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Dance training ‘drastically’ reduces Parkinson’s progression, eases symptoms
Over 3 years, weekly participation in dance training classes “drastically” reduced the expected decline in motor function and significantly improved speech, tremors, balance, and stiffness, the researchers reported.
Dance training also appeared to have benefits regarding cognition, hallucinations, depression, and anxiety.
“These findings strongly suggest the benefits of dance for people with PD as a supplement to a normal treatment regimen,” the investigators noted.
Although the mechanism of benefit is unclear, dance training may help “train neural network nodes that helps either strengthen networks damaged or builds neural road maps that pass the damage,” study investigator Joseph DeSouza, PhD, principal investigator and associate professor, department of psychology, York University, Toronto, said in an interview.
The study was published online July 7, 2021, in Brain Sciences.
Multiple benefits
PD is a neurodegenerative disease associated with progression of motor dysfunction within the first 5 years of diagnosis. The annual rate of motor decline, as determined with the Movement Disorder Society Unified Parkinson’s Disease Rating Scale (MDS-UPDRS), is between 5.2 and 8.9 points.
Prior studies that assessed various styles of dance by patients with PD showed beneficial effects regarding gait speed, balance, locomotion, and aspects of quality of life.
To investigate further, DeSouza and coauthor Karolina Bearss, a PhD candidate at York University, followed 16 patients with mild to moderate PD who participated in a weekly dance class at Canada’s National Ballet School and Trinity St. Paul’s church.
Dance for Parkinson’s Disease, which is an established dance curriculum, involves aerobic and anaerobic movements. The protocol begins with a seated warm-up, followed by barre work, and ends with moving across the floor. All participants learn choreography for an upcoming performance.
In the study, 16 patients with PD who did not participant in the dance classes served as control patients.
Over 3 years, the daily rate of motor decline, as indicated by scores on part III of the MDS-UPDRS, was zero among the dancers (slope = 0.000146), indicating no motor impairment, whereas among the nondancers, the motor decline during follow-up was as expected (P < .01), the researchers reported.
In modeling the data, the researchers determined that after completing 1,000 days of dance training, dancers will have a motor score of 19.07, compared with a score of 28.27 for nondancers.
“Our data further showed that training in dance will slow the rate of PD motor impairment progression, as measured by the UPDRS III, by close to 3 points annually in comparison to our PD subjects who did not train,” the researchers reported.
Dance training also had a beneficial effect on motor or nonmotor aspects of daily living and on motor complications, for which there was no significant decline among the PD dancers.
“For those with Parkinson’s disease, even when it’s mild, motor impairment can impact their daily functioning – how they feel about themselves. Many of these motor symptoms lead to isolation because once they get extreme, these people don’t want to go out,” Dr. DeSouza said in a news release.
“These motor symptoms lead to further psychological issues, depression, social isolation and eventually the symptoms do get worse over time. Our study shows that training with dance and music can slow this down and improve their daily living and daily function,” he added.
‘Great potential’
Reached for comment, Demian Kogutek, PhD, director of music therapy, University of Evansville (Indiana), said that these preliminary findings from a longitudinal study are “promising.”
“I believe that dance therapy has a great potential for PD. The longitudinal aspect of this study undoubtedly adds to the current literature. Although it is a standardized assessment, it is somewhat subjective,” Dr. Kogutek said in an interview.
Going forward, Dr. Kogutek said he’d like to see other objective outcomes measured, such as objective assessments of balance, gait, hand strength, and dexterity.
Also weighing in on the results, Karen Lee, PhD, president and CEO of Parkinson Canada, said her organization is “encouraged by these preliminary findings as exercise and healthy activities are important for people with Parkinson’s. This study is part of a growing body of research that explores the link between the impact of activities and both motor and nonmotor symptoms of Parkinson’s.
“This research adds to growing evidence about the importance of exercise as part of the management of Parkinson’s, and we encourage people living with Parkinson’s to incorporate exercise as part of their approach to managing their health,” Dr. Lee said in an interview.
Funding for the project is provided in part by a National Science and Engineering Research Council Discovery Grant and by donations from the Irpinia Club of Toronto and others. Dr. Dr. DeSouza, Ms. Bearss, Dr. Kogutek, and Dr. Lee disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Over 3 years, weekly participation in dance training classes “drastically” reduced the expected decline in motor function and significantly improved speech, tremors, balance, and stiffness, the researchers reported.
Dance training also appeared to have benefits regarding cognition, hallucinations, depression, and anxiety.
“These findings strongly suggest the benefits of dance for people with PD as a supplement to a normal treatment regimen,” the investigators noted.
Although the mechanism of benefit is unclear, dance training may help “train neural network nodes that helps either strengthen networks damaged or builds neural road maps that pass the damage,” study investigator Joseph DeSouza, PhD, principal investigator and associate professor, department of psychology, York University, Toronto, said in an interview.
The study was published online July 7, 2021, in Brain Sciences.
Multiple benefits
PD is a neurodegenerative disease associated with progression of motor dysfunction within the first 5 years of diagnosis. The annual rate of motor decline, as determined with the Movement Disorder Society Unified Parkinson’s Disease Rating Scale (MDS-UPDRS), is between 5.2 and 8.9 points.
Prior studies that assessed various styles of dance by patients with PD showed beneficial effects regarding gait speed, balance, locomotion, and aspects of quality of life.
To investigate further, DeSouza and coauthor Karolina Bearss, a PhD candidate at York University, followed 16 patients with mild to moderate PD who participated in a weekly dance class at Canada’s National Ballet School and Trinity St. Paul’s church.
Dance for Parkinson’s Disease, which is an established dance curriculum, involves aerobic and anaerobic movements. The protocol begins with a seated warm-up, followed by barre work, and ends with moving across the floor. All participants learn choreography for an upcoming performance.
In the study, 16 patients with PD who did not participant in the dance classes served as control patients.
Over 3 years, the daily rate of motor decline, as indicated by scores on part III of the MDS-UPDRS, was zero among the dancers (slope = 0.000146), indicating no motor impairment, whereas among the nondancers, the motor decline during follow-up was as expected (P < .01), the researchers reported.
In modeling the data, the researchers determined that after completing 1,000 days of dance training, dancers will have a motor score of 19.07, compared with a score of 28.27 for nondancers.
“Our data further showed that training in dance will slow the rate of PD motor impairment progression, as measured by the UPDRS III, by close to 3 points annually in comparison to our PD subjects who did not train,” the researchers reported.
Dance training also had a beneficial effect on motor or nonmotor aspects of daily living and on motor complications, for which there was no significant decline among the PD dancers.
“For those with Parkinson’s disease, even when it’s mild, motor impairment can impact their daily functioning – how they feel about themselves. Many of these motor symptoms lead to isolation because once they get extreme, these people don’t want to go out,” Dr. DeSouza said in a news release.
“These motor symptoms lead to further psychological issues, depression, social isolation and eventually the symptoms do get worse over time. Our study shows that training with dance and music can slow this down and improve their daily living and daily function,” he added.
‘Great potential’
Reached for comment, Demian Kogutek, PhD, director of music therapy, University of Evansville (Indiana), said that these preliminary findings from a longitudinal study are “promising.”
“I believe that dance therapy has a great potential for PD. The longitudinal aspect of this study undoubtedly adds to the current literature. Although it is a standardized assessment, it is somewhat subjective,” Dr. Kogutek said in an interview.
Going forward, Dr. Kogutek said he’d like to see other objective outcomes measured, such as objective assessments of balance, gait, hand strength, and dexterity.
Also weighing in on the results, Karen Lee, PhD, president and CEO of Parkinson Canada, said her organization is “encouraged by these preliminary findings as exercise and healthy activities are important for people with Parkinson’s. This study is part of a growing body of research that explores the link between the impact of activities and both motor and nonmotor symptoms of Parkinson’s.
“This research adds to growing evidence about the importance of exercise as part of the management of Parkinson’s, and we encourage people living with Parkinson’s to incorporate exercise as part of their approach to managing their health,” Dr. Lee said in an interview.
Funding for the project is provided in part by a National Science and Engineering Research Council Discovery Grant and by donations from the Irpinia Club of Toronto and others. Dr. Dr. DeSouza, Ms. Bearss, Dr. Kogutek, and Dr. Lee disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Over 3 years, weekly participation in dance training classes “drastically” reduced the expected decline in motor function and significantly improved speech, tremors, balance, and stiffness, the researchers reported.
Dance training also appeared to have benefits regarding cognition, hallucinations, depression, and anxiety.
“These findings strongly suggest the benefits of dance for people with PD as a supplement to a normal treatment regimen,” the investigators noted.
Although the mechanism of benefit is unclear, dance training may help “train neural network nodes that helps either strengthen networks damaged or builds neural road maps that pass the damage,” study investigator Joseph DeSouza, PhD, principal investigator and associate professor, department of psychology, York University, Toronto, said in an interview.
The study was published online July 7, 2021, in Brain Sciences.
Multiple benefits
PD is a neurodegenerative disease associated with progression of motor dysfunction within the first 5 years of diagnosis. The annual rate of motor decline, as determined with the Movement Disorder Society Unified Parkinson’s Disease Rating Scale (MDS-UPDRS), is between 5.2 and 8.9 points.
Prior studies that assessed various styles of dance by patients with PD showed beneficial effects regarding gait speed, balance, locomotion, and aspects of quality of life.
To investigate further, DeSouza and coauthor Karolina Bearss, a PhD candidate at York University, followed 16 patients with mild to moderate PD who participated in a weekly dance class at Canada’s National Ballet School and Trinity St. Paul’s church.
Dance for Parkinson’s Disease, which is an established dance curriculum, involves aerobic and anaerobic movements. The protocol begins with a seated warm-up, followed by barre work, and ends with moving across the floor. All participants learn choreography for an upcoming performance.
In the study, 16 patients with PD who did not participant in the dance classes served as control patients.
Over 3 years, the daily rate of motor decline, as indicated by scores on part III of the MDS-UPDRS, was zero among the dancers (slope = 0.000146), indicating no motor impairment, whereas among the nondancers, the motor decline during follow-up was as expected (P < .01), the researchers reported.
In modeling the data, the researchers determined that after completing 1,000 days of dance training, dancers will have a motor score of 19.07, compared with a score of 28.27 for nondancers.
“Our data further showed that training in dance will slow the rate of PD motor impairment progression, as measured by the UPDRS III, by close to 3 points annually in comparison to our PD subjects who did not train,” the researchers reported.
Dance training also had a beneficial effect on motor or nonmotor aspects of daily living and on motor complications, for which there was no significant decline among the PD dancers.
“For those with Parkinson’s disease, even when it’s mild, motor impairment can impact their daily functioning – how they feel about themselves. Many of these motor symptoms lead to isolation because once they get extreme, these people don’t want to go out,” Dr. DeSouza said in a news release.
“These motor symptoms lead to further psychological issues, depression, social isolation and eventually the symptoms do get worse over time. Our study shows that training with dance and music can slow this down and improve their daily living and daily function,” he added.
‘Great potential’
Reached for comment, Demian Kogutek, PhD, director of music therapy, University of Evansville (Indiana), said that these preliminary findings from a longitudinal study are “promising.”
“I believe that dance therapy has a great potential for PD. The longitudinal aspect of this study undoubtedly adds to the current literature. Although it is a standardized assessment, it is somewhat subjective,” Dr. Kogutek said in an interview.
Going forward, Dr. Kogutek said he’d like to see other objective outcomes measured, such as objective assessments of balance, gait, hand strength, and dexterity.
Also weighing in on the results, Karen Lee, PhD, president and CEO of Parkinson Canada, said her organization is “encouraged by these preliminary findings as exercise and healthy activities are important for people with Parkinson’s. This study is part of a growing body of research that explores the link between the impact of activities and both motor and nonmotor symptoms of Parkinson’s.
“This research adds to growing evidence about the importance of exercise as part of the management of Parkinson’s, and we encourage people living with Parkinson’s to incorporate exercise as part of their approach to managing their health,” Dr. Lee said in an interview.
Funding for the project is provided in part by a National Science and Engineering Research Council Discovery Grant and by donations from the Irpinia Club of Toronto and others. Dr. Dr. DeSouza, Ms. Bearss, Dr. Kogutek, and Dr. Lee disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
St. Jude to pay $27 million to end DOJ suit over faulty ICDs
St. Jude Medical, now part of Abbott Laboratories, will pay the American government $27 million to settle allegations that it knowingly sold defective implantable cardiac defibrillators to health care facilities, which were implanted into patients, causing injuries and two deaths, the U.S. Department of Justice (DOJ) has announced.
