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Strong support for causal role of cannabis in schizophrenia
The long-observed association between cannabis use and schizophrenia is likely partially causal in nature, new research shows.
Investigators found a clear increase in the proportion of schizophrenia cases linked to cannabis use disorder over the past 25 years.
“In my view, the association is most likely causative, at least to a large extent,” first author Carsten Hjorthøj, PhD, from the Copenhagen Research Center for Mental Health, Copenhagen University Hospital, told this news organization.
“It is, of course, nearly impossible to use epidemiological studies to actually prove causation, but all the numbers behave exactly in the way that would be expected under the theory of causation,” said Dr. Hjorthøj.
The study was published online July 21 in JAMA Psychiatry.
Far from harmless
The findings are based on Danish national health registry data. The study sample included all people in Denmark born before Dec. 31, 2000 who were aged 16 years or older at some point from Jan. 1, 1972 to Dec. 31, 2016. The data analysis was conducted from August 2020 to April 2021.
Despite some fluctuation, there was a general increase in the population-attributable risk fraction (PARF) for cannabis use disorder with regard to schizophrenia over time, the researchers report. The PARF increased from about 2% in 1995 to about 4% in 2000 and has hovered from 6% to 8% since 2010.
“Although not in itself proof of causality, our study provides evidence of the theory of cannabis being a component cause of schizophrenia,” the investigators write.
The findings are “particularly important with the increasing legalization of cannabis for both medicinal and recreational uses seeming to lead to an increase in the perception of cannabis as relatively harmless and possibly in the uptake of cannabis use, especially among youth,” they add.
“Although psychosis is not the only outcome of interest in terms of cannabis use, our study clearly indicates that cannabis should not be considered harmless,” they conclude.
Cases linked to cannabis underestimated?
In an accompanying editorial, Tyler VanderWeele, PhD, Harvard School of Public Health, Boston, notes that estimates in this study could be conservative as a result of underdiagnosis of cannabis use disorder and because it only examined cannabis use disorder.
“Cannabis use disorder is not responsible for most schizophrenia cases, but it is responsible for a nonnegligible and increasing proportion. This should be considered in discussions regarding legalization and regulation of the use of cannabis,” Dr. VanderWeele writes.
Experts with the Science Media Center, a U.K. nonprofit organization, also weighed in on the results.
Terrie Moffitt, PhD, with King’s College London, said the study “adds important evidence that patients with diagnosed cannabis use disorder are more at risk for psychosis now than they used to be.”
“ However, most cannabis users, even those who are dependent on it, never come in to clinics for treatment. Also, it is known that people who seek treatment tend to have multiple mental health problems, not solely cannabis problems,” Dr. Moffitt commented.
Emir Englund, PhD, also from King’s College London, said the study “strengthens an already well-established association between the two. However, it is unable to shed additional light on whether cannabis causes schizophrenia or not, due to the observational nature of the study.”
“In my opinion, the current scientific view of cannabis use as a ‘component cause’ which interacts with other risk factors to cause schizophrenia but is neither necessary nor sufficient to do so on its own still stands,” Dr. Englund said.
The study was supported by a grant from Lundbeckfonden. The authors have disclosed no relevant financial relationships. Dr. VanderWeele has received grants from the National Cancer Institute and the John Templeton Foundation. Dr. Moffitt and Dr. Englund have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The long-observed association between cannabis use and schizophrenia is likely partially causal in nature, new research shows.
Investigators found a clear increase in the proportion of schizophrenia cases linked to cannabis use disorder over the past 25 years.
“In my view, the association is most likely causative, at least to a large extent,” first author Carsten Hjorthøj, PhD, from the Copenhagen Research Center for Mental Health, Copenhagen University Hospital, told this news organization.
“It is, of course, nearly impossible to use epidemiological studies to actually prove causation, but all the numbers behave exactly in the way that would be expected under the theory of causation,” said Dr. Hjorthøj.
The study was published online July 21 in JAMA Psychiatry.
Far from harmless
The findings are based on Danish national health registry data. The study sample included all people in Denmark born before Dec. 31, 2000 who were aged 16 years or older at some point from Jan. 1, 1972 to Dec. 31, 2016. The data analysis was conducted from August 2020 to April 2021.
Despite some fluctuation, there was a general increase in the population-attributable risk fraction (PARF) for cannabis use disorder with regard to schizophrenia over time, the researchers report. The PARF increased from about 2% in 1995 to about 4% in 2000 and has hovered from 6% to 8% since 2010.
“Although not in itself proof of causality, our study provides evidence of the theory of cannabis being a component cause of schizophrenia,” the investigators write.
