health.
 

Higher brain volume

Previous studies examining the potential link between napping and cognition in older adults have yielded conflicting results.

To clarify this association, Ms. Paz and colleagues used Mendelian randomization to study DNA samples, cognitive outcomes, and functional magnetic resonance imaging data in participants from the ongoing UK Biobank Study.  

Starting with data from 378,932 study participants (mean age 57), investigators compared measures of brain health and cognition of those who are more genetically programmed to nap with people who did not have these genetic variations.

More specifically, the investigators examined 97 sections of genetic code previously linked to the likelihood of regular napping and correlated these results with fMRI and cognitive outcomes between those genetically predisposed to take regular naps and those who weren’t.

Study outcomes included total brain volume, hippocampal volume, reaction time, and visual memory.

The final study sample included 35,080 with neuroimaging, cognitive assessment, and genotype data.

The researchers estimated that the average difference in brain volume between individuals genetically programmed to be habitual nappers and those who were not was equivalent to 15.8 cubic cm, or 2.6-6.5 years of aging.

However, there was no difference in the other three outcomes – hippocampal volume, reaction time, and visual processing – between the two study groups.

Since investigators did not have information on the length of time participants napped, Ms. Paz suggested that “taking a short nap in the early afternoon may help cognition in those needing it.”

However, she added, the study’s findings need to be replicated before any firm conclusions can be made.

“More work is needed to examine the associations between napping and cognition, and the replication of these findings using other datasets and methods,” she said.

The investigators note that the study’s findings augment the knowledge of the “impact of habitual daytime napping on brain health, which is essential to understanding cognitive impairment in the aging population. The lack of evidence for an association between napping and hippocampal volume and cognitive outcomes (for example, alertness) may be affected by habitual daytime napping and should be studied in the future.”
 

Strengths, limitations

Tara Spires-Jones, PhD, president of the British Neuroscience Association and group leader at the UK Dementia Research Institute, said, “the study shows a small but significant increase in brain volume in people who have a genetic signature associated with taking daytime naps.”

Dr. Spires-Jones, who was not involved in the research, noted that while the study is well-conducted, it has limitations. Because Mendelian randomization uses a genetic signature, she noted, outcomes depend on the accuracy of the signature. 

“The napping habits of UK Biobank participants were self-reported, which might not be entirely accurate, and the ‘napping’ signature overlapped substantially with the signature for cognitive outcomes in the study, which makes the causal link weaker,” she said.

“Even with those limitations, this study is interesting because it adds to the data indicating that sleep is important for brain health,” said Dr. Spires-Jones.

The study was supported by Diabetes UK, the British Heart Foundation, and the Diabetes Research and Wellness Foundation. In Uruguay, it was supported by Programa de Desarrollo de las Ciencias Básicas, Agencia Nacional de Investigación e Innovación, Comisión Sectorial de Investigación Científica, and Comisión Académica de Posgrado. In the United States it was supported by the National Heart, Lung, and Blood Institute. There were no disclosures reported.

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

Daily napping may help preserve brain health, new research suggests.

Investigators at University College London, and the University of the Republic of Uruguay, Montevideo, found individuals genetically predisposed to regular napping had larger total brain volume, a surrogate of better cognitive health.

“Our results suggest that napping may improve brain health,” first author Valentina Paz, MSc, a PhD candidate at the University of the Republic of Uruguay said in an interview. “Specifically, our work revealed a 15.8 cubic cm increase in total brain volume with more frequent daytime napping,” she said.

The findings were published online in Sleep Health.
 

Higher brain volume

Previous studies examining the potential link between napping and cognition in older adults have yielded conflicting results.

To clarify this association, Ms. Paz and colleagues used Mendelian randomization to study DNA samples, cognitive outcomes, and functional magnetic resonance imaging data in participants from the ongoing UK Biobank Study.  

Starting with data from 378,932 study participants (mean age 57), investigators compared measures of brain health and cognition of those who are more genetically programmed to nap with people who did not have these genetic variations.

More specifically, the investigators examined 97 sections of genetic code previously linked to the likelihood of regular napping and correlated these results with fMRI and cognitive outcomes between those genetically predisposed to take regular naps and those who weren’t.

Study outcomes included total brain volume, hippocampal volume, reaction time, and visual memory.

The final study sample included 35,080 with neuroimaging, cognitive assessment, and genotype data.

The researchers estimated that the average difference in brain volume between individuals genetically programmed to be habitual nappers and those who were not was equivalent to 15.8 cubic cm, or 2.6-6.5 years of aging.

However, there was no difference in the other three outcomes – hippocampal volume, reaction time, and visual processing – between the two study groups.

Since investigators did not have information on the length of time participants napped, Ms. Paz suggested that “taking a short nap in the early afternoon may help cognition in those needing it.”

However, she added, the study’s findings need to be replicated before any firm conclusions can be made.

“More work is needed to examine the associations between napping and cognition, and the replication of these findings using other datasets and methods,” she said.

The investigators note that the study’s findings augment the knowledge of the “impact of habitual daytime napping on brain health, which is essential to understanding cognitive impairment in the aging population. The lack of evidence for an association between napping and hippocampal volume and cognitive outcomes (for example, alertness) may be affected by habitual daytime napping and should be studied in the future.”
 

Strengths, limitations

Tara Spires-Jones, PhD, president of the British Neuroscience Association and group leader at the UK Dementia Research Institute, said, “the study shows a small but significant increase in brain volume in people who have a genetic signature associated with taking daytime naps.”

Dr. Spires-Jones, who was not involved in the research, noted that while the study is well-conducted, it has limitations. Because Mendelian randomization uses a genetic signature, she noted, outcomes depend on the accuracy of the signature. 

“The napping habits of UK Biobank participants were self-reported, which might not be entirely accurate, and the ‘napping’ signature overlapped substantially with the signature for cognitive outcomes in the study, which makes the causal link weaker,” she said.

“Even with those limitations, this study is interesting because it adds to the data indicating that sleep is important for brain health,” said Dr. Spires-Jones.

The study was supported by Diabetes UK, the British Heart Foundation, and the Diabetes Research and Wellness Foundation. In Uruguay, it was supported by Programa de Desarrollo de las Ciencias Básicas, Agencia Nacional de Investigación e Innovación, Comisión Sectorial de Investigación Científica, and Comisión Académica de Posgrado. In the United States it was supported by the National Heart, Lung, and Blood Institute. There were no disclosures reported.

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

When used as an adjunctive treatment, probiotic supplements reduce symptoms in patients with major depression, results of a randomized, placebo-controlled trial suggest.
 

By the end of the 8-week pilot study, participants who had an incomplete response to antidepressants prior to taking probiotics scored better on measures of anxiety and depression versus placebo.

“This was a pilot study, designed as an initial exploration of whether improving gut health with probiotics could act as a new pathway for supporting mood and mental health,” study investigator Viktoriya Nikolova, PhD, Institute of Psychiatry, Psychology and Neuroscience at King’s College London, said in an interview.

“While very promising and exciting, our findings are only the first step, and larger trials are needed,” she noted.

The findings were published online in JAMA Psychiatry.
 

Gut-brain axis

It is estimated that up to 60% of people taking antidepressants for major depressive disorder (MDD) do not achieve full response.

With an eye on the so-called gut-brain axis as a treatment target for depression, the researchers conducted a meta-analysis of seven randomized controlled trials (RCT) in 2021 and found that probiotics appeared effective in reducing depressive symptoms when taken alongside antidepressants. The studies in this meta-analysis either reported poor adherence rates or did not investigate how well study participants tolerated probiotics.

To further investigate, Dr. Nikolova and team launched a pilot RCT by recruiting study participants from primary and secondary health care services, and  through general advertising in London. Data were collected from September 2019 to May 2022.

They included 49 adults diagnosed with MDD with an incomplete antidepressant response, indicated by a score of greater than 13 on the Hamilton Depression Rating Scale-17 (HAMD-17).

Half of the participants were randomly assigned to receive a widely available, proprietary, 14-strain blend probiotic supplement, and half received placebo. Both groups took their study drug four times per day during the 8-week trial.

At baseline, 4 weeks, and 8 weeks, investigators assessed the participants for depression with the HAMD-17, the Inventory of Depressive Symptomatology (IDS) Self-Report, and anxiety with the Hamilton Anxiety Rating Scale (HAMA).

The majority of participants (80%) were female with a mean age of 32 years. Adherence was high, with 97% of the doses taken as required, and no adverse events were reported.

Standardized effect sizes from linear mixed models demonstrated that, when compared with the placebo group, the probiotic group had more improvement in depressive symptoms according to the HAMD-17 (week 4: SES, 0.70; 95% confidence interval, 0.01-0.98) and IDS Self Report (week 8: SES, 0.64; 95% CI, 0.03-0.87).

When compared with the placebo group, the probiotic group also experienced greater improvements in anxiety symptoms according to the HAMA (week 4: SES, 0.67; 95% CI, 0-0.95; week 8: SES, 0.79; 95% CI, 0.06-1.05).

Dr. Nikolova said a large follow-up trial is planned to further confirm the results.

Nutritional psychiatrist Drew Ramsey, MD, author of Eat to Beat Depression and Anxiety and assistant clinical professor of psychiatry at Columbia University, New York, said in an interview: “This randomized clinical trial adds to the considerable evidence that food choices impact depression outcomes.”

He further noted that, “in nutritional psychiatry, we recommend eating fermented foods as they have been shown to improve microbiome diversity and decrease markers of inflammation.”

Dr. Ramsey noted that the RCT used the equivalent colony-forming unit of a “single serving of kombucha.”

“In our clinical group and our nutritional psychiatry course for clinicians, we recommend fermented foods over probiotics as this is the most sustainable, evidence-based way to improve microbiome diversity,” said Dr. Ramsey, citing recent research by Gardner and colleagues at Stanford (Calif.) University.

“This is an industry-funded trial that adds to the evidence base but should be interpreted by patients and clinicians as promoting consumption of more kefir, kimchi, and kombucha, not that patients should take probiotics,” he said.
 

A key place for probiotics in mental health

Commenting on the study, Uma Naidoo, MD, said: “As I shared throughout my first book, This is Your Brain on Food, there is a real place for the use of probiotics in mental health, including the importance of the gut-brain connection.”

Dr. Naidoo is the director of nutritional and metabolic psychiatry at Massachusetts General Hospital and of nutritional psychiatry at the MGH Academy, both in Boston.

She noted that, when a person stops using a probiotic after trying it out, the positive changes in the gut are reversed, so “remaining consistent in taking the probiotic is important if you have found it helpful for your mood.”

Dr. Naidoo added that “each person’s gut microbiome is so unique that it is likely not every human being will have the same reaction to a probiotic.”

“Eating foods with live probiotics may also benefit gut health and, therefore, mood,” she said. The same goes with eating fermented foods with live active cultures.”