“Medical device manufacturers have an obligation to be truthful with the Food and Drug Administration, and the U.S. government will not pay for devices that are unsafe and risk injury or death,” Jonathan F. Lenzner, Acting U.S. Attorney for the District of Maryland, said in a July 8 statement.
“The government contends that St. Jude knowingly caused the submission of false claims and failed to inform the FDA with critical information about prior injuries and a death which, had the FDA been made aware, would have led to a recall,” Mr. Lenzner added.
Those claims were submitted to the Medicare, TRICARE, and Federal Employees Health Benefits programs, according to the settlement agreement.
“The U.S. Attorney’s Office is committed to protecting Medicare and other federal health care programs from fraud, and in doing so, strengthen[ing] patient safety,” Mr. Lenzner said.
Premature battery depletion
The government alleges that St. Jude failed to disclose “serious adverse health events” related to premature battery depletion of certain models of its Fortify, Fortify Assura, Quadra, and Unify implantable defibrillators.
The government further alleges that, by 2013, St. Jude knew that lithium clusters could form on the batteries, causing them to short and run out of power. But it took until late 2014 for St. Jude to ask the FDA to approve a change to prevent lithium clusters from draining the battery.
And at this point, St. Jude told the FDA that “no serious injury, permanent harm, or deaths have been reported associated with this” issue, the government alleges.
However, according to the government’s allegations, St. Jude was aware at that time of two reported serious injuries and one death associated with the faulty batteries and continued to distribute devices that had been manufactured without the new design.
Not until August 2016 did St. Jude inform the FDA that the number of premature battery depletion events had increased to 729, including two deaths and 29 events associated with loss of pacing, the government alleges.
In October 2016, St. Jude issued a medical advisory regarding the battery problem, which the FDA classified as a Class I recall, the most serious type.
After the recall, St. Jude no longer sold the older devices, but thousands of them had been implanted into patients between November 2014 and October 2016.
In September 2017, as reported by this news organization, a nationwide class-action lawsuit was filed against St. Jude Medical and parent company Abbott Laboratories alleging that, despite knowing about a battery-depletion defect in some of its cardiac defibrillators as early as 2011, St. Jude failed to adequately report the risk and waited nearly 5 years before issuing a recall.
“To ensure the health and safety of patients, manufacturers of implantable cardiac devices must be transparent when communicating with the government about safety issues and incidents,” Acting Assistant Attorney General Brian Boynton, from the DOJ’s Civil Division, said in the DOJ statement announcing the settlement.
“We will hold accountable those companies whose conduct violates the law and puts patients’ health at risk,” Mr. Boynton said.
The civil settlement includes the resolution of claims brought under the qui tam, or whistleblower, provisions of the False Claims Act by Debbie Burke, a patient who received one of the devices that was subject to recall.
The claims resolved by the settlement are allegations only; there has been no determination of liability, the DOJ noted. St. Jude denies the allegations raised in the lawsuit.
A version of this article first appeared on Medscape.com.
St. Jude Medical, now part of Abbott Laboratories, will pay the American government $27 million to settle allegations that it knowingly sold defective implantable cardiac defibrillators to health care facilities, which were implanted into patients, causing injuries and two deaths, the U.S. Department of Justice (DOJ) has announced.
“Medical device manufacturers have an obligation to be truthful with the Food and Drug Administration, and the U.S. government will not pay for devices that are unsafe and risk injury or death,” Jonathan F. Lenzner, Acting U.S. Attorney for the District of Maryland, said in a July 8 statement.
“The government contends that St. Jude knowingly caused the submission of false claims and failed to inform the FDA with critical information about prior injuries and a death which, had the FDA been made aware, would have led to a recall,” Mr. Lenzner added.
Those claims were submitted to the Medicare, TRICARE, and Federal Employees Health Benefits programs, according to the settlement agreement.
“The U.S. Attorney’s Office is committed to protecting Medicare and other federal health care programs from fraud, and in doing so, strengthen[ing] patient safety,” Mr. Lenzner said.
Premature battery depletion
The government alleges that St. Jude failed to disclose “serious adverse health events” related to premature battery depletion of certain models of its Fortify, Fortify Assura, Quadra, and Unify implantable defibrillators.
The government further alleges that, by 2013, St. Jude knew that lithium clusters could form on the batteries, causing them to short and run out of power. But it took until late 2014 for St. Jude to ask the FDA to approve a change to prevent lithium clusters from draining the battery.
And at this point, St. Jude told the FDA that “no serious injury, permanent harm, or deaths have been reported associated with this” issue, the government alleges.
However, according to the government’s allegations, St. Jude was aware at that time of two reported serious injuries and one death associated with the faulty batteries and continued to distribute devices that had been manufactured without the new design.
Not until August 2016 did St. Jude inform the FDA that the number of premature battery depletion events had increased to 729, including two deaths and 29 events associated with loss of pacing, the government alleges.
In October 2016, St. Jude issued a medical advisory regarding the battery problem, which the FDA classified as a Class I recall, the most serious type.
After the recall, St. Jude no longer sold the older devices, but thousands of them had been implanted into patients between November 2014 and October 2016.
In September 2017, as reported by this news organization, a nationwide class-action lawsuit was filed against St. Jude Medical and parent company Abbott Laboratories alleging that, despite knowing about a battery-depletion defect in some of its cardiac defibrillators as early as 2011, St. Jude failed to adequately report the risk and waited nearly 5 years before issuing a recall.
“To ensure the health and safety of patients, manufacturers of implantable cardiac devices must be transparent when communicating with the government about safety issues and incidents,” Acting Assistant Attorney General Brian Boynton, from the DOJ’s Civil Division, said in the DOJ statement announcing the settlement.
“We will hold accountable those companies whose conduct violates the law and puts patients’ health at risk,” Mr. Boynton said.
The civil settlement includes the resolution of claims brought under the qui tam, or whistleblower, provisions of the False Claims Act by Debbie Burke, a patient who received one of the devices that was subject to recall.
The claims resolved by the settlement are allegations only; there has been no determination of liability, the DOJ noted. St. Jude denies the allegations raised in the lawsuit.
A version of this article first appeared on Medscape.com.
St. Jude Medical, now part of Abbott Laboratories, will pay the American government $27 million to settle allegations that it knowingly sold defective implantable cardiac defibrillators to health care facilities, which were implanted into patients, causing injuries and two deaths, the U.S. Department of Justice (DOJ) has announced.
“Medical device manufacturers have an obligation to be truthful with the Food and Drug Administration, and the U.S. government will not pay for devices that are unsafe and risk injury or death,” Jonathan F. Lenzner, Acting U.S. Attorney for the District of Maryland, said in a July 8 statement.
“The government contends that St. Jude knowingly caused the submission of false claims and failed to inform the FDA with critical information about prior injuries and a death which, had the FDA been made aware, would have led to a recall,” Mr. Lenzner added.
Those claims were submitted to the Medicare, TRICARE, and Federal Employees Health Benefits programs, according to the settlement agreement.
“The U.S. Attorney’s Office is committed to protecting Medicare and other federal health care programs from fraud, and in doing so, strengthen[ing] patient safety,” Mr. Lenzner said.
Premature battery depletion
The government alleges that St. Jude failed to disclose “serious adverse health events” related to premature battery depletion of certain models of its Fortify, Fortify Assura, Quadra, and Unify implantable defibrillators.
The government further alleges that, by 2013, St. Jude knew that lithium clusters could form on the batteries, causing them to short and run out of power. But it took until late 2014 for St. Jude to ask the FDA to approve a change to prevent lithium clusters from draining the battery.
And at this point, St. Jude told the FDA that “no serious injury, permanent harm, or deaths have been reported associated with this” issue, the government alleges.
However, according to the government’s allegations, St. Jude was aware at that time of two reported serious injuries and one death associated with the faulty batteries and continued to distribute devices that had been manufactured without the new design.
Not until August 2016 did St. Jude inform the FDA that the number of premature battery depletion events had increased to 729, including two deaths and 29 events associated with loss of pacing, the government alleges.
In October 2016, St. Jude issued a medical advisory regarding the battery problem, which the FDA classified as a Class I recall, the most serious type.
After the recall, St. Jude no longer sold the older devices, but thousands of them had been implanted into patients between November 2014 and October 2016.
In September 2017, as reported by this news organization, a nationwide class-action lawsuit was filed against St. Jude Medical and parent company Abbott Laboratories alleging that, despite knowing about a battery-depletion defect in some of its cardiac defibrillators as early as 2011, St. Jude failed to adequately report the risk and waited nearly 5 years before issuing a recall.
“To ensure the health and safety of patients, manufacturers of implantable cardiac devices must be transparent when communicating with the government about safety issues and incidents,” Acting Assistant Attorney General Brian Boynton, from the DOJ’s Civil Division, said in the DOJ statement announcing the settlement.
“We will hold accountable those companies whose conduct violates the law and puts patients’ health at risk,” Mr. Boynton said.
The civil settlement includes the resolution of claims brought under the qui tam, or whistleblower, provisions of the False Claims Act by Debbie Burke, a patient who received one of the devices that was subject to recall.
The claims resolved by the settlement are allegations only; there has been no determination of liability, the DOJ noted. St. Jude denies the allegations raised in the lawsuit.
A version of this article first appeared on Medscape.com.
Fitbit stats show lingering physiologic hit after COVID-19
People infected with SARS-CoV-2 can experience lingering physiologic effects after they recover, according to early data from an ongoing study that is harnessing the power of Fitbits and other wearable trackers to gauge long-term effects of COVID-19.
“To our knowledge, this is the first study to examine longer duration wearable sensor data. We found a prolonged physiological impact of COVID-19 infection, lasting approximately 2-3 months, on average, but with substantial intra-individual variability,” report Jennifer Radin, PhD, MPH, and colleagues with the Scripps Research Translational Institute, San Diego.
The study was published online July 7 in JAMA Network Open.
The DETECT study is enrolling adults from all over the United States and is collecting their health data from different wearable devices to better understand changes associated with viral illness, including COVID-19.
The current analysis focuses on a subset of 875 device wearers who reported symptoms of an acute respiratory illness and underwent testing for SARS-CoV-2. A total of 234 individuals tested positive for SARS-CoV-2; 641 were presumed to have other viral infections (COVID-19-negative symptomatic individuals).
The investigators found that among people with COVID-19, it took longer to return to baseline status with respect to resting heart rate (RHR), sleep, and activity compared with those who had symptoms of viral illness but who did not have COVID-19.
“This difference was most marked for RHR, with COVID-19-positive individuals initially experiencing a transient bradycardia followed by a prolonged relative tachycardia that did not return to baseline, on average, until 79 days after symptom onset,” Dr. Radin and colleagues reported.
Step count and sleep quantity returned to baseline values sooner than RHR, at 32 days and 24 days, respectively.
Among people with COVID-19, during recovery, trajectories differed with respect to return of RHR to normal in comparison with persons who did not have COVID-19.
The RHR of 32 COVID-19–positive participants (13.7%) remained 5 beats/min greater than their baseline RHR for more than 133 days, on average. During the acute phase of COVID-19, these individuals were more apt to report cough, body ache, and shortness of breath compared with other groups.
Limitation
The researchers say a limitation of this analysis is that symptom data were collected only during the acute phase of infection, which limits the ability to compare long-term physiologic and behavioral changes with long-term symptoms.
“In the future, with larger sample sizes and more comprehensive participant-reported outcomes, it will be possible to better understand factors associated with inter-individualized variability in COVID-19 recovery,” they concluded.
Earlier data from the DETECT study showed that pairing wearable tracker data with self-reported symptoms can improve COVID-19 prediction.
As previously reported by this news organization, DETECT investigators found that associating participant-reported symptoms with personal sensor data, such as deviation from normal sleep duration and RHR, resulted in an area under the curve of 0.80 for differentiating between symptomatic individuals who were positive and those who were negative for COVID-19.
Funding for the current study was provided by a grant from the National Center for Advancing Translational Sciences at the National Institutes of Health. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
People infected with SARS-CoV-2 can experience lingering physiologic effects after they recover, according to early data from an ongoing study that is harnessing the power of Fitbits and other wearable trackers to gauge long-term effects of COVID-19.
“To our knowledge, this is the first study to examine longer duration wearable sensor data. We found a prolonged physiological impact of COVID-19 infection, lasting approximately 2-3 months, on average, but with substantial intra-individual variability,” report Jennifer Radin, PhD, MPH, and colleagues with the Scripps Research Translational Institute, San Diego.
The study was published online July 7 in JAMA Network Open.
The DETECT study is enrolling adults from all over the United States and is collecting their health data from different wearable devices to better understand changes associated with viral illness, including COVID-19.