The findings are “particularly important with the increasing legalization of cannabis for both medicinal and recreational uses seeming to lead to an increase in the perception of cannabis as relatively harmless and possibly in the uptake of cannabis use, especially among youth,” they add.
“Although psychosis is not the only outcome of interest in terms of cannabis use, our study clearly indicates that cannabis should not be considered harmless,” they conclude.
Cases linked to cannabis underestimated?
In an accompanying editorial, Tyler VanderWeele, PhD, Harvard School of Public Health, Boston, notes that estimates in this study could be conservative as a result of underdiagnosis of cannabis use disorder and because it only examined cannabis use disorder.
“Cannabis use disorder is not responsible for most schizophrenia cases, but it is responsible for a nonnegligible and increasing proportion. This should be considered in discussions regarding legalization and regulation of the use of cannabis,” Dr. VanderWeele writes.
Experts with the Science Media Center, a U.K. nonprofit organization, also weighed in on the results.
Terrie Moffitt, PhD, with King’s College London, said the study “adds important evidence that patients with diagnosed cannabis use disorder are more at risk for psychosis now than they used to be.”
“ However, most cannabis users, even those who are dependent on it, never come in to clinics for treatment. Also, it is known that people who seek treatment tend to have multiple mental health problems, not solely cannabis problems,” Dr. Moffitt commented.
Emir Englund, PhD, also from King’s College London, said the study “strengthens an already well-established association between the two. However, it is unable to shed additional light on whether cannabis causes schizophrenia or not, due to the observational nature of the study.”
“In my opinion, the current scientific view of cannabis use as a ‘component cause’ which interacts with other risk factors to cause schizophrenia but is neither necessary nor sufficient to do so on its own still stands,” Dr. Englund said.
The study was supported by a grant from Lundbeckfonden. The authors have disclosed no relevant financial relationships. Dr. VanderWeele has received grants from the National Cancer Institute and the John Templeton Foundation. Dr. Moffitt and Dr. Englund have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The long-observed association between cannabis use and schizophrenia is likely partially causal in nature, new research shows.
Investigators found a clear increase in the proportion of schizophrenia cases linked to cannabis use disorder over the past 25 years.
“In my view, the association is most likely causative, at least to a large extent,” first author Carsten Hjorthøj, PhD, from the Copenhagen Research Center for Mental Health, Copenhagen University Hospital, told this news organization.
“It is, of course, nearly impossible to use epidemiological studies to actually prove causation, but all the numbers behave exactly in the way that would be expected under the theory of causation,” said Dr. Hjorthøj.
The study was published online July 21 in JAMA Psychiatry.
Far from harmless
The findings are based on Danish national health registry data. The study sample included all people in Denmark born before Dec. 31, 2000 who were aged 16 years or older at some point from Jan. 1, 1972 to Dec. 31, 2016. The data analysis was conducted from August 2020 to April 2021.
Despite some fluctuation, there was a general increase in the population-attributable risk fraction (PARF) for cannabis use disorder with regard to schizophrenia over time, the researchers report. The PARF increased from about 2% in 1995 to about 4% in 2000 and has hovered from 6% to 8% since 2010.
“Although not in itself proof of causality, our study provides evidence of the theory of cannabis being a component cause of schizophrenia,” the investigators write.
The findings are “particularly important with the increasing legalization of cannabis for both medicinal and recreational uses seeming to lead to an increase in the perception of cannabis as relatively harmless and possibly in the uptake of cannabis use, especially among youth,” they add.
“Although psychosis is not the only outcome of interest in terms of cannabis use, our study clearly indicates that cannabis should not be considered harmless,” they conclude.
Cases linked to cannabis underestimated?
In an accompanying editorial, Tyler VanderWeele, PhD, Harvard School of Public Health, Boston, notes that estimates in this study could be conservative as a result of underdiagnosis of cannabis use disorder and because it only examined cannabis use disorder.
“Cannabis use disorder is not responsible for most schizophrenia cases, but it is responsible for a nonnegligible and increasing proportion. This should be considered in discussions regarding legalization and regulation of the use of cannabis,” Dr. VanderWeele writes.
Experts with the Science Media Center, a U.K. nonprofit organization, also weighed in on the results.
Terrie Moffitt, PhD, with King’s College London, said the study “adds important evidence that patients with diagnosed cannabis use disorder are more at risk for psychosis now than they used to be.”
“ However, most cannabis users, even those who are dependent on it, never come in to clinics for treatment. Also, it is known that people who seek treatment tend to have multiple mental health problems, not solely cannabis problems,” Dr. Moffitt commented.
Emir Englund, PhD, also from King’s College London, said the study “strengthens an already well-established association between the two. However, it is unable to shed additional light on whether cannabis causes schizophrenia or not, due to the observational nature of the study.”