The study was funded by a Medical Research Council Industrial CASE PhD Studentship with ADM Protexin (supplier of the probiotics) as the industry partner and additional support from Freya Green. Dr. Nikolova has received grants from the Medical Research Council and ADM Protexin during the conduct of the study as well as personal fees from Janssen outside the submitted work.

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

When used as an adjunctive treatment, probiotic supplements reduce symptoms in patients with major depression, results of a randomized, placebo-controlled trial suggest.
 

By the end of the 8-week pilot study, participants who had an incomplete response to antidepressants prior to taking probiotics scored better on measures of anxiety and depression versus placebo.

“This was a pilot study, designed as an initial exploration of whether improving gut health with probiotics could act as a new pathway for supporting mood and mental health,” study investigator Viktoriya Nikolova, PhD, Institute of Psychiatry, Psychology and Neuroscience at King’s College London, said in an interview.

“While very promising and exciting, our findings are only the first step, and larger trials are needed,” she noted.

The findings were published online in JAMA Psychiatry.
 

Gut-brain axis

It is estimated that up to 60% of people taking antidepressants for major depressive disorder (MDD) do not achieve full response.

With an eye on the so-called gut-brain axis as a treatment target for depression, the researchers conducted a meta-analysis of seven randomized controlled trials (RCT) in 2021 and found that probiotics appeared effective in reducing depressive symptoms when taken alongside antidepressants. The studies in this meta-analysis either reported poor adherence rates or did not investigate how well study participants tolerated probiotics.

To further investigate, Dr. Nikolova and team launched a pilot RCT by recruiting study participants from primary and secondary health care services, and  through general advertising in London. Data were collected from September 2019 to May 2022.

They included 49 adults diagnosed with MDD with an incomplete antidepressant response, indicated by a score of greater than 13 on the Hamilton Depression Rating Scale-17 (HAMD-17).

Half of the participants were randomly assigned to receive a widely available, proprietary, 14-strain blend probiotic supplement, and half received placebo. Both groups took their study drug four times per day during the 8-week trial.

At baseline, 4 weeks, and 8 weeks, investigators assessed the participants for depression with the HAMD-17, the Inventory of Depressive Symptomatology (IDS) Self-Report, and anxiety with the Hamilton Anxiety Rating Scale (HAMA).

The majority of participants (80%) were female with a mean age of 32 years. Adherence was high, with 97% of the doses taken as required, and no adverse events were reported.

Standardized effect sizes from linear mixed models demonstrated that, when compared with the placebo group, the probiotic group had more improvement in depressive symptoms according to the HAMD-17 (week 4: SES, 0.70; 95% confidence interval, 0.01-0.98) and IDS Self Report (week 8: SES, 0.64; 95% CI, 0.03-0.87).

When compared with the placebo group, the probiotic group also experienced greater improvements in anxiety symptoms according to the HAMA (week 4: SES, 0.67; 95% CI, 0-0.95; week 8: SES, 0.79; 95% CI, 0.06-1.05).

Dr. Nikolova said a large follow-up trial is planned to further confirm the results.

Nutritional psychiatrist Drew Ramsey, MD, author of Eat to Beat Depression and Anxiety and assistant clinical professor of psychiatry at Columbia University, New York, said in an interview: “This randomized clinical trial adds to the considerable evidence that food choices impact depression outcomes.”

He further noted that, “in nutritional psychiatry, we recommend eating fermented foods as they have been shown to improve microbiome diversity and decrease markers of inflammation.”

Dr. Ramsey noted that the RCT used the equivalent colony-forming unit of a “single serving of kombucha.”

“In our clinical group and our nutritional psychiatry course for clinicians, we recommend fermented foods over probiotics as this is the most sustainable, evidence-based way to improve microbiome diversity,” said Dr. Ramsey, citing recent research by Gardner and colleagues at Stanford (Calif.) University.

“This is an industry-funded trial that adds to the evidence base but should be interpreted by patients and clinicians as promoting consumption of more kefir, kimchi, and kombucha, not that patients should take probiotics,” he said.
 

A key place for probiotics in mental health

Commenting on the study, Uma Naidoo, MD, said: “As I shared throughout my first book, This is Your Brain on Food, there is a real place for the use of probiotics in mental health, including the importance of the gut-brain connection.”

Dr. Naidoo is the director of nutritional and metabolic psychiatry at Massachusetts General Hospital and of nutritional psychiatry at the MGH Academy, both in Boston.

She noted that, when a person stops using a probiotic after trying it out, the positive changes in the gut are reversed, so “remaining consistent in taking the probiotic is important if you have found it helpful for your mood.”

Dr. Naidoo added that “each person’s gut microbiome is so unique that it is likely not every human being will have the same reaction to a probiotic.”

“Eating foods with live probiotics may also benefit gut health and, therefore, mood,” she said. The same goes with eating fermented foods with live active cultures.”

The study was funded by a Medical Research Council Industrial CASE PhD Studentship with ADM Protexin (supplier of the probiotics) as the industry partner and additional support from Freya Green. Dr. Nikolova has received grants from the Medical Research Council and ADM Protexin during the conduct of the study as well as personal fees from Janssen outside the submitted work.

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

When used as an adjunctive treatment, probiotic supplements reduce symptoms in patients with major depression, results of a randomized, placebo-controlled trial suggest.
 

By the end of the 8-week pilot study, participants who had an incomplete response to antidepressants prior to taking probiotics scored better on measures of anxiety and depression versus placebo.

“This was a pilot study, designed as an initial exploration of whether improving gut health with probiotics could act as a new pathway for supporting mood and mental health,” study investigator Viktoriya Nikolova, PhD, Institute of Psychiatry, Psychology and Neuroscience at King’s College London, said in an interview.

“While very promising and exciting, our findings are only the first step, and larger trials are needed,” she noted.

The findings were published online in JAMA Psychiatry.
 

Gut-brain axis

It is estimated that up to 60% of people taking antidepressants for major depressive disorder (MDD) do not achieve full response.

With an eye on the so-called gut-brain axis as a treatment target for depression, the researchers conducted a meta-analysis of seven randomized controlled trials (RCT) in 2021 and found that probiotics appeared effective in reducing depressive symptoms when taken alongside antidepressants. The studies in this meta-analysis either reported poor adherence rates or did not investigate how well study participants tolerated probiotics.

To further investigate, Dr. Nikolova and team launched a pilot RCT by recruiting study participants from primary and secondary health care services, and  through general advertising in London. Data were collected from September 2019 to May 2022.

They included 49 adults diagnosed with MDD with an incomplete antidepressant response, indicated by a score of greater than 13 on the Hamilton Depression Rating Scale-17 (HAMD-17).

Half of the participants were randomly assigned to receive a widely available, proprietary, 14-strain blend probiotic supplement, and half received placebo. Both groups took their study drug four times per day during the 8-week trial.

At baseline, 4 weeks, and 8 weeks, investigators assessed the participants for depression with the HAMD-17, the Inventory of Depressive Symptomatology (IDS) Self-Report, and anxiety with the Hamilton Anxiety Rating Scale (HAMA).

The majority of participants (80%) were female with a mean age of 32 years. Adherence was high, with 97% of the doses taken as required, and no adverse events were reported.

Standardized effect sizes from linear mixed models demonstrated that, when compared with the placebo group, the probiotic group had more improvement in depressive symptoms according to the HAMD-17 (week 4: SES, 0.70; 95% confidence interval, 0.01-0.98) and IDS Self Report (week 8: SES, 0.64; 95% CI, 0.03-0.87).

When compared with the placebo group, the probiotic group also experienced greater improvements in anxiety symptoms according to the HAMA (week 4: SES, 0.67; 95% CI, 0-0.95; week 8: SES, 0.79; 95% CI, 0.06-1.05).

Dr. Nikolova said a large follow-up trial is planned to further confirm the results.

Nutritional psychiatrist Drew Ramsey, MD, author of Eat to Beat Depression and Anxiety and assistant clinical professor of psychiatry at Columbia University, New York, said in an interview: “This randomized clinical trial adds to the considerable evidence that food choices impact depression outcomes.”

He further noted that, “in nutritional psychiatry, we recommend eating fermented foods as they have been shown to improve microbiome diversity and decrease markers of inflammation.”

Dr. Ramsey noted that the RCT used the equivalent colony-forming unit of a “single serving of kombucha.”

“In our clinical group and our nutritional psychiatry course for clinicians, we recommend fermented foods over probiotics as this is the most sustainable, evidence-based way to improve microbiome diversity,” said Dr. Ramsey, citing recent research by Gardner and colleagues at Stanford (Calif.) University.

“This is an industry-funded trial that adds to the evidence base but should be interpreted by patients and clinicians as promoting consumption of more kefir, kimchi, and kombucha, not that patients should take probiotics,” he said.
 

A key place for probiotics in mental health

Commenting on the study, Uma Naidoo, MD, said: “As I shared throughout my first book, This is Your Brain on Food, there is a real place for the use of probiotics in mental health, including the importance of the gut-brain connection.”

Dr. Naidoo is the director of nutritional and metabolic psychiatry at Massachusetts General Hospital and of nutritional psychiatry at the MGH Academy, both in Boston.

She noted that, when a person stops using a probiotic after trying it out, the positive changes in the gut are reversed, so “remaining consistent in taking the probiotic is important if you have found it helpful for your mood.”

Dr. Naidoo added that “each person’s gut microbiome is so unique that it is likely not every human being will have the same reaction to a probiotic.”

“Eating foods with live probiotics may also benefit gut health and, therefore, mood,” she said. The same goes with eating fermented foods with live active cultures.”

The study was funded by a Medical Research Council Industrial CASE PhD Studentship with ADM Protexin (supplier of the probiotics) as the industry partner and additional support from Freya Green. Dr. Nikolova has received grants from the Medical Research Council and ADM Protexin during the conduct of the study as well as personal fees from Janssen outside the submitted work.

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

Intranasal (IN) ketamine may be a feasible treatment alternative for people with chronic, refractory migraine who don’t respond to other medications, new research shows.

Half of the study participants who used IN ketamine for chronic, treatment-refractory migraine in a new retrospective cohort study reported it as “very effective” and over one-third said it boosted their quality of life.

“In our study, we showed that with even a few uses per day, intranasal ketamine can still improve patients’ quality of life,” lead investigator Hsiangkuo Yuan, MD, PhD, said in an interview. Dr. Yuan is associate professor of neurology at Thomas Jefferson University, Philadelphia, and director of clinical research at the Jefferson Headache Center.

He added that “multiple medications failed these patients, and the majority of patients were having daily headaches. So, if anything works, even partially and shortly, it may still give patients some relief to get through the day.”

The findings were published online in Regional Anesthesia & Pain Medicine.  
 

Daily migraine, failed medications

Use of IN ketamine has not been studied for the treatment of chronic, treatment-refractory migraine – although it has been studied in patients with cluster headache and migraine, the investigators note.