The current analysis focuses on a subset of 875 device wearers who reported symptoms of an acute respiratory illness and underwent testing for SARS-CoV-2. A total of 234 individuals tested positive for SARS-CoV-2; 641 were presumed to have other viral infections (COVID-19-negative symptomatic individuals).
The investigators found that among people with COVID-19, it took longer to return to baseline status with respect to resting heart rate (RHR), sleep, and activity compared with those who had symptoms of viral illness but who did not have COVID-19.
“This difference was most marked for RHR, with COVID-19-positive individuals initially experiencing a transient bradycardia followed by a prolonged relative tachycardia that did not return to baseline, on average, until 79 days after symptom onset,” Dr. Radin and colleagues reported.
Step count and sleep quantity returned to baseline values sooner than RHR, at 32 days and 24 days, respectively.
Among people with COVID-19, during recovery, trajectories differed with respect to return of RHR to normal in comparison with persons who did not have COVID-19.
The RHR of 32 COVID-19–positive participants (13.7%) remained 5 beats/min greater than their baseline RHR for more than 133 days, on average. During the acute phase of COVID-19, these individuals were more apt to report cough, body ache, and shortness of breath compared with other groups.
Limitation
The researchers say a limitation of this analysis is that symptom data were collected only during the acute phase of infection, which limits the ability to compare long-term physiologic and behavioral changes with long-term symptoms.
“In the future, with larger sample sizes and more comprehensive participant-reported outcomes, it will be possible to better understand factors associated with inter-individualized variability in COVID-19 recovery,” they concluded.
Earlier data from the DETECT study showed that pairing wearable tracker data with self-reported symptoms can improve COVID-19 prediction.
As previously reported by this news organization, DETECT investigators found that associating participant-reported symptoms with personal sensor data, such as deviation from normal sleep duration and RHR, resulted in an area under the curve of 0.80 for differentiating between symptomatic individuals who were positive and those who were negative for COVID-19.
Funding for the current study was provided by a grant from the National Center for Advancing Translational Sciences at the National Institutes of Health. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
People infected with SARS-CoV-2 can experience lingering physiologic effects after they recover, according to early data from an ongoing study that is harnessing the power of Fitbits and other wearable trackers to gauge long-term effects of COVID-19.
“To our knowledge, this is the first study to examine longer duration wearable sensor data. We found a prolonged physiological impact of COVID-19 infection, lasting approximately 2-3 months, on average, but with substantial intra-individual variability,” report Jennifer Radin, PhD, MPH, and colleagues with the Scripps Research Translational Institute, San Diego.
The study was published online July 7 in JAMA Network Open.
The DETECT study is enrolling adults from all over the United States and is collecting their health data from different wearable devices to better understand changes associated with viral illness, including COVID-19.
The current analysis focuses on a subset of 875 device wearers who reported symptoms of an acute respiratory illness and underwent testing for SARS-CoV-2. A total of 234 individuals tested positive for SARS-CoV-2; 641 were presumed to have other viral infections (COVID-19-negative symptomatic individuals).
The investigators found that among people with COVID-19, it took longer to return to baseline status with respect to resting heart rate (RHR), sleep, and activity compared with those who had symptoms of viral illness but who did not have COVID-19.
“This difference was most marked for RHR, with COVID-19-positive individuals initially experiencing a transient bradycardia followed by a prolonged relative tachycardia that did not return to baseline, on average, until 79 days after symptom onset,” Dr. Radin and colleagues reported.
Step count and sleep quantity returned to baseline values sooner than RHR, at 32 days and 24 days, respectively.
Among people with COVID-19, during recovery, trajectories differed with respect to return of RHR to normal in comparison with persons who did not have COVID-19.
The RHR of 32 COVID-19–positive participants (13.7%) remained 5 beats/min greater than their baseline RHR for more than 133 days, on average. During the acute phase of COVID-19, these individuals were more apt to report cough, body ache, and shortness of breath compared with other groups.
Limitation
The researchers say a limitation of this analysis is that symptom data were collected only during the acute phase of infection, which limits the ability to compare long-term physiologic and behavioral changes with long-term symptoms.
“In the future, with larger sample sizes and more comprehensive participant-reported outcomes, it will be possible to better understand factors associated with inter-individualized variability in COVID-19 recovery,” they concluded.
Earlier data from the DETECT study showed that pairing wearable tracker data with self-reported symptoms can improve COVID-19 prediction.
As previously reported by this news organization, DETECT investigators found that associating participant-reported symptoms with personal sensor data, such as deviation from normal sleep duration and RHR, resulted in an area under the curve of 0.80 for differentiating between symptomatic individuals who were positive and those who were negative for COVID-19.
Funding for the current study was provided by a grant from the National Center for Advancing Translational Sciences at the National Institutes of Health. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FDA updates label for controversial Alzheimer’s drug aducanumab (Aduhelm)
– the group studied in the clinical trials.
The FDA approved aducanumab in early June amid significant controversy and disregarding the recommendation by its own advisory panel not to approve the drug. The original prescribing information implied that the drug – which is administered intravenously and costs around $56,000 a year – could be used for treatment of any patient with Alzheimer’s disease.
The updated label now states that aducanumab should be initiated only in patients with mild cognitive impairment (MCI) or mild dementia stage of disease – the population in which treatment was initiated in the clinical trials leading to approval of the anti-amyloid drug.
The FDA granted accelerated approval of the drug based on data from clinical trials showing a reduction in amyloid beta plaques observed in patients with MCI or mild dementia stage of disease.
“Continued approval for the indication may be contingent upon verification of clinical benefit in confirmatory trial(s),” the label states. It emphasizes that there are no safety or effectiveness data on starting aducanumab treatment at earlier or later stages of the disease than were studied.
“Based on our ongoing conversations with prescribing physicians, FDA, and patient advocates, we submitted this label update with the goal to further clarify the patient population that was studied across the three Aduhelm clinical trials that supported approval,” Alfred Sandrock Jr., MD, PhD, Biogen’s head of research and development, said in a statement announcing the label update.
“We are committed to continue to listen to the community’s needs as clinical practice adapts to this important, first-in-class treatment option,” said Dr. Sandrock.
A version of this article first appeared on Medscape.com.
– the group studied in the clinical trials.
The FDA approved aducanumab in early June amid significant controversy and disregarding the recommendation by its own advisory panel not to approve the drug. The original prescribing information implied that the drug – which is administered intravenously and costs around $56,000 a year – could be used for treatment of any patient with Alzheimer’s disease.
The updated label now states that aducanumab should be initiated only in patients with mild cognitive impairment (MCI) or mild dementia stage of disease – the population in which treatment was initiated in the clinical trials leading to approval of the anti-amyloid drug.
The FDA granted accelerated approval of the drug based on data from clinical trials showing a reduction in amyloid beta plaques observed in patients with MCI or mild dementia stage of disease.
“Continued approval for the indication may be contingent upon verification of clinical benefit in confirmatory trial(s),” the label states. It emphasizes that there are no safety or effectiveness data on starting aducanumab treatment at earlier or later stages of the disease than were studied.
“Based on our ongoing conversations with prescribing physicians, FDA, and patient advocates, we submitted this label update with the goal to further clarify the patient population that was studied across the three Aduhelm clinical trials that supported approval,” Alfred Sandrock Jr., MD, PhD, Biogen’s head of research and development, said in a statement announcing the label update.
“We are committed to continue to listen to the community’s needs as clinical practice adapts to this important, first-in-class treatment option,” said Dr. Sandrock.
A version of this article first appeared on Medscape.com.
– the group studied in the clinical trials.
The FDA approved aducanumab in early June amid significant controversy and disregarding the recommendation by its own advisory panel not to approve the drug. The original prescribing information implied that the drug – which is administered intravenously and costs around $56,000 a year – could be used for treatment of any patient with Alzheimer’s disease.
The updated label now states that aducanumab should be initiated only in patients with mild cognitive impairment (MCI) or mild dementia stage of disease – the population in which treatment was initiated in the clinical trials leading to approval of the anti-amyloid drug.
The FDA granted accelerated approval of the drug based on data from clinical trials showing a reduction in amyloid beta plaques observed in patients with MCI or mild dementia stage of disease.
“Continued approval for the indication may be contingent upon verification of clinical benefit in confirmatory trial(s),” the label states. It emphasizes that there are no safety or effectiveness data on starting aducanumab treatment at earlier or later stages of the disease than were studied.
“Based on our ongoing conversations with prescribing physicians, FDA, and patient advocates, we submitted this label update with the goal to further clarify the patient population that was studied across the three Aduhelm clinical trials that supported approval,” Alfred Sandrock Jr., MD, PhD, Biogen’s head of research and development, said in a statement announcing the label update.
“We are committed to continue to listen to the community’s needs as clinical practice adapts to this important, first-in-class treatment option,” said Dr. Sandrock.
A version of this article first appeared on Medscape.com.
Magnesium is strongly tied to lower risk for intracranial aneurysm
The effects may be partially mediated by magnesium’s influence on systolic blood pressure, new research suggests.
“The modifiable risk factors for intracranial aneurysm are largely unknown. Our findings provided evidence of a causal association between increased serum magnesium levels and reduced risk of intracranial aneurysm,” said Susanna Larsson, PhD, Karolinska Institutet, Stockholm.
These results suggest that raising serum magnesium levels – through a magnesium-rich diet or magnesium supplementation – “may play a role in the primary prevention of intracranial aneurysm and associated hemorrhage,” Dr. Larsson added.
The study was published online June 22 in Neurology.
Lower risk for rupture
The researchers leveraged randomly allocated genetic variants related to serum magnesium concentrations in a two-sample Mendelian randomization (MR) study to assess whether higher genetically predicted serum magnesium correlates with reduced risk for intracranial aneurysm. They also performed a multivariable MR analysis to assess the role blood pressure might play in this association.
Source data came from a genome-wide association study (GWAS) involving 23,829 individuals that previously identified five single-nucleotide polymorphisms associated with serum magnesium. Genetic association estimates for intracranial aneurysm were derived from a GWAS in 79,429 people (7,495 case patients and 71,934 control patients), and genetic association estimates for systolic blood pressure were derived from a GWAS of 757,601 individuals.
The researchers found that higher genetically predicted serum magnesium concentrations were associated with lower risk for intracranial aneurysm.
The odds ratios per 0.1 mmol/L increment in genetically predicted serum magnesium concentrations were 0.66 (95% confidence interval, 0.49-0.91) for intracranial aneurysm (unruptured and ruptured combined), 0.57 (95% CI, 0.30-1.06) for unruptured intracranial aneurysm, and 0.67 (95% CI, 0.48-0.92) for aneurysmal subarachnoid hemorrhage.
Adjustment for genetically predicted systolic blood pressure partially attenuated the associations of genetically predicted serum magnesium with all three outcomes, suggesting that magnesium’s influence was at least partially mediated by systolic blood pressure.
“In addition to a blood pressure lowering effect, increased magnesium concentrations may reduce the risk of intracranial aneurysm rupture by improving endothelial function and reducing oxidative stress,” the investigators noted.
They caution that the data were derived from people of European ancestry, which limits the generalizability to other populations. “Caution should be taken when extrapolating findings from MR to infer the effect of a clinical intervention, and clinical trials are warranted to guide optimal practice,” they added.
Critical role in vascular health
In an accompanying editorial, Joanna Pera, MD, PhD, of Jagiellonian University Medical College, Krakow, Poland, and Christopher Anderson, MD, of Brigham and Women’s Hospital, Boston, noted that the study “adds to our understanding of the importance of magnesium in vascular health particularly related to cerebral aneurysms.”
There is a need for “both mechanistic and potentially therapeutic investigation into the role that magnesium plays in subarachnoid hemorrhage,” they added.
Further, they wrote, the results “raise interesting new questions about the links between circulating magnesium, intracranial aneurysms, and blood pressure. Arterial hypertension is a well-recognized risk factor for intracranial aneurysm development and rupture. Magnesium supplementation may lower blood pressure values.
“Could this mineral prove useful in developing interventions that could prevent intracranial aneurysm development and/or rupture over and above a simple lowering of blood pressure, perhaps through pleiotropic effects on endothelial function or other mechanisms? With these results in hand, work is clearly needed to learn more about the biology of magnesium in the vascular system and in intracranial aneurysm biology in particular,” Dr. Pera and Dr. Anderson concluded.
This study was supported by the Swedish Research Council for Health, Working Life and Welfare, the British Heart Foundation Research Center of Excellence at Imperial College London, and the National Institute for Health Research Clinical Lectureship at St. George’s, University of London. Dr. Larsson has disclosed no relevant financial relationships. Study coauthor Dipender Gill, PhD, is employed part time by Novo Nordisk. Dr. Pera has disclosed no relevant financial relationships. Dr. Anderson has received research support from the Bayer AG and has consulted for ApoPharma and Invitae.