“In my opinion, the current scientific view of cannabis use as a ‘component cause’ which interacts with other risk factors to cause schizophrenia but is neither necessary nor sufficient to do so on its own still stands,” Dr. Englund said.
The study was supported by a grant from Lundbeckfonden. The authors have disclosed no relevant financial relationships. Dr. VanderWeele has received grants from the National Cancer Institute and the John Templeton Foundation. Dr. Moffitt and Dr. Englund have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FDA OKs odevixibat for pruritus associated with rare liver disease
The U.S. Food and Drug Administration has approved odevixibat (Bylvay, Albireo Pharma), the first treatment for pruritus associated with all types of progressive familial intrahepatic cholestasis (PFIC).
PFIC is a rare disorder affecting an estimated one to two people per 100,000. The disorder usually appears within the first few months of life and causes progressive, life-threatening liver disease, often leading to cirrhosis and liver failure before age 10.
In PFIC, liver cells are unable to drain bile acids, leading to the buildup of toxic substances in the liver. While the precise cause of severe itching in patients with PFIC is unknown, it may involve increased levels of bile acids in the body and skin.
Odevixibat is a potent, nonsystemic ileal bile acid transport inhibitor that does not need refrigeration and is given as a once-daily capsule or opened and sprinkled onto soft foods, the company said in a news release announcing the approval.
There are at least three types of PFIC; all are inherited genetic conditions caused by gene mutations. Odevixibat is indicated to treat all subtypes.
“Treating children with PFIC can be difficult and frustrating given the current treatment options. Bylvay gives us a nonsurgical option and will change how we treat PFIC,” Richard Thompson, MD, principal investigator for the two trials that led to the approval, said in the news release.
“With this approval, my colleagues and I now have the opportunity to revisit how PFIC patients are being managed, and we are hopeful for better outcomes for these children,” said Dr. Thompson, professor of molecular hepatology at King’s College London.
The approval of odevixibat was supported by data from the PEDFIC 1 and PEDFIC 2 trials.
PEDFIC 1 enrolled 62 children with PFIC and severe itching, with 20 assigned to placebo and 42 to odevixibat, given once daily with a meal in the morning. Odevixibat met both of its primary endpoints, with the drug improving pruritus (P = .004) and reducing serum bile acid responses (P = .003).
In PEDFIC 2, a long-term, open-label extension study, the effects of odevixibat on pruritis and serum bile acids were sustained up to 48 weeks.
Odevixibat was well tolerated in both trials, with the most common treatment-related gastrointestinal adverse events being diarrhea/frequent stools. There were no serious treatment-related adverse events.
Children taking the drug should undergo liver test monitoring periodically during treatment, the FDA said when announcing the approval. Odevixibat may affect absorption of fat-soluble vitamins such as A, D, E, and K. Patients should be monitored for fat-soluble vitamin deficiency while taking the drug.
Full prescribing information is available online.
“Until now, invasive surgery was the only approved treatment option. With the approval of Bylvay, parents may find hope in having a less invasive treatment option available,” Emily Ventura, leader of the PFIC Advocacy and Resource Network and mother to a child with PFIC, said in the news release.
The company said it will launch odevixibat “immediately” to accelerate availability for patients and families affected by PFIC.
Odevixibat is also being studied in other rare pediatric cholestatic liver diseases, including biliary atresia and Alagille syndrome.
A version of this article first appeared on Medscape.com.
The U.S. Food and Drug Administration has approved odevixibat (Bylvay, Albireo Pharma), the first treatment for pruritus associated with all types of progressive familial intrahepatic cholestasis (PFIC).
PFIC is a rare disorder affecting an estimated one to two people per 100,000. The disorder usually appears within the first few months of life and causes progressive, life-threatening liver disease, often leading to cirrhosis and liver failure before age 10.
In PFIC, liver cells are unable to drain bile acids, leading to the buildup of toxic substances in the liver. While the precise cause of severe itching in patients with PFIC is unknown, it may involve increased levels of bile acids in the body and skin.
Odevixibat is a potent, nonsystemic ileal bile acid transport inhibitor that does not need refrigeration and is given as a once-daily capsule or opened and sprinkled onto soft foods, the company said in a news release announcing the approval.
There are at least three types of PFIC; all are inherited genetic conditions caused by gene mutations. Odevixibat is indicated to treat all subtypes.
“Treating children with PFIC can be difficult and frustrating given the current treatment options. Bylvay gives us a nonsurgical option and will change how we treat PFIC,” Richard Thompson, MD, principal investigator for the two trials that led to the approval, said in the news release.