Ketamine is not yet approved by the Food and Drug Administration to treat migraine.

To further explore ketamine’s effect in those with chronic, treatment-refractory migraine, the investigators retrospectively analyzed electronic health records of patients at the Jefferson Headache Center who had received IN ketamine for the treatment of migraine between January 2019 and February 2020.

Of 242 patients who had received IN ketamine, Dr. Yuan’s team followed up with 169 who agreed to be part of the study.

The majority (67%) had daily migraine, and 85% had tried more than three classes of preventive medications for migraine. They currently used a median of two medications, the most common of which was a CGRP monoclonal antibody.

On average, patients used six sprays per day for a median 10 days per month. Median pain relief onset was 52 minutes after dosage.

Almost three-quarters of patients reported at least one side effect from the ketamine, most commonly fatigue (22%), double/blurred vision (21%), and confusion/dissociation (21%). These effects were mostly temporary, the researchers report.

The most common reasons for initiating IN ketamine included an incomplete response to prior acute medications (59%), incomplete response to prior preventive medications (31%), and prior benefit from IV ketamine (23%).

Study investigators noted that ketamine has the potential to become addictive and indicated that “clinicians should only consider the use of a potentially addictive medication such as ketamine for significantly disabled patients with migraine.”

About half of the participants who used IN ketamine found it “very effective,” and 40% found it “somewhat effective.” Within the same group, 36% and 43% found the overall impact of IN ketamine on their quality of life was much better and somewhat better, respectively.

Among those still using ketamine during study follow-up, 82% reported that ketamine was very effective.

Compared with other acute headache medications, IN ketamine was considered much better (43%) or somewhat better (30%).

Nearly 75% of participants reported using fewer pain relievers when using IN ketamine.

Dr. Yuan said that future research might focus on finding predictors for IN ketamine response or determining the optimal effective and safe dose for the drug in those with chronic, treatment-refractory migraine.  

“We still need a prospective, randomized controlled trial to assess the efficacy and tolerability of intranasal ketamine,” he added.
 

‘Impressive result’

Commenting on the findings for this article, Richard Lipton, MD, professor of neurology, psychiatry and behavioral sciences and director of the Montefiore Headache Center at Albert Einstein College of Medicine, New York, said that “in this refractory population with multiple treatment failures, this is a very impressive, open-label result.”

“This real-world data suggests that ketamine is an effective option for people with medically intractable chronic migraine,” said Dr. Lipton, who was not part of the study. “In these very difficult to treat patients, 65% of those who started on ketamine persisted. Of those who remained on ketamine, 82% found it very effective.”

“This study makes me more confident that intranasal ketamine is a helpful treatment option, and I plan to use it more often in the future,” he added.

Like Dr. Yuan, Dr. Lipton highlighted the need for “well-designed placebo-controlled trials” and “rigorous comparative effectiveness studies.”

The study was funded by Miles for Migraine. Dr. Yuan has received institutional support for serving as an investigator from Teva and AbbVie, and royalties from Cambridge University Press and MedLink. Dr. Lipton has received compensation for consultation from Alder/Lumbeck, Axsome, Supernus, Theranica, Upsher-Smith, and Satsuma. He has participated in speaker bureaus for Eli Lilly and Amgen/Novartis and has received institutional support for serving as principal investigator from Teva, GammaCore, and Allergan/AbbVie. He has received payments for authorship or royalties from Demos Medical, Cambridge University Press, and MedLink.

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

Intranasal (IN) ketamine may be a feasible treatment alternative for people with chronic, refractory migraine who don’t respond to other medications, new research shows.

Half of the study participants who used IN ketamine for chronic, treatment-refractory migraine in a new retrospective cohort study reported it as “very effective” and over one-third said it boosted their quality of life.

“In our study, we showed that with even a few uses per day, intranasal ketamine can still improve patients’ quality of life,” lead investigator Hsiangkuo Yuan, MD, PhD, said in an interview. Dr. Yuan is associate professor of neurology at Thomas Jefferson University, Philadelphia, and director of clinical research at the Jefferson Headache Center.

He added that “multiple medications failed these patients, and the majority of patients were having daily headaches. So, if anything works, even partially and shortly, it may still give patients some relief to get through the day.”

The findings were published online in Regional Anesthesia & Pain Medicine.  
 

Daily migraine, failed medications

Use of IN ketamine has not been studied for the treatment of chronic, treatment-refractory migraine – although it has been studied in patients with cluster headache and migraine, the investigators note.

Ketamine is not yet approved by the Food and Drug Administration to treat migraine.

To further explore ketamine’s effect in those with chronic, treatment-refractory migraine, the investigators retrospectively analyzed electronic health records of patients at the Jefferson Headache Center who had received IN ketamine for the treatment of migraine between January 2019 and February 2020.

Of 242 patients who had received IN ketamine, Dr. Yuan’s team followed up with 169 who agreed to be part of the study.

The majority (67%) had daily migraine, and 85% had tried more than three classes of preventive medications for migraine. They currently used a median of two medications, the most common of which was a CGRP monoclonal antibody.

On average, patients used six sprays per day for a median 10 days per month. Median pain relief onset was 52 minutes after dosage.

Almost three-quarters of patients reported at least one side effect from the ketamine, most commonly fatigue (22%), double/blurred vision (21%), and confusion/dissociation (21%). These effects were mostly temporary, the researchers report.

The most common reasons for initiating IN ketamine included an incomplete response to prior acute medications (59%), incomplete response to prior preventive medications (31%), and prior benefit from IV ketamine (23%).

Study investigators noted that ketamine has the potential to become addictive and indicated that “clinicians should only consider the use of a potentially addictive medication such as ketamine for significantly disabled patients with migraine.”

About half of the participants who used IN ketamine found it “very effective,” and 40% found it “somewhat effective.” Within the same group, 36% and 43% found the overall impact of IN ketamine on their quality of life was much better and somewhat better, respectively.

Among those still using ketamine during study follow-up, 82% reported that ketamine was very effective.

Compared with other acute headache medications, IN ketamine was considered much better (43%) or somewhat better (30%).

Nearly 75% of participants reported using fewer pain relievers when using IN ketamine.

Dr. Yuan said that future research might focus on finding predictors for IN ketamine response or determining the optimal effective and safe dose for the drug in those with chronic, treatment-refractory migraine.  

“We still need a prospective, randomized controlled trial to assess the efficacy and tolerability of intranasal ketamine,” he added.
 

‘Impressive result’

Commenting on the findings for this article, Richard Lipton, MD, professor of neurology, psychiatry and behavioral sciences and director of the Montefiore Headache Center at Albert Einstein College of Medicine, New York, said that “in this refractory population with multiple treatment failures, this is a very impressive, open-label result.”

“This real-world data suggests that ketamine is an effective option for people with medically intractable chronic migraine,” said Dr. Lipton, who was not part of the study. “In these very difficult to treat patients, 65% of those who started on ketamine persisted. Of those who remained on ketamine, 82% found it very effective.”

“This study makes me more confident that intranasal ketamine is a helpful treatment option, and I plan to use it more often in the future,” he added.

Like Dr. Yuan, Dr. Lipton highlighted the need for “well-designed placebo-controlled trials” and “rigorous comparative effectiveness studies.”

The study was funded by Miles for Migraine. Dr. Yuan has received institutional support for serving as an investigator from Teva and AbbVie, and royalties from Cambridge University Press and MedLink. Dr. Lipton has received compensation for consultation from Alder/Lumbeck, Axsome, Supernus, Theranica, Upsher-Smith, and Satsuma. He has participated in speaker bureaus for Eli Lilly and Amgen/Novartis and has received institutional support for serving as principal investigator from Teva, GammaCore, and Allergan/AbbVie. He has received payments for authorship or royalties from Demos Medical, Cambridge University Press, and MedLink.

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

Intranasal (IN) ketamine may be a feasible treatment alternative for people with chronic, refractory migraine who don’t respond to other medications, new research shows.

Half of the study participants who used IN ketamine for chronic, treatment-refractory migraine in a new retrospective cohort study reported it as “very effective” and over one-third said it boosted their quality of life.

“In our study, we showed that with even a few uses per day, intranasal ketamine can still improve patients’ quality of life,” lead investigator Hsiangkuo Yuan, MD, PhD, said in an interview. Dr. Yuan is associate professor of neurology at Thomas Jefferson University, Philadelphia, and director of clinical research at the Jefferson Headache Center.

He added that “multiple medications failed these patients, and the majority of patients were having daily headaches. So, if anything works, even partially and shortly, it may still give patients some relief to get through the day.”

The findings were published online in Regional Anesthesia & Pain Medicine.  
 

Daily migraine, failed medications

Use of IN ketamine has not been studied for the treatment of chronic, treatment-refractory migraine – although it has been studied in patients with cluster headache and migraine, the investigators note.

Ketamine is not yet approved by the Food and Drug Administration to treat migraine.

To further explore ketamine’s effect in those with chronic, treatment-refractory migraine, the investigators retrospectively analyzed electronic health records of patients at the Jefferson Headache Center who had received IN ketamine for the treatment of migraine between January 2019 and February 2020.

Of 242 patients who had received IN ketamine, Dr. Yuan’s team followed up with 169 who agreed to be part of the study.

The majority (67%) had daily migraine, and 85% had tried more than three classes of preventive medications for migraine. They currently used a median of two medications, the most common of which was a CGRP monoclonal antibody.

On average, patients used six sprays per day for a median 10 days per month. Median pain relief onset was 52 minutes after dosage.

Almost three-quarters of patients reported at least one side effect from the ketamine, most commonly fatigue (22%), double/blurred vision (21%), and confusion/dissociation (21%). These effects were mostly temporary, the researchers report.

The most common reasons for initiating IN ketamine included an incomplete response to prior acute medications (59%), incomplete response to prior preventive medications (31%), and prior benefit from IV ketamine (23%).

Study investigators noted that ketamine has the potential to become addictive and indicated that “clinicians should only consider the use of a potentially addictive medication such as ketamine for significantly disabled patients with migraine.”

About half of the participants who used IN ketamine found it “very effective,” and 40% found it “somewhat effective.” Within the same group, 36% and 43% found the overall impact of IN ketamine on their quality of life was much better and somewhat better, respectively.

Among those still using ketamine during study follow-up, 82% reported that ketamine was very effective.

Compared with other acute headache medications, IN ketamine was considered much better (43%) or somewhat better (30%).

Nearly 75% of participants reported using fewer pain relievers when using IN ketamine.

Dr. Yuan said that future research might focus on finding predictors for IN ketamine response or determining the optimal effective and safe dose for the drug in those with chronic, treatment-refractory migraine.  

“We still need a prospective, randomized controlled trial to assess the efficacy and tolerability of intranasal ketamine,” he added.
 