A version of this article first appeared on Medscape.com.
The effects may be partially mediated by magnesium’s influence on systolic blood pressure, new research suggests.
“The modifiable risk factors for intracranial aneurysm are largely unknown. Our findings provided evidence of a causal association between increased serum magnesium levels and reduced risk of intracranial aneurysm,” said Susanna Larsson, PhD, Karolinska Institutet, Stockholm.
These results suggest that raising serum magnesium levels – through a magnesium-rich diet or magnesium supplementation – “may play a role in the primary prevention of intracranial aneurysm and associated hemorrhage,” Dr. Larsson added.
The study was published online June 22 in Neurology.
Lower risk for rupture
The researchers leveraged randomly allocated genetic variants related to serum magnesium concentrations in a two-sample Mendelian randomization (MR) study to assess whether higher genetically predicted serum magnesium correlates with reduced risk for intracranial aneurysm. They also performed a multivariable MR analysis to assess the role blood pressure might play in this association.
Source data came from a genome-wide association study (GWAS) involving 23,829 individuals that previously identified five single-nucleotide polymorphisms associated with serum magnesium. Genetic association estimates for intracranial aneurysm were derived from a GWAS in 79,429 people (7,495 case patients and 71,934 control patients), and genetic association estimates for systolic blood pressure were derived from a GWAS of 757,601 individuals.
The researchers found that higher genetically predicted serum magnesium concentrations were associated with lower risk for intracranial aneurysm.
The odds ratios per 0.1 mmol/L increment in genetically predicted serum magnesium concentrations were 0.66 (95% confidence interval, 0.49-0.91) for intracranial aneurysm (unruptured and ruptured combined), 0.57 (95% CI, 0.30-1.06) for unruptured intracranial aneurysm, and 0.67 (95% CI, 0.48-0.92) for aneurysmal subarachnoid hemorrhage.
Adjustment for genetically predicted systolic blood pressure partially attenuated the associations of genetically predicted serum magnesium with all three outcomes, suggesting that magnesium’s influence was at least partially mediated by systolic blood pressure.
“In addition to a blood pressure lowering effect, increased magnesium concentrations may reduce the risk of intracranial aneurysm rupture by improving endothelial function and reducing oxidative stress,” the investigators noted.
They caution that the data were derived from people of European ancestry, which limits the generalizability to other populations. “Caution should be taken when extrapolating findings from MR to infer the effect of a clinical intervention, and clinical trials are warranted to guide optimal practice,” they added.
Critical role in vascular health
In an accompanying editorial, Joanna Pera, MD, PhD, of Jagiellonian University Medical College, Krakow, Poland, and Christopher Anderson, MD, of Brigham and Women’s Hospital, Boston, noted that the study “adds to our understanding of the importance of magnesium in vascular health particularly related to cerebral aneurysms.”
There is a need for “both mechanistic and potentially therapeutic investigation into the role that magnesium plays in subarachnoid hemorrhage,” they added.
Further, they wrote, the results “raise interesting new questions about the links between circulating magnesium, intracranial aneurysms, and blood pressure. Arterial hypertension is a well-recognized risk factor for intracranial aneurysm development and rupture. Magnesium supplementation may lower blood pressure values.
“Could this mineral prove useful in developing interventions that could prevent intracranial aneurysm development and/or rupture over and above a simple lowering of blood pressure, perhaps through pleiotropic effects on endothelial function or other mechanisms? With these results in hand, work is clearly needed to learn more about the biology of magnesium in the vascular system and in intracranial aneurysm biology in particular,” Dr. Pera and Dr. Anderson concluded.
This study was supported by the Swedish Research Council for Health, Working Life and Welfare, the British Heart Foundation Research Center of Excellence at Imperial College London, and the National Institute for Health Research Clinical Lectureship at St. George’s, University of London. Dr. Larsson has disclosed no relevant financial relationships. Study coauthor Dipender Gill, PhD, is employed part time by Novo Nordisk. Dr. Pera has disclosed no relevant financial relationships. Dr. Anderson has received research support from the Bayer AG and has consulted for ApoPharma and Invitae.
A version of this article first appeared on Medscape.com.
The effects may be partially mediated by magnesium’s influence on systolic blood pressure, new research suggests.
“The modifiable risk factors for intracranial aneurysm are largely unknown. Our findings provided evidence of a causal association between increased serum magnesium levels and reduced risk of intracranial aneurysm,” said Susanna Larsson, PhD, Karolinska Institutet, Stockholm.
These results suggest that raising serum magnesium levels – through a magnesium-rich diet or magnesium supplementation – “may play a role in the primary prevention of intracranial aneurysm and associated hemorrhage,” Dr. Larsson added.
The study was published online June 22 in Neurology.
Lower risk for rupture
The researchers leveraged randomly allocated genetic variants related to serum magnesium concentrations in a two-sample Mendelian randomization (MR) study to assess whether higher genetically predicted serum magnesium correlates with reduced risk for intracranial aneurysm. They also performed a multivariable MR analysis to assess the role blood pressure might play in this association.
Source data came from a genome-wide association study (GWAS) involving 23,829 individuals that previously identified five single-nucleotide polymorphisms associated with serum magnesium. Genetic association estimates for intracranial aneurysm were derived from a GWAS in 79,429 people (7,495 case patients and 71,934 control patients), and genetic association estimates for systolic blood pressure were derived from a GWAS of 757,601 individuals.
The researchers found that higher genetically predicted serum magnesium concentrations were associated with lower risk for intracranial aneurysm.
The odds ratios per 0.1 mmol/L increment in genetically predicted serum magnesium concentrations were 0.66 (95% confidence interval, 0.49-0.91) for intracranial aneurysm (unruptured and ruptured combined), 0.57 (95% CI, 0.30-1.06) for unruptured intracranial aneurysm, and 0.67 (95% CI, 0.48-0.92) for aneurysmal subarachnoid hemorrhage.
Adjustment for genetically predicted systolic blood pressure partially attenuated the associations of genetically predicted serum magnesium with all three outcomes, suggesting that magnesium’s influence was at least partially mediated by systolic blood pressure.
“In addition to a blood pressure lowering effect, increased magnesium concentrations may reduce the risk of intracranial aneurysm rupture by improving endothelial function and reducing oxidative stress,” the investigators noted.
They caution that the data were derived from people of European ancestry, which limits the generalizability to other populations. “Caution should be taken when extrapolating findings from MR to infer the effect of a clinical intervention, and clinical trials are warranted to guide optimal practice,” they added.
Critical role in vascular health
In an accompanying editorial, Joanna Pera, MD, PhD, of Jagiellonian University Medical College, Krakow, Poland, and Christopher Anderson, MD, of Brigham and Women’s Hospital, Boston, noted that the study “adds to our understanding of the importance of magnesium in vascular health particularly related to cerebral aneurysms.”
There is a need for “both mechanistic and potentially therapeutic investigation into the role that magnesium plays in subarachnoid hemorrhage,” they added.
Further, they wrote, the results “raise interesting new questions about the links between circulating magnesium, intracranial aneurysms, and blood pressure. Arterial hypertension is a well-recognized risk factor for intracranial aneurysm development and rupture. Magnesium supplementation may lower blood pressure values.
“Could this mineral prove useful in developing interventions that could prevent intracranial aneurysm development and/or rupture over and above a simple lowering of blood pressure, perhaps through pleiotropic effects on endothelial function or other mechanisms? With these results in hand, work is clearly needed to learn more about the biology of magnesium in the vascular system and in intracranial aneurysm biology in particular,” Dr. Pera and Dr. Anderson concluded.
This study was supported by the Swedish Research Council for Health, Working Life and Welfare, the British Heart Foundation Research Center of Excellence at Imperial College London, and the National Institute for Health Research Clinical Lectureship at St. George’s, University of London. Dr. Larsson has disclosed no relevant financial relationships. Study coauthor Dipender Gill, PhD, is employed part time by Novo Nordisk. Dr. Pera has disclosed no relevant financial relationships. Dr. Anderson has received research support from the Bayer AG and has consulted for ApoPharma and Invitae.
A version of this article first appeared on Medscape.com.
From Neurology
Cannabis use tied to increased risk for suicidal thoughts, actions
Young adults who use cannabis – either sporadically, daily, or those who have cannabis use disorder – have a significantly increased risk for suicidal thoughts and actions, according to U.S. national drug survey data.
The risks appear greater for women than men and remained regardless of whether the individual was depressed.
“We cannot establish that cannabis use caused increased suicidality,” Nora Volkow, MD, director, National Institute on Drug Abuse (NIDA), told this news organization.
“However, it is likely that these two factors influence one another bidirectionally, meaning people with suicidal thinking might be more vulnerable to cannabis use to self-medicate their distress, and cannabis use may trigger negative moods and suicidal thinking in some people,” said Dr. Volkow.
“It is also possible that these factors are not causally linked to one another at all but rather reflect the common and related risk factors underlying both suicidality and substance use. For instance, one’s genetics may put them at a higher risk for both suicide and for using marijuana,” she added.
The study was published online June 22 in JAMA Network Open.
Marked increase in use
Cannabis use among U.S. adults has increased markedly over the past 10 years, with a parallel increase in suicidality. However, the links between cannabis use and suicidality among young adults are poorly understood.
NIDA researchers sought to fill this gap. They examined data on 281,650 young men and women aged 18 to 34 years who participated in National Surveys on Drug Use and Health from 2008 to 2019.
Status regarding past-year cannabis use was categorized as past-year daily or near-daily use (greater than or equal to 300 days), non-daily use, and no cannabis use.
Although suicidality was associated with cannabis use, even young adults who did not use cannabis on a daily basis were more likely to have suicidal thoughts or actions than those who did not use the drug at all, the researchers found.
Among young adults without a major depressive episode, about 3% of those who did not use cannabis had suicidal ideation, compared with about 7% of non-daily cannabis users, about 9% of daily cannabis users, and 14% of those with a cannabis use disorder.
Among young adults with depression, the corresponding percentages were 35%, 44%, 53%, and 50%.
Similar trends existed for the associations between the different levels of cannabis use and suicide plan or attempt.
Women at greatest risk
Gender differences also emerged. than men with the same levels of cannabis use.
Among those without a major depressive episode, the prevalence of suicidal ideation for those with versus without a cannabis use disorder was around 14% versus 4.0% among women and 10% versus 3.0% among men.
Among young adults with both cannabis use disorder and major depressive episode, the prevalence of past-year suicide plan was 52% higher for women (24%) than for men (16%).
“Suicide is a leading cause of death among young adults in the United States, and the findings of this study offer important information that may help us reduce this risk,” lead author and NIDA researcher Beth Han, MD, PhD, MPH, said in a news release.
“Depression and cannabis use disorder are treatable conditions, and cannabis use can be modified. Through better understanding the associations of different risk factors for suicidality, we hope to offer new targets for prevention and intervention in individuals that we know may be at high risk. These findings also underscore the importance of tailoring interventions in a way that takes sex and gender into account,” said Dr. Han.
“Additional research is needed to better understand these complex associations, especially given the great burden of suicide on young adults,” said Dr. Volkow.
Gender difference ‘striking’
Commenting on the findings for this news organization, Charles B. Nemeroff, MD, PhD, professor and chair, department of psychiatry and behavioral sciences, Dell Medical School, University of Texas at Austin, said this study is “clearly of great interest; of course correlation and causality are completely distinct entities, and this study is all about correlation.
“This does not, of course, mean that cannabis use causes suicide but suggests that in individuals who use cannabis, suicidality in the broadest sense is increased in prevalence rate,” said Dr. Nemeroff, who serves as principal investigator of the Texas Child Trauma Network.
Dr. Nemeroff said “the most striking finding” was the larger effect in women than men – “striking because suicide is, in almost all cultures, higher in prevalence in men versus women.”
Dr. Nemeroff said he’d like to know more about other potential contributing factors, “which would include a history of child abuse and neglect, a major vulnerability factor for suicidality, comorbid alcohol and other substance abuse, [and] comorbid psychiatric diagnosis such as posttraumatic stress disorder.”
The study was sponsored by NIDA, of the National Institutes of Health. Dr. Volkow, Dr. Han, and Dr. Nemeroff have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Young adults who use cannabis – either sporadically, daily, or those who have cannabis use disorder – have a significantly increased risk for suicidal thoughts and actions, according to U.S. national drug survey data.
The risks appear greater for women than men and remained regardless of whether the individual was depressed.
“We cannot establish that cannabis use caused increased suicidality,” Nora Volkow, MD, director, National Institute on Drug Abuse (NIDA), told this news organization.