“With this approval, my colleagues and I now have the opportunity to revisit how PFIC patients are being managed, and we are hopeful for better outcomes for these children,” said Dr. Thompson, professor of molecular hepatology at King’s College London.
The approval of odevixibat was supported by data from the PEDFIC 1 and PEDFIC 2 trials.
PEDFIC 1 enrolled 62 children with PFIC and severe itching, with 20 assigned to placebo and 42 to odevixibat, given once daily with a meal in the morning. Odevixibat met both of its primary endpoints, with the drug improving pruritus (P = .004) and reducing serum bile acid responses (P = .003).
In PEDFIC 2, a long-term, open-label extension study, the effects of odevixibat on pruritis and serum bile acids were sustained up to 48 weeks.
Odevixibat was well tolerated in both trials, with the most common treatment-related gastrointestinal adverse events being diarrhea/frequent stools. There were no serious treatment-related adverse events.
Children taking the drug should undergo liver test monitoring periodically during treatment, the FDA said when announcing the approval. Odevixibat may affect absorption of fat-soluble vitamins such as A, D, E, and K. Patients should be monitored for fat-soluble vitamin deficiency while taking the drug.
Full prescribing information is available online.
“Until now, invasive surgery was the only approved treatment option. With the approval of Bylvay, parents may find hope in having a less invasive treatment option available,” Emily Ventura, leader of the PFIC Advocacy and Resource Network and mother to a child with PFIC, said in the news release.
The company said it will launch odevixibat “immediately” to accelerate availability for patients and families affected by PFIC.
Odevixibat is also being studied in other rare pediatric cholestatic liver diseases, including biliary atresia and Alagille syndrome.
A version of this article first appeared on Medscape.com.
The U.S. Food and Drug Administration has approved odevixibat (Bylvay, Albireo Pharma), the first treatment for pruritus associated with all types of progressive familial intrahepatic cholestasis (PFIC).
PFIC is a rare disorder affecting an estimated one to two people per 100,000. The disorder usually appears within the first few months of life and causes progressive, life-threatening liver disease, often leading to cirrhosis and liver failure before age 10.
In PFIC, liver cells are unable to drain bile acids, leading to the buildup of toxic substances in the liver. While the precise cause of severe itching in patients with PFIC is unknown, it may involve increased levels of bile acids in the body and skin.
Odevixibat is a potent, nonsystemic ileal bile acid transport inhibitor that does not need refrigeration and is given as a once-daily capsule or opened and sprinkled onto soft foods, the company said in a news release announcing the approval.
There are at least three types of PFIC; all are inherited genetic conditions caused by gene mutations. Odevixibat is indicated to treat all subtypes.
“Treating children with PFIC can be difficult and frustrating given the current treatment options. Bylvay gives us a nonsurgical option and will change how we treat PFIC,” Richard Thompson, MD, principal investigator for the two trials that led to the approval, said in the news release.
“With this approval, my colleagues and I now have the opportunity to revisit how PFIC patients are being managed, and we are hopeful for better outcomes for these children,” said Dr. Thompson, professor of molecular hepatology at King’s College London.
The approval of odevixibat was supported by data from the PEDFIC 1 and PEDFIC 2 trials.
PEDFIC 1 enrolled 62 children with PFIC and severe itching, with 20 assigned to placebo and 42 to odevixibat, given once daily with a meal in the morning. Odevixibat met both of its primary endpoints, with the drug improving pruritus (P = .004) and reducing serum bile acid responses (P = .003).
In PEDFIC 2, a long-term, open-label extension study, the effects of odevixibat on pruritis and serum bile acids were sustained up to 48 weeks.
Odevixibat was well tolerated in both trials, with the most common treatment-related gastrointestinal adverse events being diarrhea/frequent stools. There were no serious treatment-related adverse events.
Children taking the drug should undergo liver test monitoring periodically during treatment, the FDA said when announcing the approval. Odevixibat may affect absorption of fat-soluble vitamins such as A, D, E, and K. Patients should be monitored for fat-soluble vitamin deficiency while taking the drug.
Full prescribing information is available online.
“Until now, invasive surgery was the only approved treatment option. With the approval of Bylvay, parents may find hope in having a less invasive treatment option available,” Emily Ventura, leader of the PFIC Advocacy and Resource Network and mother to a child with PFIC, said in the news release.
The company said it will launch odevixibat “immediately” to accelerate availability for patients and families affected by PFIC.
Odevixibat is also being studied in other rare pediatric cholestatic liver diseases, including biliary atresia and Alagille syndrome.
A version of this article first appeared on Medscape.com.
Widely prescribed meds ineffective for low back pain?