‘Impressive result’

Commenting on the findings for this article, Richard Lipton, MD, professor of neurology, psychiatry and behavioral sciences and director of the Montefiore Headache Center at Albert Einstein College of Medicine, New York, said that “in this refractory population with multiple treatment failures, this is a very impressive, open-label result.”

“This real-world data suggests that ketamine is an effective option for people with medically intractable chronic migraine,” said Dr. Lipton, who was not part of the study. “In these very difficult to treat patients, 65% of those who started on ketamine persisted. Of those who remained on ketamine, 82% found it very effective.”

“This study makes me more confident that intranasal ketamine is a helpful treatment option, and I plan to use it more often in the future,” he added.

Like Dr. Yuan, Dr. Lipton highlighted the need for “well-designed placebo-controlled trials” and “rigorous comparative effectiveness studies.”

The study was funded by Miles for Migraine. Dr. Yuan has received institutional support for serving as an investigator from Teva and AbbVie, and royalties from Cambridge University Press and MedLink. Dr. Lipton has received compensation for consultation from Alder/Lumbeck, Axsome, Supernus, Theranica, Upsher-Smith, and Satsuma. He has participated in speaker bureaus for Eli Lilly and Amgen/Novartis and has received institutional support for serving as principal investigator from Teva, GammaCore, and Allergan/AbbVie. He has received payments for authorship or royalties from Demos Medical, Cambridge University Press, and MedLink.

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

Suicidal ideation peaks during the winter but suicide attempts are most common in late spring and early summer in the early hours of the morning, new research shows.

In addition, the results from Harvard University’s Project Implicit Health also show that people are most likely to make an attempt at suicide between 4 and 6 a.m.

“No research has demonstrated a peak in suicidal ideation in winter until our paper,” study investigator Brian O’Shea, PhD, assistant professor of social psychology at the University of Nottingham, England, told this news organization.

“Most people incorrectly assume that suicide behaviours peak in winter and are surprised, as I was, when learning about this phenomenon, that suicide actually peaks in spring/early summer,” he added.

However, at least one expert cautioned that the database, which comprises mostly responses from younger women, doesn’t capture responses from those who are most likely to attempt suicide: older men with substance abuse.

The findings were published online in Translational Psychiatry.
 

New insight into suicide risk

Previous studies examining the seasonality of suicides and suicide attempts have reported a peak in spring and early summer, but there has been very little information about why this may be, the investigators noted.

Dr. O’Shea and his colleague from the University of Amsterdam, René Freichel, mined one of the databases from Project Implicit Health, which contains self-report measures on suicidal ideation, self-harm, and past suicide attempts, as well as respondents’ implicit biases on these topics.

The analysis included data from 10,000 respondents living in the United States, United Kingdom, and Canada provided between April 2012 and November 2018.

The sample was predominantly young and female, with 38% (3,247) of the sample reporting that they had made at least one suicide attempt.

The researchers found a peak in negative mood and desire to die occurring in December, especially among those who reported attempting suicide (P ≤ .001)

Suicidal ideation peaked approximately 3-4 months before the annual seasonal crest of suicide attempts in early spring and summer.

“Affected individuals may become severely depressed and experience a lack of energy throughout the winter months. Essentially, this period may put them below a threshold of severe suicide risk as the high level of suicidal ideation coincides with a low level of energy,” said Dr. O’Shea.

When the days get longer, brighter, and warmer, these changes likely improve an individuals’ mood, he explained. “Hence, the most at-risk individuals become slightly less depressed and may gain more energy to contemplate and plan their method to attempt suicide,” Dr. O’Shea noted.

A major limitation of the study is that all responses included in analysis were based on self-report.

To confirm the findings, future research should include ecological momentary assessment, which involves using a large community sample to question participants about suicidal intent at various time points, along with real-time monitoring of vital signs, said Dr. O’Shea.

Ideally, the investigators noted, the study’s findings will inform clinician assessments of patients who are at risk for suicide.
 

A research gap?

Commenting on the findings, Justin Shuster, MD, MPH, assistant professor of psychiatry at the University of Pittsburgh and medical director of two psychiatric units at Western Psychiatric Hospital, noted that the database used in the study did not include responses from those who were most likely to attempt or commit suicide: older men with a history of substance abuse, who require social supports, and who have a family history of suicide.

Though Dr. Shuster agreed with Dr. O’Shea about the possibility that spring brought energy to a desire to take one’s life, he had another theory.

“When people are depressed in the winter, they expect to feel better with the advent of the warmer weather in spring. When they don’t feel better, they may think to themselves, ‘If I’m going to feel like this forever, I may as well follow through with these plans,’ ” he said.

As for the early morning attempts, he noted that 4-6 a.m. is often when people are alone, and there are fewer distractions.

“The other thing I see a great deal of clinically is intoxication,” said Dr. Shuster. “Either intoxication with substances or alcohol, or the fact that intoxication is waning at those early morning hours, and people are becoming desperate as they face a new day,” he said.

The study was funded by a German Academic Exchange Service Scholarship and an EU Horizon 2020 Fellowship. Dr. O’Shea reports being an unpaid member of Project Implicit’s scientific advisory board and is on the executive committee of Project Implicit Health.

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

Suicidal ideation peaks during the winter but suicide attempts are most common in late spring and early summer in the early hours of the morning, new research shows.

In addition, the results from Harvard University’s Project Implicit Health also show that people are most likely to make an attempt at suicide between 4 and 6 a.m.

“No research has demonstrated a peak in suicidal ideation in winter until our paper,” study investigator Brian O’Shea, PhD, assistant professor of social psychology at the University of Nottingham, England, told this news organization.

“Most people incorrectly assume that suicide behaviours peak in winter and are surprised, as I was, when learning about this phenomenon, that suicide actually peaks in spring/early summer,” he added.

However, at least one expert cautioned that the database, which comprises mostly responses from younger women, doesn’t capture responses from those who are most likely to attempt suicide: older men with substance abuse.

The findings were published online in Translational Psychiatry.
 

New insight into suicide risk

Previous studies examining the seasonality of suicides and suicide attempts have reported a peak in spring and early summer, but there has been very little information about why this may be, the investigators noted.

Dr. O’Shea and his colleague from the University of Amsterdam, René Freichel, mined one of the databases from Project Implicit Health, which contains self-report measures on suicidal ideation, self-harm, and past suicide attempts, as well as respondents’ implicit biases on these topics.

The analysis included data from 10,000 respondents living in the United States, United Kingdom, and Canada provided between April 2012 and November 2018.

The sample was predominantly young and female, with 38% (3,247) of the sample reporting that they had made at least one suicide attempt.

The researchers found a peak in negative mood and desire to die occurring in December, especially among those who reported attempting suicide (P ≤ .001)

Suicidal ideation peaked approximately 3-4 months before the annual seasonal crest of suicide attempts in early spring and summer.

“Affected individuals may become severely depressed and experience a lack of energy throughout the winter months. Essentially, this period may put them below a threshold of severe suicide risk as the high level of suicidal ideation coincides with a low level of energy,” said Dr. O’Shea.

When the days get longer, brighter, and warmer, these changes likely improve an individuals’ mood, he explained. “Hence, the most at-risk individuals become slightly less depressed and may gain more energy to contemplate and plan their method to attempt suicide,” Dr. O’Shea noted.

A major limitation of the study is that all responses included in analysis were based on self-report.

To confirm the findings, future research should include ecological momentary assessment, which involves using a large community sample to question participants about suicidal intent at various time points, along with real-time monitoring of vital signs, said Dr. O’Shea.

Ideally, the investigators noted, the study’s findings will inform clinician assessments of patients who are at risk for suicide.
 

A research gap?

Commenting on the findings, Justin Shuster, MD, MPH, assistant professor of psychiatry at the University of Pittsburgh and medical director of two psychiatric units at Western Psychiatric Hospital, noted that the database used in the study did not include responses from those who were most likely to attempt or commit suicide: older men with a history of substance abuse, who require social supports, and who have a family history of suicide.

Though Dr. Shuster agreed with Dr. O’Shea about the possibility that spring brought energy to a desire to take one’s life, he had another theory.

“When people are depressed in the winter, they expect to feel better with the advent of the warmer weather in spring. When they don’t feel better, they may think to themselves, ‘If I’m going to feel like this forever, I may as well follow through with these plans,’ ” he said.

As for the early morning attempts, he noted that 4-6 a.m. is often when people are alone, and there are fewer distractions.

“The other thing I see a great deal of clinically is intoxication,” said Dr. Shuster. “Either intoxication with substances or alcohol, or the fact that intoxication is waning at those early morning hours, and people are becoming desperate as they face a new day,” he said.

The study was funded by a German Academic Exchange Service Scholarship and an EU Horizon 2020 Fellowship. Dr. O’Shea reports being an unpaid member of Project Implicit’s scientific advisory board and is on the executive committee of Project Implicit Health.

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

Suicidal ideation peaks during the winter but suicide attempts are most common in late spring and early summer in the early hours of the morning, new research shows.

In addition, the results from Harvard University’s Project Implicit Health also show that people are most likely to make an attempt at suicide between 4 and 6 a.m.

“No research has demonstrated a peak in suicidal ideation in winter until our paper,” study investigator Brian O’Shea, PhD, assistant professor of social psychology at the University of Nottingham, England, told this news organization.

“Most people incorrectly assume that suicide behaviours peak in winter and are surprised, as I was, when learning about this phenomenon, that suicide actually peaks in spring/early summer,” he added.

However, at least one expert cautioned that the database, which comprises mostly responses from younger women, doesn’t capture responses from those who are most likely to attempt suicide: older men with substance abuse.

The findings were published online in Translational Psychiatry.
 

New insight into suicide risk

Previous studies examining the seasonality of suicides and suicide attempts have reported a peak in spring and early summer, but there has been very little information about why this may be, the investigators noted.

Dr. O’Shea and his colleague from the University of Amsterdam, René Freichel, mined one of the databases from Project Implicit Health, which contains self-report measures on suicidal ideation, self-harm, and past suicide attempts, as well as respondents’ implicit biases on these topics.

The analysis included data from 10,000 respondents living in the United States, United Kingdom, and Canada provided between April 2012 and November 2018.

The sample was predominantly young and female, with 38% (3,247) of the sample reporting that they had made at least one suicide attempt.

The researchers found a peak in negative mood and desire to die occurring in December, especially among those who reported attempting suicide (P ≤ .001)

Suicidal ideation peaked approximately 3-4 months before the annual seasonal crest of suicide attempts in early spring and summer.

“Affected individuals may become severely depressed and experience a lack of energy throughout the winter months. Essentially, this period may put them below a threshold of severe suicide risk as the high level of suicidal ideation coincides with a low level of energy,” said Dr. O’Shea.

When the days get longer, brighter, and warmer, these changes likely improve an individuals’ mood, he explained. “Hence, the most at-risk individuals become slightly less depressed and may gain more energy to contemplate and plan their method to attempt suicide,” Dr. O’Shea noted.

A major limitation of the study is that all responses included in analysis were based on self-report.