“However, it is likely that these two factors influence one another bidirectionally, meaning people with suicidal thinking might be more vulnerable to cannabis use to self-medicate their distress, and cannabis use may trigger negative moods and suicidal thinking in some people,” said Dr. Volkow.
“It is also possible that these factors are not causally linked to one another at all but rather reflect the common and related risk factors underlying both suicidality and substance use. For instance, one’s genetics may put them at a higher risk for both suicide and for using marijuana,” she added.
The study was published online June 22 in JAMA Network Open.
Marked increase in use
Cannabis use among U.S. adults has increased markedly over the past 10 years, with a parallel increase in suicidality. However, the links between cannabis use and suicidality among young adults are poorly understood.
NIDA researchers sought to fill this gap. They examined data on 281,650 young men and women aged 18 to 34 years who participated in National Surveys on Drug Use and Health from 2008 to 2019.
Status regarding past-year cannabis use was categorized as past-year daily or near-daily use (greater than or equal to 300 days), non-daily use, and no cannabis use.
Although suicidality was associated with cannabis use, even young adults who did not use cannabis on a daily basis were more likely to have suicidal thoughts or actions than those who did not use the drug at all, the researchers found.
Among young adults without a major depressive episode, about 3% of those who did not use cannabis had suicidal ideation, compared with about 7% of non-daily cannabis users, about 9% of daily cannabis users, and 14% of those with a cannabis use disorder.
Among young adults with depression, the corresponding percentages were 35%, 44%, 53%, and 50%.
Similar trends existed for the associations between the different levels of cannabis use and suicide plan or attempt.
Women at greatest risk
Gender differences also emerged. than men with the same levels of cannabis use.
Among those without a major depressive episode, the prevalence of suicidal ideation for those with versus without a cannabis use disorder was around 14% versus 4.0% among women and 10% versus 3.0% among men.
Among young adults with both cannabis use disorder and major depressive episode, the prevalence of past-year suicide plan was 52% higher for women (24%) than for men (16%).
“Suicide is a leading cause of death among young adults in the United States, and the findings of this study offer important information that may help us reduce this risk,” lead author and NIDA researcher Beth Han, MD, PhD, MPH, said in a news release.
“Depression and cannabis use disorder are treatable conditions, and cannabis use can be modified. Through better understanding the associations of different risk factors for suicidality, we hope to offer new targets for prevention and intervention in individuals that we know may be at high risk. These findings also underscore the importance of tailoring interventions in a way that takes sex and gender into account,” said Dr. Han.
“Additional research is needed to better understand these complex associations, especially given the great burden of suicide on young adults,” said Dr. Volkow.
Gender difference ‘striking’
Commenting on the findings for this news organization, Charles B. Nemeroff, MD, PhD, professor and chair, department of psychiatry and behavioral sciences, Dell Medical School, University of Texas at Austin, said this study is “clearly of great interest; of course correlation and causality are completely distinct entities, and this study is all about correlation.
“This does not, of course, mean that cannabis use causes suicide but suggests that in individuals who use cannabis, suicidality in the broadest sense is increased in prevalence rate,” said Dr. Nemeroff, who serves as principal investigator of the Texas Child Trauma Network.
Dr. Nemeroff said “the most striking finding” was the larger effect in women than men – “striking because suicide is, in almost all cultures, higher in prevalence in men versus women.”
Dr. Nemeroff said he’d like to know more about other potential contributing factors, “which would include a history of child abuse and neglect, a major vulnerability factor for suicidality, comorbid alcohol and other substance abuse, [and] comorbid psychiatric diagnosis such as posttraumatic stress disorder.”
The study was sponsored by NIDA, of the National Institutes of Health. Dr. Volkow, Dr. Han, and Dr. Nemeroff have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Young adults who use cannabis – either sporadically, daily, or those who have cannabis use disorder – have a significantly increased risk for suicidal thoughts and actions, according to U.S. national drug survey data.
The risks appear greater for women than men and remained regardless of whether the individual was depressed.
“We cannot establish that cannabis use caused increased suicidality,” Nora Volkow, MD, director, National Institute on Drug Abuse (NIDA), told this news organization.
“However, it is likely that these two factors influence one another bidirectionally, meaning people with suicidal thinking might be more vulnerable to cannabis use to self-medicate their distress, and cannabis use may trigger negative moods and suicidal thinking in some people,” said Dr. Volkow.
“It is also possible that these factors are not causally linked to one another at all but rather reflect the common and related risk factors underlying both suicidality and substance use. For instance, one’s genetics may put them at a higher risk for both suicide and for using marijuana,” she added.
The study was published online June 22 in JAMA Network Open.
Marked increase in use
Cannabis use among U.S. adults has increased markedly over the past 10 years, with a parallel increase in suicidality. However, the links between cannabis use and suicidality among young adults are poorly understood.
NIDA researchers sought to fill this gap. They examined data on 281,650 young men and women aged 18 to 34 years who participated in National Surveys on Drug Use and Health from 2008 to 2019.
Status regarding past-year cannabis use was categorized as past-year daily or near-daily use (greater than or equal to 300 days), non-daily use, and no cannabis use.
Although suicidality was associated with cannabis use, even young adults who did not use cannabis on a daily basis were more likely to have suicidal thoughts or actions than those who did not use the drug at all, the researchers found.
Among young adults without a major depressive episode, about 3% of those who did not use cannabis had suicidal ideation, compared with about 7% of non-daily cannabis users, about 9% of daily cannabis users, and 14% of those with a cannabis use disorder.
Among young adults with depression, the corresponding percentages were 35%, 44%, 53%, and 50%.
Similar trends existed for the associations between the different levels of cannabis use and suicide plan or attempt.
Women at greatest risk
Gender differences also emerged. than men with the same levels of cannabis use.
Among those without a major depressive episode, the prevalence of suicidal ideation for those with versus without a cannabis use disorder was around 14% versus 4.0% among women and 10% versus 3.0% among men.
Among young adults with both cannabis use disorder and major depressive episode, the prevalence of past-year suicide plan was 52% higher for women (24%) than for men (16%).
“Suicide is a leading cause of death among young adults in the United States, and the findings of this study offer important information that may help us reduce this risk,” lead author and NIDA researcher Beth Han, MD, PhD, MPH, said in a news release.
“Depression and cannabis use disorder are treatable conditions, and cannabis use can be modified. Through better understanding the associations of different risk factors for suicidality, we hope to offer new targets for prevention and intervention in individuals that we know may be at high risk. These findings also underscore the importance of tailoring interventions in a way that takes sex and gender into account,” said Dr. Han.
“Additional research is needed to better understand these complex associations, especially given the great burden of suicide on young adults,” said Dr. Volkow.
Gender difference ‘striking’
Commenting on the findings for this news organization, Charles B. Nemeroff, MD, PhD, professor and chair, department of psychiatry and behavioral sciences, Dell Medical School, University of Texas at Austin, said this study is “clearly of great interest; of course correlation and causality are completely distinct entities, and this study is all about correlation.
“This does not, of course, mean that cannabis use causes suicide but suggests that in individuals who use cannabis, suicidality in the broadest sense is increased in prevalence rate,” said Dr. Nemeroff, who serves as principal investigator of the Texas Child Trauma Network.
Dr. Nemeroff said “the most striking finding” was the larger effect in women than men – “striking because suicide is, in almost all cultures, higher in prevalence in men versus women.”
Dr. Nemeroff said he’d like to know more about other potential contributing factors, “which would include a history of child abuse and neglect, a major vulnerability factor for suicidality, comorbid alcohol and other substance abuse, [and] comorbid psychiatric diagnosis such as posttraumatic stress disorder.”
The study was sponsored by NIDA, of the National Institutes of Health. Dr. Volkow, Dr. Han, and Dr. Nemeroff have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FDA fast-tracks lecanemab for Alzheimer’s disease
Lecanemab (formerly BAN2401) is a humanized monoclonal antibody that selectively binds to large, soluble aggregated Abeta protofibrils. The antibody was developed following the discovery of a mutation in amyloid precursor protein that leads to a form of Alzheimer’s disease that is marked by particularly high levels of Abeta protofibrils.
“As such, lecanemab may have the potential to have an effect on disease pathology and to slow down the progression of the disease,” Eisai and Biogen said in a joint news release.
The breakthrough therapy designation for lecanemab is based on results of a randomized, double-blind, phase 2b proof-of-concept study published April 17 in Alzheimer’s Research & Therapy.
The study enrolled 856 patients with mild cognitive impairment (MCI) due to Alzheimer’s disease and mild Alzheimer’s disease with confirmed presence of amyloid pathology.
At the highest doses, treatment with lecanemab led to a reduction in brain amyloid accompanied by a consistent reduction of clinical decline across several clinical and biomarker endpoints.
Phase 3 testing underway
In March, Eisai and Biogen completed enrollment in a phase 3 study designed to confirm the safety and efficacy of lecanemab in patients with symptomatic early Alzheimer’s disease.
The CLARITY AD study includes 1,795 patients with early Alzheimer’s disease, and initial results are expected by the end of September 2022. The core study will compare lecanemab against placebo on the change from baseline in the Clinical Dementia Rating-Sum of Boxes (CDR-SB) at 18 months. The study will also evaluate the long-term safety and tolerability of lecanemab in the extension phase and whether the long-term effects of lecanemab, as measured by the CDR-SB at the end of the core study, are maintained over time.
Additionally, the phase 3 AHEAD 3-45 clinical study is currently exploring lecanemab in adults with preclinical Alzheimer’s disease (clinically normal but with intermediate or elevated brain amyloid).
On June 7, the FDA – amid significant controversy – approved aducanumab (Aduhelm), the first anti-amyloid agent for the treatment Alzheimer’s disease, disregarding the recommendation by its own advisory panel not to approve the drug. Three members of the FDA’s Peripheral and Central Nervous System Drugs Advisory Committee subsequently resigned in protest following the agency’s approval of aducanumab.
In addition, the high-profile consumer advocacy group Public Citizen sent a letter to the secretary of the U.S. Department of Health & Human Services demanding the removal of three FDA officials, including acting FDA Commissioner Janet Woodcock, MD.
A version of this article first appeared on Medscape.com.
Lecanemab (formerly BAN2401) is a humanized monoclonal antibody that selectively binds to large, soluble aggregated Abeta protofibrils. The antibody was developed following the discovery of a mutation in amyloid precursor protein that leads to a form of Alzheimer’s disease that is marked by particularly high levels of Abeta protofibrils.
“As such, lecanemab may have the potential to have an effect on disease pathology and to slow down the progression of the disease,” Eisai and Biogen said in a joint news release.
The breakthrough therapy designation for lecanemab is based on results of a randomized, double-blind, phase 2b proof-of-concept study published April 17 in Alzheimer’s Research & Therapy.
The study enrolled 856 patients with mild cognitive impairment (MCI) due to Alzheimer’s disease and mild Alzheimer’s disease with confirmed presence of amyloid pathology.
At the highest doses, treatment with lecanemab led to a reduction in brain amyloid accompanied by a consistent reduction of clinical decline across several clinical and biomarker endpoints.
Phase 3 testing underway
In March, Eisai and Biogen completed enrollment in a phase 3 study designed to confirm the safety and efficacy of lecanemab in patients with symptomatic early Alzheimer’s disease.
The CLARITY AD study includes 1,795 patients with early Alzheimer’s disease, and initial results are expected by the end of September 2022. The core study will compare lecanemab against placebo on the change from baseline in the Clinical Dementia Rating-Sum of Boxes (CDR-SB) at 18 months. The study will also evaluate the long-term safety and tolerability of lecanemab in the extension phase and whether the long-term effects of lecanemab, as measured by the CDR-SB at the end of the core study, are maintained over time.
Additionally, the phase 3 AHEAD 3-45 clinical study is currently exploring lecanemab in adults with preclinical Alzheimer’s disease (clinically normal but with intermediate or elevated brain amyloid).
On June 7, the FDA – amid significant controversy – approved aducanumab (Aduhelm), the first anti-amyloid agent for the treatment Alzheimer’s disease, disregarding the recommendation by its own advisory panel not to approve the drug. Three members of the FDA’s Peripheral and Central Nervous System Drugs Advisory Committee subsequently resigned in protest following the agency’s approval of aducanumab.
In addition, the high-profile consumer advocacy group Public Citizen sent a letter to the secretary of the U.S. Department of Health & Human Services demanding the removal of three FDA officials, including acting FDA Commissioner Janet Woodcock, MD.
A version of this article first appeared on Medscape.com.
Lecanemab (formerly BAN2401) is a humanized monoclonal antibody that selectively binds to large, soluble aggregated Abeta protofibrils. The antibody was developed following the discovery of a mutation in amyloid precursor protein that leads to a form of Alzheimer’s disease that is marked by particularly high levels of Abeta protofibrils.