Results of a large systematic review and meta-analysis of randomized controlled trials show very “low certainty evidence” that non-benzodiazepine antispasmodics provide meaningful improvement in pain intensity in patients with low back pain – and may actually increase adverse event risk.
“We found that muscle relaxants might reduce pain in the short term, but on average, the effect is probably too small to be important, and most patients wouldn’t be able to feel any difference in their pain compared to taking a placebo,” study investigator Aidan Cashin, PhD, with the Center for Pain IMPACT, Neuroscience Research Australia, and University of New South Wales, Sydney, told this news organization. “There is also an increased risk of side effects,” he added.
The study was published online July 7 in The BMJ.
Global problem
Low back pain is a major global public health problem that burdens individuals, health care systems, and societies.
“Most people, around 80%, will have at least one episode of low back pain during their life,” Dr. Cashin noted.
Muscle relaxants, a broad class of drugs that include non-benzodiazepine antispasmodics and antispastics, are often prescribed for low back pain. In 2020 alone, prescriptions exceeded 1.3 million in England and topped 30 million in the United States.
“However, clinical practice guidelines have provided conflicting recommendations for the use of muscle relaxants to treat low back pain,” Dr. Cashin said.
To assess the efficacy and safety of muscle relaxants, the researchers conducted a detailed analysis of 31 randomized controlled trials that compared muscle relaxants with placebo, usual care, or no treatment in a total of 6,505 adults with nonspecific low back pain.
For acute low back pain, they found “very low certainty evidence” that non-benzodiazepine antispasmodics might reduce pain intensity at 2 weeks or less, but the effect is small – less than 8 points on a 0 to 100 point scale – and not clinically meaningful.
They found little to no effect of non-benzodiazepine antispasmodics on pain intensity at 3 to 13 weeks or on disability at any follow-up time points. None of the trials assessed the effect of muscle relaxants on long-term outcomes.
There was also low-certainty and very-low-certainty evidence that non-benzodiazepine antispasmodics might increase the risk of an adverse event, commonly dizziness, drowsiness, headache, and nausea (relative risk 1.6; 95% confidence interval, 1.2-2.0).
Better research needed
“We were surprised by the findings, as earlier research suggested that muscle relaxants did reduce pain intensity. But when we included all of the most up-to-date research, the results became much less certain,” said Dr. Cashin.
“We were also surprised to see that so much of the research wasn’t done very well, which means that we can’t be very certain in the results. There is a clear need to improve how research is done for low back pain so that we better understand whether medicines can help people or not,” Dr. Cashin said.
“We would encourage clinicians to discuss this uncertainty in the efficacy and safety of muscle relaxants with patients, sharing information about the possibility for a worthwhile benefit in pain reduction but increased risk of experiencing a nonserious adverse event, to allow them to make informed treatment decisions,” corresponding author James McAuley, PhD, University of New South Wales, said in an interview.
“We know that no matter what medicines people with low back pain are taking, they should avoid staying in bed, and they should try to be active and continue with their usual activities, including work, as much as they can. High-quality research shows that people who do this are more likely to recover faster and more completely,” said Dr. McAuley.
A symptom, not a diagnosis
Reached for comment, Andrew Hecht, MD, chief of spine surgery at Mount Sinai Health System, New York, noted that acute low back pain is “a symptom, not a diagnosis, and most episodes of acute low back pain without leg pain will resolve within a few weeks no matter what you do.”
“For people who have an episode of acute low back pain, we typically use anti-inflammatory medications, combined with a short, low dose course of a muscle relaxant if necessary, depending on the severity of symptoms, to help get you over the worst part of it,” Dr. Hecht said.
“We are trying to help the patient feel better in the short term and get more physically strong with therapy to try to reduce the frequency of these attacks in the future,” he added.
“But each patient is different. It’s not one-size-fits-all, and we don’t give prolonged courses of muscle relaxants because they have some side effects, like sedation,” Dr. Hecht cautioned.
The study had no specific funding. Dr. Cashin, Dr. McAuley, and Dr. Hecht have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Results of a large systematic review and meta-analysis of randomized controlled trials show very “low certainty evidence” that non-benzodiazepine antispasmodics provide meaningful improvement in pain intensity in patients with low back pain – and may actually increase adverse event risk.
“We found that muscle relaxants might reduce pain in the short term, but on average, the effect is probably too small to be important, and most patients wouldn’t be able to feel any difference in their pain compared to taking a placebo,” study investigator Aidan Cashin, PhD, with the Center for Pain IMPACT, Neuroscience Research Australia, and University of New South Wales, Sydney, told this news organization. “There is also an increased risk of side effects,” he added.
The study was published online July 7 in The BMJ.