To confirm the findings, future research should include ecological momentary assessment, which involves using a large community sample to question participants about suicidal intent at various time points, along with real-time monitoring of vital signs, said Dr. O’Shea.

Ideally, the investigators noted, the study’s findings will inform clinician assessments of patients who are at risk for suicide.
 

A research gap?

Commenting on the findings, Justin Shuster, MD, MPH, assistant professor of psychiatry at the University of Pittsburgh and medical director of two psychiatric units at Western Psychiatric Hospital, noted that the database used in the study did not include responses from those who were most likely to attempt or commit suicide: older men with a history of substance abuse, who require social supports, and who have a family history of suicide.

Though Dr. Shuster agreed with Dr. O’Shea about the possibility that spring brought energy to a desire to take one’s life, he had another theory.

“When people are depressed in the winter, they expect to feel better with the advent of the warmer weather in spring. When they don’t feel better, they may think to themselves, ‘If I’m going to feel like this forever, I may as well follow through with these plans,’ ” he said.

As for the early morning attempts, he noted that 4-6 a.m. is often when people are alone, and there are fewer distractions.

“The other thing I see a great deal of clinically is intoxication,” said Dr. Shuster. “Either intoxication with substances or alcohol, or the fact that intoxication is waning at those early morning hours, and people are becoming desperate as they face a new day,” he said.

The study was funded by a German Academic Exchange Service Scholarship and an EU Horizon 2020 Fellowship. Dr. O’Shea reports being an unpaid member of Project Implicit’s scientific advisory board and is on the executive committee of Project Implicit Health.

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

A self-led, practitioner-supported form of mindfulness therapy was more effective and more cost-effective than self-help cognitive-behavioral therapy (CBT-SH), results from a head-to-head study show.

Self-help mindfulness-based cognitive therapy (MBCT-SH) produced better outcomes for participants with depression and was more cost-effective than CBT-SH.

Practitioner-supported self-help therapy regimens are growing in popularity as a way to expand access to mental health services and to address the shortage of mental health professionals.

Generally, mindfulness-based cognitive therapy aims to increase awareness of the depression maintenance cycle while fostering a nonjudgmental attitude toward present-moment experiences, the investigators note.

In contrast, CBT aims to challenge negative and unrealistic thought patterns that may perpetuate depression, replacing them with more realistic and objective thoughts.

“Practitioner-supported MBCT-SH should be routinely offered as an intervention for mild to moderate depression alongside practitioner-supported CBT-SH,” the investigators note.

The study was published online in JAMA Psychiatry.
 

Better recovery rates?

CBT-SH traditionally had been associated with high attrition rates, and alternative forms of self-help therapy are becoming increasingly necessary to fill this treatment gap, the researchers note. To compare the efficacy and cost-effectiveness of both treatment types, the researchers recruited 410 participants with mild to moderate depression at 10 sites in the United Kingdom. Participants were randomly assigned to receive either MBCT-SH or CBT-SH between November 2017 and January 2020. A total of 204 participants received MBCT-SH, and 206 received CBT-SH.

All participants were given specific self-help workbooks, depending on the study group to which they were assigned. Those who received MBCT-SH used “The Mindful Way Workbook: An 8-Week Program to Free Yourself From Depression and Emotional Distress,” while those who received CBT-SH used “Overcoming Depression and Low Mood: A Five Areas Approach, 3rd Edition.”

Investigators asked all participants to guide themselves through six 30- to 45-minute sessions, using the information in the workbooks. Trained psychological well-being practitioners supported participants as they moved through the workbooks during the six sessions.

Participants were assessed at baseline with the Patient Health Questionnaire–9 (PHQ-9) and the Clinical Interview Schedule–Revised at 16 weeks and 24 weeks.

At 16 weeks post randomization, results showed that practitioner-supported MBCT-SH led to significantly greater reductions in depression symptom severity, compared with practitioner-supported CBT-SH (mean [standard deviation] PHQ-9 score, 7.2 [4.8] points vs. 8.6 [5.5] points; between-group difference, –1.5 points; 95% confidence interval, –2.6 to –0.4; P = .009).

Results also showed that on average, the CBT-SH intervention cost $631 more per participant than the MBCT-SH intervention over the 42-week follow-up.

The investigators explain that “a substantial proportion of this additional cost was accounted for by additional face-to-face individual psychological therapy accessed by CBT-SH participants outside of the study intervention.

“In conclusion, this study found that a novel intervention, practitioner-supported MBCT-SH, was clinically superior in targeting depressive symptom severity at postintervention and cost-effective, compared with the criterion standard of practitioner-supported CBT-SH for adults experiencing mild to moderate depression,” the investigators write.

“If study findings are translated into routine practice, this would see many more people recovering from depression while costing health services less money,” they add.
 

Clinically meaningful?

Commenting on the study for this article, Lauren Bylsma, PhD, professor of psychiatry and psychology at the University of Pittsburgh, cast doubt on the ability of such a short trial to determine meaningful change.

She said that the extra costs incurred by participants in the CBT-SH arm of the study are likely, since it is “difficult to do CBT alone – you need an objective person to guide you as you practice.”

Dr. Bylsma noted that ultimately, more real-world studies of therapy are needed, given the great need for mental health.

The study was funded by the National Institute for Health and Care Research. The original article contains a full list of the authors’ relevant financial relationships.

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

A self-led, practitioner-supported form of mindfulness therapy was more effective and more cost-effective than self-help cognitive-behavioral therapy (CBT-SH), results from a head-to-head study show.

Self-help mindfulness-based cognitive therapy (MBCT-SH) produced better outcomes for participants with depression and was more cost-effective than CBT-SH.

Practitioner-supported self-help therapy regimens are growing in popularity as a way to expand access to mental health services and to address the shortage of mental health professionals.

Generally, mindfulness-based cognitive therapy aims to increase awareness of the depression maintenance cycle while fostering a nonjudgmental attitude toward present-moment experiences, the investigators note.

In contrast, CBT aims to challenge negative and unrealistic thought patterns that may perpetuate depression, replacing them with more realistic and objective thoughts.

“Practitioner-supported MBCT-SH should be routinely offered as an intervention for mild to moderate depression alongside practitioner-supported CBT-SH,” the investigators note.

The study was published online in JAMA Psychiatry.
 

Better recovery rates?

CBT-SH traditionally had been associated with high attrition rates, and alternative forms of self-help therapy are becoming increasingly necessary to fill this treatment gap, the researchers note. To compare the efficacy and cost-effectiveness of both treatment types, the researchers recruited 410 participants with mild to moderate depression at 10 sites in the United Kingdom. Participants were randomly assigned to receive either MBCT-SH or CBT-SH between November 2017 and January 2020. A total of 204 participants received MBCT-SH, and 206 received CBT-SH.

All participants were given specific self-help workbooks, depending on the study group to which they were assigned. Those who received MBCT-SH used “The Mindful Way Workbook: An 8-Week Program to Free Yourself From Depression and Emotional Distress,” while those who received CBT-SH used “Overcoming Depression and Low Mood: A Five Areas Approach, 3rd Edition.”

Investigators asked all participants to guide themselves through six 30- to 45-minute sessions, using the information in the workbooks. Trained psychological well-being practitioners supported participants as they moved through the workbooks during the six sessions.

Participants were assessed at baseline with the Patient Health Questionnaire–9 (PHQ-9) and the Clinical Interview Schedule–Revised at 16 weeks and 24 weeks.

At 16 weeks post randomization, results showed that practitioner-supported MBCT-SH led to significantly greater reductions in depression symptom severity, compared with practitioner-supported CBT-SH (mean [standard deviation] PHQ-9 score, 7.2 [4.8] points vs. 8.6 [5.5] points; between-group difference, –1.5 points; 95% confidence interval, –2.6 to –0.4; P = .009).

Results also showed that on average, the CBT-SH intervention cost $631 more per participant than the MBCT-SH intervention over the 42-week follow-up.

The investigators explain that “a substantial proportion of this additional cost was accounted for by additional face-to-face individual psychological therapy accessed by CBT-SH participants outside of the study intervention.

“In conclusion, this study found that a novel intervention, practitioner-supported MBCT-SH, was clinically superior in targeting depressive symptom severity at postintervention and cost-effective, compared with the criterion standard of practitioner-supported CBT-SH for adults experiencing mild to moderate depression,” the investigators write.

“If study findings are translated into routine practice, this would see many more people recovering from depression while costing health services less money,” they add.
 

Clinically meaningful?

Commenting on the study for this article, Lauren Bylsma, PhD, professor of psychiatry and psychology at the University of Pittsburgh, cast doubt on the ability of such a short trial to determine meaningful change.

She said that the extra costs incurred by participants in the CBT-SH arm of the study are likely, since it is “difficult to do CBT alone – you need an objective person to guide you as you practice.”

Dr. Bylsma noted that ultimately, more real-world studies of therapy are needed, given the great need for mental health.

The study was funded by the National Institute for Health and Care Research. The original article contains a full list of the authors’ relevant financial relationships.

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

A self-led, practitioner-supported form of mindfulness therapy was more effective and more cost-effective than self-help cognitive-behavioral therapy (CBT-SH), results from a head-to-head study show.

Self-help mindfulness-based cognitive therapy (MBCT-SH) produced better outcomes for participants with depression and was more cost-effective than CBT-SH.

Practitioner-supported self-help therapy regimens are growing in popularity as a way to expand access to mental health services and to address the shortage of mental health professionals.

Generally, mindfulness-based cognitive therapy aims to increase awareness of the depression maintenance cycle while fostering a nonjudgmental attitude toward present-moment experiences, the investigators note.

In contrast, CBT aims to challenge negative and unrealistic thought patterns that may perpetuate depression, replacing them with more realistic and objective thoughts.

“Practitioner-supported MBCT-SH should be routinely offered as an intervention for mild to moderate depression alongside practitioner-supported CBT-SH,” the investigators note.

The study was published online in JAMA Psychiatry.
 

Better recovery rates?

CBT-SH traditionally had been associated with high attrition rates, and alternative forms of self-help therapy are becoming increasingly necessary to fill this treatment gap, the researchers note. To compare the efficacy and cost-effectiveness of both treatment types, the researchers recruited 410 participants with mild to moderate depression at 10 sites in the United Kingdom. Participants were randomly assigned to receive either MBCT-SH or CBT-SH between November 2017 and January 2020. A total of 204 participants received MBCT-SH, and 206 received CBT-SH.

All participants were given specific self-help workbooks, depending on the study group to which they were assigned. Those who received MBCT-SH used “The Mindful Way Workbook: An 8-Week Program to Free Yourself From Depression and Emotional Distress,” while those who received CBT-SH used “Overcoming Depression and Low Mood: A Five Areas Approach, 3rd Edition.”

Investigators asked all participants to guide themselves through six 30- to 45-minute sessions, using the information in the workbooks. Trained psychological well-being practitioners supported participants as they moved through the workbooks during the six sessions.