“As such, lecanemab may have the potential to have an effect on disease pathology and to slow down the progression of the disease,” Eisai and Biogen said in a joint news release.
The breakthrough therapy designation for lecanemab is based on results of a randomized, double-blind, phase 2b proof-of-concept study published April 17 in Alzheimer’s Research & Therapy.
The study enrolled 856 patients with mild cognitive impairment (MCI) due to Alzheimer’s disease and mild Alzheimer’s disease with confirmed presence of amyloid pathology.
At the highest doses, treatment with lecanemab led to a reduction in brain amyloid accompanied by a consistent reduction of clinical decline across several clinical and biomarker endpoints.
Phase 3 testing underway
In March, Eisai and Biogen completed enrollment in a phase 3 study designed to confirm the safety and efficacy of lecanemab in patients with symptomatic early Alzheimer’s disease.
The CLARITY AD study includes 1,795 patients with early Alzheimer’s disease, and initial results are expected by the end of September 2022. The core study will compare lecanemab against placebo on the change from baseline in the Clinical Dementia Rating-Sum of Boxes (CDR-SB) at 18 months. The study will also evaluate the long-term safety and tolerability of lecanemab in the extension phase and whether the long-term effects of lecanemab, as measured by the CDR-SB at the end of the core study, are maintained over time.
Additionally, the phase 3 AHEAD 3-45 clinical study is currently exploring lecanemab in adults with preclinical Alzheimer’s disease (clinically normal but with intermediate or elevated brain amyloid).
On June 7, the FDA – amid significant controversy – approved aducanumab (Aduhelm), the first anti-amyloid agent for the treatment Alzheimer’s disease, disregarding the recommendation by its own advisory panel not to approve the drug. Three members of the FDA’s Peripheral and Central Nervous System Drugs Advisory Committee subsequently resigned in protest following the agency’s approval of aducanumab.
In addition, the high-profile consumer advocacy group Public Citizen sent a letter to the secretary of the U.S. Department of Health & Human Services demanding the removal of three FDA officials, including acting FDA Commissioner Janet Woodcock, MD.
A version of this article first appeared on Medscape.com.
Profound brain changes found in patients who died of COVID-19
The most comprehensive molecular study to date of brain tissue from people who died of COVID-19 provides clear evidence that SARS-CoV-2 causes profound molecular changes in the brain, despite no molecular trace of the virus in brain tissue.
“The signature the virus leaves in the brain speaks of strong inflammation and disrupted brain circuits and resembles signatures the field has observed in Alzheimer’s or other neurodegenerative diseases,” senior author Tony Wyss-Coray, PhD, professor of neurology and neurological sciences, Stanford (Calif.) University, told this news organization.
The study was published online June 21 in Nature.
Signs of distress
“We know that up to a third of SARS-CoV-2-infected people show brain symptoms including brain fog, memory problems, and fatigue, and a growing number of people have such symptoms long after they [have] seemingly recovered from virus infection,” said Dr. Wyss-Coray.
“However, we have very little understanding of how the virus causes these symptoms and what its effects are on the brain at a molecular level,” he added.
Using single-cell RNA sequencing, the researchers profiled the transcriptomes of 65,309 nuclei isolated from frontal cortex and choroid plexus samples from eight patients who died of COVID-19 and 14 controls who died of other causes.
There was no molecular evidence of SARS-CoV-2 in brain tissue samples from the patients who died of COVID-19.
Yet, “we were very surprised to learn that no matter which type of cell we studied (different types of nerve cells, immune cells, or different support cells in the brain) there were prominent changes” compared with brain tissue samples from controls who died of other causes, said Dr. Wyss-Coray.
The changes in the COVID-19 brains showed signatures of inflammation, abnormal nerve cell communication, and chronic neurodegeneration.
“Across cell types, COVID-19 perturbations overlap with those in chronic brain disorders and reside in genetic variants associated with cognition, schizophrenia, and depression,” the researchers report.
“Viral infection appears to trigger inflammatory responses throughout the body that may cause inflammatory signaling across the blood–brain barrier, which in turn could ‘trip off’ neuroinflammation in the brain,” Dr. Wyss-Coray said.
The findings may help explain the brain fog, fatigue, and other neurological and psychiatric symptoms of long COVID.
“While we studied only brains from people who died of COVID-19, we believe it is likely that similar, but hopefully weaker, signs of inflammation and chronic neurodegeneration will be found in COVID-19 survivors, especially those with chronic brain symptoms,” Dr. Wyss-Coray said.
This research was funded by the Nomis Foundation, the National Institutes of Health, Nan Fung Life Sciences, the Wu Tsai Neurosciences Institute and the Stanford Alzheimer’s Disease Research Center. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The most comprehensive molecular study to date of brain tissue from people who died of COVID-19 provides clear evidence that SARS-CoV-2 causes profound molecular changes in the brain, despite no molecular trace of the virus in brain tissue.
“The signature the virus leaves in the brain speaks of strong inflammation and disrupted brain circuits and resembles signatures the field has observed in Alzheimer’s or other neurodegenerative diseases,” senior author Tony Wyss-Coray, PhD, professor of neurology and neurological sciences, Stanford (Calif.) University, told this news organization.
The study was published online June 21 in Nature.
Signs of distress
“We know that up to a third of SARS-CoV-2-infected people show brain symptoms including brain fog, memory problems, and fatigue, and a growing number of people have such symptoms long after they [have] seemingly recovered from virus infection,” said Dr. Wyss-Coray.
“However, we have very little understanding of how the virus causes these symptoms and what its effects are on the brain at a molecular level,” he added.
Using single-cell RNA sequencing, the researchers profiled the transcriptomes of 65,309 nuclei isolated from frontal cortex and choroid plexus samples from eight patients who died of COVID-19 and 14 controls who died of other causes.
There was no molecular evidence of SARS-CoV-2 in brain tissue samples from the patients who died of COVID-19.
Yet, “we were very surprised to learn that no matter which type of cell we studied (different types of nerve cells, immune cells, or different support cells in the brain) there were prominent changes” compared with brain tissue samples from controls who died of other causes, said Dr. Wyss-Coray.
The changes in the COVID-19 brains showed signatures of inflammation, abnormal nerve cell communication, and chronic neurodegeneration.
“Across cell types, COVID-19 perturbations overlap with those in chronic brain disorders and reside in genetic variants associated with cognition, schizophrenia, and depression,” the researchers report.
“Viral infection appears to trigger inflammatory responses throughout the body that may cause inflammatory signaling across the blood–brain barrier, which in turn could ‘trip off’ neuroinflammation in the brain,” Dr. Wyss-Coray said.
The findings may help explain the brain fog, fatigue, and other neurological and psychiatric symptoms of long COVID.
“While we studied only brains from people who died of COVID-19, we believe it is likely that similar, but hopefully weaker, signs of inflammation and chronic neurodegeneration will be found in COVID-19 survivors, especially those with chronic brain symptoms,” Dr. Wyss-Coray said.
This research was funded by the Nomis Foundation, the National Institutes of Health, Nan Fung Life Sciences, the Wu Tsai Neurosciences Institute and the Stanford Alzheimer’s Disease Research Center. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The most comprehensive molecular study to date of brain tissue from people who died of COVID-19 provides clear evidence that SARS-CoV-2 causes profound molecular changes in the brain, despite no molecular trace of the virus in brain tissue.
“The signature the virus leaves in the brain speaks of strong inflammation and disrupted brain circuits and resembles signatures the field has observed in Alzheimer’s or other neurodegenerative diseases,” senior author Tony Wyss-Coray, PhD, professor of neurology and neurological sciences, Stanford (Calif.) University, told this news organization.
The study was published online June 21 in Nature.
Signs of distress
“We know that up to a third of SARS-CoV-2-infected people show brain symptoms including brain fog, memory problems, and fatigue, and a growing number of people have such symptoms long after they [have] seemingly recovered from virus infection,” said Dr. Wyss-Coray.
“However, we have very little understanding of how the virus causes these symptoms and what its effects are on the brain at a molecular level,” he added.
Using single-cell RNA sequencing, the researchers profiled the transcriptomes of 65,309 nuclei isolated from frontal cortex and choroid plexus samples from eight patients who died of COVID-19 and 14 controls who died of other causes.
There was no molecular evidence of SARS-CoV-2 in brain tissue samples from the patients who died of COVID-19.
Yet, “we were very surprised to learn that no matter which type of cell we studied (different types of nerve cells, immune cells, or different support cells in the brain) there were prominent changes” compared with brain tissue samples from controls who died of other causes, said Dr. Wyss-Coray.
The changes in the COVID-19 brains showed signatures of inflammation, abnormal nerve cell communication, and chronic neurodegeneration.
“Across cell types, COVID-19 perturbations overlap with those in chronic brain disorders and reside in genetic variants associated with cognition, schizophrenia, and depression,” the researchers report.
“Viral infection appears to trigger inflammatory responses throughout the body that may cause inflammatory signaling across the blood–brain barrier, which in turn could ‘trip off’ neuroinflammation in the brain,” Dr. Wyss-Coray said.
The findings may help explain the brain fog, fatigue, and other neurological and psychiatric symptoms of long COVID.
“While we studied only brains from people who died of COVID-19, we believe it is likely that similar, but hopefully weaker, signs of inflammation and chronic neurodegeneration will be found in COVID-19 survivors, especially those with chronic brain symptoms,” Dr. Wyss-Coray said.
This research was funded by the Nomis Foundation, the National Institutes of Health, Nan Fung Life Sciences, the Wu Tsai Neurosciences Institute and the Stanford Alzheimer’s Disease Research Center. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Key driver of fish oil’s antidepressant effects revealed
A key molecular mechanism underpinning the anti-inflammatory, antidepressant, and neuroprotective effects of omega-3 fatty acids has been identified. In findings that could lead to the development of new treatments for depression, the research provides the “first evidence” that hippocampal neurons are able to produce two key lipid metabolites of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) – lipoxygenase and cytochrome P450, lead investigator Alessandra Borsini, PhD, told this news organization.
This is how EPA and DHA exert their anti-inflammatory and neurogenic properties in vitro, as well as antidepressant properties in patients with depression, said Dr. Borsini, from King’s College London.
“Indeed, we found evidence for a correlation between increased levels of these metabolites and a decrease in severity of depressive symptoms in patients with major depressive disorder,” Dr. Borsini said.
The study was published online June 16 in Molecular Psychiatry.
‘Depression in a dish’
Despite the known role of inflammation in depression, there remains a lack of data showing anti-inflammatory strategies that are effective, safe for everyday use, and with a clear mechanism of action, the researchers note.
Dr. Borsini and colleagues tested the theory that when EPA and DHA are metabolized, some of their metabolites, or lipid mediators, can protect the brain from the harmful effects of inflammation. They used a validated “depression in a dish” in vitro human hippocampal cell model to test their theory.
They found that treating human hippocampal cells with EPA or DHA before exposing them to cytokines prevented increased cell death and decreased neurogenesis. Both these impacts had been previously observed in cells exposed to cytokines alone.
They confirmed that these effects were mediated by the formation of several key lipid mediators produced by EPA and DHA – namely hydroxyeicosapentaenoic acid, hydroxydocosahexaenoic acid, epoxyeicosatetraenoic acid (EpETE), and epoxydocosapentaenoic acid (EpDPA).
It’s the first time these lipid mediators were detected in human hippocampal neurons, the researchers say.
They also found that treating the neurons with an enzyme inhibitor increased the availability of two of these metabolites (EpETE and EpDPA), suggesting a possible way by which future treatments could be optimized.
The findings were replicated in 22 patients with major depression given either EPA (3 g/day) or DHA (1.4 g/day) for 12 weeks. In both groups, EPA or DHA treatment was associated with an increase in their respective metabolites and significant improvement in depressive symptoms.
The average reduction in symptom scores was 64% and 71% in the EPA and DHA groups, respectively, and there was some evidence that higher levels of the same metabolites correlated with less severe depressive symptoms.
“For some time we have known that omega-3 [polyunsaturated fatty acid (PUFA)] can induce antidepressant and anti-inflammatory effects, but, without further understanding of how this happens in the human brain, it has been difficult to develop treatments,” Dr. Borsini said in a news release.
“ which can inform the development of potential new treatments for depression using omega-3 PUFA,” Dr. Borsini added.
“We need to be cautious when interpreting data generated from the correlation between levels of metabolites and depressive symptoms as findings require further validation in a bigger sample of patients,” Dr. Borsini said.
“It is important to highlight that our research has not shown that by simply increasing omega-3 fatty acids in our diets or through taking nutritional supplements we can reduce inflammation or depression,” study author Carmine Pariante, MD, PhD, from King’s College London, said in the news release.