Global problem
Low back pain is a major global public health problem that burdens individuals, health care systems, and societies.
“Most people, around 80%, will have at least one episode of low back pain during their life,” Dr. Cashin noted.
Muscle relaxants, a broad class of drugs that include non-benzodiazepine antispasmodics and antispastics, are often prescribed for low back pain. In 2020 alone, prescriptions exceeded 1.3 million in England and topped 30 million in the United States.
“However, clinical practice guidelines have provided conflicting recommendations for the use of muscle relaxants to treat low back pain,” Dr. Cashin said.
To assess the efficacy and safety of muscle relaxants, the researchers conducted a detailed analysis of 31 randomized controlled trials that compared muscle relaxants with placebo, usual care, or no treatment in a total of 6,505 adults with nonspecific low back pain.
For acute low back pain, they found “very low certainty evidence” that non-benzodiazepine antispasmodics might reduce pain intensity at 2 weeks or less, but the effect is small – less than 8 points on a 0 to 100 point scale – and not clinically meaningful.
They found little to no effect of non-benzodiazepine antispasmodics on pain intensity at 3 to 13 weeks or on disability at any follow-up time points. None of the trials assessed the effect of muscle relaxants on long-term outcomes.
There was also low-certainty and very-low-certainty evidence that non-benzodiazepine antispasmodics might increase the risk of an adverse event, commonly dizziness, drowsiness, headache, and nausea (relative risk 1.6; 95% confidence interval, 1.2-2.0).
Better research needed
“We were surprised by the findings, as earlier research suggested that muscle relaxants did reduce pain intensity. But when we included all of the most up-to-date research, the results became much less certain,” said Dr. Cashin.
“We were also surprised to see that so much of the research wasn’t done very well, which means that we can’t be very certain in the results. There is a clear need to improve how research is done for low back pain so that we better understand whether medicines can help people or not,” Dr. Cashin said.
“We would encourage clinicians to discuss this uncertainty in the efficacy and safety of muscle relaxants with patients, sharing information about the possibility for a worthwhile benefit in pain reduction but increased risk of experiencing a nonserious adverse event, to allow them to make informed treatment decisions,” corresponding author James McAuley, PhD, University of New South Wales, said in an interview.
“We know that no matter what medicines people with low back pain are taking, they should avoid staying in bed, and they should try to be active and continue with their usual activities, including work, as much as they can. High-quality research shows that people who do this are more likely to recover faster and more completely,” said Dr. McAuley.
A symptom, not a diagnosis
Reached for comment, Andrew Hecht, MD, chief of spine surgery at Mount Sinai Health System, New York, noted that acute low back pain is “a symptom, not a diagnosis, and most episodes of acute low back pain without leg pain will resolve within a few weeks no matter what you do.”
“For people who have an episode of acute low back pain, we typically use anti-inflammatory medications, combined with a short, low dose course of a muscle relaxant if necessary, depending on the severity of symptoms, to help get you over the worst part of it,” Dr. Hecht said.
“We are trying to help the patient feel better in the short term and get more physically strong with therapy to try to reduce the frequency of these attacks in the future,” he added.
“But each patient is different. It’s not one-size-fits-all, and we don’t give prolonged courses of muscle relaxants because they have some side effects, like sedation,” Dr. Hecht cautioned.
The study had no specific funding. Dr. Cashin, Dr. McAuley, and Dr. Hecht have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Results of a large systematic review and meta-analysis of randomized controlled trials show very “low certainty evidence” that non-benzodiazepine antispasmodics provide meaningful improvement in pain intensity in patients with low back pain – and may actually increase adverse event risk.
“We found that muscle relaxants might reduce pain in the short term, but on average, the effect is probably too small to be important, and most patients wouldn’t be able to feel any difference in their pain compared to taking a placebo,” study investigator Aidan Cashin, PhD, with the Center for Pain IMPACT, Neuroscience Research Australia, and University of New South Wales, Sydney, told this news organization. “There is also an increased risk of side effects,” he added.
The study was published online July 7 in The BMJ.
Global problem
Low back pain is a major global public health problem that burdens individuals, health care systems, and societies.
“Most people, around 80%, will have at least one episode of low back pain during their life,” Dr. Cashin noted.
Muscle relaxants, a broad class of drugs that include non-benzodiazepine antispasmodics and antispastics, are often prescribed for low back pain. In 2020 alone, prescriptions exceeded 1.3 million in England and topped 30 million in the United States.
“However, clinical practice guidelines have provided conflicting recommendations for the use of muscle relaxants to treat low back pain,” Dr. Cashin said.