Participants were assessed at baseline with the Patient Health Questionnaire–9 (PHQ-9) and the Clinical Interview Schedule–Revised at 16 weeks and 24 weeks.

At 16 weeks post randomization, results showed that practitioner-supported MBCT-SH led to significantly greater reductions in depression symptom severity, compared with practitioner-supported CBT-SH (mean [standard deviation] PHQ-9 score, 7.2 [4.8] points vs. 8.6 [5.5] points; between-group difference, –1.5 points; 95% confidence interval, –2.6 to –0.4; P = .009).

Results also showed that on average, the CBT-SH intervention cost $631 more per participant than the MBCT-SH intervention over the 42-week follow-up.

The investigators explain that “a substantial proportion of this additional cost was accounted for by additional face-to-face individual psychological therapy accessed by CBT-SH participants outside of the study intervention.

“In conclusion, this study found that a novel intervention, practitioner-supported MBCT-SH, was clinically superior in targeting depressive symptom severity at postintervention and cost-effective, compared with the criterion standard of practitioner-supported CBT-SH for adults experiencing mild to moderate depression,” the investigators write.

“If study findings are translated into routine practice, this would see many more people recovering from depression while costing health services less money,” they add.
 

Clinically meaningful?

Commenting on the study for this article, Lauren Bylsma, PhD, professor of psychiatry and psychology at the University of Pittsburgh, cast doubt on the ability of such a short trial to determine meaningful change.

She said that the extra costs incurred by participants in the CBT-SH arm of the study are likely, since it is “difficult to do CBT alone – you need an objective person to guide you as you practice.”

Dr. Bylsma noted that ultimately, more real-world studies of therapy are needed, given the great need for mental health.

The study was funded by the National Institute for Health and Care Research. The original article contains a full list of the authors’ relevant financial relationships.

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

Rheumatoid arthritis (RA) is linked to almost a twofold increased risk for Parkinson’s disease (PD), new research shows.

Claims data in 55,000 patients with RA and 273,000 age- and sex-matched controls show that those with RA were 1.74 times more likely than controls to be diagnosed with PD.

“If patients with rheumatoid arthritis begin exhibiting motor symptoms such as muscle rigidity, tremors, or slowed movement, it is imperative that they be evaluated by a qualified neurologist to rule out the possibility of developing Parkinson’s disease,” study investigator Hyungjin Kim, MD, PhD, told this news organization.

Dr. Kim is an associate professor in the department of medical humanities at Sungkyunkwan University School of Medicine in Seoul, South Korea.

The findings were published online in JAMA Neurology.
 

Conflicting findings

The investigators note that a number of studies have examined the link between RA and PD, with conflicting results – one even showing a 35% reduced risk for PD for individuals with RA. A more recent population-based study in Taiwan showed a 37% higher rate of PD in patients with rheumatic disease.

However, previous studies did not control for important variables such as body mass index or diabetes.

For the current study, the investigators analyzed claims on about 55,000 patients diagnosed with RA between 2010 and 2017, with follow-up until 2019, and compared the outcomes of this group vs. those of 273,000 controls.

The mean age of claimants was 58 years, and 75% were female.

Results showed that those diagnosed with seropositive RA were about twice as likely as controls to be diagnosed with PD. Those with seronegative RA were 1.2 times as likely as controls to be diagnosed with PD.

Dr. Kim noted that although the pathogenic link between RA and PD remains elusive, inflammation probably plays an important role. “Inflammatory cytokines such as tumor necrosis factor alpha and interleukin-6, which are increased in RA patients, can induce microglial activation, leading to neuroinflammation,” he stated.

“These inflammatory cytokines are known to be associated with the dysfunction and degeneration of nigral dopaminergic neurons, which are important in the pathogenesis of PD,” he added.

The investigators noted that patients with RA may have been subject to more frequent health care services than controls and so were more likely to obtain a PD diagnosis.

Another possibility was that because patients with health check-ups were included in the analysis, the findings may have been biased toward those who were older and who had a higher income.

Dr. Kim noted that additional research is required to clarify the pathogenic connection between RA and PD.

“Moreover, additional studies are necessary to explore the potential influence of novel therapeutic treatments for RA on Parkinson’s disease susceptibility in patients with RA,” he said.

Commenting on the findings for this news organization, David Sulzer, PhD, professor of psychiatry, neurology, and pharmacology at Columbia University in New York, said that the study adds to the growing body of evidence showing there is an autoimmune component to PD.

Dr. Sulzer pointed to data in several papers he published with others to this effect, including one showing higher rates of PD in people with inflammatory bowel disease.

The study had no specific funding. The study investigators and Dr. Sulzer report no relevant disclosures.

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

Rheumatoid arthritis (RA) is linked to almost a twofold increased risk for Parkinson’s disease (PD), new research shows.

Claims data in 55,000 patients with RA and 273,000 age- and sex-matched controls show that those with RA were 1.74 times more likely than controls to be diagnosed with PD.

“If patients with rheumatoid arthritis begin exhibiting motor symptoms such as muscle rigidity, tremors, or slowed movement, it is imperative that they be evaluated by a qualified neurologist to rule out the possibility of developing Parkinson’s disease,” study investigator Hyungjin Kim, MD, PhD, told this news organization.

Dr. Kim is an associate professor in the department of medical humanities at Sungkyunkwan University School of Medicine in Seoul, South Korea.

The findings were published online in JAMA Neurology.
 

Conflicting findings

The investigators note that a number of studies have examined the link between RA and PD, with conflicting results – one even showing a 35% reduced risk for PD for individuals with RA. A more recent population-based study in Taiwan showed a 37% higher rate of PD in patients with rheumatic disease.

However, previous studies did not control for important variables such as body mass index or diabetes.

For the current study, the investigators analyzed claims on about 55,000 patients diagnosed with RA between 2010 and 2017, with follow-up until 2019, and compared the outcomes of this group vs. those of 273,000 controls.

The mean age of claimants was 58 years, and 75% were female.

Results showed that those diagnosed with seropositive RA were about twice as likely as controls to be diagnosed with PD. Those with seronegative RA were 1.2 times as likely as controls to be diagnosed with PD.

Dr. Kim noted that although the pathogenic link between RA and PD remains elusive, inflammation probably plays an important role. “Inflammatory cytokines such as tumor necrosis factor alpha and interleukin-6, which are increased in RA patients, can induce microglial activation, leading to neuroinflammation,” he stated.

“These inflammatory cytokines are known to be associated with the dysfunction and degeneration of nigral dopaminergic neurons, which are important in the pathogenesis of PD,” he added.

The investigators noted that patients with RA may have been subject to more frequent health care services than controls and so were more likely to obtain a PD diagnosis.

Another possibility was that because patients with health check-ups were included in the analysis, the findings may have been biased toward those who were older and who had a higher income.

Dr. Kim noted that additional research is required to clarify the pathogenic connection between RA and PD.

“Moreover, additional studies are necessary to explore the potential influence of novel therapeutic treatments for RA on Parkinson’s disease susceptibility in patients with RA,” he said.

Commenting on the findings for this news organization, David Sulzer, PhD, professor of psychiatry, neurology, and pharmacology at Columbia University in New York, said that the study adds to the growing body of evidence showing there is an autoimmune component to PD.

Dr. Sulzer pointed to data in several papers he published with others to this effect, including one showing higher rates of PD in people with inflammatory bowel disease.

The study had no specific funding. The study investigators and Dr. Sulzer report no relevant disclosures.

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

Rheumatoid arthritis (RA) is linked to almost a twofold increased risk for Parkinson’s disease (PD), new research shows.

Claims data in 55,000 patients with RA and 273,000 age- and sex-matched controls show that those with RA were 1.74 times more likely than controls to be diagnosed with PD.

“If patients with rheumatoid arthritis begin exhibiting motor symptoms such as muscle rigidity, tremors, or slowed movement, it is imperative that they be evaluated by a qualified neurologist to rule out the possibility of developing Parkinson’s disease,” study investigator Hyungjin Kim, MD, PhD, told this news organization.

Dr. Kim is an associate professor in the department of medical humanities at Sungkyunkwan University School of Medicine in Seoul, South Korea.

The findings were published online in JAMA Neurology.
 

Conflicting findings

The investigators note that a number of studies have examined the link between RA and PD, with conflicting results – one even showing a 35% reduced risk for PD for individuals with RA. A more recent population-based study in Taiwan showed a 37% higher rate of PD in patients with rheumatic disease.

However, previous studies did not control for important variables such as body mass index or diabetes.

For the current study, the investigators analyzed claims on about 55,000 patients diagnosed with RA between 2010 and 2017, with follow-up until 2019, and compared the outcomes of this group vs. those of 273,000 controls.

The mean age of claimants was 58 years, and 75% were female.

Results showed that those diagnosed with seropositive RA were about twice as likely as controls to be diagnosed with PD. Those with seronegative RA were 1.2 times as likely as controls to be diagnosed with PD.

Dr. Kim noted that although the pathogenic link between RA and PD remains elusive, inflammation probably plays an important role. “Inflammatory cytokines such as tumor necrosis factor alpha and interleukin-6, which are increased in RA patients, can induce microglial activation, leading to neuroinflammation,” he stated.

“These inflammatory cytokines are known to be associated with the dysfunction and degeneration of nigral dopaminergic neurons, which are important in the pathogenesis of PD,” he added.

The investigators noted that patients with RA may have been subject to more frequent health care services than controls and so were more likely to obtain a PD diagnosis.

Another possibility was that because patients with health check-ups were included in the analysis, the findings may have been biased toward those who were older and who had a higher income.

Dr. Kim noted that additional research is required to clarify the pathogenic connection between RA and PD.

“Moreover, additional studies are necessary to explore the potential influence of novel therapeutic treatments for RA on Parkinson’s disease susceptibility in patients with RA,” he said.

Commenting on the findings for this news organization, David Sulzer, PhD, professor of psychiatry, neurology, and pharmacology at Columbia University in New York, said that the study adds to the growing body of evidence showing there is an autoimmune component to PD.

Dr. Sulzer pointed to data in several papers he published with others to this effect, including one showing higher rates of PD in people with inflammatory bowel disease.

The study had no specific funding. The study investigators and Dr. Sulzer report no relevant disclosures.

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

A brief scalable suicide risk assessment tool accurately predicts suicide risk in patients with serious mental illness (SMI), a new population-based study shows.

The 17-question Oxford Mental Illness and Suicide Tool (OxMIS) assessment is designed to predict 12-month suicide risk in people with schizophrenia spectrum disorders and bipolar disorder based on risk factors such as familial traits, antisocial traits, and information about self-harm.

“We have demonstrated the clinical utility of OxMIS in two separate studies and countries. As with any clinical risk prediction tool, it will not improve outcomes unless coupled with effective interventions,” lead investigator Amir Sariaslan, PhD, a senior research fellow in psychiatric epidemiology at the University of Oxford, England, told this news organization.