“The mechanisms behind the associations between depression and omega-3 PUFA are complicated and require further research and clinical trials to fully understand how they work and inform future therapeutic approaches,” Dr. Pariante said.
No clinical implications
Weighing in on this research in a Science Media Centre statement, Kevin McConway, emeritus professor of applied statistics, The Open University, Milton Keynes, United Kingdom, said, “The point of the study was to throw some light on the mechanisms in the body by which omega-3 fatty acids might work to reduce inflammation or depression.”
“The research mostly involved cells in laboratory dishes, but it also involved treating a small sample of patients with major depression by giving them supplements of one or other of the two omega-3 acids under investigation for 12 weeks,” he noted.
“The researchers found that the patients’ average scores on a standard set of questions, used to diagnose and measure depression, improved over that 12-week period, for each of the two fatty acids.
While depression symptoms improved over 12 weeks with omega-3 fatty acid treatment, “depression symptoms change over time anyway, for many reasons,” and depressive symptoms might have improved over 12 weeks even if the patients had not been given the omega-3 acids, Dr. McConway said.
“We just can’t tell since every patient got omega-3 fatty acids. So these results can hint that omega-3 fatty acids might help in depression, but it comes nowhere near showing that this is the case with a reasonable degree of certainty,” he cautioned.
“Indeed the researchers did not carry out this part of their study to see whether the omega-3 supplements help with depression – they did it to see whether the biochemical changes that they had seen in cell cultures in the lab might also occur in human bodies,” he noted.
This research was funded in part by grants to the investigators from the U.K. Medical Research Council, the European Commission Horizon 2020, and the National Institute for Health Research (NIHR), Maudsley Biomedical Research Centre (BRC) at South London and Maudsley NHS Foundation Trust and King’s College London. Dr. Borsini has received research funding from Johnson & Johnson for research on depression and inflammation. Dr. McConway is a trustee of the Science Media Centre and a member of its advisory committee.
A version of this article first appeared on Medscape.com.
A key molecular mechanism underpinning the anti-inflammatory, antidepressant, and neuroprotective effects of omega-3 fatty acids has been identified. In findings that could lead to the development of new treatments for depression, the research provides the “first evidence” that hippocampal neurons are able to produce two key lipid metabolites of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) – lipoxygenase and cytochrome P450, lead investigator Alessandra Borsini, PhD, told this news organization.
This is how EPA and DHA exert their anti-inflammatory and neurogenic properties in vitro, as well as antidepressant properties in patients with depression, said Dr. Borsini, from King’s College London.
“Indeed, we found evidence for a correlation between increased levels of these metabolites and a decrease in severity of depressive symptoms in patients with major depressive disorder,” Dr. Borsini said.
The study was published online June 16 in Molecular Psychiatry.
‘Depression in a dish’
Despite the known role of inflammation in depression, there remains a lack of data showing anti-inflammatory strategies that are effective, safe for everyday use, and with a clear mechanism of action, the researchers note.
Dr. Borsini and colleagues tested the theory that when EPA and DHA are metabolized, some of their metabolites, or lipid mediators, can protect the brain from the harmful effects of inflammation. They used a validated “depression in a dish” in vitro human hippocampal cell model to test their theory.
They found that treating human hippocampal cells with EPA or DHA before exposing them to cytokines prevented increased cell death and decreased neurogenesis. Both these impacts had been previously observed in cells exposed to cytokines alone.
They confirmed that these effects were mediated by the formation of several key lipid mediators produced by EPA and DHA – namely hydroxyeicosapentaenoic acid, hydroxydocosahexaenoic acid, epoxyeicosatetraenoic acid (EpETE), and epoxydocosapentaenoic acid (EpDPA).
It’s the first time these lipid mediators were detected in human hippocampal neurons, the researchers say.
They also found that treating the neurons with an enzyme inhibitor increased the availability of two of these metabolites (EpETE and EpDPA), suggesting a possible way by which future treatments could be optimized.
The findings were replicated in 22 patients with major depression given either EPA (3 g/day) or DHA (1.4 g/day) for 12 weeks. In both groups, EPA or DHA treatment was associated with an increase in their respective metabolites and significant improvement in depressive symptoms.
The average reduction in symptom scores was 64% and 71% in the EPA and DHA groups, respectively, and there was some evidence that higher levels of the same metabolites correlated with less severe depressive symptoms.
“For some time we have known that omega-3 [polyunsaturated fatty acid (PUFA)] can induce antidepressant and anti-inflammatory effects, but, without further understanding of how this happens in the human brain, it has been difficult to develop treatments,” Dr. Borsini said in a news release.
“ which can inform the development of potential new treatments for depression using omega-3 PUFA,” Dr. Borsini added.
“We need to be cautious when interpreting data generated from the correlation between levels of metabolites and depressive symptoms as findings require further validation in a bigger sample of patients,” Dr. Borsini said.
“It is important to highlight that our research has not shown that by simply increasing omega-3 fatty acids in our diets or through taking nutritional supplements we can reduce inflammation or depression,” study author Carmine Pariante, MD, PhD, from King’s College London, said in the news release.
“The mechanisms behind the associations between depression and omega-3 PUFA are complicated and require further research and clinical trials to fully understand how they work and inform future therapeutic approaches,” Dr. Pariante said.
No clinical implications
Weighing in on this research in a Science Media Centre statement, Kevin McConway, emeritus professor of applied statistics, The Open University, Milton Keynes, United Kingdom, said, “The point of the study was to throw some light on the mechanisms in the body by which omega-3 fatty acids might work to reduce inflammation or depression.”
“The research mostly involved cells in laboratory dishes, but it also involved treating a small sample of patients with major depression by giving them supplements of one or other of the two omega-3 acids under investigation for 12 weeks,” he noted.
“The researchers found that the patients’ average scores on a standard set of questions, used to diagnose and measure depression, improved over that 12-week period, for each of the two fatty acids.
While depression symptoms improved over 12 weeks with omega-3 fatty acid treatment, “depression symptoms change over time anyway, for many reasons,” and depressive symptoms might have improved over 12 weeks even if the patients had not been given the omega-3 acids, Dr. McConway said.
“We just can’t tell since every patient got omega-3 fatty acids. So these results can hint that omega-3 fatty acids might help in depression, but it comes nowhere near showing that this is the case with a reasonable degree of certainty,” he cautioned.
“Indeed the researchers did not carry out this part of their study to see whether the omega-3 supplements help with depression – they did it to see whether the biochemical changes that they had seen in cell cultures in the lab might also occur in human bodies,” he noted.
This research was funded in part by grants to the investigators from the U.K. Medical Research Council, the European Commission Horizon 2020, and the National Institute for Health Research (NIHR), Maudsley Biomedical Research Centre (BRC) at South London and Maudsley NHS Foundation Trust and King’s College London. Dr. Borsini has received research funding from Johnson & Johnson for research on depression and inflammation. Dr. McConway is a trustee of the Science Media Centre and a member of its advisory committee.
A version of this article first appeared on Medscape.com.
A key molecular mechanism underpinning the anti-inflammatory, antidepressant, and neuroprotective effects of omega-3 fatty acids has been identified. In findings that could lead to the development of new treatments for depression, the research provides the “first evidence” that hippocampal neurons are able to produce two key lipid metabolites of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) – lipoxygenase and cytochrome P450, lead investigator Alessandra Borsini, PhD, told this news organization.
This is how EPA and DHA exert their anti-inflammatory and neurogenic properties in vitro, as well as antidepressant properties in patients with depression, said Dr. Borsini, from King’s College London.
“Indeed, we found evidence for a correlation between increased levels of these metabolites and a decrease in severity of depressive symptoms in patients with major depressive disorder,” Dr. Borsini said.
The study was published online June 16 in Molecular Psychiatry.
‘Depression in a dish’
Despite the known role of inflammation in depression, there remains a lack of data showing anti-inflammatory strategies that are effective, safe for everyday use, and with a clear mechanism of action, the researchers note.
Dr. Borsini and colleagues tested the theory that when EPA and DHA are metabolized, some of their metabolites, or lipid mediators, can protect the brain from the harmful effects of inflammation. They used a validated “depression in a dish” in vitro human hippocampal cell model to test their theory.
They found that treating human hippocampal cells with EPA or DHA before exposing them to cytokines prevented increased cell death and decreased neurogenesis. Both these impacts had been previously observed in cells exposed to cytokines alone.
They confirmed that these effects were mediated by the formation of several key lipid mediators produced by EPA and DHA – namely hydroxyeicosapentaenoic acid, hydroxydocosahexaenoic acid, epoxyeicosatetraenoic acid (EpETE), and epoxydocosapentaenoic acid (EpDPA).
It’s the first time these lipid mediators were detected in human hippocampal neurons, the researchers say.
They also found that treating the neurons with an enzyme inhibitor increased the availability of two of these metabolites (EpETE and EpDPA), suggesting a possible way by which future treatments could be optimized.
The findings were replicated in 22 patients with major depression given either EPA (3 g/day) or DHA (1.4 g/day) for 12 weeks. In both groups, EPA or DHA treatment was associated with an increase in their respective metabolites and significant improvement in depressive symptoms.
The average reduction in symptom scores was 64% and 71% in the EPA and DHA groups, respectively, and there was some evidence that higher levels of the same metabolites correlated with less severe depressive symptoms.
“For some time we have known that omega-3 [polyunsaturated fatty acid (PUFA)] can induce antidepressant and anti-inflammatory effects, but, without further understanding of how this happens in the human brain, it has been difficult to develop treatments,” Dr. Borsini said in a news release.
“ which can inform the development of potential new treatments for depression using omega-3 PUFA,” Dr. Borsini added.
“We need to be cautious when interpreting data generated from the correlation between levels of metabolites and depressive symptoms as findings require further validation in a bigger sample of patients,” Dr. Borsini said.
“It is important to highlight that our research has not shown that by simply increasing omega-3 fatty acids in our diets or through taking nutritional supplements we can reduce inflammation or depression,” study author Carmine Pariante, MD, PhD, from King’s College London, said in the news release.
“The mechanisms behind the associations between depression and omega-3 PUFA are complicated and require further research and clinical trials to fully understand how they work and inform future therapeutic approaches,” Dr. Pariante said.
No clinical implications
Weighing in on this research in a Science Media Centre statement, Kevin McConway, emeritus professor of applied statistics, The Open University, Milton Keynes, United Kingdom, said, “The point of the study was to throw some light on the mechanisms in the body by which omega-3 fatty acids might work to reduce inflammation or depression.”
“The research mostly involved cells in laboratory dishes, but it also involved treating a small sample of patients with major depression by giving them supplements of one or other of the two omega-3 acids under investigation for 12 weeks,” he noted.
“The researchers found that the patients’ average scores on a standard set of questions, used to diagnose and measure depression, improved over that 12-week period, for each of the two fatty acids.
While depression symptoms improved over 12 weeks with omega-3 fatty acid treatment, “depression symptoms change over time anyway, for many reasons,” and depressive symptoms might have improved over 12 weeks even if the patients had not been given the omega-3 acids, Dr. McConway said.
“We just can’t tell since every patient got omega-3 fatty acids. So these results can hint that omega-3 fatty acids might help in depression, but it comes nowhere near showing that this is the case with a reasonable degree of certainty,” he cautioned.
“Indeed the researchers did not carry out this part of their study to see whether the omega-3 supplements help with depression – they did it to see whether the biochemical changes that they had seen in cell cultures in the lab might also occur in human bodies,” he noted.
This research was funded in part by grants to the investigators from the U.K. Medical Research Council, the European Commission Horizon 2020, and the National Institute for Health Research (NIHR), Maudsley Biomedical Research Centre (BRC) at South London and Maudsley NHS Foundation Trust and King’s College London. Dr. Borsini has received research funding from Johnson & Johnson for research on depression and inflammation. Dr. McConway is a trustee of the Science Media Centre and a member of its advisory committee.
A version of this article first appeared on Medscape.com.
Does vitamin D deficiency play a role in opioid addiction?
Vitamin D deficiency amplifies the craving for, and the effects of, opioids, potentially raising the risk for opioid dependence and addiction, new research suggests. However, some experts are urging caution in interpreting the findings.
The study, which also linked vitamin D deficiency to sun-seeking behavior, points to the potential of vitamin D supplementation to help address the opioid epidemic, the investigators note.
“Even modest rescue of vitamin D deficiency could be beneficial in the prevention and treatment of opioid addiction, especially considering that vitamin D is generally inexpensive, accessible, and safe,” they write.
The study was published online June 11 in Science Advances.
Endorphin rush
In earlier work, researchers led by David Fisher, MD, PhD, with the Massachusetts General Hospital (MGH) and Harvard Medical School, Boston, found that exposure to ultraviolet rays causes the skin to produce the hormone endorphin, which is chemically related to morphine, heroin, and other opioids.