To assess the efficacy and safety of muscle relaxants, the researchers conducted a detailed analysis of 31 randomized controlled trials that compared muscle relaxants with placebo, usual care, or no treatment in a total of 6,505 adults with nonspecific low back pain.
For acute low back pain, they found “very low certainty evidence” that non-benzodiazepine antispasmodics might reduce pain intensity at 2 weeks or less, but the effect is small – less than 8 points on a 0 to 100 point scale – and not clinically meaningful.
They found little to no effect of non-benzodiazepine antispasmodics on pain intensity at 3 to 13 weeks or on disability at any follow-up time points. None of the trials assessed the effect of muscle relaxants on long-term outcomes.
There was also low-certainty and very-low-certainty evidence that non-benzodiazepine antispasmodics might increase the risk of an adverse event, commonly dizziness, drowsiness, headache, and nausea (relative risk 1.6; 95% confidence interval, 1.2-2.0).
Better research needed
“We were surprised by the findings, as earlier research suggested that muscle relaxants did reduce pain intensity. But when we included all of the most up-to-date research, the results became much less certain,” said Dr. Cashin.
“We were also surprised to see that so much of the research wasn’t done very well, which means that we can’t be very certain in the results. There is a clear need to improve how research is done for low back pain so that we better understand whether medicines can help people or not,” Dr. Cashin said.
“We would encourage clinicians to discuss this uncertainty in the efficacy and safety of muscle relaxants with patients, sharing information about the possibility for a worthwhile benefit in pain reduction but increased risk of experiencing a nonserious adverse event, to allow them to make informed treatment decisions,” corresponding author James McAuley, PhD, University of New South Wales, said in an interview.
“We know that no matter what medicines people with low back pain are taking, they should avoid staying in bed, and they should try to be active and continue with their usual activities, including work, as much as they can. High-quality research shows that people who do this are more likely to recover faster and more completely,” said Dr. McAuley.
A symptom, not a diagnosis
Reached for comment, Andrew Hecht, MD, chief of spine surgery at Mount Sinai Health System, New York, noted that acute low back pain is “a symptom, not a diagnosis, and most episodes of acute low back pain without leg pain will resolve within a few weeks no matter what you do.”
“For people who have an episode of acute low back pain, we typically use anti-inflammatory medications, combined with a short, low dose course of a muscle relaxant if necessary, depending on the severity of symptoms, to help get you over the worst part of it,” Dr. Hecht said.
“We are trying to help the patient feel better in the short term and get more physically strong with therapy to try to reduce the frequency of these attacks in the future,” he added.
“But each patient is different. It’s not one-size-fits-all, and we don’t give prolonged courses of muscle relaxants because they have some side effects, like sedation,” Dr. Hecht cautioned.
The study had no specific funding. Dr. Cashin, Dr. McAuley, and Dr. Hecht have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Legalization of cannabis tied to drop in opioid-related ED visits
State laws permitting recreational marijuana use have not led to an increase in opioid-related emergency department visits, as many had feared.
On the contrary, states that legalize recreational marijuana may see a short-term decrease in opioid-related ED visits in the first 6 months, after which rates may return to prelegalization levels, new research suggests.
Previous research suggests that individuals may reduce the use of opioids when they have an alternative and that cannabis can provide pain relief.
“At the same time, we often hear claims from politicians that we should not legalize cannabis because it may act as a ‘gateway drug’ that leads to use of other drugs,” lead researcher Coleman Drake, PhD, Department of Health Policy and Management, University of Pittsburgh Graduate School of Public Health, told this news organization.
“Our findings indicate that cannabis legalization does not effect any increase in opioid-related ED visits, contradicting the gateway drug explanation,” Dr. Drake said.
The study was published online July 12 in Health Economics.
Significant reduction
So far, 19 states have legalized recreational cannabis, meaning that nearly half of the U.S. population lives in a state that allows recreational cannabis use.
The investigators analyzed data on opioid-related ED visits from 29 states between 2011 and 2017. Four states – California, Maine, Massachusetts, and Nevada – legalized recreational marijuana during the study period; the remaining 25 states did not.
The four states with recreational cannabis laws experienced a 7.6% reduction in opioid-related ED visits for 6 months after the law went into effect in comparison with the states that did not legalize recreational marijuana.
“This isn’t trivial – a decline in opioid-related emergency department visits, even if only for 6 months, is a welcome public health development,” Dr. Drake said in a statement.
Not surprisingly, these effects are driven by men and adults aged 25 to 44 years. “These are populations that are more likely to use cannabis, and the reduction in opioid-related ED visits that we find is concentrated among them,” Dr. Drake told this news organization.
However, the downturn in opioid-related ED visits after making marijuana legal was only temporary.