The findings were published online in Translational Psychiatry.
 

Twice validated

Dr. Sariaslan and his team originally developed and validated the OxMIS in a cohort of 75,000 people with SMI in Sweden. Recognizing the lack of externally validated prognostic models in the mental health field, the team wanted to validate the instrument in a new, population-based sample in Finland.

The investigators accessed information about patient diagnosis and treatment from the Finnish Care Register for Health Care, which contains de-identified information for all individuals between ages 15 and 65 years diagnosed with an SMI between Jan. 1, 1996, and Dec. 31, 2017.

They included 137,000 patients with somatic symptom disorder or bipolar disorder for a total of more than 5 million episodes of inpatient or outpatient treatment. Investigators linked the cohort to the Causes of Death Register to identify those who had died by suicide within 12 months of an index treatment episode, which investigators randomly selected for each person.

The investigators found that 1,475 individuals in the sample died by suicide within 1 year of their index episode (1.1%).

Each patient was assigned a clinical suicide risk score based on their clinical information, familial traits, prescription information, and comorbid conditions. Using OxMIS, the investigators found that the instrument accurately predicted suicide with an area under the curve of 0.70.

In other words, in 70% of the instances where the investigators randomly selected two people from the sample, one of whom died by suicide and the other of whom did not, the individual who died by suicide had a higher OxMIS risk score.

The investigators note the model overestimated the risk for patients who were at extremely high risk for suicide (those with a predicted suicide risk of > 5%). “In our complementary sensitivity analysis, we observed improved calibration in these patients when we assigned them a suicide risk prediction of no more than 5%,” they write.

Dr. Sariaslan said that the findings highlight the importance of safety planning interventions. “It is also essential to remember that OxMIS is not intended to replace clinical decision-making, but rather to support it,” he said.

As to whether the tool could be used in other populations, such as in the United States, Dr. Sariaslan said, “there is no good evidence that the contribution of risk factors to suicide in this population is different in the U.S. than in northern Europe, so there is no a priori reason to have to do multiple external validations before it can be used for research or clinical purposes.”
 

One size does not fit all

Commenting on the study, Ronald Kessler, PhD, McNeil Family Professor, department of health care policy at Harvard Medical School, Boston, said that he’d be “surprised” if OxMIS was adopted in the United States because there is already an existing tool that is “slightly more accurate,” which he helped develop.

Harvard Medical School

“In addition, when we start thinking about uses for such scales, it becomes clear that different scales should be used for different segments of the population, depending on intervention options,” Dr. Kessler said.

“So, for example, a different scale would probably be optimal in deciding how to manage psychiatric inpatients in the transition back to the community after hospital discharge than [it would be], say, in deciding how to respond to suicidality among patients presenting at an emergency department. No one scale will fit for all the scenarios in which prediction is desired,” he added.

The study was funded by the Academy of Finland. Dr. Kessler receives funding from the National Institute of Mental Health, Department of Defense, and Veterans Administration to develop suicide prediction models. Dr. Sariaslan has no disclosures to report.

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

A brief scalable suicide risk assessment tool accurately predicts suicide risk in patients with serious mental illness (SMI), a new population-based study shows.

The 17-question Oxford Mental Illness and Suicide Tool (OxMIS) assessment is designed to predict 12-month suicide risk in people with schizophrenia spectrum disorders and bipolar disorder based on risk factors such as familial traits, antisocial traits, and information about self-harm.

“We have demonstrated the clinical utility of OxMIS in two separate studies and countries. As with any clinical risk prediction tool, it will not improve outcomes unless coupled with effective interventions,” lead investigator Amir Sariaslan, PhD, a senior research fellow in psychiatric epidemiology at the University of Oxford, England, told this news organization.

The findings were published online in Translational Psychiatry.
 

Twice validated

Dr. Sariaslan and his team originally developed and validated the OxMIS in a cohort of 75,000 people with SMI in Sweden. Recognizing the lack of externally validated prognostic models in the mental health field, the team wanted to validate the instrument in a new, population-based sample in Finland.

The investigators accessed information about patient diagnosis and treatment from the Finnish Care Register for Health Care, which contains de-identified information for all individuals between ages 15 and 65 years diagnosed with an SMI between Jan. 1, 1996, and Dec. 31, 2017.

They included 137,000 patients with somatic symptom disorder or bipolar disorder for a total of more than 5 million episodes of inpatient or outpatient treatment. Investigators linked the cohort to the Causes of Death Register to identify those who had died by suicide within 12 months of an index treatment episode, which investigators randomly selected for each person.

The investigators found that 1,475 individuals in the sample died by suicide within 1 year of their index episode (1.1%).

Each patient was assigned a clinical suicide risk score based on their clinical information, familial traits, prescription information, and comorbid conditions. Using OxMIS, the investigators found that the instrument accurately predicted suicide with an area under the curve of 0.70.

In other words, in 70% of the instances where the investigators randomly selected two people from the sample, one of whom died by suicide and the other of whom did not, the individual who died by suicide had a higher OxMIS risk score.

The investigators note the model overestimated the risk for patients who were at extremely high risk for suicide (those with a predicted suicide risk of > 5%). “In our complementary sensitivity analysis, we observed improved calibration in these patients when we assigned them a suicide risk prediction of no more than 5%,” they write.

Dr. Sariaslan said that the findings highlight the importance of safety planning interventions. “It is also essential to remember that OxMIS is not intended to replace clinical decision-making, but rather to support it,” he said.

As to whether the tool could be used in other populations, such as in the United States, Dr. Sariaslan said, “there is no good evidence that the contribution of risk factors to suicide in this population is different in the U.S. than in northern Europe, so there is no a priori reason to have to do multiple external validations before it can be used for research or clinical purposes.”
 

One size does not fit all

Commenting on the study, Ronald Kessler, PhD, McNeil Family Professor, department of health care policy at Harvard Medical School, Boston, said that he’d be “surprised” if OxMIS was adopted in the United States because there is already an existing tool that is “slightly more accurate,” which he helped develop.

Harvard Medical School

“In addition, when we start thinking about uses for such scales, it becomes clear that different scales should be used for different segments of the population, depending on intervention options,” Dr. Kessler said.

“So, for example, a different scale would probably be optimal in deciding how to manage psychiatric inpatients in the transition back to the community after hospital discharge than [it would be], say, in deciding how to respond to suicidality among patients presenting at an emergency department. No one scale will fit for all the scenarios in which prediction is desired,” he added.

The study was funded by the Academy of Finland. Dr. Kessler receives funding from the National Institute of Mental Health, Department of Defense, and Veterans Administration to develop suicide prediction models. Dr. Sariaslan has no disclosures to report.

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

A brief scalable suicide risk assessment tool accurately predicts suicide risk in patients with serious mental illness (SMI), a new population-based study shows.

The 17-question Oxford Mental Illness and Suicide Tool (OxMIS) assessment is designed to predict 12-month suicide risk in people with schizophrenia spectrum disorders and bipolar disorder based on risk factors such as familial traits, antisocial traits, and information about self-harm.

“We have demonstrated the clinical utility of OxMIS in two separate studies and countries. As with any clinical risk prediction tool, it will not improve outcomes unless coupled with effective interventions,” lead investigator Amir Sariaslan, PhD, a senior research fellow in psychiatric epidemiology at the University of Oxford, England, told this news organization.

The findings were published online in Translational Psychiatry.
 

Twice validated

Dr. Sariaslan and his team originally developed and validated the OxMIS in a cohort of 75,000 people with SMI in Sweden. Recognizing the lack of externally validated prognostic models in the mental health field, the team wanted to validate the instrument in a new, population-based sample in Finland.

The investigators accessed information about patient diagnosis and treatment from the Finnish Care Register for Health Care, which contains de-identified information for all individuals between ages 15 and 65 years diagnosed with an SMI between Jan. 1, 1996, and Dec. 31, 2017.

They included 137,000 patients with somatic symptom disorder or bipolar disorder for a total of more than 5 million episodes of inpatient or outpatient treatment. Investigators linked the cohort to the Causes of Death Register to identify those who had died by suicide within 12 months of an index treatment episode, which investigators randomly selected for each person.

The investigators found that 1,475 individuals in the sample died by suicide within 1 year of their index episode (1.1%).

Each patient was assigned a clinical suicide risk score based on their clinical information, familial traits, prescription information, and comorbid conditions. Using OxMIS, the investigators found that the instrument accurately predicted suicide with an area under the curve of 0.70.

In other words, in 70% of the instances where the investigators randomly selected two people from the sample, one of whom died by suicide and the other of whom did not, the individual who died by suicide had a higher OxMIS risk score.

The investigators note the model overestimated the risk for patients who were at extremely high risk for suicide (those with a predicted suicide risk of > 5%). “In our complementary sensitivity analysis, we observed improved calibration in these patients when we assigned them a suicide risk prediction of no more than 5%,” they write.

Dr. Sariaslan said that the findings highlight the importance of safety planning interventions. “It is also essential to remember that OxMIS is not intended to replace clinical decision-making, but rather to support it,” he said.

As to whether the tool could be used in other populations, such as in the United States, Dr. Sariaslan said, “there is no good evidence that the contribution of risk factors to suicide in this population is different in the U.S. than in northern Europe, so there is no a priori reason to have to do multiple external validations before it can be used for research or clinical purposes.”
 

One size does not fit all

Commenting on the study, Ronald Kessler, PhD, McNeil Family Professor, department of health care policy at Harvard Medical School, Boston, said that he’d be “surprised” if OxMIS was adopted in the United States because there is already an existing tool that is “slightly more accurate,” which he helped develop.

Harvard Medical School

“In addition, when we start thinking about uses for such scales, it becomes clear that different scales should be used for different segments of the population, depending on intervention options,” Dr. Kessler said.

“So, for example, a different scale would probably be optimal in deciding how to manage psychiatric inpatients in the transition back to the community after hospital discharge than [it would be], say, in deciding how to respond to suicidality among patients presenting at an emergency department. No one scale will fit for all the scenarios in which prediction is desired,” he added.

The study was funded by the Academy of Finland. Dr. Kessler receives funding from the National Institute of Mental Health, Department of Defense, and Veterans Administration to develop suicide prediction models. Dr. Sariaslan has no disclosures to report.

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

High-dose vitamin D in patients with relapsing, remitting multiple sclerosis (RRMS) does not prevent relapse, results from a randomized control trial show. However, at least one expert believes the study’s exclusion criteria may have been too broad.

The investigation of vitamin D to prevent relapse of MS is based on older observational studies of people who already had higher blood levels of vitamin D and were less likely to develop MS, said study investigator Ellen Mowry, MD, Richard T. and Frances W. Johnson professor of neurology, Johns Hopkins University, Baltimore.

Later research where participants were given vitamin D as a therapeutic option for MS “were disappointing as the vitamin D had minimal effect,” she said.