They also observed that UV exposure raises endorphin levels in mice, which leads the animals to display behavior consistent with opioid addiction.
In their latest research, they conducted a series of animal and human studies designed to better understand the relationship between vitamin D and UV-seeking and opioid-seeking behavior.
They first compared normal laboratory mice with vitamin D–deficient mice.
“We found that modulating vitamin D levels changes multiple addictive behaviors to both UV and opioids,” lead author Lajos Kemény, MD, PhD, a postdoctoral research fellow in dermatology at MGH, said in a statement.
When the mice were conditioned with modest doses of morphine, those deficient in vitamin D continued seeking out the drug. This behavior was less common in the normal mice. When morphine was withdrawn, the vitamin D–deficient mice were far more likely to show withdrawal symptoms.
Morphine also appeared to work more effectively as a pain reliever in the vitamin D–deficient mice, suggesting that response to the opioid was exaggerated in the setting of low vitamin D.
“When we corrected vitamin D levels in the deficient mice, their opioid responses reversed and returned to normal,” Dr. Fisher said in the statement.
The animal data that suggest vitamin D deficiency increases addictive behavior was supported by several analyses using National Health and Nutrition Examination Survey data and MGH patient health records.
The results show an increase in the prevalence of vitamin D deficiency among patients diagnosed with opioid use disorder (OUD) and an inverse and dose-dependent association of vitamin D levels with self-reported opioid use.
, whereas patients who were severely vitamin D deficient were 90% more likely to use opioids, the researchers report.
“Our results imply that vitamin D–deficient individuals may be at risk for developing tolerance and physiologic opioid dependence more rapidly, experiencing more significant withdrawal and experiencing greater reward from opioid exposure,” they note.
“Vitamin D supplementation might have a preventative benefit by decreasing opioid reward and possibly diminishing the risk of OUD. Vitamin D supplementation may also improve the beneficial effects of medications for OUD,” they add.
Interpret with caution
Weighing in on this research for this news organization, Richard Saitz, MD, MPH, professor, Boston University Schools of Medicine and Public Health, urged caution in interpreting the results.
“The human studies are cross-sectional and subject to many biases and may show that opioid use and disorder are associated with vitamin D deficiency (which is not news) and does not at all show deficiency causes disorder or use,” said Dr. Saitz.
“All in all, the studies are interesting and could generate hypotheses to be tested in well-designed prospective studies of vitamin D deficiency as a risk factor and vitamin D as a treatment,” he added.
However, he cautioned that it’s “going way beyond the data” to conclude that vitamin D causes or exacerbates opioid addiction in people, “but suggesting clinical studies be done is certainly reasonable.”
Also weighing in on this research, Kenneth Stoller, MD, director of the Johns Hopkins Broadway Center for Addiction and associate professor of psychiatry and behavioral sciences at Johns Hopkins University, Baltimore, noted that “95% of patients with co-occurring disorders coming to the inpatient unit are vitamin D deficient, so it’s very common in the population.
“It’s hard to know, but I really think that it’s unlikely that vitamin D deficiency is a common pathway for development of addiction – that is, that they developed an addiction specifically because of the vitamin D deficiency,” Dr. Stoller said.
“However, it does make me think that for my patients who are experiencing maybe a partial but not a full response to medications for opioid use disorder, maybe I’ll be more likely to check the vitamin D level, and if it’s really off, try them on some supplementation,” said Dr. Stoller.
He pointed to a recent study that showed some benefit of vitamin D supplementation on cognitive function and some mental health parameters for people on methadone, “but I don’t think this is necessarily a silver bullet.”
The work was supported by a grant from the National Institutes of Health and the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation. Dr. Fisher, Dr. Saitz, and Dr. Stoller have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Vitamin D deficiency amplifies the craving for, and the effects of, opioids, potentially raising the risk for opioid dependence and addiction, new research suggests. However, some experts are urging caution in interpreting the findings.
The study, which also linked vitamin D deficiency to sun-seeking behavior, points to the potential of vitamin D supplementation to help address the opioid epidemic, the investigators note.
“Even modest rescue of vitamin D deficiency could be beneficial in the prevention and treatment of opioid addiction, especially considering that vitamin D is generally inexpensive, accessible, and safe,” they write.
The study was published online June 11 in Science Advances.
Endorphin rush
In earlier work, researchers led by David Fisher, MD, PhD, with the Massachusetts General Hospital (MGH) and Harvard Medical School, Boston, found that exposure to ultraviolet rays causes the skin to produce the hormone endorphin, which is chemically related to morphine, heroin, and other opioids.
They also observed that UV exposure raises endorphin levels in mice, which leads the animals to display behavior consistent with opioid addiction.
In their latest research, they conducted a series of animal and human studies designed to better understand the relationship between vitamin D and UV-seeking and opioid-seeking behavior.
They first compared normal laboratory mice with vitamin D–deficient mice.
“We found that modulating vitamin D levels changes multiple addictive behaviors to both UV and opioids,” lead author Lajos Kemény, MD, PhD, a postdoctoral research fellow in dermatology at MGH, said in a statement.
When the mice were conditioned with modest doses of morphine, those deficient in vitamin D continued seeking out the drug. This behavior was less common in the normal mice. When morphine was withdrawn, the vitamin D–deficient mice were far more likely to show withdrawal symptoms.
Morphine also appeared to work more effectively as a pain reliever in the vitamin D–deficient mice, suggesting that response to the opioid was exaggerated in the setting of low vitamin D.
“When we corrected vitamin D levels in the deficient mice, their opioid responses reversed and returned to normal,” Dr. Fisher said in the statement.
The animal data that suggest vitamin D deficiency increases addictive behavior was supported by several analyses using National Health and Nutrition Examination Survey data and MGH patient health records.
The results show an increase in the prevalence of vitamin D deficiency among patients diagnosed with opioid use disorder (OUD) and an inverse and dose-dependent association of vitamin D levels with self-reported opioid use.
, whereas patients who were severely vitamin D deficient were 90% more likely to use opioids, the researchers report.
“Our results imply that vitamin D–deficient individuals may be at risk for developing tolerance and physiologic opioid dependence more rapidly, experiencing more significant withdrawal and experiencing greater reward from opioid exposure,” they note.
“Vitamin D supplementation might have a preventative benefit by decreasing opioid reward and possibly diminishing the risk of OUD. Vitamin D supplementation may also improve the beneficial effects of medications for OUD,” they add.
Interpret with caution
Weighing in on this research for this news organization, Richard Saitz, MD, MPH, professor, Boston University Schools of Medicine and Public Health, urged caution in interpreting the results.
“The human studies are cross-sectional and subject to many biases and may show that opioid use and disorder are associated with vitamin D deficiency (which is not news) and does not at all show deficiency causes disorder or use,” said Dr. Saitz.
“All in all, the studies are interesting and could generate hypotheses to be tested in well-designed prospective studies of vitamin D deficiency as a risk factor and vitamin D as a treatment,” he added.
However, he cautioned that it’s “going way beyond the data” to conclude that vitamin D causes or exacerbates opioid addiction in people, “but suggesting clinical studies be done is certainly reasonable.”
Also weighing in on this research, Kenneth Stoller, MD, director of the Johns Hopkins Broadway Center for Addiction and associate professor of psychiatry and behavioral sciences at Johns Hopkins University, Baltimore, noted that “95% of patients with co-occurring disorders coming to the inpatient unit are vitamin D deficient, so it’s very common in the population.
“It’s hard to know, but I really think that it’s unlikely that vitamin D deficiency is a common pathway for development of addiction – that is, that they developed an addiction specifically because of the vitamin D deficiency,” Dr. Stoller said.
“However, it does make me think that for my patients who are experiencing maybe a partial but not a full response to medications for opioid use disorder, maybe I’ll be more likely to check the vitamin D level, and if it’s really off, try them on some supplementation,” said Dr. Stoller.
He pointed to a recent study that showed some benefit of vitamin D supplementation on cognitive function and some mental health parameters for people on methadone, “but I don’t think this is necessarily a silver bullet.”
The work was supported by a grant from the National Institutes of Health and the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation. Dr. Fisher, Dr. Saitz, and Dr. Stoller have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Vitamin D deficiency amplifies the craving for, and the effects of, opioids, potentially raising the risk for opioid dependence and addiction, new research suggests. However, some experts are urging caution in interpreting the findings.
The study, which also linked vitamin D deficiency to sun-seeking behavior, points to the potential of vitamin D supplementation to help address the opioid epidemic, the investigators note.
“Even modest rescue of vitamin D deficiency could be beneficial in the prevention and treatment of opioid addiction, especially considering that vitamin D is generally inexpensive, accessible, and safe,” they write.
The study was published online June 11 in Science Advances.
Endorphin rush
In earlier work, researchers led by David Fisher, MD, PhD, with the Massachusetts General Hospital (MGH) and Harvard Medical School, Boston, found that exposure to ultraviolet rays causes the skin to produce the hormone endorphin, which is chemically related to morphine, heroin, and other opioids.
They also observed that UV exposure raises endorphin levels in mice, which leads the animals to display behavior consistent with opioid addiction.
In their latest research, they conducted a series of animal and human studies designed to better understand the relationship between vitamin D and UV-seeking and opioid-seeking behavior.
They first compared normal laboratory mice with vitamin D–deficient mice.
“We found that modulating vitamin D levels changes multiple addictive behaviors to both UV and opioids,” lead author Lajos Kemény, MD, PhD, a postdoctoral research fellow in dermatology at MGH, said in a statement.
When the mice were conditioned with modest doses of morphine, those deficient in vitamin D continued seeking out the drug. This behavior was less common in the normal mice. When morphine was withdrawn, the vitamin D–deficient mice were far more likely to show withdrawal symptoms.
Morphine also appeared to work more effectively as a pain reliever in the vitamin D–deficient mice, suggesting that response to the opioid was exaggerated in the setting of low vitamin D.
“When we corrected vitamin D levels in the deficient mice, their opioid responses reversed and returned to normal,” Dr. Fisher said in the statement.
The animal data that suggest vitamin D deficiency increases addictive behavior was supported by several analyses using National Health and Nutrition Examination Survey data and MGH patient health records.
The results show an increase in the prevalence of vitamin D deficiency among patients diagnosed with opioid use disorder (OUD) and an inverse and dose-dependent association of vitamin D levels with self-reported opioid use.
, whereas patients who were severely vitamin D deficient were 90% more likely to use opioids, the researchers report.
“Our results imply that vitamin D–deficient individuals may be at risk for developing tolerance and physiologic opioid dependence more rapidly, experiencing more significant withdrawal and experiencing greater reward from opioid exposure,” they note.
“Vitamin D supplementation might have a preventative benefit by decreasing opioid reward and possibly diminishing the risk of OUD. Vitamin D supplementation may also improve the beneficial effects of medications for OUD,” they add.
Interpret with caution
Weighing in on this research for this news organization, Richard Saitz, MD, MPH, professor, Boston University Schools of Medicine and Public Health, urged caution in interpreting the results.
“The human studies are cross-sectional and subject to many biases and may show that opioid use and disorder are associated with vitamin D deficiency (which is not news) and does not at all show deficiency causes disorder or use,” said Dr. Saitz.
“All in all, the studies are interesting and could generate hypotheses to be tested in well-designed prospective studies of vitamin D deficiency as a risk factor and vitamin D as a treatment,” he added.
However, he cautioned that it’s “going way beyond the data” to conclude that vitamin D causes or exacerbates opioid addiction in people, “but suggesting clinical studies be done is certainly reasonable.”
Also weighing in on this research, Kenneth Stoller, MD, director of the Johns Hopkins Broadway Center for Addiction and associate professor of psychiatry and behavioral sciences at Johns Hopkins University, Baltimore, noted that “95% of patients with co-occurring disorders coming to the inpatient unit are vitamin D deficient, so it’s very common in the population.
“It’s hard to know, but I really think that it’s unlikely that vitamin D deficiency is a common pathway for development of addiction – that is, that they developed an addiction specifically because of the vitamin D deficiency,” Dr. Stoller said.
“However, it does make me think that for my patients who are experiencing maybe a partial but not a full response to medications for opioid use disorder, maybe I’ll be more likely to check the vitamin D level, and if it’s really off, try them on some supplementation,” said Dr. Stoller.
He pointed to a recent study that showed some benefit of vitamin D supplementation on cognitive function and some mental health parameters for people on methadone, “but I don’t think this is necessarily a silver bullet.”
The work was supported by a grant from the National Institutes of Health and the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation. Dr. Fisher, Dr. Saitz, and Dr. Stoller have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.