“
Encouragingly, he said, the data show that opioid-related ED visits don’t increase above baseline after recreational marijuana laws are adopted.
“We conclude that cannabis legalization likely is not a panacea for the opioid epidemic, but there are some helpful effects,” Dr. Drake said in an interview.
The study was supported by the National Institute on Drug Abuse. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
State laws permitting recreational marijuana use have not led to an increase in opioid-related emergency department visits, as many had feared.
On the contrary, states that legalize recreational marijuana may see a short-term decrease in opioid-related ED visits in the first 6 months, after which rates may return to prelegalization levels, new research suggests.
Previous research suggests that individuals may reduce the use of opioids when they have an alternative and that cannabis can provide pain relief.
“At the same time, we often hear claims from politicians that we should not legalize cannabis because it may act as a ‘gateway drug’ that leads to use of other drugs,” lead researcher Coleman Drake, PhD, Department of Health Policy and Management, University of Pittsburgh Graduate School of Public Health, told this news organization.
“Our findings indicate that cannabis legalization does not effect any increase in opioid-related ED visits, contradicting the gateway drug explanation,” Dr. Drake said.
The study was published online July 12 in Health Economics.
Significant reduction
So far, 19 states have legalized recreational cannabis, meaning that nearly half of the U.S. population lives in a state that allows recreational cannabis use.
The investigators analyzed data on opioid-related ED visits from 29 states between 2011 and 2017. Four states – California, Maine, Massachusetts, and Nevada – legalized recreational marijuana during the study period; the remaining 25 states did not.
The four states with recreational cannabis laws experienced a 7.6% reduction in opioid-related ED visits for 6 months after the law went into effect in comparison with the states that did not legalize recreational marijuana.
“This isn’t trivial – a decline in opioid-related emergency department visits, even if only for 6 months, is a welcome public health development,” Dr. Drake said in a statement.
Not surprisingly, these effects are driven by men and adults aged 25 to 44 years. “These are populations that are more likely to use cannabis, and the reduction in opioid-related ED visits that we find is concentrated among them,” Dr. Drake told this news organization.
However, the downturn in opioid-related ED visits after making marijuana legal was only temporary.
“
Encouragingly, he said, the data show that opioid-related ED visits don’t increase above baseline after recreational marijuana laws are adopted.
“We conclude that cannabis legalization likely is not a panacea for the opioid epidemic, but there are some helpful effects,” Dr. Drake said in an interview.
The study was supported by the National Institute on Drug Abuse. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
State laws permitting recreational marijuana use have not led to an increase in opioid-related emergency department visits, as many had feared.
On the contrary, states that legalize recreational marijuana may see a short-term decrease in opioid-related ED visits in the first 6 months, after which rates may return to prelegalization levels, new research suggests.
Previous research suggests that individuals may reduce the use of opioids when they have an alternative and that cannabis can provide pain relief.
“At the same time, we often hear claims from politicians that we should not legalize cannabis because it may act as a ‘gateway drug’ that leads to use of other drugs,” lead researcher Coleman Drake, PhD, Department of Health Policy and Management, University of Pittsburgh Graduate School of Public Health, told this news organization.
“Our findings indicate that cannabis legalization does not effect any increase in opioid-related ED visits, contradicting the gateway drug explanation,” Dr. Drake said.
The study was published online July 12 in Health Economics.
Significant reduction
So far, 19 states have legalized recreational cannabis, meaning that nearly half of the U.S. population lives in a state that allows recreational cannabis use.
The investigators analyzed data on opioid-related ED visits from 29 states between 2011 and 2017. Four states – California, Maine, Massachusetts, and Nevada – legalized recreational marijuana during the study period; the remaining 25 states did not.
The four states with recreational cannabis laws experienced a 7.6% reduction in opioid-related ED visits for 6 months after the law went into effect in comparison with the states that did not legalize recreational marijuana.
“This isn’t trivial – a decline in opioid-related emergency department visits, even if only for 6 months, is a welcome public health development,” Dr. Drake said in a statement.
Not surprisingly, these effects are driven by men and adults aged 25 to 44 years. “These are populations that are more likely to use cannabis, and the reduction in opioid-related ED visits that we find is concentrated among them,” Dr. Drake told this news organization.
However, the downturn in opioid-related ED visits after making marijuana legal was only temporary.
“
Encouragingly, he said, the data show that opioid-related ED visits don’t increase above baseline after recreational marijuana laws are adopted.
“We conclude that cannabis legalization likely is not a panacea for the opioid epidemic, but there are some helpful effects,” Dr. Drake said in an interview.
The study was supported by the National Institute on Drug Abuse. The authors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
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.