“While we were excited by early data suggesting that vitamin D may have an important impact on MS, it’s essential to follow those linkage studies with the gold standard clinical evidence, which we have here,” Dr. Mowry added.

The findings were published online in eClinicalMedicine.
 

No difference in relapse risk

The multisite, phase 3 Vitamin D to Ameliorate MS (VIDAMS) clinical trial included 172 participants aged 18-50 years with RRMS from 16 neurology clinics between 2012 and 2019.

Inclusion criteria were having one or more clinical episodes of MS in the past year and at least one brain lesion on MRI in the past year or having two or more clinical episodes in the past year. Eligible participants also had to have a score of 4 or less on the Kurtzke Expanded Disability Status Scale.

A total of 83 participants were randomly assigned to receive low-dose vitamin D₃ (600 IU/day) and 89 to receive high-dose vitamin D₃ (5,000 IU/day). Each participant took the vitamin tablet with glatiramer acetate, a synthetic protein that simulates myelin.

Participants were assessed every 12 weeks to measure serum 25(OH)D levels and every 24 weeks for a number of movement and coordination tests, as well as two 3T clinical brain MRIs to check for lesions.

By the trial’s end at 96 weeks, the researchers found no differences in relapse risk between the high- and low-dose groups (P = .57). In addition, there were no differences in MRI outcomes between the two groups.

Dr. Mowry said that more than a few people have asked her if she is disappointed by the results of the VIDAMS trial. “I tell them that no, I’m not – that we are scientists and clinicians, and it is our job to understand what they can do to fight their disease. And if the answer is not vitamin D, that’s OK – we have many other ideas.”

These include helping patients minimize cardiometabolic comorbidities, such as heart disease and blood pressure, she said.
 

Exclusion criteria too broad?

Commenting on the findings, Alberto Ascherio, MD, professor of epidemiology and nutrition at Harvard School of Public Health, Boston, said a key principle of recommending vitamin supplements is that they are, generally speaking, only beneficial for individuals with vitamin deficiencies.

He noted that “patients with vitamin D deficiency (25(OH)D < 15 ng/mL, which corresponds to 37.5 nmol/L) were excluded from this study. Most importantly, the baseline mean 25(OH)D levels were about 30 ng/mL (75 nmol/L), which is considered a sufficient level (the IOM considers 20 ng/mL = 50 nmol/L as an adequate level),” with the level further increasing during the trial due to the supplementation.

“It would be a serious mistake to conclude from this trial (or any of the previous trials) that vitamin D supplementation is not important in MS patients,” Dr. Ascherio said.

He added that many individuals with MS have serum vitamin D levels below 20 ng/mL (50 nmol/L) and that this was the median serum value in studies among individuals with MS in Europe.

“These patients would almost certainly benefit from moderate doses of vitamin D supplements or judicious UV light exposure. Most likely even patients with sufficient but suboptimal 25(OH)D levels (between 20 and 30 ng/mL, or 50 and 75 nmol/L) would benefit from an increase,” he said.

The study was funded by the National Multiple Sclerosis Society, Teva Neuroscience, and the National Institute of Health. Dr. Mowry reported grant support from the National MS Society, Biogen, Genentech, and Teva Neuroscience; honoraria from UpToDate; and consulting fees from BeCare Link.
 

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

High-dose vitamin D in patients with relapsing, remitting multiple sclerosis (RRMS) does not prevent relapse, results from a randomized control trial show. However, at least one expert believes the study’s exclusion criteria may have been too broad.

The investigation of vitamin D to prevent relapse of MS is based on older observational studies of people who already had higher blood levels of vitamin D and were less likely to develop MS, said study investigator Ellen Mowry, MD, Richard T. and Frances W. Johnson professor of neurology, Johns Hopkins University, Baltimore.

Later research where participants were given vitamin D as a therapeutic option for MS “were disappointing as the vitamin D had minimal effect,” she said.

“While we were excited by early data suggesting that vitamin D may have an important impact on MS, it’s essential to follow those linkage studies with the gold standard clinical evidence, which we have here,” Dr. Mowry added.

The findings were published online in eClinicalMedicine.
 

No difference in relapse risk

The multisite, phase 3 Vitamin D to Ameliorate MS (VIDAMS) clinical trial included 172 participants aged 18-50 years with RRMS from 16 neurology clinics between 2012 and 2019.

Inclusion criteria were having one or more clinical episodes of MS in the past year and at least one brain lesion on MRI in the past year or having two or more clinical episodes in the past year. Eligible participants also had to have a score of 4 or less on the Kurtzke Expanded Disability Status Scale.

A total of 83 participants were randomly assigned to receive low-dose vitamin D₃ (600 IU/day) and 89 to receive high-dose vitamin D₃ (5,000 IU/day). Each participant took the vitamin tablet with glatiramer acetate, a synthetic protein that simulates myelin.

Participants were assessed every 12 weeks to measure serum 25(OH)D levels and every 24 weeks for a number of movement and coordination tests, as well as two 3T clinical brain MRIs to check for lesions.

By the trial’s end at 96 weeks, the researchers found no differences in relapse risk between the high- and low-dose groups (P = .57). In addition, there were no differences in MRI outcomes between the two groups.

Dr. Mowry said that more than a few people have asked her if she is disappointed by the results of the VIDAMS trial. “I tell them that no, I’m not – that we are scientists and clinicians, and it is our job to understand what they can do to fight their disease. And if the answer is not vitamin D, that’s OK – we have many other ideas.”

These include helping patients minimize cardiometabolic comorbidities, such as heart disease and blood pressure, she said.
 

Exclusion criteria too broad?

Commenting on the findings, Alberto Ascherio, MD, professor of epidemiology and nutrition at Harvard School of Public Health, Boston, said a key principle of recommending vitamin supplements is that they are, generally speaking, only beneficial for individuals with vitamin deficiencies.

He noted that “patients with vitamin D deficiency (25(OH)D < 15 ng/mL, which corresponds to 37.5 nmol/L) were excluded from this study. Most importantly, the baseline mean 25(OH)D levels were about 30 ng/mL (75 nmol/L), which is considered a sufficient level (the IOM considers 20 ng/mL = 50 nmol/L as an adequate level),” with the level further increasing during the trial due to the supplementation.

“It would be a serious mistake to conclude from this trial (or any of the previous trials) that vitamin D supplementation is not important in MS patients,” Dr. Ascherio said.

He added that many individuals with MS have serum vitamin D levels below 20 ng/mL (50 nmol/L) and that this was the median serum value in studies among individuals with MS in Europe.

“These patients would almost certainly benefit from moderate doses of vitamin D supplements or judicious UV light exposure. Most likely even patients with sufficient but suboptimal 25(OH)D levels (between 20 and 30 ng/mL, or 50 and 75 nmol/L) would benefit from an increase,” he said.

The study was funded by the National Multiple Sclerosis Society, Teva Neuroscience, and the National Institute of Health. Dr. Mowry reported grant support from the National MS Society, Biogen, Genentech, and Teva Neuroscience; honoraria from UpToDate; and consulting fees from BeCare Link.
 

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

High-dose vitamin D in patients with relapsing, remitting multiple sclerosis (RRMS) does not prevent relapse, results from a randomized control trial show. However, at least one expert believes the study’s exclusion criteria may have been too broad.

The investigation of vitamin D to prevent relapse of MS is based on older observational studies of people who already had higher blood levels of vitamin D and were less likely to develop MS, said study investigator Ellen Mowry, MD, Richard T. and Frances W. Johnson professor of neurology, Johns Hopkins University, Baltimore.

Later research where participants were given vitamin D as a therapeutic option for MS “were disappointing as the vitamin D had minimal effect,” she said.

“While we were excited by early data suggesting that vitamin D may have an important impact on MS, it’s essential to follow those linkage studies with the gold standard clinical evidence, which we have here,” Dr. Mowry added.

The findings were published online in eClinicalMedicine.
 

No difference in relapse risk

The multisite, phase 3 Vitamin D to Ameliorate MS (VIDAMS) clinical trial included 172 participants aged 18-50 years with RRMS from 16 neurology clinics between 2012 and 2019.

Inclusion criteria were having one or more clinical episodes of MS in the past year and at least one brain lesion on MRI in the past year or having two or more clinical episodes in the past year. Eligible participants also had to have a score of 4 or less on the Kurtzke Expanded Disability Status Scale.

A total of 83 participants were randomly assigned to receive low-dose vitamin D₃ (600 IU/day) and 89 to receive high-dose vitamin D₃ (5,000 IU/day). Each participant took the vitamin tablet with glatiramer acetate, a synthetic protein that simulates myelin.

Participants were assessed every 12 weeks to measure serum 25(OH)D levels and every 24 weeks for a number of movement and coordination tests, as well as two 3T clinical brain MRIs to check for lesions.

By the trial’s end at 96 weeks, the researchers found no differences in relapse risk between the high- and low-dose groups (P = .57). In addition, there were no differences in MRI outcomes between the two groups.

Dr. Mowry said that more than a few people have asked her if she is disappointed by the results of the VIDAMS trial. “I tell them that no, I’m not – that we are scientists and clinicians, and it is our job to understand what they can do to fight their disease. And if the answer is not vitamin D, that’s OK – we have many other ideas.”

These include helping patients minimize cardiometabolic comorbidities, such as heart disease and blood pressure, she said.
 

Exclusion criteria too broad?

Commenting on the findings, Alberto Ascherio, MD, professor of epidemiology and nutrition at Harvard School of Public Health, Boston, said a key principle of recommending vitamin supplements is that they are, generally speaking, only beneficial for individuals with vitamin deficiencies.

He noted that “patients with vitamin D deficiency (25(OH)D < 15 ng/mL, which corresponds to 37.5 nmol/L) were excluded from this study. Most importantly, the baseline mean 25(OH)D levels were about 30 ng/mL (75 nmol/L), which is considered a sufficient level (the IOM considers 20 ng/mL = 50 nmol/L as an adequate level),” with the level further increasing during the trial due to the supplementation.

“It would be a serious mistake to conclude from this trial (or any of the previous trials) that vitamin D supplementation is not important in MS patients,” Dr. Ascherio said.

He added that many individuals with MS have serum vitamin D levels below 20 ng/mL (50 nmol/L) and that this was the median serum value in studies among individuals with MS in Europe.

“These patients would almost certainly benefit from moderate doses of vitamin D supplements or judicious UV light exposure. Most likely even patients with sufficient but suboptimal 25(OH)D levels (between 20 and 30 ng/mL, or 50 and 75 nmol/L) would benefit from an increase,” he said.

The study was funded by the National Multiple Sclerosis Society, Teva Neuroscience, and the National Institute of Health. Dr. Mowry reported grant support from the National MS Society, Biogen, Genentech, and Teva Neuroscience; honoraria from UpToDate; and consulting fees from BeCare Link.
 